Mitochondria-localized MBD2c facilitates mtDNA transcription and drug resistance.

Mitochondria contain a 16-kb double stranded DNA genome encoding 13 proteins essential for respiration, but the mechanisms regulating transcription and their potential role in cancer remain elusive. Although methyl-CpG-binding domain (MBD) proteins are essential for nuclear transcription, their role in mitochondrial DNA (mtDNA) transcription is unknown. Here we report that the MBD2c splicing variant translocates into mitochondria to mediate mtDNA transcription and increase mitochondrial respiration in triple-negative breast cancer (TNBC) cells.

Thoracoscopic Repair for Kluth Type Ⅲb3 Esophageal Atresia and Distal Tracheoesophageal Fistula.

Introduction: This report aims to present our initial miniseries of successful thoracoscopic repair for esophageal atresia (EA) and distal tracheoesophageal fistula (TEF) of Kluth type Ⅲb3 in accordance with Kluth's classification.

Methods: From January 2012 to January 2024, ten patients with Kluth type Ⅲb3 EA-TEF were treated by thoracoscopic surgery. The therapeutic methods and surgical outcomes were retrospectively reviewed.

PDHX acetylation facilitates tumor progression by disrupting PDC assembly and activating lactylation mediated gene expression.

Deactivation of the mitochondrial pyruvate dehydrogenase complex (PDC) is important for the metabolic switching of cancer cell from oxidative phosphorylation to aerobic glycolysis. Studies examining PDC activity regulation have mainly focused on the phosphorylation of pyruvate dehydrogenase (PDH, E1), leaving other post-translational modifications (PTMs) largely unexplored. Here, we demonstrate that the acetylation of Lys 488 of pyruvate dehydrogenase complex component X (PDHX) commonly occurs in hepatocellular carcinoma (HCC), disrupting PDC assembly and contributing to lactate-driven epigenetic control of gene expression.

[Inhibition of connexin 43-mediated hemichannel activity promotes odontoblast differentiation of human dental pulp cells induced by lipopolysaccharide].

Purpose: To investigate the role and mechanism of connexin 43（Cx43）in odontoblast differentiation of human dental pulp cells (hDPCs) induced by lipopolysaccharide (LPS).

Methods: The maxillary first molar injury model of SD rats was established. The expression pattern of Cx43 in dental pulp repair after injury was detected by immunofluorescence(IF) staining.

Carnosine regulation of intracellular pH homeostasis promotes lysosome-dependent tumor immunoevasion.

Tumor cells and surrounding immune cells undergo metabolic reprogramming, leading to an acidic tumor microenvironment. However, it is unclear how tumor cells adapt to this acidic stress during tumor progression. Here we show that carnosine, a mobile buffering metabolite that accumulates under hypoxia in tumor cells, regulates intracellular pH homeostasis and drives lysosome-dependent tumor immune evasion.

Lumbar Endoscopic Unilateral Laminotomy With Bilateral Decompression Surgery in Severe Lumbar Stenosis Under Electrophysiological Monitoring-Focused on Full-Visualized Trephine/Osteotome.

Objective: Although endoscopic drill has the advantages in manipulation and hemostasis, whose low efficiency and blurred vision reduce the efficacy of lumbar endoscopic unilateral laminotomy with bilateral decompression (LE-ULBD). The present study was designed to evaluate the safety and efficacy of full-visualized trephine/osteotome in the LE-ULBD surgery for severe lumbar stenosis.

Methods: Fifty-seven severe lumbar stenosis patients who underwent LE-ULBD between January 2020 to January 2023 were enrolled, who were divided into drill and visualized trephine groups.

Comparison of Imaging Characteristics of Gangliogliomas between Child/Adolescent Group and Adult Group.

Background: Ganglioglioma is a rare, slowly proliferating mixed glioneuronal tumor, with the highest incidence observed in children and young adults, but it can also occur in adults.

Objective: This study aimed to compare the imaging characteristics of ganglioglioma in children/adolescents and adults to facilitate radiographic diagnosis.

Methods: In this retrospective study, a total of 32 patients were included and divided into two groups: the child/adolescent group (age < 18 years, n=19) and the adult group (age ≥ 18 years, n=13).

PGAM5 deacetylation mediated by SIRT2 facilitates lipid metabolism and liver cancer proliferation.

Tumor metabolic reprogramming and epigenetic modification work together to promote tumorigenesis and development. Protein lysine acetylation, which affects a variety of biological functions of proteins, plays an important role under physiological and pathological conditions. Here, through immunoprecipitation and mass spectrum data, we show that phosphoglycerate mutase 5 (PGAM5) deacetylation enhances malic enzyme 1 (ME1) metabolic enzyme activity to promote lipid synthesis and proliferation of liver cancer cells.

Branched-chain amino acid catabolism breaks glutamine addiction to sustain hepatocellular carcinoma progression.

Branched-chain amino acid (BCAA) catabolism is related to tumorigenesis. However, the underlying mechanism and specific contexts in which BCAAs affect tumor progression remain unclear. Here, we demonstrate that BCAA catabolism is activated in liver cancer cells without glutamine.

Non-canonical phosphoglycerate dehydrogenase activity promotes liver cancer growth via mitochondrial translation and respiratory metabolism.

Phosphoglycerate dehydrogenase (PHGDH) is a key serine biosynthesis enzyme whose aberrant expression promotes various types of tumors. Recently, PHGDH has been found to have some non-canonical functions beyond serine biosynthesis, but its specific mechanisms in tumorigenesis remain unclear. Here, we show that PHGDH localizes to the inner mitochondrial membrane and promotes the translation of mitochondrial DNA (mtDNA)-encoded proteins in liver cancer cells.

Fluoxetine reverses hyperactivity of anterior cingulate cortex and attenuates chronic stress-induced hyperalgesia.

Somatic symptom disorder (SSD), which occurs in about 5-7 percent of the adult population, involves heightened physical and emotional sensitivity to pain. However, its neural mechanism remains elusive and thus hinders effective clinical intervention. In this study, we employed chronic restraint stress (CRS)-induced hyperalgesia as a mouse model to investigate the neural mechanism underlying SSD and its pharmacological treatment.

Intentional replantation combined root resection therapy for the treatment of type III radicular groove with two roots: A case report.

Background: A radicular groove is an anatomic malformation that usually initiates at the central fossa, extending along the root at varying lengths and depths and predisposes the involved tooth to a severe periodontal defect. Severe grooves that extend to the root apex often lead to complex combined periodontal-endodontic lesions. They are a serious challenge for doctors to diagnose and treat.

CD47 Blockade Accelerates Blood Clearance and Alleviates Early Brain Injury After Experimental Subarachnoid Hemorrhage.

Aims: Subarachnoid hemorrhage (SAH) is a devastating stroke subtype. Following SAH, erythrocyte lysis contributes to cell death and brain injuries. Blockage of the anti-phagocytic receptor Cluster of Differentiation 47 (CD47) enhances phagocyte clearance of erythrocytes, though it has not been well-studied post-SAH.

ENO1 suppresses cancer cell ferroptosis by degrading the mRNA of iron regulatory protein 1.

α-Enolase 1 (ENO1) is a critical glycolytic enzyme whose aberrant expression drives the pathogenesis of various cancers. ENO1 has been indicated as having additional roles beyond its conventional metabolic activity, but the underlying mechanisms and biological consequences remain elusive. Here, we show that ENO1 suppresses iron regulatory protein 1 (IRP1) expression to regulate iron homeostasis and survival of hepatocellular carcinoma (HCC) cells.

Microvascular decompression for pediatric onset trigeminal neuralgia: patterns and variation.

Objectives: Pediatric trigeminal neuralgia has been rarely reported in the literature, which were only 28 cases. Although microvascular decompression (MVD) has been widely accepted as effective therapy for trigeminal neuralgia, the etiology and surgical treatment of pediatric ones are seldom addressed. We report our experience with MVD for pediatric trigeminal neuralgia patients with emphasis on the vascular conflict patterns and surgical skills.

H-type congenital tracheo-oesophageal fistula associated with oesophageal stenosis: anatomical variant.

The goal of this paper was to report a new variant of oesophageal atresia: an H-type congenital tracheo-oesophageal fistula associated with oesophageal segmental stenosis distal to the fistula. Although symptoms were present from birth, we did not differentiate the new anatomical variant preoperatively. The patient was treated by fistula ligation, segmental resection of the distal oesophagus and end-to-end anastomosis of the oesophagus by thoracoscopic surgery.

How to Improve the Effect of Microvascular Decompression for Hemifacial Spasm: A Retrospective Study of 32 Cases with Unsuccessful First Time MVD.

Background:  Microvascular decompression (MVD) has become accepted as an effective therapeutic option for hemifacial spasm (HFS); however, the curative rate of MVD for HFS varies widely (50-98%) in different medical centers. This study could contribute to the improvement of the MVD procedure.

Methods:  We retrospectively analyzed 32 patients in whom initial MVD failed in other hospitals and who underwent a second MVD at our center.

Hemifacial Spasm: Comparison of Results between Patients Older and Younger than 70 Years Operated on with Microvascular Decompression.

Objective:  The aim of the present study was to evaluate the efficacy and safety of microvascular decompression (MVD) for primary hemifacial spasm (HFS) in patients aged ≥70 years and to compare the outcome with a control cohort of younger patients(<70 years).

Methods:  In this retrospective study, subjects were divided into two groups: an elderly group (patients who were ≥70 years) and a younger group. We compared demographic and clinical data, surgical outcome, MVD-related complications, and duration of operation and hospitalization after MVD between the two groups.

MYC promotes cancer progression by modulating m A modifications to suppress target gene translation.

The MYC oncoprotein activates and represses gene expression in a transcription-dependent or transcription-independent manner. Modification of mRNA emerges as a key gene expression regulatory nexus. We sought to determine whether MYC alters mRNA modifications and report here that MYC promotes cancer progression by down-regulating N6-methyladenosine (m A) preferentially in transcripts of a subset of MYC-repressed genes (MRGs).

Hypoxia-Induced Suppression of Alternative Splicing of MBD2 Promotes Breast Cancer Metastasis via Activation of FZD1.

Metastasis is responsible for the majority of breast cancer-related deaths, however, the mechanisms underlying metastasis in this disease remain largely elusive. Here we report that under hypoxic conditions, alternative splicing of MBD2 is suppressed, favoring the production of MBD2a, which facilitates breast cancer metastasis. Specifically, MBD2a promoted, whereas its lesser known short form MBD2c suppressed metastasis.

Myc-mediated SDHA acetylation triggers epigenetic regulation of gene expression and tumorigenesis.

The transcriptional role of cMyc (or Myc) in tumorigenesis is well appreciated; however, it remains to be fully established how extensively Myc is involved in the epigenetic regulation of gene expression. Here, we show that by deactivating succinate dehydrogenase complex subunit A (SDHA) via acetylation, Myc triggers a regulatory cascade in cancer cells that leads to H3K4me3 activation and gene expression. We find that Myc facilitates the acetylation-dependent deactivation of SDHA by activating the SKP2-mediated degradation of SIRT3 deacetylase.

IL-6 contributes to Na1.3 up-regulation in trigeminal nerve following chronic constriction injury.

: To verify the hypothesis that the nature of trigeminal neuralgia (TN) is an ectopic impulse induced by sodium channel modulated by cytokines, we conducted an animal study using the infraorbital nerve chronic constriction injury (CCI) model in rats.: The expression of Nav1.3 or IL-6 in the infraorbital nerve (ION) and trigeminal ganglion (TG) were detected by western blot and immunocytochemistry after administration of antisense oligodeoxynucleotide sequence (AS), IL-6 or Anti-IL-6.

Fully endoscopic microvascular decompression of the hemifacial spasm: our experience.

Purpose: Microvascular decompression (MVD) surgery has been accepted as a potentially curative method for hemifacial spasm (HFS). The primary cause of failure of MVD is incomplete decompression of the offending vessel due to inadequate visualization. This study is aimed at evaluating the benefit of endoscopic visualization and the value of fully endoscopic MVD.

Microvascular Decompression Alone without Rhizotomy Is an Effective Way of Treating Glossopharyngeal Neuralgia: Clinical Analysis of 46 Cases.

Background: Microvascular decompression (MVD) has been the right choice for glossopharyngeal neuralgia (GPN) patients. However, whether glossopharyngeal/vagal nerve root rhizotomy should be combined with MVD is still controversial.

Objective: To evaluate whether glossopharyngeal/vagal nerve root rhizotomy during MVD is necessary for the treatment of GPN.

DIS3L2 Promotes Progression of Hepatocellular Carcinoma via hnRNP U-Mediated Alternative Splicing.

DIS3-like 3'-5' exoribonuclease 2 (DIS3L2) degrades aberrant RNAs, however, its function in tumorigenesis remains largely unexplored. Here, aberrant DIS3L2 expression promoted human hepatocellular carcinoma (HCC) progression via heterogeneous nuclear ribonucleoproteins (hnRNP) U-mediated alternative splicing. DIS3L2 directly interacted with hnRNP U through its cold-shock domains and promoted inclusion of exon 3b during splicing of pre-Rac1 independent of its exonuclease activity, yielding an oncogenic splicing variant, Rac1b, which is known to stimulate cellular transformation and tumorigenesis.