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PubMed2003

Cerebral atrophy and disability in relapsing-remitting and secondary progressive multiple sclerosis over four years.

Pathology and magnetic resonance imaging (MRI) studies have provided evidence of widespread axonal loss and reductions of cerebral and spinal cord volume in multiple sclerosis (MS). Atrophy measures on MRI may be a useful surrogate marker of worsening disability in MS, but the published studies are of relatively short duration. Change in brain volume (atrophy) was measured over a four-year period in 20 patients with relapsing-remitting (RR) and 18 with secondary progressive (SP) MS using three-dimensional (3D) MRI acquired during treatment trials of interferon-beta-1a (Rebif). Brain parenchymal and lateral ventricle volume changes were determined and correlated with clinical measures. Over four years, brain parenchymal volume (BPV) decreased in RRMS and SPMS patients by 0.9% (P = 0.006) and 0.3% (P = 0.118), respectively, and the lateral ventricle volumes increased by 15% (P < 0.0001) and 13% (P < 0.0001), respectively. In RRMS patients both lateral ventricle volume (r = 0.63, P = 0.004) and BPV change (r = -0.47, P = 0.037) were related to disability change, as measured by the Expanded Disability Status Scale. Even though a small study and despite the possible confounding effects of interferon treatment, this study demonstrated an association between measures of cerebral atrophy and worsening disability. The data also provides evidence that brain atrophy can be detected early in the disease course and central white matter atrophy as reflected by ventricle enlargement appears to be a continuous process.

Adjuvants, Immunologic↗

PubMed2004

Atrophy rate in medial temporal lobe during progression of Alzheimer disease.

OBJECTIVE: To establish the progression of brain atrophy rates in patients with a known date of onset of Alzheimer disease (AD). METHODS: Each of 18 subjects had two high-resolution T1-weighted three-dimensional MRI examinations. The two MRIs were coregistered and the annual rate of brain tissue atrophy was derived both for the entire brain and regionally for the left and right medial temporal lobe (MTL). Time since onset (TSO) of AD, defined as the interval between the date of onset and the midpoint of MRI dates, ranged from -2.9 to 4.2 years. RESULTS: In patients with AD, TSO was a correlate of the atrophy rate for both the left MTL (R2 = 0.58, p = 0.001) and right MTL (R2 = 0.30, p = 0.03). When serial measurements were applied to a control group of 21 cognitively normal elderly subjects, MTL atrophy rate classified the group membership (AD vs normal cognition) with an accuracy of 92.3%. CONCLUSION: Increased annual atrophy rate in the medial temporal lobe is a potential diagnostic marker of the progression of Alzheimer disease.

Aged↗

PubMed2005

Rate of brain atrophy in relapsing MS decreases during treatment with IFNbeta-1a.

OBJECTIVE: To determine the time course of brain atrophy during treatment with once-weekly IM interferon beta-1a (IFNbeta-1a). METHODS: The MRI cohort (n = 386) of the European IFNbeta-1a dose comparison study in relapsing multiple sclerosis (MS) was analyzed. In addition to baseline and three annual scans, a frequent subgroup (n = 138) had two scans before treatment initiation and scans at months 4, 5, 6, 10, and 11. Brain parenchymal fraction (BPF), a normalized measure of whole-brain atrophy, and volume of Gd-enhancing lesions (T1Gd) and T2 hyperintense lesions (T2LL) were evaluated. RESULTS: BPF decrease was -0.686% (first year), -0.377% (second year), and -0.378% (third year). Analysis of the frequent subgroup showed that 68% of the first-year BPF decrease occurred during the first 4 months of treatment. This change was paralleled by a drop in T1Gd and T2LL. In the frequent subgroup, an annualized atrophy rate was determined by a regression slope for the pretreatment period and from month 4 of treatment onward. Annualized pretreatment rate (-1.06%) was significantly higher than the under-treatment rate (-0.33%). CONCLUSIONS: In the first year of treatment with anti-inflammatory agents, atrophy measurements are possibly confounded by resolution of inflammatory edema or more remote effects of previous damage to the CNS. The atrophy rate reduction observed after treatment month 4 may reflect a beneficial but partial effect of interferon beta-1a and was sustained over the 3-year study period.

Adult↗

PubMed2005

Association between blood pressure, white matter lesions, and atrophy of the medial temporal lobe.

BACKGROUND: Blood pressure level is associated with the risk of clinical Alzheimer disease (AD), yet the underlying mechanisms are unclear. High blood pressure levels may cause cerebral small-vessel pathology, which contributes to cognitive decline in patients with AD. Alternatively, in persons with high blood pressure, increased numbers of neurofibrillary tangles and amyloid plaques at autopsy have also been observed, suggesting direct links between blood pressure and AD. OBJECTIVE: To investigate the association of blood pressure and markers of small-vessel disease (white matter lesions [WMLs] on MRI) with hippocampal and amygdalar atrophy on MRI-potential in vivo indicators of Alzheimer pathology. METHODS: In 1995 to 1996, 511 nondemented elderly subjects (age 60 to 90) underwent MRI. The extent of WMLs was assessed, and volumes of the hippocampus and amygdala were measured. Blood pressure levels were assessed at the time of MRI and 5 years before the MRI. RESULTS: Higher diastolic blood pressure 5 years before MRI predicted more hippocampal atrophy in persons untreated for hypertension (per SD increase -0.10 mL [95% CI -0.19 to -0.02, p = 0.02]). Conversely, in persons treated for hypertension, a low diastolic blood pressure was associated with more severe atrophy. Persons with more WMLs on MRI more often had severe atrophy of the hippocampus and amygdala. CONCLUSION: Blood pressure and indicators of small-vessel disease in the brain may be associated with atrophy of structures affected by Alzheimer pathology.

Adult↗

PubMed2005

Risk factors for progression of brain atrophy in aging: six-year follow-up of normal subjects.

OBJECTIVES: To determine the rate of brain atrophy in neurologically asymptomatic elderly and to investigate the impact of baseline variables including conventional cerebrovascular risk factors, APOE epsilon4, and white matter hyperintensity (WMH) on its progression. METHODS: We assessed the brain parenchymal fraction at baseline and subsequent annual brain volume changes over 6 years for 201 participants (F/M = 96/105; 59.8 +/- 5.9 years) in the Austrian Stroke Prevention Study from 1.5-T MRI scans using SIENA (structural image evaluation using normalization of atrophy)/SIENAX (an adaptation of SIENA for cross-sectional measurement)(www.fmrib.ox.ac.uk/fsl). Hypertension, cardiac disease, diabetes mellitus, smoking, and regular alcohol intake were present in 64 (31.8%), 60 (29.9%), 5 (2.5%), 70 (39.3%), and 40 (20.7%) subjects, respectively. Plasma levels of fasting glucose (93.7 +/- 18.6 mg/dL), glycated hemoglobin A (HbA1c; 5.6 +/- 0.7%), total cholesterol (228.3 +/- 40.3 mg/dL), and triglycerides (127.0 +/- 75.2 mg/dL) were determined. WMH was rated as absent (n = 56), punctate (n = 120), early confluent (n = 14), and confluent (n = 11). RESULTS: The baseline brain parenchymal fraction of the entire cohort was 0.80 +/- 0.02 with a mean annual brain volume change of -0.40 +/- 0.29%. Univariate analysis demonstrated a higher rate of brain atrophy in older subjects (p = 0.0001), in those with higher HbA1c (p = 0.0001), higher body mass index (p = 0.02), high alcohol intake (p = 0.04), severe WMH (p = 0.03), and in APOE epsilon4 carriers (p = 0.07). Multivariate analysis suggested that baseline brain parenchymal fraction, HbA1c, and WMH score explain a major proportion of variance in the rates of brain atrophy in the cohort (corrected R2 = 0.27; p = 0.0001). CONCLUSIONS: Neurologically asymptomatic elderly experience continuing brain volume loss, which appears to accelerate with age. Glycated hemoglobin A (HbA1c) was identified as a risk factor for a greater rate of brain atrophy. Clustering of factors associated with the so-called metabolic syndrome in subjects with high HbA1c suggests a link between this syndrome and late-life brain tissue loss.

Age Distribution↗

PubMed2006

Predominant dystonia with marked cerebellar atrophy: a rare phenotype in familial dystonia.

BACKGROUND: Dystonia syndromes constitute a heterogeneous group of phenotypes that may be caused by different heredodegenerative, metabolic, or genetic diseases. OBJECTIVE: To describe the characteristics of an unusual dystonia-plus phenotype associated with cerebellar atrophy. METHODS: We selected patients with predominant dystonia and cerebellar atrophy among the 861 families referred to us for genetic testing from 1992 to 2003. The main secondary heredodegenerative causes and the major genes responsible for hereditary dystonias and autosomal dominant or recessive ataxias were excluded. RESULTS: We identified 12 patients in 8 families with an unusual dystonia-plus phenotype characterized by dystonia and cerebellar atrophy on brain MRI. The mean age at onset was 27.3 +/- 11.5 years (range: 9 to 42 years) and the mean disease duration 14.7 +/- 7.7 years (range: 4 to 30). At onset, dystonia was focal or multifocal, mainly affecting vocal cords (n = 8) and upper limbs (n = 2). During the disease course spasmodic dysphonia became severe in five patients, leading to complete aphonia in two. Dystonia became generalized in five. Cerebellar ataxia was limited to unsteadiness in most patients and progressed very slowly. The paucity of clinical cerebellar signs contrasted with the marked cerebellar atrophy on brain MRI in most patients. Four families with two affected sibs support the hypothesis of an autosomal recessive disorder. However, X-linked inheritance is possible since only men were affected. CONCLUSION: We have characterized an unusual familial phenotype associating dystonia and cerebellar atrophy in 12 male patients.

Adult↗

PubMed1999

Hippocampal and entorhinal cortex atrophy in frontotemporal dementia and Alzheimer's disease.

OBJECTIVE: To describe atrophic changes of the hippocampus and entorhinal cortex in frontotemporal dementia (FTD) and compare them with those of AD. BACKGROUND: The medial temporal lobe shows atrophic changes early in the course of AD, but whether these changes are specific to AD or occur in other degenerative dementias, and to what extent, is unclear. METHODS: The authors measured the volumes of the left and right hippocampus and entorhinal cortex from MR images (1.5 T, 2-mm-thick slices) in 12 patients with FTD, 30 with AD, and 30 elderly control subjects. RESULTS: In FTD patients, the left and right hippocampus (16% and 21% tissue loss) and the entorhinal cortex (28% and 27% loss) were more atrophic than the control subjects. Atrophy of the hippocampus in FTD was less severe than in AD, but atrophy of the entorhinal cortex was equally severe. Greater hippocampal and entorhinal cortex atrophy was present in the most severe patients in both groups (as high as a 49% tissue loss). The sensitivity of the hippocampus and the entorhinal cortex to discriminate FTD patients from control subjects was low (49% and 52%, respectively; specificity set at 90%), whereas hippocampal volumes could better differentiate AD patients from control subjects (80% sensitivity). CONCLUSIONS: At variance with AD, detectable in vivo atrophy of the hippocampus might not be an early event in FTD. Differential patterns of atrophy might help in the diagnostic process of the degenerative dementias.

Age Factors↗

PubMed2001

Seizure outcome and hippocampal atrophy in familial mesial temporal lobe epilepsy.

OBJECTIVE: To describe the clinical, genetic and MR characteristics of patients with familial mesial temporal lobe epilepsy (MTLE). DESIGN/METHODS: The familial occurrence of MTLE was identified by a systematic search of family history of seizures in patients followed in the authors' epilepsy clinic. All probands and, whenever possible, other affected family members underwent EEG and MR investigations. RESULTS: Twenty-two unrelated families with at least two individuals with MTLE were identified by clinical and EEG findings. Ninety-eight individuals with history of seizures were evaluated. Sixty-eight patients fulfilled the diagnostic criteria for MTLE. MRI was performed in 84 patients, and showed hippocampal atrophy with increased T2 signal in 48 (57%). The distribution of hippocampal atrophy according to the seizure outcome groups was 6 of 13 patients (46%) with seizure remission, 16 of 31 (51%) with good seizure control under medication, and all 16 patients with refractory MTLE. Hippocampal atrophy was found also in patients that did not fulfill the criteria for MTLE: 3 of 10 (30%) patients with febrile seizure alone, 6 of 10 (60%) patients with recurrent generalized tonic-clonic seizures, and 1 of 4 (25%) patients with a single partial seizure. CONCLUSION: Familial MTLE is a clinically heterogeneous syndrome. Hippocampal atrophy was observed in 57% of patients, including those with benign course or seizure remission, indicating that the relationship between hippocampal atrophy and severity of epilepsy might be more complex than previously suspected. In addition, these findings indicate the presence of a strong genetic component determining the development of mesial temporal sclerosis in these families.

Adolescent↗

PubMed2001

Bilateral hippocampal atrophy: consequences to verbal memory following temporal lobectomy.

BACKGROUND: Bilateral hippocampal damage is a risk factor for memory decline after anterior temporal lobectomy (ATL). OBJECTIVE: To investigate verbal memory outcome in patients with temporal lobe epilepsy (TLE) with either unilateral or bilateral hippocampal atrophy as measured by MRI. METHODS: The authors selected 60 patients with TLE who had undergone ATL (left = 31, right = 29). They determined normalized MRI hippocampal volumes by cursor tracing 1.5-mm slices from three-dimensional MRI acquisition. Hippocampal volumes were defined as atrophic if the volumes were below 2 SD for control subjects. Bilateral hippocampal atrophy was present in 10 patients with left TLE and 11 patients with right TLE. The authors assessed acquisition, retrieval, and recognition components of verbal memory both before and after ATL. RESULTS: Groups did not differ across age, education, intelligence, age at seizure onset, or seizure duration. Seizure-free rates after ATL were 70% or higher for all groups. Before surgery, patients with left TLE displayed worse verbal acquisition performance compared with patients with right TLE. Patients with left TLE with bilateral hippocampal volume loss displayed the lowest performance across all three memory components. After surgery, both groups of patients with left TLE exhibited worse verbal memory outcome compared with patients with right TLE. Bilateral hippocampal atrophy did not worsen outcome in the patients with right TLE. A higher proportion of patients with left TLE with bilateral hippocampal atrophy experienced memory decline compared with the other TLE groups. CONCLUSION: Bilateral hippocampal atrophy in the presence of left TLE is associated with worse verbal memory before and after ATL compared with patients with unilateral hippocampal volume loss or right TLE with bilateral hippocampal volume loss.

Adolescent↗

PubMed2002

Patterns of brain atrophy in frontotemporal dementia and semantic dementia.

OBJECTIVE: To identify and compare the patterns of cerebral atrophy associated with two clinical variants of frontotemporal lobar degeneration (FTLD): frontotemporal dementia (FTD) and semantic dementia (SemD). METHODS: Twenty patients with FTLD were classified as having FTD (N = 8) or SemD (N = 12) based on current clinical criteria. Both groups showed a similar spectrum of behavioral abnormalities, as indicated by the neuropsychiatric inventory. T1-weighted MRI was obtained for each patient and 20 control subjects. The regions of focal gray matter tissue loss associated with both FTD and SemD, as well as those differing between the two groups were examined using voxel-based morphometry. RESULTS: Regions of significant atrophy seen in both groups were located in the ventromedial frontal cortex, the posterior orbital frontal regions bilaterally, the insula bilaterally, and the left anterior cingulate cortex. The FTD, but not the SemD, group showed atrophy in the right dorsolateral frontal cortex and the left premotor cortex. The SemD, but not the FTD, group showed tissue loss in the anterior temporal cortex and the amygdala/anterior hippocampal region bilaterally. CONCLUSIONS: Although FTD and SemD are associated with different overall patterns of brain atrophy, regions of gray matter tissue loss in the orbital frontal, insular, and anterior cingulate regions are present in both groups. The authors suggest that pathology in the areas of atrophy associated with both FTD and SemD may underlie some the behavioral symptoms seen in the two disorders.

Adult↗

PubMed2001

Testicular atrophy in 80 HIV-positive patients: a multivariate statistical analysis.

This retrospective study of risk factors for testicular atrophy in HIV-infected men investigates the relationship between complications of AIDS such as wasting or opportunistic illness and testicular atrophy. Microscopic sections of the right testis were evaluated for testicular atrophy by assessing the mean score in each of 80 selected HIV-infected patients who underwent an autopsy during a one-year period. A significant association was observed between testicular atrophy and body mass index (BMI) (P=0.0496). Thus, underweight patients with HIV infection were 3.52 times more likely to have testicular atrophy than those with acceptable body weight. Other significant associations between other variables were not found.

Adult↗

PubMed2006

Hyaluronate fragments reverse skin atrophy by a CD44-dependent mechanism.

BACKGROUND: Skin atrophy is a common manifestation of aging and is frequently accompanied by ulceration and delayed wound healing. With an increasingly aging patient population, management of skin atrophy is becoming a major challenge in the clinic, particularly in light of the fact that there are no effective therapeutic options at present. METHODS AND FINDINGS: Atrophic skin displays a decreased hyaluronate (HA) content and expression of the major cell-surface hyaluronate receptor, CD44. In an effort to develop a therapeutic strategy for skin atrophy, we addressed the effect of topical administration of defined-size HA fragments (HAF) on skin trophicity. Treatment of primary keratinocyte cultures with intermediate-size HAF (HAFi; 50,000-400,000 Da) but not with small-size HAF (HAFs; <50,000 Da) or large-size HAF (HAFl; >400,000 Da) induced wild-type (wt) but not CD44-deficient (CD44-/-) keratinocyte proliferation. Topical application of HAFi caused marked epidermal hyperplasia in wt but not in CD44-/- mice, and significant skin thickening in patients with age- or corticosteroid-related skin atrophy. The effect of HAFi on keratinocyte proliferation was abrogated by antibodies against heparin-binding epidermal growth factor (HB-EGF) and its receptor, erbB1, which form a complex with a particular isoform of CD44 (CD44v3), and by tissue inhibitor of metalloproteinase-3 (TIMP-3). CONCLUSIONS: Our observations provide a novel CD44-dependent mechanism for HA oligosaccharide-induced keratinocyte proliferation and suggest that topical HAFi application may provide an attractive therapeutic option in human skin atrophy.

Adult↗

PubMedDate not supplied

[Comparison of scanning laser polarimetry, optical coherence tomography 1 and Stratus optical coherence tomography for the detection of axonal loss in band atrophy of the optic nerve].

PURPOSE: To compare the abilitiy of scanning laser polarimetry (GDx), optical coherence tomography (OCT) 1 and Stratus- optical coherence tomography to discriminate between healthy eyes and eyes with band atrophy of the optic nerve and temporal hemianopsia. METHODS: Twenty-three eyes with band atrophy of the optic nerve and 23 eyes from healthy subjects were included in this observational prospective case-control study. All eyes underwent retinal nerve fiber layer (RNFL) thickness analysis using GDx, optical coherence tomography-1 and Stratus-optical coherence tomography. Mean values obtained with each equipment were compared between band atrophy and normal eyes. Receiver operating characteristic (ROC) curves and sensitivities at fixed specificities (80% e 95%) were calculated for each parameter calculated with each equipment and compared. RESULTS: When compared with healthy subjects, the parameters corresponding to the global average as well as each of the four quadrant retinal nerve fiber layer thickness in eyes with band atrophy were significantly smaller (p<0.05), than in normal eyes, with the exception of GDx's temporal thickness parameter. Comparison of the areas under ROC curves (AUCs) of the parameters from the three equipments revealed significantly greater values for the Stratus-OCT when compared to the OCT-1 in the global average and in the temporal quadrant thickness measurement. Stratus-OCT was significantly more sensitive than GDx in the global average as well as in the temporal, nasal and inferior quadrant. OCT-1 was superior to GDx only in the temporal quadrant. All three equipments revealed a similar ability to identify retinal nerve fiber layer reduction in the superior quadrant. CONCLUSIONS: The Stratus OCT showed the best ability to discriminate between eyes with band atrophy of the optic nerve and healthy eyes although all three equipments were able do identify most of the abnormal eyes. OCT-1 was inferior to Stratus-OCT and superior do GDx in the temporal quadrant. Although GDx was able identify some abnormality in most studied eyes, the equipment showed poor sensitivity in the detection of axonal loss in the nasal and temporal aspect of the optic disc and should be used with caution in neuro-ophthalmic diseases that cause retinal nerve fiber layer loss in those areas of the optic disc.

Axons↗

PubMed2006

Striatal and extrastriatal atrophy in Huntington's disease and its relationship with length of the CAG repeat.

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder that affects the striatum most severely. However, except for juvenile forms, relative preservation of the cerebellum has been reported. The objective of the present study was to perform MRI measurements of caudate, putamen, cerebral, and cerebellar volumes and correlate these findings with the length of the CAG repeat and clinical parameters. We evaluated 50 consecutive patients with HD using MRI volumetric measurements and compared them to normal controls. Age at onset of the disease ranged from 4 to 73 years (mean: 43.1 years). The length of the CAG repeat ranged from 40 to 69 (mean: 47.2 CAG). HD patients presented marked atrophy of the caudate and putamen, as well as reduced cerebellar and cerebral volumes. There was a significant correlation between age at onset of HD and length of the CAG repeat, as well as clinical disability and age at onset. The degree of basal ganglia atrophy correlated with the length of the CAG repeat. There was no correlation between cerebellar or cerebral volume and length of the CAG repeat. However, there was a tendency to a positive correlation between duration of disease and cerebellar atrophy. While there was a negative correlation of length of the CAG repeat with age at disease onset and with striatal degeneration, its influence on extrastriatal atrophy, including the cerebellum, was not clear. Extrastriatal atrophy occurs later in HD and may be related to disease duration.

Adolescent↗

PubMed2006

Estrogen administration attenuates immobilization-induced skeletal muscle atrophy in male rats.

We tested the hypothesis that estrogen administration would retard immobilization-induced muscle atrophy in adult male rats. The rats were injected for 24 days with either estrogen (40 microg/kg(-1), beta-estradiol 3-benzoate in olive oil vehicle), or vehicle alone. At day 14 of estrogen treatment, the hindlimb muscles of one leg were immobilized in plantar flexion position by the use of a plaster cast. Following 10 days of immobilzation, the atrophic and the contralateral soleus muscles were both removed and analyzed to determine the level of muscle atrophy along with the measurement of the protein levels of Cu-Zn-superoxide dismutase (Cu-Zn-SOD), heat shock protein 72 (HSP72), and selected proteases. Compared to placebo animals, estrogen treatment significantly reduced (-35%) muscle atrophy. Further, estrogen significantly abridged the expression of the calcium-activated protease, calpain, in the atrophied hindlimb muscle. In contrast, estrogen treatment did not alter the protein levels of HSP72 in the immobilized soleus muscle. These results support the postulate that estrogen attenuates the rate of disuse muscle atrophy, partly because of reductions in immobilization-induced calcium-activated protease levels.

Animals↗

PubMed1991

A case of Marfan's syndrome phenotype associated with neurogenic muscle atrophy.

A 23 year-old man was admitted because of weakness and atrophy in both tights. He was 184 cm in height with arachnodactyly and had a mild dilatation of the ascending aorta which was detected by cardiac echogram and chest CT scan. A laboratory examination revealed normal serum values for mucopolysaccarides and amino acids, and 46XY chromosomes. These findings indicate a Marfan's syndrome phenotype. A neurological finding showed a proximal dominant muscle atrophy and increased deep tendon reflexes. The EMG revealed a polyphasic action potential, and a subsequent muscle biopsy demonstrated a small group atrophy and atrophy of Type II fibers. Neuroradiological studies of brain and spinal cord indicated no substantial abnormalities. Only 4 cases of Marfanoid habit accompanied by primary nervous system disturbances have been reported and these had variable complications or severe neurological deficits. The present case, which involved mild neurogenic muscle atrophy and brisk deep tendon reflexes without complications except myopia, was unique.

Adult↗

PubMed1999

Development and validation of a physical examination scale to assess vaginal atrophy and inflammation.

BACKGROUND: The assessment of vaginal atrophy is central to menopause-related research and clinical practice. However, methods of grading vaginal atrophy have not been subjected to reliability and validity assessments. OBJECTIVE: To assess the validity and reproducibility of selected vaginal examination findings proposed to represent vaginal atrophy and inflammation. DESIGN: Cross-sectional study. PARTICIPANTS: A convenience sample of 40 postmenopausal volunteers with past history of breast cancer. MEASUREMENTS: Participants completed questionnaires to assess vaginal symptoms. Pelvic examinations were carried out using specified criteria to assess the vaginal appearance. Vaginal cytological smears and pH measurements were performed using standardized techniques. RESULTS: A four-item physical examination atrophy scale had an alpha reliability of 0.48 and was statistically significantly correlated with pH (r = 0.55) and parabasal cells (r = 0.50). A three-item physical examination inflammation scale had an alpha reliability of 0.45. It was not significantly associated with vaginal smear-measured inflammation. Masked inter-rater agreement for the examination was 90%. Self-reported symptoms of itching/irritation or dryness were poorly related to findings on physical examination. CONCLUSIONS: These results offer objective validation that the physical characteristics proposed to represent atrophy are related to biomarkers of this condition. A relationship between examination characteristics believed to represent inflammation and inflammation biomarkers was not upheld.

Atrophy↗

PubMed1994

Modulation of transglutaminase expression in rat skeletal muscle by induction of atrophy and endurance training.

The persistence of muscle fiber number regardless of size reduction in muscle atrophy has not yet been fully explained. For the mechanism inherent in skeletal muscle tissues for preventing cellular death, the protective function of muscle tissue through transglutaminases has been tested, since the enzyme is responsible for structural stabilization and participates in signal transduction. In the present experiment, hindlimb suspension for two weeks caused a marked muscle atrophy in Wistar female rats. Comparison of muscle weight and histological analysis showed that suspension-induced atrophy in the hindlimb was more prominent in the soleus muscle, comprised mainly of type I fiber than that in the plantaris muscle of type II fibers. The immunohistochemical analysis with antitransglutaminase C antibody (anti TGase C Ab) showed that some atrophic bundles of soleus muscle were positively reacted with the antibody. The anti-TGase C Ab-reactive substances were observed to disappear significantly after endurance exercise, indicating their characteristic atrophy-dependency. The enzymatic analysis of transglutaminase showed the increase in activity in the atrophic soleus muscle tissue, compared with that in the normal or exercise-trained muscle tissues. From these results, the expression of TGase in the atrophic muscle is suggested to be the possible marker for muscle atrophy and its expression is probably related with the protective mechanism of the muscle tissue to prevent further cellular damage in the atrophic process.

Animals↗