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Agro-morphological attributes are the key parameters for evaluating field crops including fodders. The genetic divergence of cereal forages provide sustainability to modern intensive production systems in the worlds. Changing climate situation is challenging for sorghum and other field crops. Therefore, characterization of agro-morphological attributes of sorghum is crucial for plant fitness, adaptability, livestock and human food supply in the worlds. A field study in the regular arrangement of randomized complete block design (RCBD) with three replications was conducted at the experimental farm, RCA, Udaipur. The study was aimed to evaluate and characterize sixteen multi-cut fodder sorghum genotypes for various agro-morphological traits. As per recorded data, genotypes displayed significant variability for various traits. Additionally, green fodder yield (GFY) at first cut manifested significant and positive association with regeneration score whereas genotypic and phenotypic coefficient variation (GCV & PCV) remained high for dry fodder yield at second cut. Furthermore, high heritability (h2) along with high expected genetic gains were exhibited by dry fodder yield at second cut. Moreover, plant height exhibited the maximum direct effect on green fodder yield at first cut followed by regeneration ability score and leaf: stem ratio. To conclude, genotype SPH-1877 showed better performance for green fodder and dry fodder yield, and also exhibited better regeneration score compared to the rest of the genotypes. This study suggests that the best sorghum cultivar with better agro-morphological and yield related traits can be useful for sustainable sorghum production and ensuring the fodder supply for livestock. [ABSTRACT FROM AUTHOR]

Present investigation was made to study the nature and magnitude of genetic divergence in 66 foxtail millet genotypes using multivariate analysis through Mahalanobis „D² statistics. The analysis suggested considerable genetic divergence among thematerial. D² statistics resulted in five clusters. Based on relative magnitude of D², the genotypes were grouped into five different non-overlapping clusters. Cluster I, having 36 genotypes, emerged with highest number of entries; cluster II were constituted by 15 genotypes. Cluster III comprising 13 genotypes. Cluster IV and V having one genotype each. The maximum intra-cluster distance was observed for cluster II, followed by cluster III and cluster I. The highest inter-cluster distance was recorded between cluster IV and III followed by cluster IV and V, then cluster IV and I followed by cluster IIIand I. Among the 13 characters studied highest contribution in manifestation of genetic divergence was exhibited by grainiron content (ppm) followed by flag leaf length, grain zinc content (ppm), straw weight, flag leaf area, plant height, flag leafwidth, panicle weight and grain yield. [ABSTRACT FROM AUTHOR]

Compares the commercial source of drug information in Great Britain and India. Factors affecting the commercial scarce of drug information; Therapeutic differences between the drugs and drug groups; Side effects of the drug.

Tourette syndrome, characterized by phonic and motor tics, is a neurodevelopmental disorder that significantly affects the quality of life of people with the condition. With over 1500 articles published in the last decade alone, this study aims to analyze the gender trends in publications related to Tourette syndrome from 2013 to 2022, examining the number of female authors as first authors and predicting future changes in female participation. The aim of this study is to analyze the gender trends of the first author in publications related to "Tourette Syndrome" from PubMed-indexed publications from January 2013 to December 2022. A bibliometric analysis was conducted by the search engine PubMed for articles pertaining to "Tourette Syndrome". NamSor app V.2 (Namsor™ Applied Onomastics, NamSor SAS, Versailles, France), an application programming interface (API), was used to identify the gender of the first publishing author. Statistical analysis and graphic models were produced using R software (R Foundation for Statistical Computing, Vienna, Austria), ARIMA (Autoregressive Integrated Moving Average) model, and DataWrapper (Datawrapper GmbH, Berlin Prenzlauer Berg, Germany). Based on the analysis of 1052 publications on Tourette Syndrome, it was found that 54.8% (n=576) of the first authors were females. A significant association was observed between gender ratios and country of publication. Statistical forecasting models suggest that female participation in Tourette research is expected to rise to approximately 60 by the year 2027. Therefore, the study highlights the progress made in achieving gender parity in Tourette syndrome research, with female-led publications being on par with male-led publications. However, there is still a need to address the global gender gap and geographical disparities in research to work towards a more inclusive and diverse academic environment., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2024, Mahajan et al.)

Aims: The aim of this study was to characterise and compare the biopsychosocial characteristics of children admitted with failure to thrive (FTT), subdivided into those with underlying medical complexities (categorised as organic FTT - OFTT) and those with none (categorised as non-organic FTT - NOFTT), with a focus on the medical, nutritional, feeding skills and psychosocial domains., Methods: A retrospective review of medical records was conducted in children admitted with FTT from January 2010 to December 2020. Descriptive statistics were used for data analysis., Results: A total of 353 children were included, with the mean age of presentation 0.82 ± 2.05 years (OFTT 1.16 ± 2.50 years, NOFTT 0.49 ± 1.41 years, P = 0.002). Approximately, half of the children were classified as having OFTT. These children had lower birth weights, were more likely to have a history of intrauterine growth restriction and had longer hospital stays. The NOFTT group had significantly more abnormal feeding strategies identified in their caregivers, whereas the OFTT group had more delayed feeding skills and oral aversion. There was no significant difference in psychosocial domains, with both groups having a comparably high risk of abuse and neglect., Conclusions: The classification of FTT as non-organic or organic based purely on psychosocial parameters did not reflect the complex nature of FTT within our local population. These groups had different medical variables, and caregiver feeding strategies. A multidisciplinary team approach is recommended for the assessment and intervention for children with FTT to address these domains and the complex interactions between them., (© 2023 The Authors. Journal of Paediatrics and Child Health published by John Wiley & Sons Australia, Ltd on behalf of Paediatrics and Child Health Division (The Royal Australasian College of Physicians).)

Studies in spontaneously hypertensive rat had revealed an elevated level of ACE gene expression in the tissues and is substantiated by experimental clinical studies for a positive correlation between ACE I/D polymorphism and hypertension. Aim: To determine whether the polymorphic variant of ACE gene in intron 16 confers susceptibility to essential hypertension. I/D polymorphism at the locus intron 16 of the ACE gene were amplified from the genomic DNA of the total 571 (hypertensive patients, n: 279; controls, n: 292) participants using polymerase chain reaction and gel electrophoresis methods and were examined in a case-control approach. Suitable descriptive statistics was used for different variables. Result revealed significant heterogeneity under the allele ( p : 0.0002) and genotype ( p : 0.0001) contrast in hypertensive patients than in normal controls, with an increased frequency of D allele (62.72%; p  < 0.0001; OR: 1.8144; 95% CI: 1.4327-2.2979) and DD genotype (41.93%; p : < 0.0001). A significant association was found in the DD variant with disease phenotype ( p : 0.0018, 95% CI: 1.3303-3.4907; OR: 2.1549; Table 31) and is substantiated by the data of multivariate analysis, demonstrating a statistically significant increase in odds of hypertension with the ACE D/D genotype (OR: 2.09; 95% CI: 1.24-2.91). Conspicuously, subgroup analysis by gender did not change this pattern of results. Albeit the allele distribution resulted in a higher frequency of the D/D genotype in the cases than controls, testing genetic equilibrium between the observed and expected genotypes using Hardy-Weinberg equilibrium showed ACE gene variants were confirming to the law in hypertensive as well as in non-hypertensive participants. I/D polymorphism in the angiotensin-I-converting enzyme gene at the 16th intron can be useful for outcome predictions during diagnostic processes can be implicated in an individual's propensity for hypertension and thus implies that genetic variants of ACE I/D might serve as a predictor for the susceptibility to hypertension., (© Association of Clinical Biochemists of India 2020.)

Inflammasomes have been implicated in the detection and clearance of a variety of bacterial pathogens, but little is known about whether this innate sensing mechanism has any regulatory effect on the expression of stimulatory ligands by the pathogen. During infection with Salmonella and many other pathogens, flagellin is a major activator of NLRC4 inflammasome-mediated macrophage pyroptosis and pathogen eradication. Salmonella switches to a flagellin-low phenotype as infection progresses to avoid this mechanism of clearance by the host. However, the host cues that Salmonella perceives to undergo this switch remain unclear. Here, we report an unexpected role of the NLRC4 inflammasome in promoting expression of its microbial ligand, flagellin, and identify a role for type 1 IFN signaling in switching of Salmonella to a flagellin-low phenotype. Early in infection, activation of NLRC4 by flagellin initiates pyroptosis and concomitant release of lysophospholipids which in turn enhance expression of flagellin by Salmonella thereby amplifying its ability to elicit cell death. TRIF-dependent production of type 1 IFN, however, later represses NLRC4 and the lysophospholipid biosynthetic enzyme iPLA2, causing a decline in intracellular lysophospholipids that results in down-regulation of flagellin expression by Salmonella These findings reveal a previously unrecognized immune-modulating regulatory cross-talk between endosomal TLR signaling and cytosolic NLR activation with significant implications for the establishment of infection with Salmonella ., Competing Interests: The authors declare no competing interest.

Pathogenic Salmonella serovars are a major cause of enteric illness in humans and animals, and produce clinical manifestations ranging from localized gastroenteritis to systemic disease. T cells are a critical component of immunity against this intracellular pathogen. The mechanisms by which Salmonella modulates T-cell-mediated immune responses in order to establish systemic infection are not completely understood. We show that infection of mice with Salmonella enterica serovar Typhimurium ( S . Typhimurium) suppresses IL-2 and increases IFN-γ and IL-17 production from T cells activated in vivo or ex vivo through the T cell receptor. Infection with S . Typhimurium brings about recruitment of CD11b + Gr1 + suppressor cells to the spleen. Ex vivo depletion of these cells restores the ability of activated T cells to produce IL-2 and brings secretion of IFN-γ and IL-17 from these cells back to basal levels. The reduction in IL-2 secretion is not seen in IFN-γ -/- and iNOS -/- mice infected with Salmonella . Our findings demonstrate that sustained innate activated IFN-γ production during progression of infection with Salmonella reduces IL-2-secreting capability of T cells through an iNOS-mediated signaling pathway that can adversely affect long term immunity against this pathogen., (Copyright © 2020 Yadav, Dikshit, Ismaeel and Qadri.)

Finger millet (Eleusine coracana L. Gaertn., 2n=36) is one of the most important minor crops, commonly known as 'ragi' and used as a staple food grain in more than 25 countries including Africa and south Asia. Twenty-seven accessions of ragi were collected from different parts of India and were evaluated for morpho-genetic diversity studies. Simple sequence repeat (SSR) and random amplified polymorphic DNA (RAPD) markers were used for assessment of genetic diversity among 27 genotypes of E. coracana. High degree of similarity (90%) was obtained between 'IC49979A' and 'IC49974B' genotypes, whereas low level of similarity (9.09%) was found between 'IC204141' and 'IC49985' as evident in morphological and DNA markers. A total of 64 SSR and 301 RAPD amplicons were produced, out of which 87.50% and 77.20% DNA fragments showed polymorphism, respectively. The clustering pattern obtained among the genotypes corresponded well with their morphological and cytological data with a monophyletic origin of this species which was further supported by high bootstrap values and principal component analysis. Cluster analysis showed that ragi accessions were categorised into three distinct groups. Genotypes IC344761, IC340116, IC340127, IC49965 and IC49985 found accession specific in RAPD and SSR markers. The variation among ragi accessions might be used as potential source of germplasm for crop improvement.

Acinetobacter baumannii (A. baumannii) is a significant cause of severe nosocomial pneumonia in immunocompromised individuals world-wide. With limited treatment options available, a better understanding of host immnity to A. baumannii infection is critical to devise alternative control strategies. Our previous study has identified that intracellular Nod1/Nod2 signaling pathway is required for the immune control of A. baumannii in airway epithelial cells in vitro. In the current study, using Nod2 -/- mice and an in vivo sublethal model of pulmonary infection, we show that Nod2 contributes to the early lung defense against A. baumannii infection through reactive oxygen species (ROS)/reactive nitrogen species (RNS) production as Nod2 -/- mice showed significantly reduced production of ROS/RNS in the lungs following A. baumannii infection. Consistent with the higher bacterial load, A. baumannii-induced neutrophil recruitment, cytokine/chemokine response and lung pathology was also exacerbated in Nod2 -/- mice at early time points post-infection. Finally, we show that administration of Nod2 ligand muramyl dipeptide (MDP) prior to infection protected the wild- type mice from A. baumannii pulmonary challenge. Collectively, Nod2 is an important player in the early lung immunity against A. baumannii and modulating Nod2 pathway could be considered as a viable therapeutic strategy to control A. baumannii pulmonary infection.

This corrects the article DOI: 10.1038/ncomms15865.

Optimal regulation of the innate immune receptor nucleotide-binding oligomerization domain-containing protein 2 (NOD2) is essential for controlling bacterial infections and inflammatory disorders. Chronic NOD2 stimulation induces non-responsiveness to restimulation, termed NOD2-induced tolerance. Although the levels of the NOD2 adaptor, RIP2, are reported to regulate both acute and chronic NOD2 signalling, how RIP2 levels are modulated is unclear. Here we show that ZNRF4 induces K48-linked ubiquitination of RIP2 and promotes RIP2 degradation. A fraction of RIP2 localizes to the endoplasmic reticulum (ER), where it interacts with ZNRF4 under either 55 unstimulated and muramyl dipeptide-stimulated conditions. Znrf4 knockdown monocytes have sustained nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, and Znrf4 knockdown mice have reduced NOD2-induced tolerance and more effective control of Listeria monocytogenes infection. Our results thus demonstrate E3-ubiquitin ligase ZNRF4-mediated RIP2 degradation as a negative regulatory mechanism of NOD2-induced NF-κB, cytokine and anti-bacterial responses in vitro and in vivo, and identify a ZNRF4-RIP2 axis of fine-tuning NOD2 signalling to promote protective host immunity.

Type I interferon (IFN-I) mediated innate immune response controls virus infections by inducing the expression of interferon stimulated genes (ISGs). Although ubiquitination plays key roles in immune signaling regulation, a human genome-wide understanding of the role of E3 ubiquitin ligases in interferon mediated ISG induction is lacking. Here, we report a genome-wide profiling of the effect of ectopic expression of 521 E3 ubiquitin ligases and substrate recognition subunits encoded in the human genome (which constitutes 84.4% of all ubiquitination related genes encoded in the human genome, hereafter termed Human Ubiquitome) on IFNβ mediated induction of interferon stimulated DNA response element (ISRE) driven reporter activity. We identified 96 and 42 genes of the human ubiquitome as novel negative and positive regulators of interferon signaling respectively. Furthermore, we characterized DCST1 as a novel E3 ubiquitin ligase negatively regulating interferon response. Ectopic expression and gene silencing of DCST1 respectively attenuated and increased ISRE reporter activity. DCST1 regulated Type I interferon signaling by interacting with and promoting ubiquitination-mediated degradation of STAT2, an essential component of antiviral gene induction. In summary, this study provided a systems level view on the role of human ubiquitination associated genes in Type I interferon response.

Several lines of experimental and clinical evidence have alluded a pivotal role of renin in blood pressure homeostasis and therefore a relevance of molecular variants of the renin gene and essential hypertension have been speculated. This study was designed to evaluate the pattern, alliance and risk of renin Mbo I (10631A>G; rs2368564) polymorphism at the locus intron 9 for a possible role in modulating essential hypertension in adult population from Gujarat (India). A total of 257 consecutively enrolled essential hypertensive patients and 270 controls were genotyped using polymerase chain reaction-restriction fragment length polymorphism method for the selected marker. Suitable descriptive statistics was used for different variables. Genotypic (x(2) 10.43, p 0.0054) and allelic (x(2) 11.46, p 0.0007) distribution of this SNP displayed significant differences between cases and controls with an increased frequency of the A allele (x(2) 6.275; p 0.0122) and A/A geno-type (x(2) 8.247; p 0.0041) in hypertensive individuals. However, it showed no deviation from Hardy-Weinberg equilibrium in either affected or control group. A significant association was found in the A/A variant of rs2368564 with essential hypertension (p 0.0032), along with a statistically significant increase in odds of hypertension (OR 1.69; CI 1.46-2.28; p 0.02), even after confounding factors were adjusted in multiple logistic regression analysis and is substantiated by inter-genotypic variations in the mean systolic and diastolic blood pressure in patients. In conclusion, renin 10631A>G gene mutation at the ninth intron play critical roles in BP (dys)regulation and can be implicated in an individual's susceptibility for hypertension.

Dissecting the complexities of branched peptide-lipopolysaccharides (LPS) interactions provide rationale for the development of non-cytotoxic antibiotic adjuvants. Using various biophysical methods, we show that the branched peptide, B2088, binds to lipid A and disrupts the supramolecular organization of LPS. The disruption of outer membrane in an intact bacterium was demonstrated by fluorescence spectroscopy and checkerboard assays, the latter confirming strong to moderate synergism between B2088 and various classes of antibiotics. The potency of synergistic combinations of B2088 and antibiotics was further established by time-kill kinetics, mammalian cell culture infections model and in vivo model of bacterial keratitis. Importantly, B2088 did not show any cytotoxicity to corneal epithelial cells for at least 96 h continuous exposure or hemolytic activity even at 20 mg/ml. Peptide congeners containing norvaline, phenylalanine and tyrosine (instead of valine in B2088) displayed better synergism compared to other substitutions. We propose that high affinity and subsequent disruption of the supramolecular assembly of LPS by the branched peptides are vital for the development of non-cytotoxic antibiotic adjuvants that can enhance the accessibility of conventional antibiotics to the intracellular targets, decrease the antibiotic consumption and holds promise in averting antibiotic resistance.

Recurrent urinary tract infections (UTIs) caused by uropathogenic E. coli (UPEC) are common and morbid infections with limited therapeutic options. Previous studies have demonstrated that persistent intracellular infection of bladder epithelial cells (BEC) by UPEC contributes to recurrent UTI in mouse models of infection. However, the mechanisms employed by UPEC to survive within BEC are incompletely understood. In this study we aimed to understand the role of host vesicular trafficking proteins in the intracellular survival of UPEC. Using a cell culture model of intracellular UPEC infection, we found that the small GTPase Rab35 facilitates UPEC survival in UPEC-containing vacuoles (UCV) within BEC. Rab35 plays a role in endosomal recycling of transferrin receptor (TfR), the key protein responsible for transferrin-mediated cellular iron uptake. UPEC enhance the expression of both Rab35 and TfR and recruit these proteins to the UCV, thereby supplying UPEC with the essential nutrient iron. Accordingly, Rab35 or TfR depleted cells showed significantly lower intracellular iron levels and reduced ability to support UPEC survival. In the absence of Rab35, UPEC are preferentially trafficked to degradative lysosomes and killed. Furthermore, in an in vivo murine model of persistent intracellular infection, Rab35 also colocalizes with intracellular UPEC. We propose a model in which UPEC subverts two different vesicular trafficking pathways (endosomal recycling and degradative lysosomal fusion) by modulating Rab35, thereby simultaneously enhancing iron acquisition and avoiding lysosomal degradation of the UCV within bladder epithelial cells. Our findings reveal a novel survival mechanism of intracellular UPEC and suggest a potential avenue for therapeutic intervention against recurrent UTI.

Acinetobacter baumannii is a major extensively drug-resistant lethal human nosocomial bacterium. However, the host innate immune mechanisms controlling A. baumannii are not well understood. Although viewed as an extracellular pathogen, A. baumannii can also invade and survive intracellularly. However, whether host innate immune pathways sensing intracellular bacteria contribute to immunity against A. baumannii is not known. Here, we provide evidence for the first time that intracellular antibacterial innate immune receptors Nod1 and Nod2, and their adaptor Rip2, play critical roles in the sensing and clearance of A. baumannii by human airway epithelial cells in vitro. A. baumannii infection upregulated Rip2 expression. Silencing of Nod1, Nod2, and Rip2 expression profoundly increased intracellular invasion and prolonged the multiplication and survival of A. baumannii in lung epithelial cells. Notably, the Nod1/2-Rip2 axis did not contribute to the control of A. baumannii infection of human macrophages, indicating that they play cell type-specific roles. The Nod1/2-Rip2 axis was needed for A. baumannii infection-induced activation of NF-κB but not mitogen-activated protein kinases. Moreover, the Nod1/2-Rip2 axis was critical to induce optimal cytokine and chemokine responses to A. baumannii infection. Mechanistic studies showed that the Nod1/2 pathway contributed to the innate control of A. baumannii infection through the production of β-defensin 2 by airway epithelial cells. This study revealed new insights into the immune control of A. baumannii and may contribute to the development of effective immune therapeutics and vaccines against A. baumannii.

BRCA1 gene expression in familial breast cancer is mainly focused on mutational analysis. However in sporadic cancers BRCA1 protein expression is the main area of interest because somatic inactivation of one allele of the gene is likely to occur during the oestrogen mediated proliferation at puberty and subsequent tumourigenic events take place in the same cell. Standard immunohistochemical analysis was used to assess BRCA1 and oestrogen/progesterone receptor (ER/PR) status in familial and sporadic breast cancer patients and correlation of BRCA1 protein expression with histopathological features ER/PR status was studied in these tumours. One hundred and seventy-seven sporadic tumours (group A) and 28 familial tumours (patients with history of breast cancer in first or second degree relative ie, group B) were studied. In group A, 61 tumours had absent/reduced BRCA 1 protein expression; 30 (49%) out of these were negative for ER/PR receptors. In group B, 18 patients had absent/reduced BRCA1 protein expression, and 10 (55.6%) out of these, were ER/PR negative. Overall in 2 groups, 82 tumours were of grade 1, 61 tumours of grade 2 and 62 tumours were of grade 3 differentiation. Test of proportion showed that percentage of ER/PR negativity is significantly higher than ER/PR positivity in sporadic as well as in familial tumours with absent/ reduced BRCA 1 protein expression (p < 0.05). Sporadic tumours with deranged BRCA1 protein expression like familial tumours have more unfavourable histopathological characteristics and are likely to be of higher grade and oestrogen receptor negative

Background: Coronary artery disease is an important cause of death and disability among older women. Modification in lipid profile lowers the risk of coronary artery disease. It is claimed that yoga and transcendental meditation have a cholesterol lowering effect. This study was designed to assess the effect of raja yoga meditation of Brahmakumaris which is very simple to practice, on serum lipids in normal Indian women., Methods and Results: 49 normal female volunteers were the subjects. They were divided into pre-menopausal (n=23) and post-menopausal (n=26) groups. They were further divided into non-meditators (who had never done any kind of meditation), short-term meditators (meditating for 6 months to 5 years) and long-term meditators (meditating for more than 5 years). Lipid profile was assessed using their respective reagent sets. Serum cholesterol, triglyceride and low-density lipoprotein-cholesterol in nonmeditators were significantly more in post-menopausal women as compared to pre-menopausal women. Serum cholesterol and low density lipoprotein-cholesterol were significantly lowered in both short and long term meditators as compared to non-meditators in post-menopausal women. No significant difference was observed in lipid profile in pre-menopausal women., Conclusion: Raja yoga meditation lowered serum cholesterol and low-density lipoprotein-cholesterol in post-menopausal women thus reducing the risk of coronary artery disease in them.

In this study, respiratory functions, cardiovascular parameters and lipid profile of those practicing Raja Yoga meditation (short and long term meditators) were compared with those of nonmediators. Vital capacity, tidal volume and breath holding were significantly higher in short and long term meditators than nonmeditators. Long term mediators had significantly higher vital capacity and expiratory pressure than short term meditators. Diastolic blood pressure was significantly lower in both short and long term meditators as compared to nonmeditators. Heart rate was significantly lower in long term meditators than in short term meditators and nonmeditators. Lipid profile showed a significant lowering of serum cholesterol in short and long term meditators as compared to nonmeditators. Lipid profile of short and long term meditators was better than the profile of nonmeditators inspite of similar physical activity. This shows that Raja Yoga meditation provides significant improvements in respiratory functions, cardiovascular parameters and lipid profile.