AQP4参与卵巢激素对单胺类神经递质的调节作用

目的：探讨AQP4对卵巢激素调节神经递质作用的影响。方法：应用雌性AQP4基因敲除型CD1小鼠与野生型CD1小鼠，测定AQP4基因敲除对小鼠血浆中雌孕激素水平的影响；两种基因型小鼠实施卵巢去势手术，测定纹状体和皮层中单胺类神经递质的含量。结果：AQP4基因敲除型小鼠动情后期血浆雌、孕激素水平显著低于野生型小鼠；去势后野生型小鼠纹状体多巴胺（DA）及皮层去甲肾上腺素（NE）含量明显降低，但去势不影响AQP4基因敲除型小鼠脑内相应的递质水平。结论：AQP4参与了卵巢激素对单胺类神经递质的调节。     

Sex differences in the regulation of body weight

Obesity and its associated health disorders and costs are increasing. Males and females differ in terms of how and where body fat is stored, the hormones they secrete in proportion to their fat, and the way their brains respond to signals that regulate body fat. Fat accumulation in the intra-abdominal adipose depot is associated with the risk for developing cardiovascular problems, type-2 diabetes mellitus, certain cancers and other disorders. Men and postmenopausal women accumulate more fat in the intra-abdominal depot than do pre-menopausal women, and therefore have a greater risk of developing metabolic complications associated with obesity. The goal of this review is to explore what we know about sexual dimorphisms in adipose tissue accrual and deposition. Elucidating the mechanisms by which sex hormones may modulate the way in which fat is accumulated and stored is a critical area of research due to the prevalence of obesity and the metabolic syndrome, and the rapid increase in propensity for these diseases following menopause.     

Effect of photoperiod and temperature on gonadal activity and plasma steroid levels in a reared strain of the mummichog (Fundulus heteroclitus) during different phases of its annual reproductive cycle

Mummichog, a spring and summer spawning teleost, were exposed to various photoperiod and temperature conditions to investigate the environmental regulation of the annual reproductive cycle. In early spring, latter phases of gonadal development (vitellogenesis in females and active spermatogenesis in males) were effectively accelerated by warm temperature (16 degrees C) regardless of the photoperiod (11L or 16L), although internal factor(s) may be concerned with triggering the initiation of the development. In late summer, intense gonadal regression which leads to the termination of the spawning period was accelerated by a short day length (相似文献   

雌雄激素联合作用对高脂血症小鼠血脂水平及凝血功能的影响

目的 探讨雌雄激素联合作用对高脂血症小鼠血脂水平及凝血功能的影响。方法 对小鼠行去势手术后通过高脂饮食建立高脂血症模型,通过给予不同激素将老鼠分为5组。造模结束后采集小鼠血液,一部分小鼠分离血清检测小鼠血脂水平,一部分小鼠分离血浆检测凝血功能。结果 高脂饮食后,小鼠血清总胆固醇、甘油三酯和低密度脂蛋白水平较对照组相比明显升高,凝血酶原时间、活化部分凝血酶原时间时间明显缩短(P<0.05),给予雌雄激素联合治疗后,与造模组相比,小鼠血清总胆固醇、甘油三酯和低密度脂蛋白水平较对照组相比明显下降,凝血酶原时间、活化部分凝血酶原时间时间明显延长(P<0.05),而与对照组无明显差异。结论 雌雄激素联合治疗可以调节血脂,显著降低低密度脂蛋白的水平,调节凝血功能,提示雌雄激素联合作用可以降低冠心病的发病风险,为冠心病的激素治疗提供新思路。     

Paradoxical zinc toxicity and oxidative stress in the mammary gland during marginal dietary zinc deficiency

Zinc (Zn) regulates numerous cellular functions. Zn deficiency is common in females; ∼80% of women and 40% of adolescent girls consume inadequate Zn. Zn deficiency enhances oxidative stress, inflammation and DNA damage. Oxidative stress and inflammation is associated with breast disease. We hypothesized that Zn deficiency increases oxidative stress in the mammary gland, altering the microenvironment and architecture. Zn accumulated in the mammary glands of Zn deficient mice and this was associated with macrophage infiltration, enhanced oxidative stress and over-expression of estrogen receptor α. Ductal and stromal hypercellularity was associated with aberrant collagen deposition and disorganized e-cadherin. Importantly, these microenvironmental alterations were associated with substantial impairments in ductal expansion and mammary gland development. This is the first study to show that marginal Zn deficiency creates a toxic microenvironment in the mammary gland impairing breast development. These changes are consistent with hallmarks of potential increased risk for breast disease and cancer.     

17-β estradiol attenuates ovariectomy-induced changes in cardiomyocyte contractile function via activation of AMP-activated protein kinase

Menopause increases the risk of cardiometabolic diseases in women. This circumstance is usually attributed to a deficiency in circulating estrogen levels although the underlying mechanism remains elusive. Given the pivotal role of AMP-activated protein kinase (AMPK) in the regulation of energy metabolism and cardiac function, this study was designed to examine the role of AMPK in estrogen deficiency and replacement-exerted cardiomyocyte responses. Adult female WT and AMPK kinase dead (KD) mice were subjected to bilateral ovariectomy (OVX) or sham operation. A cohort of ovariectomized mice received 17β-estradiol (E2) (40 μg/kg/day, i.p.) for 6 weeks. Mechanical and intracellular Ca²⁺ properties were evaluated including peak shortening (PS), time-to-PS (TPS), time-to-90%-relengthening (TR₉₀), and maximal velocity of shortening/relengthening (±dL/dt). Levels of AMPK, Akt JNK, ACC, SERCA, membrane Glut4, AS160 and PGC-1α were assessed using Western blot. OVX significantly decreased PS, ±dL/dt and intracellular Ca²⁺ rise in responsible to electric stimulus, prolonged TR₉₀ and intracellular Ca²⁺ decay without affecting TPS and resting intracellular Ca²⁺, the effects of which were reconciled by E2 replacement. Western blot analysis depicted that OVX suppressed phosphorylation of Akt AMPK and ACC although it promoted JNK phosphorylation, the effects of which were mitigated or significantly attenuated by E2 treatment in WT but not KD mice. Moreover, OVX procedure downregulated SERCA2a and membrane Glut4 while inhibiting AS160 phosphorylation without affecting PGC-1α levels. In vitro study revealed that E2 corrected cardiomyocyte contractile dysfunction elicited by OVX in cardiomyocytes from WT but not the AMPK kinase dead mice. Taken together, these data suggest that E2 treatment ameliorates estrogen deficiency-induced changes in cardiac contractile function possibly through an AMPK-dependent mechanism.     

急性白血病患者雌激素受体多药耐药相关蛋白的检测及临床意义

目的 :探讨雌激素受体 (ER)、多药耐药相关蛋白 (MRP)表达与临床疗效的关系 ,为耐药白血病寻找新的治疗途径。方法 :采用免疫组化ABC法检测了 37例急性白血病 (AL)复发难治患者骨髓单个核细胞的ER与MRP表达。结果 :①ER阳性组CR率为 91.6 7% (11/ 12 ) ,阴性组为 2 8.0 0 % (7/ 2 5 ) ,ER阳性组CR率显著优于阴性组 (P <0 .0 1)。②MRP阳性组CR率为 2 3.81% (5 / 2 1) ,MRP阴性组为 81.2 5 % (13/ 16 ) ,MRP阳性组CR率明显差于阴性组 (P <0 .0 1)。③ 37例AL患者中 ,8例ER +/MRP -与 17例ER - /MRP +患者其ER与MRP表达的一致性很好 (Kappa系数 =0 .83,P <0 .0 1)。另有ER +/MRP +4例 ,ER - /MRP - 8例 ,其ER与MRP表达缺乏一致性。结论 :ER与MRP表达有一定的一致性 ,且与临床疗效有一定关系 ;ER与MRP检测有助于疗效和预后的判定     

晚期糖化终末产物在去卵巢大鼠骨质疏松发病中的作用及氨基胍防治效果

目的　探讨晚期糖化终末产物 (AGEs)在去卵巢大鼠骨质疏松发病中的作用及氨基胍防治效果。方法　选用 1 0月龄大鼠通过卵巢切除诱导骨质疏松并用氨基胍防治其骨量丢失 ,测定其骨密度及骨胶原中 AGEs的含量及血、尿生化指标。结果　卵巢切除大鼠骨密度 (0 .2 0 7g/cm2 ± 0 .0 1 6 g/cm2 )明显低于假手术大鼠 (0 .2 36 g/cm2 ± 0 .0 1 0 g/cm2 ) (P<0 .0 1 ) ,而骨胶原 AGEs含量 (59.86 RU/mg胶原± 3.1 3 RU/mg胶原 )明显高于假手术组大鼠 (53.83RU/mg胶原± 5.46RU/mg胶原 ) (P<0 .0 1 )。卵巢切除大鼠血清雌激素 (4.50 pg/ml± 1 .73pg/ml)与假手术组(8.45 pg/ml± 2 .90 pg/ml)比较明显降低 (P<0 .0 2 ) ,2 4 h尿钙、尿钙与肌酐比值、尿磷、尿磷与肌酐比值均有升高趋势。卵巢切除大鼠给予氨基胍后骨密度 (0 .2 2 1 g/cm2± 0 .0 1 7g/cm2 )明显升高 (P<0 .0 5) ,骨胶原中 AGEs含量 (51 .2 3RU/mg胶原± 7.46RU/mg胶原 )明显降低 (P<0 .0 1 ) ,血清雌激素 (8.59pg/ml± 3.0 1 pg/ml)明显升高 (P<0 .0 1 ) ,2 4 h尿钙、尿钙与肌酐比值降低 ,2 4 h尿羟脯氨酸升高 ,与手术组比较有显著差异 (P<0 .0 5)。结论　卵巢切除后 ,雌激素的降低和 AGEs的增加是导致骨质疏松的主要原因。而氨基胍通过降低体内 AGE