Estrogenic regulation of heat shock protein 90 kDa in the rat ventromedial hypothalamus and uterus.

The regulation of heat shock protein 90 kDa (hsp90) by estradiol was analyzed in the rat ventromedial hypothalamus (VMH) and uterus by one-dimensional gel electrophoresis/Western blots. Protein from VMH and uterus (35 micrograms/sample) was resolved on 8% acrylamide gels, transferred to polyvinyldifluoride filters, and processed for immunoblotting using an anti-hsp90 antibody. Hsp90-specific bands were visualized on film using enhanced chemiluminescence and quantitated using a laser scanning densitometer. Hsp90 protein levels were significantly elevated in VMH at 12 h (p less than 0.01), and in uterus at 18 h (p less than 0.05) following estradiol injection (10 micrograms, s.c.). Immunocytochemical analysis for hsp90 localization by cell types showed that, in brain, hsp90 immunoreactivity was primarily neuronal. In the uterus, hsp90 immunoreactivity was most evident following treatment with estradiol, and was found primarily in the glandular epithelia; staining was less prominent in myometrium, stroma, and in the luminal epithelium. Thus, increased hsp90 levels may mediate some cellular responses to estrogen in specific cell types in both uterus and brain.     

Axial muscle EMG responses evoked by cutaneous flank nerves in the female rat: effects of spinal transection, steroid hormones, and anesthesia.

In the lateral longissimus muscle (LL) of ovariectomized, female rats anesthetized with low surgical doses of urethane (1.0 g/kg), cutaneous reflexes with similar EMG and response patterns could be elicited from CNS-intact rats and from rats 24 h after complete thoracic spinal cord transection. The probability of eliciting a response to contralateral cutaneous nerve stimulation alone is much lower in rats with complete spinal transections compared to CNS-intact rats. For both CNS-intact and spinal-transected rats, responses to ipsilateral cutaneous nerve stimulation had a shorter latency and required significantly less current on average than responses to contralateral stimulation. The respective currents for eliciting threshold responses to ipsi- and contralateral stimulation are less for CNS-intact than spinal-transected rats. For both CNS-intact and spinal-transected rats, responses to bilateral cutaneous nerve stimulation were inconsistent in the same animal from run to run. With the variability of response at this anesthetic level, no consistent effects of progesterone (acute, i.v.) or estrogen (acute, i.v. and pretreatment, s.c.) were observed in spinal-transected rats. Intravenous progesterone reduced early, unilateral responses in CNS-intact rats anesthetized with 1.0 g of urethane/kg. For both CNS-intact and spinal-transected rats, additional anesthesia during EMG recording produced a gradual decline in response magnitude which could be recovered with a modest increase in stimulus intensity. However, spinal-transected rats appear to require less anesthesia to reduce comparable responses. The results suggest that supraspinal input is especially effective for facilitating contralateral cutaneous reflexes in back muscles, whereas it contributes more equally with afferent input and segmental circuitry to the efficacy of ipsilateral cutaneous reflexes.     

Immunocytochemical demonstration of neural cell adhesion molecule (NCAM) along the migration route of luteinizing hormone-releasing hormone (LHRH) neurons in mice.

Contact between the developing forebrain and the ingrowing central processes of the olfactory, vomeronasal and terminal nerves is preceded by a migration of neural cell adhesion molecule (NCAM)-immunoreactive cells from the epithelium of the olfactory pit and the formation of an NCAM-immunoreactive cellular aggregate in the mesenchyme between the olfactory pit and the forebrain. The axons of the olfactory, vomeronasal, and terminal nerves, also NCAM-immunoreactive, grow into the cellular aggregate, which as development proceeds, becomes continuous with the rostral tip of the forebrain. The lateral and more rostral part of the cellular aggregate receives the ingrowing axons of the olfactory nerves and becomes the olfactory nerve layer of the olfactory bulb. The medial, more caudal part receives the central processes of the vomeronasal and terminal nerves. The vomeronasal nerve ends in the accessory olfactory bulb. The central processes of the terminal nerve end in the medial forebrain. Luteinizing hormone-releasing hormone (LHRH)-immunoreactive neurons, like the vomeronasal and terminal nerves, originate from the medial part of the olfactory pit. These LHRH cells migrate into the brain along and within a scaffolding formed by the NCAM-immunoreactive axons of the vomeronasal and terminal nerves, and they are never seen independent of this NCAM scaffold as they cross the nasal lamina propria. The results suggest that: (1) NCAM is likely to be necessary for scaffold formation, and (2) the scaffold may be essential for the subsequent migration of LHRH neurons into the brain. Because they aggregate, migrating LHRH-immunoreactive neurons, on which we did not detect NCAM immunoreactivity, may interact via other cell adhesion molecules (CAM). Inasmuch as the interaction between the LHRH-immunoreactive neurons and the NCAM-immunoreactive scaffold is heterotypic, the possibility of a heterophilic (NCAM to other CAM) interaction is not ruled out. These findings focus our attention on the functional role of NCAM in this migratory system.     

Blood glucose-lowering acylaminoalkylbenzenesulfonamide derivatives with heterocyclic acyl residues

The paper reports on acylaminoalkylbenzenesulfonamide derivatives with special heterocyclic acyl substituents. The compounds are characterized by an oxygen atom in ortho position to the carboxamide group of the heterocyclic acyl moiety. Several compounds show blood glucose lowering activities in animals similarly to glibenclamide.     

Laboratory findings for the preoperative evaluation of patients with otherwise no organic disorders

The efficiency of preoperative laboratory screening of normal, healthy patients was investigated. Preoperative test results of 1311 consecutive patients were collected. Data on haemoglobin, serum potassium, serum creatinine and serum ALAT were routinely obtained. 736 patients were classified by history and physical examination as normal healthy persons not having any systemic disorder. In this group of patients no clinically relevant abnormal laboratory results were found under the age of 60 years. In the group of 60 years and older a significant number had elevated serum creatinine values.     

Recruiting and retaining GPs and patients in intervention studies: the DEPS-GP project as a case study

Background  

Recruiting and retaining GPs for research can prove difficult, and may result in sub-optimal patient participation where GPs are required to recruit patients. Low participation rates may affect the validity of research.     

Longer term progesterone treatment induces changes of GABAA receptor levels in forebrain sites in the female hamster: quantitative autoradiography study

Summary Quantitative receptor autoradiography was applied to evaluate the effects of one and three injections of 1 mg progesterone (P) on ³H muscimol binding levels in the different forebrain areas of the female hamster. The overall effect of P resulted in substantial increases in ³H muscimol binding in brain areas containing gonadal steroid receptors: medial preoptic area and ventromedial hypothalamic nucleus as well as in bed nucleus stria terminalis and subiculum. Similarly, the caudate putamen, a region where gonadal steroid receptors are not abundant, also showed substantial increases of ³H muscimol binding receptor levels. Moreover, female hamsters treated with P for 3 days presented altered ³H muscimol binding levels in the amygdala and thalamic nucleus that were, in some cases, not produced by one dose of P. P treatment also decreased GABA_A binding in two areas of the thalamus. These results are consistent with the proposal that P may alter GABAergic inhibitory activity via changes in the levels of GABA_A receptors in certain forebrain areas in the female hamster, changes which may be linked to the mediation of anxiolytic effects and to the inhibition of aggressive behavior. These data also suggest that P treatment increases the binding of high affinity GABA receptors in some forebrain sites and may be responsible for maintenance of the anxiolytic effects.