Ethnic disparities in postpartum hemorrhage after cesarean delivery: a retrospective case-control study.

PURPOSE: To explore the relationship of ethnicity and postpartum hemorrhage (PPH) for women who underwent cesarean delivery (CD) and examine the risk factors for PPH in distinct ethnic groups in China. METHODS: We conducted case-control studies with the maternity data from the 11,778 CD cases, in Xinjiang Uygur Autonomous Region. Initially, multivariable logistic regression was used to estimate the disparity of race-ethnicity on the risk of PPH in ethnic Han, Uygur, Hui and Kazakh. Then, we performed case-control studies within two major ethnic groups, identifying the specific risk factors for PPH. RESULTS: Ethnic Uygur were associated with a statistically significant increased odds [adjusted odds ratios (aOR) 2.05; 95% confidence interval (CI) 1.26-3.33] of PPH compared with ethnic Han. For subgroup analyses, in Uygur subgroup, general anesthesia (aOR 7.78; 95% CI 2.31-26.20); placenta previa (aOR 11.18; 95% CI 3.09-40.45); prenatal anemia (aOR 4.84; 95% CI 2.44-9.60); emergency surgery (aOR 4.22; 95% CI 1.95-9.13) were independently associated with PPH. In Han subgroup, general anesthesia (aOR 5.70; 95% CI 1.89-17.26); placenta previa (aOR 20.08; 95% CI 6.35-63.46); multiple pregnancy (aOR 7.21; 95% CI 1.61-32.37); body mass index (aOR 1.19; 95% CI 1.07-1.31) were the risk factors to PPH. CONCLUSION: Uygur have more tendency to PPH compared to Han, and risk factors for PPH in Uygur and Han groups may differ. Knowing these differences may be meaningful when planning interventions and resources for high-risk patients undergoing cesarean delivery, and we need more research aimed at risk factors for PPH.

Fatty-acid receptor CD36 functions as a hydrogen sulfide-targeted receptor with its Cys333-Cys272 disulfide bond serving as a specific molecular switch to accelerate gastric cancer metastasis.

BACKGROUND: Hydrogen Sulfide (H2S), a third member of gasotransmitter family along with nitric oxide (NO) and carbon monoxide (CO), exerts a wide range of cellular and molecular actions in our body. There is a large body of evidence suggesting that H2S plays an important role in cancer metastasis; however, the molecular mechanisms of H2S-mediated acceleration of cancer metastasis remain unknown. METHODS: We examined the promote effects of H2S on phenotype of gastric cancer (GC) cells (including those of express wild type CD36 and mutant CD36) in vitro and in vivo. GC patients' samples were used for clinical translational significance evaluation. FINDINGS: H2S triggered lipid metabolism reprogramming by significantly up-regulating the expression of the fatty-acid receptor CD36 (CD36) and directly activating CD36 in GC cells. Mechanistically, a disulfide bond located between cysteine (Cys)333 and Cys272 within the CD36 protein structure that was labile to H2S-mediated modification. The long chain-fatty acid (LC-FA) binding pocket was capped by a turn in the CD36 protein, located between helical and sheet structures that were stabilized by the Cys333-Cys272. This limited the secondary binding between LC-FAs and lysine (Lys)334. Breaking the Cys333-Cys272 disulfide bond restored the second LC-FA binding conformation of CD36. Targeting CD36 in vivo blocked H2S-promoted metastasis and improved animal survival. INTERPRETATION: These findings identify that the Cys333-Cys272 disulfide bond disrupted the integrity of the second LC-FA binding conformation of CD36. Therefore, CD36 can directly activate LC-FA access to the cytoplasm by acting as a direct target molecule for H2S.