Restoration of disturbed respiration in cats by thyrotrophin releasing hormone

Department of Physiology of Man and Animals, Biological Faculty, M. V. Lomonosov Moscow University. (Presented by Academician of the Academy of Medical Sciences of the USSR I. P. Ashmarin.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 106, No. 7, pp. 17–19, July, 1988.     

采用组织芯片技术分析胃癌组织中胃泌素和胃泌素释放肽的表达

目的研究胃癌组织中胃泌素(GAS)、胃泌素释放肽(GRP)的表达及其临床意义。方法采用组织芯片技术制作60例胃癌组织芯片,同时用生物素-链霉菌卵白素检测系统(SP)免疫组织化学方法检测胃癌组织芯片中GAS、GRP的表达。结果60例胃癌中GAS阳性率为30.0%;GRP阳性率为11.7%。中、低分化胃癌GAS、GRP阳性率高于高分化胃癌(P<0.05);印戒细胞癌GAS、GRP阳性率显著高于其他组织学类型胃癌(P<0.05);胃癌GAS、GRP阳性表达与淋巴结转移相关(P<0.05)。结论应用组织芯片大规模高效检测临床组织样本是可行的,具有快速、方便、经济、准确的特点。     

丙氨瑞林治疗子宫内膜癌病人的性激素及有丝分裂指数的变化

目的：观察丙氨瑞林对子宫内膜癌的治疗作用。方法：对诊刮确诊的１７例子宫内膜癌病人，予丙氨瑞林７００μｇ，ｉｍ，ｑｄ×７ｄ，用药前后作性激素测定及组织学检查。结果：绝经妇女用药后血中ＦＳＨ和ＬＨ下降（Ｐ＜０．０１和＜０．０５），雌二醇、孕酮及睾丸酮变化不明显。其中１３例内膜样腺癌用药后有丝分裂指数明显下降（Ｐ＜０．０１），有丝分裂指数变化与癌周内膜之反应有关。呈增生反应癌周内膜癌组织有丝分裂指数下降值明显高于呈萎缩状态癌周内膜。结论：丙氨瑞林治疗子宫内膜癌后能降低ＦＳＨ和ＬＨ水平，对子宫内膜癌尤其是雌激素依赖性内膜癌有一定疗效。     

伍用TRH与ICI174,864对兔失血性休克心功能的影响

采用脑室给药方法研究了促甲状腺素释放激素（ＴＲＨ）与δ－阿片受体特异性拮抗剂ＩＣＩ１７４，８６４合用对失血性休克兔心功能指标的影响，旨在探讨ＴＲＨ与ＩＣＩ１７４，８６４是否可配伍用药治疗休克。ＴＲＨ、ＩＣＩ１７４，８６４两药单用剂量各为５０μｇ，合用剂量各２５μｇ。结果显示，两药半量合用改善失血性休克兔心血管功能作用不仅可达单药５０μｇ的效果，且较单用效果更佳。表明两药可配伍用药治疗失血性休克，且有一定的协同作用。     

Endometriosis: Leuprolide in a 3-monthly versus a monthly depot formulation for the treatment of symptomatic endometriosis: a pilot study

An open-label randomized pilot study was conducted to evaluatethe efficacy and acceptability of 6 months treatment with leuprolidein a 3-monthly versus a monthly i.m. depot injection for therelief of chronic pelvic pain in women with endometriosis. Atotal of 30 women aged 18-38 years were allocated to the 3-monthlydepot arm (n = 15) or to the monthly depot arm (n = 15) afterlaparoscopic diagnosis of pelvic endometriosis. Mean (SD) deepdys-pareunia scores according to a 0–3 point verbal ratingscale decreased from 1.8 (0.9) at baseline to 1.3 (0.7) at theend of treatment in the 3-monthly depot group and from 2.1 (1.2)to 1–3 (0.7) in the monthly depot group. Correspondingvalues in non-menstrual pain scores fell from 2.1 (0.6) to 1.1(03), and from 2.1 (0.8) to 1.2 (0.4) respectively, withoutstatistically significant differences between the groups. Serumluteinizing hormone (LH) and 17-oestradiol concentrations weresignificantly suppressed at 12 and 24 weeks compared with baselinevalues, without differences between the groups. The monthlydepot caused a slightly more marked inhibition of serum folliclestimulating hormone (FSH) levels with respect to the 3-monthlypreparation. Mean (SD) endometriosis scores at baseline andat 6-month follow-up laparoscopy were respectively 32.8 (25.1)and 12.2 (9.3) in the 3-monthly depot group and 29.0 (22.7)and 13.1 (15.3) in the monthly depot group (paired Mest, P 0.05). Mean percentage decrease in lumbar spine bone mineraldensity was 5.2% in the former and 4.9% in the latter subjects.In the 3-monthly depot group, 13 women graded the tolerabilityof their treatment schedule as ‘good’ compared withseven in the monthly depot group (² = 5.40, P = 0.02).     

白细胞介素—1对大鼠下丘脑室旁核Fos癌蛋白和CRF的诱导作用

将白细胞介素-1(IL)注入大鼠侧脑室,用Fos癌蛋白抗体免疫组化法检测了下丘脑室旁核的激活神经元:大量位于含促肾上腺皮质激素释放因子(CRF)相应区域的室旁核小细胞部神经元呈Fos免疫强阳性。Fos和CRF的免疫双染色显示了许多Fos免疫阳性神经元也呈CRF免疫阳性。此外,在IL-1注射动物中,CRF的免疫阳性显著加强,提示CRF合成增加。     

Neuronal fields containing luteinizing hormone releasing hormone (LHRH) in mouse brain.

Immunocytochemical localization of the hypothalamic neurohormone luteinizing hormone releasing hormone (LHRH) was performed in mouse brain using the unlabeled peroxidase anti-peroxidase technique. Antisera derived from serum albumin conjugates to the decapeptide (or its analog) achieved by four conjugation procedures were used to determine the antigenic form of LHRH which reveals the various neuronal compartments. Antisera derived from LHRH conjugated to bovine serum albumin at the 2-histidyl position revealed a population of LHRH-containing cell bodies in the retrochiasmatic area, tuberal area and arcuate nucleus (the LHRH Field I). LHRH-positive fibers and terminals were seen in the organum vasculosum of the lamina terminalis and the median eminence. Fibers from the Field I neurons also coursed rostrally through the medial division of the hypothalamus and circumscribed the anterior commissure or projected dorsally into the thalamus. Antisera generated against conjugates to the N- or C-terminal of LHRH revealed a second population of LHRH perikarya. These were scattered throughout the medial preoptic, preoptic periventricular and medial septal areas (the LHRH Field II). A few neurons were found in the lateral arcuate nucleus. Fibers from septal and preoptic Field II neurons projected to the organum vasculosum. Immunoreactive fibers were found in the median eminence and thalamic regions in patterns similar to those previously described. Median eminence fibers appeared to arise in the regions of Field I neurons which did not stain with the end conjugate antisera. Antisera generated against a LHRH tyrosyl conjugate stained median eminence and organum vasculosum fibers but failed to stain perikarya in either field.The results of this study suggest the presence of two distinct immunoreactive populations of LHRH-containing perikarya, which are not contained within or restricted to any of the recognized hypothalamic nuclei.     

Secretion of growth hormone and thyroid-stimulating hormone in patients with dementia

We studied the growth hormone (GH) response to GH-releasing hormone (GHRH) and the thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH) in four groups of patients with dementia and examined whether GH and TSH secretion is altered in patients with Alzheimer's disease. The four groups included those with Alzheimer's disease (n=28), parkinsonism with dementia (n=10), progressive supranuclear palsy with dementia (n=10), and dementia of vascular origin (n=28). The results showed no differences among the four groups in GH response to GHRH (12.2 ± 2, 10.7 ± 2, 8.9 ±1.1, and 9.9 ± 1.9 g/ml, respectively); there was no correlation between GH response to GHRH and sex, stage of the disease, or cerebral atrophy. The proportion of patients with exaggerated, normal, or lower GH response was similar in the four groups. There were also no differences among the groups in terms of TSH response to TRH (9.2 ±0.9, 11.1 ± 1, 11.1 ± 1, and 10.3 ± 1 mU/ml, respectively), nor was there a correlation between TSH response to TRH and sex, stage of the disease, cerebral atrophy, or GH response to GHRH. The proportion of those with exaggerated, normal, or lower TSH response was similar in the four groups. Cerebrospinal somatostatin levels were similar in Alzheimer's disease and vascular dementia patients. These findings indicate that neither GH response to GHRH nor TSH response to TRH provides a useful diagnostic adjunt in Alzheimer's disease patients.Abbreviations AD Alzheimer's disease - PD parkinsonism with dementia - PSP progressive supranuclear palsy - VD dementia of vascular origin - GH growth hormone - GHRH growth hormone releasing hormone - TRH thyrotropin releasing hormone - TSH thyroid stimulating hormone Correspondence to: J.M. Gomez     

Electrical behaviour in a line of anterior pituitary cells (GH cells) and the influence of the hypothalamic peptide, thyrotrophin releasing factor

Anterior pituitary cells of the GH line, which secrete prolactin spontaneously, showed spontaneous action potential activity. Thyrotrophin releasing factor, which increases secretion in these cells, caused a prompt increase of action potential frequency. Potassium, another secretagogue, depolarized the cells and sometimes initiated a burst of action potentials at the onset of this effect. The action potentials persisted in tetrodotoxin-containing and Na-free media, but were suppressed by the Ca-channel blocker, methoxyverapamil. Moreover, elevating the extracellular Ca²⁺ concentration increased the amplitude of the action potentials. These action potentials therefore have a prominent Ca component. This endows them with a particular interest since secretory activity of these cells is known to be dependent on extracellular Ca²⁺. Ba²⁺, which can substitute for Ca²⁺ in maintaining secretion, also substituted for Ca²⁺ in the maintenance of the action potentials. In addition, Ba²⁺ prolonged action potentials remarkably: tetraethylammonium was less effective in this regard.The several parallels between known secretory behaviour and electrical phenomena encourage the view that analysis of electrical activity in anterior pituitary cells may provide useful clues to events involved in stimulus-secretion coupling and in the secretory control exerted by the brain.     

Effects of acute and chronic treatment with imipramine on 5-hydroxytryptamine nerve cell groups and on bulbospinal 5-hydroxytryptamine/substance P/thyrotropin releasing hormone immunoreactive neurons in the rat. A morphometric and microdensitometric analysis

Summary Groups of male rats were treated for a period of 14 days with imipramine (10mol/kg) given twice daily. Separate groups of rats received a single dose treatment using the same dose and experimental design as for the repeated treatment. Employing the avidin-biotin immunoperoxidase technique for immunohistochemistry 5-hydroxytryptamine (5-HT)-, substance P (SP)- and thyrotropin releasing hormone (TRH)-like immunoreactivities (IRs) were visualized in consecutive coronal sections of the brain stem and of the spinal cord. The IRs were studied by means of morphometric and microdensitometric procedures using automatic image analysis on profiles representing nerve terminal networks of the ventral horn of the cervical and lumbar enlargements of the spinal cord as well as their coexistence (5-HT/SP and 5-HT/TRH). With the same technique 5-HT IR was measured in the 5-HT nerve cell groups of the medulla oblongata (B 1, B 2, B 3) and of the nucleus raphe dorsalis (B 7) of the midbrain. In addition 5-HT and 5-hydroxyindolacetic acid (5-HIAA) levels were measured in the ventral and dorsal horns of the cervical and lumbar enlargements of the spinal cord using high performance liquid chromatography (HPLC). In the same parts of the spinal cord SP IR was studied by means of radioimmunoassay (RIA).The microdensitometric studies showed that chronic, but not acute, imipramine treatment selectively increased SP IR in the 5-HT/SP/TRH costoring nerve terminals of the medial part of the ventral horn in both the cervical and the lumbar enlargements. Furthermore, quantitative analysis of the entity of coexistence in the 5-HT nerve terminal networks of these areas showed that all the 5-HT nerve terminals contained SP and TRH IRs and that this phenomenon remained after acute and chronic imipramine treatment. The microdensitometric studies on the 5-HT nerve cell groups of the medulla oblongata and of the nucleus raphe dorsalis demonstrated that chronic, but not acute, imipramine treatment selectively increased 5-HT IR in the nerve cell bodies of the lateral part of group B 3 as evaluated from the median grey values. Acute, but not chronic, imipramine treatment significantly increased the field area of 5-HT IR of nerve cell bodies in group B 7, reflecting an increase in the mean profile area of the 5-HT IR nerve cell body profiles. Instead, the mean profile area of 5-HT IR cell bodies of group B 1 was acutely reduced by imipramine.The biochemical studies demonstrated that chronic imipramine treatment selectively reduced 5-HT utilization in the ventral horn of the spinal cord and selectively increased SP IR in the dorsal horn of the lumbar enlargement.In view of these observations it is suggested that chronic imipramine treatment specifically increases SP IR in the 5-HT/SP/TRH costoring nerve terminals of the ventral horn probably related to reduced SP release and reduced 5-HT utilization in these terminals. The results obtained in group B 7 may be explained by a regulation by the³H-imipramine raphe binding sites of fast axonal transport, an influence which may have therapeutic consequences. This mechanism may also be responsible for the increase in 5-HT IR seen upon chronic imipramine treatment in the lateral part of the 5-HT nerve cell body group B 3. Such an effect may lead to a metabolic down-regulation of group B 7, having a possible role for the antidepressant activity of imipramine. The reduction of the mean profile area of 5-HT IR cell bodies of group B 1 seen in the acute treatment can possibly be caused by, noradrenaline (NA) uptake inhibition in inhibitory NA terminals innervating the B 1 group. These results also illustrate the heterogeneities in the responses of the 5-HT nerve cell groups to antidepressant treatment. The ability of chronic imipramine treatment to increase SP IR in the dorsal horn of the lumbar enlargement may reflect the existence of a monoamine-SP interaction in the substantia gelatinosa due to the NA and/or 5-HT uptake blocking activity of imipramine. The existence of such an interaction may help to explain the antinociceptive effect of chronic imipramine treatment.Part of the paper was presented at the 17th International Congress of the International Society of Psychoneuroendocrinology, Bergen, June 29–July 4, 1986.