Decoding the regulatory role of ATP synthase inhibitory factor 1 (ATPIF1) in Wallerian degeneration and peripheral nerve regeneration.

ATP synthase inhibitory factor 1 (ATPIF1), a key modulator of ATP synthase complex activity, has been implicated in various physiological and pathological processes. While its role is established in conditions such as hypoxia, ischemia-reperfusion injury, apoptosis, and cancer, its involvement remains elusive in peripheral nerve regeneration. Leveraging ATPIF1 knockout transgenic mice, this study reveals that the absence of ATPIF1 impedes neural structural reconstruction, leading to delayed sensory and functional recovery.

Aberrant Chitinase 3-Like 1 Expression in Basal Cells Contributes to Systemic Sclerosis Fibrosis.

Systemic sclerosis (SSc) is an autoimmune disease characterized by extensive skin and internal organ fibrosis. However, the mechanism underlying fibrosis remains unclear, and effective treatments for halting or reversing fibrosis are lacking. In this study, single-cell RNA sequencing is used to obtain a comprehensive overview of skin cells from patients with SSc and healthy controls.

CTHRC1 Attenuates Tendinopathy via Enhancing EGFR/MAPK Signaling Pathway.

Tendinopathy poses a formidable challenge due to the inherent limitations of tendon regenerative capabilities post-injury. At present, effective curative approaches for tendinopathy are still lacking. Collagen triple helix repeat-containing 1 (CTHRC1) is an extracellular matrix protein with significant roles in both physiological and pathological processes.

Global trends in the burden of rheumatoid arthritis by sociodemographic index: a joinpoint and age-period-cohort analysis based on the Global Burden of Disease Study 2019.

Objective: To describe temporal trends in the incidence and disability-adjusted life years (DALYs) of rheumatoid arthritis (RA) across sociodemographic index (SDI) quintiles and sexes from 1990 to 2019.

Methods: Data on RA incidence and DALYs with a 95% uncertainty interval from 1990 to 2019 were extracted from the Global Burden of Disease 2019. Subsequently, trends across SDI quintiles and sexes from 1990 to 2019 were determined using joinpoint regression and age-period-cohort analyses.

An examination from 1990 to 2019: investigating the burden of knee dislocation on a global scale.

Background: The literature on the disease burden of knee dislocation is lacking. The aim of the study is to systematically assess the global burden, trends, causes, and influencing factors of knee dislocation.

Methods: The incidence and years lived with disability (YLDs) of knee dislocation were assessed globally, as well as at the regional and national levels from 1990 to 2019.

A systematic analysis on global epidemiology and burden of foot fracture over three decades.

Purpose: To comprehensively analyze the geographic and temporal trends of foot fracture, understand its health burden by age, sex, and sociodemographic index (SDI), and explore its leading causes from 1990 to 2019.

Methods: The datasets in the present study were generated from the Global Burden of Diseases Study 2019, which included foot fracture data from 1990 to 2019. We extracted estimates along with the 95% uncertainty interval (UI) for the incidence and years lived with disability (YLDs) of foot fracture by location, age, gender, and cause.

Exploring temporal trends and burden of traumatic shoulder dislocation: a global perspective.

Objective: To explore the geographical and temporal trends of traumatic shoulder dislocation, describe the association between the social and demographic factors and the health burden due to traumatic shoulder dislocation, and further investigate its causes.

Methods: Data on traumatic shoulder dislocation was collected from the Global Burden of Disease 2019, spanning the years 1990 to 2019. The epidemiology and disease burden were examined at global, regional, and national levels.

Protective effects of Pt-N-C single-atom nanozymes against myocardial ischemia-reperfusion injury.

Effective therapeutic strategies for myocardial ischemia/reperfusion (I/R) injury remain elusive. Targeting reactive oxygen species (ROS) provides a practical approach to mitigate myocardial damage following reperfusion. In this study, we synthesize an antioxidant nanozyme, equipped with a single-Platinum (Pt)-atom (PtsaN-C), for protecting against I/R injury.

A stretchable hardness sensor for the assessment of skin disease in systemic sclerosis.

Objective: To determine the validity of a hardness sensor to objectively assess skin induration in patients with systemic sclerosis, and to compare the hardness sensor with the modified Rodnan skin score (MRSS) and a durometer.

Methods: The skin induration was measured in two assessments: a Latin square experiment to examine the hardness sensor's intraobserver and interobserver reliability; and a longitudinal cohort to evaluate the distribution of hardness sensor measurements, the correlation between hardness sensor, durometer and MRSS, and the sensitivity to change in skin hardness. Other outcome data collected included the health assessment questionnaire (HAQ) disability index and Keitel function test (KTF) score.

SETD2 deficiency accelerates sphingomyelin accumulation and promotes the development of renal cancer.

Patients with polycystic kidney disease (PKD) encounter a high risk of clear cell renal cell carcinoma (ccRCC), a malignant tumor with dysregulated lipid metabolism. SET domain-containing 2 (SETD2) has been identified as an important tumor suppressor and an immunosuppressor in ccRCC. However, the role of SETD2 in ccRCC generation in PKD remains largely unexplored.

What's the clinical significance of VAS, AOFAS, and SF-36 in progressive collapsing foot deformity.

Background: This study aimed to ascertain the minimal clinically important difference (MCID), and substantial clinical benefit (SCB) of the American Orthopedic Foot and Ankle Society (AOFAS) scale, visual analog scale (VAS) for pain, and Short Form-36 Health Survey (SF-36) in progressive collapsing foot deformity (PCFD) surgery.

Methods: In this retrospective cohort study, a total of 84 patients with PCFD (84 feet) who underwent surgery between July 2015 and April 2021 were included. The study assessed the patients' subjective perception, as well as their VAS, AOFAS, and SF-36 scores at a minimum two-year follow-up, and these data were subjected to statistical analysis.

Surgical Treatment for Isolated Closed Multi-metatarsal Fractures: At Least 2-Year Outcomes in 79 Feet.

Multimetatarsal fractures are a particular type possibly associated with worse functional outcomes. Existing studies are scarce, fragmented, and lack control for confounders. This study aimed to explore the functional prognosis of isolated closed extra-articular multimetatarsal fractures and the different outcomes between the plate-screw and K-wire fixation.

Lactoferrin attenuates cardiac fibrosis and cardiac remodeling after myocardial infarction via inhibiting mTORC1/S6K signaling pathway.

Myocardial infarction (MI) causes a severe injury response that eventually leads to adverse cardiac remodeling and heart failure. Lactoferrin (Ltf), as a secreted protein, bears multi-pharmacological properties. Present study aims to establish the cardioprotective function and corresponding mechanism of Ltf in MI process.

Cthrc1 deficiency aggravates wound healing and promotes cardiac rupture after myocardial infarction via non-canonical WNT5A signaling pathway.

Cardiac fibroblasts are crucial for scar formation and cardiac repair after myocardial infarction (MI). Collagen triple helix repeat containing 1 (CTHRC1), an extracellular matrix protein, is involved in the pathogenesis of vascular remodeling, bone formation, and tumor progression. However, the role and underlying mechanism of CTHRC1 in post-MI wound repair are not fully clear.

Cardiac Overexpression of Chil1 Improves Wound Healing to Prevent Cardiac Rupture After Myocardial Infarction.

Timely formation of collagen-rich-scar is of importance to prevent ventricular rupture after myocardial infarction (MI). Chil1 (Chitinase 3-like 1) is a secreted protein associated with tissue remodeling response. However, its function in MI progression remains elusive.

Patients with comorbid coronary artery disease and hypertension: a cross-sectional study with data from the NHANES.

Background: Hypertension (HTN) and coronary artery disease (CAD), two common cardiovascular diseases, are often comorbid and interacted. The patients with comorbid CAD and HTN have worse outcomes and prognosis, however, the prevalence remains unclear. In the cross-sectional study, we aimed to explore the prevalence and influence factors of patients with comorbid CAD and HTN in the USA.

Nephronectin promotes cardiac repair post myocardial infarction via activating EGFR/JAK2/STAT3 pathway.

: ECM proteins are instrumental for angiogenesis, which plays momentous roles during development and repair in various organs, including post cardiac insult. After a screening based on an open access RNA-seq database, we identified Nephronectin (NPNT), an extracellular protein, might be involved in cardiac repair post myocardial infarction (MI). However, the specific impact of nephronectin during cardiac repair in MI remains elusive.