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PubMed1988

Atrophy with compensatory hypertrophy of the liver in hepatic neoplasms: radiographic findings.

Focal hepatic atrophy has numerous causes and in many cases is associated with compensatory hypertrophy. We have observed this phenomenon on CT in patients with hepatic neoplasms. Of 12 patients studied, eight had hepatic metastases, two had hepatocellular carcinoma, and two had bile-duct carcinoma. Focal changes in liver morphology (i.e., atrophy with compensatory hypertrophy) were found in five patients at presentation and developed after treatment with systemic or intraarterial chemotherapy in the others. Atrophic changes affected the right lobe in eight patients, the left lobe in three, and part of both lobes in one. Compensatory hypertrophy of part or all of the unaffected liver was found. Ten patients had obstruction of the portal vein branch to the atrophic segment, four of these 10 also had hepatic vein obstruction, and two of these 10 also had bile duct obstruction. Portal vein obstruction appears to be the most important element in the production of focal hepatic atrophy in patients with hepatic neoplasms. After treatment with chemotherapy, tumor regression and atrophy may be associated with compensatory hypertrophy and enlargement of the uninvolved part of the liver. This must not be mistaken for progression of disease.

Adaptation, Physiological↗

PubMed2004

Atrophy of foot muscles: a measure of diabetic neuropathy.

OBJECTIVE: Diabetic neuropathy is a length-dependent process that leads to reduced muscle strength and atrophy of leg muscles in some patients. We hypothesized that intrinsic foot muscles are atrophied in diabetic neuropathy and that the degree of atrophy is a measure of motor dysfunction closely related to the neuropathic process. RESEARCH DESIGN AND METHODS: Consecutive cross-sectional magnetic resonance images of the nondominant foot were obtained for stereological determination of the total volume of the intrinsic foot muscles (VFM) in 23 long-term diabetic patients with (n = 15) and without (n = 8) chronic neuropathy and in 23 matched healthy nondiabetic control subjects. Based on clinical examination, nerve conduction studies, and quantitative sensory examination, a neuropathy rank-sum score was calculated for each patient. RESULTS: Total VFM was 86 +/- 52, 165 +/- 34, and 168 +/- 42 cm3 in neuropathic patients, nonneuropathic patients, and healthy control subjects, respectively (P < 0.001). There was a close inverse relationship between the neuropathy rank-sum score and the VFM (r = -0.75, P < 1 x 10(-5)). CONCLUSIONS: Total volume of the foot muscles is halved in patients with diabetic neuropathy. Atrophy of foot muscles is closely related to the severity of neuropathy and reflects motor dysfunction.

Adult↗

PubMed2006

Overexpression of peroxisome proliferator-activated receptor gamma co-activator-1alpha leads to muscle atrophy with depletion of ATP.

Peroxisome proliferator-activated receptor-gamma co-activator-1alpha (PGC-1alpha) is a key nuclear receptor co-activator for mitochondrial biogenesis. Here we report that overexpression of PGC-1alpha in skeletal muscles increased mitochondrial number and caused atrophy of skeletal muscle, especially type 2B fiber-rich muscles (gastrocnemius, quadriceps, and plantaris). Muscle atrophy became evident at 25 weeks of age, and a portion of the muscle was replaced by adipocytes. Mice showed increased energy expenditure and reduced body weight; thyroid hormone levels were normal. Mitochondria exhibited normal respiratory chain activity per mitochondrion; however, mitochondrial respiration was not inhibited by an ATP synthase inhibitor, oligomycin, clearly indicating that oxidative phosphorylation was uncoupled. Accordingly, ATP content in gastrocnemius was markedly reduced. A similar phenotype is observed in Luft's disease, a mitochondrial disorder that involves increased uncoupling of respiration and muscle atrophy. Our results indicate that overexpression of PGC-1alpha in skeletal muscle increases not only mitochondrial biogenesis but also uncoupling of respiration, resulting in muscle atrophy.

Adenosine Triphosphate↗

PubMed1993

Aggressive behavior in schizophrenia: relationship to age of onset and cortical atrophy.

Aggressive behavior is a common feature of schizophrenia and is associated with the presence of 'soft' neurological signs. Since early age of onset of schizophrenia has been found to be associated with the negative syndrome, which according to Crow (1982) is related to structural brain abnormalities, I predicted that early age of onset may be a biological risk factor for aggressive behavior in the disease. To test this hypothesis, I investigated in 52 chronic institutionalized schizophrenic patients (mean age = 32.8 years; SD = 8.0), the association between age of onset of the disease and the severity of belligerent behavior. The age of onset was judged from the patient's histories as the age at which florid symptoms first emerged. Patients with early onset schizophrenia had a significantly higher belligerent score compared to those with later-onset schizophrenia (p < .05). These findings support the hypothesis of an association between early age of onset of schizophrenia and the risk of aggressive behavior and suggest, furthermore, that schizophrenic symptoms which emerge early may predict a higher risk of aggressive behavior. Furthermore, this study suggest that the neurochemical mechanisms which underlie the early emergence of symptoms may also predispose to aggressive behavior in schizophrenia. Specifically, since aggressive behavior has been linked to impairment of serotonergic (5-HT) functions, I propose that the timing of onset of schizophrenia may be partly associated with dysregulation of the 5-HT system. In a second study, I investigated whether schizophrenic patients with aggressive (suicide) behavior are characterized by more extensive brain damage and hence greater degree of cerebral atrophy on CT scan. The study, which involved 26 schizophrenic patients (mean age: 31.3 years; SD = 6.8), revealed that patients with aggressive behavior had a significantly greater degree of parieto-occipital atrophy on CT scan (p < .05). In contrast, ventricular size and prefrontal cortical atrophy did not distinguish aggressive from nonaggressive patients. These findings suggest that cortical atrophy may be a neuroradiological marker of aggressive behavior in schizophrenia.

Adult↗

PubMed1985

Adaptation of the small intestine to induced maldigestion in rats. Experimental pancreatic atrophy and acarbose feeding.

Intestinal adaptation has been studied in rats with pancreatic atrophy induced by feeding a copper-deficient diet and penicillamine and in rats with carbohydrate maldigestion induced by feeding of an alpha-glucosidase inhibitor (acarbose). Pancreatic atrophy led to a significant increase of weight, protein, and DNA content as well as specific activities and total amounts of the enzymes sucrase and maltase in the distal but not in the proximal part of the small intestine. Plasma levels of CCK and GIP were significantly higher in rats with pancreatic atrophy, whereas plasma levels of gastrin and insulin were lower. Tissue concentrations of gastrin in the antrum and GIP in duodenum and jejunum were unchanged. Duodenal CCK and jejunal substance P, somatostatin, and VIP and ileal substance P and somatostatin were significantly decreased in rats with acinar atrophy. Glucosidase inhibition by acarbose feeding led to weight increase of the small intestine and cecum. This was more marked when acarbose was fed together with a fiber-free diet. Under these conditions the protein and DNA content also increased significantly in both gut segments and maltase and sucrase content predominantly in the distal part. Insulin plasma concentration decreased significantly in the acarbose-fed groups, whereas GIP, gastrin, and CCK plasma concentrations remained unchanged. After fiber-rich diet tissue concentrations of gastrin in the antrum and insulin in the pancreas were significantly higher and GIP concentrations in the duodenum and jejunum significantly lower than after fiber-free diet. Acarbose increased the pancreatic insulin concentration only in the fiber-free group and did not influence gastrin and GIP concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Acarbose↗

PubMed1996

Stump length as related to atrophy and strength of the thigh muscles in trans-tibial amputees.

Stump length and the thigh muscles strength of the amputated limb are among the major factors influencing outcome of prosthetic rehabilitation of trans-tibial amputees. In the present study the authors evaluated and compared the strength of quadriceps and hamstrings muscles of both limbs in trans-tibial amputees, as measured by means of an electrical dynamometer. The obtained results showed that the thigh muscles of the sound limbs are significantly stronger than those of the amputated limbs (p < 0.01). The results obtained for amputees with shorter stumps were compared with those with longer stumps. In the group of amputees (n = 9) with a stump shorter than 15.1 cm, values of peak torque (in isokinetic contraction) and maximal average torque (in isometric contraction) were significantly (p < 0.5) weaker when compared to those (n = 9) with a stump longer than 15.1 cm. The results obtained for amputees with a higher rate of thigh muscle atrophy were compared to those with lesser atrophy. In the group of amputees where muscle atrophy was accompanied by decrease in thigh girth of over 5.9 cm, muscles strength did not significantly decrease (p < 0.5) as compared to amputees where thigh girth decrease was less than 5.9 cm. It is concluded that atrophy of the thigh muscles of trans-tibial amputees is accompanied with a significant decrease in strength. In amputees with a short stump, the short lever action provided by the stump interferes with the ability of the thigh muscles to control the prosthesis efficiently during daily activities such as standing and walking.

Activities of Daily Living↗

PubMed1985

Variable severity in autosomal dominant optic atrophy.

There are some indications in the literature on autosomal dominant optic atrophy that there are two genetic types - a congenital and a post-natal. This paper reviews the ocular findings of three affected members of a family with autosomal dominant optic atrophy - a father and two daughters - which appear to fit the criteria for a 'congenital' type of optic atrophy. Comparison with an additional 17 cases indicates that those with an early or congenital onset are at the more severe end of a distribution curve of involvement. The less severely affected patients were older and often had passed many years with little or no visual difficulties. Such variation is a recognized feature of autosomal dominant inheritance and is the basis for suggesting that there is probably only one genetic locus for autosomal dominant optic atrophy.

Adolescent↗

PubMed1994

[A longitudinal study of brain atrophy and its relation with background factors and common carotid hemodynamics].

This longitudinal study was performed to clarify the relation between brain atrophy and common carotid hemodynamics. A total of 147 patients, including 70 males and 77 females, who had neither neurologic deficits nor organic lesions on computed tomography of the brain, were enrolled in this study. The ages of the patients ranged from 47 to 76 years (mean: 62 years) at the first diagnosis of brain atrophy. The patients were divided into three groups: 66 controls without hypertension or diabetes mellitus (Group I), 60 with hypertension (Group II) and 21 with both hypertension and diabetes mellitus (Group III). Brain atrophy was diagnosed by caudate head index (CHI). Mean blood flow volume (BF) at the right common carotid artery was measured by an ultrasonic quantitative flow measurement system. Both CHI and BF were measured twice at a mean interval 6.5 years. Increment in CHI per year (delta CHI) and decrement in mean blood flow volume per year (delta BF) were calculated. delta CHI of Group I and Group II had a significant relation with aging. delta CHI of Group III showed a larger increase than that of both Group I and Group II in subjects in the sixties. delta CHI had a significant relation with delta BF in each group. These results indicate that complication of both HT and DM, or decrement in mean blood flow volume may cause brain atrophy to progress.

Aged↗

PubMed1990

Corpus callosal atrophy following closed head injury: detection with magnetic resonance imaging.

To investigate evidence for diffuse white matter injury and hemispheric disconnection sequelae after severe closed head injury (CHI), this study evaluates the degree of posttraumatic atrophy of the corpus callosum. Corpus callosal atrophy was quantitatively determined using a digitizer to measure sagittal magnetic resonance images of 32 patients with moderate-to-severe CHI and those of 31 control subjects of similar age. In the CHI patients, measurements were significantly reduced for the areas of the anterior four-fifths, the posterior one-fifth, and the total corpus callosum. Moreover, the minimum width of the callosal body was reduced in the CHI patients as compared to that of control individuals. Indices of corpus callosal atrophy were significantly correlated with the chronicity of injury and the degree of lateral ventricular enlargement. There was no difference in callosal measurements between men and women. Magnetic resonance imaging provides an in vivo determination of corpus callosal atrophy which may reflect the severity of diffuse axonal injury and predict the type and severity of hemispheric disconnection effects.

Adolescent↗

PubMed2004

Association of FAS (TNFRSF6)-670 gene polymorphism with villous atrophy in coeliac disease.

AIM: To investigate the association of FAS gene polymorphism with coeliac disease (CD) development. METHODS: FAS-G670A gene polymorphism, located in a gamma interferon activation site, was studied in 146 unrelated CD patients and 203 healthy ethnically matched controls. The restriction fragment length polymorphism (RFLP) method was used to identify FAS-G670A gene polymorphism. RESULTS: No significant difference was found in genotype frequency between CD cases and controls. In controls, however, the frequency of the GG genotype was significantly higher in women (26.5%) than in men (12.8%) (OR= 2.44, 95% CI 1.15-5.20, P=0.020) and it was also higher in men with CD than controls (OR=2.60, 95% CI 0.96-7.05, P=0.061). The GG genotype frequency was significantly higher in patients with most severe villous atrophy (Marsh IIIc lesions) (OR=3.74, 95% CI 1.19-11.82, P=0.025). A significantly less proportion of men suffered from Marsh IIIc lesions than women (OR=0.20, 95% CI 0.06-0.68, P=0.01). The risk of having severe villous atrophy increased with the additive effect of the G allele in women (P=0.027 for trend, age and gender adjusted). CONCLUSION: FAS-G670A gene polymorphism is associated with the severity of villous atrophy in CD. Female gender is also associated with the severity of villous atrophy.

Atrophy↗

PubMed2003

Epithelial cell proliferation and glandular atrophy in lymphocytic gastritis: effect of H pylori treatment.

AIM: Lymphocytic gastritis is commonly associated with Helicobacter pylori infection. The presence of glandular atrophy and foveolar hyperplasia in lymphocytic gastritis suggests abnormalities in cell proliferation and differentiation, forming a potential link with the suspected association with gastric cancer. Our aim was to compare epithelial cell proliferation and morphology in H pylori associated lymphocytic gastritis and H pylori gastritis without features of lymphocytic gastritis, and to evaluate the effect of H pylori treatment. METHODS: We studied 14 lymphocytic gastritis patients with H pylori infection. For controls, we selected 14 matched dyspeptic patients participating in another treatment trial whose H pylori infection had successfully been eradicated. Both groups were treated with a triple therapy and followed up with biopsies for 6-18 months (patients) or 3 months (controls). Blinded evaluation for histopathological features was carried out. To determine the cell proliferation index, the sections were labeled with Ki-67 antibody. RESULTS: Before treatment, lymphocytic gastritis was characterized by foveolar hyperplasia (P=0.001) and glandular atrophy in the body (P=0.008), and increased proliferation in both the body (P=0.001) and antrum (P=0.002). Proliferation correlated with foveolar hyperplasia and inflammation activity. After eradication therapy, the number of intraepithelial lymphocytes decreased in the body (P=0.004) and antrum (P=0.065), remaining higher than in controls (P<0.001). Simultaneously, the proliferation index decreased in the body from 0.38 to 0.15 (P=0.043), and in the antrum from 0.34 to 0.20 (P=0.069), the antral index still being higher in lymphocytic gastritis than in controls (P=0.010). Foveolar hyperplasia and glandular atrophy in the body improved (P=0.021), reaching the non-LG level. CONCLUSION: In lymphocytic gastritis, excessive epithelial cell proliferation is predominantly present in the body, where it associates with foveolar hyperplasia and glandular atrophy. These characteristic changes of lymphocytic gastritis are largely related to H pylori infection, as shown by their improvement after eradication. However, some residual deviation was still seen in lymphocytic gastritis, indicating either an abnormally slow improvement or the presence of some persistent abnormality.

Atrophy↗

PubMed2000

Leukemia inhibitory factor, oncostatin M, IL-6, and stem cell factor mRNA expression in human thymus increases with age and is associated with thymic atrophy.

The roles that thymus cytokines might play in regulating thymic atrophy are not known. Reversing thymic atrophy is important for immune reconstitution in adults. We have studied cytokine mRNA steady-state levels in 45 normal human (aged 3 days to 78 years) and 34 myasthenia gravis thymuses (aged 4 to 75 years) during aging, and correlated cytokine mRNA levels with thymic signal joint (sj) TCR delta excision circle (TREC) levels, a molecular marker for active thymopoiesis. LIF, oncostatin M (OSM), IL-6, M-CSF, and stem cell factor (SCF) mRNA were elevated in normal and myasthenia gravis-aged thymuses, and correlated with decreased levels of thymopoiesis, as determined by either decreased keratin-positive thymic epithelial space or decreased thymic sjTRECs. IL-7 is a key cytokine required during the early stages of thymocyte development. Interestingly, IL-7 mRNA expression did not fall with aging in either normal or myasthenia gravis thymuses. In vivo administration of LIF, OSM, IL-6, or SCF, but not M-CSF, i.p. to mice over 3 days induced thymic atrophy with loss of CD4+, CD8+ cortical thymocytes. Taken together, these data suggest a role for thymic cytokines in the process of thymic atrophy.

Adolescent↗

PubMed1997

Testicular atrophy in a mule deer population.

Monitoring mule deer (Odocoileus hemionus) on a former plutonium production site along the Columbia River at the Hanford Site, Washington (USA) revealed 27 (23%) of 116 adult males had unusually shaped, velvet-covered antlers and abnormally developed testicles. We captured 32 males to examine age-class differences and the ratio of affected to unaffected deer and determine whether affected testicles were atrophic or hypoplastic. We found testicular atrophy in most deer with velvet-covered antlers, primarily in animals older than 5 yr. Deer had marked to extreme stages of testicular atrophy, indicating permanent sterility. Decreased serum levels of testosterone and compensatory increased levels of luteininzing hormone and follicle stimulating hormone were detected in all affected males; thus, the gondopituitary hormonal pathway may have responded to abnormally low levels of testosterone in the affected animals. Brucella spp. antibodies in sera were not detected and 9 (90%) of 10 affected animals were seropositive for epizootic hemorrhagic disease virus (EHDV-2) and bluetongue virus (BTV-11) as compared to 12 (63%) of 19 unaffected animals; however, signs of other infectious diseases were not observed. Testicular degeneration generally exceeded that observed with nutritional disorders and poisons in domestic species. Also, severity of the atrophy and apparent lack of other affected tissues suggested that radiation may not be responsible. Testicular atrophy in mule deer has been reported elsewhere; however, neither prevalence has been as high nor or occurrence as well confined to a specific geographical area, as that observed at the Hanford Site. Furthermore, no physiological or age-related influences were described. Documenting the status of such variables and examining their relationships to this phenomenon is a crucial step in understanding the reproductive capacity of a wild deer population.

Age Factors↗

PubMed1976

Axonal labyrinths in the rat spinal cord: a consequence of degenerative atrophy.

Transection, crush or local colchicine treatment of a peripheral nerve induces degenerative atrophy of central terminals of primary sensory neurons in the Rolando substance of the rat spinal cord. In addition to osmiophilic alterations that occur in the course of degenerative processes in general, degenerative atrophy is characterized by the appearance of spectacular labyrinthine formations. Electron-microscopic analysis reveals that these consist of flattened axonal profiles. Axonal labyrinths are interpreted as signs of futile regenerative efforts of axon terminals undergoining degenerative atrophy. Labyrinths disappear from the Rolando substance several months after peripheral nerve injury, when degenerative atrophy of the central terminal is replaced by regenerative proliferation.

Animals↗

PubMed1999

[Role of growth hormone underproduction and support load deficit in development of muscle atrophy and osteopenia in tail-suspended rats].

In a 20-day experiment with tail-suspended male rats histological and histomorphometric techniques were used to study the effects of growth hormone, thyroxin, and graded support loads on the progress of atrophy in soleus and gastrocnemius m.m., tibial metaphyses spongiosis, and growth of tibiae. Daily injections of growth hormone at a dose of 0.5 mg/kg of the body mass were found to restore the longitudinal growth of tibiae and to suppress osteopenia in the spongiosis of metaphyses; however, they did not have any noteworthy effect on the muscular atrophy in the suspended rats. Support loading of the hind limbs for 2 hours a day in parallel to the treatment with growth hormone and thyroxin (0.02 mg/kg of the body mass per a day) suppressed the atrophy in soleus m. but not in gastrocnemius m. They were not able to oppose to osteoporosis in tibial metaphyses spongiosis; tibial growth was not normalized. Thyroxin did not appear to markedly influence muscle and bone atrophies; moreover, it made hypofunctioning of the thyroid more intense and, when combined with the growth hormone, masked the positive effect of the latter on the rats' bones.

Animals↗

PubMed1999

Alpha-synuclein immunoisolation of glial inclusions from multiple system atrophy brain tissue reveals multiprotein components.

Immunohistochemical studies have shown that oligodendroglial inclusions in multiple system atrophy contain alpha-synuclein, a synaptic protein also found in Lewy bodies in Parkinson's disease. We have now used density gradient enrichment and an anti-alpha-synuclein immunomagnetic technique to isolate pure and morphologically intact oligodendroglial inclusions from brain white matter of patients dying with multiple system atrophy. Filamentous inclusion structures were obtained only from multiple system atrophy tissue, but not from normal brain tissues, or from multiple system atrophy tissue processed without anti-alpha-synuclein antibody. We confirmed the purity and morphology of isolated inclusions by electron microscopy. The inclusions comprised multiple protein bands after separation by polyacrylamide gel electrophoresis. Immunoblotting demonstrated that these proteins included alpha-synuclein, alphaB-crystallin, tubulins, ubiquitin, and prominent, possibly truncated alpha-synuclein species as high-molecular-weight aggregates. Our study provides the first biochemical evidence that oligodendroglial inclusion filaments consist of multiple protein components, suggesting that these inclusions may form as a result of multiprotein interactions with alpha-synuclein.

Aged↗

PubMed1999

Availability of omental flap on prevention against muscular atrophy of a latissimus dorsi cardiomyoplasty.

Dynamic cardiomyoplasty (DCMP) has been performed in more than seven hundreds cases world wide. However, despite symptomatic improvement in the majority of patients surviving the procedure, objective hemodynamic effects have not been consistently demonstrated. Previous studies reported that left ventricular function deteriorated and returned to preoperative level in the chronic phase. We previously reported that atrophy of the latissimus dorsi muscular flap (LDMF) was responsible for the effect of DCMP on improvement of cardiac function in the chronic phase. Ischemia of the muscle flap was proved to induce peripheral muscular atrophy of the flap, and thus preservation of the blood flow is important in preventing muscular atrophy. In the present study, we applied omental flap to LDMF, and postulated that the omentum would improve vascularity and perfusion of latissimus dorsi and prevent peripheral muscle atrophy. In dogs, the right and left latissimus dorsi muscles were dissected free from all attachment except for its thoracodorsal pedicles, and omental flap was wrapped around peripheral part of the left LDMF. Tissue blood flow, maximal muscle isotonic strength, morphologic features, and tissue vascular endothelial growth factor (VEGF) were examined in left LDMF with omental flap (OM group) and in the right LDMF served as the control (Control group). In the distal part of the LDMF, tissue blood flow of OM was significantly preserved than Control (86.4 +/- 6.5% in OM and 33.6 +/- 3.4% in Control, p < 0.05). Maximal isotonic tension was significantly higher in OM as compared to Control. Microscopic findings of H and E stained specimen from distal part of LDMF showed that muscle fibers were preserved in OM. And in the distal part, VEGF expression of OM was 49.6 +/- 7.9 pg/100 micrograms protein and significantly higher than that of Control. Our results indicated that induced endogenous VEGF expression in the LDMF by the omental flap preserved blood perfusion and muscular strength of the LDMF, and suggested that dynamic cardiomyoplasty might not lose its long-term direct cardiac assistance when an omental flap applied for the latissimus dorsi muscle flap.

Animals↗

PubMed1999

[Consensus on the diagnosis of multi-system atrophy].

We report the results of a consensus conference on the diagnosis of multiple system atrophy. We describe the clinical features of the disease, which include four domains: autonomic failure/urinary dysfunction, parkinsonism and cerebellar ataxia, and corticospinal dysfunction. We set criteria to define the relative importance of these features. The diagnosis of possible multiple system atrophy requires one criterion plus two features from separate domains. The diagnosis of probable multiple system atrophy requires the criterion for autonomic failure/urinary dysfunction plus poor levodopa responsive parkinsonism or cerebellar ataxia. The diagnosis of definite multiple system atrophy requires pathological confirmation.

Diagnosis, Differential↗