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)

Protein catabolism in fibroblasts cultured from the skin of normal individuals and of patients with mucolipidosis II (I-cell disease) and several other lysosomal storage diseases was examined by metabolic labelling with [3H]leucine and following the fate of radioactive proteins in pulse-chase experiments. In mucolipidosis II cells, overall protein degradative rates were found to be distinctly lower than in normal control cells. To distinguish lysosomal from non-lysosomal degradation, labelling experiments were carried out in the presence and absence of 10 mM NH4Cl, an inhibitor of lysosomal function. It was found that mucolipidosis II fibroblasts exhibited a markedly reduced rate of lysosomal protein degradation, whereas the rate of nonlysosomal degradation appeared normal. Serum and amino acid starvation led to a marked increase in lysosomal protein degradation in normal cells, but had only a minimal effect on that in mucolipidosis II fibroblasts. The specific activities of cathepsins B, H and L were profoundly diminished in all mucolipidosis II cell lines tested. Lysosomal protein degradation in a mucolipidosis III cell line was impaired to a similar degree as in mucolipidosis II cells, whereas it was decreased to a lesser extent in fibroblasts from patients with mucopolysaccharidoses I and VI, galactosialidosis and GM1-gangliosidosis. We conclude that fibroblasts from patients with mucolipidosis II and III have a severely compromised capacity for endogenous lysosomal protein degradation that appears to result from multiple cathepsin deficiency. This lysosomal defect is likely to have pathophysiological consequences.
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PMID:Protein catabolism in fibroblasts cultured from patients with mucolipidosis II and other lysosomal disorders. 824 Feb 60

With the decline of the former main causes of death in early childhood--infections and starvation--sudden infant death syndrome (SIDS) has emerged as the most important single cause of postneonatal infant mortality. It has adopted the role of a major indicator for the standard of public health care. Despite extensive input into research, its pathophysiology has remained rather obscure. The resulting helplessness of scientists and health care professionals have lead to adherence to unconfirmed pathophysiological hypotheses and to pursuit of preventive strategies of doubtful efficacy. In this overview, the medical and technical background of five major hypotheses is being presented. A lot can be learnt from the history of their development, efforts to refute them, and the reasons for unreflected adherence to them. (1) Due to its illustrative nature, the so-called 'status thymico-lymphaticus', the theory of asphixation by an enlarged thymus, could not be eradicated although well-reknowned physicians--including the Austrian pathologist Paltauf--have repeatedly attempted to do so. (2) Assumed familiarity, an aspect which attracted the attention of pediatricians to SIDS initially has been excluded, but an increased risk of SIDS for the siblings of affected babies is still common belief. (3) The sleep-apnea-hypothesis has turned out a complete error with serious consequences, but home apnea monitors are still being widely recommended. (4) The rise of SIDS in the 80ies and its subsequent decline in the 90ies has been interpreted as the advent and successful control of an epidemic although significant numbers of cot death have been reported long before the turn of the century, and the apparent increase which paralleled the introduction of the 9th edition of the ICD code is most likely due to improved registration. (5) Finally, SIDS is still being considered a random event--ignoring all evidence of an obvious role of socioeconomical factors.
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PMID:[Child's sudden death in 20th century--hypothesis, dogmas, dead wood]. 1076 30

Anorexia nervosa and Bulimia nervosa are the main types of eating disorders described in the International Classification of Diseases ICD-10. The main features are eating patterns such as refusal to eat enough food or loss of control, followed by counter-regulatory measures. In addition, preoccupation with body shape and weight and with food is an important feature of eating disorders. Severe medical conditions may occur as a result to starvation, malnutrition and purging. Binge eating disorder has been included as an additional variant of disturbed eating in the American classification system of mental disorders (DSM-IV). The main characteristic of the binge eating disorder is binge eating, but without counter-regulatory measures. Patients with anorexia nervosa are foremost underweight (BMI < 17.5 kg/m2), those with a bulimia nervosa are usually in the normal weight range. On the other hand, patients with the binge eating disorder are overweight or obese. Etiological models are multifaceted and include predisposing and sustaining factors as well as triggers for the onset of the disorder. The course is variable and marked by changes between remission and clinically relevant symptoms. Psychotherapy is the treatment of choice.
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PMID:[Eating disorders--diagnosis and treatment]. 1843 6

The basic criterion for the diagnosis of anorexia (AN - anorexia nervosa) by ICD-10 (International Classification of Diseases, version 10) is the body weight less than 15% of the expected normal body weight. According to DSM-IV (Diagnostic and Statistical Manual for Mental Disorders, version IV) the basic feature of AN is a refusal to maintain body weight equal or greater than the minimal normal weight. The prevalence of anorexia nervosa is 0.3-0.5% or even 1.3-3.7% if include pre-anorexic states (eg. the phenomenon of pro-ana). The main feature of anorexia is a reduction of caloric intake. According to the recommendations of the American Psychiatric Association (APA) for nutritional treatment of patients with AN the main goals in therapy of AN are: restoration of body weight, normalization of eating patterns, achievement a normal feeling of hunger and satiety and correction of the consequences of improper nutrition. APA suggests that achievable weight gain is about 0.9-1.4 kg per week in the case of hospitalized patients and approximately 0.23-0.45 kg per week in the case of outpatients. During the nutritional treatment of AN numerous side effects including anxiety, phobia, occurrence of obsessive thoughts and compulsive behavior, suicidal thoughts and intentions may occur. According to National Institute for Clinical Excellence (NICE) the most important goal of AN therapy is weight gain in the range of 0.5-1 kg per week in hospitalized patients and 0.5 kg per week for outpatients. A person suffering from anorexia in the initial period of nutritional treatment spends twice more energy to maintain elevated body temperature, which significantly increases during the night rest. This phenomenon is called nocturnal hyperthermia and has a negative effect on the healing process. "Refeeding syndrome" is an adverse effect of nutritional treatment in anorexia. It is caused by too rapid nutrition in a patient suffering from chronic starvation. It can endanger the patient's life.
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PMID:[Contemporary criteria of the diagnosis and current recommendations for nutritional therapy in anorexia nervosa]. 2496 16