Use of prolonged closed suction drainage for synovial fluid-draining wounds around the ankle.

Objective: When synovial fluid drains through a wound, cells necessary to form tissue required for healing are washed away. This results in failure of wound closure, often necessitating a pedicled or free flap reconstruction. We hypothesised that prolonged (>48 hours post surgery) closed suction drainage can reduce the fluid draining through the wound, enabling wound healing and eliminating the need for a pedicled or free flap reconstruction.

Advances in applications of the CRISPR/Cas9 system for respiratory diseases.

Genetic and environmental factors can have an impact on lung and respiratory disorders which are associated with severe symptoms and have high mortality rates. Many respiratory diseases are significantly influenced by genetic or epigenetic factors. Gene therapy offers a powerful approach providing therapeutic treatment for lung diseases.

Single cell transcriptomics in blood of patients with chronic obstructive pulmonary disease.

Background: Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. Single-cell RNA sequencing (scRNA-seq) provides gene expression profiles at the single-cell level. Hence, we evaluated gene expression in the peripheral blood of patients with COPD.

Recombinant RAGE antagonist peptide promotes alveolar epithelial cell regeneration via the RAGE/MAPKs/MMP2 pathway in emphysema.

The progression of chronic obstructive pulmonary disease (COPD) results in irreversible pulmonary damage and sustained inflammatory responses. While alternative approaches have been explored, the specific role of alveolar epithelial cells in the pathogenesis of COPD remains unclear. Additionally, the association between emphysema and DAMP-RAGE signaling in COPD patients are not understood.

Exposure of lung fibroblasts to PM and lead (Pb) induces fibrosis and apoptosis in alveolar epithelial cells via a paracrine effect.

Exposure to fine particulate matter (PM) and heavy metals (HMs) in the air is closely associated with the incidence and exacerbation of pulmonary fibrosis. Although the specific responses of alveolar epithelial cells (AECs) and lung fibroblasts to PM or HM exposure have been well defined, the cellular responses of lung fibroblasts to PM or HM exposure and the subsequent interactions with AECs remain poorly investigated. In this study, we demonstrated that human lung fibroblasts exposed to PM or lead (Pb) induced fibrotic changes and apoptosis in AECs.

CXCL11 reprograms M2-biased macrophage polarization to alleviate pulmonary fibrosis in mice.

Background: In understanding the pathophysiology of pulmonary fibrosis (PF), macrophage plasticity has been implicated with a crucial role in the fibrogenic process. Growing evidence indicates that accumulation of M2 macrophages correlates with the progression of PF, suggesting that targeted modulation of molecules that influence M2 macrophage polarization could be a promising therapeutic approach for PF. Here, we demonstrated a decisive role of C-X-C motif chemokine ligand 11 (CXCL11) in driving M1 macrophage polarization to alleviate PF in the bleomycin-induced murine model.

Comparison of biportal endoscopic and microscopic tubular paraspinal approach for foraminal and extraforaminal lumbar disc herniation.

Objective: Foraminal and extraforaminal lumbar disc herniation (FELDH) is an important pathological condition that can lead to lumbar radiculopathy. The paraspinal muscle-splitting approach introduced by Reulen and Wiltse is a reasonable surgical technique. Minimally invasive procedures using a tubular retractor system have also been introduced.

Glyoxalase 1: Emerging biomarker and therapeutic target in cervical cancer progression.

Introduction: Cervical cancer presents a significant global health challenge, disproportionately impacting underserved populations with limited access to healthcare. Early detection and effective management are vital in addressing this public health concern. This study focuses on Glyoxalase-1 (GLO1), an enzyme crucial for methylglyoxal detoxification, in the context of cervical cancer.

Employment of diverse in vitro systems for analyzing multiple aspects of disease, hereditary hemorrhagic telangiectasia (HHT).

Background: In vitro disease modeling enables translational research by providing insight into disease pathophysiology and molecular mechanisms, leading to the development of novel therapeutics. Nevertheless, in vitro systems have limitations for recapitulating the complexity of tissues, and a single model system is insufficient to gain a comprehensive understanding of a disease.

Results: Here we explored the potential of using several models in combination to provide mechanistic insight into hereditary hemorrhagic telangiectasia (HHT), a genetic vascular disorder.

USP28 promotes tumorigenesis and cisplatin resistance by deubiquitinating MAST1 protein in cancer cells.

Cisplatin is a chemotherapy drug that causes a plethora of DNA lesions and inhibits DNA transcription and replication, resulting in the induction of apoptosis in cancer cells. However, over time, patients develop resistance to cisplatin due to repeated treatment and thus the treatment efficacy is limited. Therefore, identifying an alternative therapeutic strategy combining cisplatin treatment along with targeting factors that drive cisplatin resistance is needed.

Protocol for differentiation of functional macrophages from human induced pluripotent stem cells.

Human induced pluripotent stem cell (hiPSC)-derived macrophages provide a valuable tool for disease modeling and drug discovery. Here, we present a protocol to generate functional macrophages from hiPSCs using a feeder-free hematopoietic differentiation technique. We describe steps for preparing hiPSCs, mesodermal differentiation, hematopoietic commitment, and macrophage differentiation and expansion.

Recombinant Human Bone Morphogenetic Protein-2 Priming of Mesenchymal Stem Cells Ameliorate Acute Lung Injury by Inducing Regulatory T Cells.

Mesenchymal stromal/stem cells (MSCs) possess immunoregulatory properties and their regulatory functions represent a potential therapy for acute lung injury (ALI). However, uncertainties remain with respect to defining MSCs-derived immunomodulatory pathways. Therefore, this study aimed to investigate the mechanism underlying the enhanced effect of human recombinant bone morphogenic protein-2 (rhBMP-2) primed ES-MSCs (MSC) in promoting Tregs in ALI mice.

Human Pluripotent Stem Cell-Derived Alveolar Organoids: Cellular Heterogeneity and Maturity.

Chronic respiratory diseases such as idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, and respiratory infections injure the alveoli; the damage evoked is mostly irreversible and occasionally leads to death. Achieving a detailed understanding of the pathogenesis of these fatal respiratory diseases has been hampered by limited access to human alveolar tissue and the differences between mice and humans. Thus, the development of human alveolar organoid (AO) models that mimic in vivo physiology and pathophysiology has gained tremendous attention over the last decade.

A Study on the Monitoring of spp. in Various Children's Play Facilities in the Republic of Korea (2016-2021).

spp. is a zoonotic soil-transmitted parasite that infects canids and felids, which causes toxocariasis in humans, migrating to organ systems, including the lungs, the ocular system, and the central nervous system. Since spp.

βTrCP1 promotes SLC35F2 protein ubiquitination and inhibits cancer progression in HeLa cells.

The solute carrier family 35 F2 (SLC35F2) belongs to membrane-bound carrier proteins that are associated with multiple cancers. The main factor that determines cancer progression is the expression level of SLC35F2. Thus, identifying the E3 ligase that controls SLC35F2 protein abundance in cancer cells is critical.

E3 ubiquitin ligase APC/C regulates SLC35F2 protein turnover and inhibits cancer progression in HeLa cells.

Background: The solute carrier family 35 F2 (SLC35F2), belongs to membrane-bound carrier proteins that control various physiological functions and are activated in several cancers. However, the molecular mechanism regulating SLC35F2 protein turnover and its implication in cancer progression remains unexplored. Therefore, screening for E3 ligases that promote SLC35F2 protein degradation is essential during cancer progression.

USP19 Negatively Regulates p53 and Promotes Cervical Cancer Progression.

p53 is a tumor suppressor gene activated in response to cellular stressors that inhibits cell cycle progression and induces pro-apoptotic signaling. The protein level of p53 is well balanced by the action of several E3 ligases and deubiquitinating enzymes (DUBs). Several DUBs have been reported to negatively regulate and promote p53 degradation in tumors.

CFP1 governs uterine epigenetic landscapes to intervene in progesterone responses for uterine physiology and suppression of endometriosis.

Progesterone (P) is required for the preparation of the endometrium for a successful pregnancy. P resistance is a leading cause of the pathogenesis of endometrial disorders like endometriosis, often leading to infertility; however, the underlying epigenetic cause remains unclear. Here we demonstrate that CFP1, a regulator of H3K4me3, is required for maintaining epigenetic landscapes of P-progesterone receptor (PGR) signaling networks in the mouse uterus.

CRISPR/Cas9-based genome-wide screening of the deubiquitinase subfamily identifies USP3 as a protein stabilizer of REST blocking neuronal differentiation and promotes neuroblastoma tumorigenesis.

Background: The repressor element-1 silencing transcription factor (REST), a master transcriptional repressor, is essential for maintenance, self-renewal, and differentiation in neuroblastoma. An elevated expression of REST is associated with impaired neuronal differentiation, which results in aggressive neuroblastoma formation. E3 ligases are known to regulate REST protein abundance through the 26 S proteasomal degradation pathway in neuroblastoma.

Biportal endoscopic extraforaminal lumbar interbody fusion using a 3D-printed porous titanium cage with large footprints: technical note and preliminary results.

Purpose: The aim of this study was to introduce biportal endoscopic extraforaminal lumbar interbody fusion (BE-EFLIF), which involves insertion of a cage through a more lateral side as compared to the conventional corridor of transforaminal lumbar interbody fusion. We described the advantages and surgical steps of 3D-printed porous titanium cage with large footprints insertion through multi-portal approach, and preliminary results of this technique.

Methods: This retrospective study included 12 consecutive patients who underwent BE-EFLIF for symptomatic single-level lumbar degenerative disease.

Cyclic Phytosphingosine-1-Phosphate Primed Mesenchymal Stem Cells Ameliorate LPS-Induced Acute Lung Injury in Mice.

Background And Objectives: O-cyclic phytosphingosine-1-phosphate (cP1P) is a synthetic chemical and has a structure like sphingosine-1-phosphate (S1P). S1P is known to promote cell migration, invasion, proliferation, and anti-apoptosis through hippocampal signals. However, S1P mediated cellular-, molecular mechanism is still remained in the lung.