[Analysis of reproductive outcomes in the first IVF-ET cycle after laparoscopic treatment in patients with endometriosis].

Objective: To explore the effect of endometriosis (EM) on reproductive outcomes of young patient with EM after laparoscopic treatment in the first in vitro fertilization-embryo transfer (IVF-ET) cycle. Methods: The clinical data and reproductive outcomes of 394 infertile patients with EM after laparoscopic treatment (EM group) and 3 242 infertile patients caused by gamete transport disorder (control group) in the first IVF-ET cycle were collected in Chongqing Health Center for Women and Children from January 2016 to June 2021. The information included baseline characteristics, oocyte retrieval, embryo development, clinical pregnancy, miscarriage, and live birth. Propensity score matching (PSM) method was used to perform 1∶2 matching between EM group and control group. The impact of EM on reproductive outcomes was analyzed in the retrospective observational study. Results: In the initial data, compared with control group, the number of two pronucleus (2PN) zygotes (9.7±4.8 vs 9.0±4.4), the number of transferable embryos (6.2±3.6 vs 5.5±3.4) and the rate of transferable embryos (64.0% vs 60.8%) on the third day were significantly lower in EM group, and the differences were statistically significant (all P<0.05). After PSM was performed, there were 394 and 787 cases in EM group and control group, respectively. Compared with control group, the number of 2PN zygotes (9.7±4.9 vs 9.0±4.4), the 2PN fertility rate (77.1% vs 75.3%), the number of transferable embryos on the third day (6.2±3.6 vs 5.5±3.4), the transferable embryos rate on the third day (63.8% vs 60.8%) were significantly lower in EM group, and the differences were statically significant (all P<0.05). The study did not find the effect of EM on embryo implantation rate, pregnancy rate, early miscarriage rate, live birth rate and preterm birth rate (all P>0.05). Conclusions: EM might interfere with the development of oocytes and embryos. Obtaining top-quality embryos may be an effective way to improve the prognosis of patients with EM after laparoscopic treatment.

Comparative analysis and differentiation between SAPHO syndrome and spondyloarthropathies using whole-spine MRI.

AIM: To determine the imaging characteristics of SAPHO (synovitis, acne, pustulosis, hyperostosis, and osteitis) syndrome and seronegative spondyloarthropathies (SpAs) on whole-spine magnetic resonance imaging (WS-MRI) and evaluate the role of WS-MRI in the diagnosis and differentiation of the two diseases. MATERIALS AND METHODS: Twenty-eight patients with SAPHO and 44 with SpAs were included. All patients were symptomatic and clinically diagnosed with SAPHO or SpAs, and all underwent WS-MRI for comparison of imaging characteristics. RESULTS: The mean age of the SAPHO patients was 48.7 ± 12.7 years, while that of the SpA patients was 34.7 ± 12.3 years (p<0.001). WS-MRI showed that the frequency of cervical, thoracic, and lumbar spine involvement was 53.6% versus 52.3%, 75% versus 88.6%, and 60.7% versus 63.6%, respectively (p=0.70, 0.13, and 0.80). The frequency of sacroiliac joint involvement was 7.1% and 100% (p<0.001). Continuous spinal involvement accounted for 50% versus 43.2%, 60.7% versus 84.1%, and 39.3% versus 40.9% in the cervical, thoracic, and lumbar vertebrae, respectively (p=0.03). WS-MRI showed that bone marrow oedema of spinal anterior corner was observed in 50% versus 75% (p=0.03). Vertebral body and posterior attachment involvement accounted for 85.7% versus 93.2% and 14.3% versus 34.1% (p=0.3, 0.06). The frequency of bone erosion in mobile spine was 75% and 36.4%, respectively (p=0.02). The frequency of intervertebral disc, endplate, anterior thoracic wall, and paraspinal soft-tissue swelling was 42.9% versus 18.2%, 53.6% versus 22.7%, 85.7% versus 42.2%, and 50% versus 11.4% (p=0.02, 0.00). CONCLUSIONS: Factors differentiating the two groups at WS-MRI were bone marrow oedema of the spinal anterior corner, bone erosion, and swelling of the intervertebral disc, endplate, anterior thoracic wall, and paraspinal soft-tissue.

An update on the status of COVID-19: a comprehensive review.

The last two decades have witnessed two large-scale pandemics caused by coronaviruses, including severe acute respiratory syndrome (SARS) and the Middle East respiratory syndrome (MERS). At the end of 2019, another novel coronavirus, designated as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), hit Wuhan, a city in the center of China, and subsequently spread rapidly to the whole world. Latest reports revealed that more than 800 thousand people in over 200 countries are involved in the epidemic disease by SARS-CoV-2. Due to the high mortality rate and the lack of optimum therapeutics, it is crucial to understand the biological characteristics of the virus and its possible pathogenesis to respond to the SARS-CoV-2. Rapid diagnostics and effective therapeutics are also important interventions for the management of infection control. However, the rapid evolution of SARS-CoV-2 exerted tremendous challenges on its diagnostics and therapeutics. Therefore, there is an urgent need to summarize the existing research results to guide decision-making on the prioritization of resources for research and development. In this review, we focus on our current understanding of epidemiology, pathogenesis, diagnostics and therapeutics of coronavirus disease 2019 (COVID-19).

CXCR3-deficient mesenchymal stem cells fail to infiltrate into the nephritic kidney and do not ameliorate lupus symptoms in MRL. Faslpr mice.

Mesenchymal stem cell therapy is a promising candidate for the treatment of systemic lupus erythematosus (SLE). To exert their efficacy fully, mesenchymal stem cells must infiltrate efficiently into the lesion sites. Here, we examined the role of CXCR3 in mesenchymal stem cell infiltration into the kidney of MRL. Faslpr mice, which highly expressed CXCL10. The phenotypes, production of immunosuppressive mediators, and capacity to inhibit T and B cells of CXCR3-deficient mesenchymal stem cells were similar to those of wild-type mesenchymal stem cells. However, they showed less infiltration into the nephritic kidney, less conjugation with endothelial cells and weaker MMP-9 expression than did wild-type mesenchymal stem cells. Consequently, CXCR3-deficient mesenchymal stem cells did not ameliorate lupus symptoms in MRL. Faslpr mice in comparison with wild-type mesenchymal stem cells. In summary, our data suggest that upregulation of CXCR3 in mesenchymal stem cells will be a good strategy to increase their infiltration into the kidney, which will improve therapeutic outcomes in SLE.

Incidence, risk factors, and fracture healing of atypical femoral fractures: a multicenter case-control study.

The incidence of atypical femoral fractures (AFFs) was 2.95% among 6644 hip and femoral fractures. Independent risk factors included the use of bisphosphonates (BPs), osteopenia or osteoporosis, rheumatoid arthritis, increased femoral curvatures, and thicker femoral cortices. Patients with AFFs and BP treatment were more likely to have problematic healing than those with typical femoral fractures (TFFs) and no BP treatment. INTRODUCTION: To determine the incidence and risk factors of atypical femoral fractures (AFFs), we performed a multicenter case-control study. We also investigated the effects of bisphosphonates (BPs) on AFF healing. METHODS: We retrospectively reviewed the medical records and radiographs of 6644 hip and femoral fractures of patients from eight tertiary referral hospitals. All the radiographs were reviewed to distinguish AFFs from TFFs. Univariate and multivariate logistic regression analyses were performed to identify risk factors, and interaction analyses were used to investigate the effects of BPs on fracture healing. RESULTS: The incidence of AFFs among 6644 hip and femoral fractures was 2.95% (90 subtrochanter and 106 femoral shaft fractures). All patients were females with a mean age of 72 years, and 75.5% were exposed to BPs for an average duration of 5.2 years (range, 1-17 years). The use of BPs was significantly associated with AFFs (p < 0.001, odds ratio = 25.65; 95% confidence interval = 10.74-61.28). Other independent risk factors for AFFs included osteopenia or osteoporosis, rheumatoid arthritis, increased anterior and lateral femoral curvatures, and thicker lateral femoral cortex at the shaft level. Interaction analyses showed that patients with AFFs using BPs had a significantly higher risk of problematic fracture healing than those with TFFs and no BP treatment. CONCLUSIONS: The incidence of AFFs among 6644 hip and femoral fractures was 2.95%. Osteopenia or osteoporosis, use of BPs, rheumatoid arthritis, increased anterior and lateral femoral curvatures, and thicker lateral femoral cortex were independent risk factors for the development of AFFs. Patients with AFFs and BP treatment were more likely to have problematic fracture healing than those with TFFs and no BP treatment.

The Natural History of Severe Acute Liver Injury.

OBJECTIVES: Acute liver failure (ALF) is classically defined by coagulopathy and hepatic encephalopathy (HE); however, acute liver injury (ALI), i.e., severe acute hepatocyte necrosis without HE, has not been carefully defined nor studied. Our aim is to describe the clinical course of specifically defined ALI, including the risk and clinical predictors of poor outcomes, namely progression to ALF, the need for liver transplantation (LT) and death. METHODS: 386 subjects prospectively enrolled in the Acute Liver Failure Study Group registry between 1 September 2008 through 25 October 2013, met criteria for ALI: International Normalized Ratio (INR)≥2.0 and alanine aminotransferase (ALT)≥10 × elevated (irrespective of bilirubin level) for acetaminophen (N-acetyl-p-aminophenol, APAP) ALI, or INR≥2.0, ALT≥10x elevated, and bilirubin≥3.0 mg/dl for non-APAP ALI, both groups without any discernible HE. Subjects who progressed to poor outcomes (ALF, death, LT) were compared, by univariate analysis, with those who recovered. A model to predict poor outcome was developed using the random forest (RF) procedure. RESULTS: Progression to a poor outcome occurred in 90/386 (23%), primarily in non-APAP (71/179, 40%) vs. only 14/194 (7.2%) in APAP patients comprising 52% of all cases (13 cases did not have an etiology assigned; 5 of whom had a poor outcome). Of 82 variables entered into the RF procedure: etiology, bilirubin, INR, APAP level and duration of jaundice were the most predictive of progression to ALF, LT, or death. CONCLUSIONS: A majority of ALI cases are due to APAP, 93% of whom will improve rapidly and fully recover, while non-APAP patients have a far greater risk of poor outcome and should be targeted for early referral to a liver transplant center.

Glutathione peroxidase 1 deficiency attenuates concanavalin A-induced hepatic injury by modulation of T-cell activation.

Concanavalin A (Con A)-induced hepatitis model is well-established experimental T cell-mediated liver disease. Reactive oxygen species (ROS) is associated with T-cell activation and proliferation, but continued ROS exposure induces T-cell hyporesponsiveness. Because glutathione peroxidase 1 (Gpx1) is an antioxidant enzyme and is involved in T-cell development, we investigated the role of Gpx1 during Con A-induced liver injury in Gpx1 knockout (KO) mice. Male wild-type (WT) mice and Gpx1 KO mice were intravenously injected with Con A (10 mg/kg), and then killed after 8 h after Con A injection. Serum levels of aspartate transaminase and alanine transaminase were measured to assess hepatic injury. To identify that Gpx1 affects T cell-mediated inflammation, we pretreated Gpx1 inhibitor to Human Jurkat T cells then treated Con A. Con A-induced massive liver damage in WT mice but its damage was attenuated in Gpx1 KO mice. Con A-induced Th1 cytokines such as tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ) and interleukin (IL)-2 were also decreased in the liver and spleen of Gpx1 KO mice compared with WT mice. In Jurkat T cells, Con A-induced mRNA levels of IL-2, IFN-γ and TNF-α were downregulated by pretreatment of Gpx inhibitor, mercaptosuccinic acid. We also observed that Gpx1 KO mice showed increasing oxidative stress in the liver and spleen compared with WT mice. These results suggest that Gpx1 deficiency attenuates Con A-induced liver injury by induction of T-cell hyporesponsiveness through chronic ROS exposure.

Case-matched comparison of ABO-incompatible and ABO-compatible living donor liver transplantation.

BACKGROUND: ABO-incompatible (ABO-I) living donor liver transplantation (LDLT) has a high success rate. There are few detailed comparisons regarding biliary complications, infective complications and patient survival between ABO-compatible (ABO-C) and ABO-I LDLT. The aim was to compare the outcomes of ABO-I LDLT with those of ABO-C LDLT using the matched-pairs method. METHODS: Patients who underwent ABO-I LDLT procedures between 2010 and 2013 were studied. They were matched for significant variables with patients who had ABO-C LDLT (1:2 matching). RESULTS: Forty-seven ABO-I LDLT procedures were included. Ninety-four patients who had ABO-C LDLT were selected as a comparator group. The incidence of cytomegalovirus, bacterial and fungal infections during the first 3 months was similar after ABO-I LDLT and ABO-C LDLT (85 versus 76 per cent, 28 versus 37 per cent, and 13 versus 20 per cent, respectively). Antibody-mediated rejection occurred after two procedures within 2 weeks of transplantation, but liver function improved with plasma exchange in both patients. There were no differences in the rate of acute rejection and biliary complications between ABO-I and ABO-C groups (P = 0.478 and P = 0.511 respectively). Three patients who had ABO-I LDLT developed diffuse intrahepatic biliary complications and progressed to graft failure. The 1-, 2- and 3-year patient survival rates after ABO-I LDLT and ABO-C LDLT were 89 versus 87 per cent, 85 versus 83 per cent, and 85 versus 79 per cent, respectively. CONCLUSION: The short-term outcomes of ABO-I LDLT were comparable to those of ABO-C LDLT in this study. ABO-I LDLT is an effective and safe transplant option with the potential to expand the pool of live donors.

Seroepidemiology of varicella-zoster virus in Korean adolescents and adults using fluorescent antibody to membrane antigen test.

We conducted a cross-sectional seroepidemiological study in 2012-2013 to determine the seroprevalence of varicella-zoster virus (VZV) in adolescents and adults living in Korea, where varicella vaccination has been recommended universally at age 12-15 months since 2005. Residual serum samples were collected from 1196 healthy adults and adolescents aged ⩾10 years between November 2012 and March 2013. The fluorescent antibody to membrane antigen (FAMA) test and enzyme-linked immunosorbent assay (ELISA) were performed to determine the seroprevalence of VZV. The seroprevalences of VZV were compared between six age groups: 10-19, 20-29, 30-39, 40-49, 50-59, and ⩾60 years. The seroprevalence of VZV in the entire study cohort was 99·1% according to the FAMA test and 93·1% as determined by ELISA. The seroprevalences of the six age groups were as follows: 96·0%, 99·5%, 99·5%, 99·5%, 100%, and 100%, respectively, by the FAMA test, and 83·3%, 93·0%, 93·0%, 97·5%, 94·5%, and 97·5%, respectively, by ELISA. Seroprevalence increased significantly with age (P < 0·001); moreover, the seroprevalence in subjects aged 10-19 years was significantly lower than in other age groups (P < 0·001), as measured by both the FAMA test and ELISA. Thus, strategies to increase protective immunity against VZV in teenagers are necessary.

Physical characterization and in vitro skin permeation of solid lipid nanoparticles for transdermal delivery of quercetin.

OBJECTIVE: Quercetin, a phenolic compound isolated from plants, can act as an antioxidant to protect the skin from oxidative stress induced by ultraviolet rays. The aims of this work were (i) to compare the physical characterization of quercetin-loaded solid lipid nanoparticles (QSLNs) and (ii) to investigate the enhanced skin permeation of quercetin using QSLNs. METHODS: QSLNs were prepared with a certain amount lipid (palmitic acid) and the different ratio of surfactant (Tween(®) 80) by homogenization and ultrasonification method. RESULTS: QSLNs showed mono-dispersed particle size distribution in the ranges of 274.0-986.6 nm and zeta potential from -50.4 to -29.4 mV. Entrapment efficiency of QSLN was 15.2-46.2%, and their crystallinity index was low (0-18.2%). In vitro occlusion test showed QSLN-2 has the highest occlusive effect due to its smallest particle size (274.0 nm), and through these result, QSLN-2 was selected as the optimum formulation. Transmission electron microscopy (TEM) analysis further confirmed the uniform spherical shape of QSLN-2 particles. Field emission-scanning electron microscope (FE-SEM) analysis and histological observation of hairless rat skin showed that the lipid particles of QSLN-2 formed a fused lipid film and, subsequently, it hydrated the surface of the rat skin. Franz diffusion cell was used to measure in vitro skin permeation of quercetin dissolved in propylene glycol (QPG), QSLN-2 and QSLN-3. The results showed that QSLN-2 (33.5 µg cm(-2) , 21.9%) exhibited higher skin permeability than QPG (6.6 µg cm(-2) , 4.2%) and QSLN-3 (14.2 µg cm(-2) , 9.1%), which was visually confirmed by confocal laser scanning microscope (CLSM) image analysis as well. CONCLUSION: The results suggest that QSLN-2, prepared with a surfactant content of 2%, could be used as useful skin delivery system for transdermal delivery of hydrophobic antioxidants such as quercetin.

Loss of presenilin 2 is associated with increased iPLA2 activity and lung tumor development.

Presenilins are the enzymatic components of γ-secretase complex that cleaves amyloid precursor protein, Notch and ß-catenin, which has critical roles in the development of Alzheimer's disease and cancer cell growth. Therefore, in the present study, we studied the effects and mechanisms of PS2 knockout on lung cancer development and possible mechanisms as a key regulator of lung tumor development. We compared carcinogen-induced tumor growth between PS2 knockout mice and wild-type mice. PS2 knockout mice showed increased urethane (1 mg/g)-induced lung tumor incidence when compared with that of wild-type mice with decreased activity of γ-secretase in the lung tumor tissues. Consequently, iPLA2 activities in lung tumor tissues of PS2 knockout mice were much higher than in tumor tissues of wild-type mice. Furthermore, knockdown of PS2 using PS2 siRNA decreased γ-secretase activity with increased iPLA2 activity in the lung cancer cells (A549 and NCI-H460), leading to increased lung cancer cell growth. PS2 knockout mice and PS2 knockdown lung cancer cells showed increased DNA-binding activities of nuclear factor kappa-beta, signal transducer and activator of transcription 3 (STAT3) and AP-1 which are critical transcriptional factors of iPLA2 than those of PS2 wild-type mice and control lung cancer cells. Taken together, these results suggest that the loss of PS2 could have a critical role in lung tumor development through the upregulation of iPLA2 activity by reducing γ-secretase.

Risk factors for inadvertent hypothermia during adult living-donor liver transplantation.

BACKGROUND: Hypothermia (core temperature <35°C) causes multiple physiologic disturbances, including coagulopathy and cardiac dysfunction. Patients undergoing liver transplantation are at risk of inadvertent hypothermia and might be more vulnerable to its adverse effects. We sought to identify the factors contributing to hypothermia during living-donor liver transplantation (LDLT), which have not yet been studied in depth. METHODS: Medical records of 134 recipients who underwent adult-to-adult LDLT were reviewed. Core temperature at the following time points were taken: anesthetic induction, skin incision, start and end of the anhepatic phase, and hourly after hepatic reperfusion. RESULTS: Of 134 recipients, 29 (21.6%) developed hypothermia during surgery. Four independent risk factors for hypothermia were identified: small body weight-to-body surface area ratio, acute hepatic failure, high Model for End-Stage Liver Disease (MELD) score, and low graft-to-recipient weight ratio. The amount of core temperature drop was positively correlated with the number of involved risk factors. Each risk factor had a respective contribution according to the operative phases: body weight-to-body surface area ratio and the MELD score for the preanhepatic phase, acute deterioration of hepatic failure for the anhepatic phase, and graft-to-recipient weight ratio was for the postreperfusion phase. CONCLUSIONS: Hypothermia was independently associated with the recipient's morphometric characteristics, emergency of end-stage liver disease, MELD score, and graft volume. These factors showed a cumulative effect, and the role of each factor was different according to the operative phase. These results should aid in the development of an optimal thermal strategy during LDLT.

Brain MRI measurements at a term-equivalent age and their relationship to neurodevelopmental outcomes.

BACKGROUND AND PURPOSE: An increased prevalence of disabilities is being observed as more preterm infants survive. This study was conducted to evaluate correlations between brain MR imaging measurements taken at a term-equivalent age and neurodevelopmental outcome at 2 years' corrected age among very low-birth-weight infants. MATERIALS AND METHODS: Of the various brain MR imaging measurements obtained at term-equivalent ages, reproducible measurements of the transcerebellar diameter and anteroposterior length of the corpus callosum on sagittal images were compared with neurodevelopmental outcomes evaluated by the Bayley Scales of Infant Development (II) at 2 years' corrected age (mean ± standard deviation, 16.1 ± 6.4 months of age). RESULTS: Ninety infants were enrolled. The mean gestational age at birth was 27 weeks and the mean birth weight was 805.5 g. A short corpus callosal length was associated with a Mental Developmental Index <70 (P = .047) and high-risk or diagnosed cerebral palsy (P = .049). A small transcerebellar diameter was associated with a Psychomotor Developmental Index <70 (P = .003), Mental Developmental Index <70 (P = .004), and major neurologic disability (P = .006). CONCLUSIONS: A small transcerebellar diameter and short corpus callosal length on brain MR imaging at a term-equivalent age are related to adverse neurodevelopmental outcomes at a corrected age of 2 years and could be a useful adjunctive tool for counseling parents about future developmental outcomes.

Placenta-derived mesenchymal stem cells improve memory dysfunction in an Aß1-42-infused mouse model of Alzheimer's disease.

Mesenchymal stem cells (MSCs) promote functional recoveries in pathological experimental models of central nervous system (CNS) and are currently being tested in clinical trials for neurological disorders, but preventive mechanisms of placenta-derived MSCs (PD-MSCs) for Alzheimer's disease are poorly understood. Herein, we investigated the inhibitory effect of PD-MSCs on neuronal cell death and memory impairment in Aß1-42-infused mice. After intracerebroventrical (ICV) infusion of Aß1-42 for 14 days, the cognitive function was assessed by the Morris water maze test and passive avoidance test. Our results showed that the transplantation of PD-MSCs into Aß1-42-infused mice significantly improved cognitive impairment, and behavioral changes attenuated the expression of APP, BACE1, and Aß, as well as the activity of ß-secretase and γ-secretase. In addition, the activation of glia cells and the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were inhibited by the transplantation of PD-MSCs. Furthermore, we also found that PD-MSCs downregulated the release of inflammatory cytokines as well as prevented neuronal cell death and promoted neuronal cell differentiation from neuronal progenitor cells in Aß1-42-infused mice. These data indicate that PD-MSC mediates neuroprotection by regulating neuronal death, neurogenesis, glia cell activation in hippocampus, and altering cytokine expression, suggesting a close link between the therapeutic effects of MSCs and the damaged CNS in Alzheimer's disease.

Antitumor activity of IL-32ß through the activation of lymphocytes, and the inactivation of NF-κB and STAT3 signals.

Cytokine and activation of lymphocytes are critical for tumor growth. We investigated whether interleukin (IL)-32ß overexpression changes other cytokine levels and activates cytotoxic lymphocyte, and thus modify tumor growth. Herein, IL-32ß inhibited B16 melanoma growth in IL-32ß-overexpressing transgenic mice (IL-32ß mice), and downregulated the expressions of anti-apoptotic proteins (bcl-2, IAP, and XIAP) and cell growth regulatory proteins (Ki-67 antigen (Ki-67) and proliferating cell nuclear antigen (PCNA)), but upregulated the expressions of pro-apoptotic proteins (bax, cleaved caspase-3, and cleaved caspase-9). IL-32ß also inhibited colon and prostate tumor growth in athymic nude mice inoculated with IL-32ß-transfected SW620 colon or PC3 prostate cancer cells. The forced expression of IL-32ß also inhibited cell growth in cultured colon and prostate cancer cells, and these inhibitory effects were abolished by IL-32 small interfering RNA (siRNA). IL-10 levels were elevated, but IL-1ß, IL-6, and tumor necrosis factor-alpha (TNF-α) levels were reduced in the tumor tissues and spleens of IL-32ß mice, and athymic nude mice. The number of cytotoxic T (CD8(+)) and natural killer (NK) cells in tumor tissues, spleen, and blood was significantly elevated in IL-32ß mice and athymic nude mice inoculated with IL-32ß-transfected cancer cells. Constituted activated NF-κB and STAT3 levels were reduced in the tumor tissues of IL-32ß mice and athymic nude mice, as well as in IL-32ß-transfected cultured cancer cells. These findings suggest that IL-32ß inhibits tumor growth by increasing cytotoxic lymphocyte numbers, and by inactivating the NF-κB and STAT3 pathways through changing of cytokine levels in tumor tissues.

Clinical characteristics and antibiotic susceptibility of viridans streptococcal bacteremia in children with febrile neutropenia.

PURPOSE: This retrospective study was performed in order to investigate the clinical characteristics and antibiotic susceptibility of viridans streptococcal bacteremia (VSB) in febrile neutropenic children in the context of the increase in incidence and antibiotic resistance of VSB. METHODS: We conducted this study among neutropenic children with underlying hematology/oncology diseases who were diagnosed with VSB at a single institution from April 2009 to June 2012. Clinical and laboratory characteristics of the children as well as antibiotic susceptibility of the causative viridans streptococci were evaluated. RESULTS: Fifty-seven episodes of VSB were diagnosed in 50 children. Severe complications occurred in four children (7.0%), and a death of one child (1.8%) was attributable to VSB. Acute myeloid leukemia was the most common underlying disease (70.2% of all cases), and 71.9% of all cases received chemotherapy including high-dose cytarabine. VSB occurred at a median of 13 days (range 8-21 days) after the beginning of chemotherapy, and fever lasted for a median of 4 days (range 1-21 days). The C-reactive protein level significantly increased within a week after the occurrence of VSB (p < 0.001) and the maximum C-reactive protein level showed a positive correlation with fever duration (r = 0.362, p = 0.007). Second blood cultures were done before the use of glycopeptides in 33 children, and negative results were observed in 30 children (90.9%). Susceptibilities to cefotaxime, cefepime, and vancomycin were 58.9, 69.1, and 100%, respectively. CONCLUSIONS: Severe complications of VSB in neutropenic febrile children were rare. We suggest glycopeptide use according to the results of blood culture and antibiotic susceptibility tests based on the susceptibility to cefepime and the microbiologic response to empirical antibiotic treatment not including glycopeptides in this study.

Effect of active airway warming on body core temperature during adult liver transplantation.

INTRODUCTION: Active inspired gas humidification (AH) preserves body heat and maintains normothermia intraoperatively. However, it is unclear whether AH shows comparable influences during liver transplantation (OLT), which may be affected by both large internal heat loss and external heat supply. Thus, the aim of this study was to evaluate the effect of AH compared with passive humidification (PH) on body temperature in OLT. MATERIALS AND METHODS: Thirty-four adult patients undergoing living donor OLT were randomly enrolled into two groups: those given AH using a heated humidifier (HH group, n = 17) and those using a heat-and-moisture exchanger (HME group, n = 17). Both core and skin temperatures (Tc and Ts), as well as respiratory parameters, including static/dynamic lung compliances and PaO(2), were recorded at predetermined times. RESULTS: Both Tc and Ts were consistently higher among the HH versus the HME group after 2 hours of anesthesia. Differences in Tc and Ts between the two groups increased gradually over time. The overall Tc during surgery was higher among the HH than the HME group (P = .023). The incidences of hypothermia were lower in the HH group at 3 hours of anesthesia, 1 and 3 hours of reperfusion, and at the end of surgery (P = .037, 0.024, 0.005, and 0.010 respectively). The duration of hypothermia was lower in the HH than the HME group (3.9 ± 3.5 hours versus 6.7 ± 3.3 hours, P = .025). Both groups showed no significant intraoperative changes in respiratory parameters; there were no postoperative respiratory complications. CONCLUSION: Active humidification warms the patient's body effectively, lessening the incidence and duration of hypothermia during OLT with no respiratory risks.

4-O-methylhonokiol, a PPARγ agonist, inhibits prostate tumour growth: p21-mediated suppression of NF-κB activity.

BACKGROUND AND PURPOSE: The effects of 4-O-methylhonokiol (MH), a constituent of Magnolia officinalis, were investigated on human prostate cancer cells and its mechanism of action elucidated. EXPERIMENTAL APPROACH: The anti-cancer effects of MH were examined in prostate cancer and normal cells. The effects were validated in vivo using a mouse xenograft model. KEY RESULTS: MH increased the expression of PPARγ in prostate PC-3 and LNCap cells. The pull-down assay and molecular docking study indicated that MH directly binds to PPARγ. MH also increased transcriptional activity of PPARγ but decreased NF-κB activity. MH inhibited the growth of human prostate cancer cells, an effect attenuated by the PPARγ antagonist GW9662. MH induced apoptotic cell death and this was related to G(0) -G(1) phase cell cycle arrest. MH increased the expression of the cell cycle regulator p21, and apoptotic proteins, whereas it decreased phosphorylation of Rb and anti-apoptotic proteins. Transfection of PC3 cells with p21 siRNA or a p21 mutant plasmid on the cyclin D1/ cycline-dependent kinase 4 binding site abolished the effects of MH on cell growth, cell viability and related protein expression. In the animal studies, MH inhibited tumour growth, NF-κB activity and expression of anti-apoptotic proteins, whereas it increased the transcriptional activity and expression of PPARγ, and the expression of apoptotic proteins and p21 in tumour tissues. CONCLUSIONS AND IMPLICATION: MH inhibits growth of human prostate cancer cells through activation of PPARγ, suppression of NF-κB and arrest of the cell cycle. Thus, MH might be a useful tool for treatment of prostate cancer.