糖尿病低血糖昏迷急诊救治的临床效果

目的探讨糖尿病低血糖昏迷患者采用急诊系统干预方案实施救治的临床效果。方法对我院收治的糖尿病低血糖昏迷患者120例,按随机分组方案分为对照组和观察组,每组60例。对照组采用常规急诊干预方案进行救治,观察组采用急诊系统干预方案进行救治,比较两组糖尿病低血糖昏迷患者的急诊救治效果、救治后苏醒时间和治疗总时间、急诊救治期间不良事件发生情况。结果观察组糖尿病低血糖昏迷的急诊救治总有效率达91.7%,高于对照组的71.7%,组间比较差异有显著统计学意义(P0.05);救治后苏醒时间和治疗总时间比较,观察组均短于对照组,差异均具统计学意义(P0.05);观察组急诊救治期间发生不良事件1例,对照组发生不良事件8例,差异亦有统计学意义(P0.05)。结论糖尿病低血糖昏迷患者采用急诊系统干预方案实施救治,能促使患者短时间内苏醒,维持血糖稳定,改善患者预后。     

Impact of hypoglycemia and diabetes on CNS: Correlation of mitochondrial oxidative stress with DNA damage

Oxidative stress plays an important role in tissue damage caused by hypoglycemia and diabetes, which may be the result of deterioration in glucose homeostasis caused by these metabolic disorders. The present study examined the effects of insulin-induced hypoglycemia and streptozotocin induced diabetes on mitochondrial lipid peroxidation and antioxidant enzymes from different brain regions, namely, cerebral hemispheres, cerebellum, brain stem and diencephalon. In situ localization of DNA single strand breaks (SSBs) were also studied by DNA polymerase-I mediated biotin dATP labeled nick translation method after inducing hypoglycemia and diabetes. Significant decrease in mitochondrial catalase, manganese superoxide-dismutase (Mn-SOD) and reduced glutathione (GSH) content and increase in the lipid peroxidation (LPx) and glutathione peroxidase (GPx) activity was observed under these metabolic stress conditions with more pronounced effects in hypoglycemic group. We conclude that during severe energy deprivation following hypoglycemia and diabetes, mitochondrial free radicals scavenger system is down regulated, which leads to reactive oxygen species (ROS) generation. High levels of ROS in turn activate the processes leading to DNA damage. DNA SSBs, which indicates nuclear disintegration is an important feature of neuronal cell death.     

云南蒙自钳嘴鹳夜栖地利用及夜栖树选择

动物对夜栖地选择的灵活程度是其分布和扩散的重要因素之一。钳嘴鹳(Anastomus oscitans)为中国新分布种,要了解其扩散趋势,掌握其夜栖地需求至关重要。2015年11月至2018年7月在云南蒙自坝区,使用卫星跟踪技术对6只钳嘴鹳进行了夜栖地利用和夜栖树选择研究,结果表明:(1)钳嘴鹳可以在多种生境中夜栖,包括林地、沼泽、岛屿等。从群体水平上分析,钳嘴鹳主要夜栖于沼泽中,利用率为(51.19±12.34)%,其次为林地(31.55±11.34)%和岛屿(17.26±5.70)%;从个体水平上来看,不同钳嘴鹳的夜栖地利用方式差异较大,其中4只主要利用沼泽,而另外2只主要利用林地;(2)随机森林分析表明:影响钳嘴鹳夜栖树选择的首要因子为距觅食地距离,其次为树高、地径和最低枝高度,而人为干扰因子的影响较弱。综合来看,钳嘴鹳对夜栖地类型以及夜栖树均表现出了极强的适应性和可塑性,这可能是其能够快速扩散的重要原因之一。同时也表明夜栖树并不能成为一个有力的限制因子,钳嘴鹳有可能继续向国内的南方湿地区扩散。     

老年2型糖尿病患者发生严重低血糖相关危险因素分析

目的:研究老年2型糖尿病患者发生严重低血糖的相关危险因素。方法:选取2013年7月到2014年7月我院收治的老年2型糖尿病患者200例,根据是否发生严重低血糖将患者分为非低血糖组(138例)和低血糖组(62例),比较两组临床资料。结果:低血糖组和非低血糖组体重指数、住院时间以及糖尿病病程比较差异具有统计学意义(P0.05);低血糖组心脑血管疾病药物联用率显著高于非低血糖组,二甲双胍应用率显著低于非低血糖组,胰岛素应用率以及口服降糖药(OAD)和胰岛素的联合应用率显著高于非低血糖组,两组比较差异具有统计学意义(P0.05);低血糖组低钾血症发生率显著高于非低血糖组,肾功能有关的指标显著高于非低血糖组,低血糖组白细胞和中性粒细胞显著高于非低血糖组,两组比较差异具有统计学意义(P0.05);Logistic多因素回归分析可知,病程超过10年、胰岛素应用以及和OAD联用、果糖胺低于2.5 mmol/L、白细胞升高、肾功能受损均和严重低血糖发生具有相关关系。结论:病程超过10年、胰岛素应用以及和OAD联用、白细胞升高、果糖胺低于2.5 mmol/L、肾功能受损均和严重低血糖发生有关,在行降糖治疗时应该谨慎评估上述危险因素。     

Hypoglycemic effect of catalpol on high-fat diet/streptozotocin-induced diabetic mice by increasing skeletal muscle mitochondrial biogenesis

Catalpol, an iridoid glycoside, exists in the root of Radix Rehmanniae. Some studies have shown that catalpol has a remarkable hypoglycemic effect in the streptozotocin- induced diabetic model, but the underlying mechanism for this effect has not been fully elucidated. Because mito- chondrial dysfunction plays a vital role in the pathology of diabetes and because improving mitochondrial function may offer a new approach for the treatment of diabetes, this study was designed. Catalpol was orally administered together with metformin to high-fat diet/streptozotocin （HFD/STZ）-induced diabetic mice daily for 4 weeks. Body weight （BW）, fasting blood glucose （FBG） level, and glucose disposal （IPGTT） were measured during or after the treatment. The results showed a dose-dependent re- duction of FBG level with no apparent changes in BW through four successive weeks of catalpol administration. Catalpol treatment substantially reduced serum total chol- esterol and triglyceride levels in the diabetic mice. In add- ition, catalpol efficiently increased mitochondrial ATP production and reversed the decrease of mitochondrial membrane potential and mtDNA copy number in skeletal muscle tissue. Furthermore, catalpol （200 mg/kg） rescued mitochondrial ultrastructure in skeletal muscle, as detected with transmission electron microscopy. The relative mRNA level of peroxisome proliferator-activated receptor gamma co-activator 1 （PGC1） α was significantly decreased in muscle tissue of diabetic mice, while this effect was reversed by catalpol. resulting in a dose-dependent up-regulation. Taken together, we found that catalpol was capable of lowering FBG level via improving mitochondrial function in skeletal musde of HFD/STZ-induced diabetic mice.     

小儿推拿疗法联合中药热奄包治疗小儿夜啼的疗效及对睡眠质量和生长发育的影响

摘要 目的：探讨小儿推拿疗法联合中药热奄包治疗小儿夜啼的疗效及对睡眠质量和生长发育的影响。方法：选取2019年4月~到2021年8月期间石家庄市中医院收治的120例夜啼患儿作为研究对象。根据双色球法将患儿分为对照组（常规药物治疗）和观察组（对照组的基础上接受小儿推拿疗法联合中药热奄包治疗）,各为60例。对比两组疗效、中医证候评分、睡眠质量、生长发育相关指标和不良反应发生情况。结果：与对照组相比,观察组的临床总有效率明显升高（P<0.05）。与对照组相比,观察组治疗1周后啼哭、腹喜按摩、睡喜蜷曲、四肢欠温、大便稀溏、小便色清评分更低（P<0.05）。与对照组相比,观察组治疗1周后白天睡眠时间、夜间睡眠时间更长,夜间清醒时间更短,夜醒次数更少（P<0.05）。与对照组相比,观察组治疗6个月后年龄别体质量Z值（WAZ）、年龄别身长Z值（LAZ）、身长别体质量Z值（WLZ）和头围Z值（HCZ）更大（P<0.05）。治疗期间两组均未出现不良反应。结论：小儿推拿疗法联合中药热奄包治疗小儿夜啼,可有效改善患儿临床症状,提高睡眠质量,促进生长发育。     

2型糖尿病住院患者心脏自主神经病变的影响因素及对夜间AH和夜间VA的影响

摘要 目的：分析2型糖尿病（T2DM）住院患者心脏自主神经病变（CAN）的影响因素,探讨其对夜间无症状低血糖（AH）和夜间室性心律失常（VA）的影响。方法：选取2020年1月～2022年7月肇庆医学高等专科学校附属医院收治的174例T2DM患者,根据是否发生CAN分为CAN组和非CAN组,采用多因素Logistic回归分析T2DM住院患者CAN的影响因素。采用动态血糖监测系统监测夜间AH发生情况,动态心电图监测夜间VA发生情况。结果：174例T2DM患者CAN发生率为37.93%（66/174）。单因素分析显示,CAN组年龄大于非CAN组,病程长于非CAN组,收缩压、舒张压、糖化血红蛋白（HbA1c）、稳态模型评估-胰岛素抵抗（HOMA-IR）、血尿酸和微血管并发症比例高于非CAN组（P＜0.05）。多因素Logistic回归分析显示,年龄增加、病程延长、HOMA-IR升高、血尿酸升高、微血管并发症为T2DM住院患者CAN的独立危险因素（P＜0.05）。与非CAN组比较,CAN组夜间AH、VA发生率增加（P＜0.05）。结论：年龄、病程、HOMA-IR、血尿酸和微血管并发症为T2DM住院患者CAN的影响因素,CAN增加了T2DM住院患者夜间AH和夜间VA的发生率,早期筛查CAN可能有助于降低T2DM住院患者夜间AH和夜间VA的发生风险。     

Changes in Excitatory Amino Acid Receptor Binding in the Intact and Decorticated Rat Neostriatum Following Insulin-Induced Hypoglycemia

An involvement of excitatory amino acid (EAA) transmitter-receptor interactions in the development of hypoglycemia-induced neuronal damage has been suggested. We report here on the binding to EAA receptors in the rat caudate nucleus and cerebral cortex, during and following severe insulin-induced hypoglycemia with an isoelectric EEG of 10 or 30 min duration. The binding of alpha-[3H]amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid [( 3H]AMPA) to quisqualate receptors, [3H]kainic acid (KA) to kainate receptors, and [3H]glutamate to N-methyl-D-aspartate (NMDA)-sensitive sites was determined by quantitative autoradiography. During EEG isoelectricity, AMPA binding was reduced by approximately 40%, which could represent quisqualate receptor desensitization. One hour following glucose-induced recovery, AMPA binding was no longer different from control level. As the recovery period was prolonged to 1 or 4 weeks, AMPA binding decreased. The decrease was more pronounced in the dorsolateral than in the ventromedial part of the striatum. This correlates with the distribution of neuronal damage, and probably reflects loss of receptor binding sites due to cell death. During the period of EEG silence there was a tendency toward an increase in NMDA displaceable glutamate binding. Following 4 weeks of recovery, binding to NMDA receptors was significantly decreased. Glutamate binding to NMDA-sensitive sites was remarkably resistant to neuronal necrosis and was not significantly different from control values in the dorsolateral caudate 1 week following the hypoglycemic coma. No changes in KA binding were found until 1 week posthypoglycemia, when a significant reduction in binding was noted in the lateral striatum.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inflammatory profile in X‐linked adrenoleukodystrophy patients: Understanding disease progression

X‐linked adrenoleukodystrophy (X‐ALD) is an inherited disease characterized by progressive inflammatory demyelization in the brain, adrenal insufficiency, and an abnormal accumulation of very long chain fatty acids (VLCFA) in tissue and body fluids. Considering that inflammation might be involved in pathophysiology of X‐ALD, we aimed to investigate pro‐ and anti‐inflammatory cytokines in plasma from three different male phenotypes (CCER, AMN, and asymptomatic individuals). Our results showed that asymptomatic patients presented increased levels of pro‐inflammatory cytokines IL‐1β, IL‐2, IL‐8, and TNF‐α and the last one was also higher in AMN phenotype. Besides, asymptomatic patients presented higher levels of anti‐inflammatory cytokines IL‐4 and IL‐10. AMN patients presented higher levels of IL‐2, IL‐5, and IL‐4. We might hypothesize that inflammation in X‐ALD is related to plasmatic VLCFA concentration, since there were positive correlations between C26:0 plasmatic levels and pro‐inflammatory cytokines in asymptomatic and AMN patients and negative correlation between anti‐inflammatory cytokine and C24:0/C22:0 ratio in AMN patients. The present work yields experimental evidence that there is an inflammatory imbalance associated Th1, (IL‐2, IL‐6, and IFN‐γ), Th2 (IL‐4 and IL‐10), and macrophages response (TNF‐α and IL‐1β) in the periphery of asymptomatic and AMN patients, and there is correlation between VLCFA plasmatic levels and inflammatory mediators in X‐ALD. Furthermore, we might also speculate that the increase of plasmatic cytokines in asymptomatic patients could be considered an early biomarker of brain damage and maybe also a predictor of disease progression.