Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two sets of observations are reported as illustrations of problems encountered in behavioral toxicology. First, in an attempt to determine the contribution of methylmercury-induced ataxia to behavioral changes observed on the fixed-consecutive-number schedule, some ancillary control experiments were undertaken. Neither pharmacologically-produced incoordination (ethanol) nor mechanically-produced incoordination (foot taping) led to behavioral changes similar to those seen after exposure to methylmercury. Second, total crop impaction in a pigeon that died during a behavioral experiment on lead suggested some further work. Lead-induced crop stasis in pigeons was measured by x-raying the passage of force-fed stainless steel ball bearings through the crop. This retardation of motility reliably preceded signs of overt toxicity. These results suggest that the behavioral changes in the pigeon noted by us and reported by other investigators cannot be attributed to CNS dysfunction alone, but more likely arise from starvation, or from combined CNS damage and starvation. In addition, these results demonstrate that the appearance of behavioral effects prior to overt toxicity does not necessarily reflect CNS damage.
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PMID:Some problems in interpreting the behavioral effects of lead and methylmercury. 29 71

Three months after gastric partitioning for morbid obesity, two patients developed an unusual and severe form of polyneuropathy that affected their sense of position maximally. This disorder produced severe ataxia of the upper extremities and trunk, and pseudochorea. One patient died and the autopsy showed an extensive demyelinating polyneuropathy. Neuronal cell bodies in the anterior horns and dorsal root ganglia showed extensive accumulations of lipofuscin and Schwann cells showed extensive accumulations of lipid. This neuronal and Schwann cell lipidosis appears to result from starvation of the obese and has never been reported in other forms of human starvation or nutritional deficiency.
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PMID:Peripheral neuropathy and starvation after gastric partitioning for morbid obesity. 627 6

Magnesium deficiency may complicate many diseases. The causes include the following: inadequate intake during starvation or increased requirement during early childhood, pregnancy, or lactation; excessive losses of magnesium as a result of malabsorption from the gastrointestinal tract or from the kidneys during use of diuretics; and to a combination of the two, as in alcoholism. Most often the etiological factors have been operative for a month or more. Acute hypomagnesemia can occur without previous Mg deficiency after epinephrine, cold stress and stress of serious injury or extensive surgery. The clinical manifestations depend on the age of the patient and may begin insidiously or with dramatic suddenness, or there may be no overt symptoms or signs. The manifestations can be divided into the following categories: totally non-specific symptoms and signs ascribable to the primary disease; neuromuscular hyperactivity including tremor, myoclonic jerks, convulsions, Chvostek sign, Trousseau sign (rarely), spontaneous carpopedal spasm (rarely), ataxia, nystagmus and dysphagia; psychiatric disturbances from apathy and coma to some of all facets of delirium; cardiac arrhythmias including ventricular fibrillation and sudden death; hypocalcemia which is responsive only to Mg therapy; and hypokalemia which is not easily nor completely corrected without Mg therapy. The diversity of etiologies and the multiplicity of manifestations result in confusion and controversy. The documentation of normal renal function is absolutely necessary for maximum doses. The order of magnitude of dose is 1.0 meq Mg/kg on day 1, and 0.3 to 0.5 mEq/kg per day for 3 to 5 days. In emergencies such as convulsions or ventricular arrhythmias, a bolus injection of 1.0 gm (8.1 meq) of MgSO4 is indicated. Therapy of Mg deficiency in the presence of renal insufficiency requires smaller doses and frequent monitoring. Complete repletion occurs slowly.
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PMID:Magnesium deficiency. Etiology and clinical spectrum. 702 Mar 47

Morphological changes in rat sciatic nerve (SN) and plantar nerve (PN) induced by a thiamine deficient diet (TDD) and administration of oxythiamine (OT: 4 mg/100 g X 6 days) were observed, and thiamine (T) levels in rat nerve were simultaneously determined. Body weight gain ratio in rats which received OT fed a TDD (OTD group) was much reduced, and anorexia and ataxia were recognized in this group. Rats fed a regular diet, whose weights were restricted to be the same as those in the OTD group (EWC group), showed the symptoms of starvation. T levels of the SN and PN in the OT group, OTD group, and rats fed a TDD (TDD group) were reduced, but in the EWC group, T levels were the same as those in the control group (C group). There were myelin folds and myelin oboids in the EWC group, and these were recognized before axonal degeneration. In the TDD group, an increase in the number of mitochondria (Mit) was seen in the myelinated axon (MAx). In the TDD group, an increase in the number of mitochondria (Mit) was seen in the myelinated axon (MAx). In the OT and OTD groups, axonal degeneration (increase in the number of Mit, appearance of degenerated Mit, axonal shrinkage, and disappearance of neurofilament and neurotubule) was observed in the MAx. Degeneration of the MAx caused by TDD and OT was more severe in the PN than in the SN. Since these changes progressed from the peripheral nerve to the centripetal one, these changes in OTD group might be dying-back polyneuropathy.
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PMID:[Effect of oxythiamine on rat peripheral nerve. --Morphological changes in sciatic nerve and plantar nerve of thiamine deficiency-- (author's transl)]. 709 52

Jittery (ji) is a recessive mouse mutation on Chromosome 10 characterized by progressive ataxic gait, dystonic movements, spontaneus seizures, and death by dehydration/starvation before fertility. Recently, a viable neurological recessive mutation, hesitant, was discovered. It is characterized by hesitant, unco-ordinated movements, exaggerated stepping of the hind limbs, and reduced fertility in males. In a complementation test and by genetic mapping we have shown here that hesitant and jittery are allelic. Using several large intersubspecific backcrosses and intercrosses we have genetically mapped ji near the marker Amh and microsatellite markers D10Mit7, D10Mit21, and D10Mit23. The linked region of mouse Chromosome 10 is homologous to human 19p13.3, to which several human ataxia loci have recently been mapped. By excluding genes that map to human 21q22.3 (Pfkl) and 12q23 (Nfyb), we conclude that jittery is not likely to be a genetic mouse model for human Unverricht-Lundborg progressive myoclonus epilepsy (EPM1) on 21q22.3 nor for spinocerebellar ataxia II (SCA2) on 12q22-q24. The closely linked markers presented here will facilitate positional cloning of the ji gene.
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PMID:The neurological mouse mutations jittery and hesitant are allelic and map to the region of mouse chromosome 10 homologous to 19p13.3. 881 88

Wernicke's encephalopathy is a neurologic disorder due to a nutritional deficiency of thiamine, characterized by ocular palsies, ataxia, and altered mental activity. While Wernicke's encephalopathy is commonly attributed to alcoholism in the adult population, it has been described in children receiving prolonged parenteral nutrition and those with malignancies and AIDS. The disease, however, is rarely diagnosed in the pediatric population during life. We report a case of Wernicke's encephalopathy in a child with prolonged starvation and aim to improve awareness of a potentially fatal but treatable disease.
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PMID:A common cause of altered mental status occurring at an uncommon age. 1078 10

The yeast ATM1 protein is essential for normal mitochondrial iron homeostasis. Deletion of ATM1 results in mitochondrial iron accumulation and oxidative mitochondrial damage. Mutations in ABC7, the human homolog of ATM1, result in X-linked sideroblastic anemia and ataxia. Here we show that a deletion of ATM1 also has effects on extra-mitochondrial iron metabolism. ATM1-deficient cells have an increased iron requirement for growth. When grown in iron-rich medium, mutant cells accumulate excess mitochondrial iron and have increased expression of the genes required for both high and low affinity iron uptake. Thus, ATM1 mutant cells simultaneously demonstrate features of both iron overload and iron starvation. Yfh1p is the yeast homolog of the human frataxin protein, which is deficient in Friedreich's ataxia. As in atm1 cells, a yfh1 deletion results in both mitochondrial iron accumulation and cytosolic iron starvation. In spite of their apparent roles in cellular iron homeostasis, we find that the expression of neither ATM1 nor YFH1 is responsive to cellular iron status. Based on these observations, we propose a model in which cellular iron is prioritized for use by the mitochondrion, and available to the remainder of the cell only after mitochondrial needs have been fulfilled.
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PMID:The role of the mitochondrion in cellular iron homeostasis. 1612 Feb 68

Pesticides can modify invertebrate movement and feeding behaviour which could reduce predation in agroecosystems. Previous assays have exposed the spider Pardosa amentata (Clerck) to the synthetic pyrethroid cypermethrin and monitored prey items consumed in small containers (requiring very little movement to capture prey). The current study used larger arenas containing artificial 'vegetation' (a plastic analogue) to encourage spiders to hunt and capture prey. The period 24 h after exposure produced greatest variability in prey item consumption between treatments and was used to examine treatment effects. At this time, cypermethrin reduced prey consumption rates but these effects did not persist. Findings did not suggest that the presence of artificial vegetation in arenas modified prey consumption rates, which was consistent for individuals treated with cypermethrin and a control group. This is despite the majority of pesticide-treated individuals exhibiting both ataxia and paralysis of the hind legs (these effects persisting for a maximum of 3 and 6 days respectively). These findings were consistent for both sexes. Spider longevity under starvation conditions was not significantly reduced by cypermethrin exposure but overall females survived longer than males. The findings are discussed in the context of the arenas used and the ecology of this common predator.
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PMID:Impact of cypermethrin on feeding behaviour and mortality of the spider Pardosa amentata in arenas with artificial 'vegetation'. 1626 42

Health monitoring of spotted hyenas (Crocuta crocuta) in the Serengeti ecosystem, Tanzania, revealed Hepatozoon infection in all of 11 immature individuals examined following death from natural causes. Hepatozoon infection was probably an important factor contributing to mortality in two cases that exhibited clinical signs of ataxia, lethargy, ocular discharge, retching, and labored breathing before death. Whether Hepatozoon infection contributed to six deaths from fire, probable lion predation and unknown causes could not be determined. Four deaths from infanticide and starvation were unlikely to be associated with Hepatozoon infection. Histologic examination revealed lung tissue infected with cyst-like structures containing protozoan stages in all eight cases examined and interstitial pneumonia in most cases. Systemic spread of infection to several organs was found in three cases. Alignment of a 426 bp sequence from the parasite's 18s rRNA gene revealed a Hepatozoon species identical to that recently described from two domestic cats in Spain and only 7 bp substitutions when a 853 bp sequence was aligned to this cat Hepatozoon species. Previous reports of infection of wild carnivores in eastern and southern Africa with an unspecified Hepatozoon species similar in appearance to H. canis may have involved the species described in this study.
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PMID:A Hepatozoon species genetically distinct from H. canis infecting spotted hyenas in the Serengeti ecosystem, Tanzania. 1826 20

Introduced mosquito-borne avian disease is a major limiting factor in the recovery and restoration of native Hawaiian forest birds. Annual epizootics of avian pox (Avipoxvirus) and avian malaria (Plasmodium relictum) likely led to the extinction of some species and continue to impact populations of susceptible Hawaiian honeycreepers (Drepanidinae). The introduction of a novel pathogen, such as West Nile virus (WNV), could result in further population declines and extinctions. During September and October 2004, we infected Hawai'i' Amakihi (Hemignathus virens) with a North American isolate of WNV by needle inoculation and mosquito bite to observe susceptibility, mortality, and illness in this endemic passerine, and to determine the vector competence of the co-occurring, introduced mosquito Culex quinquefasciatus. All experimentally infected Hawai'i ;Amakihi became viremic, with a mean titer >10(5) plaque-forming units (PFU)/ml, and they experienced clinical signs ranging from anorexia and lethargy to ataxia. The fatality rate among needle-inoculated Hawai'i' Amakihi (n=16) was 31.3%, but mortality in free-ranging birds is likely to increase due to predation, starvation, thermal stress, and concomitant infections of avian malaria and pox. Surviving Hawai'i' Amakihi seem to clear WNV from the peripheral blood by 7-10 days postinfection (DPI), and neutralizing antibodies were detected from 9 to 46 DPI. In transmission trials, Hawaiian Cx. quinquefasciatus proved to be a competent vector and Hawai'i Amakihi an adequate amplification host of WNV, suggesting that epizootic WNV could readily become an additional limiting factor of some native Hawaiian bird populations.
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PMID:Experimental infection of Hawai'i 'Amakihi (hemignathus virens) with West Nile virus and competence of a co-occurring vector, culex quinquefasciatus: potential impacts on endemic Hawaiian avifauna. 1939 35


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