GSH exhaustion via inhibition of xCT-GSH-GPX4 pathway synergistically enhanced DSF/Cu-induced cuproptosis in myelodysplastic syndromes.

The clinical application of the therapeutic approach in myelodysplastic syndromes (MDS) remains an insurmountable challenge for the high propensity for progressing to acute myeloid leukemia and predominantly affecting elderly individuals. Thus, the discovery of molecular mechanisms underlying the regulatory network of different programmed cell death holds great promise for the identification of therapeutic targets and provides insights into new therapeutic avenues. Herein, we found that disulfiram/copper (DSF/Cu) significantly repressed the cell viability, increased reactive oxygen species (ROS) accumulation, destroyed mitochondrial morphology, and altered oxygen consumption rate. Further studies verified that DSF/Cu induces cuproptosis, as evidenced by the depletion of glutathione (GSH), aggregation of lipoylated DLAT, and induced loss of Fe-S cluster-containing proteins, which could be rescued by tetrathiomolybdate and knockdown of ferredoxin 1 (FDX1). Additionally, GSH contributed to the tolerance of DSF/Cu-mediated cuproptosis, while pharmacological chelation of GSH triggered ROS accumulation and sensitized cell death. The xCT-GSH-GPX4 axis is the ideal downstream component of ferroptosis that exerts a powerful protective mechanism. Notably, classical xCT inhibitors were capable of leading to the catastrophic accumulation of ROS and exerting synergistic cell death, while xCT overexpression restored these phenomena. Simvastatin, an inhibitor of HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase, has beneficial effects in repurposing for inhibiting GPX4. Similarly, the combination treatment of DSF/Cu and simvastatin dramatically decreased the expression of GPX4 and Fe-S proteins, ultimately accelerating cell death. Moreover, we identified that the combination treatment of DSF/Cu and simvastatin also had a synergistic antitumor effect in the MDS mouse model, with the reduced GPX4, increased COX-2 and accumulated lipid peroxides. Overall, our study provided insight into developing a novel synergistic strategy to sensitize MDS therapy by targeting ferroptosis and cuproptosis.

Evaluation of the clinical effect of a multimodal pre-rehabilitation program guided by the behaviour change wheel in elderly women with breast cancer.

BACKGROUND: This study aims to explore the nursing effect of a multimodal pre-rehabilitation programme guided by BCW theory on elderly women patients with breast cancer. METHODS: The participants were divided into two groups. The study group was administered with the pre-rehabilitation model guided by BCW theory; the control group was administered with conventional methods. The rehabilitation effects of the two groups were compared.. RESULTS: The scores of RISC, PTGI and FACT-B were higher in the study group(P < 0.05). The SUPPH score and ROM compliance rate were higher in the study group (P < 0.05) (96% vs 72%). The avoidance score and yield score were lower in the study group(P < 0.05). CONCLUSION: A multimodal pre-rehabilitation program guided by BCW theory can significantly improve the quality of life and functional status of elderly women patients with breast cancer, and its popularisation and application are recommended.

[Elesclomol-Cu Induces Cuproptosis in Human Acute Myeloid Leukemia Cells].

OBJECTIVE: To investigate the effects of elesclomol-Cu (ES-Cu) on the proliferation and cuproptosis of human acute myeloid leukemia (AML) cells. METHODS: The effects of ES-Cu on the proliferation of AML cells and the AML cells pre-treated with ammonium tetrathiomolybdate (TTM) were examined by CCK-8 assay. The Calcein/PI kit was used to detected the changes in activity and cytotoxicity of AML cells induced by ES-Cu. Flow cytometry and Cytation3 fully automated cell imaging multifunctional detection system were used to analyze DCFH-DA fluorescence intensity, so as to determine the level of reactive oxygen species (ROS). The GSH and GSSG detection kits were used to measure the intracellular GSH content. Western blot was used to detected the expression of cuproptosis-related proteins ATP7B, FDX1, DLAT and DPYD. RESULTS: ES-Cu inhibited the proliferation of Kasumi-1 and HL-60 cells in a concentration-dependent manner (r Kasumi-1=-0.99， r HL-60=-0.98). As the concentration of ES-Cu increased, the level of intracellular ROS also increased (P <0.01-0.001). TTM could significantly reverse the inhibitory effect of ES-Cu on cell proliferation and its promoting effect on ROS. With the increase of ES-Cu concentration, the content of GSH was decreased (r =-0.98), and Western blot showed that the protein expressions of ATP7B, FDX1, DLAT and DPYD were significantly reduced (P <0.05). CONCLUSION: ES-Cu can induce cuproptosis in AML cells, which provides a new idea for the treatment of AML.

The role of lncRNAKCNQ1OT1/miR-301b/Tcf7 axis in cardiac hypertrophy.

OBJECTIVE: Cardiac hypertrophy, acting as a pathologic process of chronic hypertension and coronary disease, and its underlying mechanisms still need to be explored. Long non-coding RNA (LncRNA) potassium voltage-gated channel subfamily Q member 1 Transcript 1 (KCNQ1OT1) has been implicated in myocardial infarction. However, its role in cardiac hypertrophy remains reported. METHOD: To explore the regulated effect of lncRNAKCNQ1OT1 and miR-301b in cardiac hypertrophy, gain-and-lose function assays were tested. The expression of lncRNAKCNQ1OT1 and miR-301b were tested by quantitative real time polymerase chain reaction (qRT-PCR). The levels of transcription factor 7 (Tcf7), Proto-oncogene c-myc (c-myc), Brainnatriureticpeptide (BNP) and ß-myosin heavy chain (ß-MHC) were detected by Western blot. Additionally, luciferase analysis revealed interaction between lncRNAKCNQ1OT1, BNPß-MHCmiR-301b, and Tcf7. RESULT: LncRNAKCNQ1OT1 overexpression significantly induced cardiac hypertrophy. Furthermore, lncRNAKCNQ1OT1 acts as a sponge for microRNA-301b, which exhibited lower expression in cardiac hypertrophy model, indicating an anti-hypertrophic role. Furthermore, the BNP and ß-MHC expression increased, as well as cardiomyocyte surface area, with Ang II treatment, while the effect was repealed by miR-301b. Moreover, the protein expression of Tcf7 was inversely regulated by miR-301b and Antisense miRNA oligonucleotides (AMO)-301b. CONCLUSION: Our study has shown that overexpression of lncRNAKCNQ1OT1 could promote the development of cardiac hypertrophy by regulating miR-301b and Tcf7. Therefore, inhibition of lncRNAKCNQ1OT1 might be a potential therapeutic strategy for cardiac hypertrophy.

Ferroptosis mechanisms and its novel potential therapeutic targets for DLBCL.

Diffuse large B-cell lymphoma (DLBCL), a heterogeneous lymphoid malignancy, poses a significant threat to human health. The standard therapeutic regimen for patients with DLBCL is rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP), with a typical cure rate of 50-70%. However, some patients either relapse after complete remission (CR) or exhibit resistance to R-CHOP treatment. Therefore, novel therapeutic approaches are imperative for managing high-risk or refractory DLBCL. Ferroptosis is driven by iron-dependent phospholipid peroxidation, a process that relies on the transition metal iron, reactive oxygen species (ROS), and phospholipids containing polyunsaturated fatty acids-containing phospholipids (PUFA-PLs). Research indicates that ferroptosis is implicated in various carcinogenic and anticancer pathways. Several hematological disorders exhibit heightened sensitivity to cell death induced by ferroptosis. DLBCL cells, in particular, demonstrate an increased demand for iron and an upregulation in the expression of fatty acid synthase. Additionally, there exists a correlation between ferroptosis-associated genes and the prognosis of DLBCL. Therefore, ferroptosis may be a promising novel target for DLBCL therapy. In this review, we elucidate ferroptosis mechanisms, its role in DLBCL, and the potential therapeutic targets in DLBCL. This review offers novel insights into the application of ferroptosis in treatment strategies for DLBCL.

The potential of targeting cuproptosis in the treatment of kidney renal clear cell carcinoma.

Renal cell carcinoma (RCC) is one of the top ten malignancies and tumor-related causes of death worldwide. The most common histologic subtype is kidney renal clear cell carcinoma (KIRC), accounting for approximately 75% of all RCC cases. Early resection is considered the basic treatment for patients with KIRC. However, approximately 30% of these patients experience recurrence post-operation. Cuproptosis, an autonomous mechanism for controlling cell death, encompasses various molecular mechanisms and multiple cellular metabolic pathways. These pathways mainly include copper metabolic signaling pathways, mitochondrial metabolism signaling pathways, and lipoic acid pathway signaling pathways. Recent evidence shows that cuproptosis is identified as a key cell death modality that plays a meaningful role in tumor progression. However, there is no published systematic review that summarizes the correlation between cuproptosis and KIRC, despite the fact that investigations on cuproptosis and the pathogenesis of KIRC have increased in past years. Researchers have discovered that exogenous copper infusion accelerates the dysfunction of mitochondrial dysfunction and suppresses KIRC cells by inducing cuproptosis. The levels of tricarboxylic acid cycle proteins, lipoic acid protein, copper, and ferredoxin 1 (FDX1) were dysregulated in KIRC cells, and the prognosis of patients with high FDX1 expression is better than that of patients with low expression. Cuproptosis played an indispensable role in the regulation of tumor microenvironment features, tumor progression, and long-term prognosis of KIRC. In this review, we summarized the systemic and cellular metabolic processes of copper and the copper-related signaling pathways, highlighting the potential targets related to cuproptosis for KIRC treatment.

Epidemic, risk factors of carbapenem-resistant Klebsiella pneumoniae infection and its effect on the early prognosis of liver transplantation.

Background: Carbapenem-resistant Klebsiella pneumoniae (CRKP) infection remains a major cause of morbidity and mortality in early-stage post-liver transplantation (LT). Methods: We retrospectively analyzed the demographic and clinical infections characteristics of all LT recipients in our hospital between January 2019 and December 2021. Results: Among the 272 LT recipients who received LT between January 2019 and December 2021, sixty-two patients had at least one infection within 3-months post-LT, with a prevalence of 22.8% (62/272). The prevalence of CRKP infections was 7.0% (19/272), and the 3-months post-LT mortality was 19.4% (12/62). The risk factors independently related to 3-months mortality were age (Odds ratio (OR)= 1.126, 95% Confidence interval (CI): 1.009~1.257; P=0.034), mechanical ventilation (MV) (OR=1.206, 95% CI: 1.039~1.401; P =0.014), and CRKP infection (OR=18.240, 95% CI: 2.206~150.842; P =0.007). In CRKP infection, the length of ICU stay (OR=1.067, 95% CI: 1.015~1.122; P=0.011), pre-operation infection (POI) (OR=6.733, 95% CI: 1.160~39.088; P=0.034), and hepatocellular carcinoma (HCC) (OR=26.772, 95% CI: 1.747~410.187; P=0.018) were the independent risk factors. With COX multivariate regression analysis, the 3-months survival rate of CRKP infected patients was significantly lower than that without CRKP infection post-LT. Conclusions: CRKP infection is closely correlated with poor prognosis in 3-months post-LT.

Investigating CENPW as a Novel Biomarker Correlated With the Development and Poor Prognosis of Breast Carcinoma.

Breast invasive carcinoma (BRCA) is a carcinoma with a fairly high incidence, and the therapeutic schedules are generally surgery and chemotherapy. However, chemotherapeutic drugs tend to produce serious toxic side effects, which lead to the cessation of treatment. Therefore, it is imperative to develop treatment strategies that are more effective and have fewer side effects at the genetic level. Centromeric protein W (CENPW) is an oncogene that plays an important part in nucleosome assembly. To date, no studies have reported the prognostic significance of CENPW in breast carcinoma. In this study, we verified that CENPW expression is up-regulated in breast carcinoma and positively associated with the level of immune cell infiltration. The clinicopathological characteristics further suggest that CENPW expression is correlated with a worse prognosis of breast carcinoma. Interestingly, the CENPW mutation contributes to the poor prognosis. Next, we discovered that the genes interacting with CENPW are mainly concentrated in the cell cycle pathway, and CENPW is co-expressed with CDCA7, which is also highly expressed in breast carcinoma and leads to a worse prognosis. Our subsequent studies verified that knockdown of CENPW significantly inhibits the proliferation and migration of breast carcinoma cells and promotes their apoptosis rate. Notably, inhibition of CEMPW sensitizes breast cancer cells to chemotherapeutic drugs that have been found to induce cell cycle arrest. In summary, these results provide extensive data and experimental evidence that CENPW can serve as a novel predictor of breast cancer and may act as a prospective therapeutic target.

A Signature for Smoking Status of Coronary Heart Disease Patients through Weighted Gene Coexpression Network Analysis.

BACKGROUND: Smoking is one of the risk factors of coronary heart disease (CHD), while its underlying mechanism is less well defined. PURPOSE: To identify and testify 6 key genes of CHD related to smoking through weighted gene coexpression network analysis (WGCNA), protein-protein interaction (PPI) network analysis, and pathway analysis. METHODS: CHD patients' samples were first downloaded from Gene Expression Omnibus (GEO). Then, genes of interest were obtained after analysis of variance (ANOVA). Thereafter, 23 coexpressed modules that were determined after genes with similar expression were incorporated via WGCNA. The biological functions of genes in the modules were researched by enrichment analysis. Pearson correlation analysis and PPI network analysis were used to screen core genes related to smoking in CHD. RESULTS: The violet module was the most significantly associated with smoking (r = -0.28, p = 0.006). Genes in this module mainly participated in biological functions related to the heart. Altogether, 6 smoking-related core genes were identified through bioinformatics analyses. Their expressions in animal models were detected through the animal experiment. CONCLUSION: This study identified 6 core genes to serve as underlying biomarkers for monitoring and predicting smoker's CHD risk.

MCT2 overexpression promotes recovery of cognitive function by increasing mitochondrial biogenesis in a rat model of stroke.

Monocarboxylate transporter 2 (MCT2) is the predominant monocarboxylate transporter expressed by neurons. MCT2 plays an important role in brain energy metabolism. Stroke survivors are at high risk of cognitive impairment. We reported previously that stroke-induced cognitive impairment was related to impaired energy metabolism. In the present study, we report that cognitive function was impaired after stroke in rats. We found that MCT2 expression, but not that of MCT1 or MCT4, was markedly decreased in the rat hippocampus at 7 and 28 days after transient middle cerebral artery occlusion (tMCAO). Moreover, MCT2 overexpression promoted recovery of cognitive function after stroke. The molecular mechanism underlying these effects may be related to an increase in adenosine monophosphate-activated protein kinase-mediated mitochondrial biogenesis induced by overexpression of MCT2. Our findings suggest that MCT2 activation ameliorates cognitive impairment after stroke.

Antiproliferative effects of mealworm larvae (Tenebrio molitor) aqueous extract on human colorectal adenocarcinoma (Caco-2) and hepatocellular carcinoma (HepG2) cancer cell lines.

Recently, insects have aroused the interest of researchers as potential therapeutic resources against malignant diseases such as cancer. In this study, the effects of aqueous extracts from mysore thorn borer (MTB) (Anoplophora chinensis) and mealworm larvae (MWL) (Tenebrio molitor) against cancer cells were investigated. MWL aqueous extract showed higher antiproliferative effects against Caco-2 and HepG2 cells compared to MTB. The IC50 (48 hr) of MWL aqueous extract were 11.44 and 20 mg/ml for Caco-2 and HepG2 respectively. Flow cytometry analysis showed that MWL aqueous extract induced apoptosis in Caco-2 and HepG2 increasing from 2.06% to 74.34% and from 0.04% to 42.14% after 24 hr respectively. Caspase activity assay showed that apoptosis was mediated via death receptor pathway mediated by caspase-8 and -9 followed by the activation of caspase-3; caspase-3 may have induced DNA damage and cell death. These effects may be correlated to its free amino acids. The results of this study demonstrate the potentials of MWL in the development of natural anticancer therapeutics in the future. PRACTICAL APPLICATIONS: Natural nutraceuticals from insects might be useful for the treatment and prevention of cancers such as colorectal and liver cancer. In recent years, edible insects have caught the attention of researchers, because of their potential as an alternative source of food and nutraceuticals. The results of our study showed that MWL extract might provide important anticancer compounds against colon and liver cancer.

A Novel Anastomosis Technique for Laparoscopic Pancreaticoduodenectomy: Case Series of Our Center's Experience.

Background: Laparoscopic pancreaticoduodenectomy has developed rapidly in recent years. Postoperative pancreatic fistula is still the most dangerous complication of laparoscopic pancreaticoduodenectomy. Baumgart pancreaticojejunostomy is considered one of the safest anastomosis procedures, with low rates of pancreatic fistula. We modified Blumgart pancreaticojejunostomy and applied the modified procedure during laparoscopic pancreaticoduodenectomy. The modified procedure entailed a longitudinal U-shaped suture through the pancreas for anastomosis of the pancreatic duct and the jejunal mucosa. Methods: We prospectively collected and retrospectively analyzed the data of 120 patients who underwent laparoscopic pancreaticoduodenectomy from January 2016. The total operative time, time for complete pancreaticojejunostomy, postoperative pancreatic fistula rate, postoperative delayed gastric emptying, postoperative bleeding, postoperative length of hospital stays, and mortality within 90 days after surgery were analyzed. An analysis of laparoscopic pancreaticojejunostomy compared with open pancreaticojejunostomy is also reported. Results: In the laparoscopic pancreaticojejunostomy group, the average total operative time, the average time for complete pancreaticojejunostomy, and the average intraoperative blood loss were 271 min, 35.3 min, and 184 ml, respectively. The total postoperative clinically relevant pancreatic fistula rate was 9.2% (Grade B and C fistulas). The incidence rates of postoperative delayed gastric emptying and postoperative biliary fistula were ~2.5 and 1.7%, respectively. The postoperative bleeding rate was 0.83%, and the average postoperative indwelling time of the abdominal drainage tube was 7.3 days. The postoperative length of hospital stay was 10.8 days, and the mortality rate within 90 days after surgery was 0.83%. The rates of clinically relevant postoperative clinically relevant pancreatic fistula are comparable between laparoscopic and open surgery, there were no other severe postoperative complications in either group. The mean postoperative length of hospital stay was significantly shorter in the laparoscopic pancreaticojejunostomy group. Conclusion: The modified laparoscopic-adapted Blumgart anastomosis simplifies and facilitates the creation of the pancreaticojejunostomy in laparoscopic pancreaticoduodenectomy. The rates of clinically relevant postoperative pancreatic fistula are comparable with those obtained by open surgery, and length of stay are shoter.

Identification of peptides interfering with the LRRK2/PP1 interaction.

Serine/threonine phosphatases are responsible for modulating the activities of the protein kinases implicated in the development of several pathologies. Here we identified by a PEP-scan approach a peptide of LRRK2, a Parkinson's disease associated protein, interacting with the phosphatase PP1. In order to study its biological activity, the peptide was fused via its N-terminal to an optimized cell penetrating peptide. We synthesized from the original peptide five interfering peptides and identified two (Mut3DPT-LRRK2-Short and Mut3DPT-LRRK2-Long) able to disrupt the LRRK2/PP1 interaction by competition in anti-LRRK2 immunoprecipitates. Using FITC-labelled peptides, we confirmed their internalization into cell lines as well as into primary cells obtained from healthy or ill human donors. We confirmed by ELISA test the association of Mut3DPT-LRRK2-Long peptide to purified PP1 protein. The peptides Mut3DPT-LRRK2-5 to 8 with either N or C-terminal deletions were not able to disrupt the association LRRK2/PP1 nor to associate with purified PP1 protein. The interfering sequences blocking the PP1/LRRK2 interaction were also fused to a shuttle peptide able to cross the blood brain barrier and showed that the newly generated peptides BBB-LRRK2-Short and BBB-LRRK2-Long were highly resistant to protease degradation. Furthermore, they blocked PP1/LRRK2 interaction and they penetrated into cells. Hence, these newly generated peptides can be employed as new tools in the investigation of the role of the LRRK2/PP1 interaction in normal and pathological conditions.

MicroRNA-1246 Promotes Melanoma Progression Through Targeting FOXA2.

INTRODUCTION: Recently, the incidence of melanoma has been rising and there is a lack of effective targeted therapies. The regulatory mechanisms of microRNA-1246 (miR-1246) have been found in many cancers, except melanoma. This study focused on the regulatory mechanism of miR-1246 in melanoma development. METHODS: The expression of miR-1246 was assessed using quantitative real-time polymerase chain reaction (RT-qPCR). Cell viability and metastasis were detected by Transwell and MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assays. The protein expression of epithelial mesenchymal transition (EMT) makers was assessed by Western blot analysis. The target gene of miR-1246 was detected using luciferase reporter assay. RESULTS: MiR-1246 expression was increased in melanoma tissues and cells. In addition, upregulation of miR-1246 promoted cell viability and metastasis in melanoma. Forkhead box protein A2 (FOXA2) was confirmed to be a direct target of miR-1246. And FOXA2 expression was decreased in melanoma and was suppressed by miR-1246. Importantly, upregulation of FOXA2 restored the carcinogenesis of miR-1246 in melanoma. CONCLUSION: MiR-1246 promoted cell viability and metastasis in melanoma by inhibiting FOXA2 expression.

Recent Advances of Chitosan and its Derivatives in Biomedical Applications.

Chitosan is the second-most abundant natural polysaccharide. It has unique characteristics, such as biodegradability, biocompatibility, and non-toxicity. Due to the existence of its free amine group and hydroxyl groups on its backbone chain, chitosan can undergo further chemical modifications to generate Chitosan Derivatives (CDs) that permit additional biomedical functionality. Chitosan and CDs can be fabricated into various forms, including Nanoparticles (NPs), micelles, hydrogels, nanocomposites and nano-chelates. For these reasons, chitosan and CDs have found a tremendous variety of biomedical applications in recent years. This paper mainly presents the prominent applications of chitosan and CDs for cancer therapy/diagnosis, molecule biosensing, viral infection, and tissue engineering over the past five years. Moreover, future research directions on chitosan are also considered.

LncRNA FOXD3-AS1 promotes proliferation, invasion and migration of cutaneous malignant melanoma via regulating miR-325/MAP3K2.

PURPOSE: The aim was to study the mechanism of LncRNA FOXD3-AS1 in cutaneous melanoma. METHODS: FOXD3-AS1 levels in 47 pairs of melanoma samples were detected. We used qRT-PCR to detect FOXD3-AS1, miR-325 and MAP3K2 expression in different staging samples and cutaneous melanoma cell lines. We used Kaplan-Meier curve to analyze survival rate in patients with FOXD3-AS1 high and low expression. Sh-FOXD3-AS1, miR-325, miR-325 inhibitor and oeMAP3K2 were transfected. The proliferation of A375 and SK-MEL-1 was detected by CCK8 and EdU labeling assay and cell clone formation assay. Dual luciferase reporter assay and pull down assay was used to confirm the binding site of FOXD3-AS1, miR-325 and MAP3K2. Flow cytometry was applied to detect the effect of lncRNA on cell cycle. The migration and invasion ability were detected by transwell assay. RESULTS: LncRNA FOXD3-AS1 highly expressed in cutaneous melanoma cells and tissues. Patients with highly expressed LncRNA FOXD3-AS1 were always with shorter overall survival time. When LncRNA FOXD3-AS1 was knockdown, proliferation, invasion and migration of cutaneous malignant melanoma, and tumor weight was inhibited, and cell cycle was arrested. LncRNA FOXD3-AS1 negatively regulated the expression of miR-325, and then improved the level of MAP3K2. MiR-325 was with similarly effects on above biological process, and MAP3K2 overexpression could rescue the influence of sh-FOXD3-AS1. Tumor volume and weight were measured to confirm the effect of sh-FOXD3-AS1 in vivo. CONCLUSION: LncRNA FOXD3-AS1 could promote proliferation, invasion and migration of cutaneous malignant melanoma via regulating miR-325/MAP3K2 axis.

Causative agents and outcome of spontaneous bacterial peritonitis in cirrhotic patients: community-acquired versus nosocomial infections.

BACKGROUND: Spontaneous bacterial peritonitis (SBP) is a serious complication and common cause of death in patients with liver cirrhosis. This study was conducted to compare the microbiological characteristics, drug resistance, and treatment outcomes for nosocomial SBP and community-acquired SBP. METHODS: A retrospective study was performed on 334 patients with culture-positive SBP at Beijing Youan Hospital, China, between January 2012 and December 2016. The medical records for these patients were reviewed, and their clinical and laboratory data were analyzed. RESULTS: A total of 155 (46.4%) patients with nosocomial SBP and 179 (53.6%) with community-acquired SBP were included in this study. From the patients' ascitic fluids, 334 pathogenic strains, including 178 Gram-negative bacterial strains, 138 Gram-positive bacterial strains and 18 other microbial strains were isolated. E. coli was the major pathogen (24.3%), followed by Klebsiella pneumoniae (12.0%) and Enterococcus faecium (10.5%). The proportion of Enterococcus was significantly higher in the patients with nosocomial SBP (6.1% vs. 27.7%, P < 0.001) than in the patients with community-acquired SBP. The main pathogens isolated from the nosocomial infections were significantly more resistant to the first-line recommended drug. Compared with community-acquired SBP, nosocomial SBP had a poorer outcome (36.8% vs. 24.6%; P = 0.016). The independent predictors for 30-day mortality included nosocomial infection, Child-Pugh classification, hepatocellular carcinoma, renal failure and hepatic encephalopathy. CONCLUSION: Gram-negative bacteria were the major pathogens involved in SBP in the cirrhotic patients. The strains isolated from the patients with nosocomial SBP displayed higher drug resistance than those isolated from patients with community-acquired SBP. Compared with community-acquired SBP, nosocomial SBP had a poorer outcome. When choosing drug treatments, the acquisition site of infection and the local epidemiological situation should be taken into account.

Segmental zoster abdominal paresis mimicking an abdominal hernia: A case report and literature review.

RATIONALE: Herpes zoster infection typically involves the posterior root ganglia and most of the symptoms are sensory. Motor involvement can occur in the same distribution but is relatively uncommon. Segmental zoster paresis is a rare motor complication of Herpes zoster, mimicking an abdominal hernia, but it needs no surgery different from the real abdominal wall hernia. PATIENT CONCERNS: We present a case of a 58-year-old man with an abdominal protrusion and characteristical herpes zoster rash. DIAGNOSES: Initially, the surgeon regarded it as an abdominal hernia, while ultrasonography excluded the abdominal wall defect, and then the dermatologist diagnosed it as segmental herpes zoster abdominal paralysis. INTERVENTIONS: He received a treatment with oral acyclovir, mecobalamin, and vitamin B1. OUTCOMES: The abdominal wall bulge disappeared after 2 months, avoiding unnecessary surgery. LESSONS: Segmental zoster abdominal paresis, mimicking an abdominal hernia needs no surgery.

Large Aggressive Angiomyxoma of the Liver: A Case Report and Brief Review of the Literature.

Aggressive angiomyxoma (AAM) is an uncommon mesenchymal myxoid tumor that almost solely involves the soft tissues of the perineum and pelvis. An AAM originating from the liver is extremely rare. Herein, we present a case of a 45-year-old female with a large mass in the left lateral lobe of the liver. She underwent a left lateral lobe hepatectomy. The histopathology of the resected specimen showed features that were characteristic of AAM. Immunohistochemical analysis of the neoplastic cells showed reactions to antibodies against CD34, smooth muscle actin (SMA), and Ki67 (2%) and showed no reactions to antibodies against Estrogen receptor (ER), C-keratin (CK), and Desmin. The patient was subsequently diagnosed with a primary AAM of the liver. This is the largest AAM of the liver that has been reported. We hereby report these findings and review the current literature.