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With the increasing incidence of kidney diseases, there is an urgent need to develop therapeutic strategies to combat post‐injury fibrosis. Immune cells, including platelets, play a pivotal role in this repair process, primarily through their released cytokines. However, the specific role of platelets in kidney injury and subsequent repair remains underexplored. Here, the detrimental role of platelets in renal recovery following ischemia/reperfusion injury and its contribution to acute kidney injury to chronic kidney disease transition is aimed to investigated. In this study, it is shown that depleting platelets accelerates injury resolution and significantly reduces fibrosis. Employing advanced single‐cell and spatial transcriptomic techniques, macrophages as the primary mediators modulated by platelet signals is identified. A novel subset of macrophages, termed "cycling M2", which exhibit an M2 phenotype combined with enhanced proliferative activity is uncovered. This subset emerges in the injured kidney during the resolution phase and is modulated by platelet‐derived thrombospondin 1 (THBS1) signaling, acquiring profibrotic characteristics. Conversely, targeted inhibition of THBS1 markedly downregulates the cycling M2 macrophage, thereby mitigating fibrotic progression. Overall, this findings highlight the adverse role of platelet THBS1‐boosted cycling M2 macrophages in renal injury repair and suggest platelet THBS1 as a promising therapeutic target for alleviating inflammation and kidney fibrosis. [ABSTRACT FROM AUTHOR]

The article focuses on exploring the spatial contribution of immune cells to gene expression in lung fibroblasts within fibrotic lesions in idiopathic pulmonary fibrosis (IPF). Topics include the characterization of "hot" and "cold" fibrotic lesions based on immune cell presence, the identification of gene expression profiles associated with these lesions, and proteomic analysis confirming the pro-proliferative and immune-mediated characteristics of "hot" lesions.

Focusing on U.S. oil and gas companies following the SEC's investigation of ExxonMobil's climate risk issues, this study investigates the impact of climate change risk (CCR) disclosure on corporate accounting choices. After examining U.S. oil and gas firms' 10-K filings, carbon disclosure project (CDP) reports, and multi-source corporate sustainability reports, we find a positive association between CCR disclosure and the full cost (FC) accounting choice, designating that oil and gas firms with greater CCR disclosures are more likely to adopt the FC method to record oil and gas exploration activities. Our study responds to the SEC's2010 and 2022 Climate Change Disclosure Guidance and encourages more oil and gas companies to disclose CCR and its impact on financial reporting to facilitate transparent transitions towards a low-carbon economy. [ABSTRACT FROM AUTHOR]

Intraoperative computed tomography scanning with O-arm and use of Stealth navigation can improve surgical outcomes in a variety of orthopedic subspecialties. In spine surgery, the accuracy, precision, and safety of pedicle screw and interbody implant placement has improved. This technology is now routinely used in percutaneous pedicle screw placement and minimally invasive sacroiliac joint fusion. Other applications include, but are not limited to, isthmic pars defect repair, lumbosacral pseudoarticulation resection in Bertolotti's syndrome, radiofrequency ablation, and en bloc tumor resection. Intraoperative navigation has numerous applications, and use of this technology should continue to evolve as the technology advances. [Orthopedics. 2023;46(2):e89–e97.] [ABSTRACT FROM AUTHOR]

Increasing public attention to climate change has led to many studies to investigate the impact of climate change in various fields. However, the topic demands a further thorough examination of the impact of climate change on firms' accounting behavior, such as firm disclosure. There are currently no mandatory U.S. accounting standards issued by accounting standards‐setting bodies such as the FASB or SEC on reporting the impact of climate change on firms' business. However, firms have started to report the impact of climate change on a voluntary basis. In order to help academia, professionals, and investors better understand voluntary climate change disclosure, this study surveys theories of corporate accounting disclosure related to corporate social responsibility and environmental reporting, particularly in the areas of voluntary climate change disclosure. This study integrates multi‐dimensional corporate climate change disclosure theories to help future policymakers, investors, and other stakeholders provide appropriate corporate climate disclosure theoretical assistance and respond to the government and society's calls for a low‐carbon economy. [ABSTRACT FROM AUTHOR]

This paper examines the influence of smog on firm earnings and information content using the data of Chinese A share listed firms and the air quality monitoring data released by the China National Environmental Monitoring Center from 2013 to 2017. The empirical results show that smog will not only negatively influence the earnings of local firms, but also result in a decrease in the information content of their earnings for market valuations. This paper further tests the role of firm size in the influence mechanism of smog on earnings and information content. The results reveal the significant moderating effect of firm size in the influence mechanism, which is reflected by large-scale firms being more likely to suffer earnings decrease and less likely to suffer earnings information content decrease due to smog, while small-scale firms tend to experience the opposite. [ABSTRACT FROM AUTHOR]

Tobacco smoking is a well-known risk factor for both fibrogenesis and fibrotic progression; however, themechanisms behind these processes remain enigmatic.RTKs (receptor tyrosine kinases) have recently been reported to drive profibrotic phenotypes in fibroblasts during pulmonary fibrosis (PF). Using a phospho-RTK array screen, we identified the RTK AXL as a top upregulated RTK in response to smoke. Both expression and signaling activity of AXL were indeed elevated in lung fibroblasts exposed to tobacco smoke, whereas no significant change to the levels of a canonicalAXLlig and, Gas6 (growth arrest-specific 6), was seen upon smoke treatment. Notably, we found that smoke-exposed human lung fibroblasts exhibited highly proliferative and invasive activities and were capable of inducing fibrotic lung lesions in mice. Conversely, genetic suppression of AXL in smoke-exposed fibroblasts cells led to suppression of AXL downstream pathways and aggressive phenotypes. We further demonstrated that AXL interacted with MARCKS (myristoylated alanine-rich C kinase substrate) and cooperated with MARCKS in regulating downstream signaling activity and fibroblast invasiveness. Pharmacological inhibition of AXL with AXL-specific inhibitor R428 showed selectivity for smoke-exposed fibroblasts. In all, our data suggest that AXL is a potential marker for smoke-associated PF and that targeting of the AXL pathway is a potential therapeutic strategy in treating tobacco smoking-related PF. [ABSTRACT FROM AUTHOR]

Cigarette smoking is a well-known risk factor for pulmonary diseases, including chronic obstructive pulmonary disease (COPD), asthma and pulmonary fibrosis. Despite major progress in dissecting the mechanisms associated with disease development and progression, findings only represent one aspect of multifaceted disease. A crucial consequence of this approach is that many therapeutic treatments often fail to improve or reverse the disease state as other conditions and variables are insufficiently considered. To expand our understanding of pulmonary diseases, omics approaches, particularly metabolomics, has been emerging in the field. This strategy has been applied to identify putative biomarkers and novel mechanistic insights. In this review, we discuss metabolic profiles of patients with COPD, asthma, and idiopathic pulmonary fibrosis (IPF) with a focus on the direct effects of cigarette smoking in altering metabolic regulation. We next present cell- and animal-based experiments and point out the therapeutic potential of targeting metabolic reprogramming in inflammatory lung diseases. In addition, the obstacles in translating these findings into clinical practice, including potential adverse effects and limited pharmacological efficacy, are also addressed. Image 1 • Smoke exposure causes inflammatory response and multiple pathophysiological processes via metabolic dysregulation. • The alteration of mitochondrial functions drives emphysema for chronic obstructive pulmonary disease. • Arginine reprogramming and mitochondrial fragmentation promote airway remodeling in allergic asthma. • TGF-β1 upregulates metabolic flux for lung fibroblast activation in pulmonary fibrosis. [ABSTRACT FROM AUTHOR]

Targeting activated fibroblasts, including myofibroblast differentiation, has emerged as a key therapeutic strategy in patients with idiopathic pulmonary fibrosis (IPF). However, there is no available therapy capable of selectively eradicating myofibroblasts or limiting their genesis. Through an integrative analysis of the regulator genes that are responsible for the activation of IPF fibroblasts, we noticed the phosphatidylinositol 4,5-bisphosphate (PIP2)-binding protein, myristoylated alanine-rich C-kinase substrate (MARCKS), as a potential target molecule for IPF. Herein, we have employed a 25-mer novel peptide, MARCKS phosphorylation site domain sequence (MPS), to determine if MARCKS inhibition reduces pulmonary fibrosis through the inactivation of PI3K/protein kinase B (AKT) signaling in fibroblast cells. We first observed that higher levels of MARCKS phosphorylation and the myofibroblast marker α-smooth muscle actin (α-SMA) were notably overexpressed in all tested IPF lung tissues and fibroblast cells. Treatment with the MPS peptide suppressed levels of MARCKS phosphorylation in primary IPF fibroblasts. A kinetic assay confirmed that this peptide binds to phospholipids, particularly PIP2, with a dissociation constant of 17.64 nM. As expected, a decrease of phosphatidylinositol (3,4,5)-trisphosphate pools and AKT activity occurred in MPS-treated IPF fibroblast cells. MPS peptide was demonstrated to impair cell proliferation, invasion, and migration in multiple IPF fibroblast cells in vitro as well as to reduce pulmonary fibrosis in bleomycin-treated mice in vivo. Surprisingly, we found that MPS peptide decreases a-SMA expression and synergistically interacts with nintedanib treatment in IPF fibroblasts. Our data suggest MARCKS as a druggable target in pulmonary fibrosis and also provide a promising antifibrotic agent that may lead to effective IPF treatments. [ABSTRACT FROM AUTHOR]

S-Arylation of cysteine residues is an increasingly powerful tool for site-specific modification of proteins, providing novel structure and electronic perturbation. The present work demonstrates an operationally-simple cysteine arylation reaction 2-nitro-substituted arylboronic acids, promoted by a simple nickel(ii) salt. The process exhibits strikingly fast reaction rates under physiological conditions in purely aqueous media with excellent selectivity toward cysteine residues. Cysteine arylation of natural proteins and peptides allows attachment of useful reactive handles for stapling, imaging, or further conjugation. [ABSTRACT FROM AUTHOR]

Cigarette smoke has been shown to trigger aberrant signaling pathways and pathophysiological processes; however, the regulatory mechanisms underlying smoke-induced gene expression remain to be established. Herein, we observed that two smoke-responsive genes, HO-1 and CYP1A1, are robustly induced upon smoke by different mechanisms in human bronchial epithelia. CYP1A1 is mediated by aryl hydrocarbon receptor signaling, while induction of HO-1 is regulated by oxidative stress, and suppressed by N-acetylcysteine treatment. In light of a pivotal role of NRF2 and BACH1 in response to oxidative stress and regulation of HO-1, we examined if smoke-induced HO-1 expression is modulated through the NRF2/BACH1 axis. We demonstrated that smoke causes significant nuclear translocation of NRF2, but only a slight decrease in nuclear BACH1. Knockdown of NRF2 attenuated smoke-induced HO-1 expression while down-regulation of BACH1 had stimulatory effects on both basal and smoke-induced HO-1 with trivial influence on NRF2 nuclear translocation. Chromatin immunoprecipitation assays showed that smoke augments promoter-specific DNA binding of NRF2 but suppresses BACH1 binding to the HO-1 promoter ARE sites, two of which at 􀀀1.0 kb and 􀀀2.6 kb are newly identified. These results suggest that the regulation of NRF2 activator and BACH1 repressor binding to the ARE sites are critical for smoke-mediated HO-1 induction. [ABSTRACT FROM AUTHOR]

There is an increasing public concern about climate change. As a response to such concern in the accounting field, in 2010, the Securities and Exchange Commission (SEC) announced the SEC 2010 Commission Guidance Regarding Disclosure Related to Climate Change (SEC 2010 Guidance), the first disclosure guidance issued by either the FASB or the SEC for U.S. listed companies. However, the publication provoked criticism and debate. Opponents point out that the SEC 2010 Guidance might have an adverse impact on corporate social responsibility (CSR) reporting "by registrants fearful of liability under securities laws for the contents of such disclosures" (Shorter, 2013). This study investigates (1) the relation between firms' climate change disclosure and corporate social responsibility (CSR) disclosures and (2) the impact of the passage of SEC 2010 Guidance on corporate social responsibility (CSR) reporting. The analysis results suggest that climate change disclosures are positively associated with corporate social responsibility concerns, strengths, and overall disclosure. In addition, we do not find empirical evidence that the SEC 2010 Guidance discourages firms' overall environmental and corporate social responsibility disclosures. [ABSTRACT FROM AUTHOR]

Given the controversy regarding whether carotid endarterectomy (CEA) or carotid artery stenting (CAS) may be superior for stroke prevention, it is uncertain how recent clinical evidence, guidelines, and reimbursement policies have influenced the volume and outcomes after these procedures.We conducted a serial, cross-sectional study with time trends of patients undergoing CAS (n=124 265) and CEA (n=1 260 647) between 2001 and 2010 from the Nationwide Inpatient Sample database. During the 10-year period, the frequency of CEA declined, whereas CAS use slowly increased. After multivariate propensity score-matched analysis, CAS was associated with an increased risk of death (odds ratio [OR], 1.69; 95% confidence interval [CI], 1.40-2.04), stroke (OR, 1.43; 95% CI, 1.23-1.66), and major adverse events including death, stroke, and myocardial infarction (OR, 1.25; 95% CI, 1.13-1.39). In asymptomatic patients, there was no significant difference in major adverse events (OR, 1.08; 95% CI, 0.92-1.20; P=0.16 [P <0.001 for interaction between procedure type and symptom status]) between CAS and CEA. Importantly, there was a significant improvement in CAS outcomes during the course of 10 years (reduction in death [OR, 0.51; 95% CI, 0.49-0.67; P for trend=0.03] and major adverse events [OR, 0.75; 95% CI, 0.66-0.84; P for trend=0.05] comparing years 2010 versus 2001).In US hospitals between 2001 and 2010, CAS was associated with worse in-hospital outcomes, partly attributable to selection and ascertainment bias. Asymptomatic patients undergoing CAS versus CEA had similar adjusted rates of major adverse events. CAS outcomes improved significantly during the course of the decade likely attributable to improvements in patient selection, operator skills, and technological advancements. [ABSTRACT FROM AUTHOR]

This paper examines a comprehensive set of environmental characteristics based on Choi and Meek's (2008, CM) framework to explain international accounting system development, which we proxy by IFRS adoption. The main finding indicates that CM's framework is fairly descriptive. Factors relating to political and economic ties, reliance on foreign-sourced debt and common law legal systems create contracting incentives for adoption. Similarly, the need for capital investment evidenced by greater economic growth and capital formation, and higher literacy rates creates signaling incentives for adoption. However, other factors relating to size of capital markets, taxation, and inflation produce disincentives for adoption, which point to internal political and practical costs of converting current accounting systems to IFRS. [ABSTRACT FROM AUTHOR]

The innate and adaptive immunities have been documented to participate in the pathogenesis of nephrotoxic acute kidney injury (AKI); however, the mechanisms controlling these processes have yet to be established. In our cisplatin-induced AKI mouse model, we show pathological damage to the kidneys, with the classical markers elevated, consistent with the response to cisplatin treatment. Through assessments of the components of the immune system, both locally and globally, we demonstrate that the immune microenvironment of injured kidneys was associated with an increased infiltration of CD4+ T cells and macrophages concomitant with decreased Treg cell populations. Our cell-based assays and animal studies further show that cisplatin exposure downregulated the protein levels of programmed death-ligand 1 (PD-L1), an immune checkpoint protein, in primary renal proximal tubular epithelial cells, and that these inhibitions were dose-dependent. After orthotopic delivery of PD-L1 gene into the kidneys, cisplatin-exposed mice displayed lower levels of both serum urea nitrogen and creatinine upon PD-L1 expression. Our data suggest a renoprotective effect of the immune checkpoint protein, and thereby provide a novel therapeutic strategy for cisplatin-induced AKI. [ABSTRACT FROM AUTHOR]

SUMO, a small ubiquitin-related modifier, is known to covalently attach to a number of nuclear regulatory proteins such as p53, 1κB, promyelocytic leukemia protein and c-Jun. The sumoylation reaction is catalyzed by the SUMO protease, which exposes the C-terminal active glycine residue of the nascent SUMO, the heterodimeric SUMO activating enzyme, the SUMO conjugating enzyme, Ubc9, and SUMO protein ligases, in a manner similar to ubiquitinylation. Identification of SUMO-regulated proteins is hampered by the fact that many sumoylated proteins are present at a level below normal detection limit. This limitation was overcome by either in vivo overexpression of Myc-SUMO or in vitro sumoylation with excess biotin-SUMO and Ubc9. Sumoylated proteins so obtained were affinity purified or isolated by immunoprecipitation. The isolated sumoylated proteins were identified by sequence analysis using mass spectrometric methods. Results reveal that several heterogeneous nuclear ribonucleoproteins (hnRNPs), zinc finger proteins, and nuclear pore complex proteins were sumoylated. The sumoylation of hnRNP A1, hnRNP F, and hnRNP K were confirmed in vivo by coimmunoprecipitation. In view of the facts that hnRNPs have been implicated in RNA splicing, transport, stability, and translation, our findings suggest that sumoylation could play an important role in regulating mRNA metabolism. [ABSTRACT FROM AUTHOR]

Smog pollution in China has drawn worldwide attention. Using companies' data from Chinese Securities Markets and Accounting Research database (CSMAR) and air quality monitoring data from China National Environmental Monitoring Centre(CNEMC), we employ the PM2.5 concentration as a proxy for smog pollution and examine the effect of smog pollution on company environmental uncertainty and operating investment in 74 key cities in China. The empirical results show that smog pollution causes an increase in company environmental uncertainty and a decrease in operating investment for Chinese listed companies, with environmental uncertainty as a mediating variable. Smog pollution can positively influence companies' environmental uncertainty through their employees and high pressure from the public and government. According to the real-options-based investment approach, companies choose to "wait and see" and, correspondingly, reduce operating investment under high environmental uncertainty such as that caused by smog pollution. Additionally, we find that state-owned enterprises are more significantly influenced by smog pollution in terms of environmental uncertainty and operating investment because of their close relationships with the government and their responsibility to set an example among Chinese companies in the fight against smog pollution. [ABSTRACT FROM AUTHOR]

Currently, Doppler ultrasound and contrast angiography are the main imaging procedues being used to evaluate arterial bypass shunts. IV radionuclide total body arteriogra- phy (TBA) is another useful imaging procedure for evaluation of bypass shunts. The authors reviewed 33 patients, 19 women and 14 men, ranging in age from forty-three to eighty-five, who had TBA done after arterial bypass surgery. Ten patients had multiple shunts and 5 had multiple follow-up studies. In total there were 80 shunts, including 43 femoropopliteal, 16 axil- lofemoral, 1 axillopopliteal, 13 cross- over femorofemoral, and 7 aortofemoral shunts. Sixty-two of the 80 shunts were patent, 14 were occluded, and 4 had partial occlusion. The results were confirmed by Dopper studies, contrast angiograms, and/or surgical exploration without false positives or false negatives. Since the radiotracer used was ‘Tc- labeled red blood cells, a MUGA study can also be performed immediately following TBA in the same injection. Twenty-eight patients had gated cardiac blood pool studies (MUGA) done; 16 had abnormal wall motion and diminished ventricular function. [ABSTRACT FROM AUTHOR]

A fifty-five-year-old male demonstrated over a three-year period marked enlargement of pulmonary aneurysms. This can be a fatal condition owing to rupture of the aneurysms. [ABSTRACT FROM AUTHOR]