Erector spinae plane block for obstetric analgesia in a patient with factor XI deficiency: a case report.

Factor XI (FXI) deficiency is a rare bleeding disorder characterized by a quantitative or qualitative deficiency of FXI. The symptoms are highly variable, and the severity and site of bleeding is unpredictable and does not necessarily correlate with FXI levels. FXI deficiency is classified by phenotype: bleeding or non-bleeding, depending on the clinical manifestations.

Deficiency of the histone H3K36 methyltransferase SETD2 inhibits the proliferation and migration of hepatocellular carcinoma cells.

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide. SETD2, the only known methyltransferase catalyzes the trimethylation of histone H3 lysine 36 (H3K36), has been reported to be associated with several cancers. However, the function of SETD2 in HCC is unclear.

A Rare Case Report of Acquired Coagulation Factor XI Deficiency.

Background: Acquired coagulation factor deficiency is an autoimmune hemorrhagic disease caused by the production of antibodies to coagulation factor. The incidence of acquired coagulation factor XI deficiency is low and rarely reported.

Case Presentation: We report a case of a patient with acquired coagulation factor XI deficiency.

A Targeted Octahedral DNA Nanostructure Co-delivers siME3 and Doxorubicin to Enhance Collateral Lethality in ME2-Deficient Pancreatic Cancer.

The genetic characteristics of pancreatic cancer (PC) are being revealed, but treatment strategies based on these profiles are developing slowly. About one-third of PC patients harbor mutations, with its homozygous deletions often accompanied by deletions of the malic enzyme 2 (ME2) gene, leading to upregulation of malic enzyme 3 (ME3) to eliminate reactive oxygen species (ROS). We designed an aptamer-modified octahedral DNA nanostructure for targeted co-delivery of siRNA targeting ME3 (siME3) and doxorubicin (DOX).

Molecular mechanism analysis of a family with hereditary coagulation FXI deficiency caused by compound heterozygous mutations.

Objective: The purpose of this study was to determine the molecular basis of a Chinese family with factor XI (FXI) deficiency.

Methods: The qRT-PCR was used to detect the transcription of F11 mRNA in transfected cells. ELISAs and western blot were used to detect the expression of FXI protein in culture media and lysates.

PTP1B Modulates Carotid Plaque Vulnerability in Atherosclerosis Through Rab5-PDGFRβ-Mediated Endocytosis Disruption and Apoptosis.

Background: Protein tyrosine phosphatase 1B (PTP1B) is a protein tyrosine phosphatase and modulates platelet-derived growth factor (PDGF)/platelet-derived growth factor receptor (PDGFR) signaling in vascular smooth muscle cells (VSMCs) via endocytosis. However, the related molecular pathways that participated in the interaction of endo-lysosome and the trafficking of PDGFR are largely unknown. This study aims to determine the subcellular regulating mechanism of PTP1B to the endo-lysosome degradation of PDGFR in atherosclerotic carotid plaques, thereby offering a potential therapeutic target for the stabilization of carotid plaques.

Novel factors affecting fibrin clot formation and their clinical implications.

Fibrin formation is pivotal in hemostasis, serving as a temporary barrier to blood loss following vascular injury, while in thrombosis this process is involved in thrombus progression, stability, and recurrence. Growing evidence shows exceptional complexity of processes that determine fibrin clot structure and function, especially lysability, both in health and disease, which might be relevant in the pathogenesis of arterial and venous thromboembolic diseases. In this review, we summarized available data on novel factors that in recent years have been suggested to contribute to prothrombotic fibrin clot properties, involving formation of compact fibrin networks (reduced clot permeability) displaying impaired susceptibility to lysis (prolonged clot lysis time).

Laboratory and Molecular Diagnosis of Factor XI Deficiency.

The prevalence of factor XI (FXI) deficiency is 1 per 10 to 20,000 in the general population, much higher than that reported in most texts. The prevalence is higher in Ashkenazi Jews where it is about 1:20. Clinically, FXI deficiency presents as a mild bleeding disorder mostly associated with posttraumatic or postsurgical hemorrhages or unexplained minor bleeding.

Therapeutic effects of Mudan granules on diabetic retinopathy: Mitigating fibrogenesis caused by FBN2 deficiency and inflammation associated with TNF-α elevation.

Ethnopharmacological Relevance: Mudan granules (MuD), a time-honored traditional Chinese patent medicine (TCPM), are widely utilized in the clinical treatment of diabetic peripheral neuropathy (DPN). In the field of biomedical diagnostics, both diabetic retinopathy (DR) and DPN are recognized as critical microvascular complications associated with diabetes. According to the principles of traditional Chinese medicine (TCM), these conditions are primarily attributed to a deficiency in Qi and the obstruction of collaterals.

Anesthetic Implications of Factor XI Deficiency: A Clinical Case Study and Review of Literature.

Factor XI deficiency, a rare but significant coagulopathy, poses unique challenges in perioperative management, particularly in obstetric settings. This review provides an in-depth exploration of the pathophysiology, diagnosis, and anesthetic implications of factor XI deficiency, thereby emphasizing the useful role of anesthesiologists. The variable bleeding phenotype of the disorder necessitates a nuanced understanding and tailored management strategies to mitigate severe perioperative bleeding risks.

The Impact of Selenium Deficiency and T-2 Toxin on Zip6 Expression in Kashin-Beck Disease.

This study investigated the expression of Zip6, a gene predominantly located in the placenta, breast, and prostate tissues, in patients with Kashin-Beck disease (KBD). Environmental risk factor models for KBD were developed using low selenium (Se) feeding (with a Se content of 0.02 mg Se/kg in the feed) and exposure to T-2 toxin (200 ng/g*BW/D).

Hepatocyte-specific NR5A2 deficiency induces pyroptosis and exacerbates non-alcoholic steatohepatitis by downregulating ALDH1B1 expression.

Nonalcoholic steatohepatitis (NASH) is a prevalent chronic disease, yet its exact mechanisms and effective treatments remain elusive. Nuclear receptor subfamily 5 group A member 2 (NR5A2), a transcription factor closely associated with cholesterol metabolism in the liver, has been hindered from comprehensive investigation due to the lethality of NR5A2 loss in cell lines and animal models. To elucidate the role of NR5A2 in NASH, we generated hepatocyte-specific knockout mice for Nr5a2 (Nr5a2) and examined their liver morphology across different age groups under a regular diet.