T-Cell Non-Hodgkin Lymphoma of the Ileum Presenting as Perforation and Peritonitis: A Case Report.

Background: Non-Hodgkin lymphoma (NHL) of the ileum, presenting as perforation and peritonitis, is a rare disease, derived from intestinal intraepithelial T lymphocytes. The degree of malignancy is extremely high. The pathogenesis of ileal perforation caused by NHL remains unclear, as well as the chromosome and immune system abnormalities, which may be related to NHL, and are indistinguishable from other benign and malignant conditions and are clinically nonspecific. Case Report: We describe an 84-year-old man with abdominal pain for 4 days, which was aggravated for 3 h. The pain was in the upper abdominal region and was initially considered to be due to gastrointestinal perforation. He had persistent insidious pain, accompanied by nausea, vomiting, and fever. Physical examination indicated that the patient had pain all over the abdomen; also, rebound pain and muscle tension, and bowel sounds were reduced on auscultation. An abdominal CT scan showed free gas in the abdominal cavity. The patient was diagnosed with peritonitis due to hollow viscus perforation. A prompt exploratory laparotomy was performed. Intraoperative findings showed perforations in the ileum that are approximately 40 cm from the ileocecal region, which were 3-8 mm in size. A segmental distribution was observed, and the intestinal contents overflowed with purulent discharge around the perforation surface. Resection and ileostomy were performed, and the clinical histopathological examination confirmed T-cell lymphoma. The patient was advised to visit the Oncology Department for further chemotherapy. Conclusion: Timely emergency surgery is the key to the treatment of ileal perforation caused by T-cell lymphoma. Resection and ileostomy were performed as intervention measures, and subsequent histopathological examination manifested T-cell lymphoma.

Long-term survival and prognostic implications of patients with invasive breast cancer in southern Taiwan.

Our objective in this study was to determine the survival rate of patients with invasive breast cancer and identify the prognostic factors related to all-cause mortality during a 10-year follow-up.Analysis was performed on the medical records of 2002 patients newly diagnosed with breast cancer at a medical center in southern Taiwan between 2006 and 2017. The Kaplan-Meier method and Cox regression analysis were used to estimate survival and the independence of prognostic factors associated with all-cause mortality.Among the 2002 patients, 257 expired during the 10-year follow-up period. The overall survival rates were as follows: 3 years (91.1%), 5 years (85.6%), and 10 years (77.9%). The median survival time was 120.41 months (95% confidence interval: 118.48-122.33 months). Older age, pathologic tumor status, regional lymph node metastasis, distant metastasis, grade/differentiation, treatment modalities, and hormone therapy were significantly related to all-cause mortality.This study identified several clinical factors related to all-cause mortality as well as its relationship to distant metastasis and poor differentiation. Early diagnosis and treatment aimed at preventing recurrence are the keys to survival.

MicroRNA-424-5p regulates aortic smooth muscle cell function in atherosclerosis by blocking APOC3-mediated nuclear factor-κB signalling pathway.

NEW FINDINGS: What is the central question of this study? What is the role of microRNA-424-5p (miR-424-5p) in aortic smooth muscle cells? How does miR-424-5p function as a suppressor of the inflammatory response? What is the main finding and its importance? Upregulation of miR-424-5p inhibits the inflammatory response in aortic smooth muscle cells. miR-424-5p inactivates the nuclear factor-κB signalling pathway through the downregulation of apolipoprotein C3. ABSTRACT: Dysregulated aortic smooth muscle cells in chronic inflammation result in plaque formation in atherosclerosis (AS), which is a systemic disease that affects the large arteries with the activation of inflammatory pathways as a key process in its pathogenesis. The aim of the study was to investigate the regulatory mechanism of microRNA-424-5p (miR-424-5p) in aortic smooth muscle cell activities and inflammation in AS via the regulation of apolipoprotein C3 (APOC3) and the nuclear factor-κB (NF-κB) signalling pathway. The results showed that miR-424-5p was poorly expressed and APOC3 highly expressed in the peripheral blood of AS patients and rat models of AS. Molecularly, our results confirmed that miR-424-5p targeted the APOC3 gene directly and inhibited APOC3 expression, which resulted in repressed activation of the NF-κB signalling pathway. The gain- and loss-of-function approaches were used to determine the effects of miR-424-5p and APOC3 on inflammation and on the proliferation, apoptosis and migration of aortic smooth muscle cells. Upregulation of miR-424-5p or silencing of APOC3 significantly suppressed proliferation, migration and inflammation and promoted apoptosis of aortic smooth muscle cells, which was achieved through inactivation of the NF-κB signalling pathway. Taken together, our results show that miR-424-5p upregulation impedes the progression of AS by blocking the APOC3-mediated NF-κB signalling pathway, which could be used as a novel target and a potential therapeutic pathway against AS.

Protective effect of atorvastatin meditated by HMGCR gene on diabetic rats with atherosclerosis: An in vivo and in vitro study.

BACKGROUND: Accelerated atherosclerosis in patients suffering from diabetes represents a major cause of morbidity and mortality. The aim of present study was to investigate the protective effects conferred by atorvastatin (AVT) meditated by the HMGCR gene in diabetic rats with atherosclerosis. METHODS: Serum triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), very-low-density lipoprotein cholesterol (VLDL-C), fasting blood glucose (FBG) and serum insulin (INS) were all determined by means of in vivo experiments. Following the establishment of the diabetic model of atherosclerosis, the expressions of HMGCR, low density lipoprotein receptor (LDLR), fatty acid synthase (FASN) were detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis in the vitro experiments. Flow cytometry was adopted in order to detect cell cycle and apoptosis. RESULTS: The in vivo experiments results indicated that FBG and INS among the diabetic arteriosclerosis rats exhibited markedly higher levels; after injected with AVT and HMGCR, decreased contents of TC, TG, LDL-C and VLDL-C, while increased contents of HDL-C as well as an increased positive rate of HMGCR protein expression were observed. In vitro experiment, the mRNA and protein expression of LDLR were increased and FASN were decreased in cells transfected with HMGCR and AVT; with a greater number of cells arrested at the S phase and less in the G0/G1 phase, as well as data indicating the rate of apoptosis was inhibited after HMGCR and AVT transfection processes. CONCLUSION: The key findings of the present study suggested that the protective effect conferred by AVT in diabetic rats with atherosclerosis was associated with the overexpression of the HMGCR gene, thus presenting a novel target for atherosclerosis treatment.

shRNA interference of NLRP3 inflammasome alleviate ischemia reperfusion-induced myocardial damage through autophagy activation.

Myocardial ischemia-reperfusion (I/R) injury always occur during the recovery of myocardial blood supply with high morbidity and mortality. Although, various therapeutic schedules were applied in clinic, there are real problems that have to be resolved on curative effect. Nod-like receptor protein 3 (NLRP3) inflammasome has moderation effects on cellular damage and inflammatory reaction after I/R injury. Our research aims to investigate a more effective approach to restrain the activation of NLRP3 inflammasome in treating myocardial I/R injury. Results indicated that cell viability, Bax/Bcl-2 expression were affected hardly by sh-NLRP3 transfection in normal cells. However, the decreased cell viability and increased Bax/Bcl-2 expression level caused by I/R were remarkably suppressed through sh-NLRP3 transfection. Besides that, the reduced levels of pro-autophagy proteins (Beclin1, Agt7, LC3II/LC3I) while enhanced level of anti-autophagy protein (p62) and apoptosis-related proteins (Bax/Bcl-2) were significantly repressed via sh-NLRP3 transfection. Nevertheless, the autophagy inhibitor 3 MA could reverse the results. Moreover, in vivo experiment suggested that NLRP3 was up-regulated in wild type (WT) rats with I/R injury. The expansion of infarct size induced by ischemia was tremendously constricted in NLRP3 knockout (KO) rats. NLRP3 silence had nearly no impact on myocardial enzymes (AST, LDH and CK) expressions, inflammatory factors (TNF-α and IL-1ß) expressions and cell apoptosis in rats without I/R injury. Nonetheless, the elevated levels of myocardial enzymes, inflammatory factors and cell apoptosis caused by I/R injury were vastly inhibited in NLRP3 KO rats. Furthermore, NLRP3 KO itself would lead to higher level of pro-autophagy proteins (Beclin1, Agt7, LC3II/LC3I) while lower level of anti-autophagy protein (p62) in vivo. The decreased expressions of pro-autophagy proteins while increased expressions of anti-autophagy protein induced by I/R injury were remarkably suppressed by NLRP3 KO. Taken together, our study indicated that shRNA interference of NLRP3 inflammasome attenuated myocardial I/R injury via autophagy activation. These findings demonstrated that NLRP3 KO may a promising therapy in myocardial I/R injury.

Mir-23a inhibition attenuates ischemic/reperfusion-induced myocardial apoptosis by targeting XIAP.

MicroRNAs are a group of single-strand, non-coding RNAs that inhibit the translation of protein-coding genes. Recent studies indicated that miRNAs are broadly involved in the development of cardiovascular diseases, including arrhythmia, hypertrophy, heart failure and cardiac injury. In this study, we report that miR-23a, a tumor suppressor, acts as an apoptotic promoter in rats undergoing ischemic/reperfusion. In rats subjected to ischemic/reperfusion injury, the expression of miR-23a in heart tissue was upregulated significantly. The infarct area and the apoptosis rate also increased. In contrast, knockdown of miR-23a by tail injection of antagomir-23a attenuated the ischemic/reperfusion injury. Moreover, we used Western blots to determine that miR-23a targeted XIAP to influence the expression of caspase and the NFkB pathway. In summary, miR-23a was shown to be part of a novel regulatory pathway that contributed to ischemic/reperfusion injury.

Short- and long-term efficacy and safety of triple vs. dual antithrombotic therapy in patients with drug-eluting stent implantation and an indication for oral anticoagulation: a meta-analysis.

BACKGROUND: The optimal antithrombotic regimen after coronary stenting in patients taking oral anticoagulants (OACs) is still unclear. Therefore, this meta-analysis focused on the short- and long-term efficacy and safety of triple therapy (TT: OAC, aspirin, and thienopyridine) and dual therapy (DT: OAC plus single antiplatelet drug or aspirin plus thienopyridine). METHODS: We searched PubMed, Embase, the Cochrane Library, Wangfang database, and Google Scholar up to December 1, 2015 (January 1, 2000 - December 2015), from randomized and nonrandomized studies comparing TT and DT in patients with OACs undergoing drug-eluting stent (DES) implantation. Major adverse cardiac and cerebrovascular events (MACCE) were the main outcome. Safety outcome was major bleeding (MB). RESULTS: Of 964 publications identified, 1 randomized study and 27 nonrandomized studies of 31,346 patients were included. Overall, TT and OAC plus clopidogrel were associated with a lower risk of MACCE, stroke, MI, and allcause mortality compared with dual antiplatelet therapy or OAC plus aspirin. Additionally, short-term use of triple antithrombotic regimen with OAC, aspirin, and clopidogrel is associated with equivalent risk of major bleeding and decreased rate of MACCE. Long-term use of OAC plus clopidogrel after TT was associated with equal or better benefit and safety outcomes. CONCLUSION: For patients on OAC after coronary stenting, triple therapy (OAC, aspirin, clopidogrel) should be considered in the short term, followed by more long-term therapy with OAC plus clopidogrel. More randomized studies are needed to confirm these findings.

[An experience nursing a patient with dengue hemorrhagic fever].

The case report presented a patient with dengue hemorrhagic fever after being bitten by an insect in a suburban area. The author observed and interviewed the patient and utilized Gorden's functional health scale to collect information, from Nov., 08 to Nov., 15 2002. Thrombocytopenia, febrile, and pain accompanied with dengue hemorrhagic fever were recorded during nursing evaluation. Lack of associated medical information contributed to the patient's anxiety status. The major nursing problems were changing of protection/ thrombocytopenia, hyperthermia, pain, and inadequacy of knowledge. The gum bleeding, fevers, and generalized bone pain were relieved by sincere listening and nursing intervention. In addition, medical information was delivered by way of a health information booklet to improve the understanding of the patient and ease the latter's anxiety status. Amid an increase in cases of dengue hemorrhagic fever in Taiwan, this case report might provide some valuable information to the nursing staff in order to enhance their ability to provide comprehensive care.