OVERHEATING IN BED AS AN IMPORTANT FACTOR IN MANY COMMON DERMATOSES

Background. Extensive questioning of patients with a wide variety of skin disorders led to the impression that nocturnal overheating was probably an important factor in the initiation and the perpetuation of many skin disorders. Methods. In order to test the hypothesis, 12 “clean-skinned” subjects (6M/6F) aged 18 to 45 years were monitored electronically every 30 seconds during an 8 hour sleep period (2300 to 0700 hours), sleeping under a standard 10 tog duvet. Results. All the subjects were too hot by 3 to 4°C. All showed changes in their EEG patterns with reduced REM sleep, increased awakenings, and all showed changes in their sleep stage patterns. In addition, they all showed evidence of increased sweating in the “heat-sink” area. Conclusions. The mechanisms where by such changes could be implicated in the precipitation and perpetuation of skin disease are discussed. “Lifestyle” modification as a very effective, noninvasive, therapeutic regime is recommended. Further research along these lines would probably be very valuable and instructive.     

Aortopulmonary window with patent ductus arteriosus and interrupted aortic arch: A case report

Indian Journal of Thoracic and Cardiovascular Surgery -     

Decreased inducibility of TNF expression in lipid-loaded macrophages

Background  

Inflammation and immune responses are considered to be very important in the pathogenesis of atherosclerosis. Lipid accumulation in macrophages of the arterial intima is a characteristic feature of atherosclerosis which can influence the inflammatory potential of macrophages. We studied the effects of lipid loading on the regulation of TNF expression in human monocyte-derived macrophages.     

Mouse homologues of the human AZF candidate gene RBM are expressed in spermatogonia and spermatids, and map to a Y chromosome deletion interval associated with a high incidence of sperm abnormalities

An RNA-binding motif (RBM) gene family has been identified on the human Y chromosome that maps to the same deletion interval as the 'azoospermia factor' (AZF). We have identified the homologous gene family (Rbm) on the mouse Y with a view to investigating the proposal that this gene family plays a role in spermatogenesis. At least 25 and probably >50 copies of Rbm are present on the mouse Y chromosome short arm located between Sry and the centromere. As in the human, a role in spermatogenesis is indicated by a germ cell-specific pattern of expression in the testis, but there are distinct differences in the pattern of expression between the two species. Mice carrying the deletion Yd1, that maps to the proximal Y short arm, are female due to a position effect resulting in non-expression of Sry ; sex-reversing such mice with an Sry transgene produces males with a high incidence of abnormal sperm, making this the third deletion interval on the mouse Y that affects some aspect of spermatogenesis. Most of the copies of Rbm map to this deletion interval, and the Yd1males have markedly reduced Rbm expression, suggesting that RBM deficiency may be responsible for, or contribute to, the abnormal sperm development. In man, deletion of the functional copies of RBM is associated with meiotic arrest rather than sperm anomalies; however, the different effects of deletion are consistent with the differences in expression between the two species.      

Bias due to incomplete follow up in a cohort study

AIM: To investigate the bias introduced by incomplete follow up in a cohort study of ocular outcome after premature birth. METHODS: A geographically defined cohort of children born before 32 weeks' gestation was prospectively recruited at birth to study the ocular outcome at 2 years. On the basis of attendance at 2 years, the children's families were allocated to one of three groups: group 1 attended for follow up, group 2 were difficult to trace, and group 3 were very reluctant for assessment. All children were examined by a single ophthalmologist, masked to these groupings. RESULTS: 558 children (98.8% of study group) were examined, of whom 505 were in group 1, 20 in group 2, and 33 in group 3. The groups which were more difficult to study (groups 2 and 3) showed a significantly higher prevalence of ocular abnormalities, including strabismus (p=0. 02) and cicatricial retinopathy of prematurity (p=0.002) compared with those attending for follow up. Further, not all of these cases could have been identified by review of the children's previous records. Ocular abnormalities would be underestimated by 16% (11.3% in group 1 compared with 13.4% in the total cohort, p=0.77). CONCLUSIONS: This study suggests that the prevalence of abnormalities would be underestimated by incomplete follow up, as those subjects who were most difficult to obtain for study had a significantly higher prevalence of abnormalities.     

Pharmacological characterization of endothelin receptor subtypes in the guinea-pig prostate gland.

Experiments have been conducted to investigate the actions of endothelins on the guinea-pig prostate gland. Saturation experiments with [125I]-endothelin-1 (2-800 pM) in guinea-pig prostatic homogenates indicated the presence of high affinity binding sites with an equilibrium dissociation constant (KD) of 230+/-50 pM, a maximum number of binding sites (Bmax) of 52+/-16 fmol mg(-1) protein or 269+/-61 fmol g(-1) tissue and a Hill coefficient (nH) of 1.01+/-0.03 (n = 3). Competition experiments revealed that binding of [125I]-endothelin-1 (20 pM) was inhibited with the following order of potency: endothelin-1 >BQ-788 (N-cis-2,6-dimethylpiperidinocarbonyl-L-gamma-methyl-Leu-D-Trp[1-+ ++CO2CH3-D-Nle-ONa])> BQ-123 (cyclo-D-Asp-L-Pro-D-Val-Leu-D-Trp) > or = sarafotoxin S6c. At concentrations with negligible influence on smooth muscle tone, endothelin-1, endothelin-2 and sarafotoxin S6b (1 nM-0.1 microM) produced concentration-dependent potentiation of the contractions evoked by electrical field stimulation with trains of 20 pulses at 10 Hz every 50 s, 0.5 ms pulse width and a dial setting of 60 V. In contrast, the endothelin ET(B) receptor-preferring agonist endothelin-3 (1 nM- 1 microM) was much less potent, and the endothelin ET(B) receptor-selective agonists sarafotoxin S6c and BQ-3020 (Ac-[Ala11,15]-endothelin-1 (6-21)), up to 1 microM, were without effect. The endothelin ET(A) receptor antagonist BQ-123 (1 microM) markedly inhibited the potentiation induced by endothelin-1, endothelin-2 and sarafotoxin S6b while the endothelin ET(B) receptor antagonist BQ-788 (1 microM) was less effective. While our binding data indicates the presence of ET(A) and ET(B) binding sites in the guinea-pig prostate, the endothelin-induced facilitation of neurotransmission to the prostatic smooth muscle is mediated largely via activation of endothelin receptors of the ET(A) subtype.