Analysis of factors related to failure in the pressure test: a six-year experience in Taiwan.

INTRODUCTION: The Republic of China Navy instituted the pressure test as one of the selection tools for diving troops and submarine crews. We analyzed factors associated with failure in the pressure test. METHODS: This was a retrospective cohort study designed to investigate pressure test failure in Navy recruits between January 2010 and August 2015. The recruits received pressurization in a hyperbaric chamber to a simulated depth of 112 feet of seawater (fsw) at a rate of 25 fsw/minute. Data describing trainee demographics, disease history, causes and depth of failure, as well as type of injury, were extracted from case notes and facility databases for statistical analysis. RESULTS: Of 3,608 trial cohorts, there were 435 failures, with an overall failure rate of 12.06%. About 95% of these failure trials were within a simulated depth of 60 fsw. Fifty-seven (57) failures did not record causes of failure. Among the other 378 failures, the most commonly identified causes were ear barotrauma (365 trials, 96.56%) and sinus barotrauma (10 trials, 2.65%). Statistical analysis revealed that recent upper respiratory tract infection, allergic rhinitis, and cigarette smoking were all significantly associated with higher incidence of middle ear barotrauma. CONCLUSIONS: Our results suggest that pressure testing to a depth of 60 fsw is effective in disqualifying personnel entering diving and submarine service. Recent infection of the upper respiratory tract, allergic rhinitis and cigarette smoking are risk factors for middle ear barotrauma, resulting in failure of the pressure test.

Periorbital emphysema after a wet chamber dive.

Although periorbital emphysema (PE) is commonly associated with orbital fractures, it may develop without any fracture or significant trauma in circumstances such as post-surgery, infection, forceful nose blowing, sneezing, and weight lifting. We report on a healthy military diver who developed PE following a wet chamber dive. A diagnosis of PE secondary to sinus barotrauma was reached. He was treated conservatively without medication and his symptoms recovered completely within 10 days. To the best of our knowledge, only five cases of diving-related PE have been reported in the literature. Analysis of these cases and ours revealed that facial trauma, repeated forceful Valsalva manoeuvres and recent upper respiratory tract infection are probable risk factors for diving-related PE.

Resveratrol Inhibition of Rac1-Derived Reactive Oxygen Species by AMPK Decreases Blood Pressure in a Fructose-Induced Rat Model of Hypertension.

Recent studies have reported that the activation of AMP-activated protein kinase (AMPK) suppressed oxidative stress. The aim of this study was to examine whether the activation of AMPK in the brain decreased Rac1-induced ROS generation, thereby reducing blood pressure (BP) in rats with fructose-induced hypertension. The inhibition of ROS by treatment with an AMPK activator (oral resveratrol, 10 mg/kg/day) for 1 week decreased the BP and increased the NO production in the rostral ventrolateral medulla (RVLM) of fructose-fed rats but not in control Wistar-Kyoto (WKY) rats. In addition, resveratrol treatment abolished the Rac1-induced increases in the activity of the NADPH oxidase subunits p22-phox and reduced the activity of SOD2, while treatment with an AMPK inhibitor (compound C, 40 µM/day) had the opposite effect, in the fructose-fed rats. Interestingly, the activation of AMPK abolished Rac1 activation and decreased BP by inducing the activities of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and ribosomal protein S6 kinase (RSK) and nNOS phosphorylation in the fructose-fed rats. We conclude that the activation of AMPK decreased BP, abolished ROS generation, and enhanced ERK1/2-RSK-nNOS pathway activity by negatively regulating Racl-induced NADPH oxidase levels in the RVLM during oxidative stress-associated hypertension.

Clinical aggressiveness of myxofibrosarcomas associates with down-regulation of p12CDK2AP1: prognostic implication of a putative tumor suppressor that induces cell cycle arrest and apoptosis via mitochondrial pathway.

BACKGROUND: Attenuated endogenous protein levels of cyclin-dependent kinase 2 associated protein 1 (p12(CDK2AP1)) and its active homodimer p25(CDK2AP1) were found in myxofibrosarcoma-derived cell lines. Clinical and biological significances of this putative tumor suppressor in myxofibrosarcoma were studied. METHODS: Plasmids carrying the CDK2AP1 gene and small hairpin RNA interference (shRNAi) targeting CDK2AP1 were transfected into NMFH-1 and/or OH931 cells to evaluate the effects on the CDK2, active caspase 3 (CASP3), cleaved-CASP8 and -CASP9 levels, cell cycle regulation, and/or apoptotic responses. Immunostaining of p12(CDK2AP1) was interpretable in 102 primary myxofibrosarcomas and correlated with clinicopathological variables, CDK2, Ki-67 and active CASP3 protein levels, and disease-specific survival. RESULTS: Exogenous expression of p12(CDK2AP1) in NMFH-1 and OH931 cells significantly induced G0/G1 cell cycle arrest and down-regulated CDK2 protein level. In NMFH-1 cells, these aspects were reversed by shRNAi targeting CDK2AP1 gene. Increased active CASP3 and cleaved-CASP9, but not -CASP8, were detected after CDK2AP1 overexpression, suggesting the cellular apoptosis were induced through the mitochondrial pathway. Immunostains of p12(CDK2AP1) were aberrantly decreased in 56.9 % of cases; positively and negatively correlated with protein levels of CDK2 (p = 0.023), Ki-67 (p = 0.001) and active CASP3 (p < 0.001), respectively. Following by high histological grades, p12(CDK2AP1) down-regulation was predictive of worse disease-specific survival in univariate (p = 0.003) and multivariate (p = 0.004) analyses. CONCLUSIONS: Through down-regulation of CDK2, high p12(CDK2AP1) level induced cell cycle arrest and the mitochondrial-dependent apoptotic pathway. Low p12(CDK2AP1) level represents a poor prognostic factor in patients with myxofibrosarcoma.

Serum heat shock protein after simulated deep diving in Navy divers.

Deep sea diving might cause a tremendous physical or psychological stress to the divers. The present study aims to evaluate the stress response to a simulated wet dive in Navy divers. Nineteen Navy divers took part in this study when they were undergoing annual deep dive training. Ten divers were exposed to 190 feet of sea water (fsw) breathing compressed air on day 1 and to 250 fsw breathing helium-oxygen (Heliox) gas mixture on day 3. Another 9 divers were exposed to 220 fsw on day 1 and 285 fsw on day 3 breathing Heliox gas mixture. The bottom time ranged from 5 to 8 min, and then the standard U.S. Navy air and Heliox decompression tables were followed for surfacing. Predive levels of serum heat shock protein 72 (sHsp72) were 9.95 +/- 0.56 ng/ml, which were significantly higher than those in the control group (8.01 +/- 0.77 ng/ml). After simulating Heliox dive, the sHsp72 increased to 10.43 +/- 0.56 ng/ml, but this was not statistically significant. Our results demonstrated that the serum level of Hsp72 is higher in the Navy divers who underwent regular intensive exercise. However, it remains unknown whether this increase of stress protein is associated with the diving stress or exercise preconditioning in the Navy divers.