Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences最新文献

Objectives: To design and synthesize peptide inhibitors targeting transient receptor potential vanilloid 1 (TRPV1) ion channel, and to validate their function.

Methods: Based on previous studies on the relation of molecular structure and function of red head toxin (RhTx), a series of peptides were rationally designed and synthesized, with positive charged amino acids linked to the N terminus of RhTx. These Nplus-RhTx peptides were functionally validated by patch-clamp recordings in live cells.

Results: Among the 8 synthesized Nplus-RhTx peptides, four inhibited TRPV1 ion channel activated by capsaicin with IC₅₀ of (188.3±4.7), (193.6±18.0), (282.8±11.9) and (299.5±6.4) µmol/L, respectively.

Conclusions: It is feasible to develop TRPV1 peptide inhibitors by using rational design based on N terminal residues of RhTx.

Chest tightness variant asthma (CTVA) is an atypical form of asthma with chest tightness as the sole or predominant symptom. The underlying receptors for chest tightness are bronchial C-fibers or rapidly adapting receptors. The nerve impulses are transmitted via the vagus nerve and processed in different regions of the cerebral cortex. Chest tightness is associated with sensory perception, and CTVA patients may have heightened ability to detect subtle changes in lung function, but such sensory perception is unrelated to respiratory muscle activity, lung hyperinflation, or mechanical loading of the respiratory system. Airway inflammation, pulmonary ventilation dysfunction (especially involving small airways), and airway hyperresponsiveness may underlie the sensation of chest tightness. CTVA patients are prone to comorbid anxiety and depression, which share similar central nervous system processing pathways with dyspnea, suggesting a possible neurological basis for the development of CTVA. This article examines the recognition and mechanisms of chest tightness, and explores the pathogenesis of CTVA, focusing on its association with airway inflammation, ventilation dysfunction, airway hyperresponsiveness, and psychosocial factors.

Ovarian tissue cryopreservation and transplantation is the only way to preserve fertility for female cancer patients in prepubertal ages and those who cannot delay radiotherapy or chemotherapy. However, the success rate of cryopreservation and transplantation of ovarian tissue is still low at present due to the risk of ischemia and hypoxia of the grafted tissues. Abnormal activation of primordial follicles and ischemia-reperfusion injury after blood supply recovery also cause massive loss of follicles in grafted ovarian tissues. Various studies have explored the use of different drugs to reduce the damage of follicles during freezing and transplantation as well as to extend the duration of endocrine and reproductive function in patients with ovarian transplantation. For example, melatonin, N-acetylcysteine, erythropoietin or other antioxidants have been used to reduce oxidative stress; mesenchymal stem cells derived from different tissues, basic fibroblast growth factor, vascular endothelial growth factor, angiopoietin 2 and gonadotropin have been used to promote revascularization; anti-Müllerian hormone and rapamycin have been used to reduce abnormal activation of primordial follicles. This article reviews the research progress on the main mechanisms of follicle loss after ovarian tissue transplantation, including hypoxia, ischemia-reperfusion injury and associated cell death, and abnormal activation of follicles. The methods for reducing follicle loss in grafted ovarian tissues are further explored to provide a reference for improving the efficiency of ovarian tissue cryopreservation and transplantation.

In the last twenty years, the cesarean section rate has been rising in China, leading to an increased prevalence of cesarean scar defect (CSD) and secondary infertility. CSD decreases receptivity of endometrium, induces adenomyosis and endometriosis, disrupts uterine micro-environment and causes difficulties in embryo transplant operation as well as has further pregnancy complications. For women undergoing assisted reproductive technology (ART), CSD significantly reduces live birth rate, clinical pregnancy rate and embryo implantation rate. CSD can be effectively treated by hysteroscopic surgery, laparoscopic surgery and transvaginal surgery to increase the pregnancy rate. This article reviews the research progress on the impact of CSD on the reproductive outcomes of ART, the potential factors and related treatments, and provides a reference for the management of CSD patients undergoing ART.