Images of women: Prostitutes and bad/ unworthy women in Lughano Mwangwegho’s poetry

The notion of prostitution in Malawian literature has been either avoided or misrepresented. The misrepresentation has mainly stemmed from conservative and patriarchal forces which have guided theory and practice in Malawi and many parts of Africa. Women have mostly been viewed in binary terms as either good or bad, constructive or destructive, civilised or backward. Only recently, there has been a change in approach to the subject of prostitution caused by the emergence of feminism and human rights bodies. Even though this change is moving towards recognition of the prostitute body as autonomous, there are still remnants of patriarchal forces that want to maintain or preserve the peripheral position of the prostitute body in Malawian literature. Apart from this prostitute body, another notion of a bad/unworthy woman has been rarely researched. It is mainly confused or included in the same bracket of prostitution. This paper dwells on these two bodies and how they have been (mis)represented in selected poems of Lughano Mwangwegho’s Echoes of a Whisper. The paper leans on sexuality by focusing on Josephine Donavan’s images of a woman in Beyond the Net: Feminist Criticism as a Moral Criticism. It also dwells on the notion of power relations expounded by Sylvia Tamale.&nbsp

Focus–specific clinical profiles in human African trypanosomiasis caused by <i>Trypanosoma brucei rhodesiense</i>

&lt;p&gt;&lt;b&gt;Background:&lt;/b&gt; Diverse clinical features have been reported in human African trypanosomiasis (HAT) foci caused by &lt;i&gt;Trypanosoma brucei rhodesiense&lt;/i&gt; (&lt;i&gt;T.b.rhodesiense&lt;/i&gt;) giving rise to the hypothesis that HAT manifests as a chronic disease in South-East African countries and increased in virulence towards the North. Such variation in disease severity suggests there are differences in host susceptibility to trypanosome infection and/or genetic variation in trypanosome virulence. Our molecular tools allow us to study the role of host and parasite genotypes, but obtaining matched extensive clinical data from a large cohort of HAT patients has previously proved problematic.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Methods/Principal Findings:&lt;/b&gt; We present a retrospective cohort study providing detailed clinical profiles of 275 HAT patients recruited in two northern foci (Uganda) and one southern focus (Malawi) in East Africa. Characteristic clinical signs and symptoms of &lt;i&gt;T.b.rhodesiense&lt;/i&gt; infection were recorded and the degree of neurological dysfunction determined on admission. Clinical observations were mapped by patient estimated post-infection time. We have identified common presenting symptoms in &lt;i&gt;T.b.rhodesiense&lt;/i&gt; infection; however, marked differences in disease progression and severity were identified between foci. HAT was characterised as a chronic haemo-lymphatic stage infection in Malawi, and as an acute disease with marked neurological impairment in Uganda. Within Uganda, a more rapid progression to meningo-encephaltic stage of infection was observed in one focus (Soroti) where HAT was characterised by early onset neurodysfunction; however, severe neuropathology was more frequently observed in patients in a second focus (Tororo).&lt;/p&gt; &lt;p&gt;&lt;b&gt;Conclusions/Significance:&lt;/b&gt; We have established focus-specific HAT clinical phenotypes showing dramatic variations in disease severity and rate of stage progression both between northern and southern East African foci and between Ugandan foci. Understanding the contribution of host and parasite factors in causing such clinical diversity in &lt;i&gt;T.b.rhodesiense&lt;/i&gt; HAT has much relevance for both improvement of disease management and the identification of new drug therapy.&lt;/p&gt

Presentation of Trypanosomiasis in Nkhotakota

In 2002, we identified 28 people in Nkhotakota District who were suffering from Human African Trypanosomiasis (HAT). Sixteen of these were identified when they presented to the District Hospital with a febrile illness. The remaining twelve were identified through a rural cross-sectional survey, in which 500 people were visited in their homes, persons found to be febrile, were examined by blood film microscopy. Of the 28 people, 50% (14) presented within a month of the onset of symptoms. Sixteen (57%) had splenomegaly, and 24 were anaemic ([Hb

The impact of aspects of education [level and type] on corruption in Zimbabwe

Undergraduate thesis submitted to the Department of Business Administration, Ashesi University, in partial fulfillment of Bachelor of Science degree in Business Administration, May 2020Zimbabwe spends much of its budget allocation on education, yet the nation faces high levels of public sector corruption, raising the question of whether corruption is immune to education. Corruption is detrimental to development and societal growth whilst education, through human development, is supposed to aid growth. Therefore, there is every need to assess whether corruption, maybe through the educational process itself, and the products it produces, is dampening the potential returns to education in Zimbabwe. This paper explores the research question: What is the impact of different aspects of education [level and type] on corruption among public service sector officials in Zimbabwe? Identifying these relationships assists policymakers to make decisions appropriate for developing ethical leaders through education and for sustainable development. The study employed a qualitative research method to assess views and experiences on the education and corruption nexus. Public sector officials in the Higher and Tertiary Education and Finance and Economic Development sectors were engaged via interviews, after purposive and snowball sampling had been administered. The results show that there is a relationship between education type and level with perceptions of education impacting corruption. This impact is evident in the following deficiencies; there are no ethics or value-based teachings in the educational curriculum, people are generally losing morals, ethics are not taught at a lower education level and the economic challenges become an enabler of corruption. The recommendations include a remodeling of the Zimbabwean academic curriculum to incorporate ethics or value teachings and mandatory anti-corruption courses at universities.Ashesi Universit

Role of Cytokines in Trypanosoma brucei-Induced Anaemia: A Review of the Literature

Background: Anaemia is an important complication of trypanosomiasis. The mechanisms through which trypanosomal infection leads to anaemia are poorly defined. A number of studies have implicated inflammatory cytokines, but these data are limited and inconsistent. In this article, we reviewed the published literature on cytokines associated with Trypanosoma brucei infections and their role in the immunopathology leading to anaemia.Methodology: Articles were searched in PubMed through screening of titles and abstracts with no limitation on date of publishing and study design. Articles in English were searched using keywords “African trypanosomiasis”, “sleeping sickness”, “Trypanosoma brucei”, in all possible combinations with “anaemia” and/or “cytokines”.Results: Twelve articles examining cytokines and their role in trypanosomeinduced anaemia were identified out of 1095 originally retrieved from PubMed. None of the articles identified were from human-based studies. A total of eight cytokines were implicated, with four cytokines (IFN-γ, IL-10, TNF-α, IL-12) showing an association with anaemia. These articles reported that mice lacking TNF-α were able to control anaemia, and that IFN-γ was linked to severe anaemia given its capacity to suppress erythropoiesis, while IL-10 was shown to regulate IFN-γ and TNF-α, providing a balance that was associated with severity of anaemia. IFN-γ and TNF-α have also been reported to work in concert with other factors such as nitric oxide and iron in order to induce anaemia.Conclusion: IFN-γ, IL-10, and TNF-α were the three major cytokines identified to beheavily involved in anaemia caused by Trypanosoma brucei infection. The anti-inflammatory cytokine, IL-10, was shown to counter the effects of proinflammatory cytokines in order to balance the severity of anaemia. The mechanism of anaemia is multifactorial and therefore requires further, more elaborate research. Data from human subjects would also shed more light

Cytosine Arabinoside reduces the numbers of granulocyte macrophage colony forming cells (GMCFC) and high proliferative potential colony forming cells (HPP-CFC) in vivo in mice

Background: Cytosine arabinoside (Ara-C) is an S-phase specific cytotoxic drug used in the treatment of malignancies. It is converted to Cytosine Arabinoside triphosphate (Ara-CTP) in the cell. Cytosine Arabinoside triphosphate, reversibly displaces deoxy cytidine triphosphate from DNA polymerase for incorporation into DNA. This process leads to cell death.Objective: To investigate the in vivo effects of Ara-C on the Granulocyte Macrophage Colony Forming Cells (GM-CFC) and High Proliferative Potential Colony Forming Cells (HPP-CFC) respectively in mice.Methodology: Ara-C (150mg/kg) was administered intraperitoneally (i.p) once to mice and bone marrow cells sampled on days 1, 3 and 6.Results: Ara-C reduced the numbers of both GM-CFC and HPP-CFC in the bone marrow. HPP-CFCs were initially more sensitive to Ara-C treatment than GM-CFCs. In the six days after treatment the effect on GM-CFC persisted, while there was a partial recovery in the number of HPP-CFCs.Conclusion: It is possible that Ara-C disturbs the stem cells niche by damaging the stromal cells of the bone marrow microenvironment. This would result in derangement of HPP-CFC proliferation

Determining the potential of wearable technologies within the disease landscape of sub-Saharan Africa

Thesis (MEng)--Stellenbosch University, 2019.ENGLISH ABSTRACT: Please refer to full text for abstract.AFRIKAANSE OPSOMMING: Raadpleeg asseblief vol teks vir opsomming

Association between social economic status and obesity in a rural South African community

Research report submitted to the Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, in partial fulfilment of the requirements for the degree of Master of Science (MSc) in Epidemiology in the field of Epidemiology and BiostatisticsObesity is an emerging problem in South Africa, particularly in women for whom prevalence rates well above 40% have been reported. Parallel to this health problem, South Africa continues to experience relatively high poverty levels of 10.5% to 48.0%. The aim of this study was to estimate the prevalence of obesity and low social economic status (SES) levels at Agincourt Health and Socio-Demographic Surveillance System site (AHDSS). The study also sought to investigate the association between low SES and obesity at AHDSS. Materials and methods This was a secondary data analysis of the original Na Nakekela HIV/Non communicable disease (NCD) study conducted at AHDSS from August 2010 to May 2011. Included in the study presented in this report were residents of AHDSS aged 15 years or older during this time period. Data from 4 502 individuals (2 683 females and 1 819 males) were analysed. Age-specific prevalences of obesity (body mass index ≥ 30kg/m2), and central obesity (waist hip ratio ≥1.0 and ≥0.85 in men and women, respectively), stratified by sex and SES, were calculated. SES was assessed by ascertaining the household assets of AHDSS residents and assigning a weighted score to the household assets, using multiple correspondence analysis (MCA). The household score was then computed and used to classify the population into SES categories. The relative ranks of households, using this score, were then used as a measure of SES. The association between SES and obesity (BMI ≥ 30) was assessed by means of chi-square tests and logistic regression. Results The overall prevalence of obesity at the AHDSS in the study period was 20.4%. Overall, sex -specific prevalences of obesity were 29.3% and 7.4% in females and males, respectively. Females aged 50-59 years and males aged 45-49 years had the highest age-specific prevalence of obesity, at 40.1% and 18.3%, respectively. The overall prevalence of central obesity was 31.1%. Sex-specific prevalence of central obesity in females was 51.1%, while in males it was 4.9%. The highest age-specific prevalence of central obesity in both sexes was for those 70 years and older: 74.3% in females and 11.1% in males. Around 50% of individuals at the AHDSS were classified as belonging to lower SES categories, with females constituting 56.6% of these individuals. The highest prevalence of individuals in the high SES category was females aged 60-69 (14.5%) and males aged 70 (16.4%) years and older. After adjusting for other variables, being in a lower SES category was inversely associated with obesity as measured by BMI, as was being male and being HIV positive. The only positive predictor of high BMI was older age. No association between central obesity and lower SES was found after adjusting for confounders and other explanatory variables. However, older age was a predictor of central obesity. Being male, HIV positive and the male head of the household were factors that were inversely associated with central obesity. Discussion The high prevalence of individuals in the lower SES group (50.5%) reported in this study is similar to the Mpumalanga provincial poverty estimate of 51%.The ratio of obese females to males was at least 2.2 in every age group. The prevalence of central obesity in females of 51.1% in the AHDSS was higher than the national estimate of 47.1% for females, while the male estimate of 4.9% was lower than the 6.8% national estimate for males. In contrast to other studies, no associations between lower SES and obesity as measured by central obesity were observed. Conclusion and Recommendations Specific interventions to reduce obesity in females should be undertaken, including the provision of educational talks. This would empower them to make better informed decisions about food and lifestyle choices. These recommendations should be integrated into already existing HIV prevention programmes because HIV prevention is currently the main focus of policy makers in South Africa. Measures to reduce the number of individuals in the lower SES group, which this study reported to be very high (especially among women), e.g. through job creation, should be considered

The regulatory role of AcSDKP and angiotensin 1-converting enzyme (ACE) inhibitors on haematopoietic stem and progenitor cell proliferation

Negative regulatory factors inhibit the proliferation of haematopoietic stem cells thus protecting them from differentiation pressures. One of the negative regulators of stem cell proliferation is the tetrapeptide Acetyl-Seryl-Aspartyl-Lysyl-Proline (AcSDKP). This peptide is endogenously produced in vivo and long term bone marrow cultures and is degraded by angiotensin 1-converting enzyme (ACE) both in vivo and in vitro. The aim of these investigations was to study the role of ACE on haematopoietic stem and progenitor cell proliferation. Since the N-domain ACE active has been implicated in AcSDKP degradation, an analysis of two ACE inhibitors (captopril and lisinopril) shown to have differential effects on the N-domain ACE active site was conducted. Both captopril and lisinopril equally reduced ACE activity in plasma in vitro. However, captopril had a lesser effect on reducing serum ACE activity in vitro than lisinopril. Captopril and AcSDKP together reduced the proportion of GM-CFC in S-phase after 7 hours of in vitro incubation. In addition, ACE resistant AcSDKP analogue (AcSDPψKP) when incubated with bone marrow cells in the absence of captopril also reduced the proportion of GM-CFC in S-phase. This finding suggest that the effect of captopril and AcSDKP on GM-CFC proliferation was due to AcSDKP alone. Haematopoietic stem cells were induced into cell cycle by in vivo administration of either 2 Gy-γ-irradiation or the two cytotoxic drugs, cytosine arabinoside (Ara-C) (100 mg/kg i.p.) or 5 flourouracil (5 FU) (150 mg/kg i.v). Bone marrow cells were sampled and incubated in vitro for up to 24 hours. Captopril together with AcSDKP reduced the proportion of high proliferative colony forming cells-1 (HPP-CFC-1) in S-phase following 2 Gy-γ-irradiation. Lisinopril together with AcSDKP had no such effect. In addition, captopril alone in vitro reduced the proportion of HPP-CFC-1 in S-phase induced into cell cycle by cytotoxic drugs. Lisinopril had no such effect. Incubation alone reduced the proportion of HPP-CFC-1 in S-phase in cytotoxic drug treated bone marrow cells. When cultures, which were incubated with captopril, were assayed for AcSDKP levels, captopril induced an increase in AcSDKP levels in both control normal bone marrow cells and cells derived from Ara-C treated mice. However, it did not affect AcSDKP levels in cultures derived from 5 FU and 2 Gy treated mice, AcSDKP together with captopril were shown to inhibit S-phase cell entry of HPP-CFC-1 when they were incubated with bone marrow cells derived from mice treated with either 2 Gy-γ-irradiation or cytotoxic drug insults. Interestingly, captopril was unable to reduce the proportion of SA2 leukaemic cells in S-phase Captopril on its own at therapeutic doses reduced the proportion of HPP-CFC- 1 in S-phase in vivo regardless of the insult used to induce HPP-CFC-1 into cell cycle. Lisinopril slightly reduced the proportion of HPP-CFC-1 in S-phase following Ai-a-C treatment only. Captopril induced an in vivo increase in AcSDKP levels in all the models tested. Captopril also reduced the proportion of HPP-CFC-1 and GM-CFC in S-phase following fractionated doses of Ara-C. Captopril's inhibitory effect on GM- CFC proliferation following fractionated dose of Ara-C was diminished after 7 days while it was sustained with HPP-CFC-1. Long-term bone marrow cultures revealed that captopril and AcSDxj/KP had the same effect on cellularities of both layers and on the proliferation of HPP-CFC and GM-CFC in both layers. From the present investigations, it can be concluded that captopril is a potent inhibitor of HPP-CFC-1 proliferation. This effect may in part be mediated by AcSDKP mechanism