Includes abstract. / Includes bibliographical references. / In Sub-Saharan Africa, the prevalence of vascular calcification (VC) in CKD-5D is unknown. We undertook to determine the effect of ethnicity on VC, the risk factors for VC, the utility of abdominal X-ray (AXR) in predicting coronary calcium score (CCS) and the effect of VC on central aortic systolic pressure (CASP) and left ventricular mass index (LVMI) in South African dialysis patients. ... Black race significantly protects from VC in South African CKD-5D patients and warrants further study. The AXR is a useful screening tool for CCS in our population. VC does not appear to influence CASP in our population.

Background The burden of leptospirosis in sub-Saharan Africa remains unclear although it is accepted that this infection is widely spread in this region. The global estimated number of cases is one million with 58 900 deaths attributable to leptospirosis annually. Objective To describe the profile of patients with suspected leptospirosis and to compare their in hospital outcomes. Methods &amp; Material We performed a retrospective study at a tertiary referral hospital in South Africa. All adults with suspected leptospirosis who had a laboratory request for leptospirosis ELISA IgM testing between 2005 and 2015 were included. Clinical and laboratory findings at presentation were correlated with the patient's subsequent clinical course and ELISA IgM status. Results During the study period 223 patients who had ELISA IgM test requests were enrolled. Leptospirosis ELISA IgM was positive in 45 (20%) patients. Enrolled patients had a median age of 38 (IQR 31 – 53) years, 147/223 (66%) were males and 80/223 (36%) were HIV positive. There were 12/45 (27%) HIV-positive patients in the IgM-positive group compared to 68/178 (38%) in the IgM-negative group, p=0.22. Compared to IgM-negative patients, patients with positive IgM were more likely to present with jaundice 37/45 (82%) vs. 82/178 (46%), p <0.01, and acute kidney injury (AKI) 34/45 (76%) vs.102/178(57%), p=0.06. The median length of hospital stay was 13 days (IQR 8-22 days) for IgM-positive compared to 10 days (IQR 6-21 days) in IgM-negative patients, p= 0.10. A total of 11/45 (24%) IgMpositive patients required ICU admission compared to 41/178 (23%) of IgM-negative patients, p=0.84 and the median length of ICU stay was 7 days (IQR 4-11) for IgM-positive compared to 6 days (IQR 3-9.5) for IgM-negative patients, p=0.51. There were 13/45 (29%) IgM-positive patients who needed dialysis compared to 42/178 (24%) of IgM-negative patients, p= 0.46. The mortality rate was 7/45 (16%) in IgM-positive compared to 52/178 (29%) in IgM-negative patients, p=0.07. Conclusion Patients with positive IgM presented predominantly with jaundice and AKI. There was no statistically significant difference in HIV status and outcomes between the two groups of patients

The 5' stem-loop (5'SL) in the 5' UTR of collagen α1(I) and α2(I) mRNAs is the key element regulating stability and translation of collagen mRNAs. LARP6 is the RNA binding protein which exhibits high affinity binding to the 5'SL of collagen α1(I) and α2(I) mRNAs. In the first part of the dissertation, we report that vimentin filaments associate with type I collagen mRNAs in a 5'SL and LARP6 dependent manner. This association is needed for stabilization of type I collagen mRNAs. Our conclusion was based on the following lines of evidence. First, RNA immunoprecipitation and cellular fractionation experiments showed that collagen α1(I) and α2(I) mRNAs exhibit specific interaction with vimentin intermediate filaments. This was substantiated by RNA-FISH experiments which showed that collagen I mRNAs colocalize with vimentin filaments. Second, we showed that the binding of collagen mRNAs to vimentin intermediate filaments is dependent on the 5' stem-loop. Collagen mRNAs from mouse embryonic fibroblasts carrying a knock-in mutation in the 5'SL failed to interact with vimentin intermediate filaments. Third, interaction of collagen mRNAs with collagen mRNAs was mediated by the RNA binding protein, LARP6, which specifically binds the 5'SL of type I collagen mRNAs. siRNA knock down of LARP6 abrogated the interaction of type I collagen mRNAs with vimentin intermediate filaments. We also found that LARP6 interacts and colocalizes with vimentin intermediate filaments. Mapping of the domain of LARP6 needed for interaction with vimentin revealed that the La domain of LARP6 is necessary and sufficient to interact with viemntin. Fourth, disruption of vimentin filaments using the vimentin disrupting drug β,β'-imminodipropionitrile or by expressing a dominant negative intermediate filament markedly reduced production of type I collagen. The reduction in collagen synthesis was due to decreased stability of collagen mRNAs. Last, but not least, we observed a marked reduction in collagen synthesis from vimentin -/- mouse fibroblasts. This reduced collagen production was also due to reduced stability of type I collagen mRNAs in vimentin deficient fibroblasts. This was consistent with the impaired wound healing phenotype displayed by vimentin deficient mice further verifying the important role of vimentin filaments in collagen synthesis. We concluded that vimentin intermediate filaments play a key role in the development of tissue fibrosis by stabilizing type I collagen mRNAs. This finding served as a basis for targeting vimentin in the investigation of a novel anti-fibrotic therapy. In the second part of the project, we examined the antifibrotic effects of Withaferin-A. The intermediate filament vimentin is the primary target of Withaferin-A. In light of our finding of the role of vimentin in stabilizing collagen mRNAs, we hypothesized that Withaferin A may reduce collagen production by disrupting vimentin filaments and decreasing the stability of collagen mRNAs. We thus aimed to determine if Withafrein-A exhibits anti-fibrotic properties in vitro and in vivo and to elucidate the molecular mechanisms by which WF-A exerts its anti-fibrotic effects. We found that, in tissue culture, Withaferin-A suppresses collagen expression, both at transcriptional and post-transcriptional level, by inhibiting the TGF-β signaling pathway and by disrupting vimentin filaments, respectively. Withaferin-A disrupted vimentin filaments and caused degradation of vimentin in fibroblasts. The toxicity of Withaferin-A is not due to disruption of vimentin filaments as the disruption occurs at concentrations lower than the toxic range. WF-A can potently inhibit the expression of type I collagen in human and rodent fibroblasts. Withaferin-A increases the rate of decay of α1(I) and α2(I) collagen mRNAs. The effect of WF-A on half-life of collagen mRNAs is dependent on the presence of vimentin. In addition to destabilizing collagen mRNAs by disrupting vimentin filaments, WF-A also interferes with TGF-β induced transcription of collagen genes. WF-A inhibits both the TGF-β induced as well as the culture induced phosphorylation of Smad3. Withaferin-A inhibits in vitro activation of hepatic stellate cells (HSCs) and decreases collagen production by HSCs. In vivo, WF-A inhibits isoproterenol-induced myocardial fibrosis and results in downregulation type I and type III collagen as well as α-smooth muscle actin. Our findings provide a strong evidence base for the further exploration of Withaferin-A as a therapeutic drug against fibroproliferative diseases, including but not limited to cardiac interstitial fibrosis. Taken together, this dissertation project gives both the basic science and translational aspect of the posttranscriptional regulation of collagen expression by a complex involving vimentin intermediate filaments, LARP6 and the 5'SL of collagen mRNAs. The findings strongly show that, in this complex, vimentin confers stability to collagen mRNAs. Importantly, the dissertation utilizes the collagen stabilizing function of vimentin for targeting by a potential ant-fibrotic drug. We discovered for the first time that Withaferin-A displays anti-fibrotic properties in vitro and in vivo in mouse model of isoproterenol-induced myocardial fibrosis. / A Dissertation submitted to the Department of Biomedical Sciences in partial fulfillment of the requirements for the degree of Doctor of Philosophy. / Fall Semester, 2011. / October 28, 2011. / collagen, fibrosis, mRNA, stability, vimentin, Withaferin-A / Includes bibliographical references. / Branko Stefanovic, Professor Directing Dissertation; Hengli Tang, University Representative; Choogon Lee, Committee Member; James Olcese, Committee Member.

Protein aggregates formation is a common characteristic of many neurodegenerative diseases including Parkinson's disease (PD), Alzheimer's disease (AD) and Amyotrophic Lateral Sclerosis (ALS). Effective clearance of those toxic protein aggregates is critical for neuronal survival. Aggresome is a newly defined cytoplasmic structure, which serves to sequester accumulated protein aggregates for further degradation. However, the mechanism of aggresome formation is poorly understood. In this study, we discover that 14-3-3 has a general role in promoting aggresome formation. Overexpressing 14-3-3, a family of conserved acidic proteins, enhances aggresome formation of several aggregation-prone proteins including alpha-SynEGFP, GFP-250 and GFP-CFTRΔF508, while blocking 14-3-3's binding ability by its antagonist suppresses aggresome formation in cells. In addition, we find that 14-3-3 interacts with both dynein intermediate chain (DIC) and a HSP70 co-chaperone Bcl-2-associated athanogene 3 (BAG3). Our biochemical and functional studies further reveal that dimeric 14-3-3 bindings bridge the interaction between BAG3 and DIC, which is crucial for both loading of misfolded protein cargos onto dynein complex and aggresome formation. Taken together, these findings suggest that 14-3-3 functions as a molecular adaptor by coupling BAG3-cargo-complex with dynein motor for targeting misfolded proteins to aggresome in cells. / A Dissertation submitted to the Department of Biomedical Sciences in partial fulfillment of the requirements for the degree of Doctor of Philosophy. / Summer Semester, 2012. / June 27, 2012. / 14-3-3, aggresome, alpha-Syn, Bag3, dynein, neurodegeneration / Includes bibliographical references. / Yi Zhou, Professor Directing Dissertation; Robert Contreras, University Representative; Mohamed Kabbaj, Committee Member; Yanchang Wang, Committee Member.

The faithful maintenance of structure and function of chromatin is crucial for maintaining genomic stability. In proliferating cells, nucleosome assembly occurs largely during S-phase with a strict coordination between DNA and histone synthesis. Histone gene transcription is induced during the G1/S transition of cell cycle and shuts off before DNA replication ends. When S-phase cells are treated with genotoxic agents that impede DNA replication, an evolutionary conserved response leads to a rapid drop in histone transcript levels. The objective of this thesis was to understand how cells achieve this regulation by unraveling the underlying molecular mechanisms. We have chosen the budding yeast as a model system to study this because of the simple organization of histone genes in this unicellular eukaryote. In particular, we have focused on the transcriptional regulation of histone genes as this is the major form of regulation for histone genes in budding yeast. A novel surveillance mechanism has been described in the budding yeast Sacccharomyces cerevisiae that monitors the accumulation of non-chromatin-bound histones and promotes their rapid degradation by the proteasome dependent on the checkpoint kinase Rad53. This led us to explore the role of DNA Damage Response kinases in histone gene regulation in response to DNA damage and replication arrest. We have uncovered that the transcriptional repression of histone genes upon DNA damage and replication arrest is dependent on Rad53 and its upstream activators Mec1/Tel1. Further, based on the identification of Hpc2, one of the components of the Hir complex as a novel target of DDR kinases, we identified the phosphorylation sites on Hpc2 that regulate histone gene transcription under replication stress. Additionally, we find that the phosphorylation at these specific sites is crucial for the recruitment of the Rsc chromatin remodeling complex to the histone promoters. Interestingly the DDR kinase dependent phosphorylation of Hpc2 leads to the stabilization of the Hpc2 protein itself upon Hydroxyurea (HU) treatment. This may provide a potential mechanism for how the Hir mediated repression is relieved at G1/S or after checkpoint recovery. Putting all the information together, we propose that DDR kinase dependent phosphorylation stabilizes Hpc2. Its stability plays a regulatory role in the Hir-dependent repression of histone genes upon replication inhibition. It remains to be determined what triggers the instability of Hpc2. Lastly, we explored the role of histone H3K56 acetylation, a mark that persists under replication stress, in the regulation of histone genes. We find histone H3 acetylation at Lysine 56 is indispensable for histone gene repression under replication stress and its removal after recovery is crucial for histone gene transcription to resume. Together the findings in this thesis highlight the important contribution of checkpoint kinases in the maintenance of genomic stability via novel mechanisms that coordinate DNA and histone synthesis. / A Dissertation submitted to the Department of Biomedical sciences in partial fulfillment of the requirements for the degree of Doctor of Philosophy. / Fall Semester, 2012. / August 9, 2012. / budding yeast, checkpoint kinases, genotoxic stress, Histones, Nucleosome assembly, Replication checkpoint / Includes bibliographical references. / Johanna Paik, Professor Directing Dissertation; Hong-Guo Yu, University Representative; Akash Gunjan, Committee Member; Myra Hurt, Committee Member; Yamchang Wang, Committee Member.

The secondary injury cascades in the acute phase of traumatic brain injury (TBI) are often the most devastating to patient outcome. These cascades include the neurobiological and neurochemical changes subsequent to the mechanical trauma inflicted whether direct, or indirect. Major secondary events include edema and inflammation, both leading to increased cell damage, demyelination, and cell death. Such secondary cascades alter blood flow, concentrations of ions, metabolism, and structural integrity ultimately leading to deteriorating patient outcome days after the injury rather than immediately. Many studies examine individual aspects of the secondary mechanisms to find potential biomarkers and/or therapeutic targets for TBI. However, no effort has proven successful at identifying a single biomarker of diagnostic or therapeutic application in part due to the heterogeneity of the condition – there remains a significant void in details about the secondary mechanisms of TBI that are still not understood. Ultimately the goal of this research is to better characterize the heterogeneous nature of TBI to allow for identification and inhibition of cell damage and death by inhibiting these secondary mechanisms. The kallikrein (human: KLK; rodent: Klk) family of serine proteases is one potential target that has not been examined with respect to TBI. Among the 15 known kallikreins (numbered 1–15), KLK6 is the most abundant in the brain and is associated with numerous aspects of the secondary TBI cascade. My primary goal is to identify a blood biomarker for diagnosing TBI and for tracking the efficacy of future drugs that prevent demyelination and cell death. To assist in this goal, the first aim of this study focused on analysis of the level of Klk6 in rodent brain and blood in three models of rat brain injury: mild (closed head), moderate (2.0 mm depth of impact), and severe (3.0 mm depth of impact). Protein assays determined levels of Klk6 at 3 and 24 h post–mild injury and 3, 6, 9, 24, 72, and 96 h post-moderate and severe injury and in sham and craniotomy-only operates. Comparison of Klk6 levels over time and across grades of injury severity are presented with respect to known substrates of Klk6 and to well-studied biomarkers of inflammatory demyelination characteristic of TBI to include: myelin basic protein (MBP) and tumor necrosis factor–α (TNFα). Immunohistochemistry determined the extent of corresponding pathology. These data supports Klk6 as a potentially important new physiological biomarker of TBI worthy of additional future study. The second aim of this study focused on analysis of the effect of neurosteroid treatment on Klk6 levels in brain and blood after severe TBI and the corresponding levels of inflammatory demyelination. Here, the indirect effect of allopregnanolone (ALLO) – an existing treatment of TBI in rodent studies which is known to increase the levels of free serpin in the brain – on Klk6 is described with respect to pathological implications. Protein assays determined reduced levels of Klk6 overall and specifically at 3, 6, and 9 h, but not at 24 h post–severe injury as compared to untreated. Immunohistochemistry determined corresponding alterations in pathology as a result of treatment with ALLO and suggest demyelination and inflammation are not significantly altered within 9 h of treatment with ALLO despite a reduction in the overall levels of Klk6. Additional studies beyond this time point are not warranted at this time due to the reductions in Klk6 by 24 h in untreated controls. However, further studies are warranted to examine the specific mechanism by which the Klk6 is reduced. Overall, the results support the hypothesis that Klk6 is involved in the secondary mechanisms of TBI and serum levels are a discrete diagnostic biomarker in rodents. Furthermore, treatment of injured rodents with ALLO decreases Klk6 acutely. However, reductions in Klk6 within 24 h were not paired with comparable improvements in inflammation or demyelination suggesting that the improvements require more than 24 h whether due to a delayed increase in serpins or by delayed remyelination potentially due to sustained inflammation. Therefore, although Klk6 appears to be a promising diagnostic biomarker, it does not appear to be a promising acute therapeutic biomarker of secondary pathology recovery. / A Dissertation submitted to the Department of Biomedical Sciences in partial fulfillment of the requirements for the degree of Doctor of Philosophy. / Summer Semester, 2013. / May 13, 2013. / concussion, cortical impact, demyelination, inflammation, neurosteroids, protease / Includes bibliographical references. / Michael Blaber, Professor Directing Dissertation; Richard L. Hyson, University Representative; Cathy Levenson, Committee Member; Richard Nowakowski, Committee Member; Jacob VanLandingham, Committee Member.

The zebra finch (Taeniopygia guttata) has long been used as an animal model for memory and cognition due to the naturally occurring process through which they acquire and produce song This process, in which song is learned from tutor finches in their environment, is thought to be highly analogous to human speech development. The areas of the zebra finch brain involved in song acquisition and production are known as song nuclei, some of which are known to contain nicotinic acetylcholine receptors (nAChRs). Some of these receptor subtypes have been shown to play important roles in memory. I explored the roles that nAChRs may play in the production of song by adult male zebra finches through behavioral long-term experiments, which monitor song production before and after in vivo nicotine administration. I found that both Inter-Syllable Duration (ISD) and Wiener Entropy (WE) were significantly altered two months after the cessation of nicotine, suggesting a possible role of nAChRs in the timing mechanisms of song. Re-exposure to nicotine further alleviated the previous observed changes in ISD and WE, which could point towards an alteration in nicotinic circuits, possibly through a change in synaptic functioning. / A Dissertation submitted to the Department of Biomedical Sciences in partial fulfillment of the requirements for the degree of Doctor of Philosophy. / Spring Semester, 2014. / November 4, 2013. / Nicotine, Song, Zebra Finch / Includes bibliographical references. / Susanne L. T. Cappendijk-van Engelen, Professor Directing Dissertation; Mohammed Kabbaj, Professor Directing Dissertation; Anke Meyer-Baese, University Representative; James F. Johnson, Committee Member; Cathy W. Levenson, Committee Member; Charles C. Ouimet, Committee Member.

OBJECTIVE: Despite recent scientific and technological advancements preterm birth remains one of the leading causes of neonatal mortality worldwide. With annual increases in the prevalence of preterm birth over the last decade further research is needed to discover the optimum management style for this complex population. The objectives of this study are to identify factors that may increase the risk of postoperative mortality or intensive care in preterm and early-term neonates undergoing surgery, and to create a predictive risk score to help clinicians and families better understand the probability of this postoperative outcome. METHODS: A retrospective analysis was performed on 653 neonates born <39 weeks gestation undergoing surgery within the first 30 days of life at Boston Children’s Hospital between January 2013 and December 2018. Multivariable logistic regression analysis was used to determine independent risk factors for postoperative intensive care or mortality. Significant independent risk factors were multiplexed into a predictive risk algorithm with scores ranging from 0 to 13 points. Probabilities of intensive care or mortality were obtained with 95% confidence intervals for each score, and model validation via 1,000 bootstrap resamples was performed to assess model discrimination and calibration. RESULTS: Among the total of 653 premature neonates undergoing surgery, 614 (94%) were deceased or required postoperative intensive care. Fifty-eight (9%) were deceased, 556 (85%) required postoperative intensive care and survived, and 39 (6%) survived without intensive care. Two hundred ninety-two neonates (45%) were female, and 356 neonates (55%) had an American Society for Anesthesiologists – Physical Status (ASA-PS) rating of IV/V. The following were determined independent predictors of postoperative mortality or intensive care: body weight < 2.5 kg (odds ratio(OR) = 0.16; 95% CI: 0.06, 0.41; P<0.001), ASA-PS IV/V (OR=14.65; 95% CI: 1.28, 168.2; P=0.031), cardiovascular condition (OR=4.44; 95% CI: 1.27, 15.55; P=0.020), neurological condition (OR=7.84; 95% CI: 1.89, 32.49; P=0.005), pulmonary condition (OR=16.11; 95% CI: 1.51, 32.06; P=0.002), and renal/urological condition (OR=6.96; 95% CI: 1.51, 32.06; P=0.013). The probability of postoperative mortality or intensive care ranged from 31.2% (95% CI: 18.6%, 47.4%) for a risk score of 0 points to 99.9% (95% CI: 99.9%, 99.9%) for a risk score of at least 9 points. The score demonstrated extremely good discriminatory performance (c-index=0.969; 95% CI: 0.950, 0.986). DISCUSSION: Our risk score can estimate postoperative survival without intensive care for preterm (PT) and early-term (ET) neonates. Providers could use this index to guide discussions with families about possible postoperative outcomes. Our model can also be applied within healthcare facilities for a variety of purposes. This score can assist in departmental standardization for the perioperative management of a PT or ET neonate to create more regular treatment patterns. If applied correctly it could increase operating room throughput and allow for more efficient healthcare resource utilization. Finally, though many severity-of-illness and mortality risk scores exist in clinical practice presently, the proposed algorithm can be applied to a broader population with less temporal restriction. CONCLUSION: The risk algorithm is a reliable and reproducible tool for the prediction of postoperative mortality or the likelihood of postoperative intensive care for PT and ET neonates meeting the inclusion criteria. / 2022-06-04T00:00:00Z

Background: International and national (South African constitution) laws mandate that the Department of Correctional Services (DCS) ensure that on remand detainees receive the same medical treatment as those who are not incarcerated, as well as adequate nutrition while incarcerated. Literature across the globe indicates that inmates are at an increased risk of health problems and malnutrition, with juveniles being at an even higher risk than the adult inmate population. To our knowledge no research on the nutritional status of juveniles at entry into correctional facilities in South Africa or internationally has been published to date. The aim of this research was to determine and compare the nutrition related health status, associated factors and predictors in juvenile male and female on remand detainees at entry into Pollsmoor correctional service facilities in the Western Cape. Methods: In this cross-sectional comparative study of 67 male and 52 female juvenile on remand detainees the following was assessed using an interviewer based questionnaire: sociodemographic information including age, ethnicity, language spoken at home, a hunger score, meal pattern and food choices in the week prior to entry into the facility using a nonquantified FFQ, understanding of healthy eating, physical activity and sedentary behaviour before entry using the GPAQv2, risk taking behaviours (smoking and alcohol an illicit substance use), body shape perception, and symptoms of depression and anxiety using the K10 tool. The following physical measures were taken: weight, height, triceps-skinfold, mid-upper arm circumference (MUAC) and maximum handgrip strength (MHGS). BMI and the corrected arm muscle area (cAMA) were calculated. All variables were analysed descriptively and compared between male and female juveniles using Pearson Chi-square test, independent samples t-test or Mann-Whitney U test as appropriate. Association tests (Spearman Rank correlation coefficient for continuous and cross-tabulations and the Pearson's Chi square test for categorical variables) were furthermore undertaken with BMI, cAMA and MHGS as the dependent variables within each gender group. The same tests were used to conduct association analysis between socio-demographic variables, dietary intake, physical activity, risk taking behaviour and symptoms of depression and anxiety within each gender group. Multiple linear regression analyses were conducted to identify predictors of BMI, cAMA and MHGS within each gender groups. The clinical significance of statistically significant predictors was assessed using novel criteria. 4 Results: A summary of the profiles of juvenile female and male on remand detainees are shown in Table A, while the predictors of malnutrition in the same population are shown in Table B following the abstract conclusion. Juvenile female on remand detainees were characterised by a double burden of malnutrition, namely undernutrition (15.4%) and overweight/obesity (23.1%). Coloured (55.8%) and black African ethnicities (42.3%) were equally represented in the sample, with Afrikaans being the most common (46.2%) and isiXhosa the second most common home language reported (32.7%). Only a few had completed grade 12, and half had given birth to one or more children. Food insecurity was reported by 30.8%. Food choices showed frequent intake of low nutrient high-energy food items (table sugar, crisps, white bread, fizzy drinks that contain sugar and non-fibre containing starches) and less frequent intake of nutrient dense foods (fruits, vegetables, dairy and quality proteins). Physical activity levels were high (67.3% classified as active with ≥3000 MET minutes/week), with walking/cycling to get to places being a major contributor to time spent doing physical activity median (IQR) 106 (51-300) minutes/day. Daily illicit substance use was the most common risk taking behaviour, especially amongst the females from the coloured ethnic group (48%). Daily smoking was also common, also specifically amongst those from the coloured ethnic group (83%), while alcohol use seemed to be less prominent. Female detainees were also characterized by the presence of depression and anxiety symptoms (74.5% moderate to very high score). The prevalence of infectious disease was reportedly low (13.7%), but may have been an underestimation Juvenile male on remand detainees were characterised by undernutrition (17.9%), but none of them were overweight or obese. The majority of males were from the coloured ethnic group (65.7%) and reported that they had Afrikaans as home language (65.7%). As was the case for the females, only a few had completed grade 12. Food insecurity was reported by 43.3%. Similar to females, food choice data showed frequent intake of low nutrient high-energy food items and less frequent intake of nutrient dense foods. Physical activity levels were high (83.6% active with ≥3000 MET min/week), with both walking/cycling to get to places (60 min/day) and recreational physical activity (26 min/day) contributing to time spent doing physical activity. Smoking was the most common risk taking behaviour followed by illicit substance use (smoking was highest in the coloured males 82%). Both smoking and illicit substance use was more frequent in the male sample, while daily alcohol intake was not common in either gender. Male detainees were also characterized by the presence of depression and anxiety symptoms (74.6%) that were positively associated with illicit substance use. As for females, the prevalence of infectious disease was reportedly low (9%). 5 Predictors of probable clinical significance for juvenile female on remand detainees were as follows: BMI - frequency of vegetable intake (+), frequency of high-fat snack intake (+), frequency of dairy food intake (-), illicit substance use (-), physical activity in MET minutes (-) and availability of fruit juice in the home (-); cAMA - having Afrikaans as home language and depression and anxiety symptoms (-); and MHGS having Afrikaans as home language (-) and anxiety and depression symptoms (-). Predictors of probable clinical significance juvenile male on remand detainees were as follows: BMI -having Afrikaans as home language (-); cAMA - frequency of snacking between meals per week (+) and having Afrikaans as home language (-); and MHGS - hunger score (-) and having Afrikaans as home language or isiXhosa as home language (-). Conclusions and recommendations: The key conclusion of this research is that both female and male juveniles were prone to be malnourished at admission to the correctional facility (Pollsmoor correctional facility). Females had a double burden of malnutrition, with both underweight and overweight/obesity being present, while underweight was the key malnutrition problem in males. It can further be concluded that being from the coloured ethic group and having Afrikaans as a home language increased the risk of being underweight at admission to the correctional facility for both male and female on remand detainees. For female detainees it can be concluded that low frequency of intake of vegetables, high levels of physical activity, frequent use of illicit substances and the presence of depression and anxiety in the month preceding the study also increased the risk of being undernourished, while greater frequency of consumption of high fat snacks increased the risk for being overweight/obese. For male detainees it can be concluded that food insecurity and lower snacking between meals also increased the risk of being undernourished. The main recommendation from this study is for the Department of Correctional Services (DCS) to implement a nutritional status screening procedure at the point of entry of a juvenile into a correctional facility for identification/diagnosis of nutrition related problems and associated factors for referral for nutrition and other health support within the facility.

Knowledge of intimate partner violence (IPV) against women in India has great importance for public health researchers and policymakers. Although there has been a substantial and growing body of scholarship, piecing together the numerous studies is complex. Many of these studies may not address findings within theoretical contexts that are important for understanding a woman’s experience of IPV in India. What is especially lacking is a comprehensive understanding of the structural inequalities and the patriarchal values that exist in India and further exacerbate women’s experience of IPV. In terms of theory, a combination of Bronfenbrenner’s social-ecological framework with radical feminism helps to fill this gap in the scholarship. In terms of empirical data, there are many studies on various individual factors of IPV in India. While many scholars have published systematic reviews of these studies, a thorough articulation of why and how a woman in India is especially susceptible to experiencing IPV is sparse. This literature review will attempt to address both of these critical needs. First, it will articulate a combination of theories (social-ecological theory and radical feminism) to aid in understanding the persistent public health crisis of IPV against women in India. Second, it will look at a broad range of studies to provide an introduction to IPV scholarship and illustrate the multiple, complex, and often overlapping factors that are associated with women’s experience of IPV in India. To do so, this literature review will address types of IPV, studies of prevalence, geographical distribution, structural violence, and risk factors, including pregnancy. It will conclude with policy recommendations and suggestions for further research.