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Preterm birth (gestational age < 37 weeks) is a public health concern that causes fetal and maternal mortality and morbidity. When this condition is detected early, suitable treatment can be prescribed to delay labour. Uterine electromyography (uEMG) has gained a lot of attention for detecting preterm births in advance. However, analyzing uEMG is challenging due to the complexities associated with inter and intra-subject variations. This work aims to investigate the applicability of cyclostationary characteristics in uEMG signals for predicting premature delivery. The signals under term and preterm situations are considered from two online datasets. Preprocessing is carried out using a Butterworth bandpass filter, and spectral correlation density function is adapted using fast Fourier transform-based accumulation method (FAM) to compute the cyclostationary variations. The cyclic frequency spectral density (CFSD) and degree of cyclostationarity (DCS) are quantified to assess the existence of cyclostationarity. Features namely, maximum cyclic frequency, bandwidth, mean cyclic frequency (MNCF), and median cyclic frequency (MDCF) are extracted from the cyclostationary spectrum and analyzed statistically. uEMG signals exhibit cyclostationarity property, and these variations are found to distinguish preterm from term conditions. All the four extracted features are noted to decrease from term to preterm conditions. The results indicate that the cyclostationary nature of the signals can provide better characterization of uterine muscle contractions and could be helpful in detecting preterm birth. The proposed method appears to aid in detecting preterm birth, as analysis of uterine contractions under preterm conditions is imperative for timely medical intervention.

In response to tissue injury, within seconds the ultra-large glycoprotein von Willebrand factor (VWF) is released from endothelial storage organelles (Weibel−Palade bodies) into the lumen of the blood vasculature, where it leads to the recruitment of platelets. The marked size of VWF multimers represents an unprecedented burden on the secretory machinery of endothelial cells (ECs). ECs have evolved mechanisms to overcome this, most notably an actomyosin ring that forms, contracts, and squeezes out its unwieldy cargo. Inhibiting the formation or function of these structures represents a novel therapeutic target for thrombotic pathologies, although characterizing proteins associated with such a dynamic process has been challenging. We have combined APEX2 proximity labeling with an innovative dual loss-of-function screen to identify proteins associated with actomyosin ring function. We show that p21 activated kinase 2 (PAK2) recruits septin hetero-oligomers, a molecular interaction that forms a ring around exocytic sites. This cascade of events controls actomyosin ring function, aiding efficient exocytic release. Genetic or pharmacological inhibition of PAK2 or septins led to inefficient release of VWF and a failure to form platelet-catching strings. This new molecular mechanism offers additional therapeutic targets for the control of thrombotic disease and is highly relevant to other secretory systems that employ exocytic actomyosin machinery.

Hematopoietic stem cell (HSC) activity is tightly controlled to ensure the integrity of the hematopoietic system during the organism's lifetime. How the HSC compartment maintains its long-term fitness in conditions of chronic stresses associated with systemic metabolic disorders is poorly understood. In this study, we show that obesity functionally affects the long-term function of the most immature engrafting HSC subpopulation. We link this altered regenerative activity to the oxidative stress and the aberrant constitutive activation of the AKT signaling pathway that characterized the obese environment. In contrast, we found minor disruptions of the HSC function in obese mice at steady state, suggesting that active mechanisms could protect the HSC compartment from its disturbed environment. Consistent with this idea, we found that FOXO proteins in HSCs isolated from obese mice become insensitive to their normal upstream regulators such as AKT, even during intense oxidative stress. We established that hyperglycemia, a key condition associated with obesity, is directly responsible for the alteration of the AKT-FOXO axis in HSCs and their abnormal oxidative stress response. As a consequence, we observed that HSCs isolated from a hyperglycemic environment display enhanced resistance to oxidative stress and DNA damage. Altogether, these results indicate that chronic metabolic stresses associated with obesity and/or hyperglycemia affect the wiring of the HSCs and modify their oxidative stress response. These data suggest that the uncoupling of FOXO from its environmental regulators could be a key adaptive strategy that promotes the survival of the HSC compartment in obesity.

Ginseng is popularly known to be the king of ancient medicines and is used widely in most of the traditional medicinal compositions due to its various pharmaceutical properties. Numerous studies are being focused on this plant's curative effects to discover their potential health benefits in most human diseases, including cancer— the most life-threatening disease worldwide. Modern pharmacological research has focused mainly on ginsenosides, the major bioactive compounds of ginseng, because of their multiple therapeutic applications. Various issues on ginseng plant development, physiological processes, and agricultural issues have also been studied widely through state-of-the-art, high-throughput sequencing technologies. Since the beginning of the 21st century, the number of publications on ginseng has rapidly increased, with a recent count of more than 6,000 articles and reviews focusing notably on ginseng. Owing to the implementation of various technologies and continuous efforts, the ginseng plant genomes have been decoded effectively in recent years. Therefore, this review focuses mainly on the cellular biomolecular sequences in ginseng plants from the perspective of the central molecular dogma, with an emphasis on genomes, transcriptomes, and proteomes, together with a few other related studies.

The plant–parasitic Root Knot Nematodes (Meloidogynespp.,) play a pivotal role to devastate vegetable crops across the globe. Considering the significance of plant–microbe interaction in the suppression of Root Knot Nematode, we investigated the diversity of microbiome associated with bioagents-treated and nematode-infected rhizosphere soil samples through metagenomics approach. The wide variety of organisms spread across different ecosystems showed the highest average abundance within each taxonomic level. In the rhizosphere, Proteobacteria, Firmicutes, and Actinobacteria were the dominant bacterial taxa, while Ascomycota, Basidiomycota, and Mucoromycota were prevalent among the fungal taxa. Regardless of the specific treatments, bacterial genera like Bacillus, Sphingomonas, and Pseudomonaswere consistently found in high abundance. Shannon diversity index vividly ensured that, bacterial communities were maximum in B. velezensisVB7-treated soil (1.4–2.4), followed by Root Knot Nematode-associated soils (1.3–2.2), whereas richness was higher with Trichoderma konigiopsisTK drenched soils (1.3–2.0). The predominant occurrence of fungal genera such as Aspergillus Epicoccum, Choanephora, Alternariaand Thanatephorushabituate rhizosphere soils. Shannon index expressed the abundant richness of fungal species in treated samples (1.04–0.90). Further, refraction and species diversity curve also depicted a significant increase with maximum diversity of fungal species in B. velezensisVB7-treated soil than T. koningiopsisand nematode-infested soil. In field trial, bioagents-treated tomato plant (60% reduction of Meloidogyne incognitainfection) had reduced gall index along with enhanced plant growth and increased fruit yield in comparison with the untreated plant. Hence, B. velezensisVB7 and T. koingiopsiscan be well explored as an antinemic bioagents against RKN.

The dynamics of the hematopoietic flux responsible for blood cell production in native conditions remains a matter of debate. Using CITE-seq analyses, we uncovered a distinct progenitor population that displays a cell cycle gene signature similar to the one found in quiescent hematopoietic stem cells. We further determined that the CD62L marker can be used to phenotypically enrich this population in the Flt3+ multipotent progenitor (MPP4) compartment. Functional in vitro and in vivo analyses validated the heterogeneity of the MPP4 compartment and established the quiescent/slow-cycling properties of the CD62L− MPP4 cells. Furthermore, studies under native conditions revealed a novel hierarchical organization of the MPP compartments in which quiescent/slow-cycling MPP4 cells sustain a prolonged hematopoietic activity at steady-state while giving rise to other lineage-biased MPP populations. Altogether, our data characterize a durable and productive quiescent/slow-cycling hematopoietic intermediary within the MPP4 compartment and highlight early paths of progenitor differentiation during unperturbed hematopoiesis.

Obesity is a chronic organismal stress that disrupts multiple systemic and tissue-specific functions. In this study, we describe the impact of obesity on the activity of the hematopoietic stem cell (HSC) compartment. We show that obesity alters the composition of the HSC compartment and its activity in response to hematopoietic stress. The impact of obesity on HSC function is progressively acquired but persists after weight loss or transplantation into a normal environment. Mechanistically, we establish that the oxidative stress induced by obesity dysregulates the expression of the transcription factor Gfi1 and that increased Gfi1 expression is required for the abnormal HSC function induced by obesity. These results demonstrate that obesity produces durable changes in HSC function and phenotype and that elevation of Gfi1 expression in response to the oxidative environment is a key driver of the altered HSC properties observed in obesity. Altogether, these data provide phenotypic and mechanistic insight into durable hematopoietic dysregulations resulting from obesity.