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This investigation was conducted under a naturally ventilated polyhouse, in the Department of Horticulture, SHUATS, Prayagraj, Uttar Pradesh. In December 2020 with records taken from the month of February to month of March 2021. There were nine treatments comprising two growth regulators Gibberellic acid (GA3) (at 200, 250, 300, and 350 ppm), and Naphthalic Acetic Acid (NAA) (at 50,100,150, and 200 ppm) along with control. The whole experiment was laid out as a Randomized Block Design (RBD) with three replications. The results revealed that among the Lilium cv. LITOUWEN, the foliar application of 250 ppm GA3 significantly increased the number of leaves per plant (66) with enhanced days to bud initiation (25.7 days). The number of bud per plant was 2.8 and stem length was 43.4cm respectively., GA3 at a concentration of 350 ppm enhanced vase life (7.9 days). and NAA at a concentration of 100 ppm enhanced the number of bulblets (3.3).

An experiment entitled " Effect of plant growth regulators on growth, yield and fruit quality of Bottle Gourd (Lagenaria siceraria) cv. MGH-4" was conducted at Horticulture Research Field, Department of Horticulture, Naini Agricultural Institute, Sam Higginbottom University of Agriculture, Technology and Sciences, Prayagraj (Uttar Pradesh) during 2019. Plant Growth regulators are regarded as one of the most important treatments, used nowadays in agriculture, which in most cases modify the plant growth and the subsequent fruiting. The experimental trial consisted two plant growth regulators having different concentration NAA (30, 40, 50, 60, 70 & 80 ppm) and GA3(30,40, 50, 60 & 70 ppm). Water was used as a control. The application of plant growth regulators significantly affects the vegetative as well as reproductive attributes of the crop. Application of plant growth regulators at the 2-4 leaf stage was found to be the most productive in terms of growth attributes of bottle gourd. Treatment T7 (80 ppm NAA) at 2-4 leaf stage showed the maximum vine length (8.20 m), Number of Leaves Per Plant (103.50) and took minimum Days to First Female Flower Initiation (53.33). However, the treatment T9 (40 ppm GA3) showed the maximum Number of Male Flowers Per Vine (54.08) and Number of Female Flowers Per vine (17.08). Plant Growth regulators are one of the most significant treatments currently used in agriculture, and they typically alter plant growth and subsequent fruiting and growth attributes.

Context: Using Visible Light to bond orthodontic attachments is now an accepted norm, the progression being Halogens, Low and High Intensity Light Emitting Diodes (LEDs). Since, clinical use of bonded brackets is pragmatically linked with Shear Bond Strength (SBS) and chair-side time, adhesives with shorter curing time are a boon. Hence, the aforementioned facets bear a more detailed study. Settings and Design: 6 Groups (2 Halogens, 2 Low Intensity LEDs and 2 High Intensity LEDs); Each Group comprised of 10 assemblies of Metal Brackets (3M Unitek, Gemini Series) bonded to facial surface of extracted human Maxillary 1st bicuspids. Methods and Material: Brackets were directly bonded using Standard Bonding Protocol to freshly extracted Human Maxillary Premolars. Shear Bond Strength (SBS) testing was done using Universal Testing Machine, Instron. The SBS values attained in Kg/F were converted into MPa and results subjected to a comparative evaluation. Results: Mean SBS values, in MPa, for Halogen Light Cure Systems were 8.51 and 8.86; for Low Intensity LEDs were 10.50 and 10.33 while for High Intensity LEDs 15.54 and 13.85.

Matricellular proteins comprise a diverse group of molecular entities secreted into the extracellular space. They interact with the extracellular matrix (ECM), integrins, and other cell-surface receptors, and can alter matrix strength, cell attachment to the matrix, and cell-cell adhesion. A founding member of this group is thrombospondin-1 (TSP-1), a high molecular-mass homotrimeric glycoprotein. Given the importance of the matrix and ECM remodeling in the lung following injury, TSP-1 has been implicated in a number of lung pathologies. This review examines the role of TSP-1 as a damage controller in the context of lung inflammation, injury resolution, and repair in noninfectious and infectious models. This review also discusses the potential role of TSP-1 in human diseases as it relates to lung inflammation and injury.

Globally, lung cancer is the second most-diagnosed cancer and is the leading cause of cancer death. Advances in science and technology have contributed to improvements in primary cancer prevention, cancer diagnosis, and cancer therapy, leading to an increase in survival and improvement in quality of life. Many of these advances have been seen in high-income countries. Accessibility, availability, and affordability are key domains in barriers to access of care between countries and within countries. The impact of these domains, as they relate to molecular testing, radiation therapy, and systemic therapy, are discussed.

Idiopathic Pulmonary Fibrosis (IPF) is a progressively fatal and incurable disease characterized by the loss of alveolar structures, increased epithelial-mesenchymal transition (EMT), and aberrant tissue repair. In this study, we investigated the role of Nuclear Factor I-B (NFIB), a transcription factor critical for lung development and maturation, in IPF. Using both human lung tissue samples from patients with IPF, and a mouse model of lung fibrosis induced by bleomycin, we showed that there was a significant reduction of NFIB both in the lungs of patients and mice with IPF. Furthermore, our in vitro experiments using cultured human lung cells demonstrated that the loss of NFIB was associated with the induction of EMT by transforming growth factor beta (TGF-β). Knockdown of NFIB promoted EMT, while overexpression of NFIB suppressed EMT and attenuated the severity of bleomycin-induced lung fibrosis in mice. Mechanistically, we identified post-translational regulation of NFIB by miR-326, a miRNA with anti-fibrotic effects that is diminished in IPF. Specifically, we showed that miR-326 stabilized and increased the expression of NFIB through its 3'UTR target sites for Human antigen R (HuR). Moreover, treatment of mice with either NFIB plasmid or miR-326 reversed airway collagen deposition and fibrosis. In conclusion, our study emphasizes the critical role of NFIB in lung development and maturation, and its reduction in IPF leading to EMT and loss of alveolar structures. Our study highlights the potential of miR-326 as a therapeutic intervention for IPF.

Stock market comprises of different purchasers and merchants of stock. Stock market expectation implies deciding the future extent of market. A framework is fundamental to be constructed which will work with most extreme exactness and it ought to consider terrifically significant variables that could impact the outcome. Different investigates have effectively been done to anticipate securities exchange costs. The examination is done over business and software engineering space. At some point the securities exchange in all actuality does well in any event, when the economy is falling on the grounds that there are different purposes behind the benefit or loss of an offer. Foreseeing the exhibition of a securities exchange is extreme as it considers different elements. The principle point is to distinguish the feelings of financial backers. It is typically troublesome as there should be thorough investigation of public and worldwide occasions. An investor actually must know the current cost and estimation of the future price.

Bioactive fractions obtained from medicinal plants which have been used for the treatment of multiple diseases could exert their effects by targeting common pathways. Prior knowledge of their usage could allow us to identify novel molecular links. In this study, we explored the molecular basis of action of one such herbal formulation Cissampelos pareira L. (Cipa), used for the treatment of female hormone disorders and fever. Transcriptomic studies on MCF7 cell lines treated with Cipa extract carried out using Affymetrix arrays revealed a downregulation of signatures of estrogen response potentially modulated through estrogen receptor α (ERα). Molecular docking analysis identified 38 Cipa constituents that potentially bind (ΔG https://clue.io/;) revealed high positive scores with translation inhibitors such as emetine (score: 99.61) and knockdown signatures of genes linked to the antiviral response such as ribosomal protein RPL7 (score: 99.92), which is a reported ERα coactivator. Further, gene knockdown experiments revealed that Cipa exhibits antiviral activity in dengue infected MCF7 cells potentially modulated through estrogen receptor 1. This approach reveals a novel pathway involving the ESR1-RPL7 axis which could be a potential target in dengue viral infection.

Objective: Comparative evaluation of antibacterial and anti-adherent properties of surface-modified stainless steel (SS) orthodontic brackets against Streptococcus mutans ( S. mutans). Materials and Methods: The study was conducted on 120 SS orthodontic McLaughlin, Bennett, Trevisi (MBT) 0.022″ slot by Leone, Italy. Orthodontic brackets that constituted the sample size were divided into 6 groups, consisting of 20 samples each in two control (non-surface coated) and four experimental groups. The experimental group’s surface coatings were photocatalytic zinc oxide (ZnO) and photocatalytic titanium oxide (TiO2), which were carried out by radiofrequency (RF) magnetron sputtering method for surface modification. Brackets were subjected to microbiological tests against S. mutans. For anti-adherence, weight change, pre- and postexposure, was evaluated to gauge the adherence of bacteria and colony-forming units/milliliter (CFU/mL) count measuring the survival rate of bacterial cells for antibacterial activity. Results: The TiO2-coated group showed statistically significant anti-adherence ( P-value < .05) against S. mutans than control and ZnO groups. The CFU count of TiO2 group was lower than control as well as ZnO group. Conclusion: TiO2 is superior to ZnO and should be continued to be considered for surface modification of orthodontic brackets against White Spot Lesions (WSLs) and gingivitis.

Severe asthma is a chronic airway disease that exhibits poor response to conventional asthma therapies. Growing evidence suggests that elevated hypoxia increases the severity of asthmatic inflammation among patients and in model systems. In this study, we elucidate the therapeutic effects and mechanistic basis of Adhatoda vasica (AV) aqueous extract on mouse models of acute allergic as well as severe asthma subtypes at physiological, histopathological, and molecular levels. Oral administration of AV extract attenuates the increased airway resistance and inflammation in acute allergic asthmatic mice and alleviates the molecular signatures of steroid (dexamethasone) resistance like IL-17A, KC (murine IL-8 homologue), and HIF-1α (hypoxia-inducible factor-1α) in severe asthmatic mice. AV inhibits HIF-1α levels through restoration of expression of its negative regulator—PHD2 (prolyl hydroxylase domain-2). Alleviation of hypoxic response mediated by AV is further confirmed in the acute and severe asthma model. AV reverses cellular hypoxia-induced mitochondrial dysfunction in human bronchial epithelial cells—evident from bioenergetic profiles and morphological analysis of mitochondria. In silico docking of AV constituents reveal higher negative binding affinity for C and O—glycosides for HIF-1α, IL-6, Janus kinase 1/3, TNF-α, and TGF-β—key players of hypoxia inflammation. This study for the first time provides a molecular basis of action and effect of AV whole extract that is widely used in Ayurveda practice for diverse respiratory ailments. Further, through its effect on hypoxia-induced mitochondrial dysfunction, the study highlights its potential to treat severe steroid-resistant asthma.

Background COVID-19 pneumonia has been associated with severe acute hypoxia, sepsis-like states, thrombosis and chronic sequelae including persisting hypoxia and fibrosis. The molecular hypoxia response pathway has been associated with such pathologies and our recent observations on anti-hypoxic and anti-inflammatory effects of whole aqueous extract of Adhatoda Vasica (AV) prompted us to explore its effects on relevant preclinical mouse models. Methods In this study, we tested the effect of whole aqueous extract of AV, in murine models of bleomycin induced pulmonary fibrosis, Cecum Ligation and Puncture (CLP) induced sepsis, and siRNA induced hypoxia-thrombosis phenotype. The effect on lung of AV treated naïve mice was also studied at transcriptome level. We also determined if the extract may have any effect on SARS-CoV2 replication. Results Oral administration AV extract attenuates increased airway inflammation, levels of transforming growth factor-β1 (TGF-β1), IL-6, HIF-1α and improves the overall survival rates of mice in the models of pulmonary fibrosis and sepsis and rescues the siRNA induced inflammation and associated blood coagulation phenotypes in mice. We observed downregulation of hypoxia, inflammation, TGF-β1, and angiogenesis genes and upregulation of adaptive immunity-related genes in the lung transcriptome. AV treatment also reduced the viral load in Vero cells infected with SARS-CoV2. Conclusion Our results provide a scientific rationale for this ayurvedic herbal medicine in ameliorating the hypoxia-hyperinflammation features and highlights the repurposing potential of AV in COVID-19-like conditions.

Introduction: Single crowns or fixed partial dentures retainers usually get dislodged due to inadequate resistance form. Hence, it is prudent to evaluate features of a tooth preparation, which can prevent these failures. Aim: To evaluate the effect of auxiliary features, occlusal surface modifications, and total occlusal convergence (TOC) on the resistance of a full veneer crown. Materials and Methods: An ivorine mandibular molar tooth was prepared with features of inadequate resistance form, i.e., 2.5 mm axial wall height and TOC of 20°. Seven auxiliary preparation features were subsequently added one by one to it. They were mesiodistal grooves, buccolingual and mesiodistal grooves, buccolingual grooves, mesiodistal boxes, occlusal inclined planes, 8° reduced TOC in the cervical aspect, and mesiodistal grooves added to 8° reduced TOC in the cervical aspect. Ten dies with their respective crowns were prepared for each group. Resistance testing of all the samples was performed on the INSTRON testing machine. Results: Modification of the overtapered die preparation by reducing the TOC to 8° in the cervical 1.5 mm of the axial wall and then subsequently adding mesiodistal grooves to the reduced TOC cervically offered the greatest resistance to dislodgment statistically. Conclusion: For an overtapered preparation, reducing the TOC to 8° in the cervical aspect and subsequently adding proximal grooves can provide maximum resistance form.

The precise molecular mechanisms behind life-threatening lung abnormalities during severe SARS-CoV-2 infections are still unclear. To address this challenge, we performed whole transcriptome sequencing of lung autopsies from 31 patients suffering from severe COVID-19 related complications and 10 uninfected controls. Using a metatranscriptome analysis of lung tissue samples we identified the existence of two distinct molecular signatures of lethal COVID-19. The dominant “classical” signature (n=23) showed upregulation of unfolded protein response, steroid biosynthesis and complement activation supported by massive metabolic reprogramming leading to characteristic lung damage. The rarer signature (n=8) potentially representing “Cytokine Release Syndrome” (CRS) showed upregulation of cytokines such IL1 and CCL19 but absence of complement activation and muted inflammation. Further, dissecting expression of individual genes within enriched pathways for patient signature suggests heterogeneity in host response to the primary infection. We found that the majority of patients cleared the SARS-CoV-2 infection, but all suffered from acute dysbiosis with characteristic enrichment of opportunistic pathogens such as Staphylococcus cohnii in “classical” patients and Pasteurella multocida in CRS patients. Our results suggest two distinct models of lung pathology in severe COVID-19 patients that can be identified through the status of the complement activation, presence of specific cytokines and characteristic microbiome. This information can be used to design personalized therapy to treat COVID-19 related complications corresponding to patient signature such as using the identified drug molecules or mitigating specific secondary infections.

Milk is globally consumed as a rich source of protein and calcium. A major protein component of milk is casein, with β-casein having 2 major variants A1 and A2. Of these, A1 casein variant has been implicated as a potential etiological factor in several pathologies, but direct effect on lungs has not been studied. The objective of the present study was to evaluate the A1and A2 β casein variants of cow milk as factors causing allergic airway disease in murine model. Mice fed with A1A1 milk exhibited increased airway hyperresponsiveness with increasing concentration of bronchoconstrictor (methacholine), which was not observed in mice fed with A2A2 milk. Significantly elevated levels of IL-4 and IL-5 were found in bronchoalveolar lavage and serum of A1A1 variant fed mice. Increased IgE and IgG levels along with increased infiltration of lymphocytes and eosinophils, leading to peribronchial inflammation was also observed in A1A1 variant fed mice, although, no goblet cell hyperplasia or airway remodeling was observed. In contrast, A2A2 milk fed mice presented phenotype matching the control group, while A1A2 milk fed group presented an intermediate phenotype. In summary, our results show that A1 form of cow milk has a proinflammatory effect on the lung resulting in phenotype closely matching with the typical allergic asthma phenotype.

Mesenchymal stem cell (MSC) transplantation alleviates metabolic defects in diseased recipient cells by intercellular mitochondrial transport (IMT). However, the effect of host metabolic conditions on MSCs in general, and IMT in particular, has largely remained unexplored. This study has identified a molecular pathway that primarily governs the metabolic function and IMT of MSCs. We found underlying mitochondrial dysfunction, impaired mitophagy, and reduced IMT in MSCs derived from high-fat diet (HFD)-induced obese mice (MSC-Ob). Mechanistically, MSC-Ob failed to sequester their damaged mitochondria into LC3-dependent autophagosomes due to decrease in mitochondrial cardiolipin content, which we propose as a putative mitophagy receptor for LC3 in MSCs. Functionally, MSC-Ob exhibited diminished potential to rescue metabolic deficits and cell death in stress-induced epithelial cells. In a small molecule screen, we found pyrroloquinoline quinone (PQQ) as a regulator of mitophagy and IMT. Long-term culture of MSC-Ob with PQQ (MSC-ObPQQ) restored cardiolipin content and sequestration of mitochondria to autophagosomes with concomitant activation of mitophagy. Upon co-culture, MSC-ObPQQ rescued cell death in stress-induced epithelial cells by enhancing IMT. The beneficial effect of PQQ was also evident in MSCs derived from human subjects in an in vitro model. In two independent mice models, the transplantation of MSC-ObPQQ restored IMT to airway epithelial cells, improved their mitochondrial metabolism and attenuated features of allergic airway inflammation (AAI). However, unmodulated MSC-Ob failed to do so. In summary, we uncover the molecular mechanism leading to the therapeutic decline of obese-derived MSCs and highlight the importance of pharmacological modulation of these cells for therapeutic intervention.

Angiotensin-converting enzyme 2 (ACE2) is a key host protein by which severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) enters and multiplies within cells. The level of ACE2 expression in the lung is hypothesised to correlate with an increased risk of severe infection and complications in COVID-19 (COrona VIrus Disease 2019). To test this hypothesis, we compared the protein expression status of ACE2 by immunohistochemistry (IHC) in post-mortem lung samples of patients who died of severe COVID-19 and lung samples obtained from non-COVID-9 patients for other indications. IHC for CD61 and CD163 were performed for assessment of platelet-rich microthrombi and macrophages, respectively. IHC for SARS-CoV-2 viral antigen was also performed. Quantification of immunostaining, random sampling, and correlation analysis was used to substantiate the morphologic findings. Our results show that among a total of 44 COVID-19 post-mortem lung tissues and 15 lung biopsies in non-COVID-19 patients included, ACE2 protein expression was significantly higher in COVID-19 patients than in controls, regardless of sample size. Histomorphology in COVID-19 lungs showed diffuse alveolar damage (DAD), acute bronchopneumonia, and acute lung injury with SARS-CoV-2 viral protein detected in a subset of cases. ACE2 expression levels positively correlated with increased expression levels of CD61 and CD163. In conclusion, our results show significantly higher ACE2 protein expression in severe COVID-19 disease, correlating with increased macrophage infiltration and microthrombi, suggesting a pathobiological role in disease severity.

Angiotensin-converting enzyme 2 (ACE2) is a key host protein by which severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) enters and multiplies within cells. The level of ACE2 expression in the lung is hypothesised to correlate with an increased risk of severe infection and complications in COrona VIrus Disease 2019 (COVID-19). To test this hypothesis, we compared the protein expression status of ACE2 by immunohistochemistry (IHC) in post-mortem lung samples of patients who died of severe COVID-19 and lung samples obtained from non-COVID-19 patients for other indications. IHC for CD61 and CD163 was performed for the assessment of platelet-rich microthrombi and macrophages, respectively. IHC for SARS-CoV-2 viral antigen was also performed. In a total of 55, 44 COVID-19 post-mortem lung samples were tested for ACE2, 36 for CD163, and 26 for CD61, compared to 15 non-covid 19 control lung sections. Quantification of immunostaining, random sampling, and correlation analysis were used to substantiate the morphologic findings. Our results show that ACE2 protein expression was significantly higher in COVID-19 post-mortem lung tissues than in controls, regardless of sample size. Histomorphology in COVID-19 lungs showed diffuse alveolar damage (DAD), acute bronchopneumonia, and acute lung injury with SARS-CoV-2 viral protein detected in a subset of cases. ACE2 expression levels were positively correlated with increased expression levels of CD61 and CD163. In conclusion, our results show significantly higher ACE2 protein expression in severe COVID-19 disease, correlating with increased macrophage infiltration and microthrombi, suggesting a pathobiological role in disease severity.