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PubMed1995

Differential cloning of novel intestine-specific genes whose expression is altered under conditions of villus atrophy.

Atrophy of the small intestinal villi occurs in a variety of disease states and is associated with diarrhea, malabsorption, and impaired barrier function. We have previously demonstrated that villus atrophy is associated with an increase in lactase and a decrease in intestinal alkaline phosphatase gene expression. Given these changes in enterocyte phenotype with villus atrophy, we speculated that there may be other intestine-specific genes whose expression is altered as a function of epithelial growth state. We have employed two molecular techniques in order to identify and clone complementary DNAs (cDNA) which are differentially expressed in atrophic compared to normal small intestinal mucosa. In differential cDNA library (+/-) screening, duplicate filters of a normal jejunal cDNA library are hybridized with radiolabeled cDNA probes from either atrophic or control tissues. Comparisons of the intensities of hybridized clones allows for the identification of differentially expressed gene products. In the mRNA differential display system, RT-PCR is used to randomly amplify mRNA species. Similar to cDNA library screening, comparisons of radiolabeled bands on a polyacrylamide sequencing gel allow for the identification of differentially expressed genes. Using these methods, we have identified a novel cDNA, called D9, which appears to be expressed exclusively in the intestinal mucosa. Northern analyses have confirmed that the expression of the D9 mRNA is dramatically decreased under conditions of villus atrophy, suggesting an underlying relationship with epithelial growth state. DNA sequence analysis (GenBank) reveals no identity to previously cloned genes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2001

Voxel-based morphometry using the RAVENS maps: methods and validation using simulated longitudinal atrophy.

Statistical analysis of anatomical maps in a stereotaxic space has been shown to be a useful tool in population-based studies for quantifying local anatomical differences or changes, without a priori assumptions about the location and extent of the regions of interest. This paper presents an extension and validation of a previously published methodology, referred to as RAVENS, for characterizing regional atrophy in the brain. A new method for elastic, volume-preserving spatial normalization, which allows for accurate quantification of very localized atrophy, is used. The RAVENS methodology was tested on images with simulated atrophy within two gyri: precentral and superior temporal. It was found to accurately determine the regions of atrophy, despite their localized nature and the interindividual variability of cortical structures. Moreover, it was found to perform substantially better than the voxel-based morphology method of SPM'99. Improved sensitivity was achieved at the expense of human effort involved in defining a number of sulcal curves that serve as constraints on the 3D elastic warping.

Atrophy↗

PubMed1993

Fetal thymic atrophy after exposure to T-2 toxin: selectivity for lymphoid progenitor cells.

Treatment of experimental animals with T-2 toxin has been found to markedly decrease thymic cellularity and to suppress cell-mediated immune function. Although T-2 toxin readily crosses the placenta, little is known about its effect on development of immunity following gestational exposure. In the present report, prenatal T-2 toxin resulted in significant fetal thymic atrophy in mice. In vitro exposure to T-2 toxin resulted in decreased thymocyte proliferation, as well as significant but transient increases in thymocyte viability. Cycloheximide increased thymocyte viability parallel to that seen after T-2 toxin, indicating that enhanced viability after T-2 toxin may be the result of inhibited endonuclease synthesis. These findings suggest that direct cytotoxic effects of T-2 toxin make limited contribution to thymic atrophy production. In support of this conclusion, in vivo T-2 toxin exposure resulted in only limited alteration of thymocyte development, as evidenced by expression of CD4, CD8, and alpha beta TCR cell-surface antigens. These data further indicate that antiproliferative effects of T-2 toxin on thymocytes may contribute limitedly to thymic atrophy observed in vivo. In vivo T-2 toxin treatment did not affect total numbers of CD44+, CD45+, or Mac-1+ fetal liver cells. However, such exposure resulted in significant decreases in CD44lo and CD45lo fetal liver prolymphoid cell subpopulations. Subsequent in vitro T-2 toxin exposure of fetal liver cells enriched for lymphoid precursors resulted in both decreased cell viability and highly significant decreased proliferation. Taken together, these data suggest that lymphocyte progenitors, in contrast to thymocytes, represent highly sensitive targets of T-2 toxin exposure, responsible for thymic atrophy.

Animals↗

PubMed1993

Thymic atrophy caused by ethanol in a mouse model for binge drinking: involvement of endogenous glucocorticoids.

Consumption of large amounts of ethanol (EtOH) in a single drinking episode is common, but very little is known about the immunological effects of such occurrences. Exposure to EtOH for several days is immunosuppressive in rodent models, and a single dose of EtOH causes substantial increases in endogenous glucocorticoid levels which might have immunosuppressive effects. In the present study, the effects of a single dose of EtOH on the thymus and the role of endogenous glucocorticoids in these effects were examined in B6C3F1 female mice. A single dose of EtOH decreased thymus weight and cellularity, predominantly by elimination of CD4+CD8+ (immature) thymocytes. This occurred over a broad range of EtOH doses and was associated with behavioral effects (ranging from mild ataxia to unresponsiveness) similar to those noted in human binge drinkers. Several lines of evidence indicate that the effects of EtOH on the thymus are mediated by endogenous glucocorticoids: (1) corticosterone levels in EtOH-treated mice increased more than 10-fold and remained significantly elevated for up to 12 hr; (2) the most glucocorticoid-sensitive thymocytes (CD4+CD8+ cells) were preferentially depleted by EtOH; (3) before thymocyte depletion was evident, substantial DNA fragmentation occurred in the thymus as would be expected in the case of glucocorticoid-induced apoptosis; (4) the glucocorticoid antagonist, RU 486, blocked thymic atrophy and DNA fragmentation in EtOH-treated mice; (5) EtOH and its major metabolites at concentrations comparable to or greater than expected in vivo did not decrease thymocyte viability in 20-hr cultures, indicating that direct action of EtOH or its metabolites on thymocytes does not play an important role in EtOH-induced thymic atrophy. These results suggest that a single dose of EtOH induces thymic atrophy which is predominantly mediated by increased levels of endogenous glucocorticoids. The mouse model described here should be useful in evaluating other effects of binge drinking on the immune system, and the experimental strategy described should be applicable in investigating the role of endogenous glucocorticoids in thymic atrophy induced by other chemicals and drugs.

Animals↗

PubMed2006

Time profile of eosinophilic neurons in the cortical layers and cortical atrophy.

Eosinophilic neurons (ENs) appear in the post-ischemic cortex; however, whether there are differences in the time profile for different cortical layers and the fate of the cortex with ENs is largely unknown. We examined the time profile of ENs in different cortical layers and evolution of cortical atrophy after transient cerebral ischemia in Mongolian gerbils. Unilateral forebrain ischemia was induced twice by 10-minute unilateral common carotid artery occlusions. Brains at 24 hours, 4 days, and 2, 4, and 16 weeks post-ischemia were prepared for morphometric analysis. Quantitative analysis of ENs in regions of interest in the rostral and caudal cortex showed the highest number of ENs at 4 days post-ischemia in layers 3 and 6. Reduction in ENs after this peak was slower in layer 6 than in layer 3 in both rostral and caudal cortex, and this difference was significant in layer 6 of the caudal cortex. Infarcts with significant atrophy appeared in the rostral cortex. In the caudal cortex, only selective neuronal death with mild but distinct atrophy was observed. We observed a significant difference between cortical layers in the time profile of ENs in the post-ischemic cortex. Selective neuronal death without infarction was sufficient to induce cortical atrophy after transient cerebral ischemia.

Animals↗

PubMed1996

The ultrastructure of parapapillary chorioretinal atrophy in eyes with secondary angle closure glaucoma.

BACKGROUND: The present study was performed to investigate the ultrastructure of deep retinal layers and choroid corresponding to the parapapillary chorioretinal atrophy in eyes with secondary angle-closure glaucoma. METHODS: The glaucomatous eyes included two eyes enucleated due to iris ring melanoma with high intraocular pressure and one eye with neovascular glaucoma enucleated due to ocular pain. The control eyes included one eye enucleated due to choroidal malignant melanoma with normal intraocular pressure and one eye enucleated during surgery for supramandibular carcinoma. These eyes were studied with light and electron microscopy. RESULTS: In the region of parapapillary chorioretinal atrophy of glaucomatous eyes, the retinal pigment epithelial cells showed degenerative changes, such as loss of basal infoldings and microvilli, degenerated mitochondria, vacuolar degeneration and irregular distribution of melanin granules. The photoreceptors were decreased in number in this area of glaucomatous eyes. The lumen of the choriocapillary vessels adjacent to the optic nerve was collapsed. CONCLUSION: These results elucidate the fine structures of deep retina and choroid in the region of parapapillary chorioretinal atrophy of glaucomatous eyes, and suggest that the reduced choroidal perfusion might be the pathogenetic mechanism of glaucomatous parapapillary chorioretinal atrophy.

Adult↗

PubMed1986

Proximal tubular atrophy: qualitative and quantitative structural changes in chronic obstructive nephropathy in the pig.

Kidneys of pigs with various degrees of induced chronic obstructive nephropathy were studied by light- and electron microscopy to assess the structural changes of proximal convoluted tubules with increasing degrees of atrophy. A particular aim was to evaluate the quantitative relationship between proximal tubular and interstitial changes in early tubular atrophy. The kidneys were subjected to varying degrees of ureteral obstruction and were fixed by in vivo vascular perfusion. Quantitative (morphometric) analyses were carried out on montages of electron micrographs representing randomly selected cortical areas and cross sections of individual proximal convoluted tubules. The results demonstrated that ureteral obstruction was followed by significant reductions in proximal tubular epithelium, in volume of proximal tubular mitochondria and in surface area of proximal tubular basolateral membranes. These changes were present even in the absence of any demonstrable increase in cortical interstitium or alterations in the relationships between proximal tubules and peritubular capillaries. With increase in the volume of cortical interstitium the proximal tubules were further simplified in ultrastructure with a reduced number of interdigitating lateral cell processes. Concomitantly there were significant quantitative changes in the spatial associations between tubules and capillaries due to increase in tubulo-capillary distances. The present study shows that ultrastructural changes in proximal tubules during early atrophy precede the volume increase in cortical interstitium associated with chronic obstructive nephropathy. It is suggested that the early tubular changes are due to decreased functional loads, whereas the further progression of tubular atrophy may be a result of impaired nourishment of the tubular cells due to increased interstitial tissue and altered relationships between tubules and capillaries.

Animals↗

PubMed1993

The topographic distribution of brain atrophy in frontal lobe dementia.

The topographic distribution of brain atrophy was quantified by image analysis of fixed brain slices from ten patients dying with dementia of frontal type (DFT) and from six other patients dying with dementia of frontal type with motor neurone disease (DFT + MND). In both groups the atrophy was maximal within frontal, anterior temporal and anterior parietal regions of cortex, although other structures such as the amygdala, caudate nucleus, thalamus and hippocampus were also affected. The magnitude of the atrophy was much greater, in all affected regions, in DFT alone than in DFT + MND. Grey and white matter were affected equally in DFT alone although in DFT + MND a preferential white matter involvement was noted. No differences in the topographic distribution of the atrophy was observed in cases of DFT showing a spongiform degeneration of the cortex compared to those showing a gliotic degeneration with, or without, Pick cells and Pick bodies.

Aged↗

PubMed1994

Asymmetrical atrophy of the renal medulla: a previously unreported abnormality.

Investigation of the smaller of a pair of unequal kidneys showed a band of atrophy in the inner medulla, sparing the papillary tip, which was viable and contained collecting ducts. The kidney had extensive cortical atrophy with glomerulocystic disease and multiple tiny renal cell neoplasms. These changes were considered secondary to the medullary lesion. Study of 85 other kidneys taken a autopsy and surgery showed 8 other cases with similar band-like atrophy in the medulla to various degrees. All 9 cases had severe vascular disease. This asymmetrical or band-like atrophy of the renal medulla seemed to be fairly common but previously unreported, could be differentiated from renal papillary necrosis, and was most likely due to an episode of severe ischaemia, possibly in kidneys with pre-existing vascular narrowing.

Adult↗

PubMed1994

Immunohistochemical analysis of the distribution of MyoD1 in muscle biopsies of primary myopathies and neurogenic atrophy.

The expression of the myogenic determination gene MyoD1 plays a primary role in the commitment of primitive mesenchymal cells to a striated muscle lineage and is down-regulated during later stages of differentiation. To determine the potential role of this gene in myopathic conditions, we examined its expression by means of immunohistochemical analysis, using a series of muscle biopsies from 14 patients with a variety of primary myopathies and neurogenic disorders. Utilizing the avidin-biotin-complex technique, cryostat sections were stained with monoclonal antibody 5.8 A, which we have previously described as having a high level of specificity for tumors with rhabdomyoblastic differentiation. Of special interest was the observation in 4 of 8 cases of neurogenic atrophy of varying levels of cytoplasmic positivity of muscle fibers, appearing to correlate with their degree of atrophy, in addition to weak nuclear staining. Muscle biopsies from 2 patients with Duchenne's muscular dystrophy and 2 patients with autoimmune inflammatory myopathies demonstrated various levels of nuclear positivity in scattered foci that appeared to correlate with areas of regeneration. A biopsy from a single case of neurogenic atrophy secondary to infantile spinal muscular atrophy (Werdnig-Hoffmann's disease) demonstrated diffuse but relatively weak staining of myofiber nuclei, in contrast to sections of normal striated muscle and muscle biopsies from patients with unexplained myoglobinuria, which exhibited only minimal amounts of staining. These data are compatible with observations that MyoD1 expression is related to electrical activity and muscle regeneration.

Adult↗

PubMed1987

Lack of correlation between formation of reactive metabolites and thymic atrophy caused by 3, 4, 3', 4'-tetrachlorobiphenyl in C57BL/6N mice.

The possible role of active metabolites of 3, 4, 3', 4'-tetrachlorobiphenyl (TCB) in causing thymic atrophy was investigated using inbred strains of mice. The generation of reactive species which bind covalently to cellular proteins was used to monitor the formation of active TCB metabolites. The amount of in vitro covalent binding of TCB to proteins by liver microsomes was increased markedly by pretreatment of AHH-responsive C57BL/6N mice with either 3-methylcholanthrene (MC) or TCB itself, although these two inducers were not effective in AHH-nonresponsive DBA/2N mice. MC treatment also caused an induction of microsomal TCB-binding activity in all of the (C57BL/6N X DBA/2N) F1 mice. Moreover, among 38 individuals of [(C57BL/6N) (DBA/2N) F1 X DBA/2N] backcross, 23 mice responded to MC with respect to microsomal TCB-binding activity while others did not. These results suggest that the conversion of TCB to protein-bound metabolites is mediated by particular form(s) of cytochrome P-450 which is (are) induced by an Ah receptor mechanism. In order to ascertain whether the active TCB metabolites play a role in causing thymic atrophy, 14C-labeled TCB was administered IP to C57BL/6N mice and the amount of covalent binding of radioactive metabolites to tissue proteins was determined. The in vivo binding was evident in the liver, particularly in the microsomal fraction, on the basis of protein content. In contrast, the thymic proteins contained no measurable amounts of bound radioactivity even when the mice showed marked thymic atrophy. These data suggest that thymic atrophy caused by TCB is not likely to result from the generation of reactive metabolites.

Animals↗

PubMed1990

An autopsy case of peroneal muscular atrophy with rigidity and tremor. Ultrastructural and systematic morphometrical studies on peripheral nerves.

An autopsy case of hereditary peroneal muscular atrophy (PMA) with rigidity and static tremor is presented. The patient developed slowly progressive distal muscular atrophy of the legs at the age of 15 years. By the age of 52 years, PMA became marked associated with pes cavus, and tremor and rigidity of the extremities were noted. Motor and sensory conduction velocities gradually depressed and lost near the end of his life. At autopsy, the major neuropathological abnormalities involved the peripheral nervous systems, and were characterized by axonal atrophy and loss of myelinated fibers. These changes involved both the proximal and distal nerves, being more severely affected in the distal. The pathological changes in other regions of the nervous systems were mainly confined to the spinal cord, dorsal ganglia and spinal nerve roots, and pigmented neurons in the brain stem. Morphometrically, the total fascicular area was much smaller than in control, but the total number of myelinated fibers greatly outnumbered that of control 75,200 to 48,200 at the proximal sciatic nerve and then gradually decreased towards the periphery; however, even in the distal sural nerve, the total number of myelinated fibers exceeded that of control (6820 to 5469). Thus, the density of myelinated fibers were much higher, being 1.5 to 2 times greater, than in control. Its abrupt decline at the distal nerve might account for neurogenic atrophy of the distal musculature. Unmyelinated fibers were slightly increased in density and not atrophic. This case is unique in its clinicopathology and does not belong to any subtypes of PMA including "neuronal plus".

Adult↗

PubMed1982

Epileptic seizures and cerebral atrophy in alcoholics.

Computed tomography was carried out in two groups of chronic alcoholics diagnosed according to the research diagnostic criteria, one with and the other without epileptic seizures. The sizes of the ventricles and the extracerebral spaces were compared with those of a control group, in order to examine the possible role of cerebral atrophy in precipitating epileptic fits in chronic alcoholics. Although a severe degree of atrophy was demonstrated in both groups, no difference was found between alcoholics with and without seizures. However, by correlating the sizes of different spaces, a more generalized atrophy was found in alcoholics with seizures. Thus, cerebral atrophy in a more generalized form may play a yet undefined role in precipitating epileptic attacks.

Adult↗

PubMed1984

Gangliosides in rabbit and human skeletal muscle with denervation atrophy.

In experimental denervation of rabbit skeletal muscle, an increase of gangliosides has been reported. Ganglioside, DNA, total lipid and protein levels were studied in experimental denervation of rabbit gastrocnemius muscle and in human skeletal muscle with denervation atrophy. In severe human denervation atrophy total ganglioside, DNA and total lipid levels were increased, and protein levels decreased as compared with controls. The ganglioside pattern was changed in severe human denervation atrophy and showed a significant increase of a GT1b-like and moderate decrease of a GM1-like compound. Findings in experimentally denervated rabbit muscle resembled results obtained in human denervation atrophy, showing a significant increase of total ganglioside levels as well as a moderate increase of GT1b-like and decrease of GM1-like compounds.

Adult↗

PubMed1989

Skeletal muscle CK-B activity in neurogenic muscular atrophies.

Creatine kinase isoenzymes were determined in skeletal muscle biopsy specimens of 34 patients suffering from neurogenic muscular atrophies. The findings were compared: (1) with those of 38 control muscle samples and (2) with those in 41 muscular dystrophies and other myopathic conditions. The measurements were made by electrophoretic separation and elution of the isoenzymes and by immunoinhibition assay. The results showed that the total and specific CK activity were significantly decreased (P less than 0.005) in neurogenic atrophies in contrast to myopathic conditions where no differences from control levels were observed. This decrease was due to a decrease of the CK-M subunit activity, while the CK-B subunit was elevated. The muscle CK-MB activity was considerably elevated in muscular dystrophies (P less than 0.02) and myositis (P less than 0.001), but it was also slightly elevated in neurogenic conditions. The similarity of the muscle CK isoenzyme pattern in neurogenic atrophies and myotonic dystrophy was noted. These findings could possibly reflect considerable difference in the regeneration process of neurogenic atrophies and muscular dystrophies.

Biopsy↗

PubMed1990

The development of infratentorial atrophy in patients with idiopathic cerebellar ataxia of late onset: a CT study.

The development of infratentorial atrophy in six patients suffering from idiopathic cerebellar ataxia of late onset was studied by a retrospective evaluation of consecutive computed tomography (CT) scans. Four patients had evidence of olivopontocerebellar atrophy (OPCA) both on clinical testing and magnetic resonance imaging (MRI). In these four patients, atrophy of the cerebellum and brain stem became visible at the same time and progressed in a roughly parallel manner, whereas in the remaining two the brain stem was left intact. In all patients with OPCA, definite brain-stem atrophy was visible earlier than the appearance of non-cerebellar clinical symptoms. The present data suggest that CT investigations at regular intervals may be of prognostic value in cerebellar ataxias.

Adult↗

PubMed1991

Brain stem atrophy in Joseph disease: a morphometric study using two-dimensional (area) measurement by computed tomography.

Eight Japanese patients with Joseph disease were studied using computed tomography (CT). Morphometric analysis using the two-dimensional (area) measurement by CT was performed in the infratentorial region. The brain-stem index, an index of brain-stem atrophy or pontine atrophy, revealed a significant decrease (P less than 0.01), with a mean of 66.7% when compared with 16 control subjects. The patients showed a significant increase (P less than 0.01), with a mean of three times that of the controls in the fourth ventricular index, an index of fourth ventricular dilatation. There were no differences in the cerebellar index, an index of cerebellar atrophy, between these patients and the controls, although the patients had an increased number of visible cerebellar vermian (2.0, SD 0.7) and hemispheric sulci (2.6 SD 0.6) as compared with the controls (vermian sulci: 0.4, SD 0.7: hemispheric sulci: 0). These data indicate severe pontine atrophy, fourth ventricular dilatation with mild involvement of the cerebellum and correlate well with the common pathological features of Joseph disease. The present morphometric evaluation by CT may be useful in the clinical diagnosis of Joseph disease.

Adult↗

PubMed1984

Atrophy of sacrospinal muscle groups in patients with chronic, diffusely radiating lumbar back pain.

After surgery necessitated by lumbar back pain syndromes, radiolucency verified by CT may appear in the sacrospinal muscle group on the operated side. This radiolucency represents muscular atrophy and is in its most severe form a result of the replacement of muscle tissue with adipose tissue. Such muscular atrophy appeared in the present series in 31 out of all 156 patients (19.9%) and in 29 out of 94 patients operated on because of radiating lumbar back pain (30.9%). The radiological appearance, extent, and HU values of this muscular atrophy are presented in detail. Only weak correlations with the multitude of clinical symptoms and signs were found in this retrospective study. The effects of irreversible muscular atrophy on the indications for surgery and physiotherapy are discussed.

Adipose Tissue↗