Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies of rabies virus in several animal models consistently showed hypothalamic infection, hypophyseal infection, dramatic growth impairment (in the form of failure to thrive), wasting syndrome, and immune depletion. Rabies virus infection was studied through routine monoclonal antinucleocapsid antibody immunofluorescence and through a peroxidase-antiperoxidase immunoperoxidase method. The latter was modified to detect the in situ production of growth hormone by uninfected and rabies virus-infected adeno-a-pituicytes (with confirmation of the results both in vivo and in vitro). Infection with rabies virus made the specialized pituicytes produce less growth hormone. Growth before rabies virus infection and its reduction due to infection were investigated in a linear regression model. The fit was statistically significant (P less than .05) in all species studied: mouse, rat, rabbit, cow, and cat. Immune depression was studied in terms of alterations in the immunotopography of the thymus and also the specific T- and B-cell homing areas of the spleen (although spleen data are not presented here). On the basis of these results and a thorough review of wasting syndromes encountered in other diseases, a primary failure to thrive and an ensuing wasting syndrome were described and characterized for rabies, and their origin was assigned to a dysfunction of the hypophyseal/hypothalamic/thymic axis associated with at least (but not necessarily only) one of the centrally controlled growth hormones.
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PMID:Failure to thrive, wasting syndrome, and immunodeficiency in rabies: a hypophyseal/hypothalamic/thymic axis effect of rabies virus. 320 86

Electromyography, muscle histochemistry and assay of all glycolytic enzymes, phosphorylase, glycogen, carnitine and several mitochondrial marker enzymes in skeletal muscle (vastus lateralis) were carried out in two groups. One group comprised chronic alcoholic patients with prominent proximal wasting, the other was an alcoholic group with normal neuromuscular examination. Biochemical results were compared with data from control groups with normal muscle histology and with non-alcohol related type 2b fibre atrophy. Either 2b atrophy factor or 2b variability coefficient were increased in all wasted alcoholic patients, with normal values in alcoholics without wasting. Electromyography studies were usually normal in proximal muscles, although several patients had mild distal neuropathies. A significant fall in activity of phosphorylase and all glycolytic enzymes was found in wasted alcoholics with reference to normal controls. In the non-ethanolic 2b atrophy group the activity of several glycolytic enzymes was also significantly lower, but for each enzyme the mean activity was not depressed to the same extent as in the wasted alcoholic group. Muscle glycogen, carnitine, and mitochondrial marker enzyme activities (isocitrate dehydrogenase, monoamine oxidase, cytochrome oxidase) were normal in alcoholics with proximal wasting. It is concluded that there is no deficiency of mitochondrial marker enzymes in wasted alcoholics and that a significant depression in glycogenolytic and glycolytic enzyme activity is seen which is explained in part, but probably not fully, by 2b fibre atrophy.
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PMID:Chronic alcoholic proximal wasting: physiological, morphological and biochemical studies in skeletal muscle. 343 19

Potassium and magnesium deficiency have been reported as risk factors for experimental gentamicin nephrotoxicity. Amiloride, a potassium-sparing diuretic, also leads to increased renal magnesium reabsorption. Amiloride, 2 mg/kg/day, was given to groups of 8-12 Fischer 344 rats receiving gentamicin, 20 mg/kg b.i.d., for 3, 7, 10 and 14 days. Control animals received the vehicle for gentamicin, amiloride alone or gentamicin alone. The degree of renal failure and weight loss were similar in gentamicin and gentamicin + amiloride groups at all time points despite increases in serum potassium and magnesium in the amiloride-treated animals. Tubular dysfunction as assessed by depression of renal cortical slice uptake of p-aminohippurate and N-methylnicotinamide was not improved by the addition of amiloride. In addition, a comparable degree of tubular necrosis and regeneration was observed in all gentamicin-treated groups. Maximum gentamicin concentrations in the renal cortex did not differ. Thus, despite reduction of urinary losses of potassium and magnesium with resultant increased serum values, amiloride did not protect against experimental gentamicin nephrotoxicity. The tubular electrolyte wasting noted clinically is likely to be a result, rather than a cause of proximal tubular cell damage.
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PMID:Effect of amiloride on experimental gentamicin nephrotoxicity. 400 Mar 46

Protein synthesis has been measured in vivo in liver and muscle of mice bearing the XK1 tumor, an appropriate model for cancer cachexia. Two different methods were used involving measurement of tracer incorporation into tissue protein either at the end of a 4-hr constant infusion of [14C]tyrosine or 10 min after i.v. injection of a flooding dose of [3H]phenylalanine. Whole-body tyrosine flux was decreased by 60% in cachectic tumor-bearing mice, and protein synthesis was depressed by 70% in muscle and by 40% in liver. The depression of protein synthesis in muscle was due to a reduction in both RNA content (i.e., protein-synthesizing capacity) and RNA activity (i.e., protein synthesized per g of RNA per hr). In liver, the depression of protein synthesis was due entirely to a decrease in RNA activity. The results also suggest that the synthesis of export proteins was affected more than the synthesis of fixed liver protein. Restriction of food intake in normal mice by up to 50% caused a loss of body weight and reductions in protein synthesis in liver and muscle which were less severe than those caused by the presence of the tumor. It is concluded that the wasting which is associated with advanced malignant disease is brought about by a reduction in the rate of protein synthesis in the tissues, and that this cannot be explained by depression of food intake alone.
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PMID:Protein synthesis measured in vivo in muscle and liver of cachectic tumor-bearing mice. 672 6

One of the stigmata of leprosy in the hand is muscular wasting between the metacarpals of the thumb and index finger. Such a deformity, which may rarely arise for other neuropathic reasons, may pass unnoticed in places where leprosy is not endemic, but is obvious to all in places where leprosy is still common, and undesirably stamps afflicted persons as lepers even if the disease is arrested. A surgical technique is described in which a buried dermal graft is used for augmentation of the depression of that muscular wasting between thumb and index finger.
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PMID:Augmentation of muscular wasting in the hand from leprosy. 701 82

A high frequency of occurrence of a wasting disease, unthriftiness, and retarded growth was observed in a group of inbred Weimaraner dogs. Affected pups had a small thymus gland, with a marked absence of thymic cortex. A litter of eight pups from a sire and dam that were known to have produced affected offspring was chosen for further study. The pups had normal concentrations of WBC and gamma-globulins and were able to produce antibody in response to Brucella abortus. Two pups in the litter developed a wasting syndrome and responded well to therapy with thymosin fraction 5. One pup that survived the wasting syndrome had a significant (P < 0.05) depression of its lymphocyte blastogenic response to phytohemagglutinin compared with its surviving littermates. Pups from this litter also lacked a normal increase in plasma growth hormone concentration after the injection of clonidine HCl. These pups had concurrent abnormalities of the thymus-dependent immune function and in growth hormone metabolism. The syndrome in these pups has some features in common with the syndrome in the Ames or Snell-Bagg strains of immunodeficient dwarf mice.
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PMID:Thymic abnormalities and growth hormone deficiency in dogs. 744 21

This article provides a clinically-oriented overview of palliative care for patients with AIDS. Indicators of decreased survival time are divided into categories of infections/illnesses, clinical signs and symptoms, immunological and serological markers, and psychosocial factors. Primary symptoms in AIDS are discussed according to etiology and treatment. However, treatments of opportunistic infections per se are not directly addressed in this article. Problems discussed include pain, confusion, depression and anxiety, fatigue, fever, dyspnea, nausea and vomiting, diarrhea, wasting, and dehydration. The article also briefly addresses clinical and ethical questions and challenges presented by AIDS to hospice or palliative care providers, and the various stages of HIV infection.
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PMID:Palliative care for patients with acquired immunodeficiency syndrome. 749 35

The objective of this investigation was to determine whether an imbalance between naive- and memory-phenotype cells occurs within CD4+ and/or CD8+ splenic T cell subsets in models of protein-energy malnutrition (PEM) which produce wasting disease (loss of approximately 1.6% of body weight per day for 14 d) and profound depression in thymus-dependent immunity. Male and female weanling mice of disparate inbred strains, CBA/J and C57BL/6J, were allocated to the following groups: zero-time control (23 d old and 19 d old, respectively), ad libitum intake of a complete purified diet (19% crude protein, 17 kJ/g gross energy), restricted intake of the complete diet, and (C57BL/6J, only) ad libitum intake of an isocaloric low protein diet (0.6% crude protein). Surface expression of isoforms of CD45, a component of the T cell receptor complex, as well as of the accessory molecule, CD2, were assessed by flow cytometry of splenic mononuclear cell suspensions. Both major T cell subsets in the malnourished groups contained a significantly higher proportion of cells expressing the surface marker, CD45RA, than was found in the spleen cells of the control groups. CD45RA+ (naive-phenotype) T cells represent the extreme of quiescence and stringent activation requirements among thymic lymphocytes. The results provide the first clear evidence of a T cell subset imbalance in PEM which is consistent with depression in acquired immunity and which occurs, apart from antigenic challenge, in a site wherein immune responses take place. The T cell receptor complex may emerge as a focal point of the depressive influence of PEM on the competence of thymic lymphocytes.
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PMID:The CD45RA+ (quiescent) cellular phenotype is overabundant relative to the CD45RA- phenotype within the involuted splenic T cell population of weanling mice subjected to wasting protein-energy malnutrition. 756 81

A new sign in Duchenne muscular dystrophy is described. The sign demonstrates a unique characteristic of this disorder: selective hypertrophy and wasting in different muscles of the same region. The patients were asked to abduct their arms to about 90 degrees with elbows flexed to 90 degrees and hands directed upwards. Those who could not abduct the arm to 90 degrees were asked to do so to the maximum that they could. In this posture, all patients had examination of pectoral girdles from behind. Some patients with spinal muscular atrophy and other forms of muscular dystrophies were also examined in the same manner. In this posture, patients with Duchenne muscular dystrophy demonstrated a linear or oval depression (due to wasting) of the posterior axillary fold with hypertrophied or preserved muscles on its 2 borders (i.e., infraspinatus inferomedially and deltoid superolaterally), as if there were a valley between the 2 mounts. The sign was specific to Duchenne muscular dystrophy with sensitivity of about 90%. It was most remarkable in patients 8-11 years of age.
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PMID:New clinical sign in Duchenne muscular dystrophy. 770 89

The main purpose of this investigation was to determine whether exogenous triiodothyronine (T3) administered according to a protocol known to prevent depression in acquired immunity in weanling murine protein-energy malnutrition (PEM) would, likewise, influence the splenic natural killer (NK) cell in this disease. Weanling mice of disparate inbred strains, C57BL/6J and CBA/J, were subjected to wasting PEM produced by means of two low-protein diets (0.5% crude protein) identical in every respect except that one diet contained supplemental T3 (0.2 micrograms/g diet). NK cell lytic activity toward YAC-1 targets was assessed in vitro using suspensions containing 0.5 x 10(6) mononuclear spleen cells. Lytic activity in this assay was low in mice fed the unsupplemented low-protein diet, but was not depressed in malnourished animals given exogenous T3. Surface marker analysis using the NK cell-specific antigen, NK 1.1 (PK 136), revealed no effect of the low-protein diet or of exogenous T3 on the proportion of splenic mononuclear cells exhibiting NK 1.1+ phenotype. Previous investigations have shown that acquired immune competence in PEM can be manipulated, by means of endocrine hormonal intervention, independently of continued wasting disease. The present results extend this fundamental new concept to include an innate immune function, namely NK cell lytic activity. In this system of experimental PEM, exogenous T3 prevented depression in NK cell lytic activity expressed on a per cell basis. The malnourished weanling rodent is a particularly powerful experimental system with which to investigate the mechanisms whereby thyroid hormones influence NK cells.
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PMID:Effects of triiodothyronine supplements on splenic natural killer cells in malnourished weanling mice. 778 50


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