On the molecular weight of thiosulfate sulfurtransferase.

Bovine liver thiosulfate sulfurtransferase (rhodanese) (EC 2.8.1.1) HAS BEEN REPORTED TO EXIST IN SOLUTION IN A RAPID, PH-dependent equilibrium between monomeric and dimeric forms of molecular weights 18 500 and 37 000 (Volini, M., DeToma, F. and Westley, J. (1967), J. Biol. Chem. 242, 5220). We have reinvestigated the proposed dissociation using sodium dodecylsulfate-polyacrylamide gel electrophoresis. The smallest rhodanese species observed has a molecular weight around 35 000, which is not reduced by severe denaturing conditions, including alkylation in 8 M guanidine-HCl or dialysis against 2% sodium dodecylsulfate and 5% mercaptoethanol. After limited CNBr cleavage, intermediate products of greater than 18 500 molecular weight are formed. The apparent molecular weight of these intermediate fragments is not changed by addition of mercaptoethanol. The total apparent molecular weights of the CNBr fragments after exhaustive cleavage is approx. 45 000 plus or minus 15 000. These results are not consistent with a monomer molecular weight of approx. 18 500 for thiosulfate sulfurtransferase.     

Predictors of ratio of placental weight to fetal weight in multiethnic community.

OBJECTIVE--To determine whether placental ratio is influenced by maternal ethnic origin, obesity, hypertension, and haematological indices of iron deficiency anaemia. DESIGN--Observational study. SETTING--District general hospital in Birmingham. SUBJECTS--692 healthy nulliparous pregnant women, of whom 367 were European, 213 Asian, 99 Afro-Caribbean, and 13 of other or undocumented ethnic origin. MAIN OUTCOME MEASURES--Placental ratio and maternal body mass index, blood pressure, and haematological indices. RESULTS--Though birth weight and placental weight were lower in Asian women than in other groups, mean placental ratio was similar in Asian (19.5% (SD 3.3%)), European (20.0% (4.0%)), and Afro-Caribbean women (20.4% (5.3%)). Gestational age at birth was the main predictor of placental ratio in the univariate analysis (r = -0.34, P < 0.001) and multivariate analysis. The only other significant predictor of placental ratio in multivariate analysis was maternal body mass index, which was positively associated with placental ratio (r = 0.1, P = 0.01). Mean (SD) placental ratio was not significantly higher in women who developed gestational hypertension (20.4% (4.5%)) and pre-eclampsia (23.3% (7.3%)) than in normal women (19.8% (3.8%)). No evidence of a relation between placental ratio and first antenatal visit haemoglobin concentration or mean cell volume was detected, and placental ratio was not associated with change in mean cell volume during pregnancy or with third trimester serum ferritin concentration. CONCLUSIONS--These data do not support the proposed association between poor maternal nutrition and increased placental ratio. The association between high placental ratio and adult hypertension may be confounded by genetic and environmental factors associated with maternal obesity (and possibly maternal hypertension).     

Estrogenic regulation of body weight in the female rat.

For a period of weeks subsequent to bilateral ovariectomy, female rats given unlimited access to food increased their food intakes and the rates at which they gained body weight; this resulted in elevated levels of body weight. Restricting ovariectomized (ovx) rats to their preoperative level of food intake (restricted diet), prevented this excessive gain in body weight. Estradiol benzoate (EB) treatments of 0.5 μg per day for 15 consecutive days partially reversed pre-occurring weight gain in obese ovx rats; this was accompanied by a reduction in food intake. In contrast, identical EB treatment for nonobese ovx rats (restricted diet) did not result in any loss of body weight or change in food intake. Oil-treated nonobese ovx rats gained a small amount of weight relative to their EB-treated counterparts, despite the similarity in their food intakes. Thus, part of the increased weight gain observed after ovariectomy may be independent of changes in food consumption, and related to removal of estrogenic influences from metabolic and behavioral processes involved in energy balance. The weight limiting actions of estradiol were far more pronounced in animals already obese or facing impending obesity than in animals in which excessive weight gain was prevented. The data also suggest that estradiol is more effective in preventing than in reversing the weight gain associated with ovariectomy, and that estrogenic influences on the body weight set point are manifested with very short latencies. These findings support earlier conclusions that estradiol does not regulate food intake directly, but secondarily controls consumption as a means of weight regulation.     

The molecular weight of bovine lactoferrin.

The molecular weight of bovine lactoferrin in a neutral solvent (e.g. 0.2 M NaC1, pH 7.8 20 degrees C) has been determined using high-speed sedimentation equilibrium at various concentrations and speeds. Under these conditions the protein behaved as a single thermodynamic component with a weight-average molecular weight [MW]C=0 = 93000 plus or minus 2000 and a second virial coefficient B = 4.3-10(-5) mol-ml(-1)-g(-2). This value of the molecular weight is in good agreement with values previously reported by Groves (J. Am. Chem. Soc. 82, 3345-3350, 1960) and Szuchet and Johnson (Eur. Polym. J. 2, 115-128, 1966); it is, however, in disagreement with the more recent value given by Castellino et al. (J. Biol. Chem. 245, 4269-4275, 1970). The possible reasons for this discrepancy are discussed.     

Excess weight and sleep-disordered breathing.

Excess weight is a well-established predictor of sleep-disordered breathing (SDB). Clinical observations and population studies throughout the United States, Europe, Asia, and Australia have consistently shown a graded increase in the prevalence of SDB as body mass index, neck girth, or other measures of body habitus increases. Clinical studies of weight loss and longitudinal population studies provide strong support for a causal association. The role of excess body weight, a modifiable risk factor, with SDB raises many questions relevant to clinical practice and public health. The topic takes on added importance with the alarming rate of weight gain in children as well as adults in industrialized nations. Among adults ages 30-69 yr, averaging over the estimated United States 2003 age, sex, and BMI distributions, we estimate that approximately 17% of adults have mild or worse SDB (apnea-hypopnea index > or = 5) and that 41% of those adults have SDB "attributable" to having a body mass index of > or =25 kg/m(2). Similarly, we estimate that approximately 5.7% of adults have moderate or worse SDB (apnea-hypopnea index > or = 15) and that 58% of those adults have SDB attributable to excess weight. Clearly, if the expanding epidemic of obesity seen in the United States continues, the prevalence of SDB will almost certainly increase, along with the proportion of SDB attributable to obesity.