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The article presents two cases of vitamin A deficiency presenting with microbial keratitis in Great Britain. The first one is that of a 10-year-old Afro-Caribbean boy suffering from an irritating left eye with epiphora. The disease didn't respond to chloramphenicol drops given by the doctor. The second case was that of a 46-year-old lady suffering from a red and itchy left eye. She was said to have a left bacterial keratitis and a large right sterile corneal epithelial defect.

Background: Numerous studies have shown that baseline drug resistance patterns may influence the outcome of antiretroviral therapy. Therefore, guidelines recommend drug resistance testing to guide the choice of initial regimen. In addition to optimizing individual patient management, these baseline resistance data enable transmitted drug resistance (TDR) to be surveyed for public health purposes. The SPREAD program systematically collects data to gain insight into TDR occurring in Europe since 2001., Methods: Demographic, clinical, and virological data from 4140 antiretroviral-naive human immunodeficiency virus (HIV)-infected individuals from 26 countries who were newly diagnosed between 2008 and 2010 were analyzed. Evidence of TDR was defined using the WHO list for surveillance of drug resistance mutations. Prevalence of TDR was assessed over time by comparing the results to SPREAD data from 2002 to 2007. Baseline susceptibility to antiretroviral drugs was predicted using the Stanford HIVdb program version 7.0., Results: The overall prevalence of TDR did not change significantly over time and was 8.3% (95% confidence interval, 7.2%-9.5%) in 2008-2010. The most frequent indicators of TDR were nucleoside reverse transcriptase inhibitor (NRTI) mutations (4.5%), followed by nonnucleoside reverse transcriptase inhibitor (NNRTI) mutations (2.9%) and protease inhibitor mutations (2.0%). Baseline mutations were most predictive of reduced susceptibility to initial NNRTI-based regimens: 4.5% and 6.5% of patient isolates were predicted to have resistance to regimens containing efavirenz or rilpivirine, respectively, independent of current NRTI backbones., Conclusions: Although TDR was highest for NRTIs, the impact of baseline drug resistance patterns on susceptibility was largest for NNRTIs. The prevalence of TDR assessed by epidemiological surveys does not clearly indicate to what degree susceptibility to different drug classes is affected., (© The Author 2015. Published by Oxford University Press for the Infectious Diseases Society of America.)

Available data on the use of maraviroc (MVC) in clinical settings are limited. In this cohort study, the clinical outcomes of HIV-1-infected patients treated with MVC were analysed and the predictive values of different tropism assays were compared. Baseline viral tropism was assessed and compared by phenotypic (Trofile and MT-2) and genotypic assays. Virological and immunological responses were evaluated. In total, 62 predominantly extensively pre-treated patients started MVC [median GSS 2.0 (IQR 2.0-2.5)]. Tropism assays were performed on baseline samples of 58 patients (93.5%). Thirty-two samples (80.0%) were classified as R5 by Trofile, 41 (80.4%) by genotypic tropism test (GTT) and 17 (81.0%) by MT-2. At least two types of tropism assay were performed on samples from 39 patients, whereas in 15 patients all three assays were performed (concordance 84.8-94.1%). Plasma HIV-RNA was <50 copies/mL in 82.1%, 85.0% and 68.8% of patients after 12, 24 and 36 months, respectively; median CD4 cell increase was 199 (IQR 108-283), 291 (IQR 187-413) and 234 (IQR 106-444)cells/μL. The predictive values of different tropism assays were comparably high: at Month 24, 92.9% (Trofile and GTT) and 100.0% (MT-2) of patients had plasma HIV-RNA <50 copies/mL. Three patients stopped MVC treatment because of suspected side effects. Five patients died during follow-up. In this heavily pre-treated cohort, treatment with MVC was well tolerated and resulted in good immunological and virological responses. Results generated by the different tropism assays correlated well with each other and had a high predictive value., (Copyright © 2015 Elsevier B.V. and the International Society of Chemotherapy. All rights reserved.)

Resveratrol pretreatment has been shown to provide neuroprotection in models of cerebral ischemia. This phenomenon, commonly termed preconditioning, promotes ischemic tolerance and may involve mild activation of endoplasmic reticulum stress pathways in the affected tissue. Systemic injection of resveratrol (2 x 10(-3), 2 x 10(-4), 1 x 10(-4) mg/kg) 30 min prior to a 4 h period of right middle cerebral artery occlusion significantly reduced infarct area in the insular region of rat prefrontal cortex. This affect was blocked when resveratrol treatment was combined with a non-selective estrogen receptor antagonist, or preceded by intracortical injection of an NMDA receptor antagonist. The neuroprotective effect of resveratrol was associated with reduced renal sympathetic nerve activity as well as induction of resident endoplasmic reticulum chaperone proteins, glucose-regulated proteins 78 and 94. The calcium-sensitive chaperone heat shock protein 70 and the cysteine protease m calpain did not respond to resveratrol pretreatment. However, a significant induction of heat shock protein 70 was observed in the contralateral cortex of resveratrol pretreated rats following 4 h of right middle cerebral artery occlusion. These data suggest that resveratrol preconditioning promotes ischemic tolerance in the short term, in part via effects mediated through activation of estrogen and NMDA receptors, as well as through mild activation of cellular stress proteins., (Copyright (c) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.)

Estrogen has received considerable attention as a potential therapeutic agent against various forms of neurodegenerative diseases including stroke. Experimental data in animal models of stroke have provided exhaustive evidence of the neuroprotective properties of this steroid hormone. Our laboratory in particular has demonstrated that acute estrogen treatment in male rats significantly reduced (approximately 50%) ischemic cell death within 4 h following permanent occlusion of the middle cerebral artery occlusion (MCAO). However, the cellular and molecular mechanisms implicated in the protective actions of estrogen in this experimental model have yet to be elucidated. Accumulating evidence suggests that in various in vivo and in vitro models, estrogen can be pro-apoptotic and that this effect may be mediated by an estrogen-induced up-regulation of the Fas/FasL system and the subsequent activation of caspase-12. We therefore hypothesized that under ischemic conditions following MCAO, estrogen would up-regulate protective endoplasmic reticulum (ER) stress pathways leading to caspase-12 activation, thus limiting infarct volume. Our results showed that estrogen significantly increased activated caspase-12 at 2, 3 and 4 h post-MCAO. Immunostaining of brain sections showed a significantly higher number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling positive cells in estrogen-treated animals at 4 h, but not at 2 h, post-MCAO. These findings correlate with previous observations that differences in infarct volume between saline and estrogen-treated animals are not seen until 3 and 4 h post-MCAO. A decrease in m-calpain expression was observed in the infarct region only at 4 h post-MCAO following estrogen pre-treatment, suggesting m-calpain may not be involved in regulating estrogen-induced caspase-12 activation. Based on these cellular changes correlated to estrogen pretreatment, we conclude that estrogen may up-regulate ER-specific apoptotic pathways, thus limiting the extent of necrotic cell death which is responsible for the spreading depression and growth of the infarct volume following MCAO.

Several studies have suggested that a potential mechanism for estrogen-mediated neuroprotection following experimental stroke is a result of modulating glutamate-mediated excitotoxicity. Our laboratory has shown that in male rats, estrogen injection (systemic or direct intracortical injection) resulted in an immediate depolarization of cortical neurons. Therefore, the present study was designed to investigate whether the estrogen-induced depolarization of cortical neurons was required in mediating the early events associated with this neuroprotection. We tested this hypothesis by co-injecting selective antagonists of the NMDA (MK-801) or AMPA (DNQX) glutamatergic receptors with estrogen. Systemic injection of estrogen significantly attenuated the MK-801-induced decrease in infarct volume following middle cerebral artery occlusion (MCAO). Similarly, when estrogen and MK-801 were co-injected directly into the cortex, no neuroprotection was observed. However, when estrogen or MK-801 was injected centrally 10 min prior to the injection of the other drug, significant neuroprotection was observed. This led us to hypothesize that estrogen-mediated neuroprotection required an initial activation of NMDA receptors. Furthermore, our results suggest that this estrogen-mediated neuroprotection was also associated with a significant increase in m-calpain and activation of an endoplasmic reticulum (ER) specific caspase-12. Finally, the results of current clamp experiments showed that estrogen significantly depolarized cortical neurons as well as enhanced NMDA-induced depolarization. Taken together, these results suggest that estrogen pretreatment may activate NMDA receptors resulting in modification of ER-associated molecular mechanisms involved in neuroprotection following MCAO.

Stroke-induced lesions of the insular cortex in the brain have been linked to autonomic dysfunction (sympathoexcitation) leading to arrhythmogenesis and sudden cardiac death. In experimental models, systemic estrogen administration in male rats has been shown to reduce stroke-induced cell death in the insular cortex as well as prevent sympathoexcitation. The central nucleus of the amygdala has been postulated to mediate sympathoexcitatory output from the insular cortex. We therefore set out to determine if endogenous estrogen levels within the central nucleus of the amygdala are altered following stroke and if microinjection of estrogen into the central nucleus of the amygdala modulates autonomic tone. Plasma estrogen concentrations were not altered by middle cerebral artery occlusion (22.86+/-0.14 pg/ml vs. 21.24+/-0.33 pg/ml; P>0.05). In contrast, estrogen concentrations in the central nucleus of the amygdala increased significantly following middle cerebral artery occlusion (from 20.83+/-0.54 pg/ml to 76.67+/-1.59 pg/ml; P<0.05). Local infusion of an aromatase inhibitor, letrozole, into the central nucleus of the amygdala at the time of middle cerebral artery occlusion prevented the increase in estrogen concentration suggesting that this increase was dependent on aromatization from testosterone. Furthermore, bilateral microinjection of estrogen (0.5 microM in 200 nl) directly into the central nucleus of the amygdala significantly decreased arterial pressure and sympathetic tone and increased baroreflex sensitivity, and these effects were enhanced following co-injection with either an N-methyl-D-aspartate or non-N-methyl-D-aspartate receptor antagonist. Taken together, the results suggest that middle cerebral artery occlusion resulted in synthesis of estrogen within the central nucleus of the amygdala and that this enhanced estrogen level may act to attenuate overstimulation of central nucleus of the amygdala neurons to prevent middle cerebral artery occlusion-induced autonomic dysfunction.

Systemic estrogen administration in male rats has been shown to normalize the autonomic dysfunction and reduce the infarct size after permanent middle cerebral artery occlusion (MCAO). Therefore, the present investigation determined if local microinjection of estrogen at the site of the infarct also promoted recovery of autonomic function and reduction of the infarct size. Experiments were done in anesthetized (thiobutabarbitol sodium; 100 mg/kg) male Sprague-Dawley rats instrumented to record baseline and reflex changes in cardiovascular and autonomic parameters. The right middle cerebral artery was permanently occluded using bipolar coagulation. Local microinjection of estrogen into the insular cortex before MCAO significantly reduced the infarct size but did not attenuate the MCAO-induced autonomic dysfunction. Injection of ICI-182,780 alone significantly increased infarct area; however, the greater infarct area was not associated with enhanced autonomic dysfunction. These results suggest that within the insula, endogenous estrogen activity can affect the extent of MCAO-induced cell death, but extracortical central nervous system sites may be responsible for mediating the beneficial effects of estrogen on the autonomic disturbances.

Several studies have provided evidence to suggest that estrogen results in a significant reduction (approximately 50%) in the size of the ischemic zone in the middle cerebral artery occlusion (MCAO) model of stroke in a rat. The current study was done to demonstrate whether this estrogen-induced reduction in infarct size is associated with normalization of the autonomic dysfunction observed in an acute model of stroke in male rats. Experiments were done in anesthetized (thiobutabarbitol sodium; 100 mg/kg) male Sprague-Dawley rats instrumented to record baseline and reflex changes in cardiovascular and autonomic parameters. Estrogen was intravenously administered 30 min before, immediately before, or 30 min after MCAO. Estrogen administration resulted in a recovery of autonomic function and prevented the detrimental changes in autonomic tone observed following a stroke. In addition, infarct size was significantly increased in the presence of the estrogen antagonist ICI-182,780. These results suggest that both pre- or poststroke estrogen administration prevents or reverses acute stroke-induced autonomic dysfunction and that endogenous estrogen levels in males can contribute to this neuroprotection.

The magnification and excellent lighting provided by the colposcope make it an excellent diagnostic tool when enhanced direct observation is required. What can be accomplished with this tool in a pediatric or adolescent patient depends upon the examiner understanding how to best perform the examination related to these age groups and knowing what they see. This article describes common techniques used in the examination of the young gynecologic patient and common normal and abnormal findings. This knowledge should be especially helpful to the practitioner who is called upon to perform a sexual abuse examination in this population.

Polychlorinated biphenyls (PCBs) are persistent environmental contaminants that bioaccumulate in the food chain and thus pose a health risk to both humans and other animals. PCB 28 was administered via the diets to male and female Sprague-Dawley rats for 13 weeks in concentrations of 0.05, 0.5, 5 and 50 ppm. The chemical was mixed in corn oil and animals that served as controls received only corn oil in their diets. Use of transmission electron microscopy and stereology revealed significant (P < 0.05) elevations in the mean volume fraction (VF) of liver smooth reticulum (SER) profiles (5 and 50 ppm groups) in the females. Also, the hepatocytes of the male rats contained a significantly greater baseline VF of SER compared to those of the females. Statistically significant alterations were not detected in VP of mitochondria, rough endoplasmic reticulum, peroxisomes or lipid droplets. We estimated in Sprague-Dawley rats a no observable adverse effect level (NOAEL) of 0.5 ppm for congener 28.

The following experiments examine the role of estrogen as a central modulator of autonomic tone and baroreflex sensitivity in the female rat. Female Sprague-Dawley rats were ovariectomized and then supplemented daily for 7 days with a fixed dose of estrogen (5 microg/kg; sc) to produce a stable level of estrogen similar to that present at proestrous (17 pg/ml). The rats were then anaesthetized with sodium thiobutabarbital (100 mg/kg) and instrumented to record blood pressure, heart rate and both vagal and renal efferent nerve activities. The sensitivity of the cardiac baroreflex was tested using intravenous injection of multiple doses of either phenylephrine hydrochloride or sodium nitroprusside. Estrogen-supplemented female rats exhibited a significantly enhanced BRS as compared to male rats from a previous study (0.78 vs. 0.5). Furthermore, bolus injection of estrogen (1x10(-2) mg/kg; iv) in estrogen-supplemented female rats produced a significant increase in vagal nerve activity and a significant decrease in renal nerve activity which together resulted in a further enhancement of the BRS (0.78 vs. 2.4). Injection of the selective estrogen receptor antagonist, ICI 182,780, into nucleus ambiguus and the intrathecal space of the spinal cord blocked the respective changes in parasympathetic and sympathetic nerve activities indicating that intravenously administered estrogen modulates baseline autonomic tone via the activation of central estrogen receptors.

PCB 128 (2,2',3,3',4,4'-hexachlorobiphenyl) prepared in 4% corn oil and mixed in diets was given to weanling Sprague-Dawley rats. The animals were placed in eight groups, each comprising 10 males or 10 females; each group received a diet that contained 0.05, 0.5 or 5 ppm PCB. Ten animals of each gender that served as the controls were given diets mixed with only corn oil. Thirteen weeks after the commencement of dosing, animals were euthanized and liver specimens were harvested and prepared for transmission electron microscopy. The architecture of the liver parenchymal cell was indistinguishable in the animals of the lowest concentration group from those in the controls. However, smooth endoplasmic reticulum profiles increased, and abnormal mitochondria were noted in the liver of rats, regardless of gender, from 0.5 and 5 ppm groups. Based on our previous work, PCB 128 is estimated to be equally toxic as PCB 153, another di-ortho substituted PCB congener.

Hepatocyte cytoplasmic alterations were morphometrically determined in male and female Sprague-Dawley rats fed PCB congener 126 (3,3',4,4',5-pentachlorobiphenyl) in concentrations of 0.1, 1.0, 10, 100 ppb or corn oil in diets for 13 weeks. A dose-dependent increase (P < 0.05) in the volume fraction of smooth endoplasmic reticulum (SER) and mitochondria was measured in the hepatocytes of the females. However, these cells of the male rats contained a significantly greater baseline volume fraction of SER compared to that in the females. Statistical differences were not detected in the volume fractions of rough endoplasmic reticulum, peroxisomes or lipid droplets of the hepatocytes in either the males or females. We conclude the increase in mitochondrial volume was a necessary cellular adaptation to meet the heightened energy demands by the SER to produce the necessary enzymes to detoxify the PCB. Morphometric analysis rather than a descriptive methodology allowed for a more accurate determination of the liver pathology induced by PCB 126.

The following experiments were done to determine whether changes in baroreflex sensitivity evoked by cervical vagus nerve stimulation are due to sympathoexcitation mediated by the parabrachial nucleus. The relative contribution of cardiopulmonary and general gastric afferents within the cervical vagus nerve to the depression in baroreflex sensitivity are also investigated. Male Sprague-Dawley rats anesthetized with thiobutabarbital sodium (50 mg/kg) were instrumented to measure blood pressure and heart rate or for the continuous monitoring of renal sympathetic nerve activity. Baroreflex sensitivity was measured using bolus injections of phenylephrine. Electrical stimulation of the cervical vagus (with or without the aortic depressor nerve) or the abdominal vagus nerve produced a significant increase in renal nerve activity and a decrease in baroreflex sensitivity. Both of these effects were blocked after the microinjection of lidocaine into the parabrachial nucleus before nerve stimulation. Therefore, we conclude that an increase in the activity of cardiac, pulmonary, or general gastric afferents mediated the increased sympathetic output and decreased baroreflex sensitivity via a pathway involving the parabrachial nucleus.

The following experiments were conducted to determine if peripherally administered estrogen has an effect on central autonomic tone and whether this change in tone results in an alteration in cardiovascular reflex control. Male Sprague-Dawley rats were anesthetized with thiobutabarbitol sodium (50 mg/kg) and instrumented to record blood pressure, heart rate, and vagal parasympathetic or renal sympathetic efferent nerve activity. Additional rats were instrumented to test the sensitivity of the cardiac baroreflex using intravenous injections of phenylephrine hydrochloride (0.025, 0.05, 0.1 mg/kg) or sodium nitroprusside (0. 0025, 0.005, 0.01 mg/kg) and plotting the cardiovascular responses. Intravenous injection of estrogen (10(-4), 10(-2), and 10(-1) mg/kg) produced a significant increase in vagal efferent activity and in baroreflex sensitivity. The bilateral microinjection of an estrogen receptor antagonist, ICI-182,780 (1 pM, 50 nl/side) into the nucleus ambiguus blocked both the estrogen-induced increase in vagal efferent activity and baroreflex sensitivity. These results demonstrate that in male rats estrogen acts centrally to enhance baroreflex sensitivity by increasing parasympathetic efferent tone.

Female mammals have an enhanced baroreflex sensitivity compared with their male counterparts, leading researchers to speculate that estrogen modulates autonomic tone. Therefore, this study tests the hypothesis that exogenous estrogen can enhance the baroreflex sensitivity of male rats. Male Sprague-Dawley rats anesthetized with thiobutabarbitol sodium (50 mg/kg) were instrumented to measure blood pressure and heart rate and for the intravenous injection of drugs. The baroreflex was tested using intravenous injections of phenylephrine (0.025, 0.05, and 0.1 mg/kg), and the cardiovascular responses were plotted to obtain a measure of the sensitivity of the cardiac baroreflex. Intravenous injection of estrogen produced dose-related increases in the baroreflex sensitivity due to an increase in the magnitude of the reflex bradycardia. In a separate group of animals, stimulation of the vagus nerve for 2 h resulted in a decrease in baroreflex sensitivity. This effect was blocked when estrogen (1 x 10(-2) mg/kg) was administered immediately before the end of stimulation. In conclusion, intravenous injection of estrogen in male rats significantly enhanced baroreflex sensitivity and blocked the attenuation in the baroreflex sensitivity observed after vagal stimulation.

Cervical vagal stimulation for 2 h results in a depressed baroreflex sensitivity produced by an enhanced sympathetic output, as indicated by increased plasma norepinephrine levels. The current study examined the role of the insular cortex in modulating the vagal stimulation-induced changes in baroreflex sensitivity. Male Sprague-Dawley rats were anesthetized with thiobutabarbitol sodium and instrumented for recording blood pressure, heart rate, intravenous drug administration, and vagal afferent nerve stimulation. Stereotaxic microinjections (300 nl) of either 5% lidocaine or 0.9% saline were made bilaterally into the insula. Thirty minutes after 2 h of vagal stimulation, the baroreflex was significantly depressed and plasma norepinephrine levels were significantly elevated in both groups. The baroreflex was also significantly depressed after bilateral lidocaine injections into the insula, independent of vagal stimulation. However, no significant change in plasma norepinephrine was observed, suggesting that an attenuated parasympathetic output contributed to the altered baroreflex. Taken together, the results suggest that the insular cortex modulates the cardiac baroreflex through a modulation of parasympathetic output.

All end-of-lay hens must be transported from the production site to the site for slaughter, usually by road. The acts of being crated and transported are likely to be novel and potentially frightening. Frightened birds can be put into tonic immobility (TI), an unlearned, catatonic state, the duration of which is positively related to the fear level of the birds. Ninety ISA Brown free-range birds (in three groups of 30) and 90 caged ISA Brown birds (in similar groups) were transported (one group from cages and free-range per day) on a journey of 68 km (74 min approximately). On their return, each of the birds was subjected to TI. Although no significant differences were recorded between free-range and caged birds after they were transported (P = 0.087), in the comparison between the same birds after 7 wk, without transport, a significant difference in fear levels was observed (P < 0.001). The free-range birds were less frightened than the caged birds. No significant difference was ever found in fear levels for caged birds from different tiers. Handling and transport on this relatively short journey was apparently equally frightening for caged and free-range birds. It cannot be assumed that just because fear levels differ between free-range and caged birds, this difference will be apparent for all novel stimuli. If all birds, at all tiers, receive the same amount of human contact during the production period, there is no reason to expect differences to occur in fear levels of birds from different tiers.

Polyhalogenated aromatic compounds such as polychlorinated biphenyls (PCBs) and polychlorinated dibenzo-p-dioxins continue to be environmental contaminants because of their bioaccumulation in the food chain and resistance to biodegradation. This study was undertaken to determine if WHO-IPCS PCB congeners or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) individually or their coadministration in rats produced morphological alterations in the liver. Groups (N = 5) of female Sprague Dawley rats received TCDD (0, 2.5, 25, 250, 1,000 ng/kg bw/day) or PCB (0, 2, 20 micrograms/kg bw/day) either alone, or each dose of PCB coadministered with that of TCDD. The test substances were dissolved in corn oil and given by gavage at 0.2 ml/100 g bw/day for 28 days. At the end of the experiment the rats were killed and liver samples were prepared for transmission electron microscopy. Electron micrographs of the liver from animals of the control groups revealed characteristic normal hepatocyte architecture. An increase in smooth endoplasmic reticulum (SER) profiles and a corresponding decrease in the profiles of rough endoplasmic reticulum (RER) proportional to the increased doses of the compounds was revealed in the micrographs. Coadministration of PCBs and TCDD induced greater SER proliferation and a greater decrease in the number of RER profiles compared to either compound administered individually. The PCBs and TCDD at the doses used apparently interacted to induce hepatic ultrastructural alterations. These changes may represent an attempt by the organism to metabolize and neutralize the effects of xenobiotics.

Twelve pregnant primiparous sows were catheterized on day 102 of gestation and randomly allocated to receive ACTH (days 112-113 of gestation [2d], days 105-parturition [10d]) or saline. At parturition the 3rd, 4th, 6th and 7th piglet born alive were sacrificed either at birth or at 6 h. The later group was fed bovine colostrum through a stomach tube at 30 min, 2 and 4 h of life. Following sacrifice, the small intestine of each piglet was excised, extended and measured. Piglets from sows in the 2d group tended to be heavier with longer small intestines than either the control or 10d groups. When the small intestine length was expressed as a function of body weight, the 10d group had the greatest ratio, suggesting that the pre-parturition maintenance of elevated cortisol levels either enhanced small intestine growth or attenuated overall weight gain. Two types of enterocyte granules were described at the level of the electron microscope: granular and opaque. Opaque granules from piglets born to sows in the 2d treatment group had both a lower volume fraction and were fewer per unit area when compared to those of either the saline or 10d treatments. The process of macromolecule uptake from the intestinal lumen appeared to have been interfered with as a result of an acute prenatal stimulation with ACTH. The above results suggest that in piglets, the level of circulating cortisol differentially controls the processes of IgG absorption, enterocyte replacement and small intestine growth through separate mechanisms. Further, these processes can be manipulated in the prenatal piglet.

The effects of prenatal adrenal stimulation and synthetic glucocorticoid supplementation on development of the gastro-intestinal tract of the piglet were investigated. Twelve pregnant sows were treated with either ACTH infusion, Isoflupredone injection or Saline between days 105 and 112 of gestation. Neonatal pigs were weighed, bled and sacrificed at 0 or at 6 h. Piglets sacrificed at 6 h were fed bovine colostrum. Transverse sections were prepared from the duodenum, jejunum and ileum for measurement of the villus amplification factor (VAF) and basal membrane circumference. Sows in the ACTH group showed an elevation in cortisol in response to infusion; this decreased after infusion and then rose again at parturition. Piglets from both the ACTH and Saline groups had more villus surface area per unit of body weight (BW) than those born to Isoflupredone-treated animals. The BW of the ACTH piglets was lower (P less than 0.05) than those of piglets in the other groups. When the weight of the stomach and the Small Intestine (SI) was expressed as a function of the body weight, the stomach and SI:BW ratio was larger (p less than 0.05) in pigs born to ACTH-treated sows. The circumference of the ileum was larger at 6 h than at 0 h. Control pigs had a higher concentration of bovine IgG at 4 and 6 h (P less than 0.05). Observations of the light microscopic preparations indicated a less organized epithelium in both ACTH and isoflupredone pigs sacrificed at 0 h. Light and EM preparations of ileum from ACTH pigs sacrificed at 6 h, showed an abundance of dark-stained vacuoles, characteristic of IgG-containing structures. These became less evident in piglets from the Isoflupredone group and even less so in the control groups. The consequences of these phenomena in terms of absorptive capacity are discussed.

The neuroleptics haloperidol and thioridazine were injected intraperitoneally in rats for 81 days. During this time the rats' water consumption was measured. Drug-treated animals drank significantly less water for the first 40 days of the experiment only. On day 82 the rats were perfused for electron microscopy. The rat's paraventricular and supraoptic nuclei were embedded, sectioned, stained for electron microscopy and viewed for morphological change. There were significantly more darkly staining neurons in the haloperidol-treated rats than in control rats. Thioridazine-treated rats had more dark neurons but the difference was not significant. These dark cells had the appearance of highly stimulated neurons. Some appeared to be degenerating.