Author: "U. Koenig" - Searchworks@Jio Institute Digital Library Search Results

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1. Phagocytic cell death leads to enhanced release of pro-inflammatory S100A12 in familial Mediterranean fever

Author: G. Varga, S. Schleifenbaum, U. Koenig, J. Waldkirch, C. Hinze, C. Kessel, W. Geluk, T. Pap, Elke Lainka, Tilmann Kallinich, D. Foell, and H. Wittkowski
Subjects: FMF, Neutrophils, ROS (reactive oxygen species), Gasdermin D (GSDMD), Pediatrics, RJ1-570
Abstract: Abstract Background Familial Mediterranean fever (FMF) is a prototypical autoinflammatory syndrome associated with phagocytic cell activation. Pyrin mutations are the genetic basis of this disease, and its expression has been shown in monocytes, granulocytes, dendritic cells, and synovial fibroblasts. Pyrin functions as a cytosolic pattern recognition receptor and forms a distinct pyrin inflammasome. The phagocyte-specific protein S100A12 is predominantly expressed in granulocytes and belongs to the group of damage associated molecular patterns (DAMP). S100A12 can be detected at massively elevated levels in the serum of FMF patients, even in clinically inactive disease. Whether this is crucial for FMF pathogenesis is as yet unknown, and we therefore investigated the mechanisms of S100A12 release from granulocytes of FMF patients presenting clinically inactive. Results We demonstrate that FMF neutrophils from patients in clinical inactive disease possess an intrinsic activity leading to cell death even in exogenously unstimulated neutrophils. Cell death resembles NETosis and is dependent on ROS and pore forming protein gasdermin D (GSDMD), as inhibitors for both are capable of completely block cell death and S100A12 release. When pyrin-activator TcdA (Clostridium difficile toxin A) is used to stimulate, neutrophilic cell death and S100A12 release are significantly enhanced in neutrophils from FMF patients compared to neutrophils from HC. Conclusions We are able to demonstrate that activation threshold of neutrophils from inactive FMF patients is decreased, most likely by pre-activated pyrin. FMF neutrophils present with intrinsically higher ROS production, when cultured ex vivo. This higher baseline ROS activity leads to increased GSDMD cleavage and subsequent release of, e.g., S100A12, and to increased cell death with features of NETosis and pyroptosis. We show for the first time that cell death pathways in neutrophils of inactive FMF patients are easily triggered and lead to ROS- and GSDMD-dependent activation mechanisms and possibly pathology. This could be therapeutically addressed by blocking ROS or GSDMD cleavage to decrease inflammatory outbreaks when becoming highly active.
Published: 2023
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2. Inferring relationships between clinical mastitis, productivity and fertility: A recursive model application including genetics, farm associated herd management, and cow-specific antibiotic treatments

Author: Rehbein, Pia, Brügemann, Kerstin, Yin, Tong, v. Borstel, U. König, Wu, Xiao-Lin, and König, Sven
Published: 2013
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3. Breed differences in maternal behaviour in relation to lamb (Ovis orientalis aries) productivity

Author: von Borstel, U. König, Moors, E., Schichowski, C., and Gauly, M.
Published: 2011
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4. Haemocompatibility testing allows selective adaption of GA-free SULEEI-preparation strategy for bovine pericardium

Author: Anett Jannasch, Sems-Malte Tugtekin, Cindy Welzel, U Koenig, Claudia Dittfeld, Klaus Matschke, Claudia Sperling, Manfred F. Maitz, and Publica
Subjects: Pathology, medicine.medical_specialty, biology, Bovine pericardium, business.industry, Inflammatory response, Inflammation, Complement C5a, pericardial sac, Fibrin, Complement system, radiation, Heart Disease, Cardiac Surgery procedures, medicine, biology.protein, Platelet, blood cells, medicine.symptom, Cardiology and Cardiovascular Medicine, business
Abstract: Background/Introduction Bovine pericardium is the main natural source for patches or valve substitutes in cardiac surgery, but still, long-term durability is limited. An alternative, glutaraldehyde (GA)-free preparation combining decellularization, riboflavin/UVA crosslinking, and low-energy electron irradiation (SULEEI) procedure was established to avoid this. Protocol optimization is ongoing to further improve the final material. Haemocompatibility in vitro testing with fresh, human whole blood has advantages for material analysis, as it provides essential information on the activation of the complement system and immune cells therefore substantiating and possibly reducing the amount of animal testing. Purpose The haemocompatibility testing system was applied to reveal advantageous protocol adaptation of GA-free SULEEI preparation of pericardia. Methods Decellularized bovine pericardia were UVA-crosslinked in riboflavin/dextran solution. Protocol SULEEI B adaption includes the addition of trypsin in decellularization buffer and a 10x reduced riboflavin/dextran concentration during prolonged UVA irradiation with reduced intensity. Electron irradiation with 36 kGy was retained. Pericardia were incubated in blood chambers with heparinized human blood (2h, 37°C, GA-fixed/native controls). Inflammation (granulocyte loss and activation [CD11b]), complement activation (C5a) and haemostasis parameters (F1+2, PF4, granulocyte/platelet conjugates, platelet loss) were analyzed via flow cytometry or ELISA. Surface cell adhesion was investigated immunohistologically and via REM-analyses. Nuclear fragments were quantified in HE-stained sections. Results Haemostasis parameters F1+2 and PF4 were significantly higher in SULEEI A-pericardium (133±25 nmol/l and 1507±677 U/ml) vs. GA-fixation (2.9±2.9 nmol/l and 320±160 U/ml). Also, granulocyte/platelet conjugates (76.3±18.8%) and platelet loss (40.4±29.7%) were significantly higher after SULEEI A preparation in comparison to GA-fixation (39.3±9.9% and 20.5±6.4%). SULEEI B treated pericardia did not differ significantly. C5a complement activation was significantly lower in SULEEI A samples but comparable in SULEEI B to GA-fixed material. This is in contrast to a higher rate of nuclear fragments in SULEEI A tissue HE stained sections. Granulocyte activation of SULEEI pericardium (A: 89.8±29.7%; B: 106.2±18.8%) was significantly higher compared to native (46.1±22.6%) and for SULEEI B higher than in GA-fixed samples (67.2±9%). Granulocyte loss was comparable to GA-fixed pericardium after SULEEI B protocol. REM-analyses and histological evaluation visualized a dense blood cell and fibrin covering particular of SULEEI A-pericardium. Conclusions Haemocompatibility testing reveals advantageous properties of SULEEI B-pericardium. The impact of treatment substances such as dextran on high inflammatory response and dense surface covering in SULEEI A protocol is focus in ongoing experiments. Funding Acknowledgement Type of funding sources: Public grant(s) – EU funding. Main funding source(s): EU/EFRE
Published: 2021

5. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Author: D. KLIONSKY, A. ABDEL-AZIZ, S. ABDELFATAH, M. ABDELLATIF, A. ABDOLI, S. ABEL, H. ABELIOVICH, M. ABILDGAARD, Y. ABUDU, A. ACEVEDO-AROZENA, I. ADAMOPOULOS, K. ADELI, T. ADOLPH, A. ADORNETTO, E. AFLAKI, G. AGAM, A. AGARWAL, B. AGGARWAL, M. AGNELLO, P. AGOSTINIS, J. AGREWALA, A. AGROTIS, P. AGUILAR, S. AHMAD, Z. AHMED, U. AHUMADA-CASTRO, S. AITS, S. AIZAWA, Y. AKKOC, T. AKOUMIANAKI, H. AKPINAR, A. AL-ABD, L. AL-AKRA, A. AL-GHARAIBEH, M. ALAOUI-JAMALI, S. ALBERTI, E. ALCOCER-GOMEZ, C. ALESSANDRI, M. ALI, M. AL-BARI, S. ALIWAINI, J. ALIZADEH, E. ALMACELLAS, A. ALMASAN, A. ALONSO, G. ALONSO, N. ALTAN-BONNET, D. ALTIERI, S. ALVES, C. DA COSTA, M. ALZAHARNA, M. AMADIO, C. AMANTINI, C. AMARAL, S. AMBROSIO, A. AMER, V. AMMANATHAN, Z. AN, S. ANDERSEN, S. ANDRABI, M. ANDRADE-SILVA, A. ANDRES, S. ANGELINI, D. ANN, U. ANOZIE, M. ANSARI, P. ANTAS, A. ANTEBI, Z. ANTON, T. ANWAR, L. APETOH, N. APOSTOLOVA, T. ARAKI, Y. ARAKI, K. ARASAKI, W. ARAUJO, J. ARAYA, C. ARDEN, M. AREVALO, S. ARGUELLES, E. ARIAS, J. ARIKKATH, H. ARIMOTO, A. ARIOSA, D. ARMSTRONG-JAMES, L. ARNAUNE-PELLOQUIN, A. AROCA, D. ARROYO, I. ARSOV, R. ARTERO, D. ASARO, M. ASCHNER, M. ASHRAFIZADEH, O. ASHUR-FABIAN, A. ATANASOV, A. AU, P. AUBERGER, H. AUNER, L. AURELIAN, R. AUTELLI, L. AVAGLIANO, Y. AVALOS, S. AVEIC, C. AVELEIRA, T. AVINWITTENBERG, Y. AYDIN, S. AYTON, S. AYYADEVARA, M. AZZOPARDI, M. BABA, J. BACKER, S. BACKUES, D. BAE, O. BAE, S. BAE, E. BAEHRECKE, A. BAEK, S. BAEK, G. BAGETTA, A. BAGNIEWSKA-ZADWORNA, H. BAI, J. BAI, X. BAI, Y. BAI, N. BAIRAGI, S. BAKSI, T. BALBI, C. BALDARI, W. BALDUINI, A. BALLABIO, M. BALLESTER, S. BALAZADEH, R. BALZAN, R. BANDOPADHYAY, S. BANERJEE, Y. BAO, M. BAPTISTA, A. BARACCA, C. BARBATI, A. BARGIELA, D. BARILA, P. BARLOW, S. BARMADA, E. BARREIRO, G. BARRETO, J. BARTEK, B. BARTEL, A. BARTOLOME, G. BARVE, S. BASAGOUDANAVAR, D. BASSHAM, R. JR, A. BASU, H. BATOKO, I. BATTEN, E. BAULIEU, B. BAUMGARNER, J. BAYRY, R. BEALE, I. BEAU, F. BEAUMATIN, L. BECHARA, G. BECK, M. BEERS, J. BEGUN, C. BEHRENDS, G. BEHRENS, R. BEI, E. BEJARANO, S. BEL, C. BEHL, A. BELAID, N. BELGAREH-TOUZE, C. BELLAROSA, F. BELLEUDI, M. PEREZ, R. BELLO-MORALES, J. BELTRAN, S. BELTRAN, D. BENBROOK, M. BENDORIUS, B. BENITEZ, I. BENITO-CUESTA, J. BENSALEM, M. BERCHTOLD, S. BEREZOWSKA, D. BERGAMASCHI, M. BERGAMI, A. BERGMANN, L. BERLIOCCHI, C. BERLIOZ-TORRENT, A. BERNARD, L. BERTHOUX, C. BESIRLI, S. BESTEIRO, V. BETIN, R. BEYAERT, J. BEZBRADICA, K. BHASKAR, I. BHATIA-KISSOVA, R. BHATTACHARYA, S. BHATTACHARYA, S. BHATTACHARYYA, M. BHUIYAN, S. BHUTIA, L. BI, X. BI, T. BIDEN, K. BIJIAN, V. BILLES, N. BINART, C. BINCOLETTO, A. BIRGISDOTTIR, G. BJORKOY, G. BLANCO, A. BLAS-GARCIA, J. BLASIAK, R. BLOMGRAN, K. BLOMGREN, J. BLUM, E. BOADA-ROMERO, M. BOBAN, K. BOESZEBATTAGLIA, P. BOEUF, B. BOLAND, P. BOMONT, P. BONALDO, S. BONAM, L. BONFILI, J. BONIFACINO, B. BOONE, M. BOOTMAN, M. BORDI, C. BORNER, B. BORNHAUSER, G. BORTHAKUR, J. BOSCH, S. BOSE, L. BOTANA, J. BOTAS, C. BOULANGER, M. BOULTON, M. BOURDENX, B. BOURGEOIS, N. BOURKE, G. BOUSQUET, P. BOYA, P. BOZHKOV, L. BOZI, T. BOZKURT, D. BRACKNEY, C. BRANDTS, R. BRAUN, G. BRAUS, R. BRAVO-SAGUA, J. BRAVO-SAN PEDRO, P. BREST, M. BRINGER, A. BRIONES-HERRERA, V. BROADDUS, P. BRODERSEN, E. ALVAREZ, J. BRODSKY, S. BRODY, P. BRONSON, J. BRONSTEIN, C. BROWN, R. BROWN, P. BRUM, J. BRUMELL, N. BRUNETTI-PIERRI, D. BRUNO, R. BRYSON-RICHARDSON, C. BUCCI, C. BUCHRIESER, M. BUENO, L. BUITRAGO-MOLINA, S. BURASCHI, S. BUCH, J. BUCHAN, E. BUCKINGHAM, H. BUDAK, M. BUDINI, G. BULTYNCK, F. BURADA, J. BURGOYNE, M. BURON, V. BUSTOS, S. BUTTNER, E. BUTTURINI, A. BYRD, I. CABAS, S. CABRERA-BENITEZ, K. CADWELL, J. CAI, L. CAI, Q. CAI, M. CAIRO, J. CALBET, G. CALDWELL, K. CALDWELL, J. CALL, R. CALVANI, A. CALVO, M. BARRERA, N. CAMARA, J. CAMONIS, N. CAMOUGRAND, M. CAMPANELLA, E. CAMPBELL, F. CAMPBELL-VALOIS, S. CAMPELLO, I. CAMPESI, J. CAMPOS, O. CAMUZARD, J. CANCINO, D. DE ALMEIDA, L. CANESI, I. CANIGGIA, B. CANONICO, C. CANTI, B. CAO, M. CARAGLIA, B. CARAMES, E. CARCHMAN, E. CARDENAL-MUNOZ, C. CARDENAS, L. CARDENAS, S. CARDOSO, J. CAREW, G. CARLE, G. CARLETON, S. CARLONI, D. CARMONA-GUTIERREZ, L. CARNEIRO, O. CARNEVALI, J. CAROSI, S. CARRA, A. CARRIER, L. CARRIER, B. CARROLL, A. CARTER, A. CARVALHO, M. CASANOVA, C. CASAS, J. CASAS, C. CASSIOLI, E. CASTILLO, K. CASTILLO, S. CASTILLO-LLUVA, F. CASTOLDI, M. CASTORI, A. CASTRO, M. CASTRO-CALDAS, J. CASTRO-HERNANDEZ, S. CASTRO-OBREGON, S. CATZ, C. CAVADAS, F. CAVALIERE, G. CAVALLINI, M. CAVINATO, M. CAYUELA, P. RICA, V. CECARINI, F. CECCONI, M. CECHOWSKA-PASKO, S. CENCI, V. CEPERUELO-MALLAFRE, J. CERQUEIRA, J. CERUTTI, D. CERVIA, V. CETINTAS, S. CETRULLO, H. CHAE, A. CHAGIN, C. CHAI, G. CHAKRABARTI, O. CHAKRABARTI, T. CHAKRABORTY, M. CHAMI, G. CHAMILOS, D. CHAN, E. CHAN, H. CHAN, M. CHAN, Y. CHAN, P. CHANDRA, C. CHANG, H. CHANG, K. CHANG, J. CHAO, T. CHAPMAN, N. CHARLET-BERGUERAND, S. CHATTERJEE, S. CHAUBE, A. CHAUDHARY, S. CHAUHAN, E. CHAUM, F. CHECLER, M. CHEETHAM, C. CHEN, G. CHEN, J. CHEN, L. CHEN, M. CHEN, N. CHEN, Q. CHEN, R. CHEN, S. CHEN, W. CHEN, X. CHEN, Y. CHEN, Z. CHEN, H. CHENG, J. CHENG, S. CHENG, W. CHENG, X. CHENG, Y. CHENG, Z. CHENG, H. CHEONG, J. CHEONG, B. CHERNYAK, S. CHERRY, C. CHEUNG, K. CHEUNG, E. CHEVET, R. CHI, A. CHIANG, F. CHIARADONNA, R. CHIARELLI, M. CHIARIELLO, N. CHICA, S. CHIOCCA, M. CHIONG, S. CHIOU, A. CHIRAMEL, V. CHIURCHIU, D. CHO, S. CHOE, A. CHOI, M. CHOI, K. CHOUDHURY, N. CHOW, C. CHU, J. CHUA, H. CHUNG, K. CHUNG, S. CHUNG, Y. CHUNG, V. CIANFANELLI, I. CIECHOMSKA, M. CIFUENTES, L. CINQUE, S. CIRAK, M. CIRONE, M. CLAGUE, R. CLARKE, E. CLEMENTI, E. COCCIA, P. CODOGNO, E. COHEN, M. COHEN, T. COLASANTI, F. COLASUONNO, R. COLBERT, A. COLELL, N. COLL, M. COLLINS, M. COLOMBO, D. COLON-RAMOS, L. COMBARET, S. COMINCINI, M. COMINETTI, A. CONSIGLIO, A. CONTE, F. CONTI, V. CONTU, M. COOKSON, K. COOMBS, I. COPPENS, M. CORASANITI, D. CORKERY, N. CORDES, K. CORTESE, M. COSTA, S. COSTANTINO, P. COSTELLI, A. COTO-MONTES, P. CRACK, J. CRESPO, A. CRIOLLO, V. CRIPPA, R. CRISTOFANI, T. CSIZMADIA, A. CUADRADO, B. CUI, J. CUI, Y. CUI, E. CULETTO, A. CUMINO, A. CYBULSKY, M. CZAJA, S. CZUCZWAR, S. D'ADAMO, M. D'AMELIO, D. D'ARCANGELO, A. D'LUGOS, G. D'ORAZI, J. DA SILVA, H. DAFSARI, R. DAGDA, Y. DAGDAS, M. DAGLIA, X. DAI, Y. DAI, J. DAL COL, P. DALHAIMER, L. DALLA VALLE, T. DALLENGA, G. DALMASSO, M. DAMME, I. DANDO, N. DANTUMA, A. DARLING, H. DAS, S. DASARATHY, S. DASARI, S. DASH, O. DAUMKE, A. DAUPHINEE, J. DAVIES, V. DAVILA, R. DAVIS, T. DAVIS, S. NAIDU, F. DE AMICIS, K. DE BOSSCHER, F. DE FELICE, L. DE FRANCESCHI, C. DE LEONIBUS, M. BARBOSA, G. DE MEYER, A. DE MILITO, C. DE NUNZIO, C. DE PALMA, M. DE SANTI, C. DE VIRGILIO, D. DE ZIO, J. DEBNATH, B. DEBOSCH, J. DECUYPERE, M. DEEHAN, G. DEFLORIAN, J. DEGREGORI, B. DEHAY, G. DEL RIO, J. DELANEY, L. DELBRIDGE, E. DELORME-AXFORD, M. DELPINO, F. DEMARCHI, V. DEMBITZ, N. DEMERS, H. DENG, Z. DENG, J. DENGJEL, P. DENT, D. DENTON, M. DEPAMPHILIS, C. DER, V. DERETIC, A. DESCOTEAUX, L. DEVIS, S. DEVKOTA, O. DEVUYST, G. DEWSON, M. DHARMASIVAM, R. DHIMAN, D. DI BERNARDO, M. DI CRISTINA, F. DI DOMENICO, P. DI FAZIO, A. DI FONZO, G. DI GUARDO, G. DI GUGLIELMO, L. DI LEO, C. DI MALTA, A. DI NARDO, M. DI RIENZO, F. DI SANO, G. DIALLINAS, J. DIAO, G. DIAZ-ARAYA, I. DIAZ-LAVIADA, J. DICKINSON, M. DIEDERICH, M. DIEUDE, I. DIKIC, S. DING, W. DING, L. DINI, M. DINIC, A. DINKOVA-KOSTOVA, M. DIONNE, J. DISTLER, A. DIWAN, I. DIXON, M. DJAVAHERI-MERGNY, I. DOBRINSKI, O. DOBROVINSKAYA, R. DOBROWOLSKI, R. DOBSON, S. EMRE, M. DONADELLI, B. DONG, X. DONG, Z. DONG, G. II, V. DOTSCH, H. DOU, J. DOU, M. DOWAIDAR, S. DRIDI, L. DRUCKER, A. DU, C. DU, G. DU, H. DU, L. DU, A. DU TOIT, S. DUAN, X. DUAN, S. DUARTE, A. DUBROVSKA, E. DUNLOP, N. DUPONT, R. DURAN, B. DWARAKANATH, S. DYSHLOVOY, D. EBRAHIMI-FAKHARI, L. ECKHART, C. EDELSTEIN, T. EFFERTH, E. EFTEKHARPOUR, L. EICHINGER, N. EID, T. EISENBERG, N. EISSA, S. EISSA, M. EJARQUE, A. EL ANDALOUSSI, N. EL-HAGE, S. EL-NAGGAR, A. ELEUTERI, E. EL-SHAFEY, M. ELGENDY, A. ELIOPOULOS, M. ELIZALDE, P. ELKS, H. ELSASSER, E. ELSHERBINY, B. EMERLING, N. EMRE, C. ENG, N. ENGEDAL, A. ENGELBRECHT, A. ENGELSEN, J. ENSERINK, R. ESCALANTE, A. ESCLATINE, M. ESCOBAR-HENRIQUES, E. ESKELINEN, L. ESPERT, M. EUSEBIO, G. FABRIAS, C. FABRIZI, A. FACCHIANO, F. FACCHIANO, B. FADEEL, C. FADER, A. FAESEN, W. FAIRLIE, A. FALCO, B. FALKENBURGER, D. FAN, J. FAN, Y. FAN, E. FANG, Y. FANG, M. FANTO, T. FARFEL-BECKER, M. FAURE, G. FAZELI, A. FEDELE, A. FELDMAN, D. FENG, J. FENG, L. FENG, Y. FENG, W. FENG, T. ARAUJO, T. FERGUSON, J. FERNANDEZ-CHECA, S. FERNANDEZVELEDO, A. FERNIE, A. FERRANTE, A. FERRARESI, M. FERRARI, J. FERREIRA, S. FERRO-NOVICK, A. FIGUERAS, R. FILADI, N. FILIGHEDDU, E. FILIPPICHIELA, G. FILOMENI, G. FIMIA, V. FINESCHI, F. FINETTI, S. FINKBEINER, E. FISHER, P. FISHER, F. FLAMIGNI, S. FLIESLER, T. FLO, I. FLORANCE, O. FLOREY, T. FLORIO, E. FODOR, C. FOLLO, E. FON, A. FORLINO, F. FORNAI, P. FORTINI, A. FRACASSI, A. FRALDI, B. 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GOGINASHVILI, J. GOLAB, D. GOLDSTONE, A. GOLEBIEWSKA, L. GOMES, R. GOMEZ, R. GOMEZ-SANCHEZ, M. GOMEZ-PUERTO, R. GOMEZ-SINTES, Q. GONG, F. GONI, J. GONZALEZ-GALLEGO, T. GONZALEZ-HERNANDEZ, R. GONZALEZ-POLO, J. GONZALEZ-REYES, P. GONZALEZ-RODRIGUEZ, I. GOPING, M. GORBATYUK, N. GORBUNOV, R. GOROJOD, S. GORSKI, S. GORUPPI, C. GOTOR, R. GOTTLIEB, I. GOZES, D. GOZUACIK, M. GRAEF, M. GRALER, V. GRANATIERO, D. GRASSO, J. GRAY, D. GREEN, A. GREENHOUGH, S. GREGORY, E. GRIFFIN, M. GRINSTAFF, F. GROS, C. GROSE, A. GROSS, F. GRUBER, P. GRUMATI, T. GRUNE, X. GU, J. GUAN, C. GUARDIA, K. GUDA, F. GUERRA, C. GUERRI, P. GUHA, C. GUILLEN, S. GUJAR, A. GUKOVSKAYA, I. GUKOVSKY, J. GUNST, A. GUNTHER, A. GUNTUR, C. GUO, H. GUO, L. GUO, M. GUO, P. GUPTA, A. FERNANDEZ, S. GUPTA, V. GUPTA, A. GUSTAFSSON, D. GUTTERMAN, H. RANJITHA, A. HAAPASALO, J. HABER, S. HADANO, A. HAFREN, M. HAIDAR, B. HALL, G. HALLDEN, A. HAMACHER-BRADY, A. HAMANN, M. HAMASAKI, W. HAN, M. HANSEN, P. HANSON, Z. HAO, M. HARADA, L. 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REN, T. RENAULT, G. RENGA, K. REUE, K. REWITZ, B. RAMOS, S. RIAZUDDIN, T. RIBEIRO-RODRIGUES, J. RICCI, R. RICCI, V. RICCIO, D. RICHARDSON, Y. RIKIHISA, M. RISBUD, R. RISUENO, K. RITIS, S. RIZZA, R. RIZZUTO, H. ROBERTS, L. ROBERTS, K. ROBINSON, M. ROCCHERI, S. ROCCHI, G. RODNEY, T. RODRIGUES, V. SILVA, A. RODRIGUEZ, R. RODRIGUEZ-BARRUECO, N. RODRIGUEZ-HENCHE, H. RODRIGUEZ-ROCHA, J. ROELOFS, R. ROGERS, V. ROGOV, A. ROJO, K. ROLKA, V. ROMANELLO, L. ROMANI, A. ROMANO, P. ROMANO, D. ROMEO-GUITART, L. ROMERO, M. ROMERO, J. RONEY, C. RONGO, S. ROPERTO, M. ROSENFELDT, P. ROSENSTIEL, A. ROSENWALD, K. ROTH, L. ROTH, S. ROTH, K. ROUSCHOP, B. ROUSSEL, S. ROUX, P. ROVERE-QUERINI, A. ROY, A. ROZIERES, D. RUANO, D. RUBINSZTEIN, M. RUBTSOVA, K. RUCKDESCHEL, C. RUCKENSTUHL, E. RUDOLF, R. RUDOLF, A. RUGGIERI, A. RUPARELIA, P. RUSMINI, R. RUSSELL, G. RUSSO, M. RUSSO, R. RUSSO, O. RYABAYA, K. RYAN, K. RYU, M. SABATER-ARCIS, U. SACHDEV, M. SACHER, C. SACHSE, A. SADHU, J. SADOSHIMA, N. SAFREN, P. SAFTIG, A. SAGONA, G. SAHAY, A. SAHEBKAR, M. SAHIN, O. SAHIN, S. SAHNI, N. SAITO, S. SAITO, T. SAITO, R. SAKAI, Y. SAKAI, J. SAKAMAKI, K. SAKSELA, G. SALAZAR, A. SALAZAR-DEGRACIA, G. SALEKDEH, A. SALUJA, B. SAMPAIO-MARQUES, M. SANCHEZ, J. SANCHEZ-ALCAZAR, V. SANCHEZ-VERA, V. SANCHO-SHIMIZU, J. SANDERSON, M. SANDRI, S. SANTAGUIDA, L. SANTAMBROGIO, M. SANTANA, G. SANTONI, A. SANZ, P. SANZ, S. SARAN, M. SARDIELLO, T. SARGEANT, A. SARIN, C. SARKAR, S. SARKAR, M. SARRIAS, D. SARMAH, J. SARPARANTA, A. SATHYANARAYAN, R. SATHYANARAYANAN, K. SCAGLIONE, F. SCATOZZA, L. SCHAEFER, Z. SCHAFER, U. SCHAIBLE, A. SCHAPIRA, M. SCHARL, H. SCHATZL, C. SCHEIN, W. SCHEPER, D. SCHEURING, M. SCHIAFFINO, M. SCHIAPPACASSI, R. SCHINDL, U. SCHLATTNER, O. SCHMIDT, R. SCHMITT, S. SCHMIDT, I. SCHMITZ, E. SCHMUKLER, A. SCHNEIDER, B. SCHNEIDER, R. SCHOBER, A. SCHOIJET, M. SCHOTT, M. SCHRAMM, B. SCHRODER, K. SCHUH, C. SCHULLER, R. SCHULZE, L. SCHURMANNS, J. SCHWAMBORN, M. SCHWARTEN, F. SCIALO, S. SCIARRETTA, M. SCOTT, K. SCOTTO, A. SCOVASSI, A. SCRIMA, A. SCRIVO, D. SEBASTIAN, S. SEBTI, S. SEDEJ, L. SEGATORI, N. SEGEV, P. SEGLEN, I. SEILIEZ, E. SEKI, S. SELLECK, F. SELLKE, A. PEREZ-LARA, J. SELSBY, M. SENDTNER, S. SENTURK, E. SERANOVA, C. SERGI, R. SERRA-MORENO, H. SESAKI, C. SETTEMBRE, S. SETTY, G. SGARBI, O. SHA, J. SHACKA, J. SHAH, D. SHANG, C. SHAO, F. SHAO, S. SHARBATI, L. SHARKEY, D. SHARMA, G. SHARMA, K. SHARMA, P. SHARMA, S. SHARMA, H. SHEN, J. SHEN, M. SHEN, W. SHEN, Z. SHEN, R. SHENG, Z. SHENG, J. SHI, X. SHI, Y. SHI, K. SHIBA-FUKUSHIMA, J. SHIEH, Y. SHIMADA, S. SHIMIZU, M. SHIMOZAWA, T. SHINTANI, C. SHOEMAKER, S. SHOJAEI, I. SHOJI, B. SHRAVAGE, V. SHRIDHAR, C. SHU, H. SHU, K. SHUI, A. SHUKLA, T. SHUTT, V. SICA, A. SIDDIQUI, A. SIERRA, V. SIERRA-TORRE, S. SIGNORELLI, P. SIL, B. SILVA, J. SILVA, E. SILVA-PAVEZ, S. SILVENTE-POIROT, R. SIMMONDS, A. SIMON, H. SIMON, M. SIMONS, A. SINGH, L. SINGH, R. SINGH, S. SINGH, D. SINHA, R. SINHA, S. SINHA, A. SIRKO, K. SIROHI, E. SIVRIDIS, P. SKENDROS, A. SKIRYCZ, I. SLANINOVA, S. SMAILI, A. SMERTENKO, M. SMITH, S. SOENEN, E. SOHN, S. SOK, G. SOLAINI, T. SOLDATI, S. SOLEIMANPOUR, R. SOLER, A. SOLOVCHENKO, J. SOMARELLI, A. SONAWANE, F. SONG, H. SONG, J. SONG, K. SONG, Z. SONG, L. SORIA, M. SORICE, A. SOUKAS, S. SOUKUP, D. SOUSA, N. SOUSA, P. SPAGNUOLO, S. SPECTOR, M. BHARATH, D. ST CLAIR, V. STAGNI, L. STAIANO, C. STALNECKER, M. STANKOV, P. STATHOPULOS, K. STEFAN, S. STEFAN, L. STEFANIS, J. STEFFAN, A. STEINKASSERER, H. STENMARK, J. STERNECKERT, C. STEVENS, V. STOKA, S. STORCH, B. STORK, F. STRAPPAZZON, A. STROHECKER, D. STUPACK, H. SU, L. SU, A. SUAREZFONTES, C. SUBAUSTE, S. SUBBIAN, P. SUBIRADA, G. SUDHANDIRAN, C. SUE, X. SUI, C. SUMMERS, G. SUN, J. SUN, K. SUN, M. SUN, Q. SUN, Y. SUN, Z. SUN, K. SUNAHARA, E. SUNDBERG, K. SUSZTAK, P. SUTOVSKY, H. SUZUKI, G. SWEENEY, J. SYMONS, S. SZE, N. SZEWCZYK, C. TABOLACCI, F. TACKE, H. TAEGTMEYER, M. TAFANI, M. TAGAYA, H. TAI, S. TAIT, Y. TAKAHASHI, S. TAKATS, P. TALWAR, C. TAM, S. TAM, D. TAMPELLINI, A. TAMURA, C. TAN, E. TAN, Y. TAN, M. TANAKA, D. TANG, J. TANG, T. TANG, I. TANIDA, Z. TAO, M. TAOUIS, L. TATENHORST, N. TAVERNARAKIS, A. TAYLOR, G. TAYLOR, J. TAYLOR, E. TCHETINA, A. TEE, I. TEGEDER, D. TEIS, N. TEIXEIRA, F. TEIXEIRA-CLERC, K. TEKIRDAG, T. TENCOMNAO, S. TENREIRO, A. TEPIKIN, P. TESTILLANO, G. TETTAMANTI, P. THARAUX, K. THEDIECK, A. THEKKINGHAT, S. THELLUNG, J. THINWA, V. THIRUMALAIKUMAR, S. THOMAS, P. THOMES, A. THORBURN, L. THUKRAL, T. THUM, M. THUMM, L. TIAN, A. TICHY, A. TILL, V. TIMMERMAN, V. TITORENKO, S. TODI, K. TODOROVA, J. TOIVONEN, L. TOMAIPITINCA, D. TOMAR, C. TOMAS-ZAPICO, B. TONG, C. TONG, X. TONG, S. TOOZE, M. TORGERSEN, S. TORII, L. TORRES-LOPEZ, A. TORRIGLIA, C. TOWERS, R. TOWNS, S. TOYOKUNI, V. TRAJKOVIC, D. TRAMONTANO, Q. TRAN, L. TRAVASSOS, C. TRELFORD, S. TREMEL, I. TROUGAKOS, B. TSAO, M. TSCHAN, H. TSE, T. TSE, H. TSUGAWA, A. TSVETKOV, D. TUMBARELLO, Y. TUMTAS, M. TUNON, S. TURCOTTE, B. TURK, V. TURK, B. TURNER, R. TUXWORTH, J. TYLER, E. TYUTEREVA, Y. UCHIYAMA, A. UGUNKLUSEK, H. UHLIG, I. ULASOV, M. UMEKAWA, C. UNGERMANN, R. UNNO, S. URBE, E. URIBE-CARRETERO, S. USTUN, V. UVERSKY, T. VACCARI, M. VACCARO, B. VAHSEN, H. VAKIFAHMETOGLU-NORBERG, R. VALDOR, M. VALENTE, A. VALKO, R. VALLEE, A. VALVERDE, G. VAN DEN BERGHE, S. VAN DER VEEN, L. VAN KAER, J. VAN LOOSDREGT, S. VAN WIJK, W. VANDENBERGHE, I. VANHOREBEEK, M. VANNIER-SANTOS, N. VANNINI, M. VANRELL, C. VANTAGGIATO, G. VARANO, I. VARELA-NIETO, M. VARGA, M. VASCONCELOS, S. VATS, D. VAVVAS, I. VEGANAREDO, S. VEGA-RUBIN-DE-CELIS, G. VELASCO, A. VELAZQUEZ, T. VELLAI, E. VELLENGA, F. VELOTTI, M. VERDIER, P. VERGINIS, I. VERGNE, P. VERKADE, M. VERMA, P. VERSTREKEN, T. VERVLIET, J. VERVOORTS, A. VESSONI, V. VICTOR, M. VIDAL, C. VIDONI, O. VIEIRA, R. VIERSTRA, S. VIGANO, H. VIHINEN, V. VIJAYAN, M. VILA, M. VILAR, J. VILLALBA, A. VILLALOBO, B. VILLAREJO-ZORI, F. VILLARROYA, J. VILLARROYA, O. VINCENT, C. VINDIS, C. VIRET, M. VISCOMI, D. VISNJIC, I. VITALE, D. VOCADLO, O. VOITSEKHOVSKAJA, C. VOLONTE, M. VOLTA, M. VOMERO, C. VON HAEFEN, M. VOOIJS, W. VOOS, L. VUCICEVIC, R. WADE-MARTINS, S. WAGURI, K. WAITE, S. WAKATSUKI, D. WALKER, M. WALKER, S. WALKER, J. WALTER, F. WANDOSELL, B. WANG, C. WANG, D. WANG, F. WANG, G. WANG, H. WANG, J. WANG, K. WANG, L. WANG, M. WANG, N. WANG, P. WANG, Q. WANG, W. WANG, X. WANG, Y. WANG, Z. WANG, G. WARNES, V. WARNSMANN, H. WATADA, E. WATANABE, M. WATCHON, T. WEAVER, G. WEGRZYN, A. WEHMAN, H. WEI, L. WEI, T. WEI, Y. WEI, O. WEIERGRABER, C. WEIHL, G. WEINDL, R. WEISKIRCHEN, A. WELLS, R. WEN, X. WEN, A. WERNER, B. WEYKOPF, S. WHEATLEY, J. WHITTON, A. WHITWORTH, K. WIKTORSKA, M. WILDENBERG, T. WILEMAN, S. WILKINSON, D. WILLBOLD, B. WILLIAMS, R. WILLIAMS, P. WILLIAMSON, R. WILSON, B. WINNER, N. WINSOR, S. WITKIN, H. WODRICH, U. WOEHLBIER, T. WOLLERT, E. WONG, J. WONG, R. WONG, V. WONG, W. WONG, A. WU, C. WU, J. WU, K. WU, M. WU, S. WU, W. WU, X. WU, Y. WU, R. XAVIER, H. XIA, L. XIA, Z. XIA, G. XIANG, J. XIANG, M. XIANG, W. XIANG, B. XIAO, G. XIAO, H. XIAO, J. XIAO, L. XIAO, S. XIAO, Y. XIAO, B. XIE, C. XIE, M. XIE, Y. XIE, Z. XIE, M. XILOURI, C. XU, E. XU, H. XU, J. XU, L. XU, W. XU, X. XU, Y. XUE, S. YAKHINE-DIOP, M. YAMAGUCHI, O. YAMAGUCHI, A. YAMAMOTO, S. YAMASHINA, S. YAN, Z. YAN, Y. YANAGI, C. YANG, D. YANG, H. YANG, J. YANG, L. YANG, M. YANG, P. YANG, Q. YANG, S. YANG, W. YANG, X. YANG, Y. YANG, H. YAO, S. YAO, X. YAO, Y. YAO, T. YASUI, M. YAZDANKHAH, P. YEN, C. YI, X. YIN, Y. YIN, Z. YIN, M. YING, Z. YING, C. YIP, S. YIU, Y. YOO, K. YOSHIDA, S. YOSHII, T. YOSHIMORI, B. YOUSEFI, B. YU, H. YU, J. YU, L. YU, M. YU, S. YU, V. YU, W. YU, Z. YU, J. YUAN, L. YUAN, S. YUAN, Y. YUAN, Z. YUAN, J. YUE, Z. YUE, J. YUN, R. YUNG, D. ZACKS, G. ZAFFAGNINI, V. ZAMBELLI, I. ZANELLA, Q. ZANG, S. ZANIVAN, S. ZAPPAVIGNA, P. ZARAGOZA, K. ZARBALIS, A. ZAREBKOHAN, A. ZARROUK, S. ZEITLIN, J. ZENG, E. ZEROVNIK, L. ZHAN, B. ZHANG, D. ZHANG, H. ZHANG, J. ZHANG, K. ZHANG, L. ZHANG, M. ZHANG, P. ZHANG, S. ZHANG, W. ZHANG, X. ZHANG, Y. ZHANG, Z. ZHANG, H. ZHAO, L. ZHAO, S. ZHAO, T. ZHAO, X. ZHAO, Y. ZHAO, G. ZHENG, K. ZHENG, L. ZHENG, S. ZHENG, X. ZHENG, Y. ZHENG, Z. ZHENG, B. ZHIVOTOVSKY, Q. ZHONG, A. ZHOU, B. ZHOU, C. ZHOU, G. ZHOU, H. ZHOU, J. ZHOU, K. ZHOU, R. ZHOU, X. ZHOU, Y. ZHOU, Z. ZHOU, B. ZHU, C. ZHU, G. ZHU, H. ZHU, W. ZHU, Y. ZHU, H. ZHUANG, X. ZHUANG, K. ZIENTARA-RYTTER, C. ZIMMERMANN, E. ZIVIANI, T. ZOLADEK, W. ZONG, D. ZOROV, A. ZORZANO, W. ZOU, Z. ZOU, S. ZURYN, W. ZWERSCHKE, B. BRAND-SABERI, C. KENCHAPPA, S. OSHIMA, Y. RONG, J. SLUIMER, and C. STALLINGS
Subjects: flux, macroautophagy, phagophore, stress, vacuole, Autophagosome, LC3, lysosome, neurodegeneration, cancer
Abstract: In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
Published: 2021

6. Fixed-time Insemination in Pasture-based Medium-sized Dairy Operations of Northern Germany and an Attempt to Replace GnRH by hCG

Author: U. Koenig von Borstel, Matthias Gauly, D. Marthold, J. Detterer, and Wolfgang Holtz
Subjects: Male, medicine.medical_specialty, Time Factors, Pregnancy Rate, medicine.medical_treatment, media_common.quotation_subject, Breeding, Luteal phase, Insemination, Buserelin, Chorionic Gonadotropin, Gonadotropin-Releasing Hormone, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, Animal science, Ovulation Induction, Pregnancy, Germany, medicine, Animals, Ovulation, Insemination, Artificial, media_common, 2. Zero hunger, Gynecology, Estrous cycle, 030219 obstetrics & reproductive medicine, business.industry, 0402 animal and dairy science, 04 agricultural and veterinary sciences, 040201 dairy & animal science, Dairying, Pregnancy rate, Herd, Cattle, Female, Animal Science and Zoology, Ovulation induction, Estrus Synchronization, business, Biotechnology, medicine.drug
Abstract: A field study was conducted aimed at (i) evaluating the practicability of a fixed-time insemination regime for medium-sized dairy operations of north-western Germany, representative for many regions of Central Europe and (ii) substituting hCG for GnRH as ovulation-inducing agent at the end of a presynch or ovsynch protocol in an attempt to reduce the incidence of premature luteal regression. Cows of two herds synchronized by presynch and two herds synchronized by ovsynch protocol were randomly allotted to three subgroups; in one group ovulation was induced by the GnRH analog buserelin, in another by hCG, whereas a third group remained untreated. The synchronized groups were fixed-time inseminated; the untreated group bred to observed oestrus. Relative to untreated herd mates, pregnancy rate in cows subjected to a presynch protocol with buserelin as ovulation-inducing agent was 74%; for hCG it was 60%. In cows subjected to an ovsynch protocol, the corresponding relative pregnancy rates reached 138% in the case of buserelin and 95% in the case of hCG. Average service interval was shortened by 1 week in the presynch and delayed by 2 weeks in the ovsynch group. It may be concluded that fixed-time insemination of cows synchronized via ovsynch protocol with buserelin as ovulation-inducing agent is practicable and may help improve efficiency and reduce the work load involved with herd management in medium-sized dairy operations. The substitution of hCG for buserelin was found to be not advisable.
Published: 2015

7. Pre-Analytic Sources of Error with the Serum PAG-Pregnancy Test for Cows

Author: U. Koenig von Borstel, Wolfgang Holtz, F. Stahmann, and Matthias Gauly
Subjects: Pregnancy test, Pregnancy, Chemistry, Heparin, Contamination, medicine.disease, Cryopreservation, Dilution, Animal science, nervous system, 13. Climate action, Immunology, medicine, Sources of error, medicine.drug, Whole blood
Abstract: The pregnancy associated glycoprotein (PAG) test for pregnancy detection in cows necessitates transportation of blood samples to the laboratory. This investigation addresses preanalytic sources of error that might compromise its reliability. During shipping blood samples undergo substantial temperature fluctuations (Experiment 1). Temperatures of whole blood beyond 0°C had no effect, whereas freezing reduced measurements by 22% at -10 °C and by 25% at -20 °C (Experiment 2). Freezing of blood with low PAG content (Experiment 3) caused an increase from 2.4 to 3.7 ng/ml (P < 0.01). Cryopreservation of serum with various PAG concentrations (Experiment 4) brought about increases to varying degrees. The presence of heparin and EDTA in collecting tubes had no effect on PAG measurements, whereas citrate caused an initial reduction, but remained stable thereafter (Experiment 5). In blood stored six months at chilling temperature no change in PAG values occurred as long as samples contained heparin or EDTA (Experiment 6). In Experiment 7 vortexing of whole blood showed no effect, whereas freezing and dilution with water seriously compromised results. In summary, to obtain reliable PAG measurements, contamination with water must be avoided; freezing of whole blood or serum and the use of collecting tubes containing citrate will result in inaccuracies without altogether distorting results. High ambient temperature, physical agitation and long term storage at chilling temperature in the presence of heparin or EDTA will have no impact. PAG determination in blood may thus be considered a reliable pregnancy test for cows in most situations.
Published: 2015

8. Schulterinstabilität — Rotatorenmanschette : Arthroskopische und offene Operationstechniken bei Schulterverletzungen des Sportlers Endoprothetik

Author: A.B. Imhoff, U. König, A.B. Imhoff, and U. König
Subjects: Sports medicine, Surgery
Abstract: Ziel der heutigen Sportorthopädie und Sporttraumatologie muß es sein, verletzten Sportlern die Rückkehr auf ihr eigenes Leistungsniveau zu ermöglichen. Erreicht wird dies durch minimalinvasive Techniken und arthroskopische Operationsmethoden mit resorbierbaren oder Titan-Ankersystemen in Kombination mit Laser-(LACS) oder elektrothermischen Sonden (ETACS). Experten aus der ganzen Welt demonstrieren den akturellen Stand - der arthorkopischen und offenen Stabilisierungsverfahren bei der instabilen oder laxen Schulter (vordere, hintere und multidirektionale Schulterinstabilität) - der perkutanen Osteosynthese von Humeruskopffrakturen - der offenen und arthroskopischen Rekonstruktion der Rotatorenmanschettenläsion mit ihren Grenzen und Möglichkeiten - des sekundären Impingements des Sportlers auf dem Boden einer superioren Instabilität - der Endoprothetik des Glenohumeralgelenkes - der Sportfähigkeit mit einer Schulterprothese. Wie das Buch'Knieinstabilität und Knorpelschaden - Das instabile Knie des Sportlers'richtet sich auch dieses Buch sowohl an den Anfänger als auch an den Fortgeschrittenen. Der Leser bekommt einen umfassenden Überblick zum aktuellen Stand der Schulterchirurgie bei sportbedingzen Verletzungen und Verschleißerscheinungen.
Published: 2013

9. Noise behavior in SiGe devices

Author: Jacques Graffeuil, L. Escotte, Olivier Llopis, Robert Plana, L. Bary, Mattia Borgarino, M. Regis, and U. Koenig
Subjects: Noise temperature, Materials science, SiGe, Physics::Instrumentation and Detectors, business.industry, Acoustics, Noise spectral density, heterojunction bipolar transistor, Condensed Matter::Mesoscopic Systems and Quantum Hall Effect, Condensed Matter Physics, Noise figure, phase noise, Electronic, Optical and Magnetic Materials, Burst noise, Noise generator, Phase noise, Materials Chemistry, Optoelectronics, Flicker noise, Electrical and Electronic Engineering, low frequency nosie, microwave noise, business, Noise (radio)
Abstract: This paper presents an overview of SiGe technologies and their corresponding noise properties both in the high frequency and low frequency range. We demonstrate that SiGe bipolar technology exhibits impressive low frequency noise performance with an excess corner noise frequency in the 1 kHz range. These results have been validated by low phase noise microwave oscillators based on SiGe material.
Published: 2001

10. Pre-Analytic Sources of Error with the Serum PAG-Pregnancy Test for Cows

Author: Stahmann, F., primary, Gauly, M., additional, Borstel, U. Koenig von, additional, and Holtz, Wolfgang, additional
Published: 2015
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11. 675 Identification of trends in the involvement and resistances of extended-spectrum beta-lactamase Escherichia coli in urinary tract infections: A 10-year follow-up study

Author: U. Koenig, C. Mrstik, Christian Radmayr, Andreas Lunacek, E. Plas, and Wolfgang Horninger
Subjects: 10 year follow up, business.industry, Urology, Urinary system, medicine.medical_treatment, medicine, Beta-lactamase, Identification (biology), medicine.disease_cause, business, Escherichia coli, Microbiology
Published: 2014

12. A technical solution for secondary arthritis due to chronic proximal tibiofibular joint instability

Author: U. Koenig, Andreas B. Imhoff, and M. Yaniv
Subjects: musculoskeletal diseases, Joint Instability, Male, medicine.medical_specialty, Arthrodesis, medicine.medical_treatment, Arthritis, Biceps, Tendons, Fascia lata, Fascia Lata, medicine, Humans, Orthopedics and Sports Medicine, Tibia, Fibula, business.industry, Middle Aged, musculoskeletal system, medicine.disease, Internal Fixators, Surgery, medicine.anatomical_structure, Orthopedic surgery, Chronic Disease, Ligaments, Articular, Ligament, business
Abstract: Chronic instability of the proximal tibiofibular joint is an uncommon diagnosis and not frequently reported in the literature. The management options of this joint instability, complicated with secondary arthritis, have rarely been discussed and consist mainly of fibular head resection or arthrodesis of this joint. We describe a new technical procedure for addressing both the instability and the joint secondary arthritis. Stability of the joint is achieved by ligament reconstruction using a biceps femoris split passed through the tibial metaphysis and fixated back to the fibular head using bone anchors. The arthritic changes are addressed by interposition of a vascularized fascia lata strip. The described procedure offers a firm stabilization with no need for postoperative restrictions and an alternative to the inadvisable joint arthrodesis or resection.
Published: 1999

13. Proximal deletion of chromosome 21 confirmed by in situ hybridization and molecular studies

Author: U. Koenig, M. B. Petersen, Pascale Cochaux, N. Van Regemorter, J. Flament‐Durand, Winnie Courtens, Franki Speleman, M. R. Verschraegen-Spae, Jean Christophe Noël, D. Delneste, N. Van Roy, and E Vamos
Subjects: medicine.medical_specialty, Monosomy, Chromosomes, Human, Pair 21, Aneuploidy, Chromosomal translocation, Gene mutation, Biology, Translocation, Genetic, Fatal Outcome, medicine, Humans, Abnormalities, Multiple, Urinary Tract, Genetics (clinical), In Situ Hybridization, Fluorescence, medicine.diagnostic_test, Cytogenetics, Infant, Newborn, Karyotype, Genitalia, Female, medicine.disease, Molecular biology, Chromosome Banding, Chromosomes, Human, Pair 1, Karyotyping, Female, Agenesis of Corpus Callosum, Chromosome Deletion, Chromosome 21, Fluorescence in situ hybridization
Abstract: Foetal blood sampling was performed at 35 weeks of gestation due to abnormal foetal ultrasound findings. There was apparent monosomy 21 (45,XX,-21) in all mitoses analyzed. The infant died at 37 weeks during delivery. Examination disclosed facial anomalies, clubfeet, hypoplasia of the left urogenital tract, agenesis of corpus callosum, ventricular dilatation, and heterotopias. Reevaluation of the karyotype showed an unbalanced translocation t(1;21) (q44;q22.11) which resulted from a maternal balanced translocation. These findings were confirmed by fluorescence in situ hybridization and molecular studies with chromosome 21 specific markers. The latter showed a proximal deletion of the maternally derived chromosome 21 including all loci from centromere down to the D21S210 locus. This case illustrates the need for complementary cytogenetic and molecular investigations in cases of apparent monosomy 21.
Published: 1994

14. UP-01.122 Trends of Increasing Resistance of E.Coli and Non-Significant Changes in Extended Spectrum Beta-Lactamase (ESBL) E.Coli in Urinary Tract Infections

Author: Andreas Lunacek, A. Nader, M. Huber, Eugen Plas, U. Koenig, and M. Schmudermaier
Subjects: business.industry, Urology, medicine.medical_treatment, Urinary system, Beta-lactamase, Medicine, business, Microbiology
Published: 2011

15. UP-01.121 Unexpected Multidrug Resistance of Methicillin-Resistant Staphylococcus Aureus (MRSA) in Urine Samples: A Single Center Study

Author: A. Nader, Eugen Plas, M. Schmudermaier, M. Huber, U. Koenig, and Andreas Lunacek
Subjects: Multiple drug resistance, business.industry, Urology, medicine, Urine, medicine.disease_cause, Single Center, business, Methicillin-resistant Staphylococcus aureus, Microbiology
Published: 2011

16. Temperature dependence of structural, electrical and magnetic properties of YBa2Cu3Ox prepared by an equilibrium method

Author: W. Reichelt, U. Koenig, T. Kopte, K. Eversmann, H. Huelz, and Mathias Doerr
Subjects: Superconductivity, Magnetic measurements, Materials science, Condensed matter physics, chemistry, Condensed Matter::Superconductivity, Thermal, chemistry.chemical_element, Electrical and Electronic Engineering, Condensed Matter Physics, Oxygen, Stoichiometry, Electronic, Optical and Magnetic Materials
Abstract: High-temperature superconducting samples of YBa2Cu3Ox with a defined oxygen stoichiometric amount have been prepared using a special equilibrium method. Results of structural investigations as well as thermal, electrical and magnetic measurements are discussed trying to understand the mechanism of the superconductivity and to make available standard values.
Published: 1994

17. ChemInform Abstract: THE INFLUENCE OF THE GROWTH PROCESS ON DOPING PROFILE AND MOBILITY PROFILE DURING LPE OF THE PSEUDOBINARY TIN-GALLIUM ARSENIDE SYSTEM

Author: E. Kubalek, U. Koenig, and K. Heime
Subjects: chemistry.chemical_compound, chemistry, business.industry, Scientific method, Optoelectronics, chemistry.chemical_element, Mineralogy, General Medicine, business, Tin, Doping profile, Gallium arsenide
Published: 1979

18. Prostaglandine und Immunabwehr

Author: R. Heicappell and U. Koenig
Abstract: Die Immunantwort umfast eine Vielzahl von regulatorischen Zellinteraktionen. Zellulare und humorale Immunitat werden durch losliche Faktoren vermittelt, die von den an der Immunreaktion beteiligten Zellen freigesetzt werden (Abb. 1).
Published: 1981

19. ChemInform Abstract: Prospects and Problems of Electrochemically Induced Cold Nuclear Fusion

Author: U. Koenig, C. van Calker, W. Kies, J.W. Schultze, and A. Hochfeld
Subjects: Chemistry, Radiochemistry, General Medicine, Cold fusion
Published: 1989

20. ChemInform Abstract: Potentiostatic Pulse Measurements of Oxide Growth on Zirconium

Author: J.W. Schultze, P. Meisterjahn, and U. Koenig
Subjects: Zirconium, chemistry.chemical_compound, chemistry, Pulse (signal processing), Analytical chemistry, Oxide, chemistry.chemical_element, General Medicine
Published: 1989

21. Sero-immunological investigations in patients with cervical cancer: higher rate of HSV-2 antibodies than in syphilis patients and evidence of IgM antibodies to an early HSV-1 antigen

Author: K E, Schneweis, A, Haag, A, Lehmköster, and U, Koenig
Subjects: Adult, Male, Complement Fixation Tests, Age Factors, Fluorescent Antibody Technique, Uterine Cervical Neoplasms, Middle Aged, Antibodies, Viral, Antibodies, Bacterial, Immunoglobulin M, Neutralization Tests, Humans, Simplexvirus, Female, Syphilis, Treponema pallidum, Antigens, Viral
Published: 1975

22. Phagocytic cell death leads to enhanced release of pro-inflammatory S100A12 in familial Mediterranean fever.

Author: Varga G, Schleifenbaum S, Koenig U, Waldkirch J, Hinze C, Kessel C, Geluk W, Pap T, Lainka E, Kallinich T, Foell D, and Wittkowski H
Abstract: Background: Familial Mediterranean fever (FMF) is a prototypical autoinflammatory syndrome associated with phagocytic cell activation. Pyrin mutations are the genetic basis of this disease, and its expression has been shown in monocytes, granulocytes, dendritic cells, and synovial fibroblasts. Pyrin functions as a cytosolic pattern recognition receptor and forms a distinct pyrin inflammasome. The phagocyte-specific protein S100A12 is predominantly expressed in granulocytes and belongs to the group of damage associated molecular patterns (DAMP). S100A12 can be detected at massively elevated levels in the serum of FMF patients, even in clinically inactive disease. Whether this is crucial for FMF pathogenesis is as yet unknown, and we therefore investigated the mechanisms of S100A12 release from granulocytes of FMF patients presenting clinically inactive., Results: We demonstrate that FMF neutrophils from patients in clinical inactive disease possess an intrinsic activity leading to cell death even in exogenously unstimulated neutrophils. Cell death resembles NETosis and is dependent on ROS and pore forming protein gasdermin D (GSDMD), as inhibitors for both are capable of completely block cell death and S100A12 release. When pyrin-activator TcdA (Clostridium difficile toxin A) is used to stimulate, neutrophilic cell death and S100A12 release are significantly enhanced in neutrophils from FMF patients compared to neutrophils from HC., Conclusions: We are able to demonstrate that activation threshold of neutrophils from inactive FMF patients is decreased, most likely by pre-activated pyrin. FMF neutrophils present with intrinsically higher ROS production, when cultured ex vivo. This higher baseline ROS activity leads to increased GSDMD cleavage and subsequent release of, e.g., S100A12, and to increased cell death with features of NETosis and pyroptosis. We show for the first time that cell death pathways in neutrophils of inactive FMF patients are easily triggered and lead to ROS- and GSDMD-dependent activation mechanisms and possibly pathology. This could be therapeutically addressed by blocking ROS or GSDMD cleavage to decrease inflammatory outbreaks when becoming highly active., (© 2023. The Author(s).)
Published: 2023
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23. A mechanism-based approach unveils metabolic routes potentially mediating chlorantraniliprole synergism in honey bees, Apis mellifera L., by azole fungicides.

Author: Haas J, Glaubitz J, Koenig U, and Nauen R
Subjects: Animals, Azoles, Bees, ortho-Aminobenzoates toxicity, Fungicides, Industrial toxicity, Insecticides toxicity
Abstract: Background: Almond production in California is an intensively managed agroecosystem dependent on managed pollination by honey bees, Apis mellifera L. A recent laboratory study reported synergism in honey bees between chlorantraniliprole, a common diamide insecticide used in almond orchards, and the fungicide propiconazole. Indeed, there is an emerging body of evidence that honey bee cytochrome P450 monooxygenases of the CYP9Q subfamily are involved in the detoxification of insecticides across a diverse range of chemical classes. The objective of the present study was to unveil the molecular background of the described synergism and to explore the potential role of CYP9Q enzymes in diamide detoxification., Results: Our study confirmed the previously reported synergistic potential of propiconazole on chlorantraniliprole in acute contact toxicity bioassays, whereas no synergism was observed for flubendiamide. Fluorescence-based biochemical assays revealed an interaction of chlorantraniliprole, but not flubendiamide, with functionally expressed CYP9Q2 and CYP9Q3. These findings were validated by an increased chlorantraniliprole tolerance of transgenic Drosophila lines expressing CYP9Q2/3, and an analytically confirmed oxidative metabolism of chlorantraniliprole by recombinantly expressed enzymes. Furthermore, we showed that several triazole fungicides used in almond orchards, including propiconazole, were strong nanomolar inhibitors of functionally expressed honey bee CYP9Q2 and CYP9Q3, whereas other fungicides such as iprodione and cyprodinil did not inhibit these enzymes., Conclusion: Honey bee CYP9Q enzymes are involved in chlorantraniliprole metabolism and inhibited by triazole fungicides possibly leading to synergism in acute contact toxicity bioassays. Our mechanistic approach has the potential to inform tier I honey bee pesticide risk assessment., (© 2021 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.)
Published: 2022
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24. Cure Is Possible: Extensively Metastatic HER2-Positive Gastric Carcinoma with 5 years of Complete Remission after Therapy with the FLOT Regimen and Trastuzumab.

Author: Schade S, Koenig U, Mekolli A, Gaedcke J, Neesse A, Reinecke J, Brunner M, Amir Hosseini AS, Kitz J, Stroebel P, Lotz J, Ghadimi M, Ellenrieder V, and Koenig A
Abstract: Gastric cancer (GC) represents one of the most fatal neoplasms in gastrointestinal oncology and affected patients can only hope for cure in limited disease. In a metastatic situation however, patients have a worse prognosis finally resulting in cancer-related death. Some improvements were made by using intensified chemotherapy such as the FLOT protocol (5-FU, leucovorin, oxaliplatin and docetaxel). However, a breakthrough in the treatment of advanced GC has been achieved by pre-therapeutical tumor analysis for potentially targetable alterations. Microsatellite instability, PD-L1 expression, Epstein Barr virus, and human epidermal growth factor receptor-2 (HER2) overexpression or amplification are the most beneficial targets, if addressed, can prolong survival in a palliative situation. Whether the combination of these targeted therapeutics with chemotherapy can bring long-term survival or even a chance of cure in a metastatic situation is not clear. Here, we report the case of a 30-year-old man with GC and extensive metastases who was cured by anti-HER2 antibody Trastuzumab combined with the FLOT regime. Initial staging showed an exophytic Siewert type III tumor and extensive hepatic metastases. Histology resulted in gastric adenocarcinoma with HER2 overexpression (2+, FISH positive). Twelve courses of chemotherapy comprising Trastuzumab and FLOT were administered. After treatment, the extensive liver metastases had disappeared with no evidence of residual tumor growth on the CT scans. Monotherapy of Trastuzumab was continued until gastrectomy with D2 lymph node dissection and probing of liver tissue, which revealed no residual tumor cells. Five years after surgery, there is continued complete remission. In conclusion, Trastuzumab in combination with FLOT may have curative potential even for metastatic stages of HER-2-positive GC., Competing Interests: The authors have no conflicts of interest to declare., (Copyright © 2022 by S. Karger AG, Basel.)
Published: 2022
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25. Effectiveness of fourth-line dual immunotherapy in hepatocellular carcinoma with simultaneous steroid administration for immune-related hepatitis.

Author: Lowes K, Reinecke J, Brunner M, Scholz M, Kitz J, Michels B, Mekolli A, Gaedcke J, Seif Amir Hosseini A, Ströbel P, Ghadimi M, Ellenrieder V, Koenig A, and Koenig U
Abstract: Medical therapy of advanced hepatocellular carcinoma (HCC) remains an emerging subject, but therapeutic sequences together with toxicity management are rarely described. Herein, we report the case of a therapeutic sequence and toxicity management in a 72-year old White male with advanced non-cirrhotic HCC. The HCC of this patient was refractory against treatment with several tyrosine kinase inhibitors, including lenvatinib and cabozantinib or immune combination of pembrolizumab and lenvatinib. Double immune combination of nivolumab and ipilimumab was effective in fourth-line treatment but resulted in immunotherapy-related grade 4 hepatitis. This toxicity responded well to high doses of corticosteroids, and reinduction of dual immune combination remained effective despite continuation of high-dose corticosteroids in a non-cirrhotic HCC. This case demonstrated the efficacy of double immune therapy in higher treatment lines in advanced non-cirrhotic HCC even if the patient was treated with other immune modulatory therapies earlier. Moreover, it can remain effective under concomitant administration of high-dose corticosteroids., Competing Interests: Conflict of interest statement: The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s), 2022.)
Published: 2022
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26. Intensified Histopathological Work-Up after Pancreatic Head Resection Reveals Relevant Prognostic Markers.

Author: Dusch N, Oldani M, Steffen T, Kitz J, Koenig U, Azizian A, König A, Ströbel P, Beissbarth T, Ghadimi M, and Gaedcke J
Subjects: Humans, Neoplasm Recurrence, Local, Pancreas diagnostic imaging, Pancreas surgery, Pancreatectomy, Pancreaticoduodenectomy, Prognosis, Retrospective Studies, Survival Rate, Pancreatic Neoplasms surgery
Abstract: Introduction: Local recurrence remains a major problem after pancreatic head resection. Intensified histopathological work-up of surgical specimens after pancreatic head resection has revealed an increased number of incomplete resections (R1) depending on tumor infiltration front at the resection margins (RMs). It remains unclear to which extent the increased R1 resection rate has a clinical relevance for the patients' prognosis., Materials and Methods: Pancreatic head resections between 2006 and 2012 were histologically intensively worked-up by a previously described protocol. The distance between the tumor infiltration front and the resection planes or organ surfaces was documented. The impact of the size of the tumor and an additional portal vein resection was analyzed. The effect of a R1 resection status on development and type of recurrence was evaluated., Results: A total of 203 pancreatic head resections were evaluated. Different definitions of R1 resection were applied. These led to significantly different prognosis for patients. A greater distance between the tumor infiltration front and the resection plane or organ surface was associated with a better outcome for the patients. For the ventral surface, the mesopancreas and the pancreatic body these differences were statistically significant comparing the different R1 definitions. For the dorsal surface, a significant difference in prognosis was found if the tumor was >2 mm away from the resection surface. A tumor size of 3 cm was identified to play a relevant role for the prognosis. Patients who had a portal vein resection without a histologically proven infiltration showed a statistically significant higher overall survival. Patients with R1 resection were at highest risk for developing local recurrence as well as distant metastasis., Conclusion: Intensified histopathological work-up with an increased number of R1 resections has a clinical relevance for patients' prognosis. Tumors with a smaller size or with a greater distance to the organ surface or RM have a better outcome., (© 2020 S. Karger AG, Basel.)
Published: 2021
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27. Cell death induced autophagy contributes to terminal differentiation of skin and skin appendages.

Author: Koenig U, Robenek H, Barresi C, Brandstetter M, Resch GP, Gröger M, Pap T, and Hartmann C
Subjects: Animals, Apoptosis physiology, Epithelial Cells physiology, Mice, Transgenic, Autophagosomes metabolism, Autophagy physiology, Cell Differentiation physiology, Lysosomes metabolism, Skin cytology
Abstract: In the adult mammalian skin, cells are constantly renewing, differentiating and moving upward, to finally die in a yet not fully understood manner. Here, we provide evidence that macroautophagy/autophagy has a dual role in the skin. In addition to its known catabolic protective role as an evolutionary conserved upstream regulator of lysosomal degradation, we show that autophagy induced cell death (CDA) occurs in epithelial lineage-derived organs, such as the inter-follicular epidermis, the sebaceous- and the Harderian gland. By utilizing GFP-LC3 transgenic and ATG7-deficient mice, we show that CDA is initiated during terminal differentiation at a stage when the cells have become highly resistant to apoptosis. In these transitional cells, the Golgi compartment expands, which accounts for the formation of primary lysosomes, and the nucleus starts to condense. During CDA a burst of autophagosome formation is observed, first the endoplasmic reticulum (ER) is phagocytosed followed by autophagy of the nucleus. By this selective form of cell death, most of the cytoplasmic organelles are degraded, but structural proteins remain intact. In the absence of autophagy, consequently, parts of the ER, ribosomes, and chromatin remain. A burst of autophagy was stochastically observed in single cells of the epidermis and collectively in larger areas of ductal cells, arguing for a coordinated induction. We conclude that autophagy is an integral part of cell death in keratinocyte lineage cells and participates in their terminal cell fate. Abbreviations: Atg7: autophagy related 7; BECN1: beclin 1; CDA: cell death-induced autophagy; Cre: Cre-recombinase; DAPI: 4',6-diamidino-2-phenylindole; ER: endoplasmatic reticulum; GFP: green fluorescent protein; HaGl: haderian gland; IVL: involucrin; KRT14: keratin 14; LD: lipid droplet; LSM: laser scanning microscope; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; PN: perinuclear space; RB: residual body; rER: rough endoplasmatic reticulum; SB: sebum; SG-SC: stratum granulosum - stratum corneum; SGl: sebaceous gland; SQSTM1: sequestosome 1; TEM: transmission electron microscopy; TUNEL: terminal deoxynucleotidyl transferase dUTP nick end labelling.
Published: 2020
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28. Clinicopathological hallmarks and biomarkers of colorectal neuroendocrine neoplasms.

Author: Koenig A, Krug S, Mueller D, Barth PJ, Koenig U, Scharf M, Ellenrieder V, Michl P, Moll R, Homayunfar K, Kann PH, Stroebel P, Gress TM, and Rinke A
Subjects: Aged, Colorectal Neoplasms blood, Disease Progression, Female, Humans, Male, Middle Aged, Neuroendocrine Tumors blood, Biomarkers, Tumor blood, Chromogranin B blood, Colorectal Neoplasms pathology, Neuroendocrine Tumors pathology
Abstract: Chromogranin A (CgA) is a well-established marker for diagnosis and follow up of patients with gastroenteropancreatic neuroendocrine neoplasms (GEP-NEN). Recently, it has been shown that plasma levels of CgA correlate with tumor load and predict survival of patients with NEN of the small bowel. It is assumed that this is as well valid for NEN of the colon and rectum, however, this is not supported by data. To evaluate this assumption, we analyzed 62 patients with NEN of the colon and rectum listed in the Marburg GEP-NEN registry for clinicopathological characteristics, expression and plasma levels of CgA. The present study demonstrates that immunohistochemical CgA and synaptophysin are good markers for histological diagnosis in patients with NEN of the colon and rectum. However, plasma CgA is a poor marker to follow-up these patients because only a minority exhibited increased levels which did not increase significantly during tumor progression. In contrast to NEN of the small bowel, there is no correlation of CgA plasma levels with tumor burden or survival. Patients with NEN of the colon and rectum displayed a relatively good prognosis resulting in a median survival of 8.5 years. However, a subset of patients affected by G3 neoplasms, exhibited a poorer prognosis with a median survival of 2.5 years. Taken together, CgA is a valuable marker for immunohistochemical diagnosis, but CgA plasma concentration is not suitable to mirror tumor burden or prognosis in patients with NEN of the colon and rectum.
Published: 2017
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29. Fixed-time Insemination in Pasture-based Medium-sized Dairy Operations of Northern Germany and an Attempt to Replace GnRH by hCG.

Author: Marthold D, Detterer J, Koenig von Borstel U, Gauly M, and Holtz W
Subjects: Animals, Breeding, Buserelin administration & dosage, Estrus Synchronization methods, Female, Germany, Insemination, Artificial methods, Male, Ovulation Induction methods, Ovulation Induction veterinary, Pregnancy, Pregnancy Rate, Time Factors, Cattle, Chorionic Gonadotropin administration & dosage, Dairying methods, Gonadotropin-Releasing Hormone administration & dosage, Insemination, Artificial veterinary
Abstract: A field study was conducted aimed at (i) evaluating the practicability of a fixed-time insemination regime for medium-sized dairy operations of north-western Germany, representative for many regions of Central Europe and (ii) substituting hCG for GnRH as ovulation-inducing agent at the end of a presynch or ovsynch protocol in an attempt to reduce the incidence of premature luteal regression. Cows of two herds synchronized by presynch and two herds synchronized by ovsynch protocol were randomly allotted to three subgroups; in one group ovulation was induced by the GnRH analog buserelin, in another by hCG, whereas a third group remained untreated. The synchronized groups were fixed-time inseminated; the untreated group bred to observed oestrus. Relative to untreated herd mates, pregnancy rate in cows subjected to a presynch protocol with buserelin as ovulation-inducing agent was 74%; for hCG it was 60%. In cows subjected to an ovsynch protocol, the corresponding relative pregnancy rates reached 138% in the case of buserelin and 95% in the case of hCG. Average service interval was shortened by 1 week in the presynch and delayed by 2 weeks in the ovsynch group. It may be concluded that fixed-time insemination of cows synchronized via ovsynch protocol with buserelin as ovulation-inducing agent is practicable and may help improve efficiency and reduce the work load involved with herd management in medium-sized dairy operations. The substitution of hCG for buserelin was found to be not advisable., (© 2015 Blackwell Verlag GmbH.)
Published: 2016
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30. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).

Author: Klionsky DJ, Abdelmohsen K, Abe A, Abedin MJ, Abeliovich H, Acevedo Arozena A, Adachi H, Adams CM, Adams PD, Adeli K, Adhihetty PJ, Adler SG, Agam G, Agarwal R, Aghi MK, Agnello M, Agostinis P, Aguilar PV, Aguirre-Ghiso J, Airoldi EM, Ait-Si-Ali S, Akematsu T, Akporiaye ET, Al-Rubeai M, Albaiceta GM, Albanese C, Albani D, Albert ML, Aldudo J, Algül H, Alirezaei M, Alloza I, Almasan A, Almonte-Beceril M, Alnemri ES, Alonso C, Altan-Bonnet N, Altieri DC, Alvarez S, Alvarez-Erviti L, Alves S, Amadoro G, Amano A, Amantini C, Ambrosio S, Amelio I, Amer AO, Amessou M, Amon A, An Z, Anania FA, Andersen SU, Andley UP, Andreadi CK, Andrieu-Abadie N, Anel A, Ann DK, Anoopkumar-Dukie S, Antonioli M, Aoki H, Apostolova N, Aquila S, Aquilano K, Araki K, Arama E, Aranda A, Araya J, Arcaro A, Arias E, Arimoto H, Ariosa AR, Armstrong JL, Arnould T, Arsov I, Asanuma K, Askanas V, Asselin E, Atarashi R, Atherton SS, Atkin JD, Attardi LD, Auberger P, Auburger G, Aurelian L, Autelli R, Avagliano L, Avantaggiati ML, Avrahami L, Awale S, Azad N, Bachetti T, Backer JM, Bae DH, Bae JS, Bae ON, Bae SH, Baehrecke EH, Baek SH, Baghdiguian S, Bagniewska-Zadworna A, Bai H, Bai J, Bai XY, Bailly Y, Balaji KN, Balduini W, Ballabio A, Balzan R, Banerjee R, Bánhegyi G, Bao H, Barbeau B, Barrachina MD, Barreiro E, Bartel B, Bartolomé A, Bassham DC, Bassi MT, Bast RC Jr, Basu A, Batista MT, Batoko H, Battino M, Bauckman K, Baumgarner BL, Bayer KU, Beale R, Beaulieu JF, Beck GR Jr, Becker C, Beckham JD, Bédard PA, Bednarski PJ, Begley TJ, Behl C, Behrends C, Behrens GM, Behrns KE, Bejarano E, Belaid A, Belleudi F, Bénard G, Berchem G, Bergamaschi D, Bergami M, Berkhout B, Berliocchi L, Bernard A, Bernard M, Bernassola F, Bertolotti A, Bess AS, Besteiro S, Bettuzzi S, Bhalla S, Bhattacharyya S, Bhutia SK, Biagosch C, Bianchi MW, Biard-Piechaczyk M, Billes V, Bincoletto C, Bingol B, Bird SW, Bitoun M, Bjedov I, Blackstone C, Blanc L, Blanco GA, Blomhoff HK, Boada-Romero E, Böckler S, Boes M, Boesze-Battaglia K, Boise LH, Bolino A, Boman A, Bonaldo P, Bordi M, Bosch J, Botana LM, Botti J, Bou G, Bouché M, Bouchecareilh M, Boucher MJ, Boulton ME, Bouret SG, Boya P, Boyer-Guittaut M, Bozhkov PV, Brady N, Braga VM, Brancolini C, Braus GH, Bravo-San Pedro JM, Brennan LA, Bresnick EH, Brest P, Bridges D, Bringer MA, Brini M, Brito GC, Brodin B, Brookes PS, Brown EJ, Brown K, Broxmeyer HE, Bruhat A, Brum PC, Brumell JH, Brunetti-Pierri N, Bryson-Richardson RJ, Buch S, Buchan AM, Budak H, Bulavin DV, Bultman SJ, Bultynck G, Bumbasirevic V, Burelle Y, Burke RE, Burmeister M, Bütikofer P, Caberlotto L, Cadwell K, Cahova M, Cai D, Cai J, Cai Q, Calatayud S, Camougrand N, Campanella M, Campbell GR, Campbell M, Campello S, Candau R, Caniggia I, Cantoni L, Cao L, Caplan AB, Caraglia M, Cardinali C, Cardoso SM, Carew JS, Carleton LA, Carlin CR, Carloni S, Carlsson SR, Carmona-Gutierrez D, Carneiro LA, Carnevali O, Carra S, Carrier A, Carroll B, Casas C, Casas J, Cassinelli G, Castets P, Castro-Obregon S, Cavallini G, Ceccherini I, Cecconi F, Cederbaum AI, Ceña V, Cenci S, Cerella C, Cervia D, Cetrullo S, Chaachouay H, Chae HJ, Chagin AS, Chai CY, Chakrabarti G, Chamilos G, Chan EY, Chan MT, Chandra D, Chandra P, Chang CP, Chang RC, Chang TY, Chatham JC, Chatterjee S, Chauhan S, Che Y, Cheetham ME, Cheluvappa R, Chen CJ, Chen G, Chen GC, Chen G, Chen H, Chen JW, Chen JK, Chen M, Chen M, Chen P, Chen Q, Chen Q, Chen SD, Chen S, Chen SS, Chen W, Chen WJ, Chen WQ, Chen W, Chen X, Chen YH, Chen YG, Chen Y, Chen Y, Chen Y, Chen YJ, Chen YQ, Chen Y, Chen Z, Chen Z, Cheng A, Cheng CH, Cheng H, Cheong H, Cherry S, Chesney J, Cheung CH, Chevet E, Chi HC, Chi SG, Chiacchiera F, Chiang HL, Chiarelli R, Chiariello M, Chieppa M, Chin LS, Chiong M, Chiu GN, Cho DH, Cho SG, Cho WC, Cho YY, Cho YS, Choi AM, Choi EJ, Choi EK, Choi J, Choi ME, Choi SI, Chou TF, Chouaib S, Choubey D, Choubey V, Chow KC, Chowdhury K, Chu CT, Chuang TH, Chun T, Chung H, Chung T, Chung YL, Chwae YJ, 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Santaguida S, Santambrogio L, Santoni G, Dos Santos CN, Saran S, Sardiello M, Sargent G, Sarkar P, Sarkar S, Sarrias MR, Sarwal MM, Sasakawa C, Sasaki M, Sass M, Sato K, Sato M, Satriano J, Savaraj N, Saveljeva S, Schaefer L, Schaible UE, Scharl M, Schatzl HM, Schekman R, Scheper W, Schiavi A, Schipper HM, Schmeisser H, Schmidt J, Schmitz I, Schneider BE, Schneider EM, Schneider JL, Schon EA, Schönenberger MJ, Schönthal AH, Schorderet DF, Schröder B, Schuck S, Schulze RJ, Schwarten M, Schwarz TL, Sciarretta S, Scotto K, Scovassi AI, Screaton RA, Screen M, Seca H, Sedej S, Segatori L, Segev N, Seglen PO, Seguí-Simarro JM, Segura-Aguilar J, Seki E, Sell C, Seiliez I, Semenkovich CF, Semenza GL, Sen U, Serra AL, Serrano-Puebla A, Sesaki H, Setoguchi T, Settembre C, Shacka JJ, Shajahan-Haq AN, Shapiro IM, Sharma S, She H, Shen CK, Shen CC, Shen HM, Shen S, Shen W, Sheng R, Sheng X, Sheng ZH, Shepherd TG, Shi J, Shi Q, Shi Q, Shi Y, Shibutani S, Shibuya K, Shidoji Y, Shieh JJ, Shih CM, Shimada Y, Shimizu S, Shin DW, Shinohara ML, Shintani M, Shintani T, Shioi T, Shirabe K, Shiri-Sverdlov R, Shirihai O, Shore GC, Shu CW, Shukla D, Sibirny AA, Sica V, Sigurdson CJ, Sigurdsson EM, Sijwali PS, Sikorska B, Silveira WA, Silvente-Poirot S, Silverman GA, Simak J, Simmet T, Simon AK, Simon HU, Simone C, Simons M, Simonsen A, Singh R, Singh SV, Singh SK, Sinha D, Sinha S, Sinicrope FA, Sirko A, Sirohi K, Sishi BJ, Sittler A, Siu PM, Sivridis E, Skwarska A, Slack R, Slaninová I, Slavov N, Smaili SS, Smalley KS, Smith DR, Soenen SJ, Soleimanpour SA, Solhaug A, Somasundaram K, Son JH, Sonawane A, Song C, Song F, Song HK, Song JX, Song W, Soo KY, Sood AK, Soong TW, Soontornniyomkij V, Sorice M, Sotgia F, Soto-Pantoja DR, Sotthibundhu A, Sousa MJ, Spaink HP, Span PN, Spang A, Sparks JD, Speck PG, Spector SA, Spies CD, Springer W, Clair DS, Stacchiotti A, Staels B, Stang MT, Starczynowski DT, Starokadomskyy P, Steegborn C, Steele JW, Stefanis L, Steffan J, Stellrecht CM, Stenmark H, Stepkowski TM, Stern ST, Stevens C, Stockwell BR, Stoka V, Storchova Z, Stork B, Stratoulias V, Stravopodis DJ, Strnad P, Strohecker AM, Ström AL, Stromhaug P, Stulik J, Su YX, Su Z, Subauste CS, Subramaniam S, Sue CM, Suh SW, Sui X, Sukseree S, Sulzer D, Sun FL, Sun J, Sun J, Sun SY, Sun Y, Sun Y, Sun Y, Sundaramoorthy V, Sung J, Suzuki H, Suzuki K, Suzuki N, Suzuki T, Suzuki YJ, Swanson MS, Swanton C, Swärd K, Swarup G, Sweeney ST, Sylvester PW, Szatmari Z, Szegezdi E, Szlosarek PW, Taegtmeyer H, Tafani M, Taillebourg E, Tait SW, Takacs-Vellai K, Takahashi Y, Takáts S, Takemura G, Takigawa N, Talbot NJ, Tamagno E, Tamburini J, Tan CP, Tan L, Tan ML, Tan M, Tan YJ, Tanaka K, Tanaka M, Tang D, Tang D, Tang G, Tanida I, Tanji K, Tannous BA, Tapia JA, Tasset-Cuevas I, Tatar M, Tavassoly I, Tavernarakis N, Taylor A, Taylor GS, Taylor GA, Taylor JP, Taylor MJ, Tchetina EV, Tee AR, Teixeira-Clerc F, Telang S, Tencomnao T, Teng BB, Teng RJ, Terro F, Tettamanti G, Theiss AL, Theron AE, Thomas KJ, Thomé MP, Thomes PG, Thorburn A, Thorner J, Thum T, Thumm M, Thurston TL, Tian L, Till A, Ting JP, Titorenko VI, Toker L, Toldo S, Tooze SA, Topisirovic I, Torgersen ML, Torosantucci L, Torriglia A, Torrisi MR, Tournier C, Towns R, Trajkovic V, Travassos LH, Triola G, Tripathi DN, Trisciuoglio D, Troncoso R, Trougakos IP, Truttmann AC, Tsai KJ, Tschan MP, Tseng YH, Tsukuba T, Tsung A, Tsvetkov AS, Tu S, Tuan HY, Tucci M, Tumbarello DA, Turk B, Turk V, Turner RF, Tveita AA, Tyagi SC, Ubukata M, Uchiyama Y, Udelnow A, Ueno T, Umekawa M, Umemiya-Shirafuji R, Underwood BR, Ungermann C, Ureshino RP, Ushioda R, Uversky VN, Uzcátegui NL, Vaccari T, Vaccaro MI, Váchová L, Vakifahmetoglu-Norberg H, Valdor R, Valente EM, Vallette F, Valverde AM, Van den Berghe G, Van Den Bosch L, van den Brink GR, van der Goot FG, van der Klei IJ, van der Laan LJ, van Doorn WG, van Egmond M, van Golen KL, Van Kaer L, van Lookeren Campagne M, Vandenabeele P, Vandenberghe W, Vanhorebeek I, Varela-Nieto I, Vasconcelos MH, Vasko R, Vavvas DG, Vega-Naredo I, Velasco G, Velentzas AD, Velentzas PD, Vellai T, Vellenga E, Vendelbo MH, Venkatachalam K, Ventura N, Ventura S, Veras PS, Verdier M, Vertessy BG, Viale A, Vidal M, Vieira HL, Vierstra RD, Vigneswaran N, Vij N, Vila M, Villar M, Villar VH, Villarroya J, Vindis C, Viola G, Viscomi MT, Vitale G, Vogl DT, Voitsekhovskaja OV, von Haefen C, von Schwarzenberg K, Voth DE, Vouret-Craviari V, Vuori K, Vyas JM, Waeber C, Walker CL, Walker MJ, Walter J, Wan L, Wan X, Wang B, Wang C, Wang CY, Wang C, Wang C, Wang C, Wang D, Wang F, Wang F, Wang G, Wang HJ, Wang H, Wang HG, Wang H, Wang HD, Wang J, Wang J, Wang M, Wang MQ, Wang PY, Wang P, Wang RC, Wang S, Wang TF, Wang X, Wang XJ, Wang XW, Wang X, Wang X, Wang Y, Wang Y, Wang Y, Wang YJ, Wang Y, Wang Y, Wang YT, Wang Y, Wang ZN, Wappner P, Ward C, Ward DM, Warnes G, Watada H, Watanabe Y, Watase K, Weaver TE, Weekes CD, Wei J, Weide T, Weihl CC, Weindl G, Weis SN, Wen L, Wen X, Wen Y, Westermann B, Weyand CM, White AR, White E, Whitton JL, Whitworth AJ, Wiels J, Wild F, Wildenberg ME, Wileman T, Wilkinson DS, Wilkinson S, Willbold D, Williams C, Williams K, Williamson PR, Winklhofer KF, Witkin SS, Wohlgemuth SE, Wollert T, Wolvetang EJ, Wong E, Wong GW, Wong RW, Wong VK, Woodcock EA, Wright KL, Wu C, Wu D, Wu GS, Wu J, Wu J, Wu M, Wu M, Wu S, Wu WK, Wu Y, Wu Z, Xavier CP, Xavier RJ, Xia GX, Xia T, Xia W, Xia Y, Xiao H, Xiao J, Xiao S, Xiao W, Xie CM, Xie Z, Xie Z, Xilouri M, Xiong Y, Xu C, Xu C, Xu F, Xu H, Xu H, Xu J, Xu J, Xu J, Xu L, Xu X, Xu Y, Xu Y, Xu ZX, Xu Z, Xue Y, Yamada T, Yamamoto A, Yamanaka K, Yamashina S, Yamashiro S, Yan B, Yan B, Yan X, Yan Z, Yanagi Y, Yang DS, Yang JM, Yang L, Yang M, Yang PM, Yang P, Yang Q, Yang W, Yang WY, Yang X, Yang Y, Yang Y, Yang Z, Yang Z, Yao MC, Yao PJ, Yao X, Yao Z, Yao Z, Yasui LS, Ye M, Yedvobnick B, Yeganeh B, Yeh ES, Yeyati PL, Yi F, Yi L, Yin XM, Yip CK, Yoo YM, Yoo YH, Yoon SY, Yoshida K, Yoshimori T, Young KH, Yu H, Yu JJ, Yu JT, Yu J, Yu L, Yu WH, Yu XF, Yu Z, Yuan J, Yuan ZM, Yue BY, Yue J, Yue Z, Zacks DN, Zacksenhaus E, Zaffaroni N, Zaglia T, Zakeri Z, Zecchini V, Zeng J, Zeng M, Zeng Q, Zervos AS, Zhang DD, Zhang F, Zhang G, Zhang GC, Zhang H, Zhang H, Zhang H, Zhang H, Zhang J, Zhang J, Zhang J, Zhang J, Zhang JP, Zhang L, Zhang L, Zhang L, Zhang L, Zhang MY, Zhang X, Zhang XD, Zhang Y, Zhang Y, Zhang Y, Zhang Y, Zhang Y, Zhao M, Zhao WL, Zhao X, Zhao YG, Zhao Y, Zhao Y, Zhao YX, Zhao Z, Zhao ZJ, Zheng D, Zheng XL, Zheng X, Zhivotovsky B, Zhong Q, Zhou GZ, Zhou G, Zhou H, Zhou SF, Zhou XJ, Zhu H, Zhu H, Zhu WG, Zhu W, Zhu XF, Zhu Y, Zhuang SM, Zhuang X, Ziparo E, Zois CE, Zoladek T, Zong WX, Zorzano A, and Zughaier SM
Subjects: Animals, Biological Assay methods, Computer Simulation, Humans, Autophagy physiology, Biological Assay standards
Published: 2016
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31. Suppression of autophagy dysregulates the antioxidant response and causes premature senescence of melanocytes.

Author: Zhang CF, Gruber F, Ni C, Mildner M, Koenig U, Karner S, Barresi C, Rossiter H, Narzt MS, Nagelreiter IM, Larue L, Tobin DJ, Eckhart L, and Tschachler E
Subjects: Aging, Premature metabolism, Animals, Autophagy-Related Protein 7, Cell Proliferation physiology, Cells, Cultured, Homeostasis physiology, Humans, In Vitro Techniques, Lipid Peroxidation physiology, Melanins metabolism, Mice, Mice, Knockout, Microtubule-Associated Proteins deficiency, Microtubule-Associated Proteins genetics, Microtubule-Associated Proteins metabolism, Models, Animal, NF-E2-Related Factor 2 metabolism, Reactive Oxygen Species metabolism, Aging, Premature physiopathology, Antioxidants metabolism, Autophagy physiology, Cellular Senescence physiology, Melanocytes metabolism, Melanocytes pathology
Abstract: Autophagy is the central cellular mechanism for delivering organelles and cytoplasm to lysosomes for degradation and recycling of their molecular components. To determine the contribution of autophagy to melanocyte (MC) biology, we inactivated the essential autophagy gene Atg7 specifically in MCs using the Cre-loxP system. This gene deletion efficiently suppressed a key step in autophagy, lipidation of microtubule-associated protein 1 light chain 3 beta (LC3), in MCs and induced slight hypopigmentation of the epidermis in mice. The melanin content of hair was decreased by 10-15% in mice with autophagy-deficient MC as compared with control animals. When cultured in vitro, MCs from mutant and control mice produced equal amounts of melanin per cell. However, Atg7-deficient MCs entered into premature growth arrest and accumulated reactive oxygen species (ROS) damage, ubiquitinated proteins, and the multi-functional adapter protein SQSTM1/p62. Moreover, nuclear factor erythroid 2-related factor 2 (Nrf2)-dependent expression of NAD(P)H dehydrogenase, quinone 1, and glutathione S-transferase Mu 1 was increased, indicating a contribution of autophagy to redox homeostasis in MCs. In summary, the results of our study suggest that Atg7-dependent autophagy is dispensable for melanogenesis but necessary for achieving the full proliferative capacity of MCs.
Published: 2015
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32. Autophagy facilitates secretion and protects against degeneration of the Harderian gland.

Author: Koenig U, Fobker M, Lengauer B, Brandstetter M, Resch GP, Gröger M, Plenz G, Pammer J, Barresi C, Hartmann C, and Rossiter H
Subjects: Animals, Cell Nucleus metabolism, Epithelial Cells cytology, Epithelial Cells metabolism, Harderian Gland drug effects, Lysosomes pathology, Mice, Proteasome Inhibitors metabolism, Vacuoles metabolism, Autophagy physiology, Harderian Gland metabolism, Lysosomes metabolism
Abstract: The epithelial derived Harderian gland consists of 2 types of secretory cells. The more numerous type A cells are responsible for the secretion of lipid droplets, while type B cells produce dark granules of multilamellar bodies. The process of autophagy is constitutively active in the Harderian gland, as confirmed by our analysis of LC3 processing in GFP-LC3 transgenic mice. This process is compromised by epithelial deletion of Atg7. Morphologically, the Atg7 mutant glands are hypotrophic and degenerated, with highly vacuolated cells and pyknotic nuclei. The mutant glands accumulate lipid droplets coated with PLIN2 (perilipin 2) and contain deposits of cholesterol, ubiquitinated proteins, SQSTM1/p62 (sequestosome 1) positive aggregates and other metabolic products such as porphyrin. Immunofluorescence stainings show that distinct cells strongly aggregate both proteins and lipids. Electron microscopy of the Harderian glands reveals that its organized structure is compromised, and the presence of large intracellular lipid droplets and heterologous aggregates. We attribute the occurrence of large vacuoles to a malfunction in the formation of multilamellar bodies found in the less abundant type B Harderian gland cells. This defect causes the formation of large tertiary lysosomes of heterologous content and is accompanied by the generation of tight lamellar stacks of endoplasmic reticulum in a pseudo-crystalline form. To test the hypothesis that lipid and protein accumulation is the cause for the degeneration in autophagy-deficient Harderian glands, epithelial cells were treated with a combination of the proteasome inhibitor and free fatty acids, to induce aggregation of misfolded proteins and lipid accumulation, respectively. The results show that lipid accumulation indeed enhanced the toxicity of misfolded proteins and that this was even more pronounced in autophagy-deficient cells. Thus, we conclude autophagy controls protein and lipid catabolism and anabolism to facilitate bulk production of secretory vesicles of the Harderian gland.
Published: 2015
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33. Management of a metastasized high grade insulinoma (G3) with refractory hypoglycemia: case report and review of the literature.

Author: Scharf M, Mueller D, Koenig U, Pfestroff A, Nimphius W, Figiel J, Rinke A, Koenig A, and Gress T
Subjects: Antineoplastic Combined Chemotherapy Protocols therapeutic use, Combined Modality Therapy, Fatal Outcome, Humans, Hypoglycemia etiology, Insulin metabolism, Insulinoma complications, Insulinoma surgery, Ki-67 Antigen analysis, Liver Neoplasms secondary, Liver Neoplasms surgery, Male, Middle Aged, Pancreatectomy, Pancreatic Neoplasms complications, Pancreatic Neoplasms surgery, Splenectomy, Hypoglycemia therapy, Insulinoma therapy, Pancreatic Neoplasms therapy
Abstract: Insulinomas represent the most common functional neuroendocrine tumor of the pancreas. They are usually solitary, benign, well differentiated (G1/G2) and curable by surgery. We describe the case of a 45 year old male Caucasian with a unique malignant, metastasized pancreatic insulinoma (Ki 67 of 70%, G3). To control excessive insulin production emanating in refractory hypoglycemia and growth of the highly proliferating tumor a multimodal therapeutic approach including the consecutive use of tumor debulking surgery, chemotherapy, TACE, SIRT, PRRT as well as a drug therapy with diazoxide, somatostatin analogs and everolimus was employed. Chemotherapy with carboplatin/etoposide plus everolimus provided the longest normoglycemic period. After progress chemotherapy with dacarbazine had the most positive effect, while debulking approaches such as surgery and liver directed therapies, as well as PRRT were less efficient with only transient success., (Copyright © 2014 IAP and EPC. Published by Elsevier B.V. All rights reserved.)
Published: 2014
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34. Unexpected Multidrug Resistance of Methicillin-Resistant Staphylococcus aureus in Urine Samples: A Single-Center Study.

Author: Lunacek A, Koenig U, Mrstik C, Radmayr C, Horninger W, and Plas E
Abstract: Purpose: Infections of methicillin-resistant Staphylococcus aureus (MRSA) are becoming an increasingly concerning clinical problem. The aim of this study was to assess the development of MRSA in urine cultures in a major public university-affiliated hospital and the therapeutical and hygiene-related possibilities for reducing resistance., Materials and Methods: This study included 243 samples from patients diagnosed with MRSA infection over a period of 6 years. An agar diffusion test measured the effects of antimicrobial agents against bacteria grown in culture. The analyses were based on the guidelines of the Clinical and Laboratory Standards Institute., Results: A regression analysis was performed, which showed 100% resistance to the following antibiotics throughout the entire testing period: carbapenem, cephalosporin (1st-4th generation), penicillin G, aminopenicillin, β-lactamase, and isoxazolyl penicillin. However, a significant decrease in resistance was found for amikacin, gentamicin, clindamycin, levofloxacin, erythromycin, and mupirocin., Conclusions: MRSA showed a decreasing trend of antimicrobial resistance, except against carbapenem, cephalosporin (1st-4th generation), penicillin G, aminopenicillin, β-lactamase, and isoxazolyl penicillin, for which complete resistance was observed.
Published: 2014
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35. Aldehyde dehydrogenase 1A3 is transcriptionally activated by all-trans-retinoic acid in human epidermal keratinocytes.

Author: Koenig U, Amatschek S, Mildner M, Eckhart L, and Tschachler E
Subjects: Cells, Cultured, Epidermal Cells, Humans, Keratinocytes drug effects, Transcription, Genetic, Tretinoin pharmacology, Aldehyde Dehydrogenase genetics, Epidermis enzymology, Gene Expression Regulation, Enzymologic, Keratinocytes enzymology, Transcriptional Activation, Tretinoin metabolism
Abstract: Retinoids are regulators of keratinocyte differentiation in the epidermis and important therapeutics in dermatology. The formation of the most active retinoid, all-trans-retinoic acid (RA) by oxidation of retinal is catalyzed by aldehyde dehydrogenases (ALDH), of which ALDH1A3 has been shown to be most efficient. Here we investigated the expression of ALDH1A3 in epidermal cultures. Three alternatively spliced mRNAs of ALDH1A3 were detected in skin cultures with the conventionally spliced mRNA being predominant. Among a panel of ALDH genes, only ALDH1A3 was upregulated by RA in primary keratinocytes. RA increased the expression of ALDH1A3 also in organotypic human skin cultures and in an epidermal explant in vitro whereas no upregulation was detected in dermal fibroblasts and HeLa cells. Our results indicate that the regulation of the retinoic acid metabolism in the epidermis involves transcriptional activation of ALDH1A3, possibly representing a positive feedback loop, which enhances the effect of exogenous RA., (Copyright © 2010 Elsevier Inc. All rights reserved.)
Published: 2010
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36. The colposcopic feature ridge sign is associated with the presence of cervical intraepithelial neoplasia 2/3 and human papillomavirus 16 in young women.

Author: Scheungraber C, Koenig U, Fechtel B, Kuehne-Heid R, Duerst M, and Schneider A
Subjects: Adolescent, Adult, Aged, Female, Humans, Middle Aged, Neoplasm Invasiveness, Observer Variation, Reproducibility of Results, Retrospective Studies, Sensitivity and Specificity, Uterine Cervical Neoplasms virology, Uterine Cervical Dysplasia virology, Colposcopy, Human papillomavirus 16, Papillomavirus Infections pathology, Uterine Cervical Neoplasms pathology, Uterine Cervical Dysplasia pathology
Abstract: Objective: Interobserver and intraobserver correlation between the colposcopic phenomenon ridge sign and its association with cervical intraepithelial neoplasia (CIN) 2 or 3, with a specific human papillomavirus (HPV) type, and with the age of the patient., Study Design: Colpophotographs, cervical smears, and histologic results of punch or cone biopsies of 592 patients were evaluated. Colpophotographs were analyzed retrospectively for the presence or absence of an opaque acetowhite ridge at the squamocolumnar junction (ridge sign) by 3 gynecologists of different experience., Results: Interobserver reliability for colposcopic grading of CIN was between 18.2% and 82.3%. Concerning the ridge sign, interobserver agreement varied between 25.3% and 49.4% according to the observers' experience, and intraobserver reliability varied between 56.4% and 67.5% (Cohen kappa=0.310-0.469). In 83 (14.0%) of 592 patients, a ridge sign was diagnosed by the most experienced investigator. Cervical intraepithelial neoplasia 2 or 3 was confirmed histologically in 53 of these 83 women (63.8%). Sensitivity of ridge sign for detection of CIN 2 or 3 was 33.1%; specificity was 93.1%. Women with ridge sign were significantly younger than women with no ridge sign (p< .001). Ridge sign was associated with the presence of HPV 16 (p< .001)., Conclusion: Ridge sign is a highly specific marker for CIN 2 or 3 and associated with HPV 16 and young age.
Published: 2009
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37. A Slicer-independent role for Argonaute 2 in hematopoiesis and the microRNA pathway.

Author: O'Carroll D, Mecklenbrauker I, Das PP, Santana A, Koenig U, Enright AJ, Miska EA, and Tarakhovsky A
Subjects: Animals, Argonaute Proteins, B-Lymphocytes cytology, B-Lymphocytes metabolism, Cell Line, Erythroblasts cytology, Erythroblasts metabolism, Erythropoiesis genetics, Erythropoiesis physiology, Eukaryotic Initiation Factor-2 deficiency, Eukaryotic Initiation Factor-2 genetics, Gene Expression Regulation, Developmental, Hematopoiesis genetics, In Vitro Techniques, Lymphopoiesis genetics, Lymphopoiesis physiology, Mice, Mice, Inbred C57BL, Mice, Knockout, MicroRNAs genetics, Eukaryotic Initiation Factor-2 physiology, Hematopoiesis physiology, MicroRNAs metabolism
Abstract: Binding of microRNA (miRNA) to mRNA within the RNA-induced silencing complex (RISC) leads to either translational inhibition or to destruction of the target mRNA. Both of these functions are executed by Argonaute 2 (Ago2). Using hematopoiesis in mice as a model system to study the physiological function of Ago2 in vivo, we found that Ago2 controls early development of lymphoid and erythroid cells. We show that the unique and defining feature of Ago2, the Slicer endonuclease activity, is dispensable for hematopoiesis. Instead, we identified Ago2 as a key regulator of miRNA homeostasis. Deficiency in Ago2 impairs miRNA biogenesis from precursor-miRNAs followed by a reduction in miRNA expression levels. Collectively, our data identify Ago2 as a highly specialized member of the Argonaute family with an essential nonredundant Slicer-independent function within the mammalian miRNA pathway.
Published: 2007
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38. Aberrant expression of caspase-14 in epithelial tumors.

Author: Koenig U, Sommergruber W, and Lippens S
Subjects: Alternative Splicing, Animals, Apoptosis, Blotting, Western, Carcinoma, Squamous Cell enzymology, Caspase 14, Caspases genetics, Cell Differentiation, Cell Line, Tumor, DNA Primers chemistry, DNA, Complementary metabolism, Gene Silencing, Humans, Immunohistochemistry, Keratin-1, Keratin-10, Keratins biosynthesis, Microscopy, Fluorescence, Mutation, Necrosis, Polymerase Chain Reaction, Skin Neoplasms enzymology, Tissue Distribution, Caspases biosynthesis, Gene Expression Regulation, Neoplastic, Neoplasms, Glandular and Epithelial enzymology
Abstract: Cysteine-dependent aspartate-specific proteases (caspases) are the cellular executors of apoptosis. Caspase-14 is the most divergent member of the family of mammalian caspases and displays a variety of unique characteristics. It is expressed in a limited number of tissues and has the shortest amino acid sequence within the caspase protein family. During induction of apoptosis, it is not processed, whereas terminal differentiation in skin leads to cleavage of caspase-14. Here we show that 40% of lung squamous cell carcinomas, 22% of breast cancers, and about 80% of cervical carcinomas express caspase-14. Immunohistochemistry reveals that caspase-14 is localized in areas of ongoing differentiation close to necrotic sites but is not strictly associated with the differentiation markers keratin-1/-10. Caspase-14 is neither mutated nor alternatively spliced in the tumors analyzed. Furthermore, caspase-14 is not processed into a small and large subunit, a process critical for the proteolytic activation of known effector caspases. We conclude that conditions exist in tumors leading to re-expression of this normally silent gene.
Published: 2005
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39. Tissue-wide expression profiling using cDNA subtraction and microarrays to identify tumor-specific genes.

Author: Amatschek S, Koenig U, Auer H, Steinlein P, Pacher M, Gruenfelder A, Dekan G, Vogl S, Kubista E, Heider KH, Stratowa C, Schreiber M, and Sommergruber W
Subjects: Adenocarcinoma metabolism, Adenocarcinoma pathology, Breast Neoplasms metabolism, Breast Neoplasms pathology, Carcinoma, Renal Cell metabolism, Carcinoma, Renal Cell pathology, Carcinoma, Squamous Cell metabolism, Carcinoma, Squamous Cell pathology, Cluster Analysis, Gene Expression Profiling, Humans, Kidney Neoplasms metabolism, Kidney Neoplasms pathology, Lung Neoplasms metabolism, Lung Neoplasms pathology, Neoplasm Staging, Nucleic Acid Hybridization, Oligonucleotide Array Sequence Analysis, RNA, Neoplasm genetics, RNA, Neoplasm isolation & purification, Reverse Transcriptase Polymerase Chain Reaction, Survival Rate, Adenocarcinoma genetics, Breast Neoplasms genetics, Carcinoma, Renal Cell genetics, Carcinoma, Squamous Cell genetics, Kidney Neoplasms genetics, Lung Neoplasms genetics
Abstract: With the objective of discovering novel putative intervention sites for anticancer therapy, we compared transcriptional profiles of breast cancer, lung squamous cell cancer (LSCC), lung adenocarcinoma (LAC), and renal cell cancer (RCC). Each of these tumor types still needs improvement in medical treatment. Our intention was to search for genes not only highly expressed in the majority of patient samples but which also exhibit very low or even absence of expression in a comprehensive panel of 16 critical (vital) normal tissues. To achieve this goal, we combined two powerful technologies, PCR-based cDNA subtraction and cDNA microarrays. Seven subtractive libraries consisting of approximately 9250 clones were established and enriched for tumor-specific transcripts. These clones, together with approximately 1750 additional tumor-relevant genes, were used for cDNA microarray preparation. Hybridizations were performed using a pool of 16 critical normal tissues as a reference in all experiments. In total, we analyzed 20 samples of breast cancer, 11 of LSCC, 11 of LAC, and 8 of RCC. To select for genes with low or even no expression in normal tissues, expression profiles of 22 different normal tissues were additionally analyzed. Importantly, this tissue-wide expression profiling allowed us to eliminate genes, which exhibit also high expression in normal tissues. Similarly, expression signatures of genes, which are derived from infiltrating cells of the immune system, were eliminated as well. Cluster analysis resulted in the identification of 527 expressed sequence tags specifically up-regulated in these tumors. Gene-wise hierarchical clustering of these clones clearly separated the different tumor types with RCC exhibiting the most homogeneous and LAC the most diverse expression profile. In addition to already known tumor-associated genes, the majority of identified genes have not yet been brought into context with tumorigenesis such as genes involved in bone matrix mineralization (OSN, OPN, and OSF-2) in lung, breast, and kidney cancer or genes controlling Ca(2+) homeostasis (RCN1,CALCA, S100 protein family). EGLN3, which recently has been shown to be involved in regulation of hypoxia-inducible factor, was found to be highly up-regulated in all RCCs and in half of the LSCCs analyzed. Furthermore, 42 genes, the expression level of which correlated with the overall survival of breast cancer patients, were identified. The gene dendogram clearly separates two groups of genes, those up-regulated such as cyclin B1, TGF-beta 3, B-Myb, Erg2, VCAM-1, and CD44 and those down-regulated such as MIG-6, Esp15, and CAK in patients with short survival time.
Published: 2004
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40. Human caspase 12 has acquired deleterious mutations.

Author: Fischer H, Koenig U, Eckhart L, and Tschachler E
Subjects: Alternative Splicing, Amino Acid Sequence, Animals, Caspase 12, Caspases biosynthesis, Chromosomes, Human, Pair 11, Humans, Mice, Molecular Sequence Data, RNA, Messenger biosynthesis, Sequence Alignment, Sequence Homology, Nucleic Acid, Tissue Distribution, Caspases genetics, Mutation
Abstract: Caspase 12 has been cloned from rodent cells, in which it mediated apoptosis in response to endoplasmic reticulum stress. Based on experiments with murine cells it was suggested that this caspase plays a central role in the pathogenesis of Alzheimer's disease. By alignment of the murine caspase 12 cDNA with the human genome sequence we localized the human caspase 12 gene at a single locus within the caspase 1/ICE gene cluster on chromosome 11q22.3. RT-PCR and molecular cloning revealed that nine alternatively spliced transcripts of this gene are expressed. A frame shift mutation and a premature stop codon which is present in all splice variants preclude the expression of a full length protein. An additional loss-of-function mutation within the SHG box, a critical site in caspases, prohibits any proteins, if they are produced, from acting catalytically. Based on our data we conclude that functional caspase 12 is lost in humans and that it can therefore not play a role in Alzheimer's disease., (Copyright 2002 Elsevier Science (USA).)
Published: 2002
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41. Evidence that caspase-13 is not a human but a bovine gene.

Author: Koenig U, Eckhart L, and Tschachler E
Subjects: Alternative Splicing, Amino Acid Sequence, Animals, Base Sequence, Cattle, Cloning, Molecular, DNA, Complementary genetics, DNA, Complementary isolation & purification, Expressed Sequence Tags, Humans, Isoenzymes genetics, Leukocytes, Mononuclear chemistry, Molecular Sequence Data, RNA, Messenger genetics, Reproducibility of Results, Reverse Transcriptase Polymerase Chain Reaction, Sequence Analysis, DNA, Sequence Homology, Species Specificity, Caspases genetics
Abstract: Caspase-13 was reported to be a member of the human caspase family of proteases (Humke, E., et al., J. Biol. Chem. 273, 15702-15707, 1998). By contrast, a recent study (Lin, X., et al., J. Biol. Chem. 275, 39920-39926, 2000) could not confirm caspase-13 expression in human tissues. When we searched the GenBank database we found several expressed sequence tags (ESTs) from bos taurus completely matching the published caspase-13 sequence. Reverse transcription polymerase chain reaction (RT-PCR) analysis revealed that bovine but not human peripheral blood mononuclear cells express caspase-13. From these cells we cloned two bovine caspase-13 splice variants and found that the sequence of the larger variant was identical to the mRNA published by Humke et al. Our findings strongly suggest that the previously published caspase-13 sequence is not of human origin but represents a bovine gene., (Copyright 2001 Academic Press.)
Published: 2001
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42. A technical solution for secondary arthritis due to chronic proximal tibiofibular joint instability.

Author: Yaniv M, Koenig U, and Imhoff AB
Subjects: Arthritis surgery, Chronic Disease, Fascia Lata transplantation, Fibula surgery, Humans, Internal Fixators, Joint Instability surgery, Ligaments, Articular surgery, Male, Middle Aged, Tendons transplantation, Tibia surgery, Arthritis etiology, Fibula pathology, Joint Instability complications, Tibia pathology
Abstract: Chronic instability of the proximal tibiofibular joint is an uncommon diagnosis and not frequently reported in the literature. The management options of this joint instability, complicated with secondary arthritis, have rarely been discussed and consist mainly of fibular head resection or arthrodesis of this joint. We describe a new technical procedure for addressing both the instability and the joint secondary arthritis. Stability of the joint is achieved by ligament reconstruction using a biceps femoris split passed through the tibial metaphysis and fixated back to the fibular head using bone anchors. The arthritic changes are addressed by interposition of a vascularized fascia lata strip. The described procedure offers a firm stabilization with no need for postoperative restrictions and an alternative to the inadvisable joint arthrodesis or resection.
Published: 1999
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43. Sero-immunological investigations in patients with cervical cancer: higher rate of HSV-2 antibodies than in syphilis patients and evidence of IgM antibodies to an early HSV-1 antigen.

Author: Schneweis KE, Haag A, Lehmköster A, and Koenig U
Subjects: Adult, Age Factors, Antibodies, Bacterial analysis, Complement Fixation Tests, Female, Fluorescent Antibody Technique, Humans, Male, Middle Aged, Neutralization Tests, Treponema pallidum immunology, Antibodies, Viral analysis, Antigens, Viral, Immunoglobulin M analysis, Simplexvirus immunology, Syphilis immunology, Uterine Cervical Neoplasms immunology
Published: 1975

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