Cross-sectional study of posterior tooth root fractures in 2015 and 2019 in a Chinese population.

OBJECTIVES: This study aimed to compare posterior tooth root fractures in endodontically treated teeth versus nonendodontically treated teeth in the Chinese population. MATERIALS AND METHODS: We investigated 500 root fractured posterior teeth in 461 Chinese patients. The clinical information (age, sex of patients, tooth type) were recorded. The fractured teeth were divided into endodontically treated root fractured (ETRF) teeth and nonendodontically treated root fractured (NETRF) teeth. The morphology of the fractured root (circular, oval, other), the orientation of fracture lines (vertical and non-vertical), the restorations performed (crown, filling, non-filling), and the position of the teeth in the dental arch (normal, misaligned) were evaluated based on cone-beam computed tomography images. These data were compared between 2015 and 2019. ETRF% was calculated as ETRF/ETRF + NETRF. Vertical% was calculated as vertical/vertical + non-vertical. RESULTS: There were 177 ETRF teeth and 323 NETRF teeth in this population. The total ETRF% was 29.3% in 2015 and 37.6% in 2019 (P = 0.087). The proportion of vertical root fracture in the ETRF group increased significantly in 2019 compared with that in 2015 (46.2% vs. 80.2%, P = 0.000). The ETRF% in female patients increased by 16.8%, but increased by only 1.2% in male patients in 2019 compared with that in 2015. The ETRF% of mandibular and maxillary premolars increased by 48.5% and 29.3%, respectively. The proportion of crown restoration increased by 2.4% in 2019 compared with that in 2015 in the ETRF group. CONCLUSIONS: The proportion of NETRF teeth and non-vertical root fractures in posterior teeth is high in this Chinese population. The number of vertical root fractures in endodontically treated teeth increased significantly from 2015 to 2019. CLINICAL RELEVANCE: More attention should be paid to endodontic treatment factors in the occurrence of root fractures, especially as female patients and premolars are more susceptible.

Abnormal Cullin1 neddylation-mediated p21 accumulation participates in the pathogenesis of recurrent spontaneous abortion by regulating trophoblast cell proliferation and differentiation.

The study explores the role of neddylation in early trophoblast development and its alteration during the pathogenesis of recurrent spontaneous abortion (RSA). Immunofluorescence and western blot were conducted to evaluate the expression pattern of NEDD8 protein in the first-trimester placentas of healthy control and RSA patients. Neddylated-cullins, especially neddylated-cullin1, were downregulated and their substrate, p21, was accumulated in RSA samples. NEDD8 cytoplasmic recruitment was observed in extravillous trophoblast (EVT) progenitors of RSA placentas. Consistent with the results of clinical samples, neddylation inhibition using MLN4924 in trophoblast cell lines caused obvious p21 accumulation and free NEDD8 cytoplasmic recruitment. Further in vitro study demonstrated neddylation inhibition attenuated proliferation of Jeg-3 cells via p21 accumulation. Moreover, when trophoblast stem (TS) cells derived from first-trimester placentas were cultured for differentiation analyses. MLN4924 impaired the differentiation of TS cells towards EVTs by downregulating HLA-G and GATA3. p21 knockdown could partly rescue MLN4924-suppressed HLA-G and GATA3 expression. In conclusion, cullin1 neddylation-mediated p21 degradation is required for trophoblast proliferation and can affect trophoblast plasticity by affecting HLA-G and GATA3 expression. The results provide insights into the pathological mechanism of RSA and the biological regulation of trophoblast development.

Efficacy and safety of desvenlafaxine treatment for hot flashes associated with menopause: a meta-analysis of randomized controlled trials.

Vasomotor symptoms, such as daytime hot flashes and nighttime awakenings due to hot flashes, are commonly associated with menopausal women. The aim of this study was to assess desvenlafaxine in moderate to severe hot flashes in postmenopausal women. Electronic databases were searched for relevant randomized controlled trials that compared desvenlafaxine to placebo for postmenopausal women affected with hot flashes. The main outcomes were mean differences (MD) or standardized mean differences (SMD) and 95% confidence interval (CI) for change of the hot flashes. Six randomized controlled trials were identified in the meta-analysis. Pooled change of moderate and severe hot flashes frequency reduced SMD of -0.49 (95% CI -0.91 to -0.07) in desvenlafaxine 100 mg and -0.36 (95% CI -0.54 to -0.19) in desvenlafaxine 150 mg at week 12. Desvenlafaxine 100 mg reduced moderate and severe hot flashes frequency SMD of -0.74 (95% CI -1.05 to -0.44) within 26 weeks. There is no evidence for an increased risk of cardiovascular, cerebrovascular, or hepatic events associated with desvenlafaxine 100 mg/day. The meta-analysis suggests that treatment with desvenlafaxine 100 mg/day is associated with a significant reduction of moderate to severe hot flashes in postmenopausal women. Desvenlafaxine appears both safe and effective for treating hot flushes for up to 12 months.

Granulocyte-macrophage colony-stimulating factor promotes endometrial repair after injury by regulating macrophages in mice.

Intrauterine adhesion (IUA) caused by endometrial injury is a common cause of female infertility and is challenging to treat. Macrophages play a critical role in tissue repair and cyclical endometrial regeneration. Granulocyte-macrophage colony-stimulating factor (GM-CSF) has significant reparative and anti-fibrotic effects in various tissues. However, there is limited research on the role of GM-CSF in the repair of endometrial injury and the involvement of macrophages in GM-CSF-mediated endometrial repair. In this study, using a mouse model of endometrial scratching injury, we found that GM-CSF treatment accelerated the repair of endometrial injury and improved fertility. At the molecular level, we observed that GM-CSF can downregulate the transcript levels of tumor necrosis factor (TNF) in mouse bone marrow-derived macrophages (BMDMs) stimulated by lipopolysaccharide (LPS) and upregulate the expression of Arginase-1 (Arg-1) and mannose receptor C-type 1 (MRC1). Importantly, during the early and middle stages of injury, GM-CSF increased the proportion of M1-like, M2-like, and M1/M2 mixed macrophages, while in the late stage of injury, GM-CSF facilitated a decline in the number of M2-like macrophages. These findings suggest that GM-CSF may promote endometrial repair by recruiting macrophages and modulating the LPS-induced M1-like macrophages into a less inflammatory phenotype. These insights have the potential to contribute to the development of novel therapeutic approaches for the treatment of intrauterine adhesion and related infertility.

TRIP6 accelerates the proliferation and migration of fetal airway smooth muscle cells by enhancing YAP activation.

The thyroid receptor interactor protein 6 (TRIP6) has emerged as a key regulator for the proliferation and migration of various cells. However, whether TRIP6 is involved in regulating the proliferation and migration of airway smooth muscle (ASM) cells in the progression of pediatric asthma remains undetermined. The present study investigated the function of TRIP6 in regulating the proliferation and migration of fetal ASM cells induced by tumor necrosis factor (TNF)-α in vitro. The results revealed that TRIP6 expression was significantly upregulated in TNF-α-stimulated ASM cells. Loss-of-function experiments demonstrated that the knockdown of TRIP6 markedly suppressed TNF-α-proliferation and migration of ASM cells. By contrast, overexpression of TRIP6 had the opposite effect. In-depth research uncovered that TNF-α stimulation promoted the activation of yes-associated protein (YAP), which could be significantly reversed by TRIP6 silencing. Moreover, inactivation of YAP significantly reversed the promotion effect of TRIP6 overexpression on TNF-α-induced ASM cell proliferation and migration. Overall, these results reveal that upregulation of TRIP6 contributes to the proliferation and migration of fetal ASM cells by enhancing YAP activation, highlighting the importance of the TRIP6/YAP axis in the airway remodeling of pediatric asthma.