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Background: Alzheimer’s disease (AD) is a growing public health concern affecting millions of individuals worldwide. This disease burden is exacerbated in countries like Bangladesh, where public awareness and knowledge about the condition remains limited.Objective: This study aimed to assess the level of AD knowledge, awareness, and perceived threat among family caregivers of individuals with chronic physical conditions of Bangladesh.Methods: A descriptive cross-sectional study was conducted among the caregivers of patients selected via convenience sampling in six public hospitals between October 2022 and March 2023. The data was collected via face-to-face interviews employing a semi-structured questionnaire that contained information about socio-demographic characteristics, personal experiences with AD, knowledge of AD, level of awareness regarding AD, and perceived threat toward AD.Results: The findings revealed a poor knowledge of AD among the study participants. Regarding AD awareness, 52.5% considered memory loss in older individuals abnormal, 26.2% attributed AD to causes like black magic, psychological distress, or bad eyes. Regarding perceived threat, 60.2% wanted to assess their AD risk, while 68.2% disagreed with the likelihood of developing the disease. Multiple linear regression analysis revealed that age, place of residence, education, and employment status significantly contribute to AD knowledge scores.Conclusions: This study highlights the urgent need for public education and awareness campaigns to address the knowledge gap and reduce stigmatization associated with AD in Bangladesh. Targeted efforts, particularly among older age groups and rural communities, can enhance understanding and improve the quality of care and support for AD patients and their caregivers.

The aggregation of amyloid-β (Aβ) peptides into decrepit plaques is distinctive of Alzheimer’s disease (AD). Aggregated Aβ fibrils are neurotoxic to the brain. This deposition of aggregates is central to AD-related neurodegeneration. Conforming to literature, amino acid residues KLVFF (16–20) in the Aβ monomer self-associate to form antiparallel β-sheet fibrils. Small molecules binding to the Aβ16–20 regions of Aβ42 can inhibit the self-assembly and disrupt Aβ fibril. Naturally occurring flavonols have shown the potential to inhibit protein aggregates found in AD. Present work investigated flavonols in complex with amyloid monomer, Aβm, and amyloid fibril Aβf using docking, followed by 100 ns molecular dynamics simulation (MDS) of the best docked Aβm-flavonol and Aβf-flavonol complexes. Molecular Mechanics Poisson–Boltzmann Surface Area (MMPBSA) method estimated the binding free energy of these complexes from MDS trajectories. These in-silico methods provided atomistic-detailed information about the binding and inhibitory properties of the selected wine-related flavonols, kaempferol (KAE), myricetin (MYR), morin (MOR), and quercetin (QUE). This selection of the flavonols was based on the structural variations in the number and placement of hydroxyl groups on the flavonoid backbone. These flavonols interacted with the residues in the hydrophobic region (Lys16 to Ala21) of the Aβm and Aβf to form complexes.

Liver fibrosis, developed in almost all chronic liver injuries. Epidermal growth factor receptors (EGFR) have been thought to contribute to cirrhosis and liver fibrosis. Therefore, using a rat model of carbon tetrachloride (CCl4)-induced liver fibrogenesis, we investigated the preventive effects of cetuximab, an inhibitor of the EGF receptor (EGFR). Ameliorative effects of cetuximab were examined in rats, brought on by biweekly doses of 50 mg/kg of carbon tetrachloride (CCl4). There were a total of 24 male Long Evans rats split up into four distinct groups such as control, CCl4,control+cetuximab and CCl4+cetuximab. After two weeks of treatment with cetuximab (100 microgram/kg), samples of tissue and blood were taken after all the rats had been sacrificed. Plasma samples were examined for the biochemical indicators of inflammation and oxidative stress. Histological staining on liver sections was performed for morphologic pathologies, and related genes expressions analysis were done with RT-PCR in liver tissue. The findings showed that cetuximab could raise the levels of glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) and considerably lower the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), malondialdehyde (MDA), and nitric oxide (NO). Sirius red staining and hematoxylin-eosin (H&E) displayed that cetuximab therapy reduced the inflammatory cells infiltration and enhanced fibrotic lesions. In the meantime, cetuximab therapy also dramatically reduces the expression of genes linked to inflammation in the liver tissue, including NF-кB, iNOS, IL-6, TNF-α, and TGF-β. To sum up, the anti-inflammatory, antifibrotic, and antioxidant properties of cetuximab confer curative efficacy against liver fibrosis.

The Forcibly Displaced Myanmar Nationals (FDMNs) residing in refugee camps face various health challenges, including a rising prevalence of scabies, exacerbated by overcrowded conditions and limited healthcare access. This study aims to assess scabies prevalence, clinical features, and environmental factors among FDMNs, aiding interventions and recommendations for better health outcomes.

Climate-induced displacement is one of the major challenges of the 21st century for the international community. The complex situations of climateinduced displacement raise questions about how well current international legal frameworks truly protect people who are displaced by the adverse impacts of climate change. The Paris Agreement is the latest international treaty adopted under the climate change regime. It has recognised the linkage between climate change and displacement. However, the Paris Agreement is not sufficient to address climate-induced displacement and other existing international legal frameworks do not fill the gaps. To protect the climate-displaced people, it is necessary to take some robust steps. Such vigorous measures could be done by adding a Protocol to the United Nations Framework Convention on Climate Change or by amending the Convention Relating to the Status of Refugees 1951. The international community should build consensus for possible solutions to address climate-induced displacement. [ABSTRACT FROM AUTHOR]

α-Synuclein is an intrinsically disordered protein whose function in a healthy brain is poorly understood. It is genetically and neuropathologically linked to Parkinson’s disease (PD). PD is manifested after the accumulation of plaques of α-synuclein aggregates in the brain cells. Aggregates of α-synuclein are very toxic and lead to the disruption of cellular homeostasis and neuronal death. α-Synuclein can also contribute to disease propagation as it may exert noxious effects on neighboring cells. Understanding the mechanism of α-synuclein aggregation will facilitate the problem of dealing with neurodegenerative diseases in general and that of PD in particular. Here, we have used molecular dynamics simulations to investigate the behavior of α-synuclein at various temperatures and in different concentrations of urea and trimethyl amine oxide. The residue region from 61 to 95 of α-synuclein is experimentally known as amyloidogenic. In our study, we have identified some other regions, which also have the propensity to form an aggregate besides this known sequence. Urea being a denaturant interacts more with these regions of α-synuclein through hydrogen bond formation and inhibits the β-sheet formation, whereas trimethyl amine oxide itself does not interact much with the protein and stabilizes the protein by preferentially distributing water molecules on the surface of the protein.

An early sign of islet failure in type 2 diabetes (T2D) is the loss of normal patterns of pulsatile insulin release. Disruptions in pulsatility are associated with a left shift in glucose sensing that can cause excessive insulin release in low glucose (relative hyperinsulinemia, a hallmark of early T2D) and β-cell exhaustion, leading to inadequate insulin release during hyperglycemia. Our hypothesis was that reducing excessive glucokinase activity in diabetic islets would improve their function. Isolated mouse islets were exposed to glucose and varying concentrations of the glucokinase inhibitor d-mannoheptulose (MH) to examine changes in intracellular calcium ([Ca2+]i) and insulin secretion. Acutely exposing islets from control CD-1 mice to MH in high glucose (20 mM) dose dependently reduced the size of [Ca2+]i oscillations detected by fura-2 acetoxymethyl. Glucokinase activation in low glucose (3 mM) had the opposite effect. We then treated islets from male and female db/db mice (age, 4 to 8 weeks) and heterozygous controls overnight with 0 to 10 mM MH to determine that 1 mM MH produced optimal oscillations. We then used 1 mM MH overnight to measure [Ca2+]i and insulin simultaneously in db/db islets. MH restored oscillations and increased insulin secretion. Insulin secretion rates correlated with MH-induced increases in amplitude of [Ca2+]i oscillations (R2 = 0.57, P < 0.01, n = 10) but not with mean [Ca2+]i levels in islets (R2 = 0.05, not significant). Our findings show that correcting glucose sensing can restore proper pulsatility to diabetic islets and improved pulsatility correlates with enhanced insulin secretion.

The relationship between gastrointestinal tract infection, the host immune response, and the clinical outcome of disease is not well understood in COVID-19. We sought to understand the effect of intestinal immune responses to SARS-CoV-2 on patient outcomes including the magnitude of systemic antibody induction. Combining two prospective cohort studies, ISARIC4C and INSTINCT, we acquired samples from 88 COVID-19 cases representing the full spectrum of disease severity and analysed viral RNA and host gut cytokine responses in the context of clinical and virological outcome measures. There was no correlation between the upper respiratory tract and faecal viral loads. Using hierarchical clustering, we identified a group of fecal cytokines including Interleukin-17A, Granulocyte macrophage colony-stimulating factor, Tumor necrosis factorα, Interleukin-23, and S100A8, that were transiently elevated in mild cases and also correlated with the magnitude of systemic anti-Spike-receptor-binding domain antibody induction. Receiver operating characteristic curve analysis showed that expression of these gut cytokines at study enrolment in hospitalised COVID-19 cases was associated negatively with overall clinical severity implicating a protective role in COVID-19. This suggests that a productive intestinal immune response may be beneficial in the response to a respiratory pathogen and a biomarker of a successful barrier response.

(Abstracted from N Engl J Med2018;379:535–546)It is unclear whether maternal vitamin D supplementation during pregnancy and lactation improves fetal and infant growth in regions where vitamin D deficiency is common.

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