Neuroendocrine control of maternal behavior in non-human and human mammals

Mammalian parental care is essentially provided by the mother and it occupies most of the reproductive period for female. The synchronization of maternal behavior with parturition and lactation ensures that the mother responds to the needs of the young at the appropriate time. This temporal synchrony is accomplished by hormonal changes that underly both the onset of maternal behavior and of parturition and lactation. The aim of this review is to describe and compare the hormonal mechanisms that regulate the onset of maternal behavior across a variety of mammals, including humans, that represent different behavioral strategies. Are involved the steroid hormones, estradiol and progesterone synthesized by the ovaries which primed the future mother to repond maternally. In response to these steroids, oxytocin release induced by vaginocervical stimulation and prolactin release affect the maternal brain. The medial preoptic area integrates the hormonal signals to regulate maternal behavior. The hormonal cocktail that stimulates maternal behavior varies across mammalian species. Because most of the studies in humans are correlative and because human environment is complex, direct causality between hormones and maternal behavior is unclear. However, one can reasonably think that hormones create a positive bias towards the baby increasing the occurrence of maternal behavior.     

What ethologically based models have taught us about the neural systems underlying fear and anxiety

Classical Pavlovian fear conditioning to painful stimuli has provided the generally accepted view of a core system centered in the central amygdala to organize fear responses. Ethologically based models using other sources of threat likely to be expected in a natural environment, such as predators or aggressive dominant conspecifics, have challenged this concept of a unitary core circuit for fear processing. We discuss here what the ethologically based models have told us about the neural systems organizing fear responses. We explored the concept that parallel paths process different classes of threats, and that these different paths influence distinct regions in the periaqueductal gray - a critical element for the organization of all kinds of fear responses. Despite this parallel processing of different kinds of threats, we have discussed an interesting emerging view that common cortical-hippocampal-amygdalar paths seem to be engaged in fear conditioning to painful stimuli, to predators and, perhaps, to aggressive dominant conspecifics as well. Overall, the aim of this review is to bring into focus a more global and comprehensive view of the systems organizing fear responses.     

颅脑损伤合并高钠血症63例临床分析

目的：探讨颅脑损伤后合并高钠血症的临床治疗及高钠血症对预后的影响。方法回顾分析该院2007年1月-2014年12月间收治的重型颅脑损伤合并高钠血症63例患者临床资料,对比血钠高低对死亡率的影响,对比控制尿量组与非控制尿量组血钠恢复时间。结果轻度高钠组、中度高钠组、重度高钠组分别有17例、24例、22例,各组的死亡率分别为29.4%、45.8%、63.6%,轻度高钠组与重度高钠组间相比,差异有统计学意义(P<0.05)。控制尿量组28例,非控制尿量组18例,两组的血钠恢复正常所需的平均天数分别为(4.57±1.86)、(6.38±1.49),两组相比差异有统计学意义(P<0.05)。结论颅脑损伤合并高钠血症血钠值越高,死亡率越高,除常规治疗外,控制尿量可明显缩短血钠恢复的时间。     

3 Tesla serial magnetic resonance imaging of human African trypanosomiasis (Trypanosoma brucei gambiense) and review of the literature

We report serial magnetic resonance imaging (MRI) findings and follow-up in a case of human African trypanosomiasis (HAT) presenting with limited lesions followed by early and complete resolution. We searched the literature for documented cases and reviewed MRI findings before treatment. A 30-year-old Lebanese man, who had lived in Gabon for six years, presented with a two-year history of rash, anorexia, weight loss, arthralgia, paresthesia, and hypersomnia. Previously, the patient had received corticosteroid therapy for unconfirmed ANCA-associated vasculitis. Physical examination revealed a painless chancre on the left arm located at the site of an old insect bite, enlarged cervical, axillar and inguinal lymph nodes, hepatosplenomegaly and impaired concentration. Blood analysis showed an elevated protein level (90 g/L) with hypoalbuminemia (24.2 g/L) and elevated IgM (26.4 g/L). Bone marrow aspirate and biopsy failed to detect any parasite. Polymerase chain reaction tests on blood and cerebrospinal fluid were positive for Trypanosoma. Serology tests confirmed the diagnosis of HAT due to Trypanosoma brucei gambiense infection. 3T MRI showed lesions in the hypothalamus and basal ganglia, the internal capsule, and the mesencephalon bilaterally. Follow-up MRI showed interval progression of the abnormalities. Treatment with melarsoprol was followed by clinical improvement with regression of the lesions on the three-month MRI, then total resolution at the 10-month follow-up. This case highlights a pattern of mild MRI lesions in T. brucei gambiense HAT with a total and rapid resolution under treatment. The literature review (16 HAT cases with sufficient radiological data, included ours) revealed an MRI pattern of brain lesion distribution that could be helpful for diagnosis and orienting biological tests.     

甲状腺激素及脑源性神经营养因子前体水平与抑郁症的关系研究

背景　随着对抑郁症了解的深入,人们发现其不仅是一种神经退行性疾病,同时还与下丘脑-垂体-甲状腺轴（HPT轴）密切相关,而抑郁症的神经营养因子假说则认为脑源性神经营养因子前体（proBDNF）在抑郁症的发病过程中发挥着一定作用,但抑郁症、HPT轴和proBDNF三者间的关系却鲜有研究。目的　探索甲状腺激素、proBDNF水平与抑郁症之间的关系。方法　选取2017年10月-2018年6月在云南省精神病医院住院及门诊治疗的抑郁症患者43例为病例组。同期选取本院健康体检者31例为对照组。测定并比较两组一般资料及甲状腺激素〔三碘甲状腺原氨酸（T3）、甲状腺素（T4）、游离三碘甲状腺原氨酸（FT3）、游离甲状腺素（FT4）、促甲状腺激素（TSH）〕、proBDNF水平;分析病例组甲状腺激素、proBDNF水平与汉密尔顿抑郁量表24项（HAMD-24）总分及其各因子评分之间的相关性,甲状腺激素与proBDNF水平的相关性。结果　两组T3、FT4水平比较,差异无统计学意义（P>0.05）;病例组T4、FT3、TSH水平低于对照组（P<0.05）。病例组FT3水平与HAMD-24总分及认知障碍评分呈正相关（P<0.05）。两组proBDNF水平比较,差异无统计学意义（P>0.05）。病例组proBDNF水平与HAMD-24总分及其各因子评分均无相关性（P>0.05）。病例组甲状腺激素水平与proBDNF水平无相关性（P>0.05）。结论　抑郁症患者更容易出现焦虑、自杀、偏执、强迫、绝望感及睡眠障碍等问题,且有并发甲状腺功能减退的可能。     

Disruption of fetal hormonal programming (prenatal stress) implicates shared risk for sex differences in depression and cardiovascular disease

Comorbidity of major depressive disorder (MDD) and cardiovascular disease (CVD) represents the fourth leading cause of morbidity and mortality worldwide, and women have a two times greater risk than men. Thus understanding the pathophysiology has widespread implications for attenuation and prevention of disease burden. We suggest that sex-dependent MDD–CVD comorbidity may result from alterations in fetal programming consequent to the prenatal maternal environments that produce excess glucocorticoids, which then drive sex-dependent developmental alterations of the fetal hypothalamic–pituitary–adrenal (HPA) axis circuitry impacting mood, stress regulation, autonomic nervous system (ANS), and the vasculature in adulthood. Evidence is consistent with the hypothesis that disruptions of pathways associated with gamma aminobutyric acid (GABA) in neuronal and vascular development and growth factors have critical roles in key developmental periods and adult responses to injury in heart and brain. Understanding the potential fetal origins of these sex differences will contribute to development of novel sex-dependent therapeutics.     

胰高血糖素样肽-1与下丘脑食欲调节

下丘脑是神经内分泌中枢,也是食欲调节中枢.胰高血糖素样肽-1(GLP-1)是一种胃肠道激素,能够在下丘脑表达并对食欲中枢有调节作用.GLP-1作为一种厌食信号肽,通过促肾上腺皮质激素释放激素(CRH)通路、组胺神经元通路、神经肽和刺鼠相关蛋白(NPY/AgRP)以及前阿片黑皮质素原和可卡因-苯丙胺调节转录肽(POMC/CART)通路及AMP活化蛋白激酶(AMPK)介导的摄食负反馈信号通路参与调节摄食活动.针对GLP-1调节摄食作用机制的研究对肥胖、胰岛素抵抗和2型糖尿病的防治有重要的理论意义.     

儿童下丘脑错构瘤三例报道及文献复习

目的 探讨儿童下丘脑错构瘤的临床表现、诊断及治疗方法.方法 回顾性分析复旦大学附属儿科医院2012年6月至2013年10月收治的3例下丘脑错构瘤患儿的临床资料,并通过PubMed检索Medline数据库、检索Springer Link,中国知网(CNKI)、万方数据库,对儿童下丘脑错构瘤的中英文文献进行系统性的综述.其中,男2例,女1例;年龄3～6岁,平均4岁;都表现为痴笑性癫痫及不同程度的性早熟.本组均采用翼点入路及经胼胝体-穹窿间入路行外科手术.结果 3例错构瘤均部分切除,术后痴笑性癫痫症状较前略有改善,其中1例并发严重脑干损伤及脑积水,行手术分流,辅以高压氧及康复训练后症状较前好转.结论 下丘脑错构瘤是婴幼儿颅内罕见的“良性肿瘤”,根据其特有的临床症状及典型的MRI表现,不难做出诊断,治疗以手术为主,总体预后良好.