Biomedical subjects

S Kaiser

Publications and source records attributed to S Kaiser.

At least 37 records · Page 2Linked to original sources

PubMed2000

UB-165: a novel nicotinic agonist with subtype selectivity implicates the alpha4beta2* subtype in the modulation of dopamine release from rat striatal synaptosomes.

Presynaptic nicotinic acetylcholine receptors (nAChRs) on striatal synaptosomes stimulate dopamine release. Partial inhibition by the alpha3beta2-selective alpha-conotoxin-MII indicates heterogeneity of presynaptic nAChRs on dopamine terminals. We have used this alpha-conotoxin and UB-165, a novel hybrid of epibatidine and anatoxin-a, to address the hypothesis that the alpha-conotoxin-MII-insensitive subtype is composed of alpha4 and beta2 subunits. UB-165 shows intermediate potency, compared with the parent molecules, at alpha4beta2* and alpha3-containing binding sites, and resembles epibatidine in its high discrimination of these sites over alpha7-type and muscle binding sites. (+/-)-Epibatidine, (+/-)-anatoxin-a, and (+/-)-UB-165 stimulated [(3)H]-dopamine release from striatal synaptosomes with EC(50) values of 2.4, 134, and 88 nM, and relative efficacies of 1:0.4:0.2, respectively. alpha-Conotoxin-MII inhibited release evoked by these agonists by 48, 56, and 88%, respectively, suggesting that (+/-)-UB-165 is a very poor agonist at the alpha-conotoxin-MII-insensitive nAChR subtype. In assays of (86)Rb(+) efflux from thalamic synaptosomes, a model of an alpha4beta2* nAChR response, (+/-)-UB-165 was a very weak partial agonist; the low efficacy of (+/-)-UB-165 at alpha4beta2 nAChR was confirmed in Xenopus oocytes expressing various combinations of human nAChR subunits. In contrast, (+/-)-UB-165 and (+/-)-anatoxin-a were similarly efficacious and similarly sensitive to alpha-conotoxin-MII in increasing intracellular Ca(2+) in SH-SY5Y cells, a functional assay for native alpha3-containing nAChR. These data support the involvement of alpha4beta2* nAChR in the presynaptic modulation of striatal dopamine release and illustrate the utility of exploiting a novel partial agonist, together with a selective antagonist, to dissect the functional roles of nAChR subtypes in the brain.

Animals↗

PubMed2000

Presynaptic nicotinic receptors modulating dopamine release in the rat striatum.

The modulation of striatal dopamine release by presynaptic nicotinic acetylcholine receptors is well documented for both synaptosomes and slices. Because the latter retain local anatomical integrity, we have compared [3H]dopamine release evoked by the nicotinic receptor agonists (-)-nicotine and (+/-)-anatoxin-a from striatal synaptosome and slice preparations in parallel. At higher agonist concentrations, mecamylamine-sensitive [3H]dopamine release was greater from slices, indicative of an additional component, and this increase was abolished by glutamate receptor antagonists. To begin to examine the localisation of specific nicotinic acetylcholine receptor subtypes in the striatum, immunogold electron microscopy was undertaken with the beta2-specific monoclonal antibody 270. In striatal sections, gold particles were associated with symmetric synapses (dopaminergic) but were absent from asymmetric synapses (glutamatergic). Surface labelling of striatal synaptosomes with gold particles was also demonstrated. Taken together, these results are consistent with dopamine release mediated by beta2-containing nicotinic acetylcholine receptors on dopamine terminals, while non-beta2-containing nicotinic acetylcholine receptors may enhance dopamine release indirectly by releasing glutamate from neighbouring terminals.

Animals↗

PubMed2000

Nicotine attenuates arachidonic acid-induced overexpression of nitric oxide synthase in cultured spinal cord neurons.

Primary spinal cord trauma can initiate a cascade of pathophysiologic events which markedly contribute to the expansion and amplification of the primary insult. The detailed mechanisms of these secondary neurochemical reactions are largely unknown; however, they involve membrane lipid derangements with the release of free fatty acids, in particular, arachidonic acid (AA). AA can induce several injury effects on spinal cord neurons. We hypothesize that upregulation of nitric oxide synthase (NOS) is among the most important mechanisms of arachidonic-acid-induced neuronal dysfunction and that nicotine can attenuate this effect. To study these hypotheses, spinal cord neurons were exposed to AA and/or nicotine, and several markers of neuronal nitric oxide synthase (nNOS) metabolism were measured. In addition, cotreatments with either inhibitors of nicotinic receptors or inhibitors of specific NOS isoforms were employed. Treatment with AA markedly increased activity of nNOS, as well as mRNA and protein levels of this enzyme. Changes in nNOS expression were accompanied by an increase in cellular cGMP and medium nitrite levels. Pretreatment with nicotine decreased AA-induced overexpression of nNOS and elevation of nitrite levels. In addition, it appeared that these nicotine effects could be partially modulated both by the alpha7 nicotinic receptors or by nonreceptor mechanisms. Alternatively, the observed changes could also be mediated by an alternate nicotinic receptor mechanism which is not blocked by alpha-bungarotoxin or mecamylamine. Results of the present study indicate that exposure to AA can lead to induction of nNOS in cultured spinal cord neurons. In addition, nicotine can exert a neuroprotective effect by attenuation of AA-induced upregulation of nNOS metabolism. These data may have therapeutic implications for the treatment of acute spinal cord trauma.

Animals↗

PubMed2000

Does clinical exposure affect medical student examination performance?

BACKGROUND: Traditionally important components of the surgical clerkship curriculum include lectures, small-group sessions, readings, clinical exposure, and testing. Time constraints require compromise among all these elements. At our institution, clinical exposure of medical students varies according to their team assignments. They differ primarily in exposure to such topics as trauma, inflammatory bowel disease (IBD), and vascular surgery. PURPOSE: The goal of this study was to quantify the influence of clinical exposure on medical student education, testing whether it influences examination performance. METHODS: At the beginning of the clerkship, students were given a written multiple-choice examination covering these three topics. They completed two 4-week blocks on surgery services in various settings. At the end of the clerkship, they were reexamined. Differences between pretest and posttest overall mean rank were analyzed using the Wilcoxon signed ranks test. Differences in improvement based on clinical exposure were analyzed using the Mann-Whitney U test. RESULTS: Statistically significant improvement was seen in overall examination performance, as well as in each of the subsections. However, these improvements could not be accounted for by clinical exposure. There was no statistically significant difference in mean rank in improvement based on clinical exposure to vascular, IBD, or trauma. CONCLUSIONS: Student examination scores improved over the course of the clerkship. No improvement could be attributed to greater clinical exposure to a topic.

Curriculum↗

PubMed2000

Molecular cloning of Schistosoma mansoni calcineurin subunits and immunolocalization to the excretory system.

In order to explain the schistosomicidal effect of cyclosporin A, the hypothesis was advanced that the drug, complexed with cyclophilin, inhibits the phosphatase activity of parasite calcineurin (CN), with mechanisms similar to those operating in its immunosuppressive action. As a preparatory step to the testing of this hypothesis, we report the molecular cloning of both CN subunits in Schistosoma mansoni. The catalytic (A) subunit has a predicted sequence of 607 amino acids and shows substantial similarity to other cloned CNs, except for the carboxy-terminal end that is highly divergent. The regulatory (B) subunit consists of 169 amino acids that are 86% identical to those of the human counterpart and, from its anomalous electrophoretic mobility, it appears to be myristoylated. The results of Southern blotting experiments are compatible with the existence of multiple genes for CNA and a single gene for CNB. Western blots showed that both subunits are present at all stages of the parasite life cycle and can be detected both in the soluble and in the membrane fraction. Immunofluorescence confocal microscopy revealed a striking concentration of the anti-CNA reactivity in 6-8 discrete spots in the schistosomula and in distinct spots along the body of the adult parasite, corresponding to the expected localization of flame cells. Both patterns were confirmed by a perfect co-localization of the anti-CNA signal with that of a previously characterized anti-flame cell monoclonal antibody. The preferential confinement of schistosome CN to the protonephridial system suggests that the enzyme in the parasite may fulfil similar functions to those performed in mammalian kidneys.

Amino Acid Sequence↗

PubMed2000

Corrected coronary flow velocity reserve: a new concept for assessing coronary perfusion.

OBJECTIVES: In order to limit the variability of coronary flow velocity reserve (CFVR), we analyzed which factors independently affect CFVR and established a new parameter integrating these factors. BACKGROUND: Coronary flow velocity reserve (CFVR) is a frequently used parameter for evaluating the physiological significance of epicardial stenosis and microvascular function. Since CFVR measurements are done in substantially different hemodynamic and clinical situations, interpretation of CFVR requires correction for major influencing factors. METHODS: In 141 patients with angina-like symptoms and angiographically unobstructed coronary arteries, intracoronary Doppler measurements were performed in at least two coronary vessels. Coronary flow velocity reserve was calculated as the ratio of hyperemic average peak velocity (hAPV), after intracoronary bolus of adenosine, to baseline average peak velocity (bAPV). RESULTS: Analysis of covariance revealed that only bAPV (p < 0.0001) and age (p < 0.0001) were independent factors influencing CFVR. Based on a regression model for estimation of predicted CFVR values, individual CFVR values (CFVRind) obtained at different bAPV and age were transformed in corrected CFVR values (CFVRcorr) by relating them to a mean bAPV of 15 cm/s and a mean age of 55 years. The transformation from CFVRind into CFVRcorr for the left anterior descending artery can be done by using the following equation: CFVRcorr = 2.85*CFVR(ind)*10(0.48*log(bAPV)+(0.0025*age)-1.16). When applying this new parameter to conditions assumed to cause microvascular dysfunction, analysis showed that only patients with diabetes showed a significant decrease of traditional CFVR and CFVRcorr, whereas a history of hypertension and current smoking habit had no influence on CFVRcorr. CONCLUSIONS: The concept of CFVRcorr standardizes CFVR for bAPV and age as the major physiological determinants. Especially in patients with microvascular dysfunction, this approach may help to discriminate between conditions directly affecting vasodilator reserve and conditions primarily affecting bAPV.

Blood Flow Velocity↗

PubMed2000

Studying the dynamics of emotional expression using synthesized facial muscle movements.

Synthetic images of facial expression were used to assess whether judges can correctly recognize emotions exclusively on the basis of configurations of facial muscle movements. A first study showed that static, synthetic images modeled after a series of photographs that are widely used in facial expression research yielded recognition rates and confusion patterns comparable to posed photos. In a second study, animated synthetic images were used to examine whether schematic facial expressions consisting entirely of theoretically postulated facial muscle configurations can be correctly recognized. Recognition rates for the synthetic expressions were far above chance, and the confusion patterns were comparable to those obtained with posed photos. In addition, the effect of static versus dynamic presentation of the expressions was studied. Dynamic presentation increased overall recognition accuracy and reduced confusions between unrelated emotions.

Adult↗

PubMed2000

alpha-bungarotoxin-sensitive nicotinic receptors indirectly modulate [(3)H]dopamine release in rat striatal slices via glutamate release.

Nicotinic agonists elicit the release of dopamine from striatal synaptosomes by acting on presynaptic nicotinic acetylcholine receptors (nAChRs) on dopamine nerve terminals. Both alpha3beta2* and alpha4beta2 nAChR subtypes (but not alpha7* nAChRs) have been implicated. Here, we compared nAChR-evoked [(3)H]dopamine release from rat striatal synaptosome and slice preparations by using the nicotinic agonist anatoxin-a. In the more integral slice preparation, the concentration-response curve for anatoxin-a-evoked [(3)H]dopamine release was best fitted to a two-site model, giving EC(50) values of 241 nM and 5.1 microM, whereas only the higher-affinity component was observed in synaptosome preparations (EC(50) = 134 nM). Responses to a high concentration of anatoxin-a (25 microM) in slices (but not in synaptosomes) were partially blocked by ionotropic glutamate receptor antagonists (kynurenic acid, 6,7-dinitroquinoxaline-2,3-dione) and by alpha7*-selective nAChR antagonists (alpha-bungarotoxin, alpha-conotoxin-ImI, methyllycaconitine) in a nonadditive manner. In contrast, the alpha3beta2-selective nAChR antagonist alpha-conotoxin-MII partially inhibited [(3)H]dopamine release from both slice and synaptosome preparations, stimulated with both low (1 microM) and high (25 microM) concentrations of anatoxin-a. Antagonism by alpha-conotoxin-MII was additive with that of alpha7*-selective antagonists. These data support a model in which alpha7* nAChRs on striatal glutamate terminals elicit glutamate release, which in turn acts at ionotropic glutamate receptors on dopamine terminals to stimulate dopamine release. In addition, non-alpha7* nAChRs on dopamine terminals also stimulate dopamine release. These observations have implications for the complex cholinergic modulation of inputs onto the major efferent neurons of the striatum.

Animals↗

PubMed2000

MR imaging and (1)H spectroscopy of brain metabolites in hepatic encephalopathy: time-course of renormalization after liver transplantation.

PURPOSE: To evaluate changes in hydrogen 1 magnetic resonance (MR) spectroscopic findings in overt or subclinical hepatic encephalopathy (HE) after liver transplantation and to compare these changes with clinical outcomes and basal ganglia high signal intensity (BGH). MATERIALS AND METHODS: Twenty-two patients scheduled for liver transplantation and 17 healthy control subjects were examined with (1)H MR spectroscopy and standard nonenhanced MR imaging. Eight patients underwent complete MR imaging and (1)H spectroscopic examinations before liver transplantation and at 3-4-week, 12-28-week, and 10-12-month follow-up after liver transplantation. RESULTS: Before liver transplantation, typical (1)H spectroscopic changes-decreased myo-inositol (mI)/creatine (Cr) and choline (Cho)/Cr ratios and an elevated glutamine and glutamate (Glx)/Cr ratio-were found in 21 patients. Eighteen patients had BGH at T1-weighted imaging. Three to 7 months after liver transplantation, the mI/Cr and Glx/Cr ratios were within the normal range in five of eight and eight of eight patients, respectively, without any residual signs of subclinical or overt HE; however, at MR imaging, seven patients still had BGH. CONCLUSION: After successful liver transplantation, renormalization of HE-specific brain metabolite changes is detected at (1)H spectroscopy and precedes the disappearance of BGH. The neuropsychologic signs of subclinical or overt HE follow the changes seen at (1)H spectroscopy rather than those seen at MR imaging.

Adult↗

PubMed2000

An integrated program for evidence-based medicine in medical school.

To provide optimal care for their patients, clinicians must be able to locate and interpret the most current literature. Teaching the necessary skills to medical students is essential, if we wish to train clinicians to be able to keep up with the expansion of biomedical knowledge for their entire working lives. In this paper, we describe our school's four-year curriculum in evidence-based medicine and the performance of three senior classes on the summative evaluation exercise devised to measure the program's success.

Curriculum↗

PubMed1999

Modeling extended sources of event-related potentials using anatomical and physiological constraints.

For the study of functional organization and reorganization of the human cortex by means of electromagnetic source imaging, a measure of the location and spatial extent of neural sources is of interest. This study evaluates the cortical patch method (CPM), an iterative procedure introduced by Lütkenhöner et al. [1995] that models EEG/MEG activity by means of extended cortical patches. Anatomical information is used to constrain estimates of location and extent of neural sources that generate the measured evoked potential. Whereas minimum norm approaches use mathematical constraints to solve the ambiguity of the inverse problem, the CPM introduces constraints based on anatomical and physiological knowledge about neural mass activity. In order to test the proposed method, the simulated activity in an artificial sulcus was subjected to the CPM. The results show that even activity on opposing walls of a sulcus can be well reconstructed. The simulations demonstrate the usefulness and limits of the CPM in estimating the spatial extent of neural sources in the cerebral cortex. As an example, an application of the method on experimental somatosensory evoked potentials is presented in the Appendix.

Brain↗

PubMed1999

4-Hydroxynonenal induces dysfunction and apoptosis of cultured endothelial cells.

Lipolytic products of triglyceride-rich lipoproteins, i.e., free fatty acids, may cause activation and dysfunction of the vascular endothelium. Mechanisms of these effects may include lipid peroxidation. One of the major and biologically active products of peroxidation of n-6 fatty acids, such as linoleic acid or arachidonic acid, is the aldehyde 4-hydroxynonenal (HNE). To study the hypothesis that HNE may be a critical factor in endothelial cell dysfunction caused by free fatty acids, human umbilical endothelial cells (HUVEC) were treated with up to160 microM of linoleic or arachidonic acid. HNE formation was detected by immunocytochemistry in cells treated for 24 h with either fatty acid, but more markedly with arachidonic acid. To study the cellulareffects of HNE, HUVEC were treated with different concentrations of this aldehyde, and several markers of endothelial cell dysfunction were determined. Exposure to HNE for 6 and 9 h resulted in increased cellular oxidative stress. However, short time treatment with HNE did not cause activation of nuclear factor-kappaB (NF-kappaB). In addition, HUVEC exposure to HNE caused a dose-dependent decrease in production of both interleukin-8 (IL-8) and intercellular adhesion molecule-1 (ICAM-1). On the other hand, HNE exerted prominent cytotoxic effects in cultured HUVEC, manifested by morphological changes, diminished cellular viability, and impaired endothelial barrier function. Furthermore, HNE treatment induced apoptosis of HUVEC. These data provide evidence that HNE does not contribute to NF-kappaB-related mechanisms of the inflammatory response in HUVEC, but rather to endothelial dysfunction, cytotoxicity, and apoptotic cell death.

Aldehydes↗

PubMed1999

Endothelial cell functions. Relationship to atherogenesis.

The vascular endothelium plays a critical role in the preservation of normal vessel wall structure and function. In particular, endothelial cells control vascular permeability, vessel tone, coagulation, fibrinolysis, and inflammatory responses. These functions are accomplished by production of a variety of biologically active substances. However, endothelial cell-mediated reactions may also lead to the development of pathological stages within the vessel wall. The current review is focused on endothelial cell metabolism in relationship to the development of atherosclerosis.

Animals↗

PubMed1999

External beam radiation after stent implantation increases neointimal hyperplasia by augmenting smooth muscle cell proliferation and extracellular matrix accumulation.

OBJECTIVES: We sought to examine the effects of high volume external beam radiation (EBR) after stent implantation on neointimal hyperplasia, smooth muscle cell (SMC) proliferation, presence of inflammatory cells and expression of extracellular matrix (ECM). BACKGROUND: Endovascular irradiation has been shown to reduce restenosis rates after angioplasty in preliminary trials, but conflicting results have been reported for the effects of external beam irradiation. METHODS: Forty-three Palmaz-Schatz stents were implanted into iliac arteries of New Zealand White rabbits. The arteries were externally irradiated after stent implantation with a single dose of 8 Gy (at day 3) or 16 Gy in two fractions (8 Gy at days 3 and 4) by means of a linear accelerator. In the control rabbits, no radiation was applied after stent implantation. Smooth muscle cells, macrophages and ECM were studied by immunohistochemistry at one and 12 weeks after stent implantation. Collagen type I and biglycan messenger ribonucleic acid (mRNA) levels were assessed by Northern blot analysis at one week. Neointimal cell densities and arterial lumen stenosis were measured by histomorphometry at 12 weeks. RESULTS: At 1 week, SMC proliferation at the site of stent implantation was increased after EBR with 8 and 16 Gy (26 +/- 5%, 32 +/- 3% vs. 17 +/- 8%; p < 0.01, 16 Gy vs. control). External beam radiation with 8 and 16 Gy augmented SMC proliferation proximal and distal to the angioplasty site (11 +/- 3%, 14 +/- 3 vs. 6 +/- 1%; p < 0.01, 16 Gy vs. control). Collagen type I and biglycan mRNA levels were elevated in stented arteries after EBR with 16 Gy. At 12 weeks, a marked decrease in neointimal cell density (248 +/- 97 vs. 498 +/- 117 SMCs/0.1 mm2 neointima; p < 0.005 vs. control) was noted after EBR with 16 Gy. Irradiation with 8 and 16 Gy increased arterial lumen stenosis compared with nonirradiated control rabbits (45 +/- 7%, 55 +/- 9% vs. 33 +/- 7%; p < 0.05, 8 Gy and p < 0.001, 16 Gy vs. control). CONCLUSIONS: High volume external beam radiation at doses of 8 or 16 Gy causes restenosis by augmenting proliferative activity at and adjacent to the site of stent implantation, and by dose-dependent up-regulation of extracellular matrix expression. The study suggests that excessive matrix accumulation is an important determinant of failure of radiation therapy to prevent restenosis.

Animals↗

PubMed1999

[MR proton spectroscopy to monitor the concentration changes in cerebral metabolites following a TIPS placement].

BACKGROUND AND AIMS: In chronic liver dysfunction with portal hypertension the risk of variceal bleeding can be lowered by intrahepatic portosystemic shunting (TIPS). Although less pronounced than in surgical shunting, hepatic encephalopathy (HE) is a well-known undesired side effect. In cerebral proton MR spectroscopy (MRS), HE can be detected by a specific pattern of brain metabolite changes (increase of glutamine/glutamate (Glx) and decrease of myo-inositol (ml) and choline (Cho)). The aim of this study was to examine whether, after TIPS implantation, there is a correlation of the reduction of the portosystemic pressure gradient (PSPG) and the cerebral metabolite changes and their correspondence to the clinical status. METHODS: We examined 10 cirrhotic patients (Child B, C) before and 3-20 days after TIPS implantation. Clinical examination was performed by a senior hepatologist. Localized MR spectra were acquired in parieto-occipital gray/white matter using a short echo time (TE = 5 ms) STEAM sequence. RESULTS: After TIPS we found an increase of Glx/(Cr + PCr) of 13%-40% and a decrease of ml(Cr + PCr) of 6%-46% with a positive (Glx: r = 0.71) respectively negative (ml: r = -0.59) correlation to the reduction of the PSPG. 7/10 patients with a reduction of the PSPG of more than 9 mmHg (9-17 mmHg) showed a clinical impairment of their HE. CONCLUSIONS: Short echo time cerebral MRS allows detection of finest HE specific metabolite changes and can therefore contribute positively to an individually optimized reduction of the PSPG during TIPS implantation.

Adult↗

PubMed1999

Hypoxia-activated apoptosis of cardiac myocytes requires reoxygenation or a pH shift and is independent of p53.

Ischemia and reperfusion activate cardiac myocyte apoptosis, which may be an important feature in the progression of ischemic heart disease. The relative contributions of ischemia and reperfusion to apoptotic signal transduction have not been established. We report here that severe chronic hypoxia alone does not cause apoptosis of cardiac myocytes in culture. When rapidly contracting cardiac myocytes were exposed to chronic hypoxia, apoptosis occurred only when there was a decrease in extracellular pH ([pH](o)). Apoptosis did not occur when [pH](o) was neutralized. Addition of acidic medium from hypoxic cultures or exogenous lactic acid stimulated apoptosis in aerobic myocytes. Hypoxia-acidosis-mediated cell death was independent of p53: equivalent apoptosis occurred in cardiac myocytes isolated from wild-type and p53 knockout mice, and hypoxia caused no detectable change in p53 abundance or p53-dependent transcription. Reoxygenation of hypoxic cardiac myocytes induced apoptosis in 25-30% of the cells and was also independent of p53 by the same criteria. Finally, equivalent levels of apoptosis, as demonstrated by DNA fragmentation, were induced by ischemia-reperfusion, but not by ischemia alone, of Langendorff-perfused hearts from wild-type and p53 knockout mice. We conclude that acidosis, reoxygenation, and reperfusion, but not hypoxia (or ischemia) alone, are strong stimuli for programmed cell death that is substantially independent of p53.

Acidosis, Lactic↗

PubMed1998

The social environment during pregnancy and lactation affects the female offsprings' endocrine status and behaviour in guinea pigs.

This study investigated the influence of the social environment during pregnancy and lactation on the female offsprings' endocrine parameters and behaviour. The subjects studied were daughters whose mothers had either lived in a stable social environment (SSE) during pregnancy and lactation (SE-mothers) or in an unstable social environment (USE) during this period of life (UE-mothers). The SSE was made by keeping the group composition (one male, five females) constant; in the USE situation every third day two females from different groups were exchanged. After weaning, 3 groups of daughters from UE-mothers (UE-daughters) and 3 groups of daughters from SE-mothers (SE-daughters), consisting of four females each, were established. From their 60th through their 80th day of age the spontaneous behaviour of the daughters was recorded in their home cages. On the endocrine level, cortisol and testosterone (T) concentration in serum as well as adrenal tyrosinehydroxylase activities in both adrenals and their weight were determined. UE-daughters displayed significantly higher amounts of male-typical courtship and play behaviour than SE-daughters. This behavioural masculinization corresponded with significantly higher T in UE- than SE-daughters. Cortisol levels did not differ between both categories of females. Significantly higher tyrosinehydroxylase activities and adrenal weight in UE- than SE-daughters pointed, however, to higher degrees of stress response in UE-daughters. Thus, the instability of the social environment during pregnancy and lactation has distinct effects on the behaviour and endocrine system of the female offspring.

Adrenal Glands↗

PubMed1998

[Results of cement-free implanted, Robert Mathys isoelastic acetabular cup].

In 163 patients--125 (76.7%) female, 38 (23.3%) male--172 cementfree isoelastic acetabular cups were implanted. The average patient age was 72.6 years (range: 16 to 96 years). Sixty-seven (41.1%) patients with 72 (41.9%) cups could be followed-up for an average of 6.0 years (range: 2.0 to 12.2 years) after the procedure. Using the Harris-hip-score we found 49 (68.1%) "very good" to "fair" results. In 23 (31.9%) hips scoring had to be classified as "bad". The rate of cup-loosenings in the collective was low at 3.5% (6/172), probably due to the reduced physical activity of our comparatively older patients. Because after the 8th year symptomatic loosening must be routinely expected, the procedure is not indicated for younger patients. In older patients with femoral neck fractures the cementfree isoelastic acetabular cup has proven itself effective in our experience.

Acetabulum↗