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ObjectiveTo assess the prevalence of depression, anxiety, insomnia, and somatic symptom disorder (SSD) in patients with benign and malignant sinonasal tumors.Materials and methodsPretreatment patients with sinonasal tumors were prospectively recruited on the rhinology ward of a tertiary hospital from July 2021 to March 2022. The electronic questionnaire which contains the rhinological symptom scale, the 22-item Sinonasal Outcome Test (SNOT-22) Scale, the Patient Health Questionnaire-9 (PHQ-9), the Generalized Anxiety Disorder-7 (GAD-7), the Insomnia Severity Index (ISI), and the Patient Health Questionnaire-15 (PHQ-15) was filled out by patients at admission. The associations between the scores of symptom/SNOT-22 and psychometric tests were assessed by the Pearson correlation coefficient (r) and simple linear regression. The receiver operating characteristic (ROC) analysis was used to evaluate the performance of the SNOT-22 score in predicting psychiatric disorders.ResultsThirteen patients with benign sinonasal tumors and 15 patients with malignant sinonasal tumors were recruited. The benign and malignant groups did not differ significantly regarding symptomatology and mental wellbeing. Of the total patients, 9 were at risk of depression (PHQ-9 > 4), 10 were at risk of anxiety (GAD-7 > 4), 11 were at risk of insomnia (ISI > 7), and 11 were at risk of SSD (PHQ-15 > 4). The overall symptom, facial pain/pressure, postnasal drip, and SNOT-22 scores were positively associated with scores of psychometric tests. Patients with a high SNOT-22 score (>18) are likely to be affected by comorbid psychiatric disorders. When interpreting the results of this study, it should be noted that screening tools, not diagnostic tools, were used to identify psychiatric risk.ConclusionDepression, anxiety, insomnia, and SSD are prevalent in patients with sinonasal tumors. Otolaryngologists should have a low threshold to ask the patient about psychiatric symptoms, especially for patients with an SNOT-22 score > 18.

Abstract. Monkeypox is usually considered as a zoonosis caused by monkeypox virus with potential threat to public health in the post–smallpox era. The recent outbreak of monkeypox began in May 7, 2022, and has been found in many countries out of Africa. The World Health Organization declared that this endemic is an “atypical” phenomenon with definite human-to-human transmission. To understand the situation more clearly, this review briefly summarizes the epidemiologic and clinical characteristics of the disease and highlights the clinical management and preventive strategies.

Abstract Systemic autoinflammatory diseases (SAIDs) are a group of monogenic diseases characterized by disordered innate immunity, which causes excessive activation of inflammatory pathways. Nucleotide-binding leucine-rich repeat-containing receptor 12-related autoinflammatory disease (NLRP12-AID) is a newly identified SAID and a rare autosomal dominant disorder caused by mutations in the NLRP12 gene, which is also known as familial cold autoinflammatory syndrome 2 (FCAS2) and mostly occurs in childhood. A total of 33 cases of NLRP12-AID in children and 21 different mutation types have been reported to date. The disease is mainly characterized by periodic fever, accompanied by multisystem inflammatory damage. NLRP12-AID is diagnosed through early clinical identification and genetic detection. Emerging drugs targeting interleukin-1-related inflammatory pathways are expected to change the treatment options and improve the quality of life of pediatric patients. This article aims to summarize the characteristics and pathogenesis of reported NLRP12-AID cases in children and provide ideas for clinical diagnosis and treatment.

AIM: To examine the clinicopathological characteristics of adult orbital xanthogranulomatous disease(AOXGD). METHODS: From January 2015 to January 2021, the researchers collected postoperative pathological diagnoses cases of AOXGD from Xi'an People's Hospital(Xi'an Fourth Hospital), retrospectively analyzed clinical pathological data, and reviewed related literature. RESULTS: A total of five AOXGD cases were collected, including three cases of adult-onset xanthogranuloma(AOX), one case of necrobiotic xanthogranuloma(NBX), and one case of Erdheim-Chester disease(ECD). The five patients were composed of middle-aged and elderly patients with local orbital lesions were treated. Microscopic examination revealed that the orbital skin and subcutaneous tissue had foam-like non-Langerhans histiocytes that exhibited diffused or nested infiltration. Immunohistochemistry revealed that the cells were positive for CD68, CD163, FXⅢa, lysozyme, negative for S100, CD1a, Langerin, HMB-45, MDM2. One ECD patient had orbital lesions as the first symptom and exhibited a combination of retroperitoneal lesions, right atrium pseudotumor, and long bones, heart, kidney lesions. The diagnosis of AOXGD depends on clinical manifestations and pathological features. The treatment was based on subtypes and clinical manifestations to select corresponding strategies, which mainly include the administration of glucocorticoids, immunosuppressants, and surgical treatment. CONCLUSION: AOXGD is relatively rare in clinical practice. AOXGD can manifest as a local orbital disease or an orbital disease combined with a systemic disease. In the clinical and pathological work of ophthalmology, the understanding and identification of this group of diseases should be strengthened, and correct diagnosis and standard treatment should be promoted.

Abstract. Background:. The scale assessment was helpful in predicting the presence of antibodies to autoimmune encephalitis. This study aimed to evaluate the application of antibody prevalence in Chinese patients with epilepsy and encephalopathy (APE2-CHN) and response to immunotherapy in Chinese patients with epilepsy and encephalopathy (RITE2-CHN) for patients with different neuronal surface antibodies. Methods:. A total of 1365 patients with epileptic seizures as the prominent feature in Xuanwu Hospital, Capital Medical University, from June 2016 to June 2020 were enrolled in our study. Of these, 915 patients with epilepsy of unknown etiology whose serum and/or cerebrospinal fluid samples were examined for autoimmune antibodies were selected. All patients were scored with antibody prevalence in patients with epilepsy and encephalopathy (APE2), response to immunotherapy with epilepsy and encephalopathy (RITE2), APE2-CHN, and RITE2-CHN scores. Results:. Of the 915 patients, 191 patients were positive for neural-surface specific antibodies (115 N-methyl-D-aspartate receptor (NMDAR) Ab, 47 leucine-rich glioma-inactivated protein 1 (LGI1) Ab, 8 contactin-associated protein 2 (CASPR2) Ab, 4 AMPA2R-Ab, and 11 GABAR-B-Ab; 3 CASPR2-Ab and LGI1-Ab, 2 NMDAR-Ab and CASPR2-Ab, and 1 NMDAR-Ab and myelin-oligodendrocyte glycoprotein [MOG] Ab). The sensitivity and specificity of APE2 ≥4 in predicting the presence of neural-surface specific antibodies in our study were 74.35% and 81.77%, respectively, and the sensitivity and specificity of APE2-CHN ≥4 were 75.92% and 84.53%, respectively. Eight cases had an APE2 score

Abstract Background The active components of Dracocephalum moldavica L. (TFDM) can inhibit myocardial ischemia by inhibiting oxidative stress. However, the effects of TFDM on astrocytes have not been investigated in vitro. The current study aimed to explore whether TFDM protects astrocytes against H2O2-induced apoptosis through a mitochondria-dependent pathway. Methods The human glioma cell line U87 was used to investigate the ability of TFDM to protect astrocytes against H2O2-induced apoptosis. The cell counting kit-8 assay and flow cytometry were used to detect cell viability, apoptosis, MMP, Ca2+ influx and reactive oxygen species (ROS). Lactate dehydrogenase (LDH) and malonic dialdehyde (MDA) levels were measured by ELISA. In addition, protein and mRNA expression changes were detected by Western blotting and qRT-PCR. Results TFDM (0.78~200 μg/ml) had limited cytotoxic effects on the viability of U87 cells. Compared with the model group (treated with H2O2 only), cells treated with medium- and high-dose TFDM exhibited reduced MDA concentrations (P

The one-leg stance is frequently used in balance training and rehabilitation programs for various balance disorders. There are some typical one-leg stance postures in Tai Chi (TC) and yoga, which are normally used for improving balance. However, the mechanism is poorly understood. Besides, the differences of one-leg stance postures between TC and yoga in training balance are still unknown. Therefore, the aim of the present study was to investigate cortical activation and rambling and trembling trajectories to elucidate the possible mechanism of improving one-leg stance balance, and compare the postural demands during one-leg stance postures between TC and yoga. Thirty-two healthy young individuals were recruited to perform two TC one-leg stance postures, i.e., right heel kick (RHK) and left lower body and stand on one leg (LSOL), two yoga postures, i.e., one-leg balance and Tree, and normal one-leg standing (OLS). Brain activation in the primary motor cortex, supplementary motor area (SMA), and dorsolateral prefrontal cortex (DLPFC) was measured using functional near-infrared spectroscopy. The center of pressure was simultaneously recorded using a force platform and decomposed into rambling and trembling components. One-way repeated-measures analysis of variance was used for the main effects. The relative concentration changes of oxygenated hemoglobin (ΔHbO) in SMA were significantly higher during RHK, LSOL, and Tree than that during OLS (p < 0.001). RHK (p < 0.001), LSOL (p = 0.003), and Tree (p = 0.006) all showed significantly larger root mean square rambling (RmRMS) than that during OLS in the medial–lateral direction. The right DLPFC activation was significantly greater during the RHK than that during the Tree (p = 0.023), OLB (p < 0.001), and OLS (p = 0.013) postures. In conclusion, the RHK, LSOL, and Tree could be used as training movements for people with impaired balance. Furthermore, the RHK in TC may provide more cognitive training in postural control than Tree and OLB in yoga. Knowledge from this study could be used and implemented in training one-leg stance balance.

AIM: To investigate the clinic opathological features of orbital soft tissue tumors.METHODS: A retrospective analysis of 455 cases of orbital soft tissue tumors in our hospital from 2003-11/2018-11 were performed to observe the clinical features, pathological classification and pathological features of rare tumors.RESULTS:All 455 patients with orbital soft tissue tumors, 421(92.5%)were benign tumors. The top 5 were 258 cases of cavernous hemangioma, 58 cases of capillary hemangioma, 16 cases of neurofibroma, 15 cases of fibroid, and 14 cases of schwannoma; 27 cases(5.9%)of intermediate type, including 23 cases of solitary fibrous tumor(SFT), 2 cases of low-grade malignant fibrous histiocytoma, 2 cases of low-grade mucinous neurofibroma; 7 cases(1.5%)of malignant type, 2 cases of orbital malignant SFT, 2 cases of orbital myeloid sarcoma(MS), mucinous liposarcoma(MLS), spindle cell undifferentiated sarcoma and peripheral primitive neuroectodermal tumor(PNET)1 case. Immunohistochemistry and molecular detection of some cases revealed that the application of new antibodies such as STAT6 and molecular detection techniques can improve the diagnostic accuracy.CONCLUSION:Benign tumors account for the majority of orbital soft tissue tumors. Cavernous hemangioma in vascular tumors is the first, and there are few soft tissue tumor pathological types such as Erdheim-Chester disease(ECD)and granulomatous ossifying fibers. Tumors(POF), leiomyomas and myxomas; intermediate and malignant tumors are rare; pathological types such as SFT, MLS, spindle cell undifferentiated sarcoma and MS are often difficult to diagnose, easy to miss diagnosis and misdiagnosis, new immunity histochemical antibodies and molecular detection techniques can improve the accuracy of the diagnosis.

Our previous study found that mutations in the PTGIS gene contributed high susceptibility to pulmonary arterial hypertension (PAH). We have generated disease-specific induced pluripotent stem cell (iPSC) lines from a PAH patient carrying the heterozygous c.1339 G > A mutation in PTGIS gene. The generated iPSC lines can be differentiated into endothelial cells to investigate the pathogenesis of PAH associated with PTGIS gene, which could provide valuable resources for personalized medicine.

Summary: Ortho-selective aromatic C-H functionalization is frequently used in organic synthesis and chemical/pharmaceutical industries. However, this reaction relies heavily on the use of directing groups suffering from limited substrate scope and extra steps to put on and remove the directing/protecting groups. Herein we present the previously neglected concept that enables good to nearly complete selective ortho position. Proton transfer was utilized to tune the electron density on the aryl ring and determine the positional selectivity of electrophilic substitution. Consistently with deuteration experiments and DFT studies, this work demonstrates that acid-promoted proton transfer directs accelerated ortho-selective halogenation of NH/OH contained aromatic amines/phenols with excellent selectivity (>40 examples; up to 98:2 ortho/para selectivity). The application potential of this Fe-catalyzed method is demonstrated by the convenient synthesis of three alkaloids and tizanidine. This report raises the possibility that proton transfer could serve as the basis of developing new selective C-H functionalization reactions.

Telomerase RNA (hTR) is transcribed as a 3′-extended precursor. Here the authors examine the processing of hTR precursors of various lengths and show that processing occurs in distinct steps involving different nucleases PARN and RRP6.

Background Cardiac fibrosis is a core pathological process associated with heart failure. The recruitment and differentiation of primitive fibroblast precursor cells of bone marrow origin play a critical role in pathological interstitial cardiac fibrosis. The KCa3.1 channels are expressed in both ventricular fibroblasts and circulating mononuclear cells in rats and are upregulated by angiotensin II. We hypothesized that KCa3.1 channels mediate the inflammatory microenvironment in the heart, promoting the infiltrated bone marrow–derived circulating mononuclear cells to differentiate into myofibroblasts, leading to myocardial fibrosis. Methods and Results We established a cardiac fibrosis model in rats by infusing angiotensin II to evaluate the impact of the specific KCa3.1 channel blocker TRAM‐34 on cardiac fibrosis. At the same time, mouse CD4+ T cells and rat circulating mononuclear cells were separated to investigate the underlying mechanism of the TRAM‐34 anti–cardiac fibrosis effect. TRAM‐34 significantly attenuated cardiac fibrosis and the inflammatory reaction and reduced the number of fibroblast precursor cells and myofibroblasts. Inhibition of KCa3.1 channels suppressed angiotensin II–stimulated expression and secretion of interleukin‐4 and interleukin‐13 in CD4+ T cells and interleukin‐4– or interleukin‐13–induced differentiation of monocytes into fibrocytes. Conclusions KCa3.1 channels facilitate myocardial inflammation and the differentiation of bone marrow‐derived monocytes into myofibroblasts in cardiac fibrosis caused by angiotensin II infusion.

Background: Myopathies with rimmed vacuoles are a heterogeneous group of muscle disorders with progressive muscle weakness and varied clinical manifestations but similar features in muscle biopsies. Here, we describe a novel autosomal dominant myopathy with rimmed vacuoles in a large family with 11 patients of three generations affected. Methods: A clinical study including family history, obstetric, pediatric, and development history was recorded. Clinical examinations including physical examination, electromyography (EMG), serum creatine kinase (CK), bone X-rays, and brain magnetic resonance imaging (MRI) were performed in this family. Open muscle biopsies were performed on the proband and his mother. To find the causative gene, the whole-exome sequencing was carried out. Results: Disease onset was from adolescence to adulthood, but the affected patients of the third generation presented an earlier onset and more severe clinical manifestations than the older generations. Clinical features were characterized as dysarthria, dysphagia, external ophthalmoplegia, limb weakness, hypophrenia, deafness, and impaired vision. However, not every patient manifested all symptoms. Serum CK was mildly elevated and EMG indicated a myopathic pattern. Brain MRI showed cerebellum and brain stem mildly atrophy. Rimmed vacuoles and inclusion bodies were observed in muscle biopsy. The whole-exome sequencing was performed, but the causative gene has not been found. Conclusions: We reported a novel autosomal dominant myopathy with rimmed vacuoles characterized by dysarthria, dysphagia, external ophthalmoplegia, limb weakness, hypophrenia, deafness, and impaired vision, but the causative gene has not been found and needs further study.

The non-coding RNA subunit of telomerase provides the template for telomerase activity. In diverse fungi, 3′ end processing of telomerase RNA involves a single cleavage by the spliceosome. Here, we examine how human telomerase RNA (hTR) primary transcripts are processed into the mature form of precisely 451 nt. We find that the splicing inhibitor isoginkgetin mimics the effects of RNA exosome inhibition and causes accumulation of long hTR transcripts. Depletion of exosome components and accessory factors reveals functions for the cap binding complex (CBC) and the nuclear exosome targeting (NEXT) complex in hTR turnover. Whereas longer transcripts are predominantly degraded, shorter precursor RNAs are oligo-adenylated by TRF4-2 and either processed by poly(A)-specific ribonuclease (PARN) or degraded by the exosome. Our results reveal that hTR biogenesis involves a kinetic competition between RNA processing and degradation and suggest treatment options for telomerase insufficiency disorders.

Based on a more practical cognitive radio network with malicious users,the spectrum sharing network model based on the cooperative spectrum sensing was studied that the secondary user can dynamically adjust its transmit power based on cooperative sensing results.To avoid significant reduction in performance of spectrum sensing system caused by malicious nodes,it is aimed to study how to improve the performance of cooperative sensing.By introducing the convex optimization problem,the secondary network throughput is maximized under the certain detection probability conditions and the corresponding power constraints.Simulation results show that whether or not there are malicious nodes,the algorithm is efficient in calculating optimal sensing time and the optimal transmit powers,and the secondary network throughput is increased when the maximum interference power limits and the maximum transmit power restrictions are decreased.

Summary: Successive point-prevalence surveys were conducted annually from 2007 to 2011 to monitor the prevalence of healthcare-associated infections (HAIs) in a university hospital in Hubei Province in China. The surveys used the case definition criteria established by the Ministry of Health of the People's Republic of China. In the 5 surveys, the overall frequency of HAIs was 3.16% (301/9533). No significant differences were identified in the point prevalence measurements of HAIs in any of the years from 2007 to 2011. Of all the cases, proportionally, the most frequent infection site was the respiratory tract (2.34%), followed by surgical sites (0.43%) and urinary tract sites (0.28%). Gram-negative aerobic bacilli were the most common organisms mentioned; the most frequently isolated organism was Pseudomonas aeruginosa, followed by Escherichia coli and Acinetobacter baumannii. Approximately one-half of the patients were receiving antibiotics at the time of the surveys. Cephalosporin, penicillin, and quinolone were most commonly used for treatment or prevention. The differences found in HAI prevalence data across the 5 surveys given in the hospital were not statistically significant. In conclusion, this successive point-prevalence survey provides information about the trend of HAI prevalence, epidemical character, and the use of antibiotics among the university hospital's in-patients. This information allows us to initiate targeted programs for infection prevention and control. Keywords: Healthcare-associated infections, Point-prevalence survey, China

Winter wheat freeze injury is one of the main agro-meteorological disasters affecting wheat production. In order to evaluate the severity of freeze injury on winter wheat systematically, we proposed a grey-system model (GSM) to monitor the degree and the distribution of the winter wheat freeze injury. The model combines remote sensing (RS) and geographic information system (GIS) technology. It gave examples of wheat freeze injury monitoring applications in Gaocheng and Jinzhou of Hebei Province, China. We carried out a quantitative evaluation method study on the severity of winter wheat freeze injury. First, a grey relational analysis (GRA) was conducted. At the same time, the weights of the stressful factors were determined. Then a wheat freezing injury stress multiple factor spatial matrix was constructed using spatial interpolation technology. Finally, a winter wheat freeze damage evaluation model was established through grey clustering algorithm (GCA), and classifying the study area into three sub-areas, affected by severe, medium or light disasters. The evaluation model were verified by the Kappa model, the overall accuracy reached 78.82% and the Kappa coefficient was 0.6754. Therefore, through integration of GSM with RS images as well as GIS analysis, quantitative evaluation and study of winter wheat freeze disasters can be conducted objectively and accurately, making the evaluation model more scientific.

In the present study, new Schiff's base derivatives: (Z)-4-amino-5-(2-(3- fluorobenzylidene)hydrazinyl)-4H-1,2,4-triazole-3-thiol (Y1), (Z)-3-((2-(4-amino-5- mercapto-4H-1,2,4-triazol-3-yl)hydrazono)methyl)phenol (Y2), (Z)-2-((2-(4-amino-5- mercapto-4H-1,2,4-triazol-3-yl)hydrazono)methyl)phenol (Y3) and 3-((Z)-(2-(4- (((E)-3-hydroxybenzylidene)amino)-5-mercapto-4H-1,2,4-triazol-3-yl)hydrazono)methyl)phenol (Y4) were synthesized and their structures were characterized by LC-MS, IR and 1H NMR. The inhibitory effects of these compounds on tyrosinase activites were evaluated. Compounds Y1, Y2 and Y3 showed potent inhibitory effects with respective IC50 value of 12.5, 7.0 and 1.5 μM on the diphenolase activities. Moreover, the inhibition mechanisms were determined to be reversible and mixed types. Interactions of the compounds with tyrosinase were further analyzed by fluorescence quenching, copper interaction, and molecular simulation assays. The results together with the anti-tyrosinase activities data indicated that substitution on the second position of benzene ring showed superior ant-ityrosinase activities than that on third position, and that hydroxyl substitutes were better than fluorine substitutes. In addition, two benzene rings connecting to the triazole ring would produce larger steric hindrance, and affect the bonding between tyrosinase and inhibitors to decrease the inhibitory effects. The anti-tyrosinase effects of these compounds were in contrast to their antioxidant activities. In summary, this research will contribute to the development and design of antityrosinase agents.

BACKGROUND: The pathological mechanism of chronic thromboembolic pulmonary hypertension (CTEPH) is not fully understood, and inflammation has been reported to be one of its etiological factors. IgG regulates systemic inflammatory homeostasis, primarily through its N-glycans. Little is known about IgG N-glycosylation in CTEPH. We aimed to map the IgG N-glycome of CTEPH to provide new insights into its pathogenesis and discover novel markers and therapies. METHODS: We characterized the plasma IgG N-glycome of patients with CTEPH in a discovery cohort and validated our results in an independent validation cohort using matrix-assisted laser desorption/ionization time of flight mass spectrometry. Thereafter, we correlated IgG N-glycans with clinical parameters and circulating inflammatory cytokines in patients with CTEPH. Furthermore, we determined IgG N-glycan quantitative trait loci in CTEPH to reveal partial mechanisms underlying glycan changes. RESULTS: Decreased IgG galactosylation representing a proinflammatory phenotype was found in CTEPH. The distribution of IgG galactosylation showed a strong association with NT-proBNP (N-terminal pro-B-type natriuretic peptide) in CTEPH. In line with the glycomic findings, IgG pro-/anti-inflammatory N-glycans correlated well with a series of inflammatory markers and gene loci that have been reported to be involved in the regulation of these glycans or inflammatory immune responses. CONCLUSIONS: This is the first study to reveal the full signature of the IgG N-glycome of a proinflammatory phenotype and the genes involved in its regulation in CTEPH. Plasma IgG galactosylation may be useful for evaluating the inflammatory state in patients with CTEPH; however, this requires further validation. This study improves our understanding of the mechanisms underlying CTEPH inflammation from the perspective of glycomics. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate keratocyte viability and proinflammatory cytokine secretion induced by HSV-1 infection. Methods: Keratocytes were separated from corneal tissues obtained with the SMILE procedure, and an in vitro system was established to study HSV-1 infection in human keratocytes. Cell viability, HSV-1 genomic DNA copy number, and the expression levels of α-SMA, ALDH1A1, phospho-p38, p38, phospho-IRF3, and IRF3 were evaluated. Antibody array and ELISA kits were used to measure the production of proinflammatory cytokines and chemokines. Results: We found that HSV-1 infection reduced cell viability and activated keratocyte transdifferentiation into corneal fibroblast-like cells. Furthermore, p38 inhibition improved cell viability and IFN-β production and played an anti-inflammatory role by reducing the production of proinflammatory cytokines and chemokines. Conclusions: Our study reveals an important role played by keratocytes during innate immune responses and identifies p38 inhibition as a potential therapeutic approach to control ocular HSV-1 infection. [ABSTRACT FROM AUTHOR]

Cardiovascular complications of type 2 diabetes mellitus (T2DM) are associated with vascular remodeling in the arteries. Perivascular sympathetic neurons release an abundance of trophic factors to regulate vascular function via a paracrine signaling. Netrin-1, a diffusible protein that can be secreted outside the cell, is one of common signals of 'conversation' between nerve and vessel. The present study investigated whether netrin-1 is a novel modulator of sympathetic neurons paracrine signaling and played a critical role in vascular adventitial remodeling under T2DM. Vascular adventitial remodeling was observed in adventitial fibroblasts (AFs) respond ing to netrin-1 deficiency in the supernatant from primary rat superior cervical ganglia (SCG) neurons, shown as AFs proliferation, migration, and collagen deposition. Conditioned medium from the high glucose (HG)-treated SCG neurons contributed to A Fs remodeling, which was effectively alleviated by exogenous netrin-1 supplementation. Further, it was found that uncoordinated-5-B (Unc5b) was mainly expressed in AFs among netrin-1 specific receptors. Treatment of netrin-1 inhibited H2O2 production derived from NADPH oxidase 4 (NOX4) through the UNC5b/CAMP/PKA signal pathway in AFs remodeling. In vivo, aorta adventitial remodeling was accompanied with the downregulation of netrin-1 in the perivascular sympathetic nerve in T2DM rats. Such abnormalities were restored by netrin-1 intervention, which was associated with the inhibition of NOX4 expression in the aorta adventitia. In conclusion, netrin-1 is a novel modulator of sympathetic neurons paracrine signaling to maintain AFs function. Vascular adventit ial remodeling was aggravated by sympathetic neurons paracrine signaling under hyperglycemia, which was ameliorated by netrin-1 treatment through the UNC5b/CAMP/PKA/NOX4 pathway. [ABSTRACT FROM AUTHOR]

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Background: Nonalcoholic steatohepatitis (NASH) is characterized by fat accumulation in the hepatocyte, inflammation, liver cell injury, and varying degrees of fibrosis, and can lead to oxidative stress in liver. Here, we investigated whether Salidroside, a natural phenolic antioxidant product, can protect rat from liver injury during NASH. Methods: NASH model was established by feeding the male SD rats with high-fat and high-cholesterol diet for 14 weeks. Four groups of male SD rats including, normal diet control group, NASH model group, and Salidroside treatment group with150mg/kg and 300 mg/kg respectively, were studied. Salidroside was given by oral administration to NASH in rats from 9 weeks to 14 weeks. At the end of 14 weeks, liver and serum were harvested, and the liver injury, oxidative stress and histological features were evaluated. Results: NASH rats exhibited significant increases in the following parameters as compared to normal diet control rats: fat droplets with foci of inflammatory cell infiltration in the liver. ALT, AST in serum and TG, TC in hepatocyte elevated. Oxidative responsive genes including CYP2E1 and Nox2 increased. Additionally, NASH model decreased antioxidant enzymes SOD, GSH, GPX, and CAT in the liver due to their rapid depletion after battling against oxidative stress. Compared to NASH model group, treatment rats with Salidroside effectively reduced lipid accumulation, inhibited liver injury in a does-dependent manner. Salidroside treatment restored antioxidant enzyme levels, inhibited expression of CYP2E1 and Nox2 mRNA in liver, which prevented the initial step of generating free radicals from NASH. Conclusion: The data presented here show that oral administration of Salidroside prevented liver injury in the NASH model, likely through exerting antioxidant actions to suppress oxidative stress and the free radical-generating CYP2E1 enzyme, Nox2 in liver. [ABSTRACT FROM AUTHOR]

Reaction of PdCl2 with N,N-bis-(diphenylphosphanylmethyl)-2-aminopyridine (bdppmapy) afforded a mononuclear complex [(bdppmapy)PdCl2] (1). Compound 1 was characterized by elemental analysis, IR, ¹H, 13C and 31P NMR, electrospray ion mass spectra (ESI-MS) and X-ray single crystal crystallography. The Pd(II) center in 1 is chelated by bdppmapy, showing a cis-square planar geometry. With the assistance of additive Cu2O, complex 1 exhibited good catalytic activity toward the decarboxylative cross-coupling reactions between 4-picolinic acid and aryl bromides. In the presence of only 2 mol% catalyst, a family of 4-aryl-pyridines could be isolated in up to 83% yield. [ABSTRACT FROM AUTHOR]

Serotonin [5-hydroxytryptamine (5-HT)] released from mast cells or platelets in peripheral tissues is one of the important inflammatory mediators in pain and hyperalgesia. The involvement of 5-HT in pain is complex because it could inhibit or facilitate nociceptive transmission, reflecting the presence of multiple 5-HT subtype receptors on peripheral and central nociceptors. The present study aimed to investigate the involvement of 5-HT2B in 5-HT-induced pain and whether the subtype exists in dorsal root ganglion (DRG) neurons. Injecting the 5-HT or 5-HT2 agonist in hindpaws of mice induced significant hyperalgesia to mechanical stimuli, which was inhibited by the 5-HT2B/2C antagonist but not by 5-HT1A , 5-HT2A , or 5-HT3A antagonists. Therefore, 5-HT2B or 5-HT2C may be involved in 5-HT-induced mechanical hyperalgesia. The 5-HT2B/2C antagonist also blocked 5-HT-induced transient [Ca2+] signaling in DRG neurons. All subtypes of 5-HT receptors except 5-HT2C and 5-HT6 are present in DRGs. In situ hybridization also demonstrated 5-HT2B mainly expressed in small- to medium-diameter DRG neurons that respond to pain. Likely, 5-HT2B mediates 5-HT-induced mechanical hyperalgesia in mice. [ABSTRACT FROM AUTHOR]

Mesenchymal stem cells can be isolated from various tissues besides bone marrow and can differentiate into cells of three germ layers. Recent studies indicate that some cells in corneal stroma express stem cell markers and can also differentiate into chondrocytes and neurocytes. This study was carried out to investigate whether mesenchymal stem cells reside in the murine corneal stroma. Corneas of BALB/c mice were treated with collagenase digestion after the epithelium and endothelium were removed. Then the single cells were harvested and further identified by reverse transcription polymerase chain reaction (RT-PCR). After the immunophenotype of passage 2 corneal stroma-derived cells was analyzed by flow cytometry, attempts were made to differentiate these cells into adipocytes and osteocytes using conditioned medium. Following induction, cells were evaluated by RT-PCR, oil red O and Alizarin Red staining. Isolated single cells were of stromal origin, not of epithelial or endothelial. Passage 2 corneal stroma-derived cells exhibited the spindle-shaped morphology and expressed CD29, CD90, CD105, and CD71; but were negative for CD34 and CD45. In addition, these cells showed the potentiality of differentiating into adipocytes and osteocytes, which was confirmed by RT-PCR and staining. This study demonstrates the presence of mesenchymal stem cell-like cells in the murine corneal stroma. Further analysis of these cells will aid elucidation of the mechanisms of some keratopathies, and these cells may be a source for bioengineering of corneal tissue and for cell-based therapeutics. [ABSTRACT FROM AUTHOR]

Ethanol oxidation on Pt is a typical multistep and multiselectivity heterogeneous catalytic process. A comprehensive understanding of this fundamental reaction would greatly benefit design of catalysts for use in direct ethanol fuel cells and the degradation of biomass-derived oxygenates. In this work, the reaction network of ethanol oxidation on different Pt surfaces, including close-packed Pt{111}, stepped Pt{211}, and open Pt{100}, is explored thoroughly with an efficient reaction path searching method, which integrates our new transition-state searching technique with periodic density functional theory calculations. Our new technique enables the location of the transition state and saddle points for most surface reactions simply and efficiently by optimization of local minima. We show that the selectivity of ethanol oxidation on Pt depends markedly on the surface structure, which can be attributed to the structure-sensitivity of two key reaction steps: (i) the initial dehydrogenation of ethanol and (ii) the oxidation of acetyl (CH3CO). On open surface sites, ethanol prefers C-C bond cleavage via strongly adsorbed intermediates (CH2CO or CHCO), which leads to complete oxidation to CO2. However, only partial oxidizations to CH3CHO and CH3COOH occur on Pt{111}. Our mechanism points out that the open surface Pt(100) is the best facet to fully oxidize ethanol at low coverages, which sheds light on the origin of the remarkable catalytic performance of Pt tetrahexahedra nanocrystals found recently. The physical origin of the structure-selectivity is rationalized in terms of both thermodynamics and kinetics. Two fundamental quantities that dictate the selectivity of ethanol oxidation are identified: (i) the ability of surface metal atoms to bond with unsaturated C-containing fragments and (ii) the relative stability of hydroxyl at surface atop sites with respect to other sites. [ABSTRACT FROM AUTHOR]

A 2D network [Zn4(OH)2(5-NO2-1,3-BDC)2(5-NO2-1,3-HBDC)2(ppene)2]n underwent a highly selective [2+2] photodimerization reaction upon UV irradiation. The coordination polymer retains its single crystallinity after photoreaction. [ABSTRACT FROM AUTHOR]

We introduce a two-dimensional Bose–Einstein condensation model consisting of massive photon and photon-pair. Based on the new nonlinear model, the traditional process of second harmonics generation is reinvestigated. In order to describe the process, a new quantum phase, the harmonic phase, is introduced. The order parameter of the new physical phase is also given in this paper. [ABSTRACT FROM AUTHOR]

A correction to the article "Frontomaxillary facial angle at 11++0 to 13++6 weeks in Chinese population," that was published in the March, 2011 issue is presented.

Treatment of [Et4N][Tp*WS3] (1) (Tp* = hydridotris(3,5-dimethylpyrazol-l-yl)borate) with 2 equiv of AgSCN in MeCN afforded a novel neutral compound [(Tp*WS2)2(μ-S2)] (2). Reactions of 2 with excess CuX (X = Cl, Br, I) in MeCN and CH2Cl2 or CHCl3 formed three neutral W/Cu/S dusters [{Tp*W(μ3-S)3Cu3(μ-Cl)}2Cu(μ-Cl)2(μ7-Cl) (MeCN)]2 (3), [{Tp*W(μ3-S)3Cu3}2Br(μ-Br)2(μ4-Br)- (MeCN)] (4), and [{Tp*W(μ3-S)3Cu3}2{Cu2(μ-I)4(μ3-I)2}] (5), respectively. On the other hand, treatment of 2 with CuX (X = Cl, Br) in the presence of Et4NX (X = Cl, Br) produced two anionic W/Cu/S clusters [Et4N][{Tp*W(μ3-S)3Cu3X}2 (μ-X)2(μ4-X)] (6, X = Cl; 7 X = Br). Compounds 2-7 were characterized by elemental analysis, IR., UV-vis, ¹H NMR, electrospray ionization (ESI) mass spectra, and single-crystal X-ray crystallography. The dimeric structure of 2 can be viewed as two [Tp*WS2] fragments in which two W atoms are connected by one S22- dianion. Compounds 3-7 all possess unique halide-bridged double cubanelike frameworks. For 3, two [Tp*W(μ3-S)3Cu3]2+ dications are linked via a μ4-Cl- bridge, two μ-Cl- bridges, and a [Cu(MeCN)(μ-C1)2]+ bridge. For 4, one [Tp*W(μ3-S)3Cu3(MeCN)]2+ dication and one [Tp*W(μ3-S)3Cu3Br]+ cation are linked via a μ4-Br- and two μ-Br bridges. For 5, the two [Tp*W(μ3-S)3Cu3]2+ dications are bridged by a linear [(μ-l)2Cu- (μ3-I)2Cu(μ-I)2]4+ species. For 6 and 7, two [Tp*W(μ3-S)3Cu3X]+ cations are linked by μ4-X- and two μ-X- bridges (x = Cl, Br). In addition, the third-order nonlinear optical (NLO) properties of 2-7 in MeCN/CH2C12 were investigated by using femtosecond degenerate four-wave mixing (DFWM) technique. [ABSTRACT FROM AUTHOR]