Sub-acute and sub-chronic toxicity assessment of the antimicrobial peptide Dermaseptin B2 on biochemical, haematological and histopathological parameters in BALB/c mice and Albino Wistar rats.

Background: Dermaseptins (Drs) are peptides found in the skin secretions of a variety of Hylid frogs, particularly those belonging to the Agalychnis and families. Dermaseptin B2 (Drs B2), an amphipathic, α-helical polypeptide was reported as the most active of the Dermaseptin B family. We have previously shown that Drs B2 has strong anti-proliferative activities against RD cells and thus required further evaluations for future medical applications.

Prevalence and factors associated with HIV-1 drug resistance mutations in treatment-experienced patients in Nairobi, Kenya: A cross-sectional study.

An estimated 1.5 million Kenyans are HIV-seropositive, with 1.1 million on antiretroviral therapy (ART), with the majority of them unaware of their drug resistance status.

Annona muricata silver nanoparticles exhibit strong anticancer activities against cervical and prostate adenocarcinomas through regulation of CASP9 and the CXCL1/CXCR2 genes axis.

Background: Green synthesized nanoparticles have been earmarked for use in nanomedicine including for the development of better anticancer drugs.

Objective: The aim of this study was to undertake biochemical evaluation of anticancer activities of green synthesized silver nanoparticles (AgNPs) from ethanolic extracts of fruits (AgNPs-F) and leaves (AgNPs-L) of Annona muricata.

Methods: Previously synthesized silver nanoparticles were used for the study.

In search of new anticancer drugs: Data for cytotoxic activities of green synthesized silver nanoparticles from ethanolic extracts of fruits and leaves of and 5-Fluorouracil against HeLa, PC3 and PNT1A cell lines.

In this article, we present data on the anticancer activities of green synthesized silver nanoparticles (AgNPs) from ethanolic extracts of fruits (AgNPs-F) and leaves (AgNPs-L) of and standard anticancer drug 5-Fluorouracil (5-FU) on two cancer cell lines, i.e. cervical adenocarcinoma (HeLa cells) and prostate adenocarcinoma (PC3 cells) as well as on an immortalized normal prostate cell line, PNT1A.

Advances in green nanobiotechnology: Data for synthesis and characterization of silver nanoparticles from ethanolic extracts of fruits and leaves of .

In this data article, data obtained from an efficient, eco-friendly and low-cost method for the synthesis and recovery of Silver nanoparticles (AgNPs) using ethanolic extracts of Annona muricata fruits and leaves as reducing, stabilizing and capping agents has been reported. 99.7% pure silver nitrate was used as the inorganic ion source.

In search of the psychosis gene in people with Prader-Willi syndrome.

The two main causes of Prader-Willi syndrome (PWS) are a paternally derived deletion in the maternally imprinted 15q11-q13 region or UPD(15)mat. Both mechanisms result in a loss of the active paternal contribution to the region. The affective psychosis associated with PWS has been found to be mainly confined to the propositi with UPD(15)mat rather than to those with a deletion.

Analysis of candidate imprinted genes in PWS subjects with atypical genetics: a possible inactivating mutation in the SNURF/SNRPN minimal promoter.

Prader-Willi syndrome (PWS) is a neurodevelopmental disorder associated with abnormalities of chromosome 15q11q13. The majority of cases result either from a deletion approximately 4 Mb in size, affecting chromosome 15 of paternal origin or from UPD(15)mat; these account for approximately 70 and approximately 20-25% of PWS cases, respectively. In the remaining 3-5% of PWS cases where neither the deletion nor UPD is detectable, PWS is thought to be caused either by a defect in the imprinting centre resulting in a failure to reset the paternally inherited chromosome 15 derived from the paternal grandmother or, very occasionally, from a balanced translocation involving a breakpoint in 15q11q13.

The transmembrane protein meckelin (MKS3) is mutated in Meckel-Gruber syndrome and the wpk rat.

Meckel-Gruber syndrome is a severe autosomal, recessively inherited disorder characterized by bilateral renal cystic dysplasia, developmental defects of the central nervous system (most commonly occipital encephalocele), hepatic ductal dysplasia and cysts and polydactyly. MKS is genetically heterogeneous, with three loci mapped: MKS1, 17q21-24 (ref. 4); MKS2, 11q13 (ref.

Tumor suppressor activity and epigenetic inactivation of hepatocyte growth factor activator inhibitor type 2/SPINT2 in papillary and clear cell renal cell carcinoma.

Following treatment with a demethylating agent, 5 of 11 renal cell carcinoma (RCC) cell lines showed increased expression of hepatocyte growth factor (HGF) activator inhibitor type 2 (HAI-2/SPINT2/Bikunin), a Kunitz-type protease inhibitor that regulates HGF activity. As activating mutations in the MET proto-oncogene (the HGF receptor) cause familial RCC, we investigated whether HAI-2/SPINT2 might act as a RCC tumor suppressor gene. We found that transcriptional silencing of HAI-2 in RCC cell lines was associated with promoter region methylation and HAI-2/SPINT2 protein expression was down-regulated in 30% of sporadic RCC.

Identification of novel VHL target genes and relationship to hypoxic response pathways.

Upregulation of hypoxia-inducible factors HIF-1 and HIF-2 is frequent in human cancers and may result from tissue hypoxia or genetic mechanisms, in particular the inactivation of the von Hippel-Lindau (VHL) tumour suppressor gene (TSG). Tumours with VHL inactivation are highly vascular, but it is unclear to what extent HIF-dependent and HIF-independent mechanisms account for pVHL tumour suppressor activity. As the identification of novel pVHL targets might provide insights into pVHL tumour suppressor activity, we performed gene expression microarray analysis in VHL-wild-type and VHL-null renal cell carcinoma (RCC) cell lines.

Mutations of the catalytic subunit of RAB3GAP cause Warburg Micro syndrome.

Warburg Micro syndrome (WARBM1) is a severe autosomal recessive disorder characterized by developmental abnormalities of the eye and central nervous system and by microgenitalia. We identified homozygous inactivating mutations in RAB3GAP, encoding RAB3 GTPase activating protein, a key regulator of the Rab3 pathway implicated in exocytic release of neurotransmitters and hormones, in 12 families with Micro syndrome. We hypothesize that the underlying pathogenesis of Micro syndrome is a failure of exocytic release of ocular and neurodevelopmental trophic factors.