6PPD induces cerebrovascular defects by triggering oxidative stress and ferroptosis in zebrafish.

N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD), which is widely used as an antiozonant in rubber tires, has recently got much attention for its acute aquatic toxicity. However, the developmental toxicity of 6PPD in cerebrovascular network remains unknown. Here, we investigated the effects of 6PPD exposure in cerebral vascular using zebrafish.

Using different zebrafish models to explore liver regeneration.

The liver possesses an impressive capability to regenerate following various injuries. Given its profound implications for the treatment of liver diseases, which afflict millions globally, liver regeneration stands as a pivotal area of digestive organ research. Zebrafish () has emerged as an ideal model organism in regenerative medicine, attributed to their remarkable ability to regenerate tissues and organs, including the liver.

Nlp-dependent ER-to-Golgi transport.

The mechanism that maintains ER-to-Golgi vesicles formation and transport is complicated. As one of the adapters, Ninein-like protein (Nlp) participated in assembly and transporting of partial ER-to-Golgi vesicles that contained specific proteins, such as β-Catenin and STING. Nlp acted as a platform to sustain the specificity and continuity of cargoes during COPII and COPI-coated vesicle transition and transportation through binding directly with SEC31A as well as Rab1B.

Perfluorooctanoic acid triggers premature ovarian insufficiency by impairing NAD+ synthesis and mitochondrial function in adult zebrafish.

High-dose perfluorooctanoic acid (PFOA) impairs oocyte maturation and offspring quality. However, the physiological concentrations of PFOA in follicular fluids of patients with premature ovarian insufficiency (POI) were detected at lower levels, thus the relationship between physiological PFOA and reproductive disorders remains elusive. Here, we investigated whether physiological PFOA exposure affects gonad function in adult zebrafish.

Cellular microenvironment: a key for tuning mesenchymal stem cell senescence.

Mesenchymal stem cells (MSCs) possess the ability to self-renew and differentiate into multiple cell types, making them highly suitable for use as seed cells in tissue engineering. These can be derived from various sources and have been found to play crucial roles in several physiological processes, such as tissue repair, immune regulation, and intercellular communication. However, the limited capacity for cell proliferation and the secretion of senescence-associated secreted phenotypes (SASPs) pose challenges for the clinical application of MSCs.

Dysregulation of cholesterol metabolism in cancer progression.

Cholesterol homeostasis has been implicated in the regulation of cellular and body metabolism. Hence, deregulated cholesterol homeostasis leads to the development of many diseases such as cardiovascular diseases, and neurodegenerative diseases, among others. Recent studies have unveiled the connection between abnormal cholesterol metabolism and cancer development.

VEGF signaling governs the initiation of biliary-mediated liver regeneration through the PI3K-mTORC1 axis.

Biliary epithelial cells (BECs) are a potential source to repair the damaged liver when hepatocyte proliferation is compromised. Promotion of BEC-to-hepatocyte transdifferentiation could be beneficial to the clinical therapeutics of patients with end-stage liver diseases. However, mechanisms underlying the initiation of BEC transdifferentiation remain largely unknown.

CDK7-YAP-LDHD axis promotes D-lactate elimination and ferroptosis defense to support cancer stem cell-like properties.

Reprogrammed cellular metabolism is essential for maintaining cancer stem cells (CSCs) state. Here, we report that mitochondrial D-lactate catabolism is a necessary initiating oncogenic event during tumorigenesis of esophageal squamous cell carcinoma (ESCC). We discover that cyclin-dependent kinase 7 (CDK7) phosphorylates nuclear Yes-associated protein 1 (YAP) at S127 and S397 sites and enhances its transcription function, which promotes D-lactate dehydrogenase (LDHD) protein expression.

TMEM92 acts as an immune-resistance and prognostic marker in pancreatic cancer from the perspective of predictive, preventive, and personalized medicine.

Background: Pancreatic cancer presents extremely poor prognosis due to the difficulty of early diagnosis, low resection rate, and high rates of recurrence and metastasis. Immune checkpoint blockades have been widely used in many cancer types but showed limited efficacy in pancreatic cancer. The current study aimed to evaluate the landscape of tumor microenvironment (TME) of pancreatic cancer and identify the potential markers of prognosis and immunotherapy efficacy which might contribute to improve the targeted therapy strategy and efficacy in pancreatic cancer in the context of predictive, preventive, and personalized medicine (PPPM).

Liver tumor-initiating cells initiate the formation of a stiff cancer stem cell microenvironment niche by secreting LOX.

Accumulating evidence has shown that the traits of tumor-initiating cells (TICs) are controlled by the microenvironment niches (MENs), but the composition and remodeling mechanisms of the MENs of TICs are poorly defined. Here, we report that the voltage-gated calcium channel α2δ1 subunit-positive TICs of hepatocellular carcinoma (HCC) specifically secret lysyl oxidase (LOX), which leads to the cross-linking of collagen, forming a stiff extracellular matrix (ECM) that is sufficient to drive the formation of TICs with a stiff mechanical trait and is subsequently required for the maintenance the properties of HCC TICs. Furthermore, the cross-linked collagen results in the upregulation of integrin α7 (ITGA7), increased phosphorylation of FAK and extracellular signal-regulated kinase 1/2 (ERK1/2).

Protective roles of mesenchymal stem cells on skin photoaging: A narrative review.

Skin is a natural barrier of human body and a visual indicator of aging process. Exposure to ultraviolet (UV) radiation in the sunlight may injure the skin tissues and cause local damage. Besides, it is reported that repetitive or long-term exposure to UV radiation may reduce the collagen production, change the normal skin structure and cause premature skin aging.

Immune landscape of advanced gastric cancer tumor microenvironment identifies immunotherapeutic relevant gene signature.

Background: Advanced gastric cancer (AGC) is a disease with poor prognosis due to the current lack of effective therapeutic strategies. Immune checkpoint blockade treatments have shown effective responses in patient subgroups but biomarkers remain challenging. Traditional classification of gastric cancer (GC) is based on genomic profiling and molecular features.

Adipose-derived stem cells regulate metabolic homeostasis and delay aging by promoting mitophagy.

Tissues undergo a process of degeneration as the body ages. Mesenchymal stem cells (MSCs) have been found to have major potential in delaying the aging process in tissues and organs. However, the mechanism underlying the anti-aging effects of MSC is not clear which limits clinical applications.

PolG Inhibits Gastric Cancer Glycolysis and Viability by Suppressing PKM2 Phosphorylation.

Purpose: Gastric cancer (GC) is the fifth most frequently diagnosed cancer and the third leading cause of cancer-related death. There is a critical need for the development of novel therapies in GC. DNA polymerase gamma (PolG) has been implicated in mitochondrial homeostasis and affects the development of numerous types of cancer, however, its effects on GC and molecular mechanisms remain to be fully determined.

The miR-204-5p/FOXC1/GDF7 axis regulates the osteogenic differentiation of human adipose-derived stem cells via the AKT and p38 signalling pathways.

Background: Human adipose-derived stem cells (hADSCs) are stem cells with the potential to differentiate in multiple directions. miR-204-5p is expressed at low levels during the osteogenic differentiation of hADSCs, and its specific regulatory mechanism remains unclear. Here, we aimed to explore the function and possible molecular mechanism of miR-204-5p in the osteogenic differentiation of hADSCs.

The Effects of Timing of Postoperative Radiotherapy on Hypertrophic Scar in a Rabbit Model.

BACKGROUND Hypertrophic scar is associated with excessive proliferation of fibroblasts, the accumulation of collagen fibers, and angiogenesis associated with chronic inflammation. Scar resection, combined with radiotherapy, is widely used in clinical practice, but timing remains controversial. This study aimed to investigate the association between the timing of postoperative radiotherapy and the effects on hypertrophic scar in a rabbit model.

BRAFi induced demethylation of miR-152-5p regulates phenotype switching by targeting TXNIP in cutaneous melanoma.

Treatment of advanced BRAF-mutant melanoma using BRAF inhibitors (BRAFi) eventually leads to drug resistance and selects for highly metastatic tumor cells. We compared the most differentially dysregulated miRNA expression profiles of vemurafenib-resistant and highly-metastatic melanoma cell lines obtained from GEO DataSets. We discovered miR-152-5p was a potential regulator mediating melanoma drug resistance and metastasis.

Surgical Treatment Strategy for Severe Rhinophyma With Bilateral Pedicled Nasolabial Flaps.

Background: Rhinophyma is a rare disease characterized by chronic inflammation and hypertrophy of sebaceous glands, blood vessels, and fibrous tissue, associated with end-stage severe acne rosacea. There are multiple approaches to treatment and repair, including dermal shaving, secondary intention healing, free skin graft, and skin flaps. However, these methods have various disadvantages, such as prolonged healing, obvious scarring, and skin texture mismatch.

CXCL11 promotes self-renewal and tumorigenicity of α2δ1 liver tumor-initiating cells through CXCR3/ERK1/2 signaling.

Tumor-initiating cells (TICs), which are responsible for sustaining tumor growth and recurrence, rely on several regulatory factors. However, the mechanism of inflammation-related molecules in the acquisition and maintenance of TIC properties in hepatocellular carcinoma (HCC) remains elusive. We previously demonstrated that the voltage-gated calcium channel α2δ1 subunit is a functional surface marker of HCC TICs.

Anthropometric labial analysis of Han Chinese young adults.

Background: Facial features vary in size and proportions between different races. This study aimed to measure the anthropometric variables of the labial region in Han Chinese young adults.

Materials And Methods: A total of 900 college students (475 male and 425 female) of Chinese Han ethnicity from the northern China were included.

High temperature requirement factor A1 (HTRA1) regulates the activation of latent TGF-β1 in keloid fibroblasts.

Scar treatments are considered a major issue in the plastic surgery field. Activation of the transforming growth factor-β (TGF-β)-mediated signaling pathway plays a key role in the scar pathogeneses, and high temperature requirement factor A1 (HTRA1) inhibits TGF-β1 activation in tumor cells. Our study aims to investigate the role of HTRA1 in the pathogenesis of scars.

Anthropometric nasal analysis of Han Chinese young adults.

Background: There are varying degrees of racial differences in the size, shape, proportions of the facial structures.

Methods: A total of 900 Han Chinese young adults (501 females and 399 males) were included in the analysis. Measurements taken of the soft tissue of the external nose included 12 items of linear distance and 5 angles.