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Results for “Atrophy”

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PubMed1995

Increase in levels of polyubiquitin and proteasome mRNA in skeletal muscle during starvation and denervation atrophy.

Most of the increased protein degradation in muscle atrophy caused by starvation and denervation is due to activation of a non-lysosomal ATP-dependent proteolytic process. To determine whether expression of the ubiquitin-proteasome-dependent pathway is activated in atrophying muscles, we measured the levels of mRNA for ubiquitin (Ub) and proteasome subunits, and Ub content. After rats had been deprived of food for 1 or 2 days, the concentration of the two polyubiquitin (polyUb) transcripts increased 2-4-fold in the pale extensor digitorum longus muscle and 1-2.5-fold in the red soleus, whereas total muscle RNA and total mRNA content fell by 50%. After denervation of the soleus, there was a progressive 2-3-fold increase in polyUb mRNA for 1-3 days, whereas total RNA content fell. On starvation or denervation, Ub concentration in the muscles also rose by 60-90%. During starvation, polyUb mRNA levels also increased in heart, but not in liver, kidney, spleen, fat, brain or testes. Although the polyUb gene is a heat-shock gene that is induced in muscles under certain stressful conditions, the muscles of starving rats or after denervation did not express other heat-shock genes. On starvation or denervation, mRNA for several proteasome subunits (C-1, C-3, C-5, C-8 and C-9) also increased 2-4-fold in the atrophying muscles. When the food-deprived animals were re-fed, levels of Ub and proteasome mRNA in their muscles returned to control values within 1 day. In contrast, no change occurred in the levels of muscle mRNAs encoding cathepsin L, cathepsin D and calpain 1 on denervation or food deprivation. Thus polyUb and proteasome mRNAs increased in atrophying muscles in co-ordination with activation of the ATP-dependent proteolytic process.

Adenosine Triphosphate↗

PubMed1997

The influence of the cervix on smear quality. I: Atrophy. An audit of cervical smears taken post-colposcopic management of intraepithelial neoplasia.

Out of 951 smears taken from women attending a hospital cytology clinic, 122 were found to be of poor quality. Twenty-eight percent of these were associated with clinical and/or cytological atrophy, and in 91% of these the main adverse factor affecting smear quality was scantiness. The relative risk of obtaining a scanty smear was found to be 4.8 times greater in women in whom clinical atrophy was identified when compared with those with no atrophy. It is suggested that a reduction in the number of scanty, and hence potentially inadequate, smears in the screening programme may be achieved by the use of more appropriate sampling implements in all women in whom there is clinical evidence of atrophy. Further review of alternative sampling methods is indicated.

Adult↗

PubMed2002

Sporadic amyotrophic lateral sclerosis with circumscribed temporal atrophy: a report of an autopsy case without dementia and with ubiquitinated intraneuronal inclusions.

This report concerns an autopsy case of amyotrophic lateral sclerosis (ALS) with circumscribed temporal atrophy. The patient was a Japanese woman without hereditary burden who was 71-year-old at the time of death. She developed dysarthria and gait disturbance at age 69, followed by dysphagia. A neurological examination about 1 year 11 months after the onset of the disease revealed absence of character change and of dementia. Neuroradiological examination disclosed circumscribed atrophy of the anterior part of the right temporal lobe. The patient died of respiratory failure 2 years after the disease onset. No respirator administration was performed throughout the clinical course. Macroscopically, neuropathological examination showed circumscribed atrophy of the right first temporal gyrus. Histologically, there was neuronal loss in the cerebral cortex, including the first temporal gyrus, the parahippocampal gyrus, subiculum, amygdala, substantia nigra, brain stem motor nuclei, and anterior horns of the spinal cord, in addition to loss of Betz cells, obvious degeneration of the pyramidal tracts, and the presence of Bunina bodies. Ubiquitin-immunoreactive intraneuronal inclusions were present in the hippocampal dentate granular cells, frontotemporal cortical layer II neurons, and motor neurons in the brain stem and spinal cord. Based on these clinicopathological findings and a review of the literature, we concluded that our case was atypical ALS without dementia, showing temporal lobe atrophy macroscopically, in addition to pathological hallmarks compatible with ALS with dementia. We also note the possibility that there is a forme fruste of ALS with dementia showing no overt dementia clinically.

Aged↗

PubMed2002

Effect of peripapillary chorioretinal atrophy on GDx parametersin patients with degenerative myopia.

PURPOSE: To determine the effect of peripapillary chorioretinal atrophy in degenerative myopia on the retinal nerve fibre layer (RNFL) thickness measurements performed by scanning laser polarimetry. METHODS: Polarimetric RNFL analysis was done in 41 degenerative myopic eyes of 25 patients with spherical refractive errors between -7.50 and -22.00 D (mean -12.50 D;SD 3.5). Analysis was also performed on 46 eyes of 24 age-matched healthy subjects with spherical refractive errors between -1.00 and +1.00 D (mean -0.25 D; SD 0.50) with GDx Nerve Fiber Analyzer (Version 1.0.12). All of the myopic patients had clinically evident peripapillary chorioretinal atrophy in their fundus examination. RESULTS: In myopic patients most of the GDx parameters were statistically different from the control group (P < 0.05). Although average thickness, ellipse average, number, inferior maximum and inferior average were found to be higher than the healthy subjects,the modulation parameters and the ratio-based parameters were significantly decreased in degenerative myopic patients (P < 0.05). The TSNIT (temporal, superior, nasal, inferior, temporal) graph showed irregular high spikes with loss of the regular double hump pattern, especially in quadrants with large chorioretinal atrophy and visible sclera. CONCLUSION: Peripapillary chorioretinal atrophy increased retardation values, which might be explained by the high reflectivity of the bare sclera in these areas.

Adolescent↗

PubMed2001

T1 lesion load and cerebral atrophy as a marker for clinical progression in patients with multiple sclerosis. A prospective 18 months follow-up study.

We investigated the relationship between local tissue destruction, diffuse cerebral atrophy and clinical progression in patients with established multiple sclerosis (MS). Twenty-nine patients with MS (13 patients with relapsing--remitting and 16 with secondary progressive disease) were included in a prospective serial study. Cerebral volumes, T1 hypointense lesion volumes, T2 hyperintense lesion volumes at baseline and at 18 months follow-up, and the volume of monthly enhancing lesions from month 0 to month 9 were assessed on magnetic resonance imaging (MRI) brain scans using highly reproducible semi-automated quantitative techniques. The main outcome measures were the MRI parameters and disability on Kurtzkes' Expanded Disability Status Scale. There was a significant correlation between the change (increase) in T1 lesion volume and progressive cerebral atrophy, whereas no correlation between the T2 lesion volume and atrophy was seen over the same follow-up period. The change in T1 lesion volume correlated more strongly than did T2 lesion volume change with the change in disability. We conclude that hypointense abnormalities detected in T1-weighted brain scans and cerebral atrophy may be directly linked. Although one should bear in mind some potential for reversibility due to inflammatory, oedematous lesions, these MR measures are a useful marker of progressive tissue damage and clinical progression in established MS.

Adult↗

PubMed2003

Volumetric quantitation by MRI in primary progressive multiple sclerosis: volumes of plaques and atrophy correlated with neurological disability.

In primary progressive multiple sclerosis (PPMS) abnormalities in brain magnetic resonance imaging (MRI) differ from abnormalities in other subtypes of multiple sclerosis (MS). It was investigated whether the extent of brain and spinal cord MRI abnormalities is reflected in the neurological disability in PPMS. Focal and diffuse changes and atrophy in central nervous system (CNS) in patients with PPMS (n = 28) and healthy controls (n = 20) were assessed by semi-automatic MRI segmentation and volumetric analysis. The measurements were related to neurological disability as expressed by the expanded disability status scale (EDSS), the regional functional scoring system (RFSS), the arm index and the ambulation index. Plaques in T1- and/or T2-weighted images were seen in all brains, while spinal plaques were detected in 23 of 28 patients (82%). The total volumes of brain and spinal cord were significantly smaller in patients than in controls (P = 0.001 and 0.000, respectively). The volumes of T1 or T2 lesions in the brain correlated to the ambulation index (r = 0.51, P = 0.005 and r = 0.53, P = 0.004, respectively). No correlations were detected between MRI measurements and total EDSS score, but relative brain atrophy correlated inversely with the total RFSS scores, poor arm index and higher cerebral disturbances (r = -0.53, P = 0.004; r = -0.53, P = 0.004; and r = -0.52, P = 0.005, respectively). Although the number of spinal T2 lesions correlated with sensory disturbances (r = 0.60, P = 0.001), no correlations were found between EDSS subscores and spinal cord atrophy. These findings show that marked atrophy of brain and spinal cord detected by volumetric quantitation correlates with neurological disability. This observation indicates the importance of neurodegenerative events in PPMS.

Activities of Daily Living↗

PubMed2000

Recombinant human interleukin-11 prevents mucosal atrophy and bowel shortening in the defunctionalized intestine.

BACKGROUND: Mucosal atrophy and bowel shortening are the hallmark of proximal intestinal diversion for extensive necrotizing enterocolitis (NEC) or Thiry-Vella fistulas (TVF), in which the ends of a defunctionalized loop of intestine are exteriorized as stomas. Recombinant human interleukin-11 (rhIL-11) is a pleiotropic cytokine that promotes epithelial regeneration and enhances adaptation after bowel resection. The authors hypothesized that rhIL-11 may prevent mucosal atrophy and bowel shortening in rats with TVF METHODS: After creation of ileal TVF, Sprague-Dawley rats were selected randomly to receive either rhIL-11 or equal volume of 0.1% bovine serum albumin (BSA) subcutaneously daily. On day 14, the TVF were excised and examined morphologically. Enterocyte apoptosis was measured using the TUNEL assay. Mucosal DNA and protein content were measured. RESULTS: Administration of rhIL-11 resulted in a significantly greater weight gain and less shortening of TVF than BSA treatment. TVF from the rhIL-11-treated group showed evidence of hyperplasia and hypertrophy and increased crypt to villus ratio. The BSA group had substantial mucosal atrophy. There was a qualitative decrease in the incidence of apoptosis in the rhIL-11 group. CONCLUSIONS: Recombinant human IL-11 prevents mucosal atrophy and shortening of defunctionalized intestinal loops. It may help reduce the incidence of short gut syndrome in infants with extensive NEC.

Animals↗

PubMed2003

[In-vivo measurement of autofluorescence in the parapapillary atrophic zone of optic discs with and without glaucomatous atrophy].

BACKGROUND: To assess the level of autofluorescence (lipofuscin) of atrophic parapapillary zones in different stages of glaucomatous optic disc atrophy. METHODS: Controlled cross-sectional prospective analysis of 79 consecutive eyes (15 normals as controls, 26 with ocular hypertension, 38 with primary open angle glaucoma). Eyes with retinal diseases or retinal pigment epithelial pathologies were excluded. The confocal scanning laser ophthalmoscope (HRA, Heidelberg Retina Angiograph) was used after lipofuscin excitation with argon blue laser (488 nm) to detect parapapillary autofluorescence in a spectrum above 500 nm. Size, extension of the parapapillary autofluorescent area and its mean distance to the optic nerve head were measured using the HRA standard software. Additional optic nerve head photographs taken with the 15 degrees Zeiss telecentric fundus camera (30 degrees camera with 2 x magnifier) were examined by two experienced ophthalmologists to determine the stage of glaucomatous optic disc atrophy (stages 0 to 4). RESULTS: Very small autofluorescent areas were found in vital discs (optic nerve glaucoma stage 0) in the parapapillary atrophic area (0.08 +/- 0.12 mm (2)) in contrast to glaucomatous discs in stage 1 (0.24 +/- 0.26 mm (2)) and stages 2, 3 and 4 (0.59 +/- 1.29 mm (2), logistic regression analysis r = 0.71; P = 0.029). The circular extension of the autofluorescent area correlated borderlined with the stage of the glaucomatous disc atrophy (higher glaucoma stages: r = 0.82; P = 0.09). The autofluorescent area was larger in OHT than in controls (0.11 mm (2) vs. 0.04 mm (2), P < 0.03). The circular extension of the autofluorescent area was longer in OHT than in controls (0.5 mm vs. 1.15 mm, P < 0.04). CONCLUSIONS: As a sign of pronounced lipofuscin accumulation in the parapapillary atrophic zone higher degrees of fundus autofluorescence can be detected in OHT and manifest primary open angle glaucoma in contrast to normals. The lipofuscin accumulation is correlated with the stage of progression of glaucoma and the stage of optic disc atrophy. The detection of active parapapillary autofluorescent areas especially in OHT may offer the ophthalmologist an important tool for early diagnosis.

Adult↗

PubMed1989

Laparoscopic observation of hepatic lobe atrophy.

From the standpoint of diagnostic laparoscopy, the frequency and etiological aspect of atrophy of a lobe of the liver was studied. The frequency of hepatic lobe atrophy was 5.3% among 1,208 laparoscopy cases at our department. Lobe atrophy of the liver can be seen not only in congenital anomaly, atrophic cirrhosis and malformation, as described in the OMED database of digestive endoscopy, but also in some other kinds of liver diseases including chronic hepatitis, idiopathic portal hypertension, primary biliary cirrhosis, drug-induced liver injury, scarred liver, autoimmune hepatitis and also in malignancies of other visceral organs. The disorders most frequently associated with hepatic lobe atrophy were idiopathic portal hypertension, and scarred liver, primary biliary cirrhosis, etc.

Atrophy↗

PubMed1999

[Psychotic symptoms as initial manifestation of a multiple system atrophy].

Multiple system atrophy is a disease characterised clinically by any combination of parkinsonian, pyramidal, autonomic or cerebellar symptoms and signs. This neurological status is often complicated by associated mental disturbances such as deficits in concentration, memory or learning. There are only very few reports in the literature describing cases of multiple system atrophy associated with psychotic symptoms. We report on two cases in which psychotic symptoms were the initial manifestation of multiple system atrophy. In view of the known neuropathologic and biochemical changes in multiple system atrophy the concurrent incidence of paranoid-hallucinatoric symptoms seems not uncommon and should be studied further.

Adult↗

PubMed1994

[Pick and focal brain atrophy].

In 1892 Arnold Pick presented the case of an elderly demented patient with severe aphasia and global brain atrophy most accentuated at the left temporal lobe. Picks main interest was the relationship between focally accentuated brain degeneration and focally accentuated neuropsychological deficits, and this was what he wanted to demonstrate. He made no effort to describe a new form of dementia. The term "Pick's disease" which was introduced 30 years later implies the existence of a nosological entity with characteristic clinical features, localisation and histology. The neuropathological causes of focally accentuated brain atrophies are varied. Neocortical pyramidal cell loss with or without spongiform changes, cortical and subcortical gliosis have commonly been described. Achromatic neuronal ballooning ("Pick's cells") and intraneuronal argentophilic inclusion bodies ("Pick's bodies"), Alzheimer type plaques and tangles and other features were found in a smaller number of cases. Several authors confirmed an association between the localisation of brain atrophy and its clinical manifestations, but no convincing relationship has been demonstrated between the clinical symptoms and the underlying histology. In several studies frontal lobe degeneration was found in 10% to 20% of the demented patients, whereas aphasia, apraxia and other pronounced deficits in the context of focally accentuated brain atrophy were described less frequently. An early clinical distinction between atypical early stages of Alzheimer's disease and other forms of slowly progressive dementing disorders is virtually impossible in these cases. Prospective studies documenting the clinical and anatomical findings are needed to examine the reliability of these surmised brain-behaviour relationships in degenerative brain diseases more reliably. A descriptive approach offers a better basis for data collection than the premature diagnosis of a poorly defined disease like "Pick's".

Alzheimer Disease↗

PubMed1984

[Independence of retinopathy and optic atrophy in the DIDMOAD syndrome].

A brother and a sister with DIDMOAD syndrome (diabetes insipidus, diabetes mellitus, optic atrophy, deafness, etc.) are described. The 15-year-old girl was suffering from severe optic atrophy, severe sensorineural hearing loss but only slight diabetic retinopathy. The 16-year-old boy presented with symptoms which were the opposite: slight optic atrophy, slight sensorineural hearing loss but severe diabetic retinopathy. These complementary impairments of neuronal and (diabetic) retinal function suggest that optic atrophy and retinopathy develop independently in DIDMOAD syndrome.

Adolescent↗

PubMed1993

Ultrasound measurement of quadriceps muscle in the first year of life. Normal values and application to spinal muscular atrophy.

Using real-time ultrasound imaging normal values were obtained for quadriceps muscle thickness and subcutaneous tissue depth in the first year of life from 120 normal infants. These values were corrected for weight and height by introduction of a "correcting factor". In addition, a "modified muscle index" was calculated by multiplying the ratio of muscle to subcutaneous tissue thickness with the correcting factor and showed a steady increase from birth (mean 2.1) to the end of the first year (mean 4.8). The study of 12 patients with spinal muscular atrophy type I (SMA I) revealed that 9 out of 12 SMA I patients failed to reach the 3rd percentile for the muscle to subcutaneous tissue ratio and 10 out of 12 were well below the 3rd percentile for the modified muscle index due to their muscle atrophy. Only the two youngest SMA I patients aged 4 and 6 weeks reached values on the 3rd percentile. In contrast, 10 patients with myopathy and one patient with holoprosencephaly showed values within the normal percentiles even in the presence of severe clinical muscle weakness and signs of atrophy on muscle histology. In the differential diagnosis of early onset myopathy, atrophy of the quadriceps muscle during the first months of life in the absence of markedly increased echodensity seems to be a pathognomonic finding for SMA.

Body Weight↗

PubMed2000

Risk factors for hyperplasia-associated versus atrophy-associated endometrial carcinoma.

OBJECTIVE: Endometrial cancer can be divided into atrophy-associated and hyperplasia-associated subtypes. It has been suggested that these subtypes have different pathologic features and prognoses. This preliminary study explores whether these subtypes are associated with different risk factors. STUDY DESIGN: Hysterectomies performed in cases of endometrial carcinoma with evaluable benign endometrium on routine processing were reviewed, and clinical data were abstracted from medical records. Forty-eight subjects with atrophy-associated and 28 subjects with hyperplasia-associated cancers were studied. RESULTS: We found younger age, higher weight, absence of cigarette smoking, and earlier menarche in subjects with hyperplasia-related cancers. CONCLUSIONS: Our findings support the idea that hyperplasia-associated endometrial cancer is estrogen-related but also suggest that atrophy-associated cases may result from a different causal pathway. Epidemiologic studies may yield more precise and accurate measures of association if atrophy-associated and hyperplasia-associated endometrial cancers are considered separately.

Adenocarcinoma↗

PubMed2001

Atrogin-1, a muscle-specific F-box protein highly expressed during muscle atrophy.

Muscle wasting is a debilitating consequence of fasting, inactivity, cancer, and other systemic diseases that results primarily from accelerated protein degradation by the ubiquitin-proteasome pathway. To identify key factors in this process, we have used cDNA microarrays to compare normal and atrophying muscles and found a unique gene fragment that is induced more than ninefold in muscles of fasted mice. We cloned this gene, which is expressed specifically in striated muscles. Because this mRNA also markedly increases in muscles atrophying because of diabetes, cancer, and renal failure, we named it atrogin-1. It contains a functional F-box domain that binds to Skp1 and thereby to Roc1 and Cul1, the other components of SCF-type Ub-protein ligases (E3s), as well as a nuclear localization sequence and PDZ-binding domain. On fasting, atrogin-1 mRNA levels increase specifically in skeletal muscle and before atrophy occurs. Atrogin-1 is one of the few examples of an F-box protein or Ub-protein ligase (E3) expressed in a tissue-specific manner and appears to be a critical component in the enhanced proteolysis leading to muscle atrophy in diverse diseases.

Amino Acid Sequence↗

PubMed1999

Age-associated neuronal atrophy occurs in the primate brain and is reversible by growth factor gene therapy.

The effects of normal aging on the primate brain are incompletely understood. Although both human and nonhuman primates demonstrate clear functional declines in selective attention, "executive" functions, and some components of declarative memory with aging, most studies have failed to demonstrate extensive neuronal atrophy or loss as a substrate for these degenerative changes in primates. In particular, extensive age-related neuronal loss in memory-related brain regions such as the hippocampus and entorhinal cortex has not been found. However, it is possible that neuronal loss or atrophy might occur in subcortical nuclei that modulate the activity of neocortical regions, thereby accounting for altered cognitive function with aging. In the present study, we describe, to our knowledge for the first time, a significant and extensive decline in the number and size of immunolabeled neurons in subcortical cholinergic basal forebrain regions of aged rhesus monkeys, the best animal model of human aging, by using stereological methods. Notably, the loss of subcortical cholinergic neuronal markers in aged monkeys was nearly completely reversed by human nerve growth factor gene delivery. These findings (i) identify reversible cellular atrophy as a potential mechanism contributing to age-related cognitive decline in primates, (ii) suggest, when considered with other studies, that subcortical brain regions exhibit greater vulnerability to the effects of aging than cortical regions, and (iii) indicate that neurotrophin gene transfer may be an effective means of preventing neuronal atrophy or degeneration in age-related neurodegenerative disorders.

Age Factors↗

PubMed2004

Insulin-like growth factor-1 (IGF-1) inversely regulates atrophy-induced genes via the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway.

Skeletal muscle size is regulated by anabolic (hypertrophic) and catabolic (atrophic) processes. We first characterized molecular markers of both hypertrophy and atrophy and identified a small subset of genes that are inversely regulated in these two settings (e.g. up-regulated by an inducer of hypertrophy, insulin-like growth factor-1 (IGF-1), and down-regulated by a mediator of atrophy, dexamethasone). The genes identified as being inversely regulated by atrophy, as opposed to hypertrophy, include the E3 ubiquitin ligase MAFbx (also known as atrogin-1). We next sought to investigate the mechanism by which IGF-1 inversely regulates these markers, and found that the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway, which we had previously characterized as being critical for hypertrophy, is also required to be active in order for IGF-1-mediated transcriptional changes to occur. We had recently demonstrated that the IGF1/PI3K/Akt pathway can block dexamethasone-induced up-regulation of the atrophy-induced ubiquitin ligases MuRF1 and MAFbx by blocking nuclear translocation of a FOXO transcription factor. In the current study we demonstrate that an additional step of IGF1 transcriptional regulation occurs downstream of mTOR, which is independent of FOXO. Thus both the Akt/FOXO and the Akt/mTOR pathways are required for the transcriptional changes induced by IGF-1.

Active Transport, Cell Nucleus↗

PubMed2003

Peripapillary choroidal atrophy in sympathetic ophthalmia and management with triple-agent immunosuppression.

PURPOSE: To describe the occurrence of peripapillary choroidal atrophy and experience with triple-agent immunosuppression in three cases of sympathetic ophthalmia. MATERIALS AND METHODS: Retrospective chart review of three cases of sympathetic ophthalmia with peripapillary choroidal atrophy. RESULTS: Three patients with sympathetic ophthalmia were managed with steroid pulse therapy and triple-agent immunosuppression. All three patients subsequently developed peripapillary choroidal atrophy. CONCLUSIONS: Peripapillary choroidal atrophy can occur in sympathetic ophthalmia and may indicate a severe form of inflammation which would benefit from triple-agent immunosuppression.

Adult↗