A Review of Government Schemes for Pregnant and Lactating Women in India

India’s current Maternal and Child Health Nutrition (MCHN) statistics reflect poorly of the country’s existing government programme. Experts recognize the phase of pregnancy and lactation as a critical window of opportunity for influencing the MCHN status. A clear identification and clinical assessment of government schemes/ programme that may have an impact on pregnant and lactating women can assist in identifying the strength, weakness, opportunities and threats in these interventions. The objective of the study was to review the government schemes for pregnant and lactating women. A review of all government programme and policies in areas of MCHN was undertaken using multiple strategies namely electronic reference libraries, journals, research papers and reports. The finding of paper identified the strength and weakness of government schemes and it proposes a coping strategy which might be useful for the policy makers in making the programme more enriching in order to implement the program with full potential. The threat analysis of these interventions has shown scope of improvement and areas of learning. The Indian government has implemented a number of measures that have a significant impact on pregnant and lactating women. However interventions focusing on health care needs, immunization, financial benefits are needed to increase the nutrition component. The necessity of nutrition was solely recognized in terms of providing adequate food, with no emphasis on macro and micro nutrients. This is an area where intervention should be strengthened. Index Terms: Government health schemes, Lactating mothers, pregnant women, Nutritional status, SWOT analysis.

The MAP Kinase Phosphatase MKP-1 Modulates Neurogenesis via Effects on BNIP3 and Autophagy

Inherited and acquired defects in neurogenesis contribute to neurodevelopmental disorders, dysfunctional neural plasticity, and may underlie pathology in a range of neurodegenerative conditions. Mitogen-activated protein kinases (MAPKs) regulate the proliferation, survival, and differentiation of neural stem cells. While the balance between MAPKs and the family of MAPK dual-specificity phosphatases (DUSPs) regulates axon branching and synaptic plasticity, the specific role that DUSPs play in neurogenesis remains unexplored. In the current study, we asked whether the canonical DUSP, MAP Kinase Phosphatase-1 (MKP-1), influences neural stem cell differentiation and the extent to which DUSP-dependent autophagy is operational in this context. Under basal conditions, Mkp-1 knockout mice generated fewer doublecortin (DCX) positive neurons within the dentate gyrus (DG) characterized by the accumulation of LC3 puncta. Analyses of wild-type neural stem cell (NSC) differentiation in vitro revealed increased Mkp-1 mRNA expression during the initial 24-h period. Notably, Mkp-1 KO NSC differentiation produced fewer Tuj1-positive neurons and was associated with increased expression of the BCL2/adenovirus E1B 19-kD protein-interacting protein 3 (BNIP3) and levels of autophagy. Conversely, Bnip3 knockdown in differentiated Mkp-1 KO NSCs reduced levels of autophagy and increased neuronal yields. These results indicate that MKP-1 exerts a pro-neurogenic bias during a critical window in NSC differentiation by regulating BNIP3 and basal autophagy levels.

Spatially and Temporally Resolved Ambient PM2.5 in Relation to Preterm Birth

Growing evidence suggests that maternal exposure to ambient fine particulate matter (PM2.5) during pregnancy is associated with preterm birth; however, few studies have examined critical windows of exposure, which can help elucidate underlying biologic mechanisms and inform public health messaging for limiting exposure. Participants included 891 mother–newborn pairs enrolled in a U.S.-based pregnancy cohort study. Daily residential PM2.5 concentrations at a 1 × 1 km2 resolution were estimated using a satellite-based hybrid model. Gestational age at birth was abstracted from electronic medical records and preterm birth (PTB) was defined as <37 completed weeks of gestation. We used Critical Window Variable Selection to examine weekly PM2.5 exposure in relation to the odds of PTB and examined sex-specific associations using stratified models. The mean ± standard deviation PM2.5 level averaged across pregnancy was 8.13 ± 1.10 µg/m3. PM2.5 exposure was not associated with an increased odds of PTB during any gestational week. In sex-stratified models, we observed a marginal increase in the odds of PTB with exposure occurring during gestational week 16 among female infants only. This study does not provide strong evidence supporting an association between weekly exposure to PM2.5 and preterm birth.

Orbital Parameters and Binary Properties of 37 FGK Stars in the Cores of Open Clusters NGC 2516 and NGC 2422

We present orbits for 24 binaries in the field of open cluster NGC 2516 (∼150 Myr) and 13 binaries in the field of open cluster NGC 2422 (∼130 Myr) using results from a multiyear radial-velocity (RV) survey of the cluster cores. Six of these systems are double-lined spectroscopic binaries. We fit these RV variable systems with orvara, a MCMC-based fitting program that models Keplerian orbits. We use precise stellar parallaxes and proper motions from Gaia EDR3 to determine cluster membership. We impose a barycentric RV prior on all cluster members; this significantly improves our orbital constraints. Two of our systems have periods between five and 15 days, the critical window in which tides efficiently damp orbital eccentricity. These binaries should be included in future analyses of circularization across similarly-aged clusters. We also find a relatively flat distribution of binary mass ratios, consistent with previous work. With the inclusion of TESS light curves for all available targets, we identity target 378–036252 as a new eclipsing binary. We also identify a field star whose secondary has a mass in the brown dwarf range, as well as two cluster members whose RVs suggest the presence of an additional companion. Our orbital fits will help constrain the binary fraction and binary properties across stellar age and across stellar environment.

Sequestration of LINE-1 in novel cytosolic bodies by MOV10 restricts retrotransposition

LINE-1 (L1) are autonomous retroelements that have retained their ability to mobilize. Mechanisms regulating L1 mobility include DNA methylation in somatic cells and the Piwi-interacting RNA pathway in the germline. During pre-implantation stages of mouse embryonic development, however, both pathways are inactivated leading to a critical window necessitating alternate means of L1 regulation. We previously reported an increase in L1 levels in Dicer_KO mouse embryonic stem cells (mESCs). Intriguingly this was accompanied by only a marginal increase in retrotransposition, suggestive of additional mechanisms suppressing L1 mobility. Here, we demonstrate that L1 Ribonucleoprotein complexes (L1 RNP) accumulate as aggregates in Dicer_KO cytoplasm along with the RNA helicase MOV10. The combined overexpression of L1 RNAs and MOV10 is sufficient to create L1 RNP aggregates in stem cells. In Dicer_KO mESCs, MOV10 is upregulated due to the loss of its direct regulation by miRNAs. The newly discovered post-transcriptional regulation of Mov10 expression, and its role in preventing L1 retrotransposition by driving novel cytosolic aggregation affords alternate routes to explore for therapy and disease progression.

One Year Follow-Up of Taste-Related Reward Associations with Weight Loss Suggests a Critical Time to Mitigate Weight Regain Following Bariatric Surgery

Background: Weight regain is a concerning issue in bariatric patients. We previously demonstrated that taste-related reward processing was associated with six-month weight loss outcomes following Roux-en-Y gastric bypass (RYGB) but not vertical sleeve gastrectomy (VSG). Here, we assessed whether these taste factors persisted in predicting weight loss, and weight regain, at one year post-surgery. Methods: Adult women enrolled in a longitudinal study of taste preferences following bariatric surgery completed behavioral and neuroimaging assessments at one year post-surgery. Results: RYGB produced better weight loss relative to VSG, with weight regain and greater weight loss variability observed from six months to one year post-VSG. Changes in liking for high fat at 2 weeks post-surgery from baseline remained a predictor of weight loss in RYGB, but other predictors did not persist. Average liking ratings rebounded to baseline and higher self-reported food cravings and dietary disinhibition correlated with poorer weight loss at one year post-surgery. Conclusion: Initial anatomical and metabolic changes resulting from RYGB that reset neural processing of reward stimuli in the mesolimbic pathway appear to be temporary and may be contingent upon post-operative eating behaviors returning to preoperative obesogenic tendencies. Six months post-surgery may be a critical window for implementing interventions to mitigate weight gain.

Post-mitotic accumulation of histone variant H3.3 in new cortical neurons establishes neuronal transcriptome, identity, and connectivity

Histone variants, which can be expressed outside of S-phase and deposited DNA synthesis-independently, provide replacement histones in terminally post-mitotic cells, including neurons. Histone variants can also serve active roles in gene regulation by modulating chromatin states or enabling nucleosome turnover at regulatory regions. Here, we find that newborn cortical excitatory neurons substantially accumulate the histone H3 variant H3.3 immediately post-mitosis. Co-deletion of H3.3-encoding genes H3f3a and H3f3b from new neurons abrogates this accumulation, and causes widespread disruptions in the developmental establishment of the neuronal transcriptome. These broad transcriptomic changes coincide with neuronal maturation phenotypes in acquisition of distinct neuronal identities and formation of axon tracts. Stage-dependent deletion of H3f3a and H3f3b from (1) cycling neural progenitor cells, (2) neurons immediately after terminal mitosis, or (3) several days later, reveals the first post-mitotic days as a critical window for de novo H3.3. After H3.3 accumulation within this developmental window, co-deletion of H3f3a and H3f3b from neurons causes progressive H3.3 depletion over several months without widespread transcriptional disruptions. Our study thus uncovers a key role for H3.3 in establishing neuronal transcriptome, identity, and connectivity immediately post-mitosis that is distinct from its role in maintaining total histone H3 levels over the neuronal lifespan.

Maternal SMCHD1 controls both imprinted Xist expression and imprinted X chromosome inactivation

Embryonic development is dependent on the maternal supply of proteins through the oocyte, including factors setting up the adequate epigenetic patterning of the zygotic genome. We previously reported that one such factor is the epigenetic repressor SMCHD1, whose maternal supply controls autosomal imprinted expression in mouse preimplantation embryos and mid-gestation placenta. In mouse preimplantation embryos, X chromosome inactivation is also an imprinted process. Combining genomics and imaging, we show that maternal SMCHD1 is required not only for the imprinted expression of Xist in preimplantation embryos, but also for the efficient silencing of the inactive X in both the preimplantation embryo and mid-gestation placenta. These results expand the role of SMCHD1 in enforcing the silencing of Polycomb targets. The inability of zygotic SMCHD1 to fully restore imprinted X inactivation further points to maternal SMCHD1's role in setting up the appropriate chromatin environment during preimplantation development, a critical window of epigenetic remodelling.

The critical window in random digraphs

We consider the component structure of the random digraph D(n,p) inside the critical window $p = n^{-1} + \lambda n^{-4/3}$ . We show that the largest component $\mathcal{C}_1$ has size of order $n^{1/3}$ in this range. In particular we give explicit bounds on the tail probabilities of $|\mathcal{C}_1|n^{-1/3}$ .