A novel combined nomogram for predicting severe acute lower respiratory tract infection in children hospitalized for RSV infection during the post-COVID-19 period.

Introduction: Off-season upsurge of respiratory syncytial virus (RSV) infection with changed characteristics and heightened clinical severity during the post-COVID-19 era are raising serious concerns. This study aimed to develop and validate a nomogram for predicting the risk of severe acute lower respiratory tract infection (SALRTI) in children hospitalized for RSV infection during the post-COVID-19 era using machine learning techniques. Methods: A multicenter retrospective study was performed in nine tertiary hospitals in Yunnan, China, enrolling children hospitalized for RSV infection at seven of the nine participating hospitals during January-December 2023 into the development dataset. Thirty-nine variables covering demographic, clinical, and laboratory characteristics were collected. Primary screening and dimension reduction of data were performed using Least Absolute Shrinkage and Selection Operator (LASSO) regression, followed by identification of independent risk factors for RSV-associated SALRTI using Logistic regression, thus finally establishing a predictive nomogram model. Performance of the nomogram was internally evaluated by receiver operating characteristic (ROC) curve, calibration curve, and decision curve analysis (DCA) based on the development dataset. External validation of our model was conducted using same methods based on two independent RSV cohorts comprising pediatric RSV inpatients from another two participating hospitals between January-March 2024. Results: The development dataset included 1102 patients, 239 (21.7%) of whom developed SALRTI; while the external validation dataset included 249 patients (142 in Lincang subset and 107 in Dali subset), 58 (23.3%) of whom were diagnosed as SALRTI. Nine variables, including age, preterm birth, underlying condition, seizures, neutrophil-lymphocyte ratio (NLR), interleukin-6 (IL-6), lactate dehydrogenase (LDH), D-dimer, and co-infection, were eventually confirmed as the independent risk factors of RSV-associated SALRTI. A predictive nomogram was established via integrating these nine predictors. In both internal and external validations, ROC curves indicated that the nomogram had satisfactory discrimination ability, calibration curves demonstrated good agreement between the nomogram-predicted and observed probabilities of outcome, and DCA showed that the nomogram possessed favorable clinical application potential. Conclusion: A novel nomogram combining several common clinical and inflammatory indicators was successfully developed to predict RSV-associated SALRTI. Good performance and clinical effectiveness of this model were confirmed by internal and external validations.

Inhalable mucin-permeable nanomicelles deliver antibiotics for effective treatment of chronic pneumonia.

Pseudomonas aeruginosa (P. aeruginosa) pneumonia can have serious physiological consequences, particularly when P. aeruginosa biofilms are formed. Although inhaled therapy is preferred, inhaled drugs tend to get trapped by pulmonary mucus, which hinders efficient antibiotic permeability through mucus and biofilms. In this study, we prepare poly[2-(pentamethyleneimino)ethyl methacrylate]-block-poly[2-(N-oxide-pentamethyleneimino)ethyl methacrylate] (PPEMA-b-PPOEMA) micelles loaded with azithromycin (AZM) using reversible addition-fragmentation chain transfer (RAFT) polymerization to achieve effective treatment of P. aeruginosa pneumonia. The zwitterionic structure on the surface of the micelle facilitates the successful traversal of the mucus and optimal concentration within the biofilm. Furthermore, the protonation of piperidine in the polymer enables the micelles to exhibit a positive charge in the acidic environment of a bacterial infection, enhancing AZM's interaction with the bacterium. Both in vivo and in vitro experiments demonstrate that this transmucosal zwitterionic polymer, in combination with a charge reversal strategy, effectively promotes the enrichment of micelles at the site of bacterial infection, thereby increasing the number of antibiotics reaching the bacterial interior and demonstrating remarkable antibacterial synergy. Overall, this work offers a promising approach for trans-airway drug delivery in the treatment of pneumonia.

Cohesin prevents cross-domain gene coactivation.

The contrast between the disruption of genome topology after cohesin loss and the lack of downstream gene expression changes instigates intense debates regarding the structure-function relationship between genome and gene regulation. Here, by analyzing transcriptome and chromatin accessibility at the single-cell level, we discover that, instead of dictating population-wide gene expression levels, cohesin supplies a general function to neutralize stochastic coexpression tendencies of cis-linked genes in single cells. Notably, cohesin loss induces widespread gene coactivation and chromatin co-opening tens of million bases apart in cis. Spatial genome and protein imaging reveals that cohesin prevents gene co-bursting along the chromosome and blocks spatial mixing of transcriptional hubs. Single-molecule imaging shows that cohesin confines the exploration of diverse enhancer and core promoter binding transcriptional regulators. Together, these results support that cohesin arranges nuclear topology to control gene coexpression in single cells.

Roles of m6A modification in regulating PPER pathway in cadmium-induced pancreatic ß cell death.

Cadmium can lead to the death of pancreatic ß cells, thus affecting the synthesis and secretion of insulin. However, the specific mechanisms underlying the cadmium-induced pancreatic ß cell death have not been fully understood. In this study, roles of m6A modification in regulating protein processing in endoplasmic reticulum (PPER) pathway in cadmium-induced pancreatic ß cell death were explored. Our results demonstrated that cell viability and RNA m6A modification level were decreased, while apoptosis rates increased after CdSO4 treatment in pancreatic ß cells (NIT-1). In addition, expressions of Bcl-2, Xbp1, Col3a1, Bax, Chop, Dnajb1, and Hsp90aa1 were all significantly changed in CdSO4 treatment cells. The m6A agonist entacapone (Ent) can prominently reverse the cytotoxicity effects of CdSO4 and alleviate the changes of protein expression induced by CdSO4 treatment. By contrast, m6A inhibitor 3-Deazaadenosine (DAA) can synergistically enhance the cytotoxicity of CdSO4 and aggravate the disorder of protein levels caused by CdSO4 treatment. Interestingly, the results of the immunoprecipitation experiment indicate that Ythdc2, one of m6A binding proteins, may regulate the PPER pathway molecules in an m6A-dependent manner. In summary, our findings provide new directions for the prevention and treatment of the impairment of pancreatic ß cell function induced by cadmium.

How does technological innovation affect the fiscal decentralization of local governments? Evidence from China.

Technological innovation is a pivotal driver of high-quality economic development, and China's distinctive fiscal decentralization model stands out as a crucial institutional factor behind the country's economic growth miracle. Despite its significant academic and practical implications, there is a noticeable scarcity of literature on examining government fiscal decentralization through the lens of technological innovation. This paper addresses fundamental research questions regarding the relationship between technological innovation and fiscal decentralization. Leveraging balanced panel data from 30 provinces in China spanning 2005 to 2020, our findings indicate that technological innovation positively impacts the fiscal decentralization of local governments. Specifically, for each standard deviation increase in technological innovation, there is a corresponding 0.1508 standard deviation in fiscal decentralization. The mechanism driving this relationship lies in technological innovation's ability to enhance enterprise profit levels, increasing tax and non-tax revenues for local governments. Importantly, when non-tax revenue at the central government level surpasses tax revenue, the resulting augmentation in local government revenue contributes to an elevated level of fiscal decentralization. In conclusion, this paper offers valuable insights into the government's endeavors to promote scientific and technological innovation while enhancing local fiscal decentralization. These insights contribute to an improved quality of economic development.

Rifampicin synergizes the toxicity of insecticides against the green peach aphid, Myzus persicae.

Myzus persicae is an important pest that has developed resistance to nearly all currently used insecticidal products. The employment of insecticide synergists is one of the effective strategies that need to be developed for the management of this resistance. Our study showed that treatment with a combination of the antibiotic, rifampicin, with imidacloprid, cyantraniliprole, or clothianidin significantly increased their toxicities against M. persicae, by 2.72, 3.59, and 2.41 folds, respectively. Rifampicin treatment led to a noteworthy reduction in the activities of multifunctional oxidases (by 32.64%) and esterases (by 23.80%), along with a decrease in the expression of the CYP6CY3 gene (by 58.57%) in M. persicae. It also negatively impacted the fitness of the aphids, including weight, life span, number of offspring, and elongation of developmental duration. In addition, bioassays showed that the combination of rifampicin and a detoxification enzyme inhibitor, piperonyl butoxide, or dsRNA of CYP6CY3 further significantly improved the toxicity of imidacloprid against M. persicae, by 6.19- and 7.55-fold, respectively. The present study suggests that development of active ingredients such as rifampicin as candidate synergists, show promise to overcome metabolic resistance to insecticides in aphids.

Identification of neuropeptides and their G protein-coupled receptors in the predatory stink bug, Arma custos (Hemiptera: Pentatomidae).

The predatory stink bug Arma custos has been selected as an effective biological control agent and has been successfully massly bred and released into fields for the control of a diverse insect pests. As a zoophytophagous generalist, A. custos relies on a complex neuropeptide signaling system to prey on distinct food and adapt to different environments. However, information about neuropeptide signaling genes in A. custos has not been reported to date. In the present study, a total of 57 neuropeptide precursor transcripts and 41 potential neuropeptide G protein-coupled receptor (GPCR) transcripts were found mainly using our sequenced transcriptome data. Furthermore, a number of neuropeptides and their GPCR receptors that were enriched in guts and salivary glands of A. custos were identified, which might play critical roles in feeding and digestion. Our study provides basic information for an in-depth understanding of biological and ecological characteristics of the predatory bug and would aid in the development of better pest management strategies based on the effective utilization and protection of beneficial natural enemies.

A role and mechanism for redox sensing by SENP1 in ß-cell responses to high fat feeding.

Pancreatic ß-cells respond to metabolic stress by upregulating insulin secretion, however the underlying mechanisms remain unclear. Here we show, in ß-cells from overweight humans without diabetes and mice fed a high-fat diet for 2 days, insulin exocytosis and secretion are enhanced without increased Ca2+ influx. RNA-seq of sorted ß-cells suggests altered metabolic pathways early following high fat diet, where we find increased basal oxygen consumption and proton leak, but a more reduced cytosolic redox state. Increased ß-cell exocytosis after 2-day high fat diet is dependent on this reduced intracellular redox state and requires the sentrin-specific SUMO-protease-1. Mice with either pancreas- or ß-cell-specific deletion of this fail to up-regulate exocytosis and become rapidly glucose intolerant after 2-day high fat diet. Mechanistically, redox-sensing by the SUMO-protease requires a thiol group at C535 which together with Zn+-binding suppresses basal protease activity and unrestrained ß-cell exocytosis, and increases enzyme sensitivity to regulation by redox signals.

Apatinib weakens proliferation, migration, invasion, and angiogenesis of thyroid cancer cells through downregulating pyruvate kinase M2.

Thyroid cancer (TC) is the most frequent malignancy of the endocrine system. Apatinib, as an anti-angiogenic agent, has been applied in the therapy of several cancers. However, the function and mechanism of Apatinib in TC have not been clearly elucidated. After processing with Apatinib alone or combined PKM2 overexpression plasmids, cell proliferation, migration, and invasion were analyzed by EdU staining, CCK-8, wound healing, and Transwell. Meanwhile. HUVECs were incubated with the conditioned medium prepared from cell culture medium, and tube formation and VEGFR2 expression in HUVECs were examined using tube formation and immunofluorescence (IF) assays. Besides, we established a nude mouse xenograft model by lentivirus-mediated PKM2 shRNAs, and tested the growth of tumors; the pathological structure was analyzed with H&E staining. And the expressions of N-cadherin, Vimentin, E-cadherin, PKM2, VEGFA, VEGFR2, and Ki67 were determined by immunohistochemistry or Western blot. Apatinib could prominently suppress proliferation, migration, invasion, and HUVEC tube formation in SW579 and TPC-1 cells. Besides, we discovered that Apatinib had a significant inhibitory role on the expression of pyruvate kinase M2 (PKM2) in TC cells. And PKM2 overexpression also could notably reverse Apatinib-mediated inhibition of TC progression. Moreover, PKM2 shRNAs were applied to TC xenografts, resulting in significant reduction in tumor volume and suppression of angiogenesis-related protein expression. In summary, Apatinib has a regulatory role in TC progression, and Apatinib can block cancer cell angiogenesis by downregulating PKM2. This will provide a theoretical basis for therapy of TC.

Association of atopy with disease severity in children with Mycoplasma pneumoniae pneumonia.

Background: Mycoplasma pneumoniae pneumonia (MPP) is common among children, but the impact of atopy on MPP severity in children is unknown. This study investigated whether atopic vs. nonatopic children had greater MPP severity. Methods: Retrospective analysis was conducted on 539 (ages 3-14 years) patients who were hospitalized in the First Affiliated Hospital of Anhui Medical University for MPP between January 2018 and December 2021, 195 were atopic and 344 were nonatopic. Of them, 204 had refractory MPP, and 335 had general MPP. And of atopic children, 94 had refractory MPP, and 101 had general MPP. Data on demographic and clinical characteristics, laboratory findings, clinical treatments were analyzed. Results: Significantly more boys with MPP were atopic than nonatopic (P < 0.05). More atopic (than nonatopic) children presented with prolonged fever and hospitalization, severe extra-pulmonary complications, asthma attaking, steroid and oxygen treatment, and increased IgE levels (all P < 0.05). In atopic (vs. nonatopic) children with MPP, the incidence of sputum plugs under the fiberoptic bronchoscopy and lobar pneumonia was significantly increased and required bronchoscopy-assisted and steroid therapy. Compared with nonatopic children, more atopic children developed refractory MPP (P < 0.05). Prolonged fever and hospitalization, severe extra-pulmonary complications, lymphocyte count, procalcitonin and lactate dehydrogenase levels, and percentages of atopy were all significantly higher (P < 0.05) among children with refractory MPP vs. general MPP. Moreover, Prolonged fever and hospitalization, lymphocyte count, procalcitonin and lactate dehydrogenase levels, and the treantment of steroid were all significantly higher (P < 0.05) among atopic children with refractory MPP vs. general MPP. Spearman correlation analysis showed strong associations between atopy and male sex, length of hospital stay, fever duration, IgE level, wheezing, lobar pneumonia, refractory MPP, and treatment with oxygen, hormones or bronchoscopy (P < 0.05). Conclusions: Atopy may be a risk factor for and was positively correlated with the severity of MPP in children.

Clinical efficacy of "Sancai therapy" for hyperplasia of the mammary glands: A systematic review and meta-analysis.

BACKGROUND: Hyperplasia of the mammary glands (HMG) is the most prevalent breast disease and can become malignant if left untreated. Although "Sancai therapy" has been widely used to treat HMG, its efficacy has not yet been systematically reviewed. This study aims to systematically evaluate the clinical efficacy of Sancai therapy for HMG treatment and provide a clinical basis for its future use. METHODS: PubMed, Cochrane Library, Web of Science, EMBASE, CNKI, CBM, VIP, and Wanfang databases were reviewed for related data collection. Chinese and English databases were searched for randomized controlled trials on Sancai therapy for HMG. The retrieval date was February 27, 2023. Exclusion criteria: (1) Non-HMG patients; (2) case reports, literature reviews, animal experiments, systematic reviews; and (3) full text could not be obtained. Data obtained after literature screening were imported into the RevMan 5.4.1 software for meta-analysis, and the included literature was assessed for methodological quality using the "bias risk assessment" tool within the software. RESULTS: The meta-analysis included 11 studies. Compared to the control group, the Sancai therapy treatment group exhibited an overall increased efficacy (relative risk = 1.36, 95% confidence interval [CI] [1.18, 1.58], P < .0001), an increased cure rate (relative risk = 3.74, 95% CI [1.70, 8.25], P = .001), a significant improvement in breast pain (standard mean difference = -2.68, 95% CI [-3.41, -1.96], P < .00001), and a reduction in breast masses (standard mean difference = -2.87, 95% CI [-3.75, -1.99], P < .00001). CONCLUSION: Sancai therapy significantly improved the overall efficacy, cure rate, and breast pain and reduced breast mass compared with the control groups. However, further large-sample, high-quality, double-blind randomized controlled trials are required to increase the level of evidence. PROTOCOL REGISTRATION NUMBER: INPLASY202380124.

Transcriptome analysis reveals salivary gland-specific neuropeptide signaling genes in the predatory stink bug, Picromerus lewisi.

Predatory stink bugs derive from phytophagous stink bugs and evolved enhanced predation skills. Neuropeptides are a diverse class of ancient signaling molecules that regulate physiological processes and behavior in animals, including stink bugs. Neuropeptide evolution might be important for the development of predation because neuropeptides can be converted to venoms that impact prey. However, information on neuropeptide signaling genes in predatory stink bugs is lacking. In the present study, neuropeptide signaling genes of Picromerus lewisi, an important predatory stink bug and an effective biological agent, were comprehensively identified by transcriptome analysis, with a total of 59 neuropeptide precursor genes and 58 potential neuropeptide receptor genes found. In addition, several neuropeptides and their receptors enriched in salivary glands of P. lewisi were identified. The present study and subsequent functional research contribute to an in-depth understanding of the biology and behavior of the predatory bugs and can provide basic information for the development of better pest management strategies, possibly including neuropeptide receptors as insecticide targets and salivary gland derived venom toxins as novel killing moleculars.

GPR84-mediated signal transduction affects metabolic function by promoting brown adipocyte activity.

The G protein-coupled receptor 84 (GPR84), a medium-chain fatty acid receptor, has garnered attention because of its potential involvement in a range of metabolic conditions. However, the precise mechanisms underlying this effect remain elusive. Our study has shed light on the pivotal role of GPR84, revealing its robust expression and functional significance within brown adipose tissue (BAT). Mice lacking GPR84 exhibited increased lipid accumulation in BAT, rendering them more susceptible to cold exposure and displaying reduced BAT activity compared with their WT counterparts. Our in vitro experiments with primary brown adipocytes from GPR84-KO mice revealed diminished expression of thermogenic genes and reduced O2 consumption. Furthermore, the application of the GPR84 agonist 6-n-octylaminouracil (6-OAU) counteracted these effects, effectively reinstating the brown adipocyte activity. These compelling in vivo and in vitro findings converge to highlight mitochondrial dysfunction as the primary cause of BAT anomalies in GPR84-KO mice. The activation of GPR84 induced an increase in intracellular Ca2+ levels, which intricately influenced mitochondrial respiration. By modulating mitochondrial Ca2+ levels and respiration, GPR84 acts as a potent molecule involved in BAT activity. These findings suggest that GPR84 is a potential therapeutic target for invigorating BAT and ameliorating metabolic disorders.

Impairment of serine transport across the blood-brain barrier by deletion of Slc38a5 causes developmental delay and motor dysfunction.

Brain L-serine is critical for neurodevelopment and is thought to be synthesized solely from glucose. In contrast, we found that the influx of L-serine across the blood-brain barrier (BBB) is essential for brain development. We identified the endothelial Slc38a5, previously thought to be a glutamine transporter, as an L-serine transporter expressed at the BBB in early postnatal life. Young Slc38a5 knockout (KO) mice exhibit developmental alterations and a decrease in brain L-serine and D-serine, without changes in serum or liver amino acids. Slc38a5-KO brains exhibit accumulation of neurotoxic deoxysphingolipids, synaptic and mitochondrial abnormalities, and decreased neurogenesis at the dentate gyrus. Slc38a5-KO pups exhibit motor impairments that are affected by the administration of L-serine at concentrations that replenish the serine pool in the brain. Our results highlight a critical role of Slc38a5 in supplying L-serine via the BBB for proper brain development.

Characteristics of Epicoccum latusicollum as revealed by genomic and metabolic phenomic analysis, the causal agent of tobacco Epicoccus leaf spot.

Epicoccum latusicollum is a fungus that causes a severe foliar disease on flue-cured tobacco in southwest China, resulting in significant losses in tobacco yield and quality. To better understand the organism, researchers investigated its optimal growth conditions and metabolic versatility using a combination of traditional methods and the Biolog Phenotype MicroArray technique. The study found that E. latusicollum exhibited impressive metabolic versatility, being able to metabolize a majority of carbon, nitrogen, sulfur, and phosphorus sources tested, as well as adapt to different environmental conditions, including broad pH ranges and various osmolytes. The optimal medium for mycelial growth was alkyl ester agar medium, while oatmeal agar medium was optimal for sporulation, and the optimum temperature for mycelial growth was 25°C. The lethal temperature was 40°C. The study also identified arbutin and amygdalin as optimal carbon sources and Ala-Asp and Ala-Glu as optimal nitrogen sources for E. latusicollum. Furthermore, the genome of E. latusicollum strain T41 was sequenced using Illumina HiSeq and Pacific Biosciences technologies, with 10,821 genes predicted using Nonredundant, Gene Ontology, Clusters of Orthologous Groups, Kyoto Encyclopedia of Genes and Genomes, and SWISS-PROT databases. Analysis of the metabolic functions of phyllosphere microorganisms on diseased tobacco leaves affected by E. latusicollum using the Biolog Eco microplate revealed an inability to efficiently metabolize a total of 29 carbon sources, with only tween 40 showing some metabolizing ability. The study provides new insights into the structure and function of phyllosphere microbiota and highlights important challenges for future research, as well as a theoretical basis for the integrated control and breeding for disease resistance of tobacco Epicoccus leaf spot. This information can be useful in developing new strategies for disease control and management, as well as enhancing crop productivity and quality.

Microwave ablation for the treatment of peripheral ground-glass nodule-like lung cancer: Long-term results from a multi-center study.

Introduction: Microwave ablation (MWA) is an effective and safe approach for the treatment of ground-glass nodule (GGN)-like lung cancer, but long-term follow-up is warranted. Therefore, this multi-center retrospective study aimed to evaluate the results of MWA for the treatment of peripheral GGN-like lung cancer with a long-term follow-up. Materials and Methods: From June 2013 to January 2018, a total of 87 patients (47 males and 40 females, mean age 64.6 ± 10.2 years) with 87 peripheral lung cancer lesions showing GGN (mean long axis diameter, 17 ± 5 mm) underwent computed tomography (CT)-guided percutaneous MWA. All GGN-like lung cancers were histologically verified. The primary endpoints were local progression-free survival (LPFS) and overall survival (OS). The secondary endpoints were cancer-specific survival (CSS) and complications. Results: During a median follow-up of 65 months, both the 3-year and 5-year LPFS rates were 96.6% and 96.6%. The OS rate was 94.3% at 3 years and 84.9% at 5 years, whereas the 3-year and 5-year CSS rates were 100% and 100%, respectively. No periprocedural deaths were observed. Complications were observed in 49 patients (51.6%). Grade 3 or higher complications included pneumothorax, pleural effusion, hemorrhage, and pulmonary infection, which were identified in ten (10.5%), two (2.1%), two (2.1%), and one (1.1%) patient, respectively. Conclusions: CT-guided percutaneous MWA is an effective, safe, and potentially curative treatment regimen for GGN-like lung cancer.

Identification of metabolizing enzyme genes associated with xenobiotics and odorants in the predatory stink bug Arma custos based on transcriptome analysis.

The predatory stink bug, Arma custos, is a highly effective beneficial predator of crop pests. The lack of gene information related to xenobiotic detoxification and odorant degrading enzymes in the predator stink bugs to date has limited our ability for more in-depth studies of biological control. Hence, we conducted de novo assembly of the A. custos transcriptome from guts, antennae, and other tiussue samples of 5th instar larvae using Illumina sequencing technology. A total of 91, 50 and 23 genes of cytochrome P450 monooxygenases (CYPs), carboxyl/choline esterases (CCEs) and glutathione S-transferases (GSTs) genes were identified, respectively. Gene expansions of CYP3 and CYP4 clans and the hormone and pheromone processing CCE class were found in A. custos. Analysis of tissue-specific expression patterns showed that 37 CYPs, 14 CCEs and 8 GSTs were enriched in guts, and 6 CYPs, 5 CCEs and 2 GSTs were up-regulated in antennae, suggesting their potential roles on xenobiotics detoxification and ordorant degradation. Gene information data presented here could be useful for a deeper understanding of the ecology, physiology and behavior of this beneficial species and could be helpful to improve their bio-control efficiency.

Allosteric activation of vinculin by talin.

The talin-vinculin axis is a key mechanosensing component of cellular focal adhesions. How talin and vinculin respond to forces and regulate one another remains unclear. By combining single-molecule magnetic tweezers experiments, Molecular Dynamics simulations, actin-bundling assays, and adhesion assembly experiments in live cells, we here describe a two-ways allosteric network within vinculin as a regulator of the talin-vinculin interaction. We directly observe a maturation process of vinculin upon talin binding, which reinforces the binding to talin at a rate of 0.03 s-1. This allosteric transition can compete with force-induced dissociation of vinculin from talin only at forces up to 10 pN. Mimicking the allosteric activation by mutation yields a vinculin molecule that bundles actin and localizes to focal adhesions in a force-independent manner. Hence, the allosteric switch confines talin-vinculin interactions and focal adhesion build-up to intermediate force levels. The 'allosteric vinculin mutant' is a valuable molecular tool to further dissect the mechanical and biochemical signalling circuits at focal adhesions and elsewhere.

Associated Risk Factors and Diagnostic Value of Fiberoptic Bronchoscopy for Protracted Bacterial Bronchitis in Children.

Objective: Untreated protracted bacterial bronchitis (PBB), a chronic wet cough prevalent in children, may lead to chronic suppurative lung disease. However, clinical diagnostic criteria are currently nonspecific; thus, PBB may be misdiagnosed. Thus, we assessed the diagnostic value of fiberoptic bronchoscopy (FOB) and the risk factors associated with PBB. Methods: Children with chronic cough at The First Affiliated Hospital of Anhui Medical University from January 2015 to May 2020 were enrolled and allocated to a suspected PBB (n = 141) or a non-PBB (n = 206) group. All children underwent extensive laboratory, chest imaging, and allergen tests. Children with suspected PBB underwent FOB with bronchoalveolar lavage; lavage and sputum samples were cultured. Results: All 347 children had a chronic wet cough for approximately 2 months. Of 141 children with suspected PBB, 140 received FOB with bronchoalveolar lavage. Visible tracheal changes included pale mucosa, mucosal congestion, edema, swelling, and increased secretions attached to the wall. Sputum was visible primarily in the left main bronchus (78.7%), left lower lobe (59.6%), right upper lobe (62.4%), and right lower lobe (64.5%). Sputum properties and amounts significantly differed between children with vs. without PBB (P < 0.05). Dermatophagoides (odds ratio (OR), 2.642; 95% CI, 1.283-5.369), milk protein (OR, 2.452; 95% CI, 1.243-4.836) allergies, and eczema (OR, 1.763; 95% CI, 1.011-3.075) were risk factors significantly associated with PBB. Conclusion: Dermatophagoides, milk protein, and eczema were associated with an increased risk of PBB. Sputum distribution and tracheal wall changes observed through FOB may distinguish PBB and assist in its diagnosis.

Identifying driving hydrogeomorphic factors of coastal wetland downgrading using random forest classification models.

Coastal wetlands provide critical ecosystem services but are experiencing disruptions caused by inundation and saltwater intrusion under intensified climate change, sea-level rise, and anthropogenic activities. Recent studies have shown that these disturbances downgraded coastal wetlands mainly through affecting their hydrological processes. However, research on what is the most critical driver for wetland downgrading and how it affects coastal wetlands is still in its infancy. This study examined drivers of three types of wetland downgrading, including woody wetland loss, emergent herbaceous wetland loss, and woody wetlands converting to emergent herbaceous wetlands. By using random forest classification models for the wetland ecosystems in the Alligator River National Wildlife Refuge, North Carolina, USA, during 1995-2019, we determined the relative importance of different hydrogeomorphic processes and the dominant variables in driving the wetland downgrading. Results showed that random forest classification models were accurate (> 97 % overall accuracy) in classifying wetland downgrading. Multiple hydrogeomorphic variables collectively contributed to the coastal wetland downgrading. However, the dominant control factors varied across different types of wetland downgrading. Woody wetlands were most susceptible to saltwater intrusion and were likely to downgrade if the saltwater table was shallower than 0.2 m below the land surface. In contrast, emergent herbaceous wetlands were most vulnerable to inundation and drought. The favorable groundwater table for emergent herbaceous wetlands was between 0.34 m above the land surface and 0.32 m below the land surface, beyond which the emergent herbaceous wetland tended to disappear. For downgraded woody wetlands, their distance to canals/ditches played a crucial role in determining their fates after downgrading. The machine learning approach employed in this study provided critical knowledge about the thresholds of hydrogeomorphic variables for the downgrading of different types of coastal wetlands. Such information can help guide effective and targeted coastal wetland conservation, management, and restoration measures.