Method for testing freeform surfaces based on a Shack-Hartmann sensor with plane wavefront scanning and stitching.

Currently, the surface error measurement technology for freeform faces a significant contradiction between measurement accuracy and dynamic range. The study proposes a non-null testing method for measuring freeform surfaces by utilizing a Shack-Hartmann wavefront sensor to emit a small aperture parallel beam and scan along the normal direction at the center of subapertures for stitching (SHPSS). A mathematical model based on ray tracing and the reflection theorem is established to calculate the sampling points on an ideal freeform surface, the reference spot array on CCD, and the corresponding relationship between microlens array and spots. An algorithm is proposed to iteratively calculate the wavefront aberration and gradually approach the actual sampling points using the established model. Theoretical analysis and numerical simulation results indicate that SHPSS can increase the dynamic range and improve the accuracy of wavefront reconstruction. The error analysis of the SHPSS method is carried out, the measurement accuracy of full aperture freeform surface is 11.45 nm. A testing system is set up and experiments are conducted on a 100 mm aperture freeform reflective mirror. The RMS of the SHPSS test results is less than λ/30 (λ=635 nm) compared to the interferometric test results. By analyzing five groups of repeated measurement experiments, the repeatability accuracy of SHPSS method is less than 1/80 λ (RMS). This demonstrates the feasibility and measurement capabilities of the method for freeform surface testing.

Development and validation of a nomogram for predicting cefoperazone/sulbactam-induced hypoprothrombinaemia in Hospitalized adult patients.

Cefoperazone/sulbactam-induced hypoprothrombinaemia is associated with longer hospital stays and increased risk of death. The aim of this study was to develop and validate a nomogram for predicting the occurrence of cefoperazone/sulbactam-induced hypoprothrombinaemia in hospitalized adult patients. This retrospective cohort study involved hospitalized adult patients at Xi'an Central Hospital from January 2020 to December 2022 based on the Chinese pharmacovigilance system developed and established by the Adverse Drug Reaction Monitoring Center in China. Independent predictors of cefoperazone/sulbactam-induced hypoprothrombinaemia were obtained using multivariate logistic regression and were used to develop and establish the nomogram. According to the same standard, the clinical data of hospitalized patients using cefoperazone/sulbactam at the Third Affiliated Hospital of Xi'an Medical University from January 1, 2023 to June 30, 2023 were collected as the external validation group. The 893 hospitalized patients included 95 who were diagnosed with cefoperazone/sulbactam-induced hypoprothrombinaemia. Our study enrolled 610 patients: 427 in the training group and 183 in the internal validation group. The independent predictors of cefoperazone/sulbactam-induced hypoprothrombinaemia were surgery (odds ratio [OR] = 5.279, 95% confidence interval [CI] = 2.597-10.729), baseline platelet count ≤50×109/L (OR = 2.492, 95% CI = 1.110-5.593), baseline hepatic dysfunction (OR = 12.362, 95% CI = 3.277-46.635), cumulative defined daily doses (OR = 1.162, 95% CI = 1.162-1.221) and nutritional risk (OR = 16.973, 95% CI = 7.339-39.254). The areas under the curve (AUC) of the receiver operating characteristic for the training and internal validation groups were 0.909 (95% CI = 0.875-0.943) and 0.888 (95% CI = 0.832-0.944), respectively. The Hosmer-Lemeshow tests yielded p = 0.475 and p = 0.742 for the training and internal validation groups, respectively, confirming the goodness of fit of the nomogram model. In the external validation group (n = 221), the nomogram was equally robust in cefoperazone/sulbactam-induced hypoprothrombinaemia (AUC = 0.837, 95%CI = 0.736-0.938). The nomogram model constructed in this study had good predictive performance and extrapolation, which can help clinicians to identify patients at high risk of cefoperazone/sulbactam-induced hypoprothrombinaemia early. This will be useful in preventing the occurrence of cefoperazone/sulbactam-induced hypoprothrombinaemia and allowing timely intervention measures to be performed.

Epileptic convulsions probably induced by desloratadine: a case report.

Desloratadine, a second generation H1-antihistamine, is generally considered to be safe. We found only one article reporting four children with a family or disease history of epilepsy who developed the condition after desloratadine treatment, with all four patients recovering well. Here we describe a healthy boy who developed left-arm convulsions on day 68 after taking desloratadine, at which point the desloratadine treatment was immediately stopped. Investigations were completed on day 83 and the patient was diagnosed with epilepsy. He was prescribed sodium valproate combined with oxcarbazepine, topiramate, lamotrigine and clonazepam for 15 months, which did not control the convulsions. During the following 3 months the patient received sodium valproate combined with lacosamide, and on day 615 the seizures stopped and no further convulsions occurred. At the follow-up, his father reported that the boy's memory was not as good as it had been previously. The convulsions continued after the withdrawal of desloratadine; therefore, the pathological mechanism of convulsion and the treatment plan need further research.

A reference human induced pluripotent stem cell line for large-scale collaborative studies.

Human induced pluripotent stem cell (iPSC) lines are a powerful tool for studying development and disease, but the considerable phenotypic variation between lines makes it challenging to replicate key findings and integrate data across research groups. To address this issue, we sub-cloned candidate human iPSC lines and deeply characterized their genetic properties using whole genome sequencing, their genomic stability upon CRISPR-Cas9-based gene editing, and their phenotypic properties including differentiation to commonly used cell types. These studies identified KOLF2.1J as an all-around well-performing iPSC line. We then shared KOLF2.1J with groups around the world who tested its performance in head-to-head comparisons with their own preferred iPSC lines across a diverse range of differentiation protocols and functional assays. On the strength of these findings, we have made KOLF2.1J and its gene-edited derivative clones readily accessible to promote the standardization required for large-scale collaborative science in the stem cell field.

Lipopolysaccharide facilitates immune escape of hepatocellular carcinoma cells via m6A modification of lncRNA MIR155HG to upregulate PD-L1 expression.

Recent studies have suggested that the initiation and progression of hepatocellular carcinoma (HCC) are closely associated with lipopolysaccharide (LPS) of intestinal bacteria. However, the role of LPS in immune regulation of HCC remains largely unknown. An orthotopic Hepa1-6 tumor model of HCC was constructed to analyze the effect of LPS on the expression of immune checkpoint molecules PD-1 and PD-L1. Then we verified the regulation of PD-L1 by LPS in HCC cells. Based on the previous finding that lncRNA MIR155HG regulates PD-L1 expression in HCC cells, we analyzed the relationship of LPS signaling pathway molecules with PD-L1 and MIR155HG by bioinformatics. The molecular mechanism of MIR155HG regulating PD-L1 expression induced by LPS was investigated by RNA pull-down followed by mass spectrometry, RNA immunoprecipitation, fluorescence in situ hybridization, and luciferase reporter assay. Finally, the HepG2 xenograft model was established to determine the role of MIR155HG on PD-L1 expression in vivo. We showed that LPS induced PD-1 and PD-L1 expression in mouse tumor tissues and induced PD-L1 expression in HCC cells. Mechanistically, upregulation of METTL14 by LPS promotes the m6A methylation of MIR155HG, which stabilizes MIR155HG relying on the "reader" protein ELAVL1 (also known as HuR)-dependent pathway. Moreover, MIR155HG functions as a competing endogenous RNA (ceRNA) to modulate the expression of PD-L1 by miR-223/STAT1 axis. Our results suggested that LPS plays a critical role in immune escape of HCC through METTL14/MIR155HG/PD-L1 axis. This study provides a new insight for understanding the complex immune microenvironment of HCC. 1. LPS plays a critical role in immune escape of HCC, especially HCC with cirrhosis. 2. Our study reveals that LPS regulates PD-L1 by m6A modification of lncRNA in HCC. 3. MIR155HG plays an important role in LPS induced PD-L1 expression. 4. LPS-MIR155HG-PD-L1 regulatory axis provides a new target for the treatment of HCC.

Beliefs about medication and their association with adherence in Chinese patients with non-dialysis chronic kidney disease stages 3-5.

ABSTRACT: There is a scarcity of research into the impact of medication beliefs on adherence in patients with non-dialysis chronic kidney disease (CKD). This study is to determine the psychometric properties of the Chinese version of the Beliefs about Medicines Questionnaire (BMQ)-Specific among patients with non-dialysis CKD stages 3-5, and to assess the beliefs of CKD patients and their association with medication adherence.A cross-sectional study was conducted in CKD patients who recruited at the nephrology clinics of Xi'an Central Hospital, Xi'an, Shaanxi, China. The original BMQ-Specific was translated into Chinese. The internal consistency and test-retest reliability of the Chinese version of the BMQ-Specific scale were assessed, while exploratory and confirmatory factor analyses were also applied to determine its reliability and validity. The Kruskal-Wallis test and multiple ordered logistic regression were performed to identify the relationship between beliefs about and adherence to medication among CKD patients.This study recruited 248 patients. Cronbach's α values of the BMQ-Specific necessity and concern subscales were 0.826 and 0.820, respectively, with intraclass correlation coefficients of 0.784 and 0.732. Factor analysis showed that BMQ-Specific provided a good fit to the two-factor model. The adherence of patients was positively correlated with perceived necessity (r = 0.264, P < .001) and negatively correlated with concern (r = -0.294, P < .001). Medication adherence was significantly higher for the accepting group (high necessity and low concern scores) than for the ambivalent group (high necessity and concern scores; ß = -0.880, 95% confidence interval [CI] = -1.475 to -0.285), skeptical group (low necessity and high concern scores; ß = -2.620, 95% CI = -4.209 to -1.031) and indifferent group (low necessity and concern scores; ß = -0.918, 95% CI = -1.724 to -0.112).The Chinese version of BMQ-Specific exhibited satisfactory reliability and validity for use in patients with non-dialysis CKD stages 3-5 and has been demonstrated to be a reliable screening tool for clinicians to use to predict and identify the non-adherence behaviors of patients.

Risk factors for linezolid-induced thrombocytopenia in adult inpatients.

Background Previous reports about risk factors for linezolid-induced thrombocytopenia have been insufficient, often due to the variability in study design and population, and some factors have not yet been studied. Aim The aims of this study are to determine potential risk factors for linezolid-induced thrombocytopenia, and to analyze the influencing factors of different thrombocytopenia definitions. Method This retrospective study involved patients who were administered intravenous linezolid for ≥ 1 day between January 1, 2015 and January 1, 2021. Their demographic and clinical data were extracted from electronic medical records. Thrombocytopenia was defined as: ①thrombocytopenia with platelet count < 100 × 109/L and a decrease in 25% or more from baseline of the platelet count (criterion 1); ②thrombocytopenia due to a platelet count drop decrease of 25% or more from baseline (criterion 2). Risk factors were determined via binary logistic regression analysis. Results This study included 320 patients. Binary logistic regression analysis indicated that baseline platelet count (p < 0.001), linezolid therapy duration (p = 0.001) and shock (patients require vasoactive medications) (p = 0.019) were independent risk factors for criterion-1thrombocytopenia, while linezolid therapy duration (p < 0.001) and shock (p = 0.015) were independent risk factors for criterion-2 thrombocytopenia. There was also a significant correlation between shock and early-onset thrombocytopenia (p = 0.005 and 0.019 for criterion 1 and criterion 2, respectively). Conclusion Linezolid therapy duration and shock were common causes of different thrombocytopenia definitions; shock was correlated with early-onset thrombocytopenia. Platelet count should be monitored during linezolid therapy especially during long-duration therapy and in shock patients.

LncRNA MIAT correlates with immune infiltrates and drug reactions in hepatocellular carcinoma.

Long non-coding RNA (lncRNA) is a kind of important molecules involved in the formation of immune landscape in tumor microenvironment. However, there are few studies on the relationship between lncRNA and immunomodulatory regulation of hepatocellular carcinoma (HCC). In this study, we combined with single cell transcriptome sequencing and TCGA data to analyze the relationship between lncRNA MIAT and immune cells in HCC. TIMER database analysis indicated that the expression of MIAT in HCC was negatively correlated with tumor purity, positively correlated with the number of immune cells such as B cells, T lymphocytes and macrophages, and positively correlated with the expression of immune checkpoint molecules such as PD-1, PD-L1 and CTLA4. Analysis of single cell sequencing data of immune cells in HCC showed that MIAT was mainly distributed in tumor, and enriched in FOXP3+CD4+T cells and PDCD1+CD8+, GZMK+CD8+T cells, indicating that MIAT may be involved in the immune escape process of HCC. Besides, through the construction of transcription factor (TF) regulatory network, MIAT-TF-mRNA, we found that the interaction of MIAT and TFs may affect the immune microenvironment of LIHC by regulating the expression of target genes JAK2, SLC6A6, KCND1, MEIS3 or RIN1; LncMAP and CARE analysis showed that MIAT was highly related to the sensitivity of many anticancer drugs, especially sorafenib. In addition, the effect of MIAT on PD-L1 and its relationship with sorafinib were verified in clinical specimens and cells. This study made a meaningful attempt to reveal the immune escape mechanism and to find the effectiveness of targeted drugs in patients with HCC.

2,5-dimethylcelecoxib improves immune microenvironment of hepatocellular carcinoma by promoting ubiquitination of HBx-induced PD-L1.

BACKGROUND: 2,5-dimethylcelecoxib (DMC) is a targeted inhibitor of microsomal prostaglandin E synthase-1 (mPGES-1), a key enzyme in the PGE2 synthesis pathway of inflammatory mediators. Previous studies have confirmed that DMC can inhibit the growth of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). However, it is not known whether DMC is involved in the changes of tumor immune microenvironment. METHODS: In this study, we explored the effects of DMC on HBV-related HCC immune microenvironment, and deeply analyzed its unique effect and mechanism on programmed death receptor 1 (PD-1)/and its ligand 1 (PD-L1) pathway. RESULTS: Clinical hepatoma tissues detection showed that compared with non-virus-related HCC, the level of CD8 of HBV-related HCC was significantly lower, while the levels of PD-L1 and CD163 were higher. In vivo experiments indicated that DMC could increase the level of tumor infiltrating CD8+ T cells in hepatitis B virus X (HBx) (+) hepatoma cells implanted mouse models, and inhibit the expression of PD-L1 and CD163 in tumor tissues. DMC combined with atezolizumab had more significant antitumor effect and stronger blocking effect on PD-1/PD-L1 pathway. Mechanism studies have shown that DMC can promote ubiquitin degradation of HBx-induced PD-L1 protein in HCC cells by activating adenosine 5'-monophosphate-activated protein kinase pathway. Further experiments confirmed that this process was mainly mediated by E3 ligase RBX1. CONCLUSIONS: Our results uncover a role for DMC in promoting HBV-related HCC immune microenvironment, which not only enrich the relationship between inflammatory factors (mPGES-1/PGE2 pathway) and immunosuppression (PD-L1), but also provide an important strategic reference for multitarget or combined immunotherapy of HBV-related HCC.

Hepatitis B virus X protein (HBx) promotes ST2 expression by GATA2 in liver cells.

At present, most studies on the relationship between hepatitis B virus (HBV) and IL-33/ST2 axis focus on clinical detection, but the underlying molecular mechanisms of HBx and IL-33/ST2 axis regulation and Th cell function regulation have not been explored. In this study, serum samples of patients with chronic hepatitis B (CHB) and HBV-related liver cancer (HBV-HCC), and healthy controls, as well as the supernatant solutions of HL7702-WT, HL7702-NC, and HL7702-HBx cells were collected to detect the content of soluble ST2 (sST2). The contents of Th1 cytokines (TNF-α and TNF-γ) and Th2 cytokines (IL-6 and IL-10) in the supernatant of different co-culture groups were detected. The effects of GATA2 on ST2 promoter transcription were investigated by upregulation or interference with GATA2 expression, dual-luciferase reporting, and ChIP experiments. The combined detection of sST2 and FIB-4 was beneficial to the non-invasive diagnosis of liver fibrosis. HBx promotes sST2 expression in liver cells, upregulates Th2 cell function, and inhibits Th1 cell function through IL-33/ST2 axis. HBx interacts with GATA2 to influence the activity of ST2 promoter. Serum sST2 detection is an invaluable indicator for the assessment of the progress of HBV infectious diseases, and the IL-33/ST2 axis plays an important role in changing the cellular immune function caused by HBV infection.

Assessment of direct oral anticoagulants administered as potentially inappropriate medications to elderly inpatients.

Background There is evidence that direct oral anticoagulants administered as potentially inappropriate medications increase the risk of bleeding and thromboembolic complications, which represent serious threats to human health. Objective To identify direct oral anticoagulants administered as potentially inappropriate medications for hospitalized patients aged ≥ 65 years in our hospital, and to determine associated factors and the correlation between potentially inappropriate medications and adverse reactions. Setting Xi'an Central Hospital, China. Method A retrospective cross-sectional study of elderly hospitalized patients who received either dabigatran or rivaroxaban at Xi'an Central Hospital between June 1, 2018 and June 1, 2019. The evaluation criteria of direct oral anticoagulants were formulated based on drug labels, disease guidelines and the 2019 American Geriatrics Society Beers Criteria, and any non-compliance with the criteria was considered to be potentially inappropriate medications. The Pearson chi-square test and a binary logistic regression model were used. Main outcome measure Factors associated with potentially inappropriate medications and correlation between potentially inappropriate medications and adverse reactions. Results This study analysed 315 patients aged ≥ 65 years. The application of our evaluation criteria identified 155 (49.2%) instances of potentially inappropriate medications, comprising 5 different types of potentially inappropriate medications. Fifteen adverse drug reactions occurred in the study participants. The Pearson chi-square test revealed significant differences in number of medications (p = 0.021) and creatinine clearance rate (p = 0.002) between potentially inappropriate medications and non-potentially inappropriate medications groups. In the binary logistic regression model, potentially inappropriate medications use was associated with creatinine clearance (creatinine clearance < 30: OR = 3.590, 95% CI = 1.214-10.615, p = 0.021), and there was no significant correlation between potentially inappropriate medications and adverse drug reactions after eliminating the confounding factors (age, length of hospitalization, number of disease combined) with p values of less than 0.25 (adjusted OR = 0.372, 95% CI = 0.117-1.182, p = 0.094). Conclusion This study revealed that the incidence of potentially inappropriate medications was relatively high, number of medications and creatinine clearance differed significantly between potentially inappropriate medications and non-potentially inappropriate medications groups, and potentially inappropriate medications was associated with creatinine clearance (creatinine clearance < 30 mL/min), but there was no significant correlation between potentially inappropriate medications and adverse drug reactions after eliminating the confounding factors.

SOD2 promotes the expression of ABCC2 through lncRNA CLCA3p and improves the detoxification capability of liver cells.

Superoxide dismutase 2 (SOD2) is a key enzyme for scavenging reactive oxygen species produced by mitochondria, which plays an important role in maintaining cellular homeostasis. However, its effects on the detoxification capability of liver cells have not been reported. In this study, we found that change in SOD2 expression affects the proliferation of liver cells. Genome-wide microarray analysis showed that SOD2 positively regulates the drug transporter ABCC2, and co-expression analysis suggested that lncRNA CLCA3P participates in the process. Further experiments showed that SOD2 can promote the expression of CLCA3P, which increases the transcription of ABCC2 by interacting with the transcription factor IRF1. By increasing ABCC2 expression SOD2 facilitates drugs efflux of liver cells and thus promotes their survival under a drug-toxic environment. This study elucidates the improvement of the detoxification of liver cells by a regulatory axis, SOD2-CLCA3P-IRF1-ABCC2, and provides novel insight into the modification of human liver cells that can be applied to bioartificial liver system or the study of SOD2 in drug metabolism.

Photo/thermo-responsive and size-switchable nanoparticles for chemo-photothermal therapy against orthotopic breast cancer.

Tumor penetration of nanocarriers is still an unresolved challenge for effective drug delivery. Herein, we described a size-switchable nanoplatform in response to an external near-infrared (NIR) laser for transcellular drug delivery. The nanoplatform was constructed with a poly(N-isopropylacrylamide) (PNIPAM)-based nanogel encapsulating chitosan-coated single-walled carbon nanotubes, followed by loading a chemotherapeutic drug, doxorubicin (DOX). In mice bearing orthotopic breast tumors, the photothermal effect from single-walled carbon nanotubes upon NIR irradiation potently inhibited tumor growth. The antitumor effect of the nanomedicine with NIR irradiation might be attributed to its capability of transcellular transport and tumor penetration in mice. In addition, the nanomedicine with NIR irradiation could elicit an antitumor response by increasing cytotoxic T cells and decreasing myeloid-derived suppressor cells. These results validated the application of photo/thermo-responsive nanomedicine in the orthotopic model of breast cancer.

MIR155HG is a prognostic biomarker and associated with immune infiltration and immune checkpoint molecules expression in multiple cancers.

In recent years, immune checkpoint inhibitor has achieved remarkable success in multiple cancer treatment. However, how to pre-judge which patients are suitable for immune checkpoint inhibitor is a difficult problem. We use the existing public bioinformatics database to comprehensively analyze the relationship between clinical data of various cancers with immune checkpoint blocking molecules and long non-coding RNAs (lncRNAs), and try to find the potential predictive value of lncRNA for immunotherapy with checkpoint inhibitors. In this study, we found that: (a) high expression of lncRNA MIR155 host gene (MIR155HG) was closely related to better overall survival (OS) in cholangiocarcinoma (CHOL), lung adenocarcinoma (LUAD), and skin cutaneous melanoma (SKCM), and have better disease-free survival (DFS) in CHOL. Meanwhile, the high level of MIR155HG was associated with poorer OS in glioblastoma multiforme (GBM), kidney renal clear cell carcinoma (KIRC), brain lower grade glioma (LGG), and uveal melanoma (UVM). (b) The expression of MIR155HG was significantly correlated with infiltrating levels of immune cells and immune molecules, especially with immune checkpoint molecules such as programmed cell death protein 1 (PD-1), PD-1 ligand 1 (PD-L1), and cytotoxic T lymphocyte-associated antigen 4 (CTLA4) in most kinds of cancers. (c) Detection of clinical CHOL and liver hepatocellular carcinoma tissues confirmed that there was a strong positive correlation between MIR155HG expression and the levels of CTLA4 and PD-L1. MIR155 host gene can be used as a prognostic marker in multiple cancers, and of great value in predicting the curative effect of immune checkpoint inhibitor therapy owing to it is closely related with immune cells infiltration and immune checkpoint molecules expression.

The influence of concomitant antiepileptic drugs on lamotrigine serum concentrations in Northwest Chinese Han population with epilepsy.

OBJECTIVE: The aims of this study were to identify the influencing factors such as gender, age, dose and combinations of other antiepileptic drugs (AEDs), especially in triple combinations on the pharmacokinetic of Lamotrigine (LTG) in epilepsy patients of Northwest Chinese Han population. METHODS: Data of the LTG concentration and clinical information were analyzed retrospectively from a therapeutic drug monitoring (TDM) database at the Clinical Pharmacy Laboratory of Xi'an Central Hospital between January 1, 2016 and January 1, 2018. The independent-sample t-test, one-way ANOVA analysis and Bonferroni and Tamhane T3 post-hoc test, the stepwise multivariate regression analysis were adopted by IBM SPSS, version 22.0. RESULTS: 226 serum samples met the inclusion criteria and were evaluated. The mean LTG serum concentration was 5.48±3.83 µg/mL. There were no gender differences (P = 0.64), and there were no significant effects by age on LTG serum concentration after age stratification (3-14 years old, 14-45 years old, 45-59 years old) (P = 0.05). Multiple regression analysis showed that the daily LTG dose and co-administration of other AEDs significantly affected LTG serum concentrations. Combination with enzyme-inducer AEDs, the mean steady-state LTG concentration could be decreased by 30.73% compared with LTG monotherapy. Among enzyme-inducer AEDs, particularly strong inducer Carbamazepine (CBZ) could decrease the mean LTG concentration by 53.65%, but weak inducer AEDs such as Oxcarbazepine (OXC) and Topiramate (TPM) had no effect, Valproic acid (VPA) could increase the mean LTG concentration by 93.95%, and the inducer only partially compensated for the inhibitory effect of VPA in triple combination. CONCLUSIONS: There were no significant gender and age effects, but the LTG daily dose and co-administration of other AEDs significantly affected LTG serum concentration. Combination with enzyme-inducer AEDs, especially CBZ could significantly decrease LTG serum concentrations, VPA could significantly increase LTG serum concentrations, and the inducer only partially compensated for the inhibitory effect of VPA in triple combination. In the clinical setting, these findings can help to estimate LTG concentrations and adjust dosage and evaluate adverse drug reactions.

Histone Deacetylase SIRT1 Targets Plk2 to Regulate Centriole Duplication.

The protein deacetylase SIRT1 (Sirtuin 1) regulates many cellular processes, including cell-cycle progression, DNA damage response, and metabolism. Although the centrosome is a key regulator of cell-cycle progression and genome stability, little is known concerning SIRT1 controlled centrosome-associated events. Here we report that the centrosome protein Plk2 is acetylated and undergoes deacetylation by SIRT1. Acetylation protects Plk2 from ubiquitination, and SIRT1-mediated deacetylation promotes ubiquitin-dependent degradation of Plk2. SIRT1 controls centriole duplication by temporally modulating centrosomal Plk2 levels. AURKA phosphorylates SIRT1 and promotes the SIRT1-Plk2 interaction in mitosis. In early-mid G1, phosphorylated SIRT1 deacetylates and promotes Plk2 degradation. In late G1, SIRT1 is hypophosphorylated and its affinity to Plk2 is decreased, resulting in a rapid accumulation of centrosomal Plk2, which contributes to the timely initiation of centriole duplication. Collectively, our findings uncover a critical role of SIRT1 in centriole duplication and provide a mechanistic insight into SIRT1-mediated centrosome-associated functions.

Diaphragmatic hernia as a rare complication of colonoscopy: Case report and literature review.

RATIONALE: Diaphragmatic Hernia is rare as complication of Colonoscopy. Diaphragmatic hernia as a complication of colonoscopy has been reported only few cases. Additionally, it is often misdiagnosed as other disease by clinicians due to their lack of related knowledge, which delays diagnosis of Diaphragmatic hernia and thus exacerbates the prognosis. PATIENT CONCERNS: We report the case of a 66-year-old man with fecal occult blood. In the case, sudden epigastric pain after colonoscopy owing to diaphragmatic hernia in a left hemidiaphragm. DIAGNOSES: The diagnoses made by a CT scan without delay. It showed marked protrusion of the large bowel into the left thoracic cavity along with elevation of the left diaphragm. INTERVENTIONS: The diaphragmatic defect was repaired by simple closure and intestinal adhesions release surgery. OUTCOMES: Five days after surgery, the patient was discharged in good condition. LESSONS: Most of diaphragmatic hernia is congenital with high mortality. However, there are a few cases of Diaphragmatic hernia caused by previous trauma or surgery. We herein report an unusual case of diaphragmatic hernia related to colonoscopy but usually life-threatening complication.

Preventive Antibiotics for Poststroke Infection in Patients With Acute Stroke: A Systematic Review and Meta-analysis.

AIMS: To determine if preventive antibiotics is effective in poststroke infection in patients with acute stroke in comparison with no prophylaxis. MATERIALS AND METHODS: MEDLINE (1950 to January 2017), the Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library, Issue 1, 2017) and EMBASE (1974 to January 2017) databases were used to search for randomized controlled trials with intervening measures related to the preventive antibiotics in patients with acute stroke. Besides, the reference lists of the retrieved publications were manually searched to explore other relevant studies. RESULTS: We included 6 randomized controlled trials involving 4110 stroke patients. The study population, study design, intervening measures, and definition of infection were different. Preventive antibiotics significantly reduced the incidence of algorithm-defined infection in patients with acute stroke from 11.14% (220/1975) to 7.43% (149/2006); odds ratio (OR)=0.41; 95% confidence interval (CI), 0.20-0.87; P=0.02. There was no difference in mortality between 2 groups, the mortality in preventive antibiotics group was 17.03% (347/2037) and control group was 16.10% (328/2037); OR=1.07; 95% CI, 0.90-1.27; P=0.44. And preventive antibiotics did not improve the proportion of good outcome, the proportion of good outcome in preventive antibiotics group was 45.47% (909/1999) and control group was 45.76% (913/1995); OR=0.89; 95% CI, 0.62-1.28; P=0.53. None of the studies reported severe adverse relevant to the study antibiotics. CONCLUSIONS: Preventive antibiotics significantly reduced the incidence of algorithm-defined infection in patients with acute stroke, but did not decrease the mortality or improve the proportion of good outcome. Future research should aim to identify the group of stroke patients who will benefit most from antibiotic prophylaxis.

First case of Stevens-Johnson syndrome after rabies vaccination.

We describe the first case of Stevens-Johnson syndrome (SJS) occurring 8 days after the first dose of a three-dose rabies vaccination series. She had no history of vaccine-related rash or other adverse drug reactions, nor had she received any other drug therapy. The temporal relationship between the development of SJS and the vaccination suggests that the rabies vaccination probably was the causal agent. This case serves as a warning of a distinct cutaneous reaction of rabies vaccination.