Enough is enough ... or is it?
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Biomedical subjects
S Scully
Publications and source records attributed to S Scully.
Rotary subluxation of the scaphoid resulting in persistent carpal tunnel syndrome.
Rotary subluxation of the scaphoid has not been previously reported in the English-language literature as a factor causing persistent or recurrent carpal tunnel syndrome. This report describes a sixty-seven-year-old man with persistent carpal tunnel syndrome. X-ray films showed a scapholunate gap and the scaphoid maintained a flexed position. At surgery the median nerve was found to be fixed to the undersurface of the transverse carpal ligament on the lateral side and was being compressed by the distal pole of the scaphoid.
Aged↗
Expression of mRNA for glial fibrillary acidic protein after experimental cerebral injury.
This study was undertaken to determine whether a mRNA for glial fibrillary acidic protein (GFAP) was present in increased amounts as a response to injury and, if so, how was its temporal expression related to the demonstration of GFAP by immunocytochemical techniques. A cerebral freeze-injury was produced in mice and at intervals thereafter the animals were anesthetized, perfused with formalin and histological sections of the brain through the injured area were prepared. A riboprobe for GFAP mRNA labeled with S35 and an immunocytochemical probe for GFAP were utilized to localize mRNA and GFAP immunoreactivity, respectively. For mRNA studies, the histological slide exposed to either sense or antisense probe was overlaid with x-ray film or dipped in photographic emulsion. The developed film was quantitated by digital image analysis. Emulsions were examined by dark-field microscopy. The results indicate that mRNA for GFAP is increased in the cortex in the environs of the injury by 6 hours, becomes maximal at 4-5 days, and is present in increased amounts up to 14 days. The message is enhanced in the adjacent cortex, the subpial region, the adjacent corpus callosum and in the ipsilateral and contralateral callosal radiations. This pattern of enhancement follows the distribution of post-injury edema. Glial fibrillary acidic protein is demonstrable at 24-48 hours after injury. Thus, there is a rapid response of the astrocyte to injury with increased mRNA expression that is followed by expression of GFAP immunoreactivity.
Animals↗
Prevalence of disordered eating in girls: a survey of middle-class children.
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Adolescent↗
Transferrin gene expression and secretion by rat brain cells in vitro.
We have previously shown by immunocytochemistry in rat primary glial cultures that transferrin (Tf) is an early developmental marker for oligodendrocytes. The present work addresses the issue of Tf gene expression and synthesis by neural cells in vitro. For this purpose, we used rat embryonic neuronal cultures and newborn glial cultures of astrocytes and oligodendrocytes. Cultured fibroblasts and C6 glioma cells were used as negative controls. We found that Tf mRNA is present in oligodendrocytes, astrocytes, and neurons. However, oligodendrocytes and astrocytes, but not neurons, were shown to synthesize and secrete Tf. Neither fibroblasts nor C6 glioma cells expressed detectable amounts of Tf mRNA. Tf mRNA levels in astrocyte cultures appeared to be under hormonal control since hydrocortisone markedly reduced message levels. These results show that both astrocytes and oligodendrocytes can synthesize and secrete Tf under cell culture conditions. However, epigenetic factors, such as hydrocortisone, may repress the expression of Tf in astrocytes in vivo.
Animals↗
Developmental regulation of myelin-associated genes in the normal and the myelin deficient mutant rat.
Oligodendrocyte development and myelinogenesis, both in vivo and in vitro, are characterized by the sequential and coordinate expression of markers which participate in the differentiation of oligodendrocytes as a prerequisite for myelination. The myelin deficient (md) rat shows greatly reduced mRNA expression for several oligodendrocyte markers: glycerol phosphate dehydrogenase (GPDH), myelin basic protein (MBP) and proteolipid protein (PLP). Brain GPDH mRNA levels are initially equivalent in md and unaffected littermates, but the mutant rats fail to display the normal developmental increase in gene expression. Immunostaining of brain tissue sections also reveals decreased expression of these oligodendrocyte markers. The number of oligodendrocytes containing GPDH-like immunoreactivity is reduced in mutant rats, and in general these cells appear morphologically less complex with shorter processes. However, the intensity of staining in many oligodendrocytes appears equivalent to that observed in unaffected rats. Expression of the neuronal marker, glutamic acid decarboxylase, and the astrocyte markers, glutamine synthetase and glial fibrillary acidic protein, are largely unaffected at either the mRNA or protein level. Mixed glial cultures prepared from the brains of neonatal male md rats possess fewer oligodendrocytes compared to cultures derived from unaffected littermates, and the temporal sequence of marker development is delayed. Although an abnormality in the PLP gene is suspected in the md rat, these findings document profound deficits in many oligodendrocyte gene products.
Animals↗
Induction of glutamine synthetase in rat astrocytes by co-cultivation with embryonic chick neurons.
Co-cultivation of confluent rat astrocyte cultures with embryonic chick neurons resulted in induction of glutamine synthetase activity in the astrocytes. This induction of glutamine synthetase in astrocytes by neurons was independent of induction by hydrocortisone and forskolin, but was dependent on the length of co-cultivation and the number of neurons present in the co-culture. Cycloheximide and actinomycin D inhibited the induction of glutamine synthetase in astrocytes by neurons, whereas cytosine arabinoside had no apparent effect. Results suggest that this induction of glutamine synthetase in astrocytes is mediated by cell contact with neurons and may represent a specific neuronal and glial interaction.
Animals↗
The hormonal regulation of gene expression of glial markers: glutamine synthetase and glycerol phosphate dehydrogenase in primary cultures of rat brain and in C6 cell line.
Increases in the mRNA levels of two neuroglial markers, glutamine synthetase (EC 6.3.1.2; GS) and glycerolphosphate dehydrogenase (EC 1.1.1.8; GPDH), were observed in hydrocortisone-treated cultures of astrocytes and oligodendrocytes, respectively, and in C6 cells by Northern blot analysis and in situ hybridization. In vitro transcription assays demonstrated increased GS transcription in isolated nuclei from hydrocortisone (HC)-treated primary cultures of astrocytes and C6 cells, relative to untreated cells. This increased transcription is reflected in increased GS mRNA levels in the cytoplasm and increased levels of GS protein synthesis. Sodium butyrate (NaB) blocked the glucocorticoid-mediated increase in GS transcription in the primary cultures of astrocytes but not in C6 cells. From our earlier observations (Kumar et al: J Neurochem 43:1455-1463, 1984) we found NaB in combination with HC to increase the levels of GS mRNA and GS protein synthesis (Weingarten et al: FEBS Lett 126:289-291, 1981). We now report that NaB, alone or in combination with HC, does not increase the rate of transcription, suggesting that NaB plays a role in post-transcriptional regulation of GS in C6. In addition, we report the presence of two distinct sizes of GS mRNA, 2.9 and 1.8 kb, in the primary cultures of astrocytes and C6 cells.
Animals↗
Regulation by glucocorticoids of rat-liver phenylalanine hydroxylase in vivo.
Phenylalanine hydroxylase, a liver-associated enzyme, is induced markedly by glucocorticoids in two permanent rat-hepatoma cell lines. In order to gain evidence that this phenomenon also occurs in vivo, we examined the effect of adrenalectomy and/or hormone supplementation on the levels of phenylalanine hydroxylase in the livers of adult rats: glucocorticoid administration increases, and adrenal ablation reduces, the activity of the hepatic enzyme, and the diminution occurring in the latter instance is entirely prevented by concurrent hormone replacement. These results thus corroborate earlier findings from a single experiment and are consistent with the hypothesis that adrenal corticosteroid hormones participate in modulating phenylalanine-hydroxylase levels within the diploid hepatocyte.
Adrenalectomy↗
Evidence for a charge-shift electrochromic mechanism in a probe of membrane potential.
Extrinsic optical probes have become important tools for monitoring membrane potential, with probes now available for many tissue or cell suspension systems. In each case that has been studied in detail, it seems that the mechanism involves a shift in the equilibrium population of the probe from one chemical environment to another in response to the transmembrane potential; the environments perturb the probe's spectrum differently. As this indirect mechanism involves a redistribution of dye between chemical environments that are likely to vary if a given probe is transferred from one membrane to another, a potential probe that is effective and calibrated for all membrane systems has not been realised. We present here evidence for a direct response of a probe chromophore to the electric field across membrane systems. The results suggest it might be possible to develop a universal set of membrane probes.
Cholesterol↗
Keratinocyte growth factor enhances early gut adaptation in a rat model of short bowel syndrome.
OBJECTIVE: To evaluate the effects of keratinocyte growth factor (KGF) on intestinal adaptation after resection of 85% of the small intestine and consider its potential application in short bowel syndrome (SBS). STUDY DESIGN: Experimental study using a known model of SBS. ANIMAL POPULATION: Thirty male Sprague Dawley rats. METHODS: Four groups of animals were designated. Two groups underwent 85% resection of the small intestine, while the other two groups were sham-operated, undergoing transection and reanastomosis. Resected and sham-operated groups then received either 3 mg/kg KGF or vehicle subcutaneously daily for 3 days. Gut adaptation was evaluated by measurements of mucosal cellularity and biochemical activity in duodenal, jejunal, and ileal segments. RESULTS: Significant small intestinal growth after bowel resection alone was confirmed in resected versus sham-operated rats. KGF further augmented this growth in the resected animals. Mucosal wet weight of the small intestine increased with resection and was further increased (by 20% or more) with KGF administration. Mucosal thickness, villus length, and crypt depth exhibited similar patterns of response. The KGF-induced increase in mucosal morphology was accompanied by increased mucosal DNA and protein content, followed by a trend toward increased mucosal enzyme activity. Histology demonstrated an increase in goblet cells in KGF-treated animals. In situ hybridization analysis demonstrated that KGF markedly increased mucosal expression of intestinal trefoil protein (ITF) mRNA. CONCLUSIONS: KGF enhances gut growth, differentiation, and gene regulation during adaptation in rat small intestine after massive resection. CLINICAL RELEVANCE: KGF may be beneficial in the management of veterinary and human patients undergoing massive intestinal resection.
Adaptation, Physiological↗
Enteral nutrition and keratinocyte growth factor regulate expression of glutathione-related enzyme messenger RNAs in rat intestine.
BACKGROUND: Malnutrition is associated with increased reactive oxygen species (ROS) formation and depletion of the critical antioxidant glutathione (GSH) in the intestine. The malnutrition-induced decrease in gut GSH levels is prevented by recombinant keratinocyte growth factor (KGF) administration. We investigated whether enzymes that are induced by oxidants and modulate tissue GSH supply are regulated by enteral nutrients or KGF at the messenger RNA (mRNA) level. METHODS: Adult rats were fasted for 3 days alone or fasted for 3 days then refed ad libitum. In a second model, rats were fasted for 3 days and then refed ad libitum or 25% of ad libitum intake with daily intraperitoneal saline or recombinant KGF (5 mg/kg/d) for 3 subsequent days. mRNA levels for gamma-glutamylcysteine synthetase (gamma-GCS), gamma-glutamyl transpeptidase (gamma-GT), glutathione-S-transferase Ya-subunit, gastrointestinal glutathione peroxidase (GI-GPx), and non-selenium-dependent glutathione peroxidase (ns-GPx) were determined in ileum and colon by ribonuclease protection assay. RESULTS: Fasting increased ileal gamma-GCS, ns-GPx, and glutathione-S-transferase mRNAs (by 36%, 165%, and 130% of controls) and decreased GI-GPx mRNA (to 55% of controls). In the colon, mRNAs for GSH-related enzymes were unchanged by fasting or refeeding. Prolonged enteral nutrient restriction (25% refeeding after a 3-day fast) increased gamma-GCS and glutathione-S-transferase mRNAs (by >270% of controls), decreased GI-GPx mRNA (to <50% of controls) in ileum and colon and increased ns-GPx mRNA (by 180%) in colon. KGF treatment increased ns-GPx mRNA in the ileum and colon and glutathione-S-transferase mRNA in the colon (by >200% of controls). CONCLUSIONS: Enteral nutrient intake regulates GSH-related enzyme mRNA levels in the intestine, which may contribute to the decrease in mucosal GSH during malnutrition. Increased ns-GPx and glutathione-S-transferase mRNA levels during malnutrition and with KGF administration may increase detoxifying functions in the gut under these conditions.
Analysis of Variance↗