With less than two years remaining from 2027-the year which the government has targeted to achieve zero Indigenous cases, we map the malaria indicators across the 700 + districts for five years betwee Show more
With less than two years remaining from 2027-the year which the government has targeted to achieve zero Indigenous cases, we map the malaria indicators across the 700 + districts for five years between 2019 and 2023 using spatiotemporal maps and also assess the potential drivers of malaria transmission in different regions. We used the annual district-wise malaria data from the National Center for Vector Borne Disease Control Programme (NCVBDC) and the cross-sectional socio-economic data from the National Family Health Survey. We also collated the meteorological and land-use land-cover data from the MERRA-2 and Sentinel-LPA satellites, respectively. We then developed region-specific ensembles of spatiotemporal models that allowed us to identify the associated covariates while the regions were identified using the Getis-Ord Gi* statistics. With 0.33 million malaria cases in 2019, the COVID-19 pandemic led to a significant reduction in reported cases. The P. falciparum affected regions are widespread in North-eastern and Central India. However, after the pandemic, an emerging geographical expansion into the north-eastern parts is observed for the P. vivax, which is evident from the clusters and the spatiotemporal ensemble models. Population belonging to scheduled castes and scheduled tribes and those economically marginalised are among the most vulnerable, but lifestyle habits such as drinking water practices, maternal education, and healthcare accessibility are associated with malaria transmission. We also developed a digital dashboard that allows the general public and the stakeholders to track the malaria indicators for each district and the corresponding year. Show less
Most published results have revealed variations in the association of serum/plasma levels of malondialdehyde (MDA), apolipoprotein B (ApoB), and oxidized low-density lipoprotein (OxLDL) and systemic l Show more
Most published results have revealed variations in the association of serum/plasma levels of malondialdehyde (MDA), apolipoprotein B (ApoB), and oxidized low-density lipoprotein (OxLDL) and systemic lupus erythematosus (SLE). This study was performed to establish MDA, ApoB, and OxLDL levels in systemic lupus erythematosus (SLE) patients. Electronic databases were searched for the included articles up to 27th February 2023. The meta-analysis included 48 articles with 2358 SLE patients and 2126 healthy controls considered for MDA, ApoB, and OxLDL levels. There were significantly higher MDA, ApoB, and OxLDL levels in SLE patients than those in the control groups. Subgroup analysis indicated that European/American SLE patients and patients of both ages <36 and ≥36 exhibited higher MDA, ApoB, and OxLDL levels. Arab and Asian SLE patients had higher ApoB and MDA/OxLDL levels. African SLE patients recorded higher OxLDL levels than the control groups. SLE patients with a body mass index (BMI) of ≥23 and a disease duration of <10 recorded significantly higher MDA, ApoB, and OxLDL levels. Patients with systemic lupus erythematosus disease activity index (SLEDAI) ≥8 of SLE had higher MDA and ApoB levels, whereas SLE patients with SLEDAI <8 showed significantly higher ApoB levels. Patients with BMI <23 of SLE had higher MDA and OxLDL levels. This study established significantly higher MDA, ApoB, and OxLDL levels in SLE patients, suggesting a possible role of MDA, ApoB, and OxLDL in the disease. Show less
Mutations in GATA6 are associated with congenital heart disease, most notably conotruncal structural defects. However, how GATA6 regulates cardiac morphology during embryogenesis is undefined. We used Show more
Mutations in GATA6 are associated with congenital heart disease, most notably conotruncal structural defects. However, how GATA6 regulates cardiac morphology during embryogenesis is undefined. We used knockout and conditional mutant zebrafish alleles to investigate the spatiotemporal role of gata6 during cardiogenesis. Loss of gata6 specifically impacts atrioventricular valve formation and recruitment of epicardium, with a prominent loss of arterial pole cardiac cells, including those of the ventricle and outflow tract. However, there are no obvious defects in cardiac progenitor cell specification, proliferation or death. Conditional loss of gata6 starting at 24 h is sufficient to disrupt the addition of late differentiating cardiomyocytes at the arterial pole, with decreased expression levels of anterior secondary heart field (SHF) markers spry4 and mef2cb. Conditional loss of gata6 in the endoderm is sufficient to phenocopy the straight knockout, resulting in a significant loss of ventricular and outflow tract tissue. Exposure to a Dusp6 inhibitor largely rescues the loss of ventricular cells in gata6-/- larvae. Thus, gata6 functions in endoderm are mediated by FGF signaling to regulate the addition of anterior SHF progenitor derivatives during heart formation. Show less