Extensive pathological changes of the colon in cystic fibrosis and high-strength pancreatic enzymes.
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Child↗
Biomedical subjects
B Beck
Publications and source records attributed to B Beck.
True trisomy 15 mosaicism, detected by amniocentesis at 12 weeks of gestation and fetal echocardiography.
A case of mosaicism of trisomy 15, with two-thirds of the cells trisomic, was detected at 12 weeks of gestation in amniotic fluid cell cultures obtained with the filtration technique. Ultrasound examination at 13 weeks showed a nodule protruding into the amniotic cavity which was speculated to be remnants of a co-twin, causing the trisomic cell line. At 20 weeks of gestation, a malformation scan (level III) was normal, but supplementary fetal echocardiography revealed a severe cardiac defect (mitral atresia and a ventricular septal defect). Fetal lymphocytes obtained by cordocentesis showed trisomy 15 mosaicism, but only in 5 per cent of the mitoses. After termination, the same percentage of trisomy 15 mosaicism was found in cells from skin and tendon as in the original early amniocentesis. No sign of earlier twinning was found in the placenta or membranes. We conclude that mosaicism in early amniotic fluid obtained by the filter technique in this case reflected the true karyotype accurately and that supplementary echocardiography added significantly to the interpretation of the clinical implications.
Adult↗
Macronutrient type independently of energy intake modulates hypothalamic neuropeptide Y in Long-Evans rats.
Neuropeptide Y (NPY) induces a robust feeding response when it is injected in the hypothalamus. It stimulates both carbohydrate and fat intakes. Diets rich in either macronutrient are known to induce obesity and to modify feeding behavior. The aim of the present study was to determine the effects of long-term ingestion of these diets on hypothalamic NPY in relation with food intake and body weight gain and composition. For this purpose, three groups of weanling Long-Evans rats were fed either a well-balanced diet, a high-carbohydrate (HC) diet (high starch plus 25% sucrose solution), or a high-fat (HF) diet during 14 weeks. Body weight and food intake were recorded during this period. At the end of the experiment, NPY was measured in several microdissected brain areas, and some adipose tissues (AT) depots were sampled. HF rats weighed significantly more than the two other groups (p < 0.02). They were also fattier (+ 30-50% in AT weights; p < 0.01). Energy intake (EI) of the HC rats was significantly greater than that of the control (+ 15%; p < 0.02) and HF rats (+ 34%; p < 0.01) during the week preceding killing. EI of HF rats over the whole experiment was lower than that of the two groups (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Paget's disease in a squamous metaplasia of the urinary bladder. The first published case of a disease which is usually found in the epidermis.
Extramammary Paget's disease is usually found in epidermis and is often associated with malignancy in visceral organs. We report the first case with Paget's disease developed in metaplastic squamous epithelium in the urinary bladder.
Carcinoma, Transitional Cell↗
Reversals of blood-brain barrier disruption by catalase: a serial magnetic resonance imaging study of experimental optic neuritis.
PURPOSE: To investigate serially the role of catalase detoxification of endogenous H2O2 in the disruption of the blood-brain barrier (BBB) and demyelination of experimental optic neuritis. METHODS: Serial contrast-enhanced magnetic resonance imaging (MRI) of the optic nerves (T1 weighted) and T2 weighted MRI without contrast were performed on 18 guinea pigs 3 to 14 days after sensitization with central myelin for experimental allergic encephalomyelitis. Sex and age-matched littermates were paired and sensitized with the identical antigenic emulsion. To detoxify endogenous hydrogen peroxide (H2O2), animals received daily intraperitoneal injections of polyethylene glycol (PEG)-catalase at a dose of 12,000 U/kg per day for 3 days, then 1,200 U/kg daily for the next week, commencing 3 days after antigenic sensitization. Littermates received an equal volume of preservative-free saline. The intensity of gadolinium-DTPA (Gd-DTPA) enhancement was quantitated by obtaining the value for a region of interest (ROI) of the right optic nerve and the left optic nerve. The effect of H2O2 detoxification by catalase was evaluated by differences in the intensity of Gd-DTPA enhancement and T2 weighted signal in the ROI of the right and the left optic nerves at 7, 10, and 14 days after antigenic sensitization, from the pretreatment value obtained at day 3. The effectiveness of catalase detoxification of H2O2 was assessed with quantitative ultracytochemical localization of electron-dense, H2O2-derived cerium perhydroxide in the optic nerves. RESULTS: With PEG-catalase treatment, mean differences for Gd-DTPA enhancement in the ROI at 7, 10, and 14 days after antigenic sensitization were significantly reduced from the pretreatment values obtained 3 days after antigenic sensitization compared with the comparable interval values for untreated littermates. For T2 weighted signal intensity, only the 7- and 14-day values were significantly less with PEG-catalase compared with values for littermates obtained at comparable intervals. Quantitative ultracytochemical localization of H2O2-derived cerium perhydroxide reaction product revealed significant reductions in the medium number of cerium particle counts of the optic nerve head, sheath, and myelinated retrobulbar nerve. CONCLUSIONS: PEG-catalase reduced H2O2-derived cerium perhydroxide reaction product in the optic nerve but did not eliminate it, reversed disruption of the BBB as measured by Gd-DTPA enhancement, and reduced demyelination and edema as measured by T2 weighted signal intensity, suggesting detoxification of H2O2 as a new treatment strategy for disorders of primary demyelination of the central nervous system.
Animals↗
Disruption of the blood-brain barrier in experimental optic neuritis: immunocytochemical co-localization of H2O2 and extravasated serum albumin.
PURPOSE: To probe the role of endogenous hydrogen peroxide (H2O2) in the pathogenesis of disruption of the blood-brain barrier (BBB) associated with experimental allergic encephalomyelitis (EAE), an animal model for primary central nervous system demyelination. METHODS: Strain-13 guinea pigs were sensitized for EAE with central myelin in complete Freund's adjuvant. Magnetic resonance imaging with Gd-DTPA was performed twice a week for 2 weeks to assess disruption of the BBB, in vivo, by the enhancement of the optic nerves. Two weeks after antigenic sensitization, ultracytochemical localization of endogenous H2O2 was performed using the cerium perhydroxide method, with co-localization of endogenous serum albumin extravasation using gold-labeled antibodies against serum albumin. Examination of blood vessels for perivascular immunogold-labeled serum albumin and H2O2 derived reaction product began in the optic nerve head and proceeded toward the retrobulbar optic nerve until a total of 20 vessels were evaluated per animal. RESULTS: Magnetic resonance imaging revealed Gd-DTPA enhancement of the optic nerves in all animals sensitized for EAE. Optic nerve ultrastructure revealed colloidal gold-labeled antibodies against serum albumin in the perivascular and adjacent interstitial spaces of capillaries and small venules in which H2O2 derived cerium perhydroxide reaction product was also simultaneously evident. Immunogold-labeled serum albumin was predominantly confined to the intravascular compartment of the optic nerve in the absence of perivascular H2O2 and/or perivascular foci of inflammatory cells. The difference between the mean percentage of blood vessels (61.8%) with co-localization of perivascular immunogold-labeled serum albumin and cerium perhydroxide reaction product, to the mean percentage of blood vessels (9.5%) with perivascular immunogold-labeled serum albumin in the absence of cerium perhydroxide, was statistically significant (P = 0.0019). CONCLUSIONS: Endogenous H2O2, found at the foci of BBB disruption, may be one of the mediators involved in the alteration of vascular permeability in experimental optic neuritis.
Animals↗
Neuropeptide Y projection from arcuate nucleus to parvocellular division of paraventricular nucleus: specific relation to the ingestion of carbohydrate.
Neuropeptide Y (NPY) injection into the hypothalamic paraventricular nucleus (PVN) stimulates feeding behavior and specifically carbohydrate intake in rats. The present study investigated the relation between endogenous levels of NPY and natural ingestion for carbohydrate. It also examined the possible importance of a specific NPY projection in this relationship, which traverses from cell bodies in the arcuate nucleus (ARC) to terminals in the parvocellular division of the PVN (pPVN). Sprague-Dawley rats were given pure macronutrient diets (carbohydrate, protein and fat), and their daily nutrient intake was recorded for 3 weeks. The rats were sacrificed, and 8 hypothalamic nuclei were micropunched and examined via RIA for endogenous NPY levels. The results demonstrate a strong, positive correlation between daily carbohydrate intake and hypothalamic NPY levels. The relationship was specific to the pPVN (r = +0.71; P < 0.001), ARC (r = +0.57; P < 0.001) and dorsomedial nucleus (DMN, r = +0.52; P < 0.01), and was not observed in any other hypothalamic area, including the magnocellular division of the PVN. In the pPVN, the NPY levels of animals that consumed > 50 kcal of carbohydrate (49 pg/microgram protein) were almost twice that of animals that consumed < 20 kcal of carbohydrate (28 pg/microgram protein: P < 0.01). Furthermore, NPY levels in the ARC were positively correlated with NPY in the pPVN and DMN but not any other nuclei. No relation between hypothalamic NPY and measures of protein or fat ingestion was detected. Levels of NPY were also unrelated to total caloric intake, to body weight at sacrifice, and to body weight gain during the 3-week measurement period. These results, together with other findings, provide support for a role of endogenous NPY and its projection from the ARC to the pPVN, perhaps via the DMN, in controlling natural appetite for carbohydrate.
Animals↗
Microdialysis in the estimation of interstitial myocardial neuropeptide Y release.
The purpose of this study was to investigate the feasibility of cardiac microdialysis for the in vivo estimation of cardiac interstitial peptide concentrations, and, to determine the changes in neuropeptide Y release in myocardial tissue during experimental brain death in pigs. Using a specifically designed concentric flexible probe, perfused with Ringer solution containing 0.5% of bovine serum albumin at a flow rate of 2 microliters/min, allowed us to obtain a 23 +/- 2% relative recovery rate in vitro. Based on these in vitro recovery data, a regional study of the kinetics of interstitial NPY levels following brain death was obtained by monitoring the changes in NPY dialysate levels recorded from dialysis probes implanted into the right and left ventricular walls of the beating heart in vivo. Basal dialysate NPY levels determined by radioimmunoassay were of 95.2 +/- 7.0 and 93.2 +/- 9.1 pmol/l in left and right ventricle, respectively. Brain death was followed by a sustained 2 h increase in NPY dialysate levels in both ventricles (peak levels: 173.2 +/- 30.9 pmol/l in left ventricle, and 149.7 +/- 23.9 pmol/l in right ventricle), which then returned to control levels. We conclude that cardiac microdialysis is a simple and promising new tool for evaluating the role of peptides in cardiovascular regulation.
Animals↗
Galanin in the hypothalamus of fed and fasted lean and obese Zucker rats.
Galanin (GAL), a 29 aminoacid peptide, is widely distributed in the central nervous system and especially in the hypothalamus. It strongly stimulates food intake when it is injected in the paraventricular nucleus (PVN) of normal rats. The obese Zucker rat with a well-established hyperphagia is characterized by a general dysregulation of some important neuropeptides involved in the regulation of feeding behavior e.g. neurotensin, NPY or CCK and the aim of this study was to measure GAL in different microdissected brain areas in lean (Fa/Fa) and obese (fa/fa) male Zucker rats. As feeding status may modulate the central peptide concentrations, it was measured in ad libitum fed rats and in 48-h fasted rats of both genotypes. GAL was measured by a specific radioimmunoassay in the arcuate nuclei (ARC) and parvocellular (PVNp) and magnocellular (PVNm) parts of the PVN as well as in the median eminence (ME), median preoptic area (MPOA), supraoptic (SON) and dorsomedian (DMN) nuclei. Two-way analysis of variance revealed a very significant effect of genotype in the PVNp (P < 0.001), SON (P < 0.001) and in the ME (P < 0.02). No significant variations at all were noted in the ARC, PVNm, MPOA and DMN. GAL concentrations were more than doubled in the PVNp and SON of ad lib obese rats when compared to the ad lib lean rats (P < 0.005). On the other hand, in the ME where GAL concentration was about 4-fold greater than in the other areas, there was a 20 to 30% decrease in GAL concentrations in the obese rat (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Analysis of Variance↗
K(+)-stimulated neuropeptide Y release into the paraventricular nucleus and relation to feeding behavior in free-moving rats.
Neuropeptide Y (NPY) strongly stimulates food intake when it is injected in the central nervous system and especially in the hypothalamus. The major site of NPY synthesis in the hypothalamus is the arcuate nucleus which projects to the paraventricular nucleus. These two nuclei form the arcuate-paraventricular axis, a local circuit in the control of food intake. It was demonstrated that neuropeptide Y concentration in the paraventricular nucleus can be modified by ingestive or metabolic factors. Actually, these modifications cannot be associated with the existence of a release of neuropeptide Y in this nucleus. That is why we used push-pull perfusion during the light phase in freely-behaving rats with food and water available. Perfusates were collected with standard artificial cerebrospinal fluid (CSF) as medium and hyperosmotic CSF obtained by addition of potassium chloride (55 mM). Hyperosmotic perfusion was repeated a second time for some animals. Results clearly demonstrated that neuropeptide Y is released into the paraventricular nucleus during normal perfusion with a mean value of 35.5 +/- 1.5 pg/tube. The potassium perfusion produced an increase in the release of neuropeptide Y (peak at 71.4 +/- 7.1 pg/tube; p < 0.01), and this phenomenon was reproduced with the second potassium stimulation (peak at 47.7 +/- 2.3 vs pg/tube; p < 0.05). Neuropeptide Y release returned to normal values after or between stimulations. Behavioral analysis showed that these stimulations were associated with an increase in food intake. Neuropeptide Y is therefore physiologically released into the paraventricular nucleus of the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Elevated neuropeptide Y in the arcuate nucleus of young obese Zucker rats may contribute to the development of their overeating.
Neuropeptide Y (NPY) mediates feeding behavior through a local hypothalamic network formed by the arcuate and paraventricular nuclei (the AP axis). In the hypothalamus, NPY is mainly synthesized in neurons of the arcuate nucleus. These neurons project to the paraventricular nucleus, the site where NPY has the strongest stimulatory effects on food intake of Sprague-Dawley rats. In the adult Zucker fatty rat (a genetic model of obesity with a well-established hyperphagia), NPY concentrations in these nuclei are higher than in its lean counterpart. We measured hypothalamic NPY before the appearance of altered eating behavior, e.g., in very young (16-d-old) lean and obese Zucker pups, and in pups at an age when overeating had begun, e.g., a few days after weaning at 30 d. At 30 d, NPY concentrations were significantly higher in obese than in lean rats in the arcuate nucleus (14.2 +/- 0.7 vs. 11.6 +/- 0.5 pmol/mg protein, P < 0.01). This difference was not observed at 16 d. A 160% increase was noted in the paraventricular nuclei of obese rats between 16 and 30 d of life compared with a 100% increase in the lean rats (P < 0.001). Neuropeptide Y concentration was greater in 30-d-old rats than in 16-d-old rats in other areas involved in the regulation of feeding behavior, such as the dorsomedian nuclei and lateral hypothalamus, but the values did not differ between genotypes. Higher NPY concentration was therefore detected early in young obese rats in the main hypothalamic site of NPY synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
Aging↗
Anti-cardiolipin antibodies (IgG and IgA) in women with recurrent fetal loss correlate to clinical and serological characteristics of SLE.
AIM OF STUDY: We investigated to which degree IgG, IgA and IgM anti-cardiolipin antibodies (aCL) are associated in recurrent abortion or late fetal death with other signs of autoimmune disease and in particular SLE. MATERIAL AND METHODS: Serological variables typical of SLE and of the anti-phospholipid antibody syndrome were measured once eight to 16 weeks after the last fetal loss in 158 women with recurrent abortion or late fetal death; women with manifest autoimmune rheumatic disease were excluded. RESULTS: (1) Positive values, i.e. above the 99th percentile of reference material, of IgG aCL and IgA aCL were observed in 4% and 7%, respectively, whereas 26% had positive values of IgM aCL. (2) IgG aCL and IgA aCL but not IgM aCL correlated to anti-nuclear antibodies and to anti-double stranded DNA. (3) Anti-double stranded DNA, IgG aCL and IgA aCL but not IgM aCL correlated to previous occurrence of thrombosis. (4) ANA correlated to lower blood platelet concentrations and higher erythrocyte sedimentation rates. CONCLUSIONS: Women with recurrent abortion or late fetal death who have higher but not necessarily abnormally high levels of IgG aCL or IgA aCL constitute a group with increased occurrence of clinical and serological characteristics of SLE. We suggest that these women be kept under surveillance for future development of autoimmune disease especially SLE. The women with high IgM aCL constitute another group without these characteristics.
Abortion, Habitual↗
In vivo monitoring of myocardial interstitial neuropeptide tyrosine release following brain death.
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Animals↗
[Reliability of the Child Behavior Checklist in a population of 6 to 8-year-old special education students].
66 children attending first grade at a special school for educationally subnormal children were examined medically and psychologically. Classification was done according to ICD-10. In addition, the parents were asked to rate their children's behavior with the "Child Behavior Checklist" by Achenbach and Edelbrock. The most common symptoms rated in this group of 6- to 8-year-old children were lack of concentration, speech and language problems, hyperactivity, demand for attention and arguing. The mean total score (cut-off score: 30) and the number of crucial items (cut-off score: at least two crucial items) differed significantly between the children with and those without psychiatric disorders. No significant correlation was found between the mean total score or the number of crucial items and the sex of the children or the other axes of the Multi-axial Classification of Child Psychiatric Disorders.
Affective Symptoms↗
[Multiple diagnoses and stresses in children of primary school age].
The study was conducted to assess the consequences of multiple diagnoses and handicaps in children aged 6 to 8 years. Children were considered to be "multiply handicapped" if they suffered from two or more disorders or impairments included in the Multi-axial Classification Scheme. To this end children in special schools were compared with a random sample of children from three communities in Bavaria. As expected, all prevalences found in the population of children from special schools were substantially higher than those found in the random sample. Furthermore, the proportion of children with multiple handicaps in the special schools far exceeded what one would have expected based on the findings for the random sample. Most of the disturbances did not differ in respect to their comorbidity. But the mentally retarded children in the special schools were all "multiply handicapped". The importance of "multiple handicaps" for the assignment to special schools is discussed, as are the implications for the planning of services.
Child↗
Early modification of neuropeptide Y but not of neurotensin in the suprachiasmatic nucleus of the obese Zucker rat.
Hyperphagia in the obese Zucker rat is characterized by the early modification of the dark/light (D/L) rhythm of food intake. This rhythm is mainly driven by the suprachiasmatic nucleus (SCN) and, more controversially, by the ventromedian nucleus (VMN). In the SCN of adult obese Zucker rat, the concentrations of neuropeptide Y (NPY), a potent stimulator of food intake, are increased whereas those of neurotensin (NT), an anorexigenic peptide, are decreased. However, nothing is actually known about the synchronicity of the dysregulation of the D/L rhythm and variations of these peptides. That is why we measured NPY and NT in the microdissected SCN and VMN of lean (n = 16) and obese (n = 15) Zucker rats before the occurrence of hyperphagia (day 16 of age) and a few days after weaning (day 30 of age) when the modifications are apparent. For NPY, there was a very significant effect of age (P less than 0.001) for both nuclei and a significant effect of genotype (P less than 0.02) for the SCN only. NPY concentrations increased between 16 and 30 days in both nuclei (+74% (SCN) and +70% (VMN) in the obese rat; +57% (SCN) and +67% (VMN) in the lean rat; P less than 0.001). NPY in the SCN was not different at 16 days of age between lean and obese rats but significantly increased at 30 days in the obese rat (22.6 +/- 1.2 vs. 18.6 +/- 1.5 ng/mg protein; P less than 0.05). NT was not detected in the SCN of either group at 16 days or at 30 days.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Unexpected regulation of hypothalamic neuropeptide Y by food deprivation and refeeding in the Zucker rat.
Neuropeptide Y strongly stimulates food intake when it is injected in the hypothalamic paraventricular (PVN) and ventromedian (VMN) nuclei. In Sprague-Dawley (SD) rats, NPY synthesis in the arcuate nucleus (ARC) is increased by food deprivation and is normalized by refeeding. We have previously shown that the obese hyperphagic Zucker rat is characterized by higher NPY concentrations in this nucleus. NPY might therefore play an important role in the development of hyperphagia. The aim of the present study was to determine if the regulation by the feeding state works in the obese Zucker rat. For this purpose, 10 weeks-old male lean (n = 30) and obese (n = 30) Zucker rats were either fed ad libitum, either food-deprived (FD) for 48 hours or food-deprived for 48 h and refed (RF) for 6 hours. NPY was measured in several microdissected brain areas involved in the regulation of feeding behavior. NPY concentrations in the ARC was about 50% greater in obese rats than in lean rats (p less than 0.02) whatever the feeding state. In the VMN, NPY concentrations were higher in the lean FD rats than in the obese FD rat (p less than 0.001). Food deprivation or refeeding did not modify NPY in the ARC, in the VMN or in the dorsomedian nucleus whatever the genotype considered. On the other hand, food deprivation induced a significant decrease in NPY concentrations in the PVN of lean rats. This decrease was localized in the parvocellular part of this nucleus (43.0 +/- 1.9 (FD) vs 54.2 +/- 2.1 (Ad lib) ng/mg protein; p less than 0.005). Ad lib levels were restored by 6 hours of refeeding. These variations were not observed in the obese rat. The regulation of NPY by the feeding state in the Zucker rat was therefore very different from that described in the SD rats. Strain or age of the animals used might explain these differences. High NPY levels and absence of regulation in obese Zucker rats could contribute to the abnormal feeding behavior of these rats.
Animals↗
Central effects of monosodium glutamate on feeding behavior in adult Long-Evans rats.
Monosodium glutamate (MSG) is known as a neurotoxic molecule when injected neonatally in rats, where it produces a marked decrease in food intake and an increase in adipose tissue mass. But, in adult rats subcutaneous injections of MSG produce a small, dose-dependent increase in food intake. It is not known if this action is centrally or systemically mediated. Therefore, the feeding pattern of adult rats injected intracerebroventricularly with MSG was measured. Seven days after installation of a cannula in the right lateral ventricle, rats were injected either with artificial cerebrospinal fluid or twice with 3 mg/brain MSG within a 3-day interval. The feeding pattern was recorded via a complete computerized system during 24 h. Feeding behavior was significantly modified by MSG treatments. These effects were observed immediately after drug injections, that is, upon the first meal, as well as during the 24 h that followed. For the first meal, modifications in meal size (+285%; p = 0.0001), meal duration (x10; p = 0.0005), postmeal interval (x4; p = 0.0005), and the satiety ratio (-50%; p = 0.01) were observed. During the 24-h postinjection period, modifications in meal number (-3; p = 0.0007), total amount of food eaten (+21%,; p = 0.007), time spent eating (+40%; p = 0.007), meal duration (+53%; p = 0.005), and meal size (+44%; p = 0.01) were noted. When the two MSG injections were compared, differences were also noted. For the first meal, postmeal interval (-50%; p < 0.005) and satiety ratio (-50%; p < 0.005) were decreased after the second injection.(ABSTRACT TRUNCATED AT 250 WORDS)
Adipose Tissue↗