Factors influencing hypothermia in very low/extremely low birth weight infants: a meta-analysis.

Introduction: Previous studies have explored factors that influence the occurrence of hypothermia in very low/extremely low birth weight (VLBW/ELBW) infants, but the factors associated with hypothermia in VLBW or ELBW infants remain inadequately evaluated due to limited prospective data and inconsistency in study populations. Therefore, it is necessary to systematically evaluate the risk factors of hypothermia in VLBW/ELBW infants in order to provide a theoretical basis for clinical practice. Methods: PubMed and other databases were used to search for case-control or cohort studies on factors influencing the occurrence of hypothermia in VLBW/ELBW infants. The search time was set from database creation to June 30th, 2022. Literature screening, quality evaluation, and data extraction were performed independently by two investigators according to predefined inclusion and exclusion criteria. Meta-analysis was performed using RevMan 5.3. Results: A total of 10 papers were finally included in this study and 12 factors were established by meta-analysis: body weight (six papers), failure to keep warm in time (three papers), neonatal resuscitation (seven papers), gestational age (three papers), premature rupture of membranes (three papers), maternal combined complications (four papers), cesarean section (six papers), antenatal steroids (four papers), multiple birth (two papers), small for gestational age (two papers), 1 min Apgar score (three papers), and 5 min Apgar score (three papers). Since only one study included race, age (hour), socio-economic status, and spontaneous labor, these factors could not be fitted into RevMan 5.3 for the analysis. Conclusion: Although there were differences in the study design of the included literature, the influencing factors described in each study were relatively similar. The influencing factors identified in this study may contribute to the construction of related intervention strategies for hypothermia in VLBW/ELBW infants.

E2F1-mediated up-regulation of TOP2A promotes viability, migration, and invasion, and inhibits apoptosis of gastric cancer cells.

Previous studies have reported that E2F transcription factor 1 (E2F1) and DNA topoisomerase II alpha (TOP2A) are up-regulated in gastric cancer (GC), the corresponding unexplored regulatory mechanisms and the interactions of which in GC are worth figuring out. In this study, the expressions of E2F1 and TOP2A in GC tissues were assessed by real-time PCR (RT-PCR), and E2F1 binding sites in the TOP2A promoter region were predicted via bioinformatics analyses and confirmed using dual-luciferase reporter and ChIP assays. The viability, apoptosis, migration, and invasion of GC cells after transfection with sh-E2F1 or TOP2A plasmid were measured using methyl thiazolyl tetrazolium (MTT) assay, Hoechst 33258 staining/Annexin V/PI staining, and transwell assay. The expressions of E2F1, TOP2A, Cleaved caspase-3, Proliferating cell nuclear antigen (PCNA), E-cadherin, N-cadherin, and Vimentin in transfected cells were assessed by reverse transcription quantitative PCR (RT-qPCR) and western blot. Concretely, E2F1, as a transcription factor, has binding sites in the TOP2A promoter region. E2F1 and TOP2A levels were up-regulated and positively correlated with each other in GC tissues, i.e., overexpressed E2F1 increased TOP2A levels and E2F1 silencing decreased TOP2A levels in GC cells. Moreover, E2F1 silencing hindered GC cell viability, migration, and invasion, enhanced apoptosis, diminished the levels of PCNA, N-cadherin and Vimentin, and elevated those of Cleaved caspase-3 and E-cadherin in GC cells. However, overexpressed TOP2A reversed the above effects of E2F1 silencing. To sum up, E2F1-mediated up-regulation of TOP2A promotes the viability, migration, and invasion, and inhibits the apoptosis of GC cells.

Overexpressing miR-122-5p Inhibits the Relaxation of Vaginal Smooth Muscle in Female Sexual Arousal Disorder by Targeting Vasoactive Intestinal Peptide Receptor 1.

INTRODUCTION: Female sexual arousal disorder (FSAD) is a common issue causing physical and psychological pain, but it has no standard diagnostic criteria or treatment. So its pathogenesis desiderates to be explored. AIM: To investigate the specific function of miR-122-5p in FSAD. METHODS: 18 subjects were grouped into FSAD and normal control groups according to the Chinese version of the Female Sexual Function Index, and the expression levels of miR-122-5p and vasoactive intestinal peptide receptor 1 (VIPR1) protein in their tissue were verified through real-time quantitative polymerase chain reaction (qRT-PCR) and western blot (WB) analysis. Then in vitro experiment, miR-122-5p was overexpressed or inhibited in rat vaginal smooth muscle cells (SMCs). The relaxation of rat vaginal SMCs was reflected by the cell morphology, intracellular free cytosolic calcium ion (Ca2+) levels, cell proliferation and apoptosis, together with the cyclic adenosine monophosphate (cAMP) concentration and protein kinase A (PKA) activities. Additionally, the expression levels of relaxation-related proteins, including VIPR1, stimulatory G protein (Gs), adenylate cyclase (AC), and PKA, were detected based on WB analysis. Furthermore, a rescue experiment that simultaneously overexpressed or silenced miR-122-5p and VIPR1 was conducted, and all the indicators were evaluated. MAIN OUTCOMES MEASURE: The expression level of VIPR1 and downstream proteins, cell morphology, cell proliferation and apoptosis, and intracellular free Ca2+ levels were examined. RESULTS: We verified that women with FSAD had higher miR-122-5p and lower VIPR1 protein. Then overexpressing miR-122-5p decreased relaxation of rat vaginal SMCs, which was manifested as a contractile morphology of cells, an increased intracellular free Ca2+ concentration, and lower cAMP concentration and PKA activity. Moreover, by rescue experiments, we inferred that VIPR1 was the target of miR-122-5p and affected the relaxation function of vaginal SMCs. CONCLUSION: miR-122-5p regulates the relaxation of vaginal SMCs in FSAD by targeting VIPR1, ulteriorly providing an underlying diagnostic and therapeutic target for FSAD. Cong S, Gui T, Shi Q, et al. Overexpressing miR-122-5p Inhibits the Relaxation of Vaginal Smooth Muscle in Female Sexual Arousal Disorder by Targeting Vasoactive Intestinal Peptide Receptor 1. Sex Med 2021;9:100390.

Gua Sha attenuates thermal hyperalgesia and decreases proinflammatory cytokine expression in serum in rats with lumbar disc herniation induced by autologous nucleus pulposus.

OBJECTIVE: To investigate the analgesic effect of Gua Sha and its underlying mechanism in rats with noncompressive lumbar disk herniation induced by autologous nucleus pulposus. METHODS: A rat model of noncompressive lumbar disk herniation was established and rats were randomly divided into model group, sham group, and Gua Sha group (24 in each group). Gua Sha was performed from the 5th day after the surgery, once every other day, 3 times for a course of treatment, and totally 3 courses. The thermal withdrawal latency was evaluated using the intelligent hot plate one day before the surgery, and on days 4 (the day before the treatment), 10 (the end of the first course), 16 (the end of the second course) and 22 (the end of the third course). On days 4, 10, 16 and 22, six rats in each group were picked randomly and their blood samples were drawn to assess the expression of interleukin-1¦Â (IL-1¦Â), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-¦Á). RESULTS: Compared to rats in the sham group, the application of nucleus pulposus to right L5 dorsal root ganglion induced prolonged thermal hyperalgesia, and up-regulated the expression of IL-1¦Â, IL-6 and TNF-¦Á in serum (P < 0.01). The therapy of Gua Sha attenuated thermal hyperalgesia potently, inhibited the expression of IL-1¦Â, IL-6 and TNF-¦Á in a time-dependent manner (P < 0.01). There were no significant differences in the thermal withdrawal latency and the expression of inflammatory cytokines between the sham and Gua Sha groups at the end of the treatment (P > 0.01). CONCLUSION: The current study showed that Gua Sha might alleviate thermal hyperalgesia in rats with lumbar disc herniation induced by autologous nucleus pulposus via inhibiting the expression of proinflammatory cytokins.