Epidemiological Interactions between Urogenital and Intestinal Human Schistosomiasis in the Context of Praziquantel Treatment across Three West African Countries

© 2015 Knowles et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The attached file is the published version of the article

A Theoretical Analysis of the Geography of Schistosomiasis in Burkina Faso Highlights the Roles of Human Mobility and Water Resources Development in Disease Transmission

We study the geography of schistosomiasis across Burkina Faso by means of a spatially explicit model of water-based disease dynamics. The model quantitatively addresses the geographic stratification of disease burden in a novel framework by explicitly accounting for drivers and controls of the disease, including spatial information on the distributions of population and infrastructure, jointly with a general description of human mobility and climatic/ecological drivers. Spatial patterns of disease are analysed by the extraction and the mapping of suitable eigenvectors of the Jacobian matrix subsuming the stability of the disease-free equilibrium. The relevance of the work lies in the novel mapping of disease burden, a byproduct of the parametrization induced by regional upscaling, by model-guided field validations and in the predictive scenarios allowed by exploiting the range of possible parameters and processes. Human mobility is found to be a primary control at regional scales both for pathogen invasion success and the overall distribution of disease burden. The effects of water resources development highlighted by systematic reviews are accounted for by the average distances of human settlements from water bodies that are habitats for the parasite's intermediate host. Our results confirm the empirical findings about the role of water resources development on disease spread into regions previously nearly disease-free also by inspection of empirical prevalence patterns. We conclude that while the model still needs refinements based on field and epidemiological evidence, the proposed framework provides a powerful tool for large-scale public health planning and schistosomiasis management

Diet and the diabetic.

SCOPUS: le.jinfo:eu-repo/semantics/publishe

The effect of hypothalamic luteinizing hormone releasing hormone (LH-RH) on plasma gonadotrophin levels in normal subjects

The release of gonadotrophin following the injection of synthetic LH‐RH (Hoechst) was studied in various physiological and experimental circumstances. In the male, 25 μg of LH‐RH led to simultaneous release of FSH and LH prior to and during puberty. In adults, on the other hand, the same dose led only to an increase in LH while FSH levels remained unchanged. At higher doses there was FSH release and an increase in LH proportional to the amount of LH‐RH injected. When FSH was released the increase was clearly less than that of LH and often occurred considerably later. In the female, 25 μg of LH‐RH led to a clear‐cut release of FSH and a small release of LH prior to puberty. After the onset of puberty the degree of response was inverted: the increase in LH was greater than that of FSH. In normally menstruating women the FSH and LH response was greater during the luteal phase than during the preovulatory phase. Treatment with non‐sequential hormonal contraceptives blocked FSH and LH release normally produced by the injection of 50 μg of LH‐RH. There was no effect when a dose of 100 μg was injected. In post‐menopausal women, only LH rose following the administration of 25 μg of LH‐RH. After 5 days of treatment with 200 μg ethinyl oestradiol the same dose of LH‐RH led to simultaneous release of LH and of FSH. From the above studies it can be concluded that the secretory response of the gonadotrophins to LH‐RH is influenced by the endocrine equilibrium and more particularly by the interaction of the gonadal steroids which can alter the synthesis and/or the release of the pituitary gonadotrophins. Copyright © 1974, Wiley Blackwell. All rights reserve

Action of luteinizing hormone releasing hormone (LH-RH) on the gonadotrophin secretion in normal subjects

Gonadotrophin release was studied after synthetic luteinizing hormone releasing hormone (LH RH) injection in several physiological and experimental conditions. In male subjects, 25 μg of LH RH induced a follicle stimulating hormone (FSH) and luteinizing hormone (LH) release before and during puberty. With higher doses of LH RH, FSH was then released and the LH increment was proportional to the dose. When FSH was released, its increase was always less marked and later than that of LH. In female subjects, 25 μg of LH RH induced marked increase of FSH and a weak increment of LH before puberty. In girls entering puberty, LH response became higher than that of FSH. In eugonadal women, the FSH and LH response, was more marked during luteal phase than during preovulatory phase. Hormonal non sequential contraceptive drugs inhibited FSH and LH response induced by 50 μg of LH RH whereas they could not depress the gonadotrophin response to 100 μg of LH RH. In postmenopausal women, LH only increased after 25 μg of LH RH; pretreatment with 200 μg of ethinyloestradiol for 5 days allowed a release of both FSH and LH. From these data, it may be accepted that gonadotrophin response to LH RH depends on the endocrine equilibrium and on gonadal steroids which could modify the synthesis and/or the release of pituitary gonadotrophin. Furthermore on the basis of selective LH response to small doses of LH RH we may speculate that an FSH releasing factor exists.Gonadotropin release after synthetic LH-RH injection was studied under a variety of experimental conditions. In male subjects, LH-RH (25 mcg) induces release of LH and FSH before and during puberty, but only of LH in adults. Larger doses of LH-RH do induce FSH release, with LH release proportional to LH-RH dose; FSH release is smaller than LH release and follows it. In prepuberal females, LH-RH induces a large release of FSH and a weak release of LH. In puberty, LH response becomes greater than FSH. In eugonadal women, FSH and LH responses are more marked during luteal phase than during preovulatory phase. Nonsequential hormonal contraceptives inhibit FSH and LH response to 50 mcg of LH-RH, but not to 100 mcg. In postmenopausal women, LH increases after 25 mcg of LH-RH; 200 mcg ethinyl estradiol for 5 days permits an increase of both gonadotropins. These results suggest that gonadotropin response to LH-RH depends on endocrine equilibrium and gonadal steroids which may modify the synthesis and/or release of pituitary gonadotropins. On the basis of selective LH response to small doses of LH-RH, ti is speculated that an FSH releasing factor may exist