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The Ordovician Craighead Limestone Formation of southwest Scotland was formed on a carbonate platform on the eastern tropical margin of the Laurentia palaeocontinent during the early Katian (c. 456 Ma). It yields the most diverse and well-preserved ostracod fauna yet recovered from the Scottish Ordovician succession, with some 25 species divisible into two distinct marine biotopes comprising shallow lagoonal and deeper platform margin settings, respectively. The ostracods show strong biogeographic links at species-level with Sandbian and early Katian faunas of North America, including Krausella arcuata, Steusloffina cuneata, Monoceratella teres and species of Levisulculus and Platybolbina. However, many of the ostracod genera that characterize the Craighead Limestone Formation have earlier origins in the Baltica palaeocontinent, suggesting enhanced migration of species from mid- (Baltica about 30[degrees]S) to low (Laurentia) latitudes in the late Sandbian and early Katian interval. Such Baltica-origin genera include Distobolbina, Kiesowia and Platybolbina. Notable is the wide biogeographic occurrence of Steusloffina cuneata, extending from warm tropical Laurentia to cooler high-latitude Gondwana, an enormous latitudinal range for a shelf-dwelling marine species. The possible Tvaerenellidae taxon Duoarcus levigatus gen. et sp. nov. is described. Keywords: ostracods, Ordovician, Scotland, palaeogeography, palaeoecology. doi: 10.1017/S0016756810000385

Intraepithelial lymphocytes (IELs) bearing the [gamma][delta] TCR are more abundant in the small intestinal mucosa of patients with celiac disease (CD) compared with healthy individuals. However, their role in disease pathogenesis is not well understood. Here, we investigated the functional attributes of [TCR[gamma][delta].sup.+] IELs isolated from intestinal biopsies of patients with either active celiac disease (ACD) or those on a gluten-free diet (GFD). We found that compared with individuals with ACD, individuals on GFD have a higher frequency of [CD8.sup.+][TCR[gamma][delta].sup.+] IELs that express the inhibitory NK receptor NKG2A and intracellular TGF-[beta]1. TCR triggering as well as cross-linking of NKG2A increased both TGF-[beta]1 intracellular expression and secretion in vitro. Coculture of sorted [TCR[gamma][delta].sup.+][NKG2A.sup.+] IELs, IL-15-stimulated [TCR[alpha][beta].sup.+] IELs, and [HLA-E.sup.+] enterocytes resulted in a decreased percentage of cytotoxic [CD8.sup.+][TCR[alpha][beta].sup.+] IELs expressing intracellular IFN-[gamma] and granzyme-B and surface NKG2D. This inhibition was partially abrogated by blocking either TGF-[beta] alone or both NKG2A and HLA-E. Thus, our data indicate that suppression was at least partially mediated by TGF-[beta] secretion as a result of engagement of NKG2A with its ligand, HLA-E, on enterocytes and/or [TCR[alpha][beta].sup.+] IELs. These findings demonstrate that human small intestinal [CD8.sup.+][TCR[gamma][delta].sup.+] IELs may have regulatory potential in celiac disease., Introduction Celiac disease (CD), or gluten-sensitive enteropathy, is a malabsorption syndrome that occurs in genetically susceptible individuals who are intolerant to dietary gluten (1). The disease is triggered by exposure [...]

Rhizobacterial phosphate solubilization supports plant nutrition under phosphorus (P) deficiency stress. In this filed study we evaluated wheat response to ACC-deaminase-containing rhizobacterial strains, with or without phosphate-solubilizing activity, under varying levels of soil applied phosphatic fertilizer. The experiment was conducted on a P-deficient soilby using randomized complete block split plot design involving two factors. Factor Ainvolved three P doses (in main plots), i.e. 0(Control), 42.5 and 85 kg P[sub 2]O[sub 5]g ha[sup -1]. Factor B included three rhizobacterial treatments (in sub plots), i.e. No rhizobacterial seed inoculation (control) and wheat seed inoculation with ACC-deaminase Pseudomonas fluorescens with or without P-solubilizing activity. P nutrition of wheat plants at half and full recommended dose increased various plant growth and yield parameters of wheat in a range of 7.4 to128% and 9.6 to 144%, respectively, against control. ACC-deaminase Pseudomonas fluorescens without or with P-solubilizing activity increased various traits of wheat plants in a range of 1.4 to38% and 2.9 to86%, respectively, against control. The study concluded that Pseudomonas fluorescens with dual activities of ACC-demainase and phosphate solubilization play significant role in enhancing wheat growth and yield under both low- and high-P sustainable agriculture. [ABSTRACT FROM AUTHOR]

Background:Individuals with active celiac disease (CD+) have an increased incidence of thyroid dysfunction, which improves on a gluten-free diet (CD−). We investigated whether tissue transglutaminase-2 IgA antibodies (anti-TGase II) present in sera of patients with celiac disease react with thyroid tissue and possibly contribute to thyroid disease.Methods:Serum from 40 active celiac patients taken before a gluten-free diet (CD+), 46 patients on a gluten-free diet (CD−), 40 normal controls (NC), and 25 with Crohn's disease (CROHN) was used. All sera were screened for antithyroperoxidase antibodies (TPO-AB) and thyroglobulin antibodies (TG-AB), and indirect immunofluorescence (IIF) was performed on primate thyroid tissue sections using TPO-AB– and TG-AB–negative sera.Results:IIF with thyroid seronegative, anti-TGase II–positive CD+ sera (n= 23) demonstrated staining of thyroid follicular cells and extracellular matrix, in an identical pattern with monoclonal anti-human TGase II antibody. Evidence of TGase II as the antigen in thyroid tissue was supported by elimination of the IIF pattern when sera were depleted of anti-TGase II by pretreatment with human recombinant TGase II. No staining of thyroid tissue was observed when sera from CD+ patients that were negative for TGase II antibodies, or sera from NC subjects were used. Thyroid antibodies were found in 43% of CD+ patients, significantly higher than NC and CROHN patients (p< 0.0001). In addition, a positive correlation was observed between anti-TGase II and TPO-AB titers (p= 0.0001; r= 0.63).Conclusions:Anti-TGase II antibodies bind to TGase II in thyroid tissue, and titers correlate with TPO antibody titers. These findings suggest that anti-TGase II antibodies could contribute to the development of thyroid disease in celiac disease. [ABSTRACT FROM AUTHOR]

Soybean [ Glycine max (L.) Merr.] cultivars show differences in their resistance to both the leaf scorch and root rot of sudden death syndrome (SDS). The syndrome is caused by root colonization by Fusarium virguliforme (ex. F. solani f. sp. glycines). Root susceptibility combined with reduced leaf scorch resistance has been associated with resistance to Heterodera glycines HG Type 1.3.6.7 (race 14) of the soybean cyst nematode (SCN). In contrast, the rhg1 locus underlying resistance to Hg Type 0 was found clustered with three loci for resistance to SDS leaf scorch and one for root infection. The aims of this study were to compare the inheritance of resistance to leaf scorch and root infection in a population that segregated for resistance to SCN and to identify the underlying quantitative trait loci (QTL). “Hartwig”, a cultivar partially resistant to SDS leaf scorch, F. virguliforme root infection and SCN HG Type 1.3.6.7 was crossed with the partially susceptible cultivar “Flyer”. Ninety-two F5-derived recombinant inbred lines and 144 markers were used for map development. Four QTL found in earlier studies were confirmed. One contributed resistance to leaf scorch on linkage group (LG) C2 (Satt277; P = 0.004, R 2 = 15%). Two on LG G underlay root infection at R8 (Satt038; P = 0.0001 R 2 = 28.1%; Satt115; P = 0.003, R 2 = 12.9%). The marker Satt038 was linked to rhg1 underlying resistance to SCN Hg Type 0. The fourth QTL was on LG D2 underlying resistance to root infection at R6 (Satt574; P = 0.001, R 2 = 10%). That QTL was in an interval previously associated with resistance to both SDS leaf scorch and SCN Hg Type 1.3.6.7. The QTL showed repulsion linkage with resistance to SCN that may explain the relative susceptibility to SDS of some SCN resistant cultivars. One additional QTL was discovered on LG G underlying resistance to SDS leaf scorch measured by disease index (Satt130; P = 0.003, R 2 = 13%). The loci and markers will provide tagged alleles with which to improve the breeding of cultivars combining resistances to SDS leaf scorch, root infection and SCN HG Type 1.3.6.7. [ABSTRACT FROM AUTHOR]

Endothelial cells have been shown to activate T cell responses to alloantigens, triggering transplant rejection. However, they may also play a role in tolerance induction. Using RT–PCR we show here that alloantigen specific CD8+CD28− T suppressor cells generated in vitro are FOXP3 positive and interact with human endothelial cells. This interaction results in the induction of inhibitory receptors and down-regulation of costimulatory and adhesion molecules, thus rendering endothelial cells tolerogenic. In turn, tolerized endothelial cells elicit the differentiation of CD8+CD28− FOXP3+ T suppressor cells. Taken together our data demonstrate a functional and phenotypic overlap between tolerogenic dendritic cells and endothelial cells. Furthermore, alloantigen specific CD8+CD28− FOXP3+ T cells, which trigger the upregulation of inhibitory receptors in endothelial cells, are present in the circulation of heart allograft recipients in quiescence as demonstrated by flow cytometry, RT–PCR and luciferase transcription assays. Their detection facilitates the identification of patients who may benefit from partial or complete cessation of immunosuppressive therapy, a goal of obvious importance given the morbidity and mortality associated with chronic immunosuppression. Modulation of endothelial cells in favor of promoting tolerance may be important for long-term survival of organ allografts. [ABSTRACT FROM AUTHOR]

Focuses on the role of T-cells in the induction of ILT3+ ILT4+ tolerogenic endothelial cells in organ allografts. Pathways of allorecognition; Factors preventing the proliferation of T-cell clones specific for DR1 peptide; Contribution of the indirect pathway of allorecognition to alloimmunity.

Scar tissue formation is a hallmark of wound repair in adults and can chronically affect tissue architecture and function. To understand the general phenomena, we sought to explore scar-driven imbalance in tissue homeostasis caused by a common, and standardized surgical procedure, the uterine scar due to cesarean surgery. Deep uterine scar is associated with a rapidly increasing condition in pregnant women, placenta accreta spectrum (PAS), characterized by aggressive trophoblast invasion into the uterus, frequently necessitating hysterectomy at parturition. We created a model of uterine scar, recapitulating PAS-like invasive phenotype, showing that scar matrix activates mechanosensitive ion channel, Piezo1, through glycolysis-fueled cellular contraction. Piezo1 activation increases intracellular calcium activity and Protein kinase C activation, leading to NF-κB nuclear translocation, and MafG stabilization. This inflammatory transformation of decidua leads to production of IL-8 and G-CSF, chemotactically recruiting invading trophoblasts towards scar, initiating PAS. Our study demonstrates aberrant mechanics of scar disturbs stroma-epithelia homeostasis in placentation, with implications in cancer dissemination., (© 2024. The Author(s).)

Hypoxia is one of the key factors in the tumor microenvironment regulating nearly all steps in the metastatic cascade in many cancers, including in breast cancer. The hypoxic regions can however be dynamic with the availability of oxygen fluctuating or oscillating. The canonical response to hypoxia is relayed by transcription factor Hypoxia-Inducible Factor 1 (HIF-1), which is stabilized in hypoxia and acts as the master regulator of a large number of downstream genes. However, HIF-1 transcriptional activity can also fluctuate either due to unstable hypoxia, or by lactate mediated noncanonical degradation of HIF-1. Our understanding of how oscillatory hypoxia or HIF-1 activity specifically influences cancer malignancy is very limited. Here, using MDA-MB-231 cells as a model of triple negative breast cancer characterized by severe hypoxia, we measured the gene expression changes induced specifically by oscillatory hypoxia. We found that oscillatory hypoxia can specifically regulate gene expression differently, and at times opposite to stable hypoxia. Using the Cancer Genome Atlas RNAseq data of human cancer samples, we show that the oscillatory specific gene expression signature in MDA-MB-231 is enriched in most human cancers, and prognosticates low survival in breast cancer patients. In particular, we found that oscillatory hypoxia, unlike stable hypoxia, induces unfolded protein folding response in cells resulting in gene expression predicting reduced survival., (© 2024 Wiley Periodicals LLC.)

Hypoxia is one of the key factors in the tumor microenvironment regulating nearly all steps in the metastatic cascade in many cancers, including in breast cancer. The hypoxic regions can however be dynamic with the availability of oxygen fluctuating or oscillating. The canonical response to hypoxia is relayed by transcription factor HIF-1, which is stabilized in hypoxia and acts as the master regulator of a large number of downstream genes. However, HIF-1 transcriptional activity can also fluctuate either due to unstable hypoxia, or by lactate mediated non-canonical degradation of HIF-1. Our understanding of how oscillatory hypoxia or HIF-1 activity specifically influence cancer malignancy is very limited. Here, using MDA-MB-231 cells as a model of triple negative breast cancer characterized by severe hypoxia, we measured the gene expression changes induced specifically by oscillatory hypoxia. We found that oscillatory hypoxia can specifically regulate gene expression differently, and at times opposite to stable hypoxia. Using The Cancer Genome Atlas (TCGA) RNAseq data of human cancer samples, we show that the oscillatory specific gene expression signature in MDA-MB-231 is enriched in most human cancers, and prognosticate low survival in breast cancer patients. In particular, we found that oscillatory hypoxia, unlike stable hypoxia, induces unfolded protein folding response (UPR) in cells resulting in gene expression predicting reduced survival.

Proton exchange membranes (PEMs) have emerged as very promising membranes for automotive applications because of their notable proton conductivity at low temperatures. These membranes find extensive utilization in fuel cells. Several polymeric materials have been used, but their application is constrained by their expense and intricate synthetic processes. Affordable and efficient synthetic methods for polymeric materials are necessary for the widespread commercial use of PEM technology. The polymeric combination of hexachlorocyclotriphosphazene (HCCP) and 4,4-diamino-2,2-biphenyldisulfonic acid facilitated the synthesis of PP-(PhSO 3 H) 2 , a polyphosphazene with built-in -SO 3 H moieties. Characterization revealed that it was a porous organic polymer with high stability. PP-(PhSO 3 H) 2 exhibited a proton conductivity of up to 8.24 × 10 -2 S cm -1 (SD = ±0.031) at 353 K under 98% relative humidity (RH), which was more than two orders of magnitude higher than that of its -SO 3 H-free analogue, PP-(Ph) 2 (2.32 × 10 -4 S cm -1 ) (SD = ±0.019) under identical conditions. Therefore, for application in a PEM fuel cell, PP-(PhSO 3 H) 2 -based matrix-mixed membranes (PP-(PhSO 3 H) 2 -MMMs) were fabricated by mixing them with polyacrylonitrile (PAN) in various ratios. The proton conductivity could reach up to 6.11 × 10 -2 S cm -1 (SD = ±0.0048) at 353 K and 98%RH, when the weight ratio of PP-(PhSO 3 H) 2  : PAN was 3 : 1, the value of which was comparable with those of commercially available electrolytes used in PEM fuel cells. PP-(PhSO 3 H) 2 -MMM (3 : 1) had an extended lifetime of reusability. Using phosphazene and bisulfonated multiple-amine modules as precursors, we demonstrated that a porous organic polymer with a highly effective proton-conductive matrix-mixed membrane for PEM fuel cells could be produced readily by an intuitive polymeric reaction., Competing Interests: There are no conflicts to declare., (This journal is © The Royal Society of Chemistry.)

Tumor hypoxia is a common microenvironmental factor in breast cancers, resulting in stabilization of Hypoxia-Inducible Factor 1 (HIF-1), the master regulator of hypoxic response in cells. Metabolic adaptation by HIF-1 results in inhibition of citric acid cycle, causing accumulation of lactate in large concentrations in hypoxic cancers. Lactate can therefore serve as a secondary microenvironmental factor influencing cellular response to hypoxia. Presence of lactate can alter the hypoxic response of breast cancers in many ways, sometimes in opposite manners. Lactate stabilizes HIF-1 in oxidative condition, as well as destabilizes HIF-1 in hypoxia, increases cellular acidification, and mitigates HIF-1-driven inhibition of cellular respiration. We therefore tested the effect of lactate in MDA-MB-231 under hypoxia, finding that lactate can activate pathways associated with DNA replication, and cell cycling, as well as tissue morphogenesis associated with invasive processes. Using a bioengineered nano-patterned stromal invasion assay, we also confirmed that high lactate and induced HIF-1α gene overexpression can synergistically promote MDA-MB-231 dissemination and stromal trespass. Furthermore, using The Cancer Genome Atlas, we also surprisingly found that lactate in hypoxia promotes gene expression signatures prognosticating low survival in breast cancer patients. Our work documents that lactate accumulation contributes to increased heterogeneity in breast cancer gene expression promoting cancer growth and reducing patient survival., (© 2024. The Author(s) under exclusive licence to Japan Human Cell Society.)

Background: Frequent premature atrial complexes (PACs) are associated with future incident atrial fibrillation (AF), but whether PACs contribute to development of AF through adverse atrial remodeling has not been studied. This study aimed to explore the effect of frequent PACs from different sites on atrial remodeling in a swine model., Methods: Forty swine underwent baseline electrophysiologic studies and echocardiography followed by pacemaker implantations and paced PACs (50% burden) at 250-ms coupling intervals for 16 weeks in 4 groups: (1) lateral left atrium (LA) PACs by the coronary sinus (Lat-PAC; n=10), (2) interatrial septal PACs (Sep-PAC; n=10), (3) regular LA pacing at 130 beats/min (Reg-130; n=10), and (4) controls without PACs (n=10). At the final study, repeat studies were performed, followed by tissue histology and molecular analyses focusing on fibrotic pathways., Results: Lat-PACs were associated with a longer P-wave duration (93.0±9.0 versus 74.2±8.2 and 58.8±7.6 ms; P <0.001) and greater echocardiographic mechanical dyssynchrony (57.5±11.6 versus 35.7±13.0 and 24.4±11.1 ms; P <0.001) compared with Sep-PACs and controls, respectively. After 16 weeks, Lat-PACs led to slower LA conduction velocity (1.1±0.2 versus 1.3±0.2 [Sep-PAC] versus 1.3±0.1 [Reg-130] versus 1.5±0.2 [controls] m/s; P <0.001) without significant change in atrial ERP. The Lat-PAC group had a significantly increased percentage of LA fibrosis and upregulated levels of extracellular matrix proteins (lysyl oxidase and collagen 1 and 8), as well as TGF-β1 (transforming growth factor-β1) signaling proteins (latent and monomer TGF-β1 and phosphorylation/total ratio of SMAD2/3; P <0.05). The Lat-PAC group had the longest inducible AF duration (terminal to baseline: 131 [interquartile range 30, 192] seconds versus 16 [6, 26] seconds [Sep-PAC] versus 22 [11, 64] seconds [Reg-130] versus -1 [-16, 7] seconds [controls]; P <0.001)., Conclusions: In this swine model, frequent PACs resulted in adverse atrial structural remodeling with a heightened propensity to AF. PACs originating from the lateral LA produced greater atrial remodeling and longer induced AF duration than the septal-origin PACs. These data provide evidence that frequent PACs can cause adverse atrial remodeling as well as AF, and that the location of ectopic PACs may be clinically meaningful., Competing Interests: Disclosures Pacemakers and leads used in the study were donated by Medtronic, Inc. The authors report no disclosures.

In developing nations with an abundance of natural water resources, fishing is a major source of income. When distributing resources between fisheries and other sectors, and preserving competitiveness in the fisheries industry, access to livelihood assets continues to be a key factor. However, vulnerability of livelihood assets and other economic and social variables have been severely affecting fishermen's livelihood. This article examines livelihood income vulnerability in the context of capital assets and the effects on local fishermen's livelihood and well-being. A survey sample size of 532 rural households based on a descriptive research design was used. Financial capital, human capital, social capital, and natural capital all made an enormous contribution to the earnings of fishermen and household heads in the Manchar Lake basin. The use of multiple regression analysis enabled new insights into how the livelihood assets characteristics affected their household income choices. The main objective of this investigation is to see whether access of livelihood capital assets affect local fishermen's livelihood income in the Manchar Lake basin. In the coastal belt of the Manchar Lake basin, resource acquisition plays a critical role in eradicating poverty. For the fishermen in the Manchar Lake basin, the current regime could further prioritize investing in fish trading infrastructure and improving essential facilities like social networks, education, skillsets, improved technology, and credit facilities in order to raise the livelihood income of fishermen and either reduce or alleviate poverty. These findings provide insight into fishermen's entry and exit for those who are planning livelihood shifts, and offer recommendations on how to overcome the constraints faced by the fisheries industry. Furthermore, insight into livelihood sustainability in order to improve the quality of life and income of fishermen domestically and nationally is also suggested., Competing Interests: No conflict of interest regarding the paper., (© 2023 The Authors.)

Background: Cardiovascular disease is the most common cause of death globally. Traditionally, centre-based cardiac rehabilitation programmes are offered to individuals after cardiac events to aid recovery and prevent further cardiac illness. Home-based and technology-supported cardiac rehabilitation programmes have been introduced in an attempt to widen access and participation, especially during the SARS-CoV-2 pandemic. This is an update of a review previously published in 2009, 2015, and 2017., Objectives: To compare the effect of home-based (which may include digital/telehealth interventions) and supervised centre-based cardiac rehabilitation on mortality and morbidity, exercise-capacity, health-related quality of life, and modifiable cardiac risk factors in patients with heart disease SEARCH METHODS: We updated searches from the previous Cochrane Review by searching the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE (Ovid), Embase (Ovid), PsycINFO (Ovid) and CINAHL (EBSCO) on 16 September 2022. We also searched two clinical trials registers as well as previous systematic reviews and reference lists of included studies. No language restrictions were applied., Selection Criteria: We included randomised controlled trials that compared centre-based cardiac rehabilitation (e.g. hospital, sports/community centre) with home-based programmes (± digital/telehealth platforms) in adults with myocardial infarction, angina, heart failure, or who had undergone revascularisation., Data Collection and Analysis: Two review authors independently screened all identified references for inclusion based on predefined inclusion criteria. Disagreements were resolved through discussion or by involving a third review author. Two authors independently extracted outcome data and study characteristics and assessed risk of bias. Certainty of evidence was assessed using GRADE., Main Results: We included three new trials in this update, bringing a total of 24 trials that have randomised a total of 3046 participants undergoing cardiac rehabilitation. A further nine studies were identified and are awaiting classification. Manual searching of trial registers until 16 September 2022 revealed a further 14 clinical trial registrations - these are ongoing. Participants had a history of acute myocardial infarction, revascularisation, or heart failure. Although there was little evidence of high risk of bias, a number of studies provided insufficient detail to enable assessment of potential risk of bias; in particular, details of generation and concealment of random allocation sequencing and blinding of outcome assessment were poorly reported. No evidence of a difference was seen between home- and centre-based cardiac rehabilitation in our primary outcomes up to 12 months of follow-up: total mortality (risk ratio [RR] = 1.19, 95% confidence interval [CI] 0.65 to 2.16; participants = 1647; studies = 12/comparisons = 14; low-certainty evidence) or exercise capacity (standardised mean difference (SMD) = -0.10, 95% CI -0.24 to 0.04; participants = 2343; studies = 24/comparisons = 28; low-certainty evidence). The majority of evidence (N=71 / 77 comparisons of either total or domain scores) showed no significant difference in health-related quality of life up to 24 months follow-up between home- and centre-based cardiac rehabilitation. Trials were generally of short duration, with only three studies reporting outcomes beyond 12 months (exercise capacity: SMD 0.11, 95% CI -0.01 to 0.23; participants = 1074; studies = 3; moderate-certainty evidence). There was a similar level of trial completion (RR 1.03, 95% CI 0.99 to 1.08; participants = 2638; studies = 22/comparisons = 26; low-certainty evidence) between home-based and centre-based participants. The cost per patient of centre- and home-based programmes was similar., Authors' Conclusions: This update supports previous conclusions that home- (± digital/telehealth platforms) and centre-based forms of cardiac rehabilitation formally supported by healthcare staff seem to be similarly effective in improving clinical and health-related quality of life outcomes in patients after myocardial infarction, or revascularisation, or with heart failure. This finding supports the continued expansion of healthcare professional supervised home-based cardiac rehabilitation programmes (± digital/telehealth platforms), especially important in the context of the ongoing global SARS-CoV-2 pandemic that has much limited patients in face-to-face access of hospital and community health services. Where settings are able to provide both supervised centre- and home-based programmes, consideration of the preference of the individual patient would seem appropriate. Although not included in the scope of this review, there is an increasing evidence base supporting the use of hybrid models that combine elements of both centre-based and home-based cardiac rehabilitation delivery. Further data are needed to determine: (1) whether the short-term effects of home/digital-telehealth and centre-based cardiac rehabilitation models of delivery can be confirmed in the longer term; (2) the relative clinical effectiveness and safety of home-based programmes for other heart patients, e.g. post-valve surgery and atrial fibrillation., (Copyright © 2023 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.)

Metabolic acidosis (MA) is a highly prevalent disorder in a significant proportion of the population, resulting from imbalance in blood pH homeostasis. The heart, being an organ with very low regenerative capacity and high metabolic activity, is vulnerable to chronic, although low-grade, MA. To systematically characterize the effect of low-grade MA on the heart, we treated male and female mice with NH 4 Cl supplementation for 2 weeks and analyzed their blood chemistry and transcriptomic signature of the heart tissue. The reduction of pH and plasma bicarbonate levels without an associated change in anion gap indicated a physiological manifestation of low-grade MA with minimal respiratory compensation. On transcriptomic analysis, we observed changes in cardiac-specific genes with significant gender-based differences due to MA. We found many genes contributing to dilated cardiomyopathy to be altered in males, more than in females, while cardiac contractility and Na/K/ATPase-Src signaling were affected in the opposite way. Our model presents a systems-level understanding of how the cardiovascular tissue is affected by MA. As low-grade MA is a common ailment with many dietary and pharmaceutical interventions, our work presents avenues to limit chronic cardiac damage and disease manifestation, as well as highlighting the sex differences in MA-induced cardiovascular damage.

Objective: Mannose-binding lectin deficiency may predispose children to having increased infection susceptibility. However, there is no conclusive evidence that mannose-binding lectin deficiency is associated with adverse respiratory consequences in children. We aimed to evaluate the effects of mannose-binding lectin deficiency (defined as a level of less than 0.6 mg/L) on clinical, radiological, and microbiological characteristics in children presenting with troublesome respiratory symptoms, as compared to those who are mannosebinding lectin-sufficient., Material and Methods: We conducted a retrospective cohort study to investigate the association between mannose-binding lectin deficiency and respiratory outcomes in children over a period of 10 years in a large teaching hospital. Children presenting with frequent or persistent respiratory symptoms such as a chronic wet cough lasting more than 4 weeks, recurrent lower respiratory tract infections (≥4 infections in a year), or severe respiratory tract infections requiring admission to intensive care or to high dependency unit were included in the study., Results: The study showed no significant difference in clinical outcomes with mannose-binding lectin deficiency and sufficiency. Thirty-two percent of children with mannose-binding lectin deficiency and 30% of those with mannose-binding lectin sufficiency had positive respiratory microbiology. Twenty-three percent of children with mannose-binding lectin deficiency and 24% of those with mannose-binding lectin sufficiency had radiological changes on plain radiographs; also the prevalence of bronchiectasis was similar in both groups. The rates of admission to pediatric intensive care unit were comparable in the 2 groups., Conclusions: Children with mannose-binding lectin deficiency and sufficiency showed similar clinical, radiological, and microbiological characteristics. Our study suggests that there are no childhood adverse respiratory consequences with mannose-binding lectin deficiency.

The following work is based on real-time temperature monitoring during the construction and during the operation of a dam. For this purpose, we have proposed a sensing model named: the "complex wireless sensors model (CWSM)" for measuring the value of different factors like temperature, humidity and pressure on the dam. The installation of the proposed model has been discussed with its wireless networking. The model contains five types of sensors i.e. humidity, temperature, pressure, sun and irradiance sensors for measuring the variation of different factors. The computation modeling of CWSM has been discussed in the paper. 3-D Finite Element method is used for thermal analysis. As the result, it is concluded that the wireless network will be more suitable for measuring and analyzing the effects of temperature, humidity, water pressure and solar radiation on the dam., Competing Interests: The authors declare no conflict of interest., (© 2023 The Authors.)