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Purpose: We investigated the effects of early postnatal administration of erythropoietin (EPO) on neurodevelopmental outcomes and morbidities in preterm infants with severe grades of intraventricular hemorrhage (IVH). Methods: We retrospectively reviewed the medical records of preterm infants of gestational age 23+0 weeks to 31+6 weeks, who were diagnosed with severe grades of IVH and received EPO over at least 2 weeks. We compared clinical characteristics, major complications, and neurodevelopmental impairment between the two groups. The primary outcome was severe neurodevelopmental impairment at 18 to 26 months of corrected age. Severe neurodevelopmental impairment was defined as a mental developmental index or psychomotor developmental index of <70 on the Bayley Scales of Infant Development II or diagnosis of cerebral palsy. Results: The study included 33 preterm infants (mean gestational age 25.2±1.6 weeks and mean birth weight 775.1±224.5 g). EPO was administered at a dose of 400 or 1,000 IU/kg thrice weekly and was maintained over a mean period of 58.6± 25.9 days beginning from 10.7±6.9 days after birth. We observed no difference in perinatal characteristics between the EPO (n=14) and the control group (n=19). Similarly, severe neurodevelopmental impairment rates did not differ between the EPO (85.7%) and control groups (78.9%). The incidence of neonatal morbidities including bronchopulmonary dysplasia, necrotizing enterocolitis, and retinopathy of prematurity was also similar between the EPO and control groups. Conclusion: Early administration of EPO did not reduce the risk of severe neurodevelopmental impairment in preterm infants with severe IVH. [ABSTRACT FROM AUTHOR]

Nasopharyngeal tuberculosis can arise from both a primary infection and a secondary spread via the lymphatic or hematogenous system from a primary pulmonary lesion. Primary nasopharyngeal tuberculosis is rare and difficult to detect earlier because of the nonspecific presentations of the disease. As upper airway tuberculosis can be contagious, early initial diagnosis and suspicion of the physicians are needed in clinical practice. Recently, we successfully diagnosed and treated the disease by antitubercular medications of two cases of primary nasopharyngeal tuberculosis. Herein, we report our experience with a literature review. [ABSTRACT FROM AUTHOR]

Campomelic dysplasia (CD) is a rare genetic disease characterized by skeletal dysplasia that also affects several other organ systems. CD is caused by a SOX9 mutation. We here report a case of CD with a 46, XY karyotype and female external genitalia. This child was born with a weight of 3.12 kg after 37 weeks of gestation. She exhibited a number of characteristic features including a small thoracic cage, bowing of both femurs, clubbed feet, hypoplastic scapula, 11 pairs of ribs, a bell-shaped narrow thorax, micrognathia, macroglossia, a cleft palate, a flattened nasal bridge, and low set ears. She experienced additional distress because of the presence of a tracheal ring and because she had tracheomalacia. CD was diagnosed through nucleotide sequence analysis. A frameshift mutation, c.235delC (p.Gln79Argfs*31), was identified in the SOX9 gene that has not previously been reported. [ABSTRACT FROM AUTHOR]

A key event required for effective resolution of inflammation is efferocytosis, which is defined as phagocytic removal of apoptotic cells mostly by macrophages acquiring an alternatively activated phenotype (M2). c-Myc has been reported to play a role in alternative activation of human macrophages and is proposed as one of the M2 macrophage markers. We found that M2-like peritoneal macrophages from zymosan A-treated mice exhibited a marked accumulation of Myc-nick, a truncated protein generated by a Calpain-mediated proteolytic cleavage of full-length c-Myc. Further, ectopic expression of Myc-nick in murine bone marrow-derived macrophages promoted the M2 polarization and, consequently, enhanced their efferocytic capability. Notably, Myc-nick-induced efferocytosis was found to be tightly associated with α-tubulin acetylation by K acetyltransferase 2a (Kat2a/Gcn5) activity. These findings suggest Myc-nick as a novel proresolving mediator that has a fundamental function in maintaining homeostasis under inflammatory conditions. [ABSTRACT FROM AUTHOR]

Purpose: This study reports the development of the Korean Version of the Treatment Satisfaction Visual Analogue Scale (TSVAS) and the Overactive Bladder Satisfaction with Treatment Questionnaire (OAB-SAT-q) based on the original versions, with subsequent linguistic validation by Korean patients with overactive bladder receiving active treatment from a physician. Methods: Translation and linguistic validation were performed in 2016. The validation process included permission for translation, forward translation, reconciliation, backward translation, cognitive debriefing, and proofreading. The original versions of the TS-VAS and OAB-SAT-q were independently translated into Korean by 2 bilingual translators and were then reconciled into a single version. The third bilingual translator performed a backward translation of the reconciled version into English. A trained interviewer and 5 Korean-speaking patients with OAB carried out the cognitive debriefing. Results: During the forward translation process, the terms used in the 2 questionnaires were adjusted to use more appropriate expressions in the Korean language than were used in the original versions. During the backward translation process, no changes were made in terms of semantic equivalence. In the cognitive debriefing session, 5 patients were asked to fill in the answers within 8 minutes; most of them reported that the translated questions were clear and easy to understand. Conclusions: The present study presents successful linguistic validation of the Korean version of the TS-VAS and OAB-SAT-q, which could be useful tools for evaluating treatment satisfaction in patients. [ABSTRACT FROM AUTHOR]

Proinflammatory cytokine overproduction and excessive cell death, coupled with impaired clearance of apoptotic cells, have been implicated as causes of failure to resolve gut inflammation in inflammatory bowel diseases. Here we have found that dendritic cells expressing the apoptotic cell-recognizing receptor CD300f play a crucial role in regulating gut inflammatory responses in a murine model of colonic inflammation. CD300f-deficient mice failed to resolve dextran sulfate sodium-induced colonic inflammation as a result of defects in dendritic cell function that were associated with abnormal accumulation of apoptotic cells in the gut. CD300f-deficient dendritic cells displayed hyperactive phagocytosis of apoptotic cells, which stimulated excessive TNF-α secretion predominantly from dendritic cells. This, in turn, induced secondary IFN-γ overproduction by colonic T cells, leading to prolonged gut inflammation. Our data highlight a previously unappreciated role for dendritic cells in controlling gut homeostasis and show that CD300f-dependent regulation of apoptotic cell uptake is essential for suppressing overactive dendritic cell-mediated inflammatory responses, thereby controlling the development of chronic gut inflammation. [ABSTRACT FROM AUTHOR]

A knotted ureteral stent is an extremely rare condition, with fewer than 20 cases reported in the literature; however, it is difficult to treat. We report a case in which a folded Terumo guidewire was successfully used to remove a knotted stent percutaneously without anesthesia. We also review the current literature on predisposing factors and management strategies for knotted ureteral stents. [ABSTRACT FROM AUTHOR]

Phagocytosis of apoptotic neutrophils, termed efferocytosis, is essential for the resolution of inflammation as it prevents the tissues surrounding the inflamed site from being exposed to the toxic contents of lytic cells. Resolvin D1 (RvD1), endogenously generated from docosahexaenoic acid during resolution of inflammation, is known to stimulate efferocytosis. However, the molecular mechanism underlying RvD1-mediated enhancement of efferocytosis remains largely unresolved. In the present study, murine macrophage-like RAW264.7 cells treated with lipopolysaccharide (LPS) exhibited markedly reduced efferocytic activity, but this was restored by coincubation with RvD1. RvD1-induced restoration of the efferocytic activity appears to be mediated by downregulation of LPS-induced TNF-α expression. The inhibitory effect of RvD1 on LPS-induced TNF-α expression was associated with enhanced nuclear localization of p50/p50 homodimer and concomitant reduction of p65/p50 heterodimer accumulation in the nucleus. RvD1 triggered phosphorylation and proteasomal degradation of nuclear factor kB1 (NF-kB1) p105 to generate p50, which was subsequently translocated to the nucleus as a p50/p50 homodimer. Knockdown of NF-kB p50 abolished the ability of RvD1 to suppress TNF-a expression and also to restore efferocytosis, suggesting that the replacement of p65/p50 with p50/p50 homodimer in the nucleus is crucial for RvD1-mediated stimulation of efferocytosis. In a murine peritonitis model, intraperitoneal administration of RvD1 abolished the zymosan-A-induced TNF-α production, thereby stimulating efferocytosis. Taken together, these findings indicate that RvD1 expedites resolution of inflammation through induction of efferocytosis by p50/p50-homodimer-mediated repression of TNF-α production. [ABSTRACT FROM AUTHOR]

The adenomatous polyposis coli gene (APC) was initially identified through its link to colon cancer. It is associated with the regulation of cell cycle progression, survival, and differentiation of normal tissues. Recent studies have demonstrated that APC is also expressed in the adult brain at high levels. However, its role in glial cells under pathological progression remains unclear. In this study, we evaluated the expression of APC and its association with β-catenin signaling pathway, following the induction of an excitotoxic lesion by kainic acid (KA) injection, which cause pyramidal cell degeneration. APC was predominantly present in oligodendrocytes in the normal brain, but was specifically associated with activated astrocytes in the KA-treated brain. Our quantitative analysis revealed that APC significantly increased from 1 day post lesion (PI), reached peak values at 3 days PI, and decreased thereafter. The phospho-GSK3β levels also showed similar spatiotemporal patterns while β-catenin expression was reduced at 1 and then increasingly returned to normal levels at 3, 7 days PI. For the first time, our data demonstrate the injury-induced astrocytic changes in the levels of APC, GSK3β, and β-catenin in vivo, which may actively be participate in cell adhesion and in the signaling pathway regulating cell survivals during brain insults. [ABSTRACT FROM AUTHOR]

While failure in resolution of inflammation is considered to increase the risk of tumorigenesis, there is paucity of experimental as well as clinical evidence supporting this association. Resolvin D1 (RvD1) is a representative pro-resolving lipid mediator that is endogenously generated from docosahexaenoic acid for the resolution of inflammation. Here, we report a decreased level of RvD1 in the blood from colorectal cancer patients and mice having inflammation-induced colon cancer, suggesting plasma RvD1 as a potential biomarker for monitoring colorectal cancer. Administration of RvD1 attenuated dextran sodium sulfate (DSS)-induced colitis and azoxymethane (AOM) plus DSS-induced colorectal carcinogenesis by suppressing the production of interleukin-6 (IL-6) and IL-6-mediated chromosomal instability. The protective effect of RvD1 against chromosomal instability is associated with downregulation of IL-6-induced Cyclin D1 expression, which appears to be mediated by blocking the Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) axis. RvD1 inhibited the STAT3 signaling pathway by interfering with the binding of IL-6 to its receptor (IL-6R), suggesting the novel function of RvD1 as a putative IL-6R antagonist. Together, our findings suggest that RvD1-mediated blockade of IL-6 signal transmission may contribute to inhibition of chromosomal instability and tumorigenesis. [ABSTRACT FROM AUTHOR]

Purpose: Given the importance of evaluating the severity of overactive bladder (OAB) symptoms and outcomes after treatment, several questionnaires have been developed to evaluate OAB patients. However, only limited questionnaires are available in Korea for use with Korean patients. Therefore, this study aimed to develop Korean versions of OAB questionnaires through a rigorous linguistic validation process. Methods: The Indevus Urgency Severity Scale, Urgency Perception Scale, Urgency Severity Scale, and Patient Perception of Intensity of Urgency Scale underwent translation and linguistic validation. The linguistic validation procedure consisted of permission for translation, forward translations, reconciliation, back-translation, cognitive debriefing, and proofreading. Two independent bilingual translators translated the original version of each questionnaire, and a panel then discussed and reconciled the 2 initial translations. Next, a third independent bilingual translator performed a backward translation of the reconciled version into English. Five Korean patients diagnosed with OAB were interviewed for cognitive debriefing. Results: Each item of the questionnaires was translated into 2 Korean versions in the forward translation process. Terms such as 'urgency' and 'wetting' were translated into ordinary language by the translators and adjusted by the panel members to more conceptually equivalent terms in a medical context. In the back-translation process, the panel made a few changes regarding details based on a comparison of the back-translated and original versions. During the cognitive debriefing process, 5 patients provided a few pieces of feedback on the naturalness of the wording of the questionnaires, but generally agreed on the translated terms. Conclusions: In this study, the panel produced a successful linguistic validation of Korean versions of multiple OAB questionnaires, which can be utilized to evaluate the severity and treatment outcomes of OAB. [ABSTRACT FROM AUTHOR]

Purpose 17β-Estradiol (E2) supplementation suppresses MC38 tumor growth by downregulating the expression of programmed death-ligand 1 (PD-L1). This study aims to figure out the gut microbiota that respond to anti-PD-L1 and/or estrogen treatment in MC38 colon cancer model. Materials and Methods A syngeneic colon tumor model was developed by injection of MC38 cells into C57BL/6 background male and female mice. Three days before MC38 cells injection, E2 was supplemented to male mice daily for 1 week. Male and female mice with MC38 tumors (50-100 mm3) were injected with anti-PD-L1 antibody. Fresh feces were collected 26 days after injection of MC38 cells and 16S rRNA metagenomics sequencing of DNA extracted from feces was used to assess gut microbial composition. Results At the taxonomic family level, Muribaculaceae was enriched only in the MC38 male control group. In male mice, linear discriminant analysis effect size analysis at the species level revealed that the four microorganisms were commonly regulated in single and combination treatment with anti-PD-L1 and/or E2; a decrease in PAC001068_g_uc and PAC001070_s (family Muribaculaceae) and increase in PAC001716_s and PAC001785_s (family Ruminococcaceae). Interestingly, in the anti-PD-L1 plus E2 group, a decrease in opportunistic pathogens (Enterobacteriaceae group) and an increase in commensal bacteria (Lactobacillus murinus group and Parabacteroides goldsteinii) were observed. Furthermore, the abundance of Parabacteroides goldsteinii was increased in both males and females in the anti-PD-L1 group. Conclusion Our results suggest that gut microbial changes induced by the pretreatment of estrogen before anti-PD-L1 might contribute to treatment of MC38 colon cancer. [ABSTRACT FROM AUTHOR]

The article describes a highly selective fluorescent chemosensor for pyrophosphate that has the ability to function in a 100 percent aqueous solution. The chemosensor demonstrates an excimer peak at 490 nm only in the presence of pyrophosphate. The unique 2+2 type excimer was induced by four zinc sites as well as a π-π interaction in the presence of pyrophosphate. Moreover, the detection of pyrophosphate is selective over ATP or phosphate.

Purpose: Extremely low birth weight (ELBW) infants exhibit immature thermoregulation and are easily exposed to hypothermia. We investigated the association between hypothermia on admission with short- and long-term outcomes. Methods: Medical records of ELBW infants admitted to the neonatal intensive care unit of a tertiary medical center between June 2012 and February 2017 were retrospectively analyzed. Upon admission, the axillary body temperature was measured. Moderate hypothermia was defined as admission temperature below 36 °C. Results: A total of 208 infants with gestational age of 26.4±2.3 weeks and birth weight of 746.7±154.9 g were included. Admission temperature ranged from 33.5 to 36.8? (median 36.1 ?). Univariate analyses of maternal and infant characteristics were performed for moderately hypothermic and control (normothermic to mildly hypothermic) infants. Lower gestational age, lower birth weight, and vaginal delivery correlated with moderate hypothermia. Logistic regression analyses adjusted for confounders revealed that the incidence of hemodynamically significant patent ductus arteriosus (hsPDA) was associated with moderate hypothermia in ELBW infants. Moreover, abnormal mental developmental index scores on the Bayley Scales of Infant Development II at a corrected age of 18 to 24 months were associated with moderate hypothermia, but not with the psychomotor developmental index, incidence of blindness, deafness, or cerebral palsy. Conclusion: Moderate hypothermia at admission is not only correlated with shortterm neonatal morbidities such as hsPDA, but may also be associated with longterm neurodevelopmental impairment in ELBW infants. Future large-scale studies are required to clarify the long-term consequences of hypothermia upon admission. [ABSTRACT FROM AUTHOR]

Purpose Sex hormones are known to affect the gut microbiota. Previously, we reported that endogenous and exogenous testosterone are associated with colorectal cancer (CRC) development and submucosal invasion. In the present study, we investigated whether the gut microbiota is affected by orchiectomy (ORX) and testosterone propionate (TP) administration using an azoxymethane/dextran sulfate sodium (AOM/DSS)-induced CRC mouse model. Materials and Methods Gut microbiota was evaluated by means of 16S rRNA gene sequencing of stool DNA extracted from feces that were obtained at 13 weeks after AOM injection (from 22-week-old animals) and stored in a gas-generating pouch. Results The increase in microbial diversity (Chao1 and Phylogenetic Diversity index) and Firmicutes/Bacteroidetes (F/B) ratio upon AOM/DSS treatment in ORX mice was significantly decreased by TP supplementation. The ratio of commensal bacteria to opportunistic pathogens was lower in the TP-administered females and ORX mice than in the AOM/DSS group. Opportunistic pathogens (Mucispirillum schaedleri or Akkermansia muciniphila) were identified only in the TP group. In addition, microbial diversity and F/B ratio were higher in male controls than in female and ORX controls. Flintibacter butyricus, Ruminococcus bromii, and Romboutsia timonensis showed similar changes in the male control group as those in the female and ORX controls. Conclusion In conclusion, testosterone determines the dysbiosis of gut microbiota, which suggests that it plays a role in the sexrelated differences in colorectal carcinogenesis. [ABSTRACT FROM AUTHOR]

Breast cancer cells possess a deregulated apoptotic pathway with increased expression levels of anti-apoptotic B-cell lymphoma-2 (Bcl-2) family proteins and ribosomal S6 kinase 1 (S6K1) protein activity. Therefore, combined interference of anti-apoptotic Bcl-2 family and S6K1 protein expression may be a reasonable therapeutic strategy for the treatment of patients with breast cancer. In the present study, it was identified that the administration of a combination of ABT263 [navitoclax; a Bcl-2/Bcl-extra large (Bcl-xL) inhibitor] and PF4708671 (an S6K1 inhibitor) markedly increased apoptotic cell death in the BT474 breast cancer cells compared with the administration of either agent alone. Furthermore, the downregulation of Bcl-2/Bcl-xL and S6K1 with small interfering RNA induced a significant increase in cell death compared with RNA interference of either agent alone. Notably, combination treatment with ABT263 and PF4708671 decreased the expression level of survivin protein, with this ectopic expression of survivin attenuating cell death. Thus, the present study determined that the combined inhibition of Bcl-2/Bcl-xL and S6K1 may be a good strategy for treating patients with breast cancer. [ABSTRACT FROM AUTHOR]

Background/Aims: Heme oxygenase-1 (HO-1) plays a central role in cellular defense against inflammatory insults, and its induction in macrophages potentiates their efferocytic activity. In this study, we explored the potential role of macrophage HO-1 in the resolution of experimentally induced colitis. Methods: To induce colitis, male C57BL/6 mice were treated with 2% dextran sulfate sodium (DSS) in the drinking water for 7 days. To investigate efferocytosis, apoptotic colon epithelial CCD 841 CoN cells were coincubated with bone marrow-derived macrophages (BMDMs). Results: Administration of the HO-1 inhibitor zinc protoporphyrin IX (ZnPP) blunted the resolution of DSS-induced intestinal inflammation and expression of the proresolving M2 macrophage marker CD206. BMDMs treated with apoptotic colonic epithelial cells showed significantly elevated expression of HO-1 and its regulator Nrf2. Under the same experimental conditions, the proportion of CD206-expressing macrophages was also enhanced. ZnPP treatment abrogated the upregulation of CD206 expression in BMDMs engulfing apoptotic colonic epithelial cells. This result was verified with BMDMs isolated from HO-1-knockout mice. BMDMs, when stimulated with lipopolysaccharide, exhibited increased expression of CD86, a marker of M1 macrophages. Coculture of lipopolysaccharide-stimulated BMDMs with apoptotic colonic epithelial cell debris dampened the expression of CD86 as well as the pro-inflammatory cytokines in an HO-1-dependent manner. Genetic ablation as well as pharmacologic inhibition of HO-1 significantly reduced the proportion of efferocytic BMDMs expressing the scavenger receptor CD36. Conclusions: HO-1 plays a key role in the resolution of experimentally induced colitis by modulating the polarization of macrophages. [ABSTRACT FROM AUTHOR]

The outcome of an encounter with Mycobacterium tuberculosis (Mtb) depends on the pathogen's ability to adapt to the variable immune pressures exerted by the host. Understanding this interplay has proven difficult, largely because experimentally tractable animal models do not recapitulate the heterogeneity of tuberculosis disease. We leveraged the genetically diverse Collaborative Cross (CC) mouse panel in conjunction with a library of Mtb mutants to create a resource for associating bacterial genetic requirements with host genetics and immunity. We report that CC strains vary dramatically in their susceptibility to infection and produce qualitatively distinct immune states. Global analysis of Mtb transposon mutant fitness (TnSeq) across the CC panel revealed that many virulence pathways are only required in specific host microenvironments, identifying a large fraction of the pathogen's genome that has been maintained to ensure fitness in a diverse population. Both immunological and bacterial traits can be associated with genetic variants distributed across the mouse genome, making the CC a unique population for identifying specific host-pathogen genetic interactions that influence pathogenesis. [ABSTRACT FROM AUTHOR]

Introduction and hypothesis: This prospective multicenter study was conducted to evaluate the efficacy and safety of an adjustable mid-urethral sling (MUS) using transobturator adjustable tape (TOA) in women with severe stress urinary incontinence or combined stress urinary incontinence (SUI) and voiding dysfunction (VD). Methods: One day after placement of TOA, the tension was adjusted. Six months after surgery, changes in several questionnaires and uroflowmetry (UFM) parameters were evaluated. Results: Among the 65 women enrolled in the study, 27 (41.5%) required postoperative tension readjustments. At 6 months, the complete cure rate of SUI was 84.4%, and patient satisfaction with the operation was 86.2%. There was improvement in the total scores on several questionnaires. There were no significant changes in postoperative UFM parameters. Conclusion: Our results support the use of TOA as an effective modality for the treatment of SUI in women at risk for persistent postoperative SUI or obstructive symptoms. [ABSTRACT FROM AUTHOR]

Purpose This study demonstrates that estradiol downregulates inflammation and inhibits colorectal cancer (CRC) development in azoxymethane/dextran sulfate sodium (AOM/DSS) mouse model. Materials and Methods AOM/DSS-treated male and female mice were sacrificed at weeks 2, 10, and 16, to assess estrogen effects on colitis and carcinogenesis. Macroscopic and histologic severity of colitis and Western blot and quantitative real-time polymerase chain reaction were evaluated, to measure inflammatory mediators and cytokines. Results Compared with AOM/DSS-treated male mice (M-AOM/DSS group), AOM/DSS-treated male mice with estradiol administration (M-AOM/DSS+estr group) displayed at week 2 significantly decreased severity of colitis. At weeks 10 and 16, AOM/DSS-treated female mice (F-AOM/DSS group) and the M-AOM/DSS+estr group showed significantly lower tumor multiplicity compared with the M-AOM/DSS group. At week 2, F-AOM/DSS group had a lower level of nuclear factor-B (NF-B) expression and higher level of nuclear factor erythroid 2-related factor 2 (Nrf2) expression, compared to the M-AOM/DSS group. At week 2, expression levels of NF-B and its related mediators decreased in the M-AOM/DSS+estr group, while levels of Nrf2 and Nrf2-related anti-oxidant enzymes increased. In addition, estradiol significantly increased Nod-like receptor protein 3 (NLRP3) inflammasome expressions in AOM/DSS-treated male mice. In contrast, at weeks 10 and 16, Nrf2 and its-related anti-oxidant enzymes and NLRP3 inflammasome were highly expressed in M-AOM/DSS group and in F-AOM/DSS group, who developed cancer. Conclusion The data suggest that estradiol inhibits the initiation of CRC by regulating Nrf2-related pathways. Moreover, these imply the dual role of Nrf2 and NLRP3 inflammasome, including promotion of tumor progression upon tumor initiation. [ABSTRACT FROM AUTHOR]

Background/Aims: The aim of this study was to investigate the protective effect of açaí against azoxymethane (AOM)/ dextran sulfate sodium (DSS)-induced colorectal cancer development. Methods: The effect of açaí on tumorigenesis was assessed by evaluating tumor incidence, multiplicity and invasiveness in the mouse colon. The levels of myeloperoxidase (MPO) and proinflammatory cytokines (tumor necrosis factor α [TNF-α], interleukin [IL]-1β, and IL-6) were measured via enzyme-linked immunosorbent assay. Protein levels of cyclooxygenase 2 (COX-2), proliferating cell nuclear antigen (PCNA), B-cell lymphoma 2 (Bcl-2), Bcl-2-associated death promoter (Bad) and cleaved-caspase-3 were assessed by immunoblotting. Results: Administration of pellets containing 5% açaí powder reduced the incidences of both colonic adenoma and cancer (adenoma, 23.1% vs 76.9%, respectively, p=0.006; cancer, 15.4% vs 76.9%, respectively, p=0.002). In the açaí-treated mice, the MPO, TNF-α, IL-1β and IL-6 levels in the colon were significantly down-regulated. Açaí inhibited PCNA and Bcl-2 expression and increased Bad and cleaved-caspase-3 expression. In vitro studies demonstrated that açaí treatment reduced lipopolysaccharide-induced expression of TNF-α, IL-1β, IL-6 and COX-2 in murine macrophage RAW 264.7 cells. Conclusions: Açaí demonstrated protective effects against AOM/DSS-induced colon carcinogenesis, which suggests that the intake of açaí may be beneficial for the prevention of human colon cancer. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the efficacy and safety of the Holmium: yttrium-aluminium-garnet (YAG) laser for the treatment of urethral/bladder neck strictures after high-intensity focused ultrasound for prostate cancer. Methods: Between February 2007 and July 2010, Holmium: YAG laser urethrotomies were performed in eleven patients for bladder neck strictures or prostatic urethral strictures. Te laser was used with a 550-μm fiber at 2 J and frequency 30 to 50 Hz. Te medical records were retrospectively reviewed for medical history, perioperative and postoperative data, urofowmetry, International Prostate Symptoms Score/quality of life, and stricture recurrence. Results: At a median follow-up of 12.0 months (range, 4 to 35 months), the mean postoperative maximal flow rate and residual volume were improved significantly (P<0.05). Te mean postoperative total, voiding and quality of life of international prostate symptom score were improved significantly (P<0.05). Of the 11 patients, 7 patients required one treatment, 4 patients two treatment, and 1 patients three treatment. 2 patients who had a documented urinary incontinence prior to the laser treatment subsequently required artificial urinary sphincter implantation and reported satisfaction without developing any recurrent strictures or artificial urinary sphincter erosion. All patients exhibited well-healed strictures and could void without difficulty. Conclusions: Holmium: YAG laser therapy represents a safe, effective and minimally invasive treatment for urethral/bladder neck strictures occurring secondary to high-intensity focused ultrasound for prostate cancer. [ABSTRACT FROM AUTHOR]

The first examples of boronic acid-linked fluorescent and colorimetric chemosensors for copper ions are reported; the monoboronic acid-conjugated rhodamine probe displays a highly selective fluorescent enhancement with Cu2+among the various metal ions whereas the fluorescence of the bisboronic acid-conjugated fluorescein probe is selectively quenched by Cu2+, probably by way of a PET mechanism. [ABSTRACT FROM AUTHOR]