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)

We conducted a case-control study of clinically diagnosed Alzheimer's disease (AD) on 170 cases aged 52 to 96 years, and 170 controls matched for age, sex and, where possible, the general practice of origin. Trained lay interviewers naive to the hypotheses and to the clinical status of the elderly person carried out risk-factor interviews with informants. Significant odds ratios were found for 4 variables: a history of either dementia, probable AD, or Down's syndrome in a 1st-degree relative, and underactivity as a behavioral trait in both the recent and more distant past. Previously reported or suggested associations not confirmed by this study include head injury, starvation, thyroid disease, analgesic abuse, antacid use (aluminum exposure), alcohol abuse, smoking, and being left-handed.
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PMID:A case-control study of Alzheimer's disease in Australia. 214 25

A group of 47 patients suffering from chronic recurrent duodenal ulcers was subdivided into two groups according to whether the first manifestation of the disorder occurred early or late in the life of each individual. A comparison of the two groups revealed that the patients in group I (early manifestation) had a larger number of constitutional handicaps along with a higher incidence of dispositional prior experience with regard to object loss and that they assumed social responsibility at an early age. Group II (late manifestation) was characterized by a larger number of depressive psychoses, a higher incidence of alcohol abuse, and by attempts at suicide. Apart from this, the patients in group II often complained of muscular pain syndromes. Patients in group I frequently exhibited the characteristics of the ulcer type described by Alexander as well as chronic anger. Patients in group II most often had the personality structure of so-called psychosomatic patients or suffered from depressive disorders affecting their personalities and from chronic anxiety. The two characteristics which were most typical for recidivation were: 1. Actualization of experienced bereavement and 2. unspecific activation as a result of the will to assert themselves in stress situations. In 41% of the cases there was evidence of somatic factors as e.g. starvation, abuse of alcohol or abuse of analgetics. Long-term prophylaxis has been effected by psychopharmacological agents as well as by psychotherapeutic techniques.
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PMID:[Ulcer disease. Studies of patients with chronic recurrent duodenal ulcer in an attempt to differentiate subgroups based on age at disease onset, psychopathologic and biographical data]. 376 11

The purpose of this paper is to review clinical studies on hypophosphatemia in pediatric intensive care unit patients with a view to verifying prevalence and risk factors associated with this disorder. We searched the computerized bibliographic databases Medline, Embase, Cochrane Library, and LILACS to identify eligible studies. Search terms included critically ill, pediatric intensive care, trauma, sepsis, infectious diseases, malnutrition, inflammatory response, surgery, starvation, respiratory failure, diuretic, steroid, antiacid therapy, mechanical ventilation. The search period covered those clinical trials published from January 1990 to January 2004. Studies concerning endocrinological disorders, genetic syndromes, rickets, renal diseases, anorexia nervosa, alcohol abuse, and prematurity were not included in this review. Out of 27 studies retrieved, only 8 involved pediatric patients, and most of these were case reports. One clinical trial and one retrospective study were identified. The prevalence of hypophosphatemia exceeded 50%. The commonly associated factors in most patients with hypophosphatemia were refeeding syndrome, malnutrition, sepsis, trauma, and diuretic and steroid therapy. Given the high prevalence, clinical manifestations, and multiple risk factors, the early identification of this disorder in critically ill children is crucial for adequate replacement therapy and also to avoid complications.
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PMID:Hypophosphatemia in critically ill children. 1554 5

The tragic life of Vincent van Gogh is summarized, emphasizing his early departure from formal education, failure as a successful salesman in the art world, attempt at religious studies, difficulty with female and family relationships, return to the art world, and tendencies toward extremes of poor nutrition or near self-starvation and excessive drinking and smoking. In Paris he joined the Impressionists, but drank very heavily both absinthe and cognac. Southward he went to Arles and was joined by Paul Gauguin, with whom he had major personality problems, causing van Gogh to cut off part of his left ear. He experienced paranoid ideation and confinement in mental institutions in Arles, and then returned to Paris and onto Auvers-sur-Oise, where he committed suicide at age 37. Possible physical diagnoses include glaucoma, Meniere's disease, acute intermittent porphyria, and chronic lead poisoning, but these diagnoses seem unlikely. Possible psychiatric diagnoses include borderline personality disorder, anxiety-depressive disorder with episodes of depression and hypomania, and also paranoid schizophrenia. Van Gogh did not have spontaneous seizures and, therefore, did not have epilepsy. Before he began to drink heavily, when he was near starvation, he had "fainting fits," and after drinking, especially absinthe, a convulsant drug, he continued to have similar attacks. His episodes of unconsciousness can be well explained by chronic malnutrition and alcohol abuse, only possibly exacerbated by drinking large quantities of absinthe. Although van Gogh is an excellent example of the Geschwind syndrome, at times associated with temporal lobe epilepsy, this fact does not establish such an epilepsy. Thus, the syndrome is an orphan without the parent condition.
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PMID:A reappraisal of the possible seizures of Vincent van Gogh. 1590 45

Metabotropic glutamate receptors (mGluRs) are a class of G-protein-coupled receptors that possess a seven transmembrane region involved in the modulation of excitatory synaptic transmission in the nervous system. mGluR orthologs have been identified in Drosophila, Caenorhabditis elegans, and higher organisms. Drosophila possesses two mGluR genes, DmGluRA and DmXR. We screened the Dictyostelium genome data base using the ligand binding domain of rat mGluR1 as bait, and identified a new receptor, DdmGluPR, belonging to the mGluR family. Similar to Drosophila DmXR, the residues of mGluRs involved in the binding of the alpha-carboxylic and alpha-amino groups of glutamate were well conserved in DdmGluPR, but the residues interacting with the gamma-carboxylic group of glutamate were not. The phylogenetic analysis suggests that DdmGluPR diverged after the mGluR family-GABA(B) receptors split but before mGluR family divergence. DdmGluPR mRNA was expressed in vegetative cells and throughout starvation-induced development, but the level of the expression was relatively high until 4 h after starvation. DdmGluPR was localized to the plasma membrane of axenically grown Ax-2 cells expressed as a green fluorescent protein fusion protein. DdmGluPR-null cells grew faster at high cell density and reached higher densities than wild-type cells. DdmGluPR-null cells exhibited delayed aggregates formation upon starvation and impaired chemotaxis toward cAMP. Although expressions of cAR1 and aca, cAMP-signaling components, were rapidly induced and peaked at 2-4 h in wild-type cells, DdmGluPR-null cells displayed sustained and peaked at 8 h of the expressions of these genes. Our findings suggest the involvement of DdmGluPR in the early development of Dictyostelium discoideum.
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PMID:A metabotropic glutamate receptor family gene in Dictyostelium discoideum. 1652 14

Alcohol is the most abused substance worldwide and a significant source of liver injury; the mechanisms of alcohol-induced liver disease are not fully understood. Significant cellular toxicity and impairment of protein synthesis and degradation occur in alcohol-exposed liver cells, along with changes in energy balance and modified responses to pathogens. Autophagy is the process of cellular catabolism through the lysosomal-dependent machinery, which maintains a balance among protein synthesis, degradation, and recycling of self. Autophagy is part of normal homeostasis and it can be triggered by multiple factors that threaten cell integrity, including starvation, toxins, or pathogens. Multiple factors regulate autophagy; survival and preservation of cellular integrity at the expense of inadequately folded proteins and damaged high-energy generating intracellular organelles are prominent targets of autophagy in pathological conditions. Coincidentally, inadequately folded proteins accumulate and high-energy generating intracellular organelles, such as mitochondria, are damaged by alcohol abuse; these alcohol-induced pathological findings prompted investigation of the role of autophagy in the pathogenesis of alcohol-induced liver damage. Our review summarizes the current knowledge about the role and implications of autophagy in alcohol-induced liver disease.
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PMID:Autophagy in alcohol-induced liver diseases. 2255 Oct 4

Ketoacidotic syndromes are frequently encountered in acute care medicine. This article focuses on ketosis and ketoacidotic syndromes associated with intoxications, alcohol abuse, starvation, and certain dietary supplements as well as inborn errors of metabolism. Although all of these various processes are characterized by the accumulation of ketone bodies and metabolic acidosis, there are differences in the mechanisms, clinical presentations, and principles of therapy for these heterogeneous disorders. Pathophysiologic mechanisms that account for these disorders are presented, as well as guidance regarding identification and management.
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PMID:Toxigenic and metabolic causes of ketosis and ketoacidotic syndromes. 2299 93

The serum glucose level is regulated within a narrow range by multiple factors under physiological conditions, but is greatly modified in the death process and after death. The present study comprehensively investigated glucose levels in blood and body fluids, including pericardial fluid (PCF), cerebrospinal fluid (CSF) and vitreous humor, reviewing forensic autopsy cases (n=672). Right heart blood glucose level was often higher than at other sites, and the CSF glucose level was the lowest, showing greater dissociation in acute/subacute death cases. The glucose level was higher in the diabetic (high HbA1c) than in the non-diabetic (low HbA1c) group at each site (p<0.01-0.0001). Fatal diabetic ketoacidosis cases had evidently high glucose levels at each site; whereas in the non-diabetic group, blood glucose level was higher in fatal alcohol abuse, saltwater drowning, electrocution, cerebrovascular disease and sudden cardiac death due to ischemic heart disease. Fatal methamphetamine (MA) abuse, sepsis, malnutrition (starvation) and hypoglycemia due to antidiabetics showed markedly lower blood glucose levels. Ketones in bilateral cardiac blood and PCF were increased in diabetic ketoacidosis and fatal alcohol abuse as well as in most cases of hyperthermia (heatstroke), hypothermia (cold exposure) and malnutrition. These findings suggest that combined analysis of glucose, HbA1c and ketones in blood and body fluids is useful to investigate not only fatal diabetic metabolic disorders but also death processes due to other causes, including alcohol and MA abuse, as well as thermal disorders, sepsis and malnutrition.
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PMID:Comprehensive investigation of postmortem glucose levels in blood and body fluids with regard to the cause of death in forensic autopsy cases. 2659 93

The use of sodium-glucose cotransporter 2 inhibitors is associated with an increased risk of diabetic ketoacidosis. This risk has been reported in particular in off-label use of these agents in type 1 diabetes, but reports of risks in type 2 diabetes patients also exist. In type 2 diabetes ketoacidosis is rare and is present particularly in patients who have undergone prolonged starvation, serious infection, alcohol abuse or surgery. The pleiotropic advantages of sodium-glucose cotransporter 2 inhibitors do not outweigh the risk for a diabetic ketoacidosis, but caution is warranted.
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PMID:Sodium-glucose Cotransporter 2 Inhibitors and Ketoacidosis - Clinical Implications in the Treatment of Patients with Type 2 Diabetes. 2963 85

Reactive oxygen species- (ROS-) mediated autophagy physiologically contributes to management of cell homeostasis in response to mild oxidative stress. Cancer cells typically engage autophagy downstream of ROS signaling derived from hypoxia and starvation, which are harsh environmental conditions that need to be faced for cancer development and progression. Hepatocellular carcinoma (HCC) is a solid tumor for which several environmental risk factors, particularly viral infections and alcohol abuse, have been shown to promote carcinogenesis via augmentation of oxidative stress. In addition, ROS burst in HCC cells frequently takes place after administration of therapeutic compounds that promote apoptotic cell death or even autophagic cell death. The interplay between ROS and autophagy (i) in the disposal of dysfunctional mitochondria via mitophagy, as a tumor suppressor mechanism, or (ii) in the cell survival adaptive response elicited by chemotherapeutic interventions, as a tumor-promoting event, will be depicted in this review in relation to HCC development and progression.
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PMID:Oxidative Stress-Driven Autophagy acROSs Onset and Therapeutic Outcome in Hepatocellular Carcinoma. 3120 85


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