To determine whether Tonopen intraocular pressure (IOP) measurements by Ophthalmic technicians are interchangeable with Goldmann applanation tonometry (GAT) by a specialist in our glaucoma clinic.
 
  Ophthalmic technician Tonopen and glaucoma specialist GAT IOP measurements were performed on both undilated eyes of 300 consecutive patients during the same visit to our glaucoma clinic.
 
  Among all 600 eyes of 300 patients (age 65.4, range 23-92years, male 44.3%), Tonopen and GAT IOPs were similar (15.5 ± 0.6 vs. 15.4 ± 0.7mmHg, respectively, p = 0.63) and directly correlated (r
   = 0.58, p < 0.0001). However, among 120 patients with bilateral primary open-angle glaucoma GAT IOP was significantly higher than Tonopen in the right eyes (17.1 ± 1.1 vs. 16.2 ± 0.9mmHg, p = 0.024) and in the left eyes (17.0 ± 1.0 vs. 16.3 ± 1.0mmHg, p = 0.029). In all 300 right eyes, Tonopen underestimated IOP in 48.3% of eyes and overestimated in 39% (difference range ( - )14 to ( + )12mmHg), with IOP difference >  ± 3mmHg inersity of New York, Buffalo, NY does not require this retrospective study to register.HOXC-AS3 has been reported to be an oncogenic lncRNA in several types of cancer, while its role in ovarian cancer (OC) is unknown. This study aimed to explore the involvement of HOXC-AS3 in OC. The expression levels of HOXC-AS3, mature miR-96, and miR-96 precursor (premature miR-96) in OC and paired non-tumor tissues from 62 OC patients were determined by RT-qPCR. Correlations were analyzed by linear regression. The expression levels of mature miR-96 and miR-96 precursor in OC cells with the overexpression of HOXC-AS3 were determined by RT-qPCR. The roles of HOXC-AS3 and mature miR-96 in regulating the proliferation of OC cells were explored by CCK-8 assay.  https://www.selleckchem.com/products/trastuzumab-deruxtecan.html  HOXC-AS3 was upregulated in OC, while mature miR-96 and miR-96 precursor were downregulated in OC. In OC tissues, HOXC-AS3 was inversely correlated with mature miR-96, but not miR-96 precursor. In OC cells, overexpression of HOXC-AS3 reduced the expression levels of mature miR-96, but not miR-96 precursor. Cell proliferation analysis showed that overexpression of HOXC-AS3 resulted in increased cell proliferation, while overexpression of miR-96 suppressed cell proliferation. In addition, overexpression of HOXC-AS3 attenuated the effects of overexpression of miR-96. HOXC-AS3 suppresses the formation of mature miR-96 in OC cells to promote cell proliferation.Meta-analyses suggest that the published literature represents only a small minority of the total data collected in biomedical research, with most becoming 'dark data' unreported in the literature. Dark data is due to publication bias toward novel results that confirm investigator hypotheses and omission of data that do not. Publication bias contributes to scientific irreproducibility and failures in bench-to-bedside translation. Sharing dark data by making it Findable, Accessible, Interoperable, and Reusable (FAIR) may reduce the burden of irreproducible science by increasing transparency and support data-driven discoveries beyond the lifecycle of the original study. We illustrate feasibility of dark data sharing by recovering original raw data from the Multicenter Animal Spinal Cord Injury Study (MASCIS), an NIH-funded multi-site preclinical drug trial conducted in the 1990s that tested efficacy of several therapies after a spinal cord injury (SCI). The original drug treatments did not produce clear positive results and MASCIS data were stored in boxes for more than two decades. The goal of the present study was to independently confirm published machine learning findings that perioperative blood pressure is a major predictor of SCI neuromotor outcome (Nielson et al., 2015). We recovered, digitized, and curated the data from 1125 rats from MASCIS. Analyses indicated that high perioperative blood pressure at the time of SCI is associated with poorer health and worse neuromotor outcomes in more severe SCI, whereas low perioperative blood pressure is associated with poorer health and worse neuromotor outcome in moderate SCI. These findings confirm and expand prior results that a narrow window of blood-pressure control optimizes outcome, and demonstrate the value of recovering dark data for assessing reproducibility of findings with implications for precision therapeutic approaches.Activation of CX43 signaling protects myocardial cells from myocardial ischemia/reperfusion (I/R) injury. However, the underlying mechanism remains unclear. MicroRNAs (miRNAs) are well known to play important roles in the progression of diverse diseases. Here, we first confirmed the expression profile of CX43 in rat heart tissues with I/R injury. Then, microRNAs (miRNAs) that target CX43 were predicted using miRDB, miRWalk, and TargetScan. The candidate miR-23a was selected, and its expression level in I/R samples was investigated. To determine the role of miR-23a, rat primary myocardial cells were transfected with miR-23a mimics after they were subjected to hypoxia-reoxygenation (H/R) injury. Transfection of miR-23a mimics stimulated mitophagy through the PINK1/Parkin pathway and downregulated the protein level of CX43. Treatment of miR-23a-transfected cells with NF-kB inhibitors completely abolished miR-23a-mediated mitophagy after H/R. Moreover, miR-23a transfection significantly suppressed CX43 expression and enhanced mitophagy in the model heart in vivo. Therefore, miR-23a plays a detrimental role in myocardial I/R injury by enhancing mitophagy and inhibiting CX43 mRNA.Melatonin is a hormone of the pineal gland that contributes to the regulation of physiological activities, such as sleep, circadian rhythm, and neuroendocrine processes. Melatonin is found in several plants and has pharmacological activities including antioxidant, anti-inflammatory, hepatoprotective, cardioprotective, and neuroprotective. It also has shown therapeutic efficacy in treatment of cancer and diabetes. Melatonin affects several molecular pathways to exert its protective effects. The NLRP3 inflammasome is considered a novel target of melatonin. This inflammasome contributes to enhanced level of IL-1β, caspase-1 activation, and pyroptosis stimulation. The function of NLRP3 inflammasome has been explored in various diseases, including cancer, diabetes, and neurological disorders. By inhibiting NLRP3, melatonin diminishes inflammation and influences various molecular pathways, such as SIRT1, microRNA, long non-coding RNA, and Wnt/β-catenin. Here, we discuss these molecular pathways and suggest that melatonin-induced inhibition of NLRP3 should be advanced in disease therapy.