Additional file 1: of Establishment of reference intervals of thyroid function tests from cord blood of neonates in two selected hospitals, Addis Ababa, Ethiopia

TSH, fT4 and fT3 results of Study participants. (XLSX 15 kb

Additional file 1 of Awareness, attitudes towards genetic diseases and acceptability of genetic interventions among pregnant women in Burera district, Rwanda

Supplementary Material

Current Efavirenz (EFV) or Ritonavir-Boosted Lopinavir (LPV/r) Use Correlates with Elevate Markers of Atherosclerosis in HIV-Infected Subjects in Addis Ababa, Ethiopia

<div><p>Background</p><p>HIV patients on antiretroviral therapy have shown elevated incidence of dyslipidemia, lipodystrophy, and cardiovascular disease (CVD). Most studies, however, focus on cohorts from developed countries, with less data available for these co-morbidities in Ethiopia and sub-Saharan Africa.</p><p>Methods</p><p>Adult HIV-negative (<i>n</i> = 36), treatment naïve (<i>n</i> = 51), efavirenz (EFV)-treated (<i>n</i> = 91), nevirapine (NVP)-treated (<i>n</i> = 95), or ritonavir-boosted lopinavir (LPV/r)-treated (<i>n</i>=44) subjects were recruited from Black Lion Hospital in Addis Ababa, Ethiopia. Aortic pressure, augmentation pressure, and pulse wave velocity (PWV) were measured via applanation tonometry and carotid intima-media thickness (cIMT) and carotid arterial stiffness, and brachial artery flow-mediated dilation (FMD) were measured via non-invasive ultrasound. Body mass index, waist-to-hip circumference ratio (WHR), skinfold thickness, and self-reported fat redistribution were used to quantify lipodystrophy. CD4+ cell count, plasma HIV RNA levels, fasting glucose, total-, HDL-, and LDL-cholesterol, triglycerides, hsCRP, sVCAM-1, sICAM-1, leptin and complete blood count were measured.</p><p>Results</p><p>PWV and normalized cIMT were elevate and FMD impaired in EFV- and LPV/r-treated subjects compared to NVP-treated subjects; normalized cIMT was also elevated and FMD impaired in the EFV- and LPV/r-treated subjects compared to treatment-naïve subjects. cIMT was not statistically different across groups. Treated subjects exhibited elevated markers of dyslipidemia, inflammation, and lipodystrophy. PWV was associated with age, current EFV and LPV/r used, heart rate, blood pressure, triglycerides, LDL, and hsCRP, FMD with age, HIV duration, WHR, and glucose, and cIMT with age, current EFV use, skinfold thickness, and blood pressure.</p><p>Conclusions</p><p>Current EFV- or LPV/r-treatment, but not NVP-treatment, correlated with elevated markers of atherosclerosis, which may involve mechanisms distinct from traditional risk factors.</p></div

Preclinical markers of atherosclerosis are elevated in EFV-treated and LPV/r-treated subjects compared to HAART-naïve and NVP-treated.

<p>Wilcoxon rank sum test <i>p</i>-values are shown. *Note: Although the pairwise Wilcoxon rank sum test showed differences in cIMT between EFV- and LPV/r-treated and NVP-treated subject, ANOVA yielded a <i>p</i> = 0.12, which is above the defined criteria of <i>p</i><0.05 for statistical significance. When normalized to carotid artery diameter (cIMT-norm = cIMT/(<i>D</i>/2), where <i>D</i> = carotid diameter), EFV- and LPV/r-treated subjects exhibited significantly increased values compared to NVP-treated and HAART-naïve subject.</p

Baseline characteristics, body composition.

<p>Continuous variables are reported as median (interquartile range). BMI = body mass index, and WHR = waist-to-hip ratio, mm = millimeters.</p><p>A, a = p<0.005 or p<0.05 versus HIV-negative controls, respectively;</p><p>B, b = p<0.005 or p<0.05 versus HAART-naive, respectively;</p><p>D, d = p<0.005 or p<0.05 versus EFV, respectively;</p><p>E, e = p<0.005 or p<0.05 versus NVP, respectively.</p><p>Baseline characteristics, body composition.</p

Improved glucose metabolism by <i>Eragrostis tef</i> potentially through beige adipocyte formation and attenuating adipose tissue inflammation

<div><p>Background</p><p>Teff is a staple food in Ethiopia that is rich in dietary fiber. Although gaining popularity in Western countries because it is gluten-free, the effects of teff on glucose metabolism remain unknown.</p><p>Aim</p><p>To evaluate the effects of teff on body weight and glucose metabolism compared with an isocaloric diet containing wheat.</p><p>Results</p><p>Mice fed teff weighed approximately 13% less than mice fed wheat (<i>p</i> < 0.05). The teff-based diet improved glucose tolerance compared with the wheat group with normal chow but not with a high-fat diet. Reduced adipose inflammation characterized by lower expression of <i>TNFα</i>, <i>Mcp1</i>, and <i>CD11c</i>, together with higher levels of cecal short chain fatty acids such as acetate, compared with the control diet containing wheat after 14 weeks of dietary treatment. In addition, beige adipocyte formation, characterized by increased expression of <i>Ucp-1</i> (~7-fold) and <i>Cidea</i> (~3-fold), was observed in the teff groups compared with the wheat group. Moreover, a body-weight matched experiment revealed that teff improved glucose tolerance in a manner independent of body weight reduction after 6 weeks of dietary treatment. Enhanced beige adipocyte formation without improved adipose inflammation in a body-weight matched experiment suggests that the improved glucose metabolism was a consequence of beige adipocyte formation, but not solely through adipose inflammation. However, these differences between teff- and wheat-containing diets were not observed in the high-fat diet group.</p><p>Conclusions</p><p>Teff improved glucose tolerance likely by promoting beige adipocyte formation and improved adipose inflammation.</p></div

Cardiovascular metrics.

<p>Continuous variables are reported as median (interquartile range). bpm = beats per minute, mmHg = millimeters of mergury, SBP = systolic blood pressure, DBP = diastolic blood pressure, MP = mean preasure, PP = pulse pressure, AP = augmentation pressure, AIx = augmentation index, AIx = 75 = augmentation index, normalize to a heart rate of 75 bpm, mm = millimeters, kPa = kiloPascals, TC = total cholesterol, TG = triglycerides, HDL = high density lipoprotein cholesterol, LDL = low density lipoprotein cholesterol, hs-CRP = high sensitivity C-reactive protein, sICAM = soluble intercellular adhesion molecule-1, sVCAM = soluble vascular cell adhesion molecule-1, mg = milligrams, ug = micrograms, ng = nanograms, dL = deciliter, mL = milliliters.</p><p>A, a = p<0.005 or p<0.05 versus HIV-negative controls, respectively;</p><p>B, b = p<0.005 or p<0.05 versus HAART-naive, respectively;</p><p>D, d = p<0.005 or p<0.05 versus EFV, respectively;</p><p>E, e = p<0.005 or p<0.05 versus NVP, respectively.</p><p>Cardiovascular metrics.</p

Adipose tissue inflammation in mice fed a chow diet with wheat (CD-wheat) or chow diet with teff (CD-teff) for 14 weeks.

<p>A: Immunostaining of the macrophage marker F4/80 (brown) in adipose tissue (scale bar = 100 μM). B: mRNA levels of the macrophage marker, <i>F4/80</i> and <i>CD11c</i>, tumor necrosis factor α (<i>TNF</i>α), monocyte chemoattractant protein-1 (<i>Mcp-1</i>), Forkhead Boxprotein P3 <i>(Foxp3</i>), and adiponectin in adipose tissue. All mRNA expression data were normalized to <i>36B4</i>. C: Immunofluorescence staining for DAPI (blue), F4/80 (red) and TNFα (green) in adipose tissue (scale bar, 100 μm). * <i>p</i> < 0.05. n.s. = not significant.</p

Comparison of body weight and glucose metabolism between mice fed a chow diet with wheat (CD-wheat: Blue) or teff (CD-teff: Red).

<p>A: Study design. B: Body weight. C: Energy intake. D: Intraperitoneal glucose tolerance test (IPGTT) at week 6 (2.0 g/kg). E: Blood glucose levels after oral mixed meal administration of each assigned diet (2.2g/kg body weight, 33% solution in dH₂O) after 16 h of fasting at week 6. F: Plasma insulin levels during OMTT. G: Oral glucose tolerance test (OGTT) at week 9 (2 g/kg). H: Insulin concentration during OGTT. I: Intraperitoneal insulin tolerance test (IPITT) at week 9 (0.5 U/kg). * <i>p</i> < 0.05, n.s. = not significant. n = 5–9 in each groups.</p

Composition and energy density of experimental diets.

<p>Composition and energy density of experimental diets.</p