Preparation of the Hypoallergenic Enzymatic Hydrolyzate of Cra a 4 with the Potential to Induce Immune Tolerance.

Sarcoplasmic calcium-binding protein identified in , is a stable allergen; the methods to reduce its allergenicity are still limited. The present study aimed to develop the hypoallergenic enzymatic hydrolyzate of Cra a 4 (ECra a 4) by enzymolysis. After screening of proteases by bioinformatics and optimization of enzymolysis conditions, ECra a 4 was obtained by enzymolysis with Trypsin.

Antigenic epitopes and cross-reactivity analysis of tropomyosin from .

Tropomyosin (TM) has been determined as the major allergen in . However, little information is available about its antigenic epitopes and cross-reactivity. In this study, recombinant TM was obtained through genetic engineering and its IgG-/IgE-binding activity was similar to native TM.

Efficacy of Endoscopic Tissue Adhesive in Patients with Gastrointestinal Tumor Bleeding.

Background: Gastrointestinal tumors bleeding remains a significantly clinical challenge due to its resistance to conventional endoscopic hemostasis methods. While the efficacy of endoscopic tissue adhesives (ETA) in variceal bleeding has been established, its role in gastrointestinal tumor bleeding (GITB) remains ambiguous.

Aims: This study aims to assess the feasibility and effectiveness of ETA in the treatment of GITB.

Mutation of Disulfide Bond Sites Reduces the Immunoreactivity of Cra a 4 by Changing the Structural Characteristics.

Sarcoplasmic calcium-binding protein (Cra a 4) from belongs to the EF-hand superfamily, and understanding of its structure-allergenicity relationship is still insufficient. In this study, chemical denaturants were used to destroy the structure of Cra a 4, showing that disruption of the structure reduced its IgG-/IgE-binding activity. To explore which critical amino acid site affects the allergenicity of Cra a 4, the mutants were obtained by site-directed mutations in the disulfide bonds site (C), conformational epitopes (I, D), or Ca-binding region (D, D) and their IgG-/IgE-binding activity was reduced significantly using serological tests.

Circ-EIF3I Promotes Hepatocellular Carcinoma Progression Through Modulating miR-361-3p/DUSP2 Axis.

Hepatocellular carcinoma (HCC) is one of the most common malignant cancers globally. Circular RNAs (circRNAs) have been implicated in the development of HCC. Previous studies have confirmed that circ-EIF3I plays an important role in the progress of lung cancer.

CircRNA DONSON contributes to cisplatin resistance in gastric cancer cells by regulating miR-802/BMI1 axis.

Background: Circular RNA downstream neighbor of SON (circDONSON) has been revealed to promote gastric cancer (GC) growth and invasion, while the role and molecular mechanism underlying circDONSON in GC cisplatin (DDP) resistance remain unclear.

Methods: Levels of circDONSON, microRNA (miR)-802, and B lymphoma Mo-MLV insertion region 1 (BMI1) mRNA were detected using quantitative real-time polymerase chain reaction. Cell viability and apoptosis were measured by cell counting kit-8 assay, colony formation assay and flow cytometry, respectively.

Electrostatic explanation of D1228V/H/N-induced c-Met resistance and sensitivity to type I and type II kinase inhibitors in targeted gastric cancer therapy.

The c-Met D1228V/H/N mutation clinically causes acquired resistance to type I tyrosine kinase inhibitors (TKIs), while maintaining sensitivity to type II TKIs in targeted gastric cancer therapy. The mutation is located in the activation loop (A-loop) region of the c-Met kinase domain, which substitutes the negatively charged residue Asp1228 with electroneutral amino acid Val, His, or Asn, thus electrostatically destabilizing the DFG-in conformation of A-loop and inducing its transition to DFG-out state. The transition is spontaneous in a dynamics point of view and the A-loop exhibits a large intrinsic disorder during the transitional dynamics course.

Association between functional PSMD10 Rs111638916 variant regulated by MiR-505 and gastric cancer risk in a Chinese population.

Background/aims: Gankyrin is an oncoprotein involved in regulating the cell cycle through protein-protein interactions with cyclin-dependent kinase 4 and p53. However, its association with gastric cancer (GC) risk has not yet been determined. In this study, we investigated micro RNA (miRNA)-associated single nucleotide polymorphisms (SNPs) in the 3'-untranslated region (UTR) of the gankyrin gene PSMD10 to clarify the relationship between these SNPs and miRNAs in Chinese patients with GC.

Risk of hepatitis B virus (HBV) reactivation in non-Hodgkin lymphoma patients receiving rituximab-chemotherapy: a meta-analysis.

Background: The addition of Rituximab to standard chemotherapy (C) has been reported to improve the end of treatment outcome in non-Hodgkin lymphoma (NHL) patients. Nevertheless, rituximab has been associated with hepatitis B virus reactivation (HBV-R).

Objectives: The aim of this systematic review and meta-analysis is to research the relationship between rituximab and HBV-R.

Chronic myeloid leukemia patients sensitive and resistant to imatinib treatment show different metabolic responses.

The BCR-ABL tyrosine kinase inhibitor imatinib is highly effective for chronic myeloid leukemia (CML). However, some patients gradually develop resistance to imatinib, resulting in therapeutic failure. Metabonomic and genomic profiling of patients' responses to drug interventions can provide novel information about the in vivo metabolism of low-molecular-weight compounds and extend our insight into the mechanism of drug resistance.

Multidrug resistance gene (MDR1) polymorphisms correlate with imatinib response in chronic myeloid leukemia.

The human multidrug resistance gene (MDR1, ABCB1) codes for P-glycoprotein (P-gp) that affects the pharmacokinetics of many drugs. MDR1 single nucleotide polymorphisms (SNPs) are associated with drug clearance. Imatinib is a substrate of P-gp-mediated efflux.