Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Atrophy”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2005

Quantification of hormone-induced atrophy of large myotubes from C2C12 and L6 cells: atrophy-inducible and atrophy-resistant C2C12 myotubes.

Myofiber atrophy is the final outcome of muscle wasting induced by catabolic factors such as glucocorticoids and thyroid hormones. We set up an in vitro system to define the catabolic reaction based on myotube atrophy. Both mouse C(2)C(12) and rat L6 cells were used. C(2)C(12) myotube formation was improved by replacing horse serum with the serum substitute Ultroser G. A new method was developed to quantify size changes of large (0.5-1 mm) myotubes only, excluding remaining myoblasts and small myotubes. Dexamethasone reduced myotube size by 30% in L6 but not in C(2)C(12) myotubes. Expression of the glucocorticoid receptor was twofold higher in L6 myotubes than in C(2)C(12) myotubes. In both cell lines, 3,3',5-triiodo-l-thyronine (T(3)) did not induce a significant size reduction. Expression of the major T(3) receptor (T(3)Rbeta1) was higher in L6 myotubes. We investigated whether the changes in myotube size are related to changes in atrogin-1 expression, as this enzyme is thought to be a key factor in the initiation of muscle atrophy. Dexamethasone induced a twofold increase of atrogin-1 mRNA; again, only L6 myotubes were susceptible. Interestingly, atrogin-1 expression in Ultroser G-fused C(2)C(12) myotubes was lower than that in horse serum-fused myotubes. Furthermore, dexamethasone treatment increased atrogin-1 expression only in horse serum-fused myotubes but not in Ultroser G-fused myotubes. Ultroser G-induced fusion may result in atrophy-resistant C(2)C(12) myotubes. Therefore, C(2)C(12) myotubes offer an ideal system in which to study skeletal muscle atrophy because, depending on differentiation conditions, C(2)C(12) cells produce atrophy-inducible and atrophy-resistant myotubes.

Animals↗
PubMedDate not supplied

Differential diagnosis of diffuse choroidal atrophies. Diffuse choriocapillaris atrophy, choroideremia, and gyrate atrophy of the choroid and retina.

Three young children showed a similar fundus appearance of sharply defined, yellowish-white, patchy or geographic atrophy of the retina and choroid and visible large choroidal vessels in almost the entire fundus. Fluorescein angiography disclosed atrophy of the retinal pigment epithelium and loss of choriocapillaris. Their visual functions and electrophysiologic findings were also similar. Family A was diagnosed as having diffuse choriocapillaris atrophy with autosomal dominant inheritance; family B, choroideremia with X-linked recessive heredity; and family C, gyrate atrophy of the choroid and retina with hyperornithinemia and autosomal recessive transmission. It became evident that diffuse choriocapillaris atrophy, choroideremia, and gyrate atrophy sometimes show a similar fundus appearance. Fluorescein angiography, serum ornithine levels, and family history were particularly helpful to differentiate these diffuse choroidal atrophies.

Adolescent↗
PubMed1992

[Multivariate analysis of the clinical signs in late cortical cerebellar atrophy (LCCA) in Japan--compared with olivo-ponto-cerebellar atrophy (OPCA) and hereditary cortical cerebellar atrophy (HCCA)].

We investigated the clinical features of 179 patients with late cortical cerebellar atrophy (LCCA) comparing with 382 patients with olivo-ponto-cerebellar atrophy (OPCA) and 91 patients with hereditary cortical cerebellar atrophy (HCCA) using multivariate analysis. They had no significant difference in durations from onset. Disorders of finger-nose test were of more severity and disorders of heel-knee test were less involved in LCCA than in HCCA. Eye movements tended to be normal in LCCA. LCCA showed more depressive and euphoric character than OPCA and HCCA. Analysis of LCCA and OPCA demonstrated that LCCA revealed hypotonia in muscles, normal or weak reactions of muscle stretch reflexes. There existed 21.4 percent of cases which could not be discriminated by multivariate analysis using clinical signs in LCCA and OPCA. Multivariate analysis of LCCA and HCCA, which are very similar in clinical signs, showed 66.3 percent of discriminatory rate. Thus, we could diagnose them to a certain extent only by clinical signs.

Aged↗
PubMed2006

Longitudinal MRI in progressive supranuclear palsy and multiple system atrophy: rates and regions of atrophy.

The rate of brain atrophy and its relationship to clinical disease progression in progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) is not clear. Twenty-four patients with PSP, 11 with MSA-P (Parkinsonian variant), 12 with Parkinson's disease, and 18 healthy control subjects were recruited for serial MRI scans, clinical assessments and formal neuropsychological evaluations in order to measure brain atrophy during life and its association with disease progression in PSP and MSA-P. Serial scans were registered and rates of whole brain atrophy calculated from the brain-boundary shift integral. Regional rates of atrophy were calculated in the brainstem (midbrain and pons), the cerebellum, the lateral and third ventricles as well as frontal and posterior inferior brain regions, by locally registering to a region of interest in order to derive a local boundary shift integral (BSI). 82% of recruited subjects completed serial MRI scans (17 PSP, 9 MSA-P, 9 Parkinson's disease patients and 18 healthy controls). Mean (SD) annualized rates of whole-brain atrophy were greatest in PSP: 1.2% (1.0%), three times that in controls. Mean (SD) midbrain atrophy rates in PSP, 2.2% (1.5%), were seven times greater than in healthy controls. In MSA-P, atrophy rates were greatest in the pons: 4.5% (3.2%), over 20 times that in controls and three times the rate of pontine atrophy in PSP. Atrophy rates in Parkinson's disease were not significantly different from control rates of atrophy. Variability in the atrophy rates was lower when calculated using the BSI rather than manual measurements. Worsening motor deficit was associated with midbrain atrophy in PSP, and ponto-cerebellar atrophy in MSA-P. Worsening executive dysfunction was associated with increased rates of frontal atrophy in PSP. Cerebellar atrophy rates were better discriminators of MSA-P than cross-sectional volumes. We confirm that serial MRI can be applied to measure whole brain and regional atrophy rates in PSP and MSA-P. Regional rather than whole-brain atrophy rates better discriminate PSP and MSA-P from healthy controls. Clinico-radiological associations suggest these regional atrophy rates have potential as markers of disease progression in trials of novel therapies.

Aged↗
PubMedDate not supplied

Computed tomographic myelography characteristics of spinal cord atrophy in juvenile muscular atrophy of the upper extremity.

Although atrophy of the lower cervical and upper thoracic cord in juvenile muscular atrophy of distal upper extremity has been reported, the atrophic patterns of the cord, especially in the transverse section, have not been studied extensively. The aim of this study is to clarify the atrophic patterns of the cord by CT myelography (CTM) and to discuss the pathogenesis of cord atrophy. Sixteen patients with juvenile muscular atrophy of distal upper extremity were examined by CTM. Atrophy of the lower cervical and upper thoracic cord, consistent with the segmental weakness, was seen in all patients. Flattening of the ventral convexity was a characteristic atrophic pattern of the cord. Bilateral cord atrophy was commonly observed; eight of 12 patients with unilateral clinical form and all four patients with bilateral form showed bilateral cord atrophy with dominance on the clinical side. There was no correlation between the degree of cord atrophy and duration of symptoms. Flattening of the ventral convexity, associated with purely motor disturbances, reflects selective atrophy of the anterior horns in the cord, which is attributable to chronic ischemia. Cord atrophy proved to precede clinical manifestations. The characteristic atrophy of the cord provides useful information to confirm the diagnosis without long-term observation.

Adolescent↗
PubMed1994

Localization of atrophy-prone areas in the aging mouse brain: comparison between the brain atrophy model SAM-P/10 and the normal control SAM-R/1.

Mouse inbred strain "SAM-P/10" (Senescence Accelerated Mouse) is a model of age-related brain atrophy. In this strain there is an earlier and more severe age-related deterioration in the conditional avoidance learning than the normal control inbred SAM-R/1 strain. The present study analysed age-related changes in brain area size using a computerized morphometric method. The region most vulnerable to age-related atrophy in SAM-P/10 was the frontal region of the cerebral cortex, including the prefrontal cortex. Other neocortical regions underwent diffuse atrophy. Posterior piriform cortex, entorhinal cortex, anterior olfactory nucleus, amygdala, caudate-putamen, nucleus accumbens and cerebellar cortex were atrophy-prone regions. The septum also underwent atrophy but other basal forebrain structures were intact. The hippocampus, diencephalon and brainstem structures showed no atrophic change. White matter structures did not change in size with aging except for the forceps minor of the corpus callosum, which showed age-related atrophy. On the contrary, SAM-R/1 showed a significant age-related atrophy only in a restricted part of the cerebral cortex, mainly in the parietal region. Other cortical regions, subcortical structures, diencephalon, brainstem structures, cerebellum and white matter were atrophy-resistant in SAM-R/1. The prefrontal cortex, entorhinal cortex, piriform cortex and striatum are closely interconnected and also connect with the amygdala which plays a key role in conditioning in the rodent. Age-related atrophy in all these structures in SAM-P/10 presumably accounts for the age-related deficits in conditional avoidance learning in this strain of mouse. Comparison between SAM-P/10 and SAM-R/1 or other well-known rodents indicates that SAM-P/10 is a unique rodent that spontaneously and rapidly develops progressive generalized cerebral atrophy, which is considered to be a pathological process rather than an accelerated aging process.

Aging↗
PubMed1999

Enlargement of atrophy and visual acuity loss in the geographic atrophy form of age-related macular degeneration.

OBJECTIVE: To describe the progression of geographic atrophy (GA) from age-related macular degeneration (AMD) with respect to visual acuity (VA) loss and enlargement of atrophy. DESIGN: A prospectively observed case series. SETTING: Tertiary retinal referral center. PARTICIPANTS: One hundred twenty-three patients with GA due to AMD who completed at least 1 year of follow-up (median follow-up, 3 years) were examined annually. METHODS: At each examination, a protocol best-corrected VA of each eye was measured, a clinical examination was performed, and color fundus photographs were taken. The areas of atrophy were drawn and measured. MAIN OUTCOME MEASURES: Visual acuity loss and enlargement of total and central atrophy. RESULTS: At baseline, median VA was poorer with larger areas of atrophy, but there was wide variation related to sparing of the fovea. Thirty-one percent of all study eyes suffered a three-line VA loss from baseline by 2 years, and 53% had a three-line loss by 4 years. Those eyes with VA better than 20/50 had the highest rate of acuity loss; 27% of these eyes had acuities of 20/200 or worse at 4 years. Visual acuity loss in the GA study eye was similar in patients with bilateral GA and in those with choroidal neovascularization in the fellow eye. Total atrophy enlarged a median of 1.8 Macular Photocoagulation Study disc areas (DA) at 2 years; atrophy within a 4-DA circle centered on the fovea enlarged a median of 0.9 DA. Two (22%) of nine patients with GA in one eye and only drusen without advanced AMD in the fellow eye developed GA in the fellow eye at 2 years. CONCLUSIONS: Geographic atrophy is associated with a significant decline in VA over time in many eyes. Areas of atrophy continue to enlarge over time, even when already large at baseline. The combination of reduced VA with enlargement of atrophy, occurring bilaterally in most patients, can lead to significant impairment of visual function.

Aged↗
PubMed2002

[Quantitative MRI study of progressive cerebral atrophy in multiple system atrophy].

We investigated cerebral atrophy in multiple system atrophy (MSA) by quantitative analysis of MRI. The subjects were 28 patients with MSA (14 striato-nigral degeneration; SND, 14 olivo-ponto-cerebellar atrophy; OPCA. 106 MRI examinations were performed totally) and 85 normal persons for control. The ratios of the ventral pons to the infratentorial space in the sagittal section, the putamen, cerebrum, frontal lobe and parietal & occipital lobes to the intracranial space in the horizontal section, and the temporal lobe to the intracranial space in the coronal section were measured. In the early stage of the disease, OPCA showed significant atrophy of the ventral pons compared with SND, and conversely, SND demonstrated significantly smaller putamen than that in OPCA. According to the progression of the disease, the atrophy of these neural tissues progressed, which resulted in no significant differences between SND and OPCA. The cerebral atrophy was observed in 17 MSA patients. The atrophy of the frontal lobe was much frequent and prominent to that in the temporal lobe and parietal & occipital lobes. SND showed higher incidence of the cerebral atrophy than OPCA in the early stage of the disease. In long period follow-up cases, one case showed cerebral atrophy in earlier stage, and another case in late stage. We indicated the involvement of the cerebral hemispheres in MSA, especially the frontal lobe.

Aged↗
PubMed2006

[An autopsy case of long-course multiple system atrophy (MSA) with remarkable atrophy and numerous NCI in the temporal lobe].

The patient was 66 year-old man with no family history of neurological diseases. At age 51, he showed initial symptom of parkinsonism, and was revealed a cerebellar atrophy by CT at age 52. He was suffered from malignant syndrome followed by renal dysfunction, which needed hemodialysis therapy. At age 54, he admitted to our hospital, when he showed parkinsonism, ataxia and dysautonomia. Neuroimaging study disclosed typical findings of multiple system atrophy (MSA), and dilatation of inferior horn of the lateral ventricle. In the next year, he lost of amburatory function, and showed low cognitive function of 5 scores in HDSR. At age 57, he was tracheostomised because of complete paralysis of the vocal cord abductor muscles. MRI study disclosed marked temporal lobe atrophy. He was complicated with bladder carcinoma, and died of multiple organ failure at age 66. The brain weight was 1,115 g. Gross neuropathological findings were temporal lobe dominant cerebral atrophy and marked pontocerebellar atrophy. Meningitis and sepsis were seen in the cerebrum, and some infarctions in the temporal and frontal lobes. Besides the typical degenerative findings of MSA, remarkable temporal lobe atrophy with enlargement of the inferior horn of lateral ventricle was observed. There were numerous number of neuron containing neuronal inclusion body (NCI) in the hippocampal cortex, dentate fascia and parahippocampal gyrus. In spite of small amount of NFT in the parahippocampal gyrus, there were no se- nile plaque, tau-positive structure except NFT, argyrophilic grain or Pick body. This case was a long-survived MSA with remarkable atrophy of the temporal lobe. The characteristic neuropathological finding was numerous numbers of neurons containing NCI in the cotices arround the inferior horn. Although frontal lobe dominant cerebral lobe atrophy is common in the long-survived MSA cases, extreme temporal lobe atrophy is rare condition. There may be a MSA subtype strongly affecting temporal lobe with numerous NCI.

Aged↗
PubMed1975

Lipo-atrophy of the ankles and its relation to other lipo-atrophies.

Two typical cases of lipo-atrophy of the ankles are described, one case of atrophy of the ankles with associated atrophy of the whole extremity, and one case of localized atrophy of the knee. For comparison, we present one case of atrophy in a diabetic patient due to insulin injections but developing at distant sites, and in one case, a child in whom atrophy followed antibiotic injections. Primary inflammatory vascular changes in the subcutaneous tissue were demonstrated in atrophy of the ankles, as in the early period of insulin-induced lipo-atrophy. Attention is called to the possible relation of the described lipo-atrophies.

Adolescent↗
PubMed2003

Voxel-based morphometry detects cortical atrophy in the Parkinson variant of multiple system atrophy.

To determine magnetic resonance imaging (MRI) patterns of brain atrophy in parkinsonian syndromes, we applied voxel-based morphometry (VBM) to segmented gray matter, white matter, and cerebrospinal fluid compartments of T(1)-weighted brain volumes of 12 patients with probable multiple system atrophy-parkinson variant (MSA-P) and 12 Parkinson's disease patients, comparing them with 12 normal controls matched for age. In comparison to controls, a cortical atrophy pattern was observed in MSA-P patients with significant clusters of volume loss in primary sensorimotor cortices bilateral, supplementary motor areas bilateral, right premotor cortex, prefrontal cortex bilateral (middle frontal gyri) and insular cortices bilateral; subcortical atrophy occurred bilaterally in caudate nuclei and putamen as well as in the midbrain. Furthermore, an enlargement of the cerebrospinal fluid compartment was found in the lateral ventricles, third ventricle, perimesencephalic and cerebellomedullar cavities. In PD patients, significant atrophy only occurred in left caudate head with enlargement of left lateral ventricle. Comparing MSA-P to PD patients, MSA-P showed a similar cortical pattern of atrophy as compared to controls. We conclude that VBM reveals selective cortical atrophy in patients with MSA-P affecting primary and higher order motor areas as well as prefrontal and insular cortices. Further studies are required to determine clinical and/or subclinical correlates of cortical atrophy in MSA-P.

Aged↗
PubMed2006

PGC-1alpha protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription.

Maintaining muscle size and fiber composition requires contractile activity. Increased activity stimulates expression of the transcriptional coactivator PGC-1alpha (peroxisome proliferator-activated receptor gamma coactivator 1alpha), which promotes fiber-type switching from glycolytic toward more oxidative fibers. In response to disuse or denervation, but also in fasting and many systemic diseases, muscles undergo marked atrophy through a common set of transcriptional changes. FoxO family transcription factors play a critical role in this loss of cell protein, and when activated, FoxO3 causes expression of the atrophy-related ubiquitin ligases atrogin-1 and MuRF-1 and profound loss of muscle mass. To understand how exercise might retard muscle atrophy, we investigated the possible interplay between PGC-1alpha and the FoxO family in regulation of muscle size. Rodent muscles showed a large decrease in PGC-1alpha mRNA during atrophy induced by denervation as well as by cancer cachexia, diabetes, and renal failure. Furthermore, in transgenic mice overexpressing PGC-1alpha, denervation and fasting caused a much smaller decrease in muscle fiber diameter and a smaller induction of atrogin-1 and MuRF-1 than in control mice. Increased expression of PGC-1alpha also increased mRNA for several genes involved in energy metabolism whose expression decreases during atrophy. Transfection of PGC-1alpha into adult fibers reduced the capacity of FoxO3 to cause fiber atrophy and to bind to and transcribe from the atrogin-1 promoter. Thus, the high levels of PGC-1alpha in dark and exercising muscles can explain their resistance to atrophy, and the rapid fall in PGC-1alpha during atrophy should enhance the FoxO-dependent loss of muscle mass.

Animals↗
PubMed2000

Prospective analysis of strength in spinal muscular atrophy. DCN/Spinal Muscular Atrophy Group.

Spinal muscular atrophy is a genetic disorder of the motor neurons that causes profound hypotonia, severe weakness, and often fatal restrictive lung disease. Patients with spinal muscular atrophy present a spectrum of disease from the most severe infantile-onset type, called Werdnig-Hoffmann disease (type 1), associated with a mortality rate of up to 90%, to a late-onset mild form (type 3), wherein patients remain independently ambulatory throughout adult life. Although many clinicians agree that patients with spinal muscular atrophy lose motor abilities with age, it is unknown whether progressive weakness occurs in all patients with spinal muscular atrophy. We present here results of the first prospective study of muscle strength in patients with spinal muscular atrophy. There was no loss in muscle strength as determined by a quantitative muscle test during the observation period. However, motor function diminished dramatically in some patients with spinal muscular atrophy. Explanations for this loss of function could not be determined from our data. Decrease in motor function could be caused by factors other than loss of strength. Therefore, it is not clear from our results whether spinal muscular atrophy is a neurodegenerative disease. We conclude that treatment trials in spinal muscular atrophy should be designed with consideration of the natural history of strength and motor function in this disorder.

Adolescent↗