Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyponatremia with simultaneous renal sodium loss was associated with the inappropriate secretion of antidiuretic hormone in a dog with heartworm disease. Antidiuresis caused expansion of extracellular fluid volume, which induced renal salt wasting and a negative sodium balance. The combination of water retention, salt wasting, and inactivation of intracellular solute contributes to the decrease in serum sodium concentration. Water intoxication due to hypotonicity of body gluids induced anorexia, depression, weakness, and incoordination.
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PMID:Inappropriate secretion of antidiuretic hormone in a dog. 50 Apr 39

The authors report a case of Charcot-Marie-Tooth disease that mimicked Friedreich's ataxia and featured impaired tendon reflexes in the limbs, incoordination mimicking cerebellar disease in the extremities, extensor plantar responses on both sides, bilateral foot deformity, imparied position sense in the toes, absent vibratory sense in the distal parts of the legs and minimal distal weakness with wasting. Motor conduction velocity in the upper limbs was substantially reduced. Other cases similar in nature reported in the literature resemble spino-cerebellar degeneration in general, and Friedreich's ataxia, in particular. It is emphasized that the natural history, EMG, motor conduction velocity studies and examination of other affected members of the family permit the correct diagnosis to be made in such cases. It is also emphasized that patients similar to the one reported here may also resemble, and should be differentiated from, cases of familial dorsal column ataxia (Biemond type). Stress is put upon the fact that when Charcot-Marie-Tooth disease mimicks spino-cerebellar degeneration, substantial slowing of motor conduction in the upper limbs is generally sufficient to establish the diagnosis. The relation between Friedreich's ataxia an Charcot-Marie-Tooth disease is reviewed and it is concluded that these two disorders are distinct clinical and pathological entities.
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PMID:A case of Charcot-Marie-Tooth disease mimicking Friedreich's ataxia: is there any association between friedreich's ataxia and Charcot-Marie-Tooth disease? 710 97

Two patients are reported presenting with incoordination mimicking cerebellar disease in the upper and lower limbs, ataxia of gait, absent tendon reflexes and little or no clinically detectable wasting. Motor conduction velocity in the upper limbs was substantially reduced in one patient whereas it was normal and slightly reduced in the other. It is concluded that in Charcot-Marie Tooth disease incoordination may mimic cerebellar disease and when this is so it is due to the association of varying degrees of proprioceptive deafferentation and a dyskinesia similar to that produced by familial (essential) tremor.
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PMID:Unusual presentation of Charcot Marie-Tooth disease-incoordination with absent of minimal wasting-Report of 2 cases. 722 62

Following an outbreak of wobbly possum disease in a colony of brush tail possums (Trichosurus vulpecula), the disease was established experimentally in captive possums by inoculating the animals intraperitoneally with tissue homogenates. Crude tissue homogenates of liver remained infectious after freezing at -75 degrees C or filtration through a 0.22 micron filter. The disease was characterised by docility, incoordination, loss of balance and wasting. Fifteen of 16 infected animals had to be euthanased owing to the severity of clinical signs. Cachexia was the only change observed postmortem. Histology revealed widespread perivascular infiltrations with plasma cells and lymphocytes which were severe in the liver and kidney and moderate to mild in a variety of other tissues, including skeletal and cardiac muscle. Changes in the brain consisted of a mild to moderate mononuclear perivascular cuffing. Most of the animals had small to large numbers of circulating nucleated red blood cells and eosinopenia when they were euthanased. There was a consistent decrease in serum albumin concentration and an increase in serum globulins, which resulted in a decreased albumin:globulin ratio. Virus-like particles were observed in preparations of liver from two animals; they appeared to be spherical or icosahedral and were 45 nm in diameter.
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PMID:Pathological studies of wobbly possum disease in New Zealand brushtail possums (Trichosurus vulpecula). 930 Oct 11

To faithfully recreate the features of the human neurodegenerative disease spinocerebellar ataxia type 1 (SCA1) in the mouse, we targeted 154 CAG repeats into the endogenous mouse locus. Sca1(154Q/2Q) mice developed a progressive neurological disorder that resembles human SCA1, featuring motor incoordination, cognitive deficits, wasting, and premature death, accompanied by Purkinje cell loss and age-related hippocampal synaptic dysfunction. Mutant ataxin-1 solubility varied with brain region, being most soluble in the neurons most vulnerable to degeneration. Solubility decreased overall as the mice aged; Purkinje cells, the most affected in SCA1, did not form aggregates of mutant protein until an advanced stage of disease. It appears that those neurons that cannot sequester the mutant protein efficiently and thereby curb its toxicity suffer the worst damage from polyglutamine-induced toxicity.
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PMID:A long CAG repeat in the mouse Sca1 locus replicates SCA1 features and reveals the impact of protein solubility on selective neurodegeneration. 1208 39

This is a critique of a study by Howlett, Nkya, Mmuni, Missalek, published in AIDS (1989), which reports on clinical findings in 200 AIDS patients at the Kilimanjaro Christian Medical Center in Tanzania between 1985-88. For 135 of these patients, the study concentrates on the clinical neurological symptoms of AIDS. General symptoms included weakness (98%); wasting (92%); fever (79%); diarrhea (75%); maculo-papulor rash (71%); and candidiasis (57%). Neurological symptoms included AIDS dementia complex (54%); retinal abnormalities (23%); areflexia (21%); pyramidal tract signs (19%) and tremor and incoordination (19%). This study is the most detailed published examination to date of the clinical neurological symptoms associated with AIDS in African patients. In spite of the weaknesses of the study the paucity of laboratory investigations and the lack of autopsy information and the frequency of different infections affecting the nervous system in African AIDS patients, the study will be referenced in all future works on the neurology of AIDS in Africa. (Author's modified).
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PMID:Neurological disorders in AIDS and HIV disease in the northern zone of Tanzania. 1228 84