Aga Khan University is a non-profit institution and an agency of the Aga Khan Development Network. It was Founded in 1983 as Pakistan's first private university. Starting in 2000, the university expanded to Kenya, Tanzania, Uganda, the United Kingdom and Afghanistan.AKU began life as a health-sciences university. It is among the largest private health-care providers in Pakistan and East Africa. AKU hospitals were the first in those regions accredited by U.S.-based Joint Commission International.More recently, the university has initiated programmes in teacher education, the study of Muslim civilisations, journalism, early childhood development and public policy. In the near future, the university plans to launch an undergraduate liberal-arts programme to educate future leaders in a wide range of fields and establish additional graduate professional schools.
Temporal Lobe Epilepsy with Hippocampal Sclerosis (TLE-HS) presents a significant therapeutic challenge, primarily due to pharmacoresistance and progressive hippocampal neurodegeneration. Since current anti-seizure therapies often provide limited seizure control in TLE-HS, there is increasing interest in exploring alternative and complementary treatment approaches. Chinese herbal medicine (CHM) or Traditional Chinese medicine (TCM) has gained attention for its multifaceted therapeutic potential, particularly its neuroprotective and anticonvulsant effects. This review explores preclinical and emerging clinical evidence supporting the efficacy of TCM in modulating key molecular targets involved in epileptogenesis. Several TCM-derived bioactive compounds exhibit anti-inflammatory properties by downregulating proinflammatory cytokines and damage-associated molecular patterns. Additionally, TCMs promote neurotrophic factor expression and enhance synaptic plasticity, thereby supporting neuronal survival. By balancing excitatory (glutamatergic) and inhibitory (GABAergic) neurotransmission, TCM may reduce seizure susceptibility and progression. Notably, herbs such as Gastrodia elata and Uncaria rhynchophylla demonstrate promising mechanistic effects. Although encouraging, these findings necessitate further pharmacological validation and clinical trials to substantiate TCM as a complementary, evidence-based intervention for patients with pharmacoresistant TLE-HS.
This chapter reviews the most recent data on malnutrition and catch-up growth published between July 1, 2015 and June 30, 2016. Catch-up growth is defined as height velocity above the expected for age that occurs after a period of growth retardation during childhood and puberty. The first paper in this chapter deals with research priorities in the field of malnutrition and highlights the most rated questions for future studies by experts (Angood et al., 2016). This is followed by research studies providing new insights into various aspects of the field: meaningful parameters for the measurement of population-level catch-up in linear growth in children (Leroy et al., 2015); new postnatal growth standards for preterm infants (Villar et al., 2015); the consequences of marginally low birth weight on weight and height in childhood (Berglund et al., 2016); important components of the malnutrition rehabilitation diet, especially proteins (Ghosh 2016; Manary et al., 2016; Stobaugh et al., 2016; Batra et al, 2016; Masarwi et al., 2016; Bortolotti et al., 2016; Semba et al., 2016), micronutrients (Shafique et al., 2016), and prebiotics (Bryk et al., 2015); and the link between the gut macrobiota and malnutrition (Blanton et al, 2016).
The hypothalamus serves as a central regulator of metabolism, integrating signals pertinent to food intake and energy balance. Brain-Derived Neurotrophic Factor (BDNF) is widely distributed in brain, including expression in hypothalamic nuclei, which regulates feeding behavior. Chronic ethanol (EtOH) consumption has adverse effects on metabolic function, affecting the hypothalamus and striatum, a reward-associated region. Virgin coconut oil (VCO), a dietary lipid rich in medium-chain triglycerides, which have been shown to modulate BDNF expression. Based on these findings, we hypothesized that chronic EtOH consumption would impair metabolic regulation and causes oxidative stress, while VCO would counteract these effects. To test this, water drinking control and EtOH drinking Wistar male rats received water as vehicle or VCO by gavage (12 days). Growth, diet and fluid consumption were recorded throughout the experiment. Hypothalamic BDNF, striatal oxidative stress, and serum metabolic markers following EtOH and VCO exposure were examined. Statistical analysis utilized t-test, two-way ANOVA and Kruskal-Wallis test. Findings revealed that VCO reduced hypothalamic BDNF, decreased food and food caloric intake, and led to weight loss in EtOH exposed rats. Metabolic effects were further modulated by alterations in serum glucose, cholesterol, and triglycerides, where EtOH lowered glucose and cholesterol due to reduced caloric intake, while VCO increased all three markers. Additionally, VCO restored oxidative stress markers in the striatum, potentially mitigating EtOH- induced neurotoxicity by normalizing catalase and peroxide levels. This study highlights the complex interaction between EtOH and VCO in metabolic regulation, oxidative stress, and neuroendocrine function, warranting further research to explore its potential therapeutic implications.
Iron deficiency anemia (IDA) remains a significant global health issue among children aged 24–59 months. It can lead to systemic metabolic changes that hinder neurodevelopment and growth. This study examined serum metabolomic profiles and hepcidin levels in young children with IDA to identify the metabolic pathways affected by iron deficiency. This observational case–control study was conducted at the pediatric clinic of University Teaching Hospital in Karachi, Pakistan, from July to September 2024. We initially recruited and screened 100 children aged 24–59 months (50 with IDA and 50 healthy controls). After applying predefined clinical and laboratory exclusion criteria, all 50 eligible IDA cases and 38 controls were included in the final analysis. Hemoglobin and ferritin levels were measured as markers of iron status. Serum hepcidin was quantified using ELISA. Untargeted metabolomic profiling was performed with gas chromatography − mass spectrometry (GC–MS). Statistical analyses were performed using SPSS (v26.0), R (v4.4.3), and MetaboAnalyst (v6.0). Children with IDA had significantly lower body weight, hemoglobin, and ferritin levels than controls (p < 0.001). Serum hepcidin levels were lower in IDA but did not differ significantly between groups (p = 0.10). Metabolomic analysis identified twelve metabolites that were significantly downregulated in IDA (p < 0.05). Pathway analysis revealed that cholesterol is a key metabolite linked to bile acid and steroid biosynthesis. Ferritin demonstrated strong positive correlations with cholesterol and 9, 12, 15-octadecatrienoic acid (r = 0.70). Conclusions: Children with IDA showed alterations in lipid-related metabolites, with cholesterol emerging as a key associated metabolite. However, pathway-level interpretations based primarily on a single sterol signal should be interpreted cautiously. Hepcidin levels were not significantly different, indicating complex regulatory influences in early childhood.
Circulating microRNAs (miRNAs) have emerged as potential non-invasive biomarkers for type 2 diabetes mellitus (T2DM), but reported diagnostic performance varies across studies. We conducted a systematic review and meta-analysis to evaluate the diagnostic accuracy of circulating miRNAs for identifying T2DM and its complications. Three databases (PubMed, Scopus, and the Cochrane Library) were searched from inception to December 2024. Studies assessing circulating miRNA expression in adults with T2DM compared with healthy or pre-diabetic controls were included. The meta-analysis only included studies reporting AUC values. Diagnostic accuracy data were synthesized using a bivariate random-effects model. Risk of bias was assessed using QUADAS-2. Thirty studies comprising 3,090 participants were included in the meta-analysis. The pooled sensitivity and specificity of circulating miRNAs for diagnosing T2DM were 0.88 (95
