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PubMed1978

Central papillary atrophy of the tongue and denture stomatitis.

A retrospective study of the epidemiologic data of 4,417 subjects has been undertaken to study the possibility of a link existing between glossal central papillary atrophy (median rhomboid glossitis) and denture stomatitis. Neither the association between glossal central papillary atrophy and denture stomatitis nor the association between glossal central papillary atrophy and denture use was statistically significant. However, the correlation between wearing removable dental prostheses and finding candidal mycelia in smears from these tongue lesions was statistically highly significant. Debilitation caused by general age changes would not appear to predispose to atrophy of the pappillae of the middle portion of the tongue-dorsum.

Atrophy↗

PubMed1986

A possible role for endogenous glucocorticoids in orchiectomy-induced atrophy of the rat levator ani muscle: studies with RU 38486, a potent and selective antiglucocorticoid.

We employed RU 38486, a potent and selective antiglucocorticoid, to study a possible role for endogenous glucocorticoids in atrophy of the levator ani muscle secondary to castration of male rats. RU 38486 was shown to block [3H]triamcinolone acetonide binding to cytosol from levator ani muscle. Daily oral administration of RU 38486 to castrated rats partially prevented atrophy of the levator ani muscle, as well as a decrease in RNA concentration. In a control group receiving RU 38486 alone, the levator ani underwent significant (20%) hypertrophy. Administration of exogenous dexamethasone also caused pronounced atrophy of the levator ani muscle. This atrophy was prevented, to a significant degree, by simultaneous oral administration of RU 38486. It is concluded that endogenous glucocorticoids, the actions of which are blocked by RU 38486, may be involved in regulation of the mass of the levator ani muscle in intact rats.

Animals↗

PubMed1988

Inhibition of TPN-associated intestinal mucosal atrophy with monoacetoacetin.

Total parenteral nutrition (TPN) is associated with intestinal mucosal atrophy. Acetoacetate is oxidized in preference to glucose by both enterocytes and colonocytes and is not present in TPN. The purpose of this study was to determine whether replacement of a portion of glucose calories with monoacetoacetin, the glycerol ester of acetoacetate, could inhibit TPN-associated intestinal atrophy. Male Sprague-Dawley rats (200-250 g) underwent superior vena caval cannulation and were assigned to receive chow ad libitium (CHOW), TPN with 0.86 M monoacetoacetin (ACAC), or TPN with 0.86 M glycerol to control for the glycerol component of monoacetoacetin (GLYC). Nitrogen balance was measured over 7 days after which time the animals were weighed and sacrificed. Jejunal and colonic segments were harvested and the mucosal weight, protein, RNA, and DNA contents measured. All groups showed comparable weight gain. Cumulative nitrogen balance was positive for both TPN groups. Significant decreases in mucosal parameters occurred in both TPN groups compared to the CHOW group, but atrophy was significantly inhibited in both jejunum and colon of the ACAC group compared to the GLYC group. Thus, the substitution of monoacetoacetin for glucose calories in parenteral nutrition solutions inhibited TPN-related atrophy of intestinal mucosa while maintaining normal growth.

Acetoacetates↗

PubMed1976

Isoelectric focusing and electrophoresis of cerebrospinal fluid proteins in muscular dystrophies and spinal muscular atrophies.

In the very few previous investigations of the CSF-proteins in muscular dystrophies the results have generally been reported as normal. In spinal muscular atrophies a barrier-damage pattern of CSF-proteins has been found in amyotrophic lateral sclerosis (ALS). In the present investigation the CSF-proteins were examined by isoelectric focusing and quantitative paper electrophoresis in 13 patients with muscular dystrophies and in 11 patients with spinal muscular atrophies. On isoelectric focusing, CSF-protein abnormalities were found in 85% of the cases with muscular dystrophies and in all patients with spinal muscular atrophies. Differences in the CSF-protein patterns were observed within the group of muscular dystrophies and between these and the cases of spinal muscular atrophies. In ALS and in myotonic dystrophy, abnormal CSF-protein fractions occurred mainly in the alkaline pH-range, while in limb-girdle dystrophy and the patient with facioscapulohumeral dystrophy, aberrant fractions appeared mainly in the acidic region. CSF-protein abnormalities were found in both the alkaline fractions (HAFs) with pI 9.2-9.6 and a fraction with PI 7.1 were found in half of the patients with myotonic dystrophy. The CSF electrophoresis in myotonic dystrophy showed increased levels of beta1-globulin in all cases examined. Signs of barrier-damage were commonly encountered in ALS in contrast to the muscular dystrophies, except for myotonic dystrophy. The results are discussed in terms of possible diagnostic value and with regard to pathogenetic significance, particularly in relation to the current hypothesis of a neural involvement in muscular disorders.

Adult↗

PubMed1983

Chronic asymmetrical spinal muscular atrophy.

The clinical and neurophysiological features of 18 cases of chronic asymmetrical spinal muscular atrophy are described. These were patients presenting with asymmetrical neurogenic atrophy involving one or more limbs who had no evidence of pyramidal tract dysfunction after 3 or more years of symptoms. There were twice as many males as females and the mean age of onset of the disorder was about 32 years. None of the patients had bulbar involvement. The tendon reflexes tended to be depressed. The distribution of muscle weakness in the limbs was very variable, and only slowly progressive. In 5 cases symptoms and signs were confined to the hands and forearms. Motor nerve conduction velocities to wasted muscles were slightly reduced but there was no evidence of generalised neuropathy. A diagnosis of chronic asymmetrical spinal muscular atrophy, as opposed to that of classical motor neurone disease, is favoured by an age of onset under 40 years, an absence of pyramidal signs or bulbar involvement after 3 years or more of symptoms, and depressed or absent tendon reflexes. The 2 conditions appear to be clinically distinct and prognosis is considerably better in chronic asymmetrical spinal muscular atrophy. The aetiology of this condition in unknown; it may be of relevance that 2 patients in this series had close relatives with Werdnig-Hoffmann disease.

Adult↗

PubMed1986

Atrophy of the cerebellar vermis in ageing. A morphometric and histologic study.

Morphometric analysis of the cerebellar vermis in 67 non-alcoholic men between 36 and 94 years of age showed a significant decline in Purkinje cell densities with increasing age in all parts of the cerebellar vermis. However, the nerve cell loss was much more severe in the superior than in the inferior part. There were large individual variations and one-half of the subjects over 80 years showed densities similar to those in the sixties. By independent evaluation, atrophy of the superior vermis was diagnosed histologically in 16 cases, 13 of whom were over 70 years of age. There was a good correspondence between the histologic diagnoses and the morphometric findings. The atrophy involved all 3 cortical layers and the changes were identical to those seen in alcoholics. The diagnosis of alcoholic cerebellar atrophy must therefore be made with great caution in subjects over 70 years of age. Cases with malignant tumours had significantly lower Purkinje cell densities in the superior vermis than those without tumours but the decline with age was of the same magnitude in the 2 groups. The age-dependent atrophy of the superior vermis seemed to be correlated to age alone and not to other known conditions. It probably was sufficiently severe to be recognized radiologically and clinically in a considerable number of the cases.

Adult↗

PubMed1987

Progressive neurogenic muscle atrophy with fasciculation in mice treated with IDPN.

Spontaneous discharges recorded on the EMG appeared in experimental mice given repeated doses of IDPN according to a time schedule. Spontaneous discharges showing a polyphasic pattern and duration of over 10 ms were considered to be fasciculations. One group of mice, treated with IDPN for 4 weeks became active with an increase in muscle volume 2 months after initiation of experiment; spontaneous discharges were recorded in this group at 3-4 weeks after first IDPN injection and disappeared at 4 months. Histologically, neurogenic muscle atrophy, in terms of group atrophy of muscles, was seen in muscles of mice exhibiting spontaneous discharge patterns. Peripheral nerves showed marked atrophy with degeneration. Dissociation of neurofilaments and other organelles was observed. Axonal swellings, filled with numerous maloriented neurofilaments, were confirmed in the lumbar cord. IDPN given repeatedly to mice at a certain dose causes degeneration of the peripheral nerves and results in neurogenic muscle atrophy.

Action Potentials↗

PubMed1990

Different mechanisms of increased proteolysis in atrophy induced by denervation or unweighting of rat soleus muscle.

Mechanisms of accelerated proteolysis were compared in denervated and unweighted (by tail-cast suspension) soleus muscles. In vitro and in vivo proteolysis were more rapid and lysosomal latency was lower in denervated than in unweighted muscle. In vitro, lysosomotropic agents (eg, chloroquine, methylamine) did not lessen the increase in proteolysis caused by unweighting, but abolished the difference in proteolysis between denervated and unweighted muscle. Leucine methylester, an indicator of lysosome fragility, lowered latency more in denervated than in unweighted muscle. 3-Methyladenine, which inhibits phagosome formation, increased latency similarly in all muscles tested. Mersalyl, a thiol protease inhibitor, and 8-(diethylamino)octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8), which antagonizes sarcoplasmic reticulum release of Ca2+, reduced accelerated proteolysis caused by unweighting without diminishing the faster proteolysis due to denervation. Calcium ionophore (A23187) increased proteolysis more so in unweighted than control muscles whether or not Ca2+ was present. Different mechanisms of accelerated proteolysis were studied further by treating muscles in vivo for 24 hours with chloroquine or mersalyl. Chloroquine diminished atrophy of the denervated but not the unweighted muscle, whereas mersalyl prevented atrophy of the unweighted but not of the denervated muscle, both by inhibiting in vivo proteolysis. These results suggest that (1) atrophy of denervated, but not of unweighted, soleus muscle involves increased lysosomal proteolysis, possibly caused by greater permeability of the lysosome, and (2) cytosolic proteolysis is important in unweighting atrophy, involving some role of Ca2(+)-dependent proteolysis and/or thiol proteases.

Animals↗

PubMed1991

Skeletal muscle atrophy in old rats: differential changes in the three fiber types.

This study was undertaken to reevaluate the effects of ageing on skeletal muscle mass and on mitochondrial and glycolytic enzyme levels in the different types of skeletal muscle in rats. It was found that some muscles atrophy with ageing, while others do not, in male rats. Atrophy appears to occur in weight-bearing muscles, and is most marked in those with a high proportion of type IIb fibers. The muscles that did not atrophy are non-weight-bearing, and include the epitrochlearis (predominantly type IIb fibers) and the adductor longus (predominantly type I fibers). The average cross-sectional area of muscle fibers in the plantaris muscles of 28-30-month-old rats was approximately 30% smaller than that of 9-10-month-old animals, providing evidence that the approximately 30% lower weight of the plantaris in the old group was entirely due to fiber atrophy. The proportion of type IIa fibers was decreased and the proportion of type I fibers was increased in the plantaris of the old rats. The respiratory capacity of the soleus muscle (predominantly type I fibers), and the glycolytic capacity of the superficial, white (type IIb) and deep, red (predominantly type IIa) portions of the vastus lateralis, were reduced in the old rats. Our results provide evidence that ageing has differential effects on the three types of skeletal muscle fiber, and on weight-bearing and non-weight-bearing muscles, in the rat.

Aging↗

PubMed1987

Emotion control and cerebellar atrophy in senile dementia.

New research increasingly indicates that the cerebellum coordinates and integrates a wide range of processes not confined to the motor sphere. Since satisfying correlations between affective disturbances and signs of cerebral atrophy have not been found, the relationship of CT-indicated cerebellar atrophy to certain psychopathologic indicators, in patients suffering from senile dementia, has been studied. The patients participating in the study were 21 women and 18 men with a mean age of 69.4 years. Each patient showed a definite pathologic score in at least one cerebral CT-measurement. The Spearman rank correlations between affective incontinency, lability of affect, and cerebellar atrophy suggest substantial relationships between affective symptoms and cerebellar pathology. This seems all the more remarkable since all of the various indicators of cerebral cortical and subcortical atrophy lacked to show any strong relationship to affective symptoms at all. The implications of the findings for research and clinical purposes are discussed.

Affective Symptoms↗

PubMed1991

Atrophy of outer hair cell stereocilia and hearing loss in hydropic cochleae.

We have earlier described selective atrophy of short and middle stereocilia on outer hair cells of the three upper cochlear turns in hydropic cochleae of guinea pigs. The present study describes sequential early stages of stereocilia degeneration leading to this specific atrophy. Comparison of the morpho-pathology with the ultimate CAP audiograms taken before sacrifice indicated a close association between the low frequency hearing loss and this atrophy of stereocilia. The atrophy appeared to be associated first with the short and then the middle stereocilia of the 2nd and 3rd rows of outer hair cells between 0.5 kHz and 2 kHz and with time included the 1st row of all outer hair cells of the upper cochlear turns down to the 8 kHz region.

Acoustic Stimulation↗

PubMed2004

Endoscopic release for carpal tunnel syndrome accompanied by thenar muscle atrophy.

PURPOSE: The objective of this study was to ascertain whether endoscopic carpal tunnel release (ECTR) is indicated for treatment of carpal tunnel syndrome accompanied by thenar muscle atrophy. TYPE OF STUDY: Prospective cohort study. METHODS: Two-portal ECTR was performed on 67 hands in 52 patients with carpal tunnel syndrome accompanied by thenar muscle atrophy. RESULTS: Preoperative severity of thenar muscle atrophy was severe in 24 hands, moderate in 23 hands, and mild in 20 hands. Postoperative severity of thenar muscle atrophy was severe in 6 hands, moderate in 2 hands, mild in 23 hands, and none in 36 hands. CONCLUSIONS: Improvements with thenar muscle function in most cases of carpal tunnel syndrome can be expected with 2-portal ECTR. LEVEL OF EVIDENCE: Level IV.

Adult↗

PubMed2005

Skeletal muscle hypertrophy and atrophy signaling pathways.

Skeletal muscle hypertrophy is defined as an increase in muscle mass, which in the adult animal comes as a result of an increase in the size, as opposed to the number, of pre-existing skeletal muscle fibers. The protein growth factor insulin-like growth factor 1 (IGF-1) has been demonstrated to be sufficient to induce skeletal muscle hypertrophy. Over the past few years, signaling pathways which are activated by IGF-1, and which are responsible for regulating protein synthesis pathways, have been defined. More recently, it has been show that IGF-1 can also block the transcriptional upregulation of key mediators of skeletal muscle atrophy, the ubiquitin-ligases MuRF1 and MAFbx (also called Atrogin-1). Further, it has been demonstrated recently that activation of the NF-kappaB transcription pathway, activated by cachectic factors such as TNFalpha, is sufficient to induce skeletal muscle atrophy, and this atrophy occurs in part via NF-kappaB-mediated upregulation of MuRF1. Further work has demonstrated a trigger for MAFbx expression upon treatment with TNFalpha--the p38 MAPK pathway. This review will focus on the recent progress in the understanding of molecular signalling, which governs skeletal muscle atrophy and hypertrophy, and the known instances of cross-regulation between the two systems.

Gene Expression Regulation↗

PubMed2006

Study of skeletal muscle glycogenolysis and glycolysis in chronic steroid myopathy, non-steroid histochemical type-2 fiber atrophy, and denervation.

OBJECTIVE: Muscle biopsies from chronic steroid (glucocorticoid) myopathy, non-steroid histochemical type-2 fiber atrophy, and muscle denervation patients were studied to determine if their glycogen contents, or enzymes involved in glycogenolysis and glycolysis might be related to their fiber atrophy. DESIGN AND METHODS: Fast frozen muscle biopsies from the above patients and from patients later judged by histochemistry to be normal were assayed enzymatically for glycogen content, for enzymes involved in glycogenolysis, and for 6 of the enzymes involved in glycolysis. RESULTS AND CONCLUSION: All three groups of patients had glycogen content, but only the chronic steroid myopathy muscle had statistically less glycogen content than did normal human muscle. All 3 groups had statistically low mean values compared to normal muscles for glycogen phosphorylase activity. This suggests that the biosynthesis and phosphorolysis of glycogen are not involved in muscle fiber atrophy, and glucocorticoid administration does not activate muscle glycogen biosynthesis. Histochemical type-2 fiber atrophy muscles were low compared to normal muscles in three glycogenolysis enzyme activities plus four glycolysis enzyme activities. Muscles from denervation patients were low compared to normal muscles in three glycogenolysis enzyme activities plus five glycolysis enzyme activities. This suggests that muscle denervation may lower the rate of glycolysis enough to fail to provide sufficient pyruvate for mitochondrial ATP biosynthesis, resulting in insufficient protein biosynthesis in both fiber types.

Adult↗

PubMed2005

Camptocormia or Pisa syndrome in multiple system atrophy.

Although a mild stooped posture is a hallmark of parkinsonism, extreme trunk forward flexion is not common. This phenomenon was described in different etiological entities and called camptocormia. Other similar presentations called Pisa syndrome and antecollis were described mainly in extrapyramidal disorders. Authors present two cases of probable multiple system atrophy (MSA) with predominant parkinsonism and Pisa syndrome (or camptocormia). Both of them were previously misdiagnosed as idiopathic Parkinson's disease (PD) and one was reported 1 year earlier. The typical clinical presentation fulfilling the diagnostic criteria for multiple system atrophy, rapid progression with lack of responsiveness to L-DOPA and apomorphine and typical MRI putaminal pathology observed in both cases allowed us to make a diagnosis. Accuracy of clinical diagnosis in multiple system atrophy is still very poor. Therefore, unusual or rare clinical presentations may support the final diagnosis. The camptocormia, Pisa syndrome and antecollis may represent the continuum of the same motor phenomenon and most of the authors refer them to unusual form of axial dystonia. According to many clinical presentations on different forms of camptocormia/Pisa syndrome authors conclude that not etiology, but the localization of specific lesion, probably within putamen is responsible for that form of dystonia. In cases of parkinsonism and severe forward flexion of trunk multiple system atrophy, diagnosis should be considered.

Diagnosis, Differential↗

PubMed2006

Restricted feeding may induce serous fat atrophy in male Göttingen minipigs.

Serous atrophy of the fatty tissue of bone marrow is occasionally seen in minipigs. It is not associated with compound toxicity, as it has been observed in both dosing and healthy control groups in toxicity studies, but the etiology and pathogenesis are unknown. However, a nutritional factor is suspected, since minipigs are generally diet restricted. In order to investigate this, newly weaned minipigs were fed different amounts of feed for nine months, after which the bone marrow was evaluated. Serous atrophy was observed in diet-restricted male minipigs fed on a diet based on the nutrient requirements of production pigs, but not in males fed on a diet specially designed for minipigs, at similarly restricted levels. No serous atrophy was observed in females. It was concluded that nutrient requirements of production pigs are not necessarily suitable for minipigs, as a diet based on these nutrient requirements caused total depletion of perirenal fat depots, as well as serous atrophy of the fatty tissue of bone marrow in male Göttingen minipigs at a restricted feeding level.

Adipose Tissue↗

PubMed2004

Effects of ventricular unloading on apoptosis and atrophy of cardiac myocytes.

BACKGROUND: Ventricular unloading decreases cardiac ventricular mass. This loss of ventricular mass can be due to either atrophy (a reversible process) or apoptosis (an irreversible process) of the cardiac myocytes. We investigated the effect of ventricular unloading on atrophy and apoptosis of cardiac myocytes, using working and nonworking transplant heart models in rats. MATERIALS AND METHODS: ACI rats underwent heterotopic heart transplantation with two different techniques to create working and nonworking cardiac grafts. Cardiac grafts were harvested at different time points after transplantation. TUNEL, caspase-3 assay, and electron microscopy were used to assess the degree of apoptosis while cellular atrophy was estimated by calculation of the cytoplasmic index (CI = mean sectional cytoplasmic area/nucleus). RESULTS: Ventricular mass reduction was more pronounced in nonworking than in working hearts (P < 0.05). Apoptotic index and caspase-3 activities increased in both groups, peaking at 3 days after transplantation, but were not significantly different between the two models. The cytoplasmic index was significantly lower in nonworking than in working grafts (P < 0.05). CONCLUSIONS: These data suggest that cellular atrophy is the primary mechanism that accounts for myocardial weight reduction following ventricular unloading. The inference is that ventricular unloading by ventricular assist devices may not cause permanent loss of cardiac myocytes, thus allowing for functional recovery.

Animals↗

PubMed2004

Cyclin expression in the atrophying and proliferating lobes of the liver after portal vein branch ligation and hepatectomy in rats.

BACKGROUND: Portal vein branch ligation causes atrophy of the portal vein ligated lobes (PVL) and proliferation of the nonligated lobes (PVNL) of the liver. However, the mechanisms underlying atrophy of the PVL and proliferation of PVNL after portal vein branch ligation have not been clarified except that interleukin-6 (IL-6), nuclear factor kappa B (NF-kappaB), signal transducer and activator of transcription 3 (STAT3), and immediate-early gene expression are similarly induced in both the PVL and the PVNL. Thus, it is still unclear what factors cause the subsequent atrophy and proliferation. MATERIALS AND METHODS: Male Wistar rats were randomly separated into a portal vein branch ligation group and partial hepatectomy group. In the portal vein branch ligation group, the branch of portal vein supplying the median and left lateral lobes of the liver was ligated. In the partial hepatectomy group, the correspondent lobes of the liver were excised. We examined cyclin expression in the PVL and PVNL after portal vein branch ligation in comparison to cyclin expression in the remaining liver (HEP) after partial hepatectomy. Cyclin D1, E, and A mRNA and protein expressions were analyzed by RT-PCR and Western blotting, respectively. RESULTS: The mRNA and protein expressions of cyclin D1 and A were not up-regulated in the PVL, whereas those in the PVNL and HEP were up-regulated. Cyclin D1 mRNA and protein expressions were significantly lower in the PVL than in the PVNL and HEP at 18 h. The levels of mRNA and protein expression of cyclin A were significantly lower in the PVL than in the PVNL and HEP at 36 h. Liver regeneration, assessed by the relative liver weight, thymidine incorporation into DNA, and proliferating cell nuclear antigen (PCNA) labeling index was delayed significantly in the PVNL compared to that in the HEP. Cyclin D1 mRNA and protein expressions were significantly lower in the PVNL than in the HEP at 12 and 18 h, respectively. CONCLUSIONS: Cell-cycle progression might be inhibited at G(1)-phase accompanied by impaired cyclin D1 expression in the PVL, which results in atrophy. The fact that liver proliferation of the PVNL is delayed in comparison to that of the HEP is likely due to delayed expression of cyclin D1.

Animals↗