Distribution modelling of Aedes aegypti in three dengue-endemic areas in Sumatera, Indonesia.

Ae. aegypti is a dengue virus vector and a public health threat in Indonesia. Furthermore, the Dengue Haemoragic Fever (DHF) has spread to all cities in the country, including Bandar Lampung. A species distribution model, Maximum Entropy (MaxEnt), was used to predict the geographic distribution of this vector in three dengue-endemic areas, namely Sukarame, Kemiling, and Tanjung Seneng. Previously, surveillance was conducted to determine the presence of Ae. aegypti. Therefore, this study suggested that environmental variables such as rainfall, temperature, land cover, and population density have influenced the widespread of Ae. aegypti and facilitate its proliferation in the study areas. The influence of the environmental variables was analyzed using a response curve. The model performance was measured by percent contribution, the importance of permutations, and the jackknife test. This study's evaluation indicates that the certainty models for the presence of Ae. aegypti in Sukarame, Kemiling, and Tanjung Seneng were developed extremely well, with respective values of 0.989, 0.993, and 0.969. The results showed that Ae. aegypti is widespread in the three endemic areas. The high population density and land conversion into settlements are influential environmental variables essential in determining the distribution of the vector in three areas of Bandar Lampung. Climatic factors such as rainfall and temperature are supporting aspects in maintaining the habitat of Ae. aegypti in the area. Mapping areas at risk of this dengue vector can aid in planning disease management strategies and identifying priority locations for entomological surveys to control epidemics.

Tissue compartment-specific estrogen receptor-alpha participation in the mouse uterine epithelial secretory response.

17Beta-estradiol (E2) acts through the estrogen receptor (ER) to regulate uterine epithelial cell growth, proliferation, differentiation, and secretory protein production. We have previously shown that E2-induced uterine epithelial proliferation is mediated indirectly by ER alpha-positive stroma; epithelial ER alpha is neither necessary nor sufficient for E2-induced uterine epithelial mitogenesis. In the present study, we addressed the question of whether production of uterine epithelial secretory proteins and their messenger RNAs (mRNAs) requires ER alpha in stroma, epithelium, or both by analyzing tissue recombinations composed of uterine tissue from adult ER alpha knockout (ko) and neonatal BALB/c (wt) mice. Stroma (S) and epithelium (E) were separated by trypsinization, and four types of uterine tissue recombinants were prepared: wt-S + wt-E, wt-S + ko-E, ko-S + wt-E, and ko-S + ko-E. These tissue recombinants were grown as subrenal capsule grafts in intact female nude mice for 4 weeks, at which time the hosts were ovariectomized. To assess the production of secretory proteins and their mRNAs, 1 week after ovariectomy the hosts were given three daily injections of oil or E2 (100 ng), and then 24 h later the grafts were recovered and used for either ER or lactoferrin (LF) immunohistochemistry. To assess steady state mRNA levels by Northern blotting, hosts received one injection of oil or E2 24 h before harvest. ER immunohistochemistry was used to monitor the completeness of tissue separation. In wt-S + wt-E tissue recombinants from E2-treated hosts, the epithelium stained intensely for LF (an abundant E2-dependent uterine secretory protein), whereas similar tissue recombinants from oil-treated hosts showed minimal immunostaining. Conversely, LF immunostaining was minimal in wt-S + ko-E grafts from both oil- and E2-treated hosts. LF staining was also minimal in ko-S + ko-E and ko-S + wt-E tissue recombinants regardless of hormone treatment. For Northern analyses, the epithelial content of the tissue recombinants was monitored using the reference epithelial transcript, E-cadherin. While all tissue recombinant groups expressed E-cadherin mRNA, wt-S + wt-E tissue recombinants from E2-treated hosts produced a strong, single 2.6-kb band of LF mRNA. LF transcripts were minimal or absent in all other tissue recombinant types. Northern blotting results identical to those seen for LF were also observed for the uterine secretory protein complement component C3. Our data demonstrate that both stromal and epithelial ER alpha are required for the production of LF protein and of LF or C3 mRNAs in response to E2. Thus, in contrast to E2-induced epithelial mitogenesis, which requires only stromal ER alpha, both epithelial and stromal ER alpha are necessary for the production of E2-dependent epithelial secretory proteins.

Quantitation of adsorption and conjugation of plasma proteins by residual glutaraldehyde in fixed collagenous tissue with radioiodinated plasma proteins.

Residual glutaraldehyde (GA) in collagenous cardiovascular tissue prostheses after multiple saline rinses remains in the prostheses and accounts for adsorption and conjugation of a variety of plasma proteins. This may account for later beneficial or adverse effects. Human serum albumin (SA), gamma globulin (GG), and fibrinogen (FB) were iodinated with 125I using the iodogen-transfer technique. Bovine pericardium (PC) was fixed with 0.5% GA for 24 hr and rinsed to remove excess GA. Fresh and GA-fixed PC (FRPC, GAPC: 1 x 1 cm2), in triplicate, were incubated with 0.5-1.0 microCi of tracers in human, porcine, or bovine blood (2 ml) for a period of 0.5, 1, 2, and 3 hr and washed (5x) with saline. Maximum adsorbed proteins per unit weight of collagen (pmol/mg of PC, mean +/- SD) at 3 hr on FRPC and GAPC were quantified with a gamma counter. Fixed PC absorbed significantly more plasma proteins from blood than fresh PC. These conjugated plasma proteins are tightly bound to fixed PC. The adsorbed and conjugated plasma proteins for GAPC and FRPC have the same sequence: SA > GG > FB vs SA > GG > FB. Protein conjugation may affect the remodeling of collagenous cardiovascular tissue prostheses post implantation.

Challenges to the implementation of the integrated management of childhood illness (IMCI) at community health centres in West Java province, Indonesia.

BACKGROUND: The integrated management of childhood illness (IMCI) is a comprehensive approach to child health, which has been adopted in Indonesia since 1997. This study aims to provide an overview of IMCI implementation at community health centres (puskesmas) in West Java province, Indonesia. METHODS: Data were derived from a cross-sectional study conducted in 10 districts of West Java province, from November to December 2012. Semi-structured interviews were used to obtain information from staff at 80 puskesmas, including the heads (80 informants), pharmacy staff (79 informants) and midwives/nurses trained in IMCI (148 informants), using semi-structured interviews. Quantitative data were analysed using frequency tabulations and qualitative data were analysed by identifying themes that emerged in informants' responses. RESULTS: Almost all (N = 79) puskesmas implemented the IMCI strategy; however, only 64% applied it to all visiting children. Several barriers to IMCI implementation were identified, including shortage of health workers trained in IMCI (only 43% of puskesmas had all health workers in the child care unit trained in IMCI and 40% of puskesmas conducted on-the-job training). Only 19% of puskesmas had all the essential drugs and equipment for IMCI. Nearly all health workers acknowledged the importance of IMCI in their routine services and very few did not perceive its benefits. Lack of supervision from district health office staff and low community awareness regarding the importance of IMCI were reported. Complaints received from patients'families were generally related to the long duration of treatment and no administration of medication after physical examination. CONCLUSION: Interventions aiming to create local regulations endorsing IMCI implementation; promoting monitoring and supervision; encouraging on-the-job training for health workers; and strengthening training programmes, counselling and other promotional activities are important for promoting IMCI implementation in West Java province, and are also likely to be useful elsewhere in the country.

Distribution modelling of Aedes aegypti in three dengue-endemic areas in Sumatera, Indonesia

@#Ae. aegypti is a dengue virus vector and a public health threat in Indonesia. Furthermore, the Dengue Haemoragic Fever (DHF) has spread to all cities in the country, including Bandar Lampung. A species distribution model, Maximum Entropy (MaxEnt), was used to predict the geographic distribution of this vector in three dengue-endemic areas, namely Sukarame, Kemiling, and Tanjung Seneng. Previously, surveillance was conducted to determine the presence of Ae. aegypti. Therefore, this study suggested that environmental variables such as rainfall, temperature, land cover, and population density have influenced the widespread of Ae. aegypti and facilitate its proliferation in the study areas. The influence of the environmental variables was analyzed using a response curve. The model performance was measured by percent contribution, the importance of permutations, and the jackknife test. This study’s evaluation indicates that the certainty models for the presence of Ae. aegypti in Sukarame, Kemiling, and Tanjung Seneng were developed extremely well, with respective values of 0.989, 0.993, and 0.969. The results showed that Ae. aegypti is widespread in the three endemic areas. The high population density and land conversion into settlements are influential environmental variables essential in determining the distribution of the vector in three areas of Bandar Lampung. Climatic factors such as rainfall and temperature are supporting aspects in maintaining the habitat of Ae. aegypti in the area. Mapping areas at risk of this dengue vector can aid in planning disease management strategies and identifying priority locations for entomological surveys to control epidemics.

Stromal estrogen receptors mediate mitogenic effects of estradiol on uterine epithelium.

Estradiol-17beta (E2) acts through the estrogen receptor (ER) to regulate uterine growth and functional differentiation. To determine whether E2 elicits epithelial mitogenesis through epithelial ER versus indirectly via ER-positive stromal cells, uteri from adult ER-deficient ER knockout (ko) mice and neonatal ER-positive wild-type (wt) BALB/c mice were used to produce the following tissue recombinants containing ER in epithelium (E) and/or stroma (S), or lacking ER altogether: wt-S + wt-E, wt-S + ko-E, ko-S + ko-E, and ko-S + wt-E. Tissue recombinants were grown for 4 weeks as subrenal capsule grafts in intact female nude mice, then the hosts were treated with either E2 or oil a week after ovariectomy. Epithelial labeling index and ER expression were determined by [3H]thymidine autoradiography and immunohistochemistry, respectively. In tissue recombinants containing wt-S (wt-S + wt-E, wt-S + ko-E), E2 induced a similar large increase in epithelial labeling index compared with oil-treated controls in both types of tissue recombinants despite the absence of epithelial ER in wt-S + ko-E tissue recombinants. This proliferative effect was blocked by an ER antagonist, indicating it was mediated through ER. In contrast, in tissue recombinants prepared with ko-S (ko-S + ko-E and ko-S + wt-E), epithelial labeling index was low and not stimulated by E2 despite epithelial ER expression in ko-S + wt-E grafts. In conclusion, these data demonstrate that epithelial ER is neither necessary nor sufficient for E2-induced uterine epithelial proliferation. Instead, E2 induction of epithelial proliferation appears to be a paracrine event mediated by ER-positive stroma. These data in the uterus and similar studies in the prostate suggest that epithelial mitogenesis in both estrogen and androgen target organs are stromally mediated events.