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Results for “Atrophy”

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At least 1,621 records · Page 90Linked to original sources

PubMed2006

Accurate quantification methods to evaluate cervical cord atrophy in multiple sclerosis patients.

OBJECT: Automatic accurate measurement techniques are needed to increase reproducibility in the quantification of cervical cord area (CCA) with magnetic resonance (MR) imaging in the assessment of central nervous system (CNS) atrophy in multiple sclerosis (MS) patients. MATERIALS AND METHODS: Two segmentation methods were implemented: (1) spatial mean brightness level estimation (SMBLE), and (2) partial-volume modeling (PVM). These were evaluated with the inclusion of spinal cord inclination and/or partial-volume-effect corrections. An averaged manually segmented set was considered as reference. Thirty MR studies were used to compare the different methods. A set of 15 MS patients and 15 control subjects within a two-year longitudinal study were used to evaluate cord atrophy with the best method. Statistical evaluation was made by using an intraclass correlation coefficient and Bland-Altman comparisons. RESULTS: Partial-volume modeling with spinal cord inclination correction and partial-volume spinal-cord contour contribution estimation was the most accurate method. The longitudinal test showed a 4% decrease in CCA in MS patients with no significant reduction in control subjects. CONCLUSION: The automatic PVM cord-segmentation approach, taking into consideration the spinal-cord inclination and partial-volume treatment, provides reproducibility and increased accuracy in the evaluation of cord atrophy, allowing the monitoring of changes in MS patients.

Adolescent↗

PubMed2005

Gastric pit cell hyperplasia and glandular atrophy in carbonic anhydrase IX knockout mice: studies on two strains C57/BL6 and BALB/C.

Carbonic anhydrase (CA) isoenzyme IX is a hypoxia-inducible enzyme, which is expressed in the human and rodent gastrointestinal tract and overexpressed in several different tumors. Functionally, it has probably an effect on proliferation and differentiation of gastrointestinal epithelial cells. It may also participate in gastric morphogenesis, since a recent study has shown gastric pit cell hyperplasia and glandular atrophy in CA IX-knockout mice. However, it is not known whether CA IX produces morphological changes in the gastric mucosa, which can turn into a dysplasia or malignancy in the presence of some carcinogenic factors. High-salt diet is considered such a factor which has been shown to modulate Helicobacter pylori-associated carcinogenesis. We produced two strains of CA IX-knockout mice, C57/BL6 and BALB/c, and the mice ate either standard or high-salt feed for 20 weeks. Stomach samples were collected from 40 Car 9(-/-) knockout mice and 37 wildtype littermates, and the tissue sections were examined for histology. CA IX-deficiency caused gastric pit cell hyperplasia and glandular atrophy in both BALB/c and C57/BL6 strains. Excess dietary salt had no significant effect on the severity of pit cell hyperplasia. No dysplasia was found in any of the groups. In C57/BL6 mice, CA IX-deficiency was associated with gastric submucosal inflammation. The results indicate that CA IX-deficiency provides a useful model to study the mechanisms of gastric morphogenesis and epithelial integrity. Further studies are needed to see whether CA IX has a role in the regulation of immune response. The findings suggest that although CA IX-deficiency is not a tumor-promoting factor per se, it induces glandular atrophy in the body mucosa, a lesion which is considered to be a preneoplastic alteration in the stomach.

Animals↗

PubMed1997

Effect of atrophy and contractions on myogenin mRNA concentration in chick and rat myoblast omega muscle cells.

The skeletal rat myoblast omega (RMo) cell line forms myotubes that exhibit spontaneous contractions under appropriate conditions in culture. We examined if the RMo cells would provide a model for studying atrophy and muscle contraction. To better understand how to obtain contractile cultures, we examined levels of contraction under different growing conditions. The proliferation medium and density of plating affected the subsequent proportion of spontaneously contracting myotubes. Using a ribonuclease protection assay, we found that exponentially growing RMo myoblasts contained no detectable myogenin or herculin mRNA, while differentiating myoblasts contained high levels of myogenin mRNA but no herculin mRNA. There was no increase in myogenin mRNA concentration in either primary chick or RMo myotubes whose contractions were inhibited by depolarizing concentrations of potassium (K+). Thus, altered myogenin mRNA concentrations are not involved in atrophy of chick myotubes. Depolarizing concentrations of potassium inhibited spontaneous contractions in both RMo cultures and primary chick myotube cultures. However, we found that the myosin concentration of 6-d-old contracting RMo cells fed medium plus AraC was 11 +/- 3 micrograms myosin/microgram DNA, not significantly different from 12 +/- 4 micrograms myosin/microgram DNA (n = 3), the myosin concentration of noncontracting RMo cells (treated with 12 mM K+ for 6 d). Resolving how RMo cells maintained their myosin content when contraction is inhibited may be important for understanding atrophy.

Animals↗

PubMed1977

Progressive bilateral essential iris atrophy.

Bilateral progressive essential iris atrophy, more advanced in one eye than in the other, occurred in a 24-year-old white man. Histopathologic examination of the iris from the eye with the more advanced iris atrophy disclosed no vascular abnormalities in that the vessels were patent and appeared normal except for accumulated perivascular connective tissue. Fluorescein angiographic examination of the fellow eye that was undergoing the earliest changes of iris atrophy failed to reveal any vascular abnormalities. However, tonographic examination indicated a markedly decreased outflow facility. There does not appear to be any vascular abnormality involved in the pathogenesis.

Adult↗

PubMed1978

The corneal endothelium and the spectrum of essential iris atrophy.

We found that the spectrum of essential iris atrophy (progressive essential iris atrophy, Chandler's syndrome, and the Cogan-Reese syndrome) began as a corneal endothelial degeneration, which, with ectopic endothelial membrane overgrowth over an open angle, followed by contraction of this membrane and further growth onto the iris, accounted for all aspects of the syndrome. The contractile membrane caused the synechiae, the glaucoma, the corectopia, the ectropion uveae, the occasional iris nodules, and the iris atrophy. Thus we found this disease to be primarily of the cornea, and only secondarily of the iris. The results of this study led us to propose a new designation for this spectrum: primary proliferative endothelial degeneration.

Adult↗

PubMed1979

Hereditary pigmented paravenous retinochoroidal atrophy.

A father and son with pigmented paravenous retinochoroidal atrophy demonstrated the classical fundus appearance of bilateral sharply circumscribed patches of retinochoroidal atrophy and pigmentation along the retinal veins. Our patients, and the preponderance of males in previously reported cases of this disease, suggest the possibility of Y-chromosome mediated male-to-male transmission. Electrophysiologic findings in our patients included elevated dark-adaptation thresholds, slightly reduced electroretinographic amplitudes, slightly prolonged a- and b-wave implicit times, and (in Case 1) abnormal electro-oculographic ratios. These findings indicate a diffuse tapetoretinal degeneration, and suggest that pigmented paravenous retinochoroidal atrophy is another incomplete form of retinitis pigmentosa.

Adolescent↗

PubMed1989

Primary sclerosing cholangitis associated with liver atrophy.

Of 27 patients with primary sclerosing cholangitis, 4 were found on investigation and subsequently at operation to have gross lobar atrophy. The disease was particularly severe in the hilar region. Three of the four patients were asymptomatic prior to the onset of jaundice. The presence of atrophy precipitated laparotomy to exclude cancer in two cases. Marked disparity in size between liver lobes precluded a hilar approach to relieve extrahepatic obstruction in two patients. Prolonged follow-up excluded coincident malignant disease. Selective liver atrophy should be considered part of the disease spectrum in primary sclerosing cholangitis.

Adolescent↗

PubMed1989

Nonoperative approach to hilar cancer determined by the atrophy-hypertrophy complex.

Twenty-seven of 135 patients with malignant hilar stricture who had associated liver atrophy or hypertrophy or both were treated by the percutaneous insertion of an endoprosthesis in the hypertrophied lobe only. The procedure was successful in 25 patients. Three patients died within 30 days of drainage. Procedure-related nonfatal complications occurred in seven patients. Effective decompression was accomplished in 21 patients, with complete relief of jaundice in 15. Late complications were experienced by 10 patients. The median total hospital stay was 22 days. Thirteen patients survived from 6 weeks to 12 months (median 5 months), 8 were alive from 3 to 18 months (median 8 months), and 1 patient was lost to follow-up. On the available evidence, we suggest that the preoperative demonstration of the atrophy-hypertrophy complex in jaundiced patients with irresectable hilar cancer is an indication for nonoperative therapy. Patients without the atrophy-hypertrophy complex and those with the complex but associated nonneoplastic disease are likely to fare better with surgical decompression and direct mucosa-to-mucosa anastomosis.

Adenoma, Bile Duct↗

PubMed1996

Deltamethrin-induced thymus atrophy in male Balb/c mice.

The action of deltamethrin, a potent type II synthetic pyrethroid insecticide, on the thymus of the Balb/c mouse was studied in vivo and in vitro. We found that deltamethrin produced atrophy in the thymus in a dose- and time-dependent fashion. The lowest effective dose was found to be 6 mg/kg, 24 hr after a single intraperitoneal treatment. Treated animals did not recover during the time-course of the experiment (365 days after treatment); however, deltamethrin did not affect the body weight of the treated animals during the course of the study. To determine if deltamethrin-induced [Ca2+]i signaling could lead to thymic atrophy via programmed cell death, mice were treated with 25 mg deltamethrin/kg for 24 hr or the isolated thymocyte suspension was treated with 50 microM deltamethrin. A significant stimulation of inositol 1,4,5-triphosphate (IP3) and inositol 1,4-diphosphate (IP2) production was found after 24 hr of deltamethrin-1R (active isomer) treatment. An inactive stereoisomer of deltamethrin (i.e. 1S) did not cause a significant rise in the production of 1P3 and 1P2. In addition, deltamethrin-1R induced a transient increase of [Ca2+]i mobilization in the thymocyte suspension after 10 min of in vitro treatment, and substantially reduced the rate of calcium-calmodulin (Ca/CaM)-dependent protein dephosphorylation in in vivo treated animals (25 mg deltamethrin/kg for 24 hr). The in vivo effects of deltamethrin treatment demonstrated induction of DNA fragmentation and cell death in thymocytes. Moreover, using a histochemical approach, it was evident that deltamethrin at 25 mg/kg was able to produce cell death in the thymus of treated animals 72 hr after treatment. In the present work, we found that cell death was apoptotic in nature as noted first by the inhibition of deltamethrin-induced cell death by aurintricarboxylic acid, an inhibitor of apoptosis, and second, by internucleosomal DNA fragmentation, a hallmark of apoptosis, produced by deltamethrin in treated animals as well in thymocyte suspensions. In addition, the involvement of the Ca/CaM-dependent protein phosphorylation-dephosphorylation cascade in the induction of apoptosis by deltamethrin was supported by the protective role of the calmodulin inhibitor trifluoperazine against the apoptotic effect of deltamethrin on thymocyte suspension. Our results suggest that deltamethrin induced thymus atrophy and altered the Ca/CaM-dependent protein kinase-phosphatase cascade, which might induce programmed cell death.

Animals↗

PubMed1985

Muscle atrophy and histopathology of the soleus in 6-mercaptopurine-treated rats.

This study was conducted to examine the histochemical changes occurring due to neonatal 6-mercaptopurine (6-MP) treatment (2 mg/kg, sc, between 2 and 22 days after birth) in the slow-twitch muscle (soleus) of adult male and female rats. At 6 months of age, the control and the 6-MP-treated rats were evaluated for the sciatic nerve conduction to the soleus and for the soleus atrophy and histopathology of the type I (slow-twitch) and type II (fast-twitch) muscle fibers. Compared to the normal controls, the 6-MP-treated male and female rats showed similar sciatic nerve conduction to the soleus. However, there was a significant muscle atrophy (57-60%, P less than 0.01) and a decrease in fiber areas of the type I (42-54%, P less than 0.05) and type II (41-71%, P less than 0.01) fibers. The number of type II fibers declined significantly (7.4-14.8%, P less than 0.05). It is proposed that the soleus muscle atrophy and histopathology in 6-MP-treated rats is unrelated to nerve conduction defects and may be related to growth inhibition caused by an interference of the drug during normal differentiation of muscle fibers.

Adenosine Triphosphatases↗

PubMed1994

Hydroxyl radical generation in skeletal muscle atrophied by immobilization.

Male Wistar rats (15 weeks old), the ankle joints of one hindlimb of which were immobilized in the extended position for 12 days, were injected with salicylate as a trapping agent for hydroxyl radicals before sacrifice. Atrophied and contralateral soleus, typical slow red muscles were collected and their levels of 2,3-dihydroxybenzoic acid (2,3-DHB), one of the main reaction products formed by the attack of hydroxyl radical on salicylate, were determined using high-performance liquid chromatography with an electrochemical detector. There was a significant increase in 2,3-DHB in the atrophied muscle. This result strongly suggests the enhanced generation in vivo of hydroxyl radicals in atrophied muscle.

Animals↗

PubMed1979

Residual alveolar ridge atrophy: classification and influence of facial morphology.

A method for grading residual alveolar ridge atrophies of edentulous maxillae and mandible has been devised for men and women. Comparisons were made in women and in men between the degree of atrophy and the vertical facial morphology. The study suggests some relationship between the total facial height (TFH), the vertical facial type determined by the Frankfort horizontal mandibular plan (FMA), and the atrophy of the alveolar ridges, especially for the mandible. Certain practical applications of these findings were suggested.

Adolescent↗

PubMed1975

The CSF lipid content in brain atrophy.

Significantly low CSF values for cholesterol and total lipids were found in a group of patients with brain atrophy in comparison with a control group. It is possible that these changes are a function of reduced brain mass or of defect in brain lipid metabolism in brain atrophy patients. Further metabolic studies are required to clarify the biochemical aspects of brain atrophy.

Adult↗

PubMed1978

Disuse atrophy of skeletal muscle. A morphometric study using image analysis.

A morphometric study of disuse atrophy was done on the rat anterior tibilalis muscle over a 13-day period after immobilization of the hind leg by pinning the knee and ankle joints. Cross-sectional areas of individual muscle fibers were measured using image analysis, a new and precise technique. Three types of muscle fibers, light, medium and dark, were defined using a modified myosin-ATPase reaction on cryostat-cut sections. Each of the 3 fiber types was found to show a degree and time course of atrophy unique to itself. At the 0.01 confidence level, the dark fibers (with strongest ATPase reaction) did not shrink significantly. Both the light (ATPase negative) and medium fiber did show significant atrophy at that level; the light shrinking more than the medium. Simple visualization of the light microscopic images was often found to be misleading. Thus, the need was documented for a precise technique for analysis of fiber size distribution.

Animals↗

PubMed1978

Autosomal dominant spinal muscular atrophy: a clinical and genetic study.

A clinical and genetic study of 6 kindreds (13 patients) with autosomal dominant spinal muscular atrophy is presented. Evidence is presented to indicate that two separate autosomal dominant genes are involved. One of these causes clinical disease with onset in early childhood (birth--8 years), which is relatively benign and in which proximal selectively of muscle involvement is not marked. A separate autosomal dominant gene causes a disease with onset in adult life (median age 37 years), showing marked initial proximal selectively; this disease may be more rapid in its clinical progression. Penetrance of both genes approaches 100%. Incidence figures are presented; less than 2% of all cases of childhood onset spinal muscular atrophy, but 30% of adult onset cases, are due to an autosomal dominant gene transmitted from an affected parent. Implications for prognosis, diagnosis and genetic counselling are discussed. A review of 11 kindreds of dominant spinal muscular atrophy in the literature is presented.

Adolescent↗

PubMed1978

Hereditary optic atrophy with probable association with a specific HLA haplotype.

A family with hereditary optic atrophy in 4 members of 3 generations is described. The clinical findings differ from those previously observed in hereditary optic atrophy and in Leber's disease, indicating that the hereditary optic atrophy described in this report represents a new disease entity, which is inherited in an autosomal, dominant way with incomplete penetrance. Analyses of the cerebrospinal fluid and serum did not reveal signs of immunoglobulin synthesis within the central nervous system, i.e. findings encountered in a considerable proportion of patients with optic neuritis. An association was found between the family members affected by the disease and the major histocompatibility system haplotype A2 B8. A linkage thus occurred between the disease and the HLA region on human chromosome No. 6.

Adolescent↗

PubMed1981

A quantitative study of cerebral atrophy in old age and senile dementia.

Cerebral atrophy was measured by comparing brain volume and cranial capacity at necropsy on 20 severely demented patients aged 64--92 years and 18 non-demented controls of similar age. The volumes of cerebral cortex and white matter and of the lobes of the cerebral hemispheres were found by point-counting morphometry. Patients with Alzheimer type dementia aged less than 80 years mainly showed pathological cerebral atrophy with global loss of cerebral tissue (P less than 0.001) whereas over 80 years of age they generally showed selective atrophy of temporal cortex (P less than 0.005). The findings support the view that disease processes, not exaggerated age change, underlie primary neuronal dementia of Alzheimer type.

Age Factors↗

PubMed1988

Histological investigations of muscle atrophy and end plates in two critically ill patients with generalized weakness.

We describe pathological alterations at the light microscopical and ultrastructural level of motor end plates and muscle fibres in 2 critically ill patients with generalized muscular atrophy and weakness. Axonal degeneration of intramuscular nerve fibres was not conspicuous. The sural nerve in one patient showed only minor abnormalities. There was a marked atrophy of type 1 and especially type 2 muscle fibres. Nodal and ultraterminal nerve sprouts were seen in both biopsies. Motor end plates showed features of regeneration. They were enlarged in one patient. This patient was treated for a prolonged period with vecuronium bromide. Pharmacological denervation may explain the presence of fibrillation potentials, and, partially, of the histological abnormalities. Another factor which must be considered is inhibition of neuromuscular transmission by antibiotics. In addition to disuse atrophy and a minor degree of axonal neuropathy, the production of muscle proteolytic factors may be involved in the rapidly occurring massive loss of muscle fibre size in critically ill patients.

Atrophy↗