Determinants Of Under Nutrition Among School Age Children In A Nairobi Peri-Urban Slum

Background: Malnutrition is a major public health concern affecting a significant number of school age children influencing their health, growth and development, and school academic performance. Objective: To establish the determinants of under nutrition among school age children between 6-12 years in a low-income urban community. Design: A cross-sectional descriptive study. Setting: Kawangware peri-urban slum, Nairobi, Kenya. Subjects: Three hundred and eighty four school children aged 6 - 12 years. Results: A total of 4.5% were wasted, 14.9% underweight and 30.2% stunted. The children who were over nine years of age were more underweight (72.4%, p=0.000) and stunted (77.2%, p=0.000) than those below eight years. The girls were more wasted (29.1%, p=0.0 13) than the boys (18.2%), whereas the boys were more stunted (65.7%, p=0.003) than the girls (50.7%). The other variables found to have had significant association with the nutritional status of the children were: monthly household income (p=0.008), food prices (p=0.012), morbidity trends (p=0.045), mode of treatment (p=0.036) and school attendance (p=0.044). Conclusion: The findings of this study show evidently that there is under nutrition among school age children, with stunting being the most prevalent. The Ministry of Education and Ministry of Health therefore need to develop policies which can alleviate under nutrition among school age children. We also recommend that awareness be created among the school age children, parents and teachers, on the dietary requirements of both boys and girls. East African Medical Journal Vol. 85 (10) 2008: pp. 471-47

Reversal of tenofovir induced nephrotoxicity: case reports of two patients

The use of the antiretroviral drug tenofovir has been associated with nephrotoxicity. However, the overall impact of this adverse effect has not been comprehensively evaluated. Some researchers have reported that it is quite severe to warrant monitoring for renal toxicity, while others have concluded that the magnitude may not be that significant. We report two clinical cases seen in our renal clinic with high creatinine levels suggestive of nephrotoxicity who reverted back to normality upon withdrawal of tenofovir.Keywords: Case report, HIV/AIDS, tenofovir, nephrotoxicity, reversa

The Assessment of Community Development Policies in Kenya

This paper gives a discussion of the role of community development policies in Kenya. The paper traces the genesis and rationale of community development policies. Particular emphasis is paid on the implementation of the policies and their contribution to community development since independence. The paper presents a discussion of the performance of the various community development strategies adopted by the Kenya government since independence. Strengths and weaknesses of each of the strategies adopted by the government are assessed. The paper further discusses the major challenges encountered in the implementation of policies which include inadequate financial resources and the non-inclusion of the local people. The paper concludes by highlighting the importance of public participation in the implementation of policies. Recommendations on the way forward with regard to community development work in Kenya are presented. Keywords: Community development, Public participation, Policies and Strategies

YouTube Vloggers as Brand Influencers on Consumer Purchase Behaviour

Objective: The increasing influence of YouTube vloggers on consumer purchase behaviour and the specificity of the vloggers _ viewers/subscribers relationship are under-researched. Addressing this gap in knowledge, this paper explores the role of vloggers as brand influencers on consumer (their viewers) purchase behaviour. It aims to investigate the interaction between vloggers and viewers/subscribers in terms of brand awareness and consumers’ purchase behaviour. Methodology: A mixed-method approach (often connected with netnography) incorporated non-participant observation of vloggers’ activities and vloggers-viewers interactions within selected popular vlogs, supported by an online survey with both vloggers and viewers. Findings: We have observed specific brand endorsements and experiences, depending on the vloggers’ context, leading to both positive and negative feedback. This interaction and the consistently positive perception of reasons behind the vloggers’ choice of the endorsed brands underpin the credibility of the vloggers – viewers/subscribers relationship. Value added: Our results show not only the significance of vloggers as brand influencers, providing their audiences information perceived as trustworthy and convincing in terms of purchase recommendations but also explore the factors affecting this process. Recommendations: This research directed our attention into the viewer-viewer interaction on the vlogs platforms. It is a very dynamic and challenging (difficult to control) part of vlog marketing activities (including various eWOM aspects) which can be very influential in the analysed context and stays a task for the future research

HOXB13 is downregulated in colorectal cancer to confer TCF4-mediated transactivation

Mutations in the Wnt signalling cascade are believed to cause aberrant proliferation of colorectal cells through T-cell factor-4 (TCF4) and its downstream growth-modulating factors. HOXB13 is exclusively expressed in prostate and colorectum. In prostate cancers, HOXB13 negatively regulates β-catenin/TCF4-mediated transactivation and subsequently inhibits cell growth. To study the role of HOXB13 in colorectal tumorigenesis, we evaluated the expression of HOXB13 in 53 colorectal tumours originated from the distal left colon to rectum with their matching normal tissues using quantitative RT–PCR analysis. Expression of HOXB13 is either lost or diminished in 26 out of 42 valid tumours (62%), while expression of TCF4 RNA is not correlated with HOXB13 expression. TCF4 promoter analysis showed that HOXB13 does not regulate TCF4 at the transcriptional level. However, HOXB13 downregulated the expression of TCF4 and its target gene, c-myc, at the protein level and consequently inhibited β-catenin/TCF-mediated signalling. Functionally, forced expression of HOXB13 drove colorectal cancer (CRC) cells into growth suppression. This is the first description of the downregulation of HOXB13 in CRC and its mechanism of action is mediated through the regulation of TCF4 protein stability. Our results suggest that loss of HOXB13 may be an important event for colorectal cell transformation, considering that over 90% of colorectal tumours retain mutations in the APC/β-catenin pathway

Beta-Catenin Phosphorylated at Threonine 120 Antagonizes Generation of Active Beta-Catenin by Spatial Localization in trans-Golgi Network

The stability and subcellular localization of beta-catenin, a protein that plays a major role in cell adhesion and proliferation, is tightly regulated by multiple signaling pathways. While aberrant activation of beta-catenin signaling has been implicated in cancers, the biochemical identity of transcriptionally active beta-catenin (ABC), commonly known as unphosphorylated serine 37 (S37) and threonine 41 (T41) β-catenin, remains elusive. Our current study demonstrates that ABC transcriptional activity is influenced by phosphorylation of T120 by Protein Kinase D1 (PKD1). Whereas the nuclear β-catenin from PKD1-low prostate cancer cell line C4-2 is unphosphorylated S37/T41/T120 with high transcription activity, the nuclear β-catenin from PKD1-overexpressing C4-2 cells is highly phosphorylated at T120, S37 and T41 with low transcription activity, implying that accumulation of nuclear β-catenin alone cannot be simply used as a read-out for Wnt activation. In human normal prostate tissue, the phosphorylated T120 β-catenin is mainly localized to the trans-Golgi network (TGN, 22/30, 73%), and this pattern is significantly altered in prostate cancer (14/197, 7.1%), which is consistent with known down regulation of PKD1 in prostate cancer. These in vitro and in vivo data unveil a previously unrecognized post-translational modification of ABC through T120 phosphorylation by PKD1, which alters subcellular localization and transcriptional activity of β-catenin. Our results support the view that β-catenin signaling activity is regulated by spatial compartmentation and post-translational modifications and protein level of β-catenin alone is insufficient to count signaling activity

The androgen receptor can signal through Wnt/β-Catenin in prostate cancer cells as an adaptation mechanism to castration levels of androgens

<p>Abstract</p> <p>Background</p> <p>A crucial event in Prostate Cancer progression is the conversion from a hormone-sensitive to a hormone-refractory disease state. Correlating with this transition, androgen receptor (AR) amplification and mutations are often observed in patients failing hormonal ablation therapies. β-Catenin, an essential component of the canonical Wnt signaling pathway, was shown to be a coactivator of the AR signaling in the presence of androgens. However, it is not yet clear what effect the increased levels of the AR could have on the Wnt signaling pathway in these hormone-refractory prostate cells.</p> <p>Results</p> <p>Transient transfections of several human prostate cancer cell lines with the AR and multiple components of the Wnt signaling pathway demonstrate that the AR overexpression can potentiate the transcriptional activities of Wnt/β-Catenin signaling. In addition, the simultaneous activation of the Wnt signaling pathway and overexpression of the AR promote prostate cancer cell growth and transformation at castration levels of androgens. Interestingly, the presence of physiological levels of androgen or other AR agonists inhibits these effects. These observations are consistent with the nuclear co-localization of the AR and β-Catenin shown by immunohistochemistry in human prostate cancer samples. Furthermore, chromatin immunoprecipitation assays showed that Wnt3A can recruit the AR to the promoter regions of Myc and Cyclin D1, which are well-characterized downstream targets of the Wnt signalling pathway. The same assays demonstrated that the AR and β-Catenin can be recruited to the promoter and enhancer regions of a known AR target gene PSA upon Wnt signaling. These results suggest that the AR is promoting Wnt signaling at the chromatin level.</p> <p>Conclusion</p> <p>Our findings suggest that the AR signaling through the Wnt/β-Catenin pathway should be added to the well established functional interactions between both pathways. Moreover, our data show that via this interaction the AR could promote prostate cell malignancy in a ligand-independent manner.</p

WNT signaling regulates self-renewal and differentiation of prostate cancer cells with stem cell characteristics

Prostate cancer cells with stem cell characteristics were identified in human prostate cancer cell lines by their ability to form from single cells self-renewing prostaspheres in non-adherent cultures. Prostaspheres exhibited heterogeneous expression of proliferation, differentiation and stem cell-associated makers CD44, ABCG2 and CD133. Treatment with WNT inhibitors reduced both prostasphere size and self-renewal. In contrast, addition of Wnt3a caused increased prostasphere size and self-renewal, which was associated with a significant increase in nuclear Β-catenin, keratin 18, CD133 and CD44 expression. As a high proportion of LNCaP and C4-2B cancer cells express androgen receptor we determined the effect of the androgen receptor antagonist bicalutamide. Androgen receptor inhibition reduced prostasphere size and expression of PSA, but did not inhibit prostasphere formation. These effects are consistent with the androgen-independent self-renewal of cells with stem cell characteristics and the androgen-dependent proliferation of transit amplifying cells. As the canonical WNT signaling effector Β-catenin can also associate with the androgen receptor, we propose a model for tumour propagation involving a balance between WNT and androgen receptor activity. That would affect the self-renewal of a cancer cell with stem cell characteristics and drive transit amplifying cell proliferation and differentiation. In conclusion, we provide evidence that WNT activity regulates the self-renewal of prostate cancer cells with stem cell characteristics independently of androgen receptor activity. Inhibition of WNT signaling therefore has the potential to reduce the self-renewal of prostate cancer cells with stem cell characteristics and improve the therapeutic outcome.Peer reviewe