Surgical treatment of four segment lumbar spondylolysis: A case report

BACKGROUNDFour-level lumbar spondylolysis is extremely rare. So far, only 1 case has been reported in the literature. CASE SUMMARYA 19-year-old man presented with severe back pain irresponsive to conservative therapies for 2 years. Lumbar radiographs and two-dimensional computed tomography scan showed four segment lumbar spondylolysis on both sides of L2-L5. Lumbar magnetic resonance imaging showed normal signal in all lumbar discs. Because daily activities were severely limited, surgery was recommended for the case. The patient underwent four-level bilateral isthmic repair at L2-L5. During surgery, L2-L5 isthmi were curetted bilaterally, freshened, and then grafted with autologous iliac bone that was bridged and compressed with a pedicular screw connected to a sub-laminar hook by a short rod. The symptoms of back pain almost disappeared. He has been followed-up for 96 mo, and his symptoms have never recurred. Fusion was found in all repaired isthmi 14 mo after surgery according to evaluation of lumbar radiography and computed tomography scan.CONCLUSIONWe report here 1 case of four-level lumbar spondylolysis that was treated successfully with direct isthmic repair.     

Oncentra近距离计划系统和MIM系统间DVH参数差异的分析

目的对近距离治疗计划的剂量参数在Oncentra治疗计划系统与MIM系统间产生的差异进行分析和研究。方法选取本院的43例妇科肿瘤患者近距离治疗计划,按照临床要求所有病例的靶区D₉₀达到处方剂量。评估参数包括:靶区体积和D₉₀,处方剂量总体积,靶区内的处方剂量体积以及危及器官包括:直肠,膀胱,小肠的D_0.01cc,D_1cc,D_2cc。结果计划系统中的靶区体积和处方剂量值均明显小于MIM系统中相应的值(P<0.05),两系统显示出的处方体积相差不大。MIM系统中的靶区D₉₀(676.74±54.82)cGy小于处方剂量,危及器官的受量则正好相反,即计划系统比MIM系统中相应的参数要小,其中直肠和膀胱的D_0.01cc,D_1cc,D_2c,小肠的D_0.01cc,D_2cc的在两系统显示的值的差异均有统计学意义(P<0.05)。结论不同系统间传输相同的剂量和轮廓文件,DVH参数存在一定的差异,其主要原因是在不同系统对已勾画的各种器官轮廓计算体积存在算法上的不同。基于此,建议近距离计划在CT扫描时,尽量小的层厚可以消除或减少这种差异。     

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.     

The endogenous inflammatory reflex inhibits the inflammatory response to different immune challenges in mice

The splanchnic anti-inflammatory pathway, the efferent arm of the endogenous inflammatory reflex, has been shown to suppress the acute inflammatory response of rats to systemic lipopolysaccharide (LPS). Here we show for the first time that this applies also to mice, and that the reflex may be engaged by a range of inflammatory stimuli. Experiments were performed on mice under deep anaesthesia. Half the animals were subjected to bilateral section of the splanchnic sympathetic nerves, to disconnect the splanchnic anti-inflammatory pathway, while the remainder underwent a sham operation. Mice were then challenged intravenously with one of three inflammatory stimuli: the toll-like receptor (TLR)-4 agonist, LPS (60 µg/kg), the TLR-3 agonist Polyinosinic:polycytidylic acid (Poly I:C, 1 mg/kg) or the TLR-2 and -6 agonist dipalmitoyl-S-glyceryl cysteine (Pam2cys, 34 µg/kg). Ninety minutes later, blood was sampled by cardiac puncture for serum cytokine analysis. The splanchnic anti-inflammatory reflex action was assessed by comparing cytokine levels between animals with cut versus those with intact splanchnic nerves. A consistent pattern emerged: Tumor necrosis factor (TNF) levels in response to all three challenges were raised by prior splanchnic nerve section, while levels of the anti-inflammatory cytokine interleukin 10 (IL-10) were reduced. The raised TNF:IL-10 ratio after splanchnic nerve section indicates an enhanced inflammatory state when the reflex is disabled. These findings show for the first time that the inflammatory reflex drives a coordinated anti-inflammatory action also in mice, and demonstrate that its anti-inflammatory action is engaged, in similar fashion, by inflammatory stimuli mimicking a range of bacterial and viral infections.     

Pregnancy induced TMA in severe preeclampsia results from complement-mediated thromboinflammation

Preeclampsia is a multifactorial vascular disease unique to human pregnancy. While genetic and antiangiogenic factors are important contributors to preeclampsia susceptibility, recent studies have shown that dysregulation and/or over-activation of the complement system has an integral role in disease etiology. Furthermore, the role of the coagulation cascade may be underappreciated in the development of the disease. Traditionally, for research purposes, the pool of preeclampsia cases has been divided into non-severe and severe disease depending on the onset and severity of the symptoms. However, of particular interest are a small but important minority of cases that present with symptoms likening to those of hemolysis, elevated liver enzymes and low platelets syndrome, atypical hemolytic uremic syndrome, or thrombotic thrombocytopenic purpura, all thrombotic microangiopathy (TMA) diseases, with the hallmark mechanisms of endothelial dysfunction and aberrant activation of complement and coagulation cascades. We therefore propose a third class, severe TMA-like preeclampsia to be included in the categorization of preeclampsia patients. Identifying these patients would target research, diagnostic differentiation, and novel treatment options to the subclass of patients with life-threatening disease that are most likely to benefit from next-generation drug development.     

Neuromodulation in Psychiatric disorders: Experimental and Clinical evidence for reward and motivation network Deep Brain Stimulation: Focus on the medial forebrain bundle

Deep brain stimulation (DBS) in psychiatric illnesses has been clinically tested over the past 20 years. The clinical application of DBS to the superolateral branch of the medial forebrain bundle in treatment‐resistant depressed patients—one of several targets under investigation—has shown to be promising in a number of uncontrolled open label trials. However, there are remain numerous questions that need to be investigated to understand and optimize the clinical use of DBS in depression, including, for example, the relationship between the symptoms, the biological substrates/projections and the stimulation itself. In the context of precision and customized medicine, the current paper focuses on clinical and experimental research of medial forebrain bundle DBS in depression or in animal models of depression, demonstrating how clinical and scientific progress can work in tandem to test the therapeutic value and investigate the mechanisms of this experimental treatment. As one of the hypotheses is that depression engenders changes in the reward and motivational networks, the review looks at how stimulation of the medial forebrain bundle impacts the dopaminergic system.     

结核性脑膜炎临床诊断评分体系的建立及评价研究

背景 结核性脑膜炎（TM）是临床常见的中枢性感染的一种，其起病较慢，症状不典型，病原学诊断困难，误诊率高。目前有效的TM诊断工具较少。利用常见的临床症状、检查指标等建立诊断评分系体可提高诊断准确率，减少误诊。 目的 建立TM临床诊断评分体系（TMCDS），并对其应用价值进行初步评价。 方法 选取2011年11月至2021年9月在柳州市人民医院感染病科住院并诊断为脑膜炎的患者187例为研究对象，采用SPSS 21.0统计软件将患者随机分成建模组（147例）和验模组（40例）。根据是否为TM将建模组分为非TM亚组（76例）和TM亚组（71例）。收集患者的一般资料，主要包括性别、年龄、临床症状（发热、头痛、意识障碍、颈抵抗），实验室及影像学检查结果，包括人类免疫缺陷病毒（HIV）感染情况、CD4+ T淋巴细胞计数、C反应蛋白、颅内压、脑脊液常规生化检查（糖、氯、蛋白、细胞数）。建模组采用多因素Logistic回归分析探讨TM的影响因素；根据每个因素的β值所占比重设立相应分值，建立TMCDS；采用受试者工作特征曲线（ROC曲线）分析TMCDS诊断TM的价值。 结果 两亚组头痛、HIV感染、CD4+ T淋巴细胞计数<200/μl、C反应蛋白升高、颅内压>200 mm H2O（1 mm H2O=0.009 8 kPa）、脑脊液糖降低、脑脊液氯降低、脑脊液蛋白升高、脑脊液单核细胞升高情况比较，差异有统计学意义（P<0.05）。多因素Logistic回归分析结果显示，头痛、CD4+ T淋巴细胞<200/μl、C反应蛋白升高、脑脊液糖降低、脑脊液蛋白升高均是TM的影响因素（P<0.05）。将以上5个影响因素同时结合临床经验纳入脑脊液氯、脑脊液细胞数再次进行多因素Logistic回归分析，结果显示，头痛、CD4+ T淋巴细胞<200/μl、C反应蛋白升高、脑脊液糖降低、脑脊液蛋白升高均是TM的影响因素（P<0.05）。根据上述7个因素β值建立评分系统，将脑脊液氯降低β值设定为1分，其他因素β值与其的倍数即为该因素所对应的分值，因2个影响因素评分为负值，为方便临床，每个因素对应分值增加2.5分，最终建立TMCDS。TMCDS诊断建模组TM的ROC曲线下面积（AUC）为0.807〔95%CI（0.735，0.879），标准误=0.037，P<0.001〕，最佳诊断界值为21.50分。TMCDS诊断验模组TM的AUC为0.766〔95%CI（0.610，0.921），标准误=0.079，P=0.004〕，灵敏度为0.789，特异度为0.667。 结论 通过7个变量建立的TMCDS简单易行，对于早期TM具有较高的临床诊断价值。