Building a Strong Undergraduate Research Culture in African Universities

Africa had a late start in the race to setting up and obtaining universities with research quality fundamentals. According to Mamdani [5], the first colonial universities were few and far between: Makerere in East Africa, Ibadan and Legon in West Africa. This last place in the race, compared to other continents, has had tremendous implications in the development plans for the continent. For Africa, the race has been difficult from a late start to an insurmountable litany of problems that include difficulty in equipment acquisition, lack of capacity, limited research and development resources and lack of investments in local universities. In fact most of these universities are very recent with many less than 50 years in business except a few. To help reduce the labor costs incurred by the colonial masters of shipping Europeans to Africa to do mere clerical jobs, they started training ―workshops‖ calling them technical or business colleges. According to Mamdani, meeting colonial needs was to be achieved while avoiding the ―Indian disease‖ in Africa -- that is, the development of an educated middle class, a group most likely to carry the virus of nationalism. Upon independence, most of these ―workshops‖ were turned into national ―universities‖, but with no clear role in national development. These national ―universities‖ were catering for children of the new African political elites. Through the seventies and eighties, most African universities were still without development agendas and were still doing business as usual. Meanwhile, governments strapped with lack of money saw no need of putting more scarce resources into big white elephants. By mid-eighties, even the UN and IMF were calling for a limit on funding African universities. In today‘s African university, the traditional curiosity driven research model has been replaced by a market-driven model dominated by a consultancy culture according to Mamdani (Mamdani, Mail and Guardian Online). The prevailing research culture as intellectual life in universities has been reduced to bare-bones classroom activity, seminars and workshops have migrated to hotels and workshop attendance going with transport allowances and per diems (Mamdani, Mail and Guardian Online). There is need to remedy this situation and that is the focus of this paper

Faculty Workshops for Teaching Information Assurance through Hands-On Exercises and Case Studies

Though many Information Assurance (IA) educators agree that hands-on exercises and case studies improve student learning, hands-on exercises and case studies are not widely adopted due to the time needed to develop them and integrate them into curriculum. Under the support of the National Science Foundation (NSF) Scholarship for Service program, we organized two faculty development workshops to disseminate effective hands-on exercises and case studies developed through multiple previous and ongoing grants. To develop faculty expertise in IA, the workshop covered a wide range of IA topics. This paper describes the hands-on exercises and case studies we disseminated through the workshops and reports our experiences of holding the faculty summer workshops. The evaluation results show that workshop participants demonstrated high levels of satisfaction with knowledge and skills gained in both the 2012 and 2013 workshops. Workshop participants also reported use of hands-on lab and case study materials in our follow-up survey and interviews. The workshops provided a valuable opportunity for IA educators to communicate and form collaborations in teaching and research in IA

High CD56++CD16- natural killer (NK) cells among suboptimal immune responders after four years of suppressive antiretroviral therapy in an African adult HIV treatment cohort

BACKGROUND: Up to 40% of HIV-infected individuals receiving Highly Active Antiretroviral Therapy (HAART) have poor CD4+ T-cell recovery. The role of natural killer (NK) cells in immune recovery during HAART is not well understood. We described the profiles of NK cell subsets and their expression of activating receptor, NKG2D and cytotoxicity receptor NKp46 among suboptimal immune responders to despite four years of suppressive HAART. METHODS: A case control study utilized frozen peripheral blood mononuclear cells (PBMC) from a cohort of HIV-infected adults that initiated HAART in 2004/5, at CD4 < 200 cells/μl. Cases were ‘suboptimal’ responders; patients within the lowest quartile of CD4+ T-cell reconstitution, with a median CD4 count increase of 129 (-43-199) cells/μl (difference between CD4 count at baseline and after 4 years of HAART) and controls were ‘super-optimal’ responders; patients within the highest quartile of CD4 T-cell reconstitution with a median CD4 count increase of 528 (416-878) cells/μl). Expression of NK cell lineage markers (CD56(+/-)CD16(+/-)) and receptors NKG2D and NKp46, was measured among PBMC from 29 cases of ‘suboptimal’ responders’ and 23 controls of ‘super-optimal responders’, and compared among ‘suboptimal’ and ‘super-optimal’ responders. NK cell populations were compared using the Holm Sidak multiple comparison test and p values < 0.05 were considered statistically significant. Data was analyzed using FLOWJO and GraphPad Prism 6. RESULTS: ‘Suboptimal responders’ had a higher proportion of cytokine producing CD56(++)CD16(+/-) (CD56(bri)) NK cells than the ‘super-optimal responders’ p = 0.017, and CD56(neg) NK cells were lower among suboptimal than super-optimal responders (p = 0.007). The largest NK cell subset, CD56(dim), was comparable among suboptimal responders and ‘super-optimal immune responders’. Expression of NKG2D and NKp46 receptors on NK cell subsets (CD56(bri), CD56(neg) and CD56(dim)), was comparable among ‘suboptimal’ and ‘super-optimal’ immune responders. CONCLUSIONS: The pro-inflammatory CD56(++)CD16(--) NK cells were higher among ‘suboptimal’ responders relative to ‘super-optimal’ responders, despite four years of suppressive HAART. Alteration of NK cell populations could inhibit host immune responses to infections among suboptimal responders. We recommend further analysis of NK cell function among suboptimal immune responders in order to inform targeted interventions to optimize immune recovery among HAART-treated adults

Prevalence and risk factors of latent Tuberculosis among adolescents in rural Eastern Uganda

Background: Latent Tuberculosis treatment is a key tuberculosis control intervention. Adolescents are a high risk group that is not routinely treated in low income countries. Knowledge of latent Tuberculosis (TB) burden among adolescents may influence policy. Objectives: We determined the prevalence and risk factors of latent TB infection among adolescents in rural Uganda. Methods: We analyzed baseline data from a study that assessed the prevalence and incidence of Tuberculosis disease among adolescents. We extracted socio-demographics, medical assessment information, and tuberculin skin test results and estimated prevalence ratios (PR) of latent TB infection risk factors by binomial regression. Results: The prevalence of latent TB was 16.1%, 95% CI (15.1 \u2013 17.2). Significant risk factors were: a BCG scar, APR 1.29 (95% CI 1.12 \u2013 1.48); male gender, APR 1.37 (95% CI 1.21 \u2013 1.56); age 17 -18 years, APR 1.46 (95% CI 1.24 \u2013 1.71) and 15-16 years, APR 1.25 (95% CI 1.07 \u2013 1.46) compared to 12-14 years; being out of school, APR 1.31 (95% CI 1.05 \u2013 1.62); and a known history of household TB contact in last 2 years, APR 1.91 (95% CI 1.55 \u2013 2.35) Conclusion: Targeted routine latent TB treatment among adolescents out of school may be crucial for TB disease control in low income countries

Global burden of disease of HIV-associated cryptococcal meningitis: an updated analysis.

BACKGROUND: Cryptococcus is the most common cause of meningitis in adults living with HIV in sub-Saharan Africa. Global burden estimates are crucial to guide prevention strategies and to determine treatment needs, and we aimed to provide an updated estimate of global incidence of HIV-associated cryptococcal disease. METHODS: We used 2014 Joint UN Programme on HIV and AIDS estimates of adults (aged >15 years) with HIV and antiretroviral therapy (ART) coverage. Estimates of CD4 less than 100 cells per μL, virological failure incidence, and loss to follow-up were from published multinational cohorts in low-income and middle-income countries. We calculated those at risk for cryptococcal infection, specifically those with CD4 less than 100 cells/μL not on ART, and those with CD4 less than 100 cells per μL on ART but lost to follow-up or with virological failure. Cryptococcal antigenaemia prevalence by country was derived from 46 studies globally. Based on cryptococcal antigenaemia prevalence in each country and region, we estimated the annual numbers of people who are developing and dying from cryptococcal meningitis. FINDINGS: We estimated an average global cryptococcal antigenaemia prevalence of 6·0% (95% CI 5·8-6·2) among people with a CD4 cell count of less than 100 cells per μL, with 278 000 (95% CI 195 500-340 600) people positive for cryptococcal antigen globally and 223 100 (95% CI 150 600-282 400) incident cases of cryptococcal meningitis globally in 2014. Sub-Saharan Africa accounted for 73% of the estimated cryptococcal meningitis cases in 2014 (162 500 cases [95% CI 113 600-193 900]). Annual global deaths from cryptococcal meningitis were estimated at 181 100 (95% CI 119 400-234 300), with 135 900 (75%; [95% CI 93 900-163 900]) deaths in sub-Saharan Africa. Globally, cryptococcal meningitis was responsible for 15% of AIDS-related deaths (95% CI 10-19). INTERPRETATION: Our analysis highlights the substantial ongoing burden of HIV-associated cryptococcal disease, primarily in sub-Saharan Africa. Cryptococcal meningitis is a metric of HIV treatment programme failure; timely HIV testing and rapid linkage to care remain an urgent priority. FUNDING: None

HIV, tuberculosis, diabetes mellitus and hypertension admissions and premature mortality among adults in Uganda from 2011 to 2019: is the tide turning?

BACKGROUND: The growing burden of diabetes mellitus (DM) and hypertension (HTN) on the background of endemic Human Immuno-deficiency Virus (HIV) and tuberculosis (TB) is a concern in low- and middle-income countries. We aimed to describe annual trends in admissions, mortality rates and premature mortality (years of potential life lost-YPLLs) due to HIV, tuberculosis (TB), diabetes mellitus (DM) and hypertension (HTN) in Uganda. METHODS: We conducted a retrospective cohort study, retrieving electronic records of adults admitted to Mulago and Kiruddu national referral hospitals medical wards between 1st January 2011 and 31st December 2019. We used STATA BE 17.0 and GraphPad Prism 8.0.2 to compute total admissions, inpatient crude mortality rates, and YPLLs; and demonstrate trends using Mann-Kendall test. RESULTS: Of 108,357 admissions, 55,620 (51.3%) were female, 15,300 (14.1%) were recorded in 2012, and 22,997 (21.2%) were aged 21-30 years. HIV, TB, DM and HTN accounted for 26,021 (24.0%); 9537 (8.8%); 13,708 (12.7) and 13,252 (12.2%) of all admissions, respectively. Overall inpatient mortality was 16.7% (18,099/108,357), 53.5% (9674/18,099) were male, 21.5% (3898) were aged 31-40 years and 2597 (14.4%) were registered in 2013. HIV, TB, DM and HTN accounted for 35.6% (6444), 14.6% (2646), 9.1% (1648) and 11.8% (2142) of all deaths, respectively. Total admissions (Kendall's tau-B = - 0.833, p < 0.001) and deaths declined (Kendall's tau-B = - 0.611, p = 0.029). A total of 355,514 (mean = 20.8 years, SD 30.0) YPLLs were recorded, of which 54.6% (191,869) were in males; 36.2% (128,755) were among those aged 21-30 years and were recorded in 2012 (54,717; 15.4%). HIV, TB, DM and HTN accounted for 46.5% (165,352); 19.5% (69,347); 4.8% (16,991) and 4.5% (16,167) of YPLLs, respectively. Proportionate contribution of HIV to deaths and YPLLs declined, remained stagnant for TB; and increased for both DM and HTN. CONCLUSION: TB and HIV account for higher though declining, while DM and HTN account for lower albeit rising morbidity and premature mortality among adult medical patients in Uganda. TB prevention and treatment; and DM/HTN service integration in HIV care should be optimized and scaled up

Computer network security and cyber ethics. Fourth edition

ix, 227 p.: bibl., index; 23 c

On the lower bound for the number ofn-ominoes

Unit squares having their vertices at integer points in the Cartesian plane are called cells. A finite set of integer points forming a vertex set of a connected subgraph of the square-lattice-graph G in the Cartesian plane is called a polyomino. A polyomino with exactly n cells is called an n-omino. Two n-ominoes are considered the same if there is an isometry which maps one onto the other. Let (r,s) be fixed integer points in $Z \times Z$ and define \tau\sb{r,s}: $Z \times Z \to\ Z \times Z$ as \tau\sb{r,s}(x,y) = (x + r,y + s) for all (x,y) $\in\ Z \times Z$. The set T = $\{(r,s)$: $(r,s) \in Z \times Z\}$ is a translation group. Two subsets of $Z \times Z$, say P and Q are said to be translationally equivalent just when there exists \tau\sb{r,s} \in T such that P = \{\tau\sb{r,s}(x,y): $(x,y) \in Q\}$. If P and Q are two finite sets of points corresponding to polyominoes, and P and Q are translationally equivalent, we say the polyominoes are translations. Let t(n) be the number of all translation equivalence classes of n-ominoes. It is known that lim\sb{n\to\infty}(t(n))\sp{1/n}=\theta exists and this limit is known as the Klarner Constant. The value of $\theta$ itself is not known. Let t\sb{k}(n) denote the number of all translational type n-ominoes that fit in a strip of width k. For all k and n, t\sb{k}(n)\leq t(n). One can show that lim\sb{n\to\infty}(t\sb{k}(n))\sp{1/n}=\tau\sb{k} exists also. Hence \tau\sb{k}\leq\theta for all k. We will show that lim\sb{n\to\infty}(t\sb{k}(n))\sp{1/n} tends to a limit \tau\sb{k}. Also that \tau\sb{k}\leq\tau\sb{k+1}