A meta-analysis examined the effect of intrawound vancomycin on surgical site wound infections in non-spinal neurosurgical operation.

To assess the impact of intrawound vancomycin on surgical site wound infections in non-spinal neurosurgical operations, we conducted a meta-analysis. A thorough review of the literature up to September 2022 showed that 4286 participants had a non-spinal neurosurgical operation at the start of the investigations; 1975 of them used intrawound vancomycin, while 2311 were control. Using dichotomous or contentious methods and a random or fixed-effect model, odds ratios (OR) and mean difference (MD) with 95% confidence intervals (CIs) were estimated to evaluate the impact of intrawound vancomycin on surgical site wound infections in non-spinal neurosurgical operation. The intrawound vancomycin had significantly lower surgical site wound infections (OR, 0.28; 95% CI, 0.19-0.40; P < .001) with low heterogeneity (I2 = 32%) compared with the control in non-spinal neurosurgical operation. The intrawound vancomycin had significantly lower surgical site wound infections compared with control in non-spinal neurosurgical operation. The low sample size of 2 out of 13 researches in the meta-analysis calls for care when analysing the results.

Glycosaminoglycan-Based Hydrogel Delivery System Regulates the Wound Microenvironment to Rescue Chronic Wound Healing.

Chronic wounds cannot proceed through the normal, orderly, and timely sequence of repair. The adverse cycle between excess reactive oxide species (ROS) and a persistent inflammatory response is an important mechanism of impaired wound healing. Herein, by combining the intrinsic bioactivities of natural polysaccharides and natural drugs, a glycosaminoglycan-based hydrogel delivery system is proposed to regulate the wound microenvironment. Dynamic supramolecular cross-linking enables the hydrogel to easily encapsulate the drug and fully fill the wound area. As the backbone of the hydrogel, heparin captures inflammatory chemokines at the wound site, while hyaluronic acid mimics the function of ECM. The hydrophobic drug curcumin has been ingeniously encapsulated in the hydrogel through micellization, thereby exerting good ROS scavenging ability and anti-inflammatory activity. Evaluations in diabetic mice showed that this antioxidant and anti-inflammatory hydrogel was effective in reducing the influx of immune cells at the wound site and in down-regulating the inflammatory response. Accelerated wound healing was also observed, as evidenced by faster re-epithelialization and better ECM remodeling. The proposed hydrogel can regulate the microenvironment of wounds from multiple aspects and thereby achieve regression of wound repair, which may provide a new therapeutic strategy for chronic wounds.

ELAV-like RNA binding protein 1 regulates osteogenesis in diabetic osteoporosis: Involvement of divalent metal transporter 1.

Diabetic osteoporosis (DOP) is a complication of diabetes mellitus (DM) and occurs due to alterations in bone metabolism under hyperglycemic condition. ELAV-like RNA binding protein 1 (ELAVL1) is abnormally up-regulated in diabetes-related diseases. Bioinformatics prediction indicates that divalent metal transporter 1 (DMT1) is a potential target of ELAVL1. To explore the role of ELAVL1 and the involvement of ELAVL1/DMT1 axis in DOP, we established a mouse model of DM by administration of high-fat diet and intraperitoneal injection with streptozotocin (STZ). The expression of ELAVL1 and DMT1 was increased in the bone tissues of DM mice. Knockdown of ELAVL1 reduced iron level and oxidative stress, promoted osteogensis, and prevented bone mass loss, thus mitigating DOP in DM mice. In vitro, mouse pre-osteoblast MC3T3-E1 cells were treated with high glucose (25 mM) and ferric ammonium citrate (FAC, 200 µM). The inhibitory effects of ELAVL1 knockdown on iron accumulation and oxidative stress were evidenced in MC3T3-E1 cells. Knockdown of ELAVL1 enhanced osteoblast viability, differentiation and mineralization. Notably, the expression of DMT1 was positively correlated with that of ELAVL1 in vivo and in vitro. Overexpression of DMT1 abolished the effect of ELAVL1 knockdown on the behaviors of MC3T3-E1 cells, suggesting that ELAVL1 might function through regulating DMT1. In conclusion, knockdown of ELAVL1 likely alleviated DOP by inhibiting iron overload and oxidative stress and promoting osteogenesis, and DMT1 might be involved in this process. These findings provide insights into the pathogenesis of DOP and suggest a potential therapeutic target for DOP treatment.

Prediction of iatrogenic preterm birth in patients with scarred uterus: a retrospective cohort study in Northeast China.

BACKGROUND: To build a novel and simple model to predict iatrogenic preterm birth in pregnant women with scarred uteri. METHODS: In this retrospective, observational, single-centre cohort study, data from 2315 patients with scarred uteri were collected. Multiple logistic regression analysis and mathematical modelling were used to develop a risk evaluation tool for iatrogenic preterm birth. After modelling, the calibration and discrimination of the model along with decision curve analysis were checked and performed to ensure clinical applicability. RESULTS: Among the 2315 patients, 417 (18.0%) had iatrogenic preterm births. The following variables were included in the model: interpregnancy interval (0 to < 12 months, OR 5.33 (95% Cl 1.79-15.91), P = 0.003; 13 to < 24 months (reference), 25 to < 60 months, OR 1.80 (95% CI 0.96-3.40), P = 0.068; ≥ 60 months, OR 1.60 (95% Cl 0.86-2.97), P = 0.14), height (OR 0.95, (95% CI 0.92-0.98), P = 0.003), parity (parity ≤1 (reference), parity = 2, OR 2.92 (95% CI 1.71-4.96), P < 0.0001; parity ≥3, OR 8.26, (95% CI 2.29-29.76), P = 0.001), number of vaginal bleeding (OR 1.81, (95% Cl 1.36-2.41), P < 0.0001), hypertension in pregnancy (OR 9.52 (95% CI 6.46-14.03), P < 0.0001), and placenta previa (OR 4.21, (95% CI 2.85-6.22), P < 0.0001). Finally, a nomogram was developed. CONCLUSIONS: In this study, we built a model to predict iatrogenic preterm birth for pregnant women with scarred uteri. The nomogram we created can assist doctors in evaluating the risk of iatrogenic preterm birth and help in making referrals; thus, better medical care can be given to improve the prognosis of patients and foetuses.

MORC2 regulates C/EBPα-mediated cell differentiation via sumoylation.

The expression and activity of CCAAT/enhancer-binding protein α (C/EBPα) are involved in sumoylation modification, which is critical to divert normal cells from differentiation to proliferation. However, the role and underlying mechanism of C/EBPα in cancer is poorly understood. Human MORC2 (microrchidia family CW-type zinc-finger 2), is a member of the MORC proteins family containing a CW-type zinc-finger domain. Here, we found that MORC2 interacted with TE-III domain of C/EBPα, and the overexpression of MORC2 promoted wild-type C/EBPα sumoylation and its subsequent degradation, which didn't significantly observe in mutant C/EBPα-K161R. Furthermore, the overexpression of MORC2 inhibited C/EBPα-mediated C2C12 cell differentiation to maintain cell cycle progression. Moreover, the striking correlation between the decreased C/EBPα expression and the increased MORC2 expression was also observed in the poor differentiation status of gastric cancer tissues. Most notably, the high expression of MORC2 is correlated  with an aggressive phenotype of clinical gastric cancer and shorter overall survival of patients. Taken together, our findings demonstrated that MORC2 expression regulated C/EBPα-mediated the axis of differentiation/proliferation via sumoylation modification, and affected its protein stability, causing cell proliferation and tumorigenesis.