新生儿低血糖脑损伤的MRI诊断及鉴别

目的:探讨新生儿低血糖脑损伤的MRI特征及扩散加权成像(DWI)在低血糖脑损伤诊断中的应用价值。方法:回顾性分析13例经临床确诊的新生儿低血糖脑损伤病例的MRI资料,所有病例均在出生后38h～7d行MRI检查,扫描序列包括常规T1WI、T2WI及DWI序列。结果:常规T1WI表现为受累部位稍低信号4例,稍高信号2例;9例T2WI表现为受累部位稍高信号或灰白质分界不清。13例在DWI图上出现异常高信号,受累部位在ADC图上呈低信号(其中2例低信号范围内出现部分高信号),受累脑区包括双侧枕顶叶皮层及皮层下脑白质10例、双侧顶枕叶皮层下脑白质1例、双侧颞叶后部皮层下脑白质4例、双侧额叶后部皮层下脑白质4例、胼胝体压部13例(整个胼胝体受累1例)、双侧内囊后肢5例、双侧内囊前肢1例、双侧外囊1例、脑干1例,13例中10例病变呈对称性分布。结论:新生儿低血糖脑损伤以双侧枕顶叶后部脑组织及胼胝体压部最常受累,常对称性分布,具有一定特征性。DWI序列较常规T1WI及T2WI序列在低血糖脑损伤的诊断及评估上更具优越性。     

The effect of the human menstrual cycle on nutrient intake

The dietary intakes of eight human females were obtained by interview each day for 60 days to determine whether the menstrual cycle affected nutrient intake. Analysis showed that over the menstrual cycle there were fluctuations in carbohydrate consumption, but not in protein and fat consumption. The mean post period (preovulation) intake was between 51.6% to 56.4% of the preperiod (postovulation) consumption. The evidence indicates that women eat more carbohydrate per day after they ovulate than before.     

Agraphia with reversible splenial corpus callosum lesion caused by hypoglycemia

Background

Neurological manifestations caused by hypoglycemia range from reversible focal deficits and transient encephalopathy to irreversible coma or death. Recently, high signal intensity lesions in the splenium of the corpus callosum on diffusion-weighted magnetic resonance imaging were reported in adults experiencing hypoglycemia. However, patients presenting with agraphia are rare.

胰岛素自身免疫综合征3例报告及文献复习

目的 总结分析国内胰岛素自身免疫综合征(insulin autoimmune syndrome,IAS)病人的临床资料,以期提高临床对IAS的认识.方法 对2013年6月至2018年12月于西安高新医院确诊为IAS的3例病人和2009年6月至2019年6月于各大数据库中检索到关于IAS的87例国内个案报道进行回顾性分析...     

Stress-induced increases in hypothalamic IL-1: a systematic analysis of multiple stressor paradigms

Exposure to stressors such as footshock, tailshock, and immobilization have been shown to induce hypothalamic IL-1 production, while other stressors such as restraint, maternal separation, social isolation, and predator exposure have no effect on hypothalamic IL-1 levels. This disparity of findings has led to considerable controversy regarding the ability of stressors to induce hypothalamic IL-1 expression. Thus, the goal of the following experiments was to examine hypothalamic IL-1 responses in adult male Sprague-Dawley rats following exposure to a diverse set of stressors. Our data indicate that exposure to 2h of restraint in a Plexiglas tube, glucoprivic challenge induced by administration of 2-deoxyglucose (2-DG), or insulin-induced hypoglycemia all fail to alter hypothalamic IL-1 levels despite robust activation of the pituitary-adrenal response. However, when restraint was administered on an orbital shaker or in combination with insulin-induced hypoglycemia, robust increases in hypothalamic IL-1 were observed. No effects of glucoprivic (2-DG) challenge were observed when combined with restraint, indicating some specificity in the hypothalamic IL-1 response to stress. We also provide a preliminary validation of the ELISA detection method for IL-1, showing that (a) Western blot analyses confirmed strong immunopositive banding at the apparent molecular weight of both mature IL-1beta and the IL-1beta prohormone, and (b) footshock led to a two-fold increase in mRNA for IL-1 in the hypothalamus as detected by RT-PCR. These data provide novel insight into the characteristics of a stressor that may be necessary for the observation of stress-induced increases in hypothalamic IL-1.     

Zinc release contributes to hypoglycemia-induced neuronal death

Neurons exposed to zinc exhibit activation of poly(ADP-ribose) polymerase-1 (PARP-1), an enzyme that normally participates in DNA repair but promotes cell death when extensively activated. Endogenous, vesicular zinc in brain is released to the extracellular space under conditions causing neuronal depolarization. Here, we used a rat model of insulin-induced hypoglycemia to assess the role of zinc release in PARP-1 activation and neuronal death after severe hypoglycemia. Zinc staining with N-(6-methoxy-8-quinolyl)-para-toluenesulfonamide (TSQ) showed depletion of presynaptic vesicular zinc from hippocampal mossy fiber terminals and accumulation of weakly bound zinc in hippocampal CA1 cell bodies after severe hypoglycemia. Intracerebroventricular injection of the zinc chelator calcium ethylene-diamine tetraacetic acid (CaEDTA) blocked the zinc accumulation and significantly reduced hypoglycemia-induced neuronal death. CaEDTA also attenuated the accumulation of poly(ADP-ribose), the enzymatic product of PARP-1, in hippocampal neurons. These results suggest that zinc translocation is an intermediary step linking hypoglycemia to PARP-1 activation and neuronal death.     

Metabolic sensors: viewing glucosensing neurons from a broader perspective

Glucose is a critical substrate for brain and organ function. Specialized glucosensing neurons, which are involved in the control of energy homeostasis and neuroendocrine function, are located in specific anatomic locations in the brain. Glucose-excited neurons increase their firing rate when ambient glucose levels rise. This glucosensing capacity appears to be regulated by a combination of glucokinase and an ATP-sensitive K(+) (K(ATP)) channel whose activity is regulated by ATP derived from glucose metabolism. Glucose inhibited neurons decrease their firing rate when glucose levels rise, although it is unclear what mechanism is used to control this function. Neuropeptide Y and proopiomelanocortin neurons in the hypothalamic arcuate nucleus are examples of neurons that are capable of sensing both glucose and a host of other peripheral metabolic signals, possibly by their actions on the K(ATP) channel. These metabolic sensing neurons are intimately involved in energy homeostasis, and it is postulated that glucose is only one of several peripheral metabolic signals involved in this process under physiologic conditions. However, when glucose supply is severely limited, glucose appears to assume primacy as a stimulant of glucosensing in order to activate the counterregulatory and ingestive processes necessary to restore the vital supply of glucose. Thus, the role of glucosensing is postulated to be a relative one that is dependent upon the supply of peripheral glucose.     

Hipoglucemias en un caso con insulinomas benignos múltiples

Riassunto Vengono descritti il quadro clinico, le indagini eseguite, il trattamento praticato, i reperti anatomo-patologici e l’evoluzione in una paziente 19enne, affetta da crisi ipoglicemiche dovute ad insulomi multipli benigni. Le indagini di laboratorio hanno messo in evidenza: a) livelli glicemici molto bassi sia in condizioni di base che in periodo postprandiale e durante le crisi; b) risultati delle prove di sovraccarico orale con glucosio, tolbutamide e glucagone compatibili con la diagnosi di insuloma; c) insulinemia basale elevata. La risposta insulinica nel corso delle prove dinamiche viene discussa. L’arteriografia selettiva ha dimostrato la presenza di immagini tumorali intra- ed extrapancreatiche. è stata praticata pancreatectomia corporo-caudale, seguìta da scomparsa della sintomatologia. L’esame del tessuto prelevato ha confermato la diagnosi di insuloma. Il quadro clinico è scomparso ed i parametri studiati si sono normalizzati nella fase postoperatoria.

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Summary The clinical pattern, tests performed, management, pathology and evolution in an 19-year-old patient with hypoglycemic attacks due to multiple benign insulomata are described. Laboratory investigations showed: a) very low blood glucose levels in basal conditions, postprandially and during the crises; b) the results of the oral glucose tolerance, tolbutamide, and glucagon tests were compatible with the diagnosis of insuloma; c) basal plasma insulin was high. The insulin response to the dynamic tests is discussed. Selective arteriography provided evidence of intra- and extrapancreatic tumors. Corporocaudal pancreatectomy was performed leading to the complete disappearance of the symptoms. Examination of the excised structures confirmed the diagnosis of insuloma. Clinical manifestations subsided and the parameters studied returned to normal after surgery.

Traduzione a cura della Redazione.     

地塞米松改变胆源性脓毒症时宿主糖代谢反应

将４０只日本大耳白兔随机分为胆源性脓毒症组（ｎ＝１５，以下简称非治疗组）、地塞米松治疗组（ｎ＝１５）和正常对照组（ｎ＝１０），并将前两组复制成胆源性脓毒症模型。治疗组于伤后３和２４小时按１０ｍｇ／ｋｇ剂量分两次腹腔注射地塞米松，动态检测和比较三组动物血糖水平的变化，用原代肝细胞培养法分析伤后４８小时感染肝叶和非感染肝叶肝细胞糖异生功能。结果显示；伤后２４小时起，非治疗组血糖水平持续显著降低，而治疗组至伤后４８小时才出现血糖降低；伤后４８小时，治疗组感染肝叶肝细胞糖异生的基础速率及激素刺激速率与非治疗组无显著性差异，但非感染肝叶肾上腺素和胰高糖素刺激的肝细胞糖异生速率分别较非治疗组提高了２５．０％和４６．０％，然而两者仍低于正常对照组水平。本实验结果表明，地塞米松对胆源性脓毒症时宿主糖代谢的稳态具有保护效应。     

Pediatric epilepsy — an Indian perspective

Prevalence studies from India suggest that epilepsy prevalence is similar to developed nations. Neurocysticercosis (NCC) predominates as an etiology. A large treatment gap is still a public health problem. Benign epilepsies and West syndrome appear to be underrepresented in studies on classification of seizures/syndromes. Febrile seizures prevalence in India is similar to other countries and appear to be as benign. Risk factors of intractable epilepsy (IE) in Indian studies include early age of onset, neurodevelopmental abnormalities and certain seizure types. Perinatal injuries underlie many IE. Many IE are not truly intractable and respond to simple therapeutic measures. The ketogenic diet and surgery are other methods now being used in Indian centers. Neurocysticercosis and neonatal hypoglycemic brain injury, two widely prevalent etiologies are reviewed in detail