Apelin-13 inhibits apoptosis and excessive autophagy in cerebral ischemia/reperfusion injury

Apelin-13 is a novel endogenous ligand for an angiotensin-like orphan G-protein coupled receptor, and it may be neuroprotective against cerebral ischemia injury. However, the precise mechanisms of the effects of apelin-13 remain to be elucidated. To investigate the effects of apelin-13 on apoptosis and autophagy in models of cerebral ischemia/reperfusion injury, a rat model was established by middle cerebral artery occlusion. Apelin-13(50 μg/kg) was injected into the right ventricle as a treatment. In addition, an SH-SY5 Y cell model was established by oxygen-glucose deprivation/reperfusion, with cells first cultured in sugar-free medium with 95% N2 and 5% CO2 for 4 hours and then cultured in a normal environment with sugar-containing medium for 5 hours. This SH-SY5 Y cell model was treated with 10–7 M apelin-13 for 5 hours. Results showed that apelin-13 protected against cerebral ischemia/reperfusion injury. Apelin-13 treatment alleviated neuronal apoptosis by increasing the ratio of Bcl-2/Bax and significantly decreasing cleaved caspase-3 expression. In addition, apelin-13 significantly inhibited excessive autophagy by regulating the expression of LC3 B, p62, and Beclin1. Furthermore, the expression of Bcl-2 and the phosphatidylinositol-3-kinase(PI3 K)/Akt/mammalian target of rapamycin(mTOR) pathway was markedly increased. Both LY294002(20 μM) and rapamycin(500 nM), which are inhibitors of the PI3 K/Akt/mTOR pathway, significantly attenuated the inhibition of autophagy and apoptosis caused by apelin-13. In conclusion, the findings of the present study suggest that Bcl-2 upregulation and mTOR signaling pathway activation lead to the inhibition of apoptosis and excessive autophagy. These effects are involved in apelin-13-induced neuroprotection against cerebral ischemia/reperfusion injury, both in vivo and in vitro. The study was approved by the Animal Ethical and Welfare Committee of Jining Medical University, China(approval No. 2018-JS-001) in February 2018.     

Robotic-assisted central pancreatectomy: A minimally invasive approach for benign and low-grade lesions

BackgroundCentrally located pancreatic lesions are often treated with extended pancreaticoduodenectomy or distal pancreatectomy resulting in loss of healthy parenchyma and a high risk of diabetes and exocrine insufficiency. Robotic central pancreatectomy (RCP) is a parenchyma sparring alternative that has been shown safe and feasible [[1], [2]].MethodsIn this article, we describe our operative technique and the perioperative outcomes of a series of RCP for low-grade or benign pancreatic tumors.ResultsSix patients (5 female and 1 man) with a median age of 51.5 (44–68) years underwent a RCP for 2 serous cystadenomas, 2 mucinous cystic tumors, 1 neuroendocrine tumor, and 1 autoimmune pancreatitis. There were no conversions, intraoperative complications, or perioperative transfusions. Median operative time and was 240 (230–291) minutes and median blood loss was 100 (100–400) ml. The median hospital stay was 8 (5–27) days. There were no mortalities, reoperations, or readmissions. One patient developed a grade B pancreatic fistula which was successfully managed conservatively. All resections had free margins and the median tumor size was 2.5 (1.5–3.5) cm. After a mean follow-up of 46 months, no patients presented new-onset diabetes or exocrine insufficiency.ConclusionsRCP represents the least invasive option for both the patient and the pancreatic parenchyma. With a standardized technique, RCP results in low postoperative morbidity and excellent long-term pancreatic function. Although our results are excellent, POPF still represents the main complication of central pancreatectomy with an incidence ranging from 0 to 80% depending on multiple factors such as the surgeon, technique, and pancreatic texture.     

HIV相关淋巴瘤诊治进展

[摘要]　HIV相关淋巴瘤是常见的HIV相关肿瘤之一，在联合抗反转录病毒治疗（combination antiretroviral therapy, cART）出现之前，其治疗效果极差。在cART时代，HIV相关淋巴瘤的基础及临床研究取得了重大进展，这些为挖掘治疗新靶点提供了依据，使优化HIV相关淋巴瘤的诊治成为可能。本文对近年来HIV相关淋巴瘤的诊断和治疗进展进行综述。     

Long-Term Follow-Up of Cerebral Amyloid Angiopathy-Associated Intracranial Hemorrhage Reveals a High Prevalence of Atrial Fibrillation

Goal: Cerebral amyloid angiopathy (CAA) is the second-most common cause of nontraumatic intracerebral hemorrhages (ICH), surpassed only by uncontrolled hypertension. We characterized the percentage, risk factors, and comorbidities of patients suffering from CAA-related ICH in relation to long-term outcomes. Material and Methods: We performed retrospective analyses and clinical follow-ups of individuals suffering from ICH who were directly admitted to neurosurgery between 2002 and 2016. Findings: Seventy-four of 174 (42%) spontaneous nontraumatic lobar ICH cases leastwise satisfied the modified Boston criteria definition for at least “possible CAA.” Females suffered a higher risk of CAA-caused ICH (42 of 74, 56.8%, P= .035). Atrial fibrillation as a major comorbidity was observed in 19 patients (25.7%). Recovery (decrease of modified Rankin scale [mRS]) was highest during hospitalization in the acute clinic. One-year mortality was as follows: 14 of 25 patients (56%) with probable CAA without supporting pathology, 6 of 18, and 8 of 31 patients with supporting pathology and possible CAA, respectively. Only 10 of 74 (13.6%) had favorable long-term outcomes (mRS ≤2). Increasing numbers of lobar hemorrhages, low initial Glasgow Coma Scale, and subarachnoid hemorrhage were significantly associated with poor survivability, whereas statins, antithrombotic agents, an intraventricular hemorrhage, and midline shift played seemingly minor roles. Conclusions: Symptomatic ICH is a serious stage in CAA progression with high mortality. The high incidence of concurrent atrial fibrillation in these patients may support data on more widespread vascular pathology in CAA.