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At least 1,027 records · Page 57Linked to original sources
PubMed2001

Chaperone overload is a possible contributor to 'civilization diseases'.

Molecular chaperones dampen the effect of damaging mutations that would otherwise be removed from the population by natural selection. Here, I propose that the development of modern medical practice depressed this process, leading to a rise of phenotypically silent mutations in the genome. The background of misfolded proteins increases during ageing and, by competition, prevents the chaperone-mediated buffering of silent mutations. Phenotypically exposed mutations contribute to a more-abundant manifestation of multigene-diseases. This 'chaperone overload' hypothesis emphasizes the need for efficient ways to enhance chaperone capacity in ageing subjects, and will hopefully lead to the identification and 'repair' of silent mutations.

Aging↗
PubMed1978

Some missile injuries due to civil unrest in Northern Ireland.

Some missile injuries are reviewed after nearly 8 years of continuous warfare. A feature of many of these injuries is the early admission to hospital which has had a profound effect on the survival rate and the recovery period. Some examples are given of injuries inflicted by rubber bullets. The effects of wounding by low and high velocity missiles are described and examples given. An injury caused by a missile incorporated in a bomb is also shown.

Adolescent↗
PubMed2004

The impact of tuberculosis on civilization.

Tuberculosis is an ancient disease that has spread in epidemic form among susceptible peoples but has had a little demographic or political impact on the populations it has inflicted. The disease continues to have a large economic impact on societies in which it is prevalent. Tuberculosis has left its mark on human creativity; on the lives of individuals in music, art, and literature; and dramatically on the advance of biomedical science and healthcare.

Civilization↗
PubMed2003

Hyperinsulinemic diseases of civilization: more than just Syndrome X.

Compensatory hyperinsulinemia stemming from peripheral insulin resistance is a well-recognized metabolic disturbance that is at the root cause of diseases and maladies of Syndrome X (hypertension, type 2 diabetes, dyslipidemia, coronary artery disease, obesity, abnormal glucose tolerance). Abnormalities of fibrinolysis and hyperuricemia also appear to be members of the cluster of illnesses comprising Syndrome X. Insulin is a well-established growth-promoting hormone, and recent evidence indicates that hyperinsulinemia causes a shift in a number of endocrine pathways that may favor unregulated tissue growth leading to additional illnesses. Specifically, hyperinsulinemia elevates serum concentrations of free insulin-like growth factor-1 (IGF-1) and androgens, while simultaneously reducing insulin-like growth factor-binding protein 3 (IGFBP-3) and sex hormone-binding globulin (SHBG). Since IGFBP-3 is a ligand for the nuclear retinoid X receptor alpha, insulin-mediated reductions in IGFBP-3 may also influence transcription of anti-proliferative genes normally activated by the body's endogenous retinoids. These endocrine shifts alter cellular proliferation and growth in a variety of tissues, the clinical course of which may promote acne, early menarche, certain epithelial cell carcinomas, increased stature, myopia, cutaneous papillomas (skin tags), acanthosis nigricans, polycystic ovary syndrome (PCOS) and male vertex balding. Consequently, these illnesses and conditions may, in part, have hyperinsulinemia at their root cause and therefore should be classified among the diseases of Syndrome X.

Civilization↗
PubMed1993

Juror competence in civil trials: effects of preinstruction and evidence technicality.

Forty-eight jury-eligible adults heard 1 of 4 versions of a tort trial. The design combined high and moderate levels of evidence technicality and the placement of substantive judicial instructions either before or after evidence presentation. Jurors given instructions before hearing the evidence for liability and before the evidence for compensation made clear distinctions among 4 differentially worthy plaintiffs, whereas jurors instructed after evidence presentation were not able to distinguish among the plaintiffs. Preinstructions enabled jurors to devise a causal model, as measured by both verbal representation of the evidence and recognition tests, that contained more probative evidence and less nonprobative and evaluative information than the models constructed by jurors who were postinstructed. Preinstructed jurors were better able than postinstructed jurors to correctly reject recognition items not part of the trial text and to correctly identify items from the trial.

Adult↗