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PubMed1998

Correlation of the peripapillary atrophy area with optic disc cupping and disc hemorrhage.

PURPOSE: To investigate the association of the peripapillary atrophy area with disc cupping area and disc hemorrhage in subjects who underwent ocular examination as part of a routine physical examination. METHODS: We reviewed plain color fundus photographs taken of 12,140 eyes of 6,070 subjects as part of a routine health examination. The refractive error in these eyes was not known. Using a computerized image analysis system, we measured the area of peripapillary atrophy (zone beta), the optic disc, and optic disc cupping by means of planimetry in 8,842 eyes of 4,421 subjects with fundus images of good quality. RESULTS: The ratio of cup area to disc area was significantly greater in eyes with peripapillary atrophy (0.36 + 0.09) than in eyes without peripapillary atrophy (0.34 + 0.07), and the ratio of peripapillary atrophy area to disc area was significantly greater in eyes with disc hemorrhage (0.26 + 0.34) than in those without disc hemorrhage (0.09 + 0.18). Moreover, in eyes with peripapillary atrophy, the ratio of cup area to disc area was significantly larger in eyes with disc hemorrhage (0.48 + 0.08) than in those without disc hemorrhage (0.36 + 0.09). These results remained statistically unchanged even after "glaucomatous" eyes were excluded from the study. CONCLUSION: Peripapillary atrophy appears to be associated with a higher degree of cupping of the optic disc and disc hemorrhage, and the results suggest an association between peripapillary atrophy and glaucomatous optic neuropathy.

Female↗

PubMed1995

Frontal lobe degeneration of non-Alzheimer type and Pick's atrophy: lumping or splitting?

We report six cases of presenile (five) and senile (one) progressive dementia with a mild-to-marked frontal or frontotemporal atrophy and ventricular dilation (Frontal Lobe Degeneration [FLD]). The most prominent microscopic features were layer-dependent neuronal depletion of the cortex, spongiosis, and cortical and subcortical gliosis. Five cases showed additional degeneration of the S. nigra, and two also had motor neuron disease. Despite the absence of Pick cells and bodies, such cases have many features in common with Pick atrophy. Because Pick cells and bodies are inconstantly occurring features in otherwise typical cases of Pick atrophy, they cannot be regarded as inevitable markers of the latter. In our opinion, cases with mild frontal or frontotemporal atrophy as described herein and by others match the grades 1 and 2 in terms of Schneider's classification of Pick atrophy [37]. As long as the etiology of both Pick atrophy and the so-called FLD is unknown, and we finally have to follow morphological criteria for classification, there is apparently no convincing reason to introduce a separate category, such as FLD or FTA, for the cases with moderate or mild frontal atrophy and dementia of frontal lobe type, which can be sufficiently classified with the Pick spectrum of lobar atrophy.

Adult↗

PubMed2006

Endoscopic markers of villous atrophy are not useful for the detection of celiac disease in patients with dyspeptic symptoms.

BACKGROUND AND STUDY AIMS: Celiac disease can manifest with nonspecific symptoms, including functional gastrointestinal disorders such as dyspepsia. The aim of our study was to assess the usefulness of duodenal endoscopic markers of villous atrophy for the selection of dyspeptic patients for histological assessment. PATIENTS AND METHODS: Esophagogastroduodenoscopy was performed in dyspeptic patients, in patients considered to be at risk of having celiac disease, and in healthy controls. At least three duodenal biopsies were performed for histological assessment of villous atrophy in all patients and controls. We looked for the following four duodenal endoscopic markers of celiac disease: reduction in the number of folds, scalloping of folds, mosaic-pattern mucosa, and nodular mucosa. RESULTS: A total of 175 people were enrolled (75 patients with dyspepsia; 75 patients who were "at risk" of having celiac disease; and 25 healthy volunteers, or "controls"). Of the dyspeptic patients, four had endoscopic markers of celiac disease with no histologically confirmed villous atrophy, while one patient without endoscopic markers was found to have Marsh type I villous atrophy. Of the patients at risk of having celiac disease, 16 had at least one endoscopic marker and 10/16 were found to have histological villous atrophy. In this group, the sensitivity and specificity of the endoscopic markers were 100 % and 90.8 % respectively. "At-risk" patients with two or more endoscopic markers all had histologically confirmed villous atrophy. Neither endoscopic markers nor villous atrophy were found in any of the control patients. CONCLUSIONS: Additional endoscopic markers are valuable for diagnosis in patients with clinical symptoms suggestive of celiac disease. In contrast, endoscopic markers of villous atrophy are not useful for selecting a subgroup of dyspeptic patients for screening for celiac disease by duodenal histological assessment. These patients should be screened using other protocols.

Adolescent↗

PubMed2003

Prevention of muscle disuse atrophy by low-frequency electrical stimulation in rats.

When muscles lose neural drive, they atrophy rapidly. Neuromuscular electrical stimulation (NMS) has been used in attempts to prevent or reverse the atrophy, but optimal stimulation programs and parameters are not well defined. In this study, we investigated the effects of four different stimulation patterns on disuse atrophy produced in the tibialis anterior, lateral gastrocnemius, and soleus muscles of rats paralyzed with tetrodotoxin for seven days. Stimulation paradigms differed from one another by their stimulation frequency (2 or 10 pulses/s) and by their stimulation period (2 or 10 h a day). Results showed that stimulation with 2 pulses/s, paradigms were more effective at preventing disuse muscle atrophy than higher-frequency stimulation. The most marked difference was in the slow soleus muscle, which had only 10% mean atrophy when stimulated at 2 pulses/s for 10 h, compared to 26% atrophy when stimulated at 10 pulses/s for either 2 or 10 h and 32% atrophy in unstimulated, paralyzed controls. The level of atrophic change was not correlated with the levels of serum creatine kinase, used as an index of muscle damage. Results suggest that remediation of disuse atrophy may be accomplished using unphysiologically low rates of motor-unit activation despite the relatively low force produced by such unfused contractions. This may have significant implications for the design of therapies for muscle paralysis consequent to upper-motoneuron lesions.

Adaptation, Physiological↗

PubMed2005

Interleukin-2 gene polymorphisms associated with increased risk of gastric atrophy from Helicobacter pylori infection.

BACKGROUND: Gastric atrophy induced by Helicobacter pylori is thought to predispose patients to noncardiac gastric cancer development. However, the host genetic factors that influence the progression of gastric atrophy have not been elucidated. In this study, we examined the effects of cytokine polymorphisms on H. pylori-induced gastric atrophy. METHODS: Blood samples were taken from 454 Japanese subjects. The interleukin-2 (IL-2; T-330G), IL-4 (C-33T), and IL-13 (C-1111T) polymorphisms were genotyped by polymerase chain reaction with confronting two-pair primers (PCR-CTPP). Anti-H. pylori IgG antibody and pepsinogen I and II were measured to diagnose H. pylori infection and atrophic gastritis. RESULTS: The odds ratios (ORs) for the association between IL-2 polymorphism [OR = 2.78, 95% CI (confidence interval) = 1.26-6.17 (T/T to G/G)] or IL-4 polymorphism [OR = 2.22, 95% CI = 1.01-4.89 (T/C to C/C)] were increased significantly with gastric atrophy, whereas the corresponding OR of IL-13 polymorphism was decreased with gastric atrophy [OR = 0.61, 95% CI = 0.39-0.96 (C/T and T/T to C/C)]. There were no significant H. pylori seropositivity-related differences between these polymorphisms. We examined the relationship between these polymorphisms and gastric atrophy separately in H. pylori-seropositive and -seronegative groups. In the H. pylori-seropositive group, the IL-2 T/T (OR = 2.78, 95% CI = 1.12-6.93) had a significant association with gastric atrophy. CONCLUSIONS: These results reveal that the IL-2 gene polymorphism is associated with an increased risk of gastric atrophy induced by H. pylori infection and might predispose to gastric cancer.

Adult↗

PubMed1999

Gastric cellular turnover and the development of atrophy after 31 years of follow-up: a case-control study.

OBJECTIVE: Why only some patients colonized with Helicobacter pylori (H. pylori) develop atrophy, a preneoplastic change, is not known. Because gastric mucosal mass is dependent upon a balance between epithelial proliferation and turnover, we hypothesized that atrophy may develop due to increased apoptosis relative to proliferation. METHODS: Gastric epithelial apoptosis was measured by terminal deoxyuridine nucleotide nick end labeling (TUNEL) assay and proliferation by Ki-67 immunohistochemistry in gastric corpus biopsies in a unique cohort of patients followed for 31 yr (1952-1983). Sixteen patients who developed atrophy over this time were selected (cases), with two matched controls, who did not develop atrophy, for each. Apoptosis and proliferation were measured in the corpus biopsies taken in 1952. RESULTS: Cases (N = 16) and controls (N = 32) were well matched for age, sex, initial histology, and severity of H. pylori infection. In the initial (1952) biopsies, 4.3 +/- 1.7 cells (mean +/- SEM) per gland were Ki-67-positive in the cases, compared with 2.1 +/- 0.4 in controls (p = 0.48). 9.2 +/- 2.3 cells per gland were terminal deoxyuridine nucleotide nick end labeling-positive in cases, compared with 6.3 +/- 0.8 in controls (p = 0.29). Proliferation to apoptosis ratios were similar in both groups (cases, 0.38 +/- 0.16; controls 0.39 +/- 0.08, p = 0.37). CONCLUSIONS: Patients who later developed atrophy, initially had mildly (but not statistically significant) increased gastric epithelial cell proliferation and apoptosis, compared with those patients who did not develop atrophy, suggesting increased cellular turnover in the atrophy group. However, in these patients with gastritis, the ratio of apoptosis to proliferation was not a determinant of risk for development of atrophy decades later.

Adolescent↗

PubMedDate not supplied

Glucocorticoid-induced muscle atrophy: mechanisms and therapeutic strategies.

OBJECTIVE: To analyze the mechanisms of action of glucocorticoids in causing muscle atrophy and to examine the therapeutic effect of testosterone as well as other treatment modalities in counteracting this adverse effect. METHODS: We reviewed selected publications to analyze the mechanisms of glucocorticoid-induced muscle atrophy in animal models and in humans. The pathophysiologic features of glucocorticoid-induced hypogonadism and the possible relationship to the muscle atrophy in patients receiving glucocorticoids were assessed. The beneficial effects of testosterone on the muscles of hypogonadal and eugonadal men were also reviewed. Other measures such as exercise and glutamine and their possible therapeutic and preventive effects were examined in the context of hypercortisolemia. RESULTS: Glucocorticoids induce rapid muscle breakdown and proximal muscle atrophy. The mechanism of glucocorticoid-induced muscle atrophy relies on the degradation of the myosin heavy chain (catabolic effect), the most important contractile protein in muscle, associated with a decrease of its synthesis (antianabolic effect). One of the contributing factors in the development of muscle atrophy is hypogonadism that is induced by long-term glucocorticoid use. Androgen possesses anabolic and anticatabolic effects in vitro and in animal models. Androgens can be used safely to counteract the catabolic effects of cortisol. Other measures such as exercise, glutamine, and alanyl-glutamine are promising in animal models of glucocorticoid-induced muscle atrophy. CONCLUSION: This study suggests the possible efficacy of testosterone and glutamine on glucocorticoid-induced muscle atrophy. Testosterone and glutamine are natural biologic products with safe pharmacologic profiles, and their bioefficacy merits active research in humans.

Journal Article↗

PubMed1994

Cerebellar atrophy in patients with long-term phenytoin exposure and epilepsy.

OBJECTIVE: Cerebellar atrophy has been noted in patients with phenytoin exposure. This finding has been attributed by some investigators to seizures, but by others to phenytoin. Previous studies included patients with mental retardation and convulsive seizures. We undertook a study in a group of nonretarded patients with partial epilepsy to better elucidate the cause of the cerebellar atrophy. DESIGN: Case control study. SETTING: Referral population from an epilepsy center. PATIENTS: Thirty-six patients with partial epilepsy and long-term phenytoin exposure were selected from a consecutive sample of admissions to an epilepsy center. Patients with histories of ethanol abuse, perinatal distress, anoxia, status epilepticus, or neurodegenerative disorders were excluded. Age- and sex-matched controls were selected from a pool of healthy volunteers and patients who had undergone magnetic resonance imaging for complaints of headache and dizziness. INTERVENTIONS: All patients and controls underwent magnetic resonance imaging. MAIN OUTCOME MEASURE: Degree of cerebellar atrophy. RESULTS: The magnetic resonance imaging scans were reviewed in a blind fashion. A rating was assigned to each scan based on the degree of cerebellar atrophy. Cerebellar atrophy was significantly more pronounced in patients than in controls. No correlation was found between cerebellar atrophy and variables reflective of seizure severity or degree of phenytoin exposure. CONCLUSIONS: Cerebellar atrophy may be seen in phenytoin-exposed patients with epilepsy in the absence of generalized tonic-clonic seizures or preexistent brain damage. Whether it is the phenytoin or the seizures that play the primary etiologic role remains unanswered. These factors may be synergistic.

Adult↗

PubMed1996

Atrophy of the corpus callosum associated with cognitive impairment and widespread cortical hypometabolism in carotid artery occlusive disease.

OBJECTIVE: To investigate whether atrophy of the corpus callosum is associated with cognitive impairment and widespread cerebral cortical hypometabolism in carotid artery occlusive disease. PATIENTS: Twelve patients with unilateral internal carotid artery occlusive disease (1 with severe stenosis and 11 with occlusion) and no cortical infarction in the chronic stage (mean +/- SD age, 64 +/- 5 years). MAIN OUTCOME MEASURES: Midsagittal corpus callosum area-skull area ratio (on T1-weighted magnetic resonance images), the sum of the scaled scores of the 6 subtests on the Wechsler Adult Intelligence Scale-Revised (Digit Span, Arithmetic, Picture Arrangement, Object Assembly, Block Design, and Digit Symbol), and cerebral metabolic rate of oxygen (measured with position emission tomography by using the oxygen 15 steady-state technique). RESULTS: The degree of cognitive impairment varied but was strongly correlated with the severity of callosal atrophy (r = 0.92, P < .001). Patients with callosal atrophy and cognitive decline also showed decreased oxygen consumption in the bilateral cerebral cortices. Stepwise regression analysis revealed that the severity of white matter lesions, especially in the centrum semiovale, and that of cortical atrophy in the hemisphere with arterial disease were 2 important factors for callosal atrophy. CONCLUSIONS: Callosal atrophy is associated with cognitive impairment and widespread cerebral cortical hypometabolism in carotid artery occlusive disease without cortical infarction. Callosal atrophy might reflect the severity of the disconnection between cortical regions, and this may be an important factor in the development of cognitive impairment with widespread cortical hypometabolism in carotid artery occlusive disease without large cortical lesions.

Aged↗

PubMed2002

Progression of corpus callosum atrophy in Alzheimer disease.

BACKGROUND: Atrophy of the corpus callosum in the absence of primary white matter degeneration reflects loss of intracortical projecting neocortical pyramidal neurons in Alzheimer disease (AD). OBJECTIVES: To determine individual rates of atrophy progression of the corpus callosum in patients with AD and to correlate rates of atrophy progression with clinical disease severity and subcortical disease. METHODS: Magnetic resonance imaging-derived measurements of corpus callosum size were studied longitudinally in 21 patients clinically diagnosed as having AD (mean observation time, 17.0 +/- 8.5 months) and 10 age- and sex-matched healthy controls (mean observation time, 24.1 +/- 6.8 months). RESULTS: Corpus callosum size was significantly reduced in AD patients at baseline. Annual rates of atrophy of total corpus callosum, splenium, and rostrum were significantly larger in AD patients (-7.7%, -12.1%, and -7.3%, respectively) than in controls (-0.9%, -1.5%, and 0.6%, respectively). Rates of atrophy of the corpus callosum splenium were correlated with progression of dementia severity in AD patients (rho = 0.52, P<.02). The load of subcortical lesions at baseline (P<.05) predicted rate of anterior corpus callosum atrophy in healthy controls. Rates of atrophy of corpus callosum areas were independent of white matter hyperintensity load in patients with AD. CONCLUSIONS: Measurement of corpus callosum size allows in vivo mapping of neocortical neurodegeneration in AD over a wide range of clinical dementia severities and may be used as a surrogate marker for evaluation of drug efficacy.

Aged↗

PubMed2003

Cinguloparietal atrophy distinguishes Alzheimer disease from semantic dementia.

BACKGROUND: Progressive brain atrophy is associated with Alzheimer disease (AD) and other dementias. Regional differences in brain atrophy may reflect clinical features of disease. OBJECTIVE: To identify regions of cerebral atrophy that are associated with AD vs other dementias. SETTING: University hospital dementia clinic. PARTICIPANTS: Eleven patients with AD and 11 with semantic dementia (SD), matched for age, sex, education, and degree of overall cognitive impairment and 15 normal controls. METHODS: Voxel-based morphometry was used to compare patterns of gray matter loss, measured on T1-weighted magnetic resonance images, between patients with AD or SD, a subtype of frontotemporal lobar degeneration, and controls. Statistically significant differences in regional gray matter concentration, after multiple-comparisons correction, between groups of subjects were identified. RESULTS: Patients with AD were more impaired than those with SD on tests of visuospatial function and on simple calculations. Consistent with these neuropsychological deficits, the most significant area of atrophy in the AD group was the left parietal cortex vs controls (z = 5.0; P =.04). Compared with SD, AD was associated with more atrophy in the left parietal lobe (z = 5.6; P =.04) and bilaterally in the posterior cingulate/precuneus (z = 5.1; P =.04). A discriminant function analysis demonstrated that the degree of atrophy of right posterior cingulate, left parietal lobe, right amygdala, and right anterior temporal lobe structures correctly classified 96% of the patients. CONCLUSION: Alzheimer disease is associated with a specific pattern of cortical atrophy compared with SD.

Aged↗

PubMed2005

Different patterns of magnetic resonance imaging atrophy for frontotemporal lobar degeneration syndromes.

BACKGROUND: Frontotemporal lobar degeneration (FTLD) is an uncommon degenerative dementia that presents with focal cognitive and behavioral deficits. OBJECTIVE: To determine the correlation of the different presentations of FTLD with structural neuroimaging findings. DESIGN AND PATIENTS: In a blinded study, we retrospectively evaluated the clinical presentations and magnetic resonance imaging (MRI) patterns of atrophy in 59 patients with FTLD and 26 patients with probable Alzheimer disease at a memory disorders clinic. RESULTS: Analysis of variance revealed a significant difference in the patterns of atrophy in the FTLD and Alzheimer disease groups. Patients with FTLD presenting with altered personal conduct had significant bifrontal atrophy, whereas patients presenting with semantic dementia had significant left temporal and bifrontal atrophy compared with other groups. Disinhibited behavior and hyperphagia correlated with right frontal atrophy, and fluent, anomic aphasia correlated with left temporal atrophy. CONCLUSIONS: We found that the type of clinical presentation of FTLD correlates with specific areas of atrophy. Our method of analysis may be useful to elicit further anatomic-behavioral relationships in degenerative brain disorders.

Aged↗

PubMed1997

Parapapillary chorioretinal atrophy in patients with ocular hypertension. I. An evaluation as a predictive factor for the development of glaucomatous damage.

OBJECTIVE: To determine whether parapapillary chorioretinal atrophy is a risk factor for the development of glaucomatous optic disc or visual field damage. METHODS: The initial morphometric parameters of the optic disc and parapapillary atrophy were retrospectively investigated in 350 eyes of 175 patients with ocular hypertension. The prognostic value of parapapillary atrophy at the baseline examination and its relationship with known risk factors for the development of glaucomatous damage were analyzed by multivariate analysis. RESULTS: Visual field loss, optic disc damage, or both were detected in 98 eyes of 53 patients during the follow-up period of at least 10 years. By univariate analysis, the presence of parapapillary atrophy, as well as higher parapapillary atrophy area-disc area, zone beta area-disc area, and parapapillary atrophy length-disc circumference ratios, at the baseline examination was associated with the conversion to glaucoma. In addition, higher intraocular pressure, larger vertical cup-disc ratio, and smaller neural rim area-disc area ratio at the baseline examination were associated with subsequent glaucomatous optic nerve damage. In a multivariate regression model adjusted for other factors, intraocular pressure (relative risk, 1.19), neural rim area-disc area ratio (relative risk, 0.72), and zone beta area-disc area ratio (relative risk, 1.32) were found to be associated with the development of optic disc damage, visual field damage, or both. CONCLUSION: The presence and the size of parapapillary atrophy are related to the development of subsequent optic disc or visual field damage in patients with ocular hypertension.

Choroid↗

PubMed1997

Parapapillary chorioretinal atrophy in patients with ocular hypertension. II. An evaluation of progressive changes.

OBJECTIVE: To determine whether parapapillary chorioretinal atrophy in patients with ocular hypertension remained stationary or progressed along with glaucomatous optic nerve damage. METHODS: The morphometric parameters and progression of parapapillary atrophy were retrospectively investigated, using serial photographs, in 350 eyes of 175 patients with ocular hypertension. The association of parapapillary atrophy progression with subsequent glaucomatous conversion and with other baseline patient- and eye-specific characteristics was analyzed. RESULTS: Progression in the area and extension of parapapillary atrophy before noticeable optic disc or visual field changes was observed in 48 (49.0%) of 98 eyes that converted to glaucoma, while parapapillary atrophy progression was noted in 25 (9.9%) of 252 ocular hypertensive eyes that did not develop glaucomatous damage (P<.001). The predictive sensitivity and specificity of this observation were 49% and 90%, respectively. In a logistic multiple regression model, the progression of parapapillary atrophy was associated with a family history of glaucoma (odds ratio, 2.7) and the initial size of zone beta (odds ratio, 1.64, for an increase of 0.10 of the zone beta area-disc area ratio). CONCLUSION: The progression of parapapillary chorioretinal atrophy may be an early glaucomatous finding in some patients with ocular hypertension.

Choroid↗

PubMed1998

A worse prognosis for men with testicular atrophy at therapeutic orchiectomy for prostate carcinoma.

BACKGROUND: The significance of testicular atrophy at the time of therapeutic orchiectomy for prostate carcinoma has not been examined even though pretreatment hypogonadism has been associated with poor prognosis during chemical androgen ablation for these tumors. METHODS: Survival after therapeutic orchiectomy was determined for 78 men with prostate carcinoma and related to the histologic severity of testicular atrophy. Included in analysis were the presence or absence of prior radiation therapy, tumor grade and stage at diagnosis, host age, obesity, and smoking habits. RESULTS: Among 35 men who underwent therapeutic orchiectomy for progressive disease after primary radiation therapy to the prostate bed, the 25 men with testicular atrophy had worse 5-year, tumor specific, postorchiectomy survival than the 10 men without testicular atrophy (30% vs. 89%) (P=0.02). These 25 men had tumors of more advanced stage and greater undifferentiation at the time of diagnosis an average of 45 months before orchiectomy, but neither characteristic was related to postorchiectomy survival. Among 25 men with Stage D2 disease (American Urologic Association staging system) with orchiectomy as the primary treatment, the 7 men with testicular atrophy more often had undifferentiated tumors and had lower 2-year tumor specific survival than the 18 men without atrophy (43% vs. 72% ) (P > 0.10). CONCLUSIONS: Testicular atrophy at the time of therapeutic orchiectomy for prostate carcinoma is associated with poor postorchiectomy prognosis in men with prior prostate bed radiation therapy and perhaps in men without prior radiation. The association may reflect a high frequency of inherently more aggressive tumors (often relatively nonandrogen-dependent) among those tumors that are progressing in hypogonadal men.

Aged↗

PubMed1998

Testicular atrophy in therapeutic orchiectomy specimens from men with prostate carcinoma: association with prior prostate bed radiation and older age.

BACKGROUND: The significance of testicular atrophy at the time of therapeutic orchiectomy for prostate carcinoma has not been examined even though hypogonadism may occur after prostate bed radiation therapy for these tumors, may itself be symptomatic, and also may be associated with poor tumor prognosis. METHODS: Therapeutic orchiectomy specimens from 78 men with prostate carcinoma and no preceding hormonal therapy were evaluated histologically for atrophy. Observations were related to prior radiation therapy, tumor grade and stage diagnosis, host age, obesity, and smoking habits. RESULTS: Thirty-five men who previously received radiation therapy to the prostate bed had testicular atrophy more frequently than 43 men without prior radiation (71% vs. 28%) (P < 0.001). In men without prior radiation, atrophy was less common in specimens from those age < 70 years than in specimens from men age > 70 years (7% vs. 38%) (P < 0.04). In men with prior radiation, prominent atrophy occurred with similar frequency in specimens from both younger and older men, and was more frequent in specimens obtained within 3 years after radiation therapy than in specimens obtained after longer postradiation intervals (89% vs. 53%) (P < 0.001). CONCLUSIONS: Testicular atrophy at the time of therapeutic orchiectomy for men with prostate carcinoma is much more common in patients with prior prostate bed radiation therapy. Available evidence suggests that this association may reflect both radiation-induced testicular injury and more frequent early tumor recurrence in men with atrophy preceding their radiation therapy.

Aged↗

PubMed1997

Myonuclear loss in atrophied soleus muscle fibers.

BACKGROUND: A skeletal muscle fiber consists of many successive "territories," each controlled by the nucleus residing in that territory. Because nuclei appear to control a specific amount of territory (nuclear domain), nuclei must be added to accommodate an increase in fiber size. Because growth and hypertrophy require the addition of nuclei to fibers, it is of interest to determine whether atrophy causes a decrease in myonuclear number. This study compared the myonuclear population in the soleus muscles of rats that had undergone atrophy due to 10 days of spaceflight in the space shuttle, Endeavour, with muscles of ground-based control animals (10 rats each). METHODS: Myofibrillar ATPase activity was used to determine the major skeletal muscle fiber types in control rats and those having spent 10 days in space, and dystrophin antibodies were used to label the sarcolemma to identify underlying myonuclei. RESULTS: Type I and II fibers were atrophied after the flight, but type I fibers were atrophied twice as much as type II. Myonuclei were counted in identified and measured fibers, and the distribution normalized to number per millimeter of fiber circumference; this was significantly greater in type II than in type I fibers in both groups of rats. However, although the muscle fibers from flight animals were significantly atrophied, the normalized number of nuclei were identical between control and flight animals, indicating that nuclei decreased in numbers as the fibers atrophied. CONCLUSION: The nuclear domain is under strict control, and a decrease in the domain, as induced by atrophy, will cause nuclear degeneration and loss, which maintains a relatively constant size of the nuclear domain.

Adenosine Triphosphatases↗

PubMed2002

Accumulation of 14-3-3 proteins in glial cytoplasmic inclusions in multiple system atrophy.

Glial cytoplasmic inclusions are the pathological hallmark of multiple system atrophy. However, the molecular mechanisms underlying the formation of glial cytoplasmic inclusions remain unclear. Alpha-synuclein, a major component of glial cytoplasmic inclusions, has the ability to interact with 14-3-3 proteins, which mediate several types of signal transduction pathways. To elucidate the role of these 14-3-3 proteins in patients with multiple system atrophy, we performed immunohistochemical studies on 14-3-3 in brain tissue specimens from 7 control subjects and from 15 patients with multiple system atrophy. In both control and multiple system atrophy cases, 14-3-3 immunoreactivity was observed mainly in the neuronal somata and proximal processes, as well as the nerve fibers. Even in the severely affected regions of patients with multiple system atrophy, 14-3-3 immunoreactivity generally was spared in the surviving neurons, some of which were strongly immunolabeled. In addition, numerous glial cytoplasmic inclusions were intensely immunostained, and neuronal cytoplasmic inclusions and dystrophic neurites were also immunoreactive for 14-3-3. Our results suggest that an aberrant accumulation of 14-3-3 proteins may occur in brains affected by multiple system atrophy, and that 14-3-3 proteins may be associated with the pathogenesis of multiple system atrophy.

14-3-3 Proteins↗