Causes of B chromosome variant substitution in the grasshopper Eyprepocnemis plorans

We have analysed B chromosome frequency for three consecutive years, B transmission rate at population and individual levels, clutch size, egg fertility and embryo–adult viability in a natural population of the grasshopper Eyprepocnemis plorans containing two different B chromosome variants, i.e. B₂ and B₂₄, the second being derived from the first and having replaced it in nearby populations. From 2002 to 2003 the relative frequency of both variants changed, although the differences did not reach significance. A mother–offspring analysis showed no significant effect of any of the two B variants on clutch size, egg fertility or embryo–adult viability, but B₂₄ was more efficiently transmitted than B₂ through males from the 2002 season, which explains the observed frequency change. Controlled crosses, at individual level, showed significant drive through some females for B₂₄ but not for B₂, suggesting that this difference in transmission rate might also be important for the substitution process. The analysis of relative fitness for B₂ and B₂₄ carriers for all fitness components, as a whole, showed a significantly better performance of B₂₄-carrying individuals, suggesting that the cumulative effect of these slight differences might contribute to the replacement of B₂ by B₂₄. Electronic Supplementary Material Supplementary material is available for this article at .     

Anal polypoid tumor formation as the form of presentation of rectal gastric heterotopia]

Heterotopic gastric epithelium occurs in all portions of the alimentary tract, but it is extremely rare in the rectum. The authors report the finding of a pedunculated anal polyp in a 9-year-old girl with a six-month history of rectal bleeding. Microscopically, the polyp consisted of epithelium of the fundic type. Both the age of the patient and the finding of heterotopic epithelium of the fundic type alone supports a congenital malformation and not an inflammatory condition.     

Relative weight of glucose, insulin and parathyroid hormone in the urinary loss of phosphate by chronically diabetic rats

This report deals with the relationships between glucose (G) and insulin on the tubular transport of phosphate (P) in chronically diabetic rats with high plasma levels of parathyroid hormone (PTH). Alloxan-induced diabetes leads to phosphorus depletion of the soft tissues. This phenomenon appears associated with weight loss and negative P balances caused by the increased urinary P excretion. Administration of 2 IU of insulin/100 g body weight (bw) to diabetic rats normalized their P balance and body weight. The effect of parathyroid function on the P metabolism of diabetic rats was investigated with balance experiments. Diabetic rats, intact or thyroparathyroidectomized (TPTX), have a greater urinary excretion of P than their controls. However, in control rats, the ratio intact:TPTX for urinary P is 1.0:0.76, showing the antiphosphaturic effect of parathyroid ablation. For diabetic animals, on the other hand, the ratio is 1.0:1.44. The simultaneous deficit of insulin and PTH thus quadruples the urinary P loss, instead of compensating for each other. The contribution of insulin deficit and hyperglycemia to the defect in tubular reabsorption (TRP) was investigated with clearance experiments (done on anesthetized, perfused rats). Five experimental groups were used: Controls (C), diabetics (D), controls+glucose (C+G), diabetics+insulin (D+I) and diabetics+insulin+glucose (D+I+G). All experimental groups showed a linear relationship between the TRP of P and G. The regression equation for C is significantly different (F=40.1, P<0.001) from that of D animals. The slope value measure the number of μmoles of P per μmol of G reabsorbed. For C and D rats, the ratio P:G approximates 1:4 and 1:20, respectively. The increase in P:G ratios represents the competition between both substrates for tubular resorption. Glycemias up to 11 mM (C and D+I) exist concurrent with the P:G ratio 1:4. Glycemias above 25 mM (D, C+G and D+I+G) produce a P:G ratio of 1:20. Fractional excretion of P (FEP) increased significantly in untreated, chronically diabetic rats (0.47± 0.12 vs controls=0.05±0.01, P<0.001). After a single intramuscular injection of insulin, the FEP decreased as a function of insulin levels. To normalize the FEP of diabetic rats in short-term experiments, insulin had to be administered in doses that produce plasma insulin levels 25 times greater than normal. The general information afforded by the present experiments shows that in untreated, chronically diabetic rats, insulin deficit plays an indirect role. The absence of PTH enhances the effect of hyperglycemia. The latter and the concurrent tubular overload of glucose are the cause of hyperphosphaturia in these animals. Received: 10 September 1996 / Accepted in revised form: 18 April 1997     

CD4+ T-cell lymphopenia in Q fever endocarditis.

Valvular endocarditis is the most serious complication of chronic Q fever, an infectious disease due to Coxiella burnetii. Although its pathogenesis is poorly understood, the role of the immune system has been evoked. The aim of this study was to investigate lymphocyte subsets in the peripheral blood of infected patients by analyzing the distribution of T- and B-lymphocyte subsets. Since various infectious diseases have been found to be associated with modified antigen expression, we also measured the antigen density of the main lymphocyte markers by quantitative flow cytometry. The absolute values of CD3+ T cells and CD19+ B cells were lower in infected subjects than in controls. The decrease in the CD4+ T-cell count was more pronounced than that in the CD8+ T-cell count, leading to a significantly lower CD4/CD8 ratio in patients. The decreases in CD4+ T cells and CD19+ B cells were correlated with levels of C. burnetii-specific immunoglobulin G, showing that CD4+ lymphopenia is related to the activity of chronic Q fever. Quantitation of antigen expression on lymphocytes showed that CD3, CD4, CD8, and CD19 were expressed similarly in patients and controls. In contrast, CD2 and CD11a expression levels, which are both related to naive and memory phenotypes, were modified in patients. The study of CD45RO and CD45RA expression by CD4+ T cells provided evidence that lymphopenia preferentially affected unprimed lymphocytes.     

Fatness and fat distribution in Mexican-American children and youths from the Hispanic health and nutrition examination survey

Mexican-American children are shorter but relatively heavier than non-Hispanic white children. The excess relative weight is probably due to increased fat rather than lean body mass and, more specifically, to increased fat deposition on the upper trunk sites. The objective of this paper is to describe the level of fatness and fat distribution in a large, representative sample of Mexican- American children and adolescents from the recently completed Hispanic Health and Nutrition Examination Survey (HHANES). As expected, Mexican-American children are generally fatter than white children measured in previous national surveys (National Health and Nutrition Examination Survey [NHANES] II, Health Examination Survey [HES]). Differences are particularly evident for trunk skinfold thicknesses and generally increase with age. Indices of fat distribution clearly show a centralized, upper body adiposity pattern among Mexican-Americans, a cause for concern since greater fat deposition on the trunk has been associated with increased risk of certain chronic disease.     

Contribution of molecular analyses to the estimation of the risk of congenital myotonic dystrophy.

A molecular analysis of the maternal and child CTG repeat size and intergenerational amplification was performed in order to estimate the risk of having a child with congenital myotonic dystrophy (CMD). In a study of 124 affected mother-child pairs (42 mother-CMD and 82 mother-non-CMD) the mean maternal CTG allele in CMD cases was three times higher (700 repeats) than in non-CMD cases (236 repeats). When the maternal allele was in the 50-300 repeats range, 90% of children were non-CMD. In contrast, when the maternal allele was greater than 300 repeats, 59% inherited the congenital form. Furthermore, the risk of having a CMD child is also related to the intergenerational amplification, which was significantly greater in the mother-CMD pairs than in the mother-non-CMD pairs. Although the risk of giving birth to a CMD child always exists for affected mothers, our data show that such a risk is considerably higher if the maternal allele is greater than 300 repeats.     

Influence of the sex of the transmitting grandparent in congenital myotonic dystrophy.

To analyse the influence of the sex of the transmitting grandparents on the occurrence of the congenital form of myotonic dystrophy (CDM), we have studied complete three generation pedigrees of 49 CDM cases, analysing: (1) the sex distribution in the grandparents' generation, and (2) the intergenerational amplification of the CTG repeat, measured in its absolute and relative values, between grandparents and the mothers of CDM patients and between the latter and their CDM children. The mean relative intergenerational increase in the 32 grandparent-mother pairs was significantly greater than in the 56 mother-CDM pairs (Mann-Whitney U test, p < 0.001). The mean expansion of the grandfathers (103 CTG repeats) was also significantly different from that seen in the grandmothers' group (154 CTG repeats) (Mann-Whitney U test, p < 0.01). This excess of non-manifesting males between the CDM grandparents' generation with a smaller CTG length than the grandmothers could suggest that the premutation has to be transmitted by a male to reach the degree of instability responsible for subsequent intergenerational CTG expansions without size constraints characteristic of the CDM range.