HHP (hypobaric hypoxia preconditioning) induces the overexpression of HSP70 (heat-shock protein 70), as well as tolerance to cerebral ischaemia. In the present study, we hypothesized that HHP would protect against HAE (high-altitude exposure)-induced acute lung injury and oedema via promoting the expression of HSP70 in lungs prior to the onset of HAE. At 2 weeks after the start of HHP, animals were exposed to a simulated HAE of 6000 m in a hypobaric chamber for 24 h. Immediately after being returned to ambient pressure, the non-HHP animals had higher scores of alveolar oedema, neutrophil infiltration and haemorrhage, acute pleurisy (e.g. increased exudate volume, increased numbers of polymorphonuclear cells and increased lung myeloperoxidase activity), increased pro-inflammatory cytokines [e.g. TNF-α (tumour necrosis factor-α), IL (interleukin)-1β and IL-6], and increased cellular ischaemia (i.e. glutamate and lactate/pyruvate ratio) and oxidative damage [glycerol, NOx (combined nitrate+nitrite) and 2,3-dihydroxybenzoic acid] markers in the BALF (bronchoalveolar fluid). HHP, in addition to inducing overexpression of HSP70 in the lungs, significantly attenuated HAE-induced pulmonary oedema, inflammation, and ischaemic and oxidative damage in the lungs. The beneficial effects of HHP in preventing the occurrence of HAE-induced pulmonary oedema, inflammation, and ischaemic and oxidative damage was reduced significantly by pretreatment with a neutralizing anti-HSP70 antibody. In conclusion, HHP may attenuate the occurrence of pulmonary oedema, inflammation, and ischaemic and oxidative damage caused by HAE in part via up-regulating HSP70 in the lungs.

Ta/TaN bilayers have been deposited by a commercial self-ionized plasma (SIP) system. The microstructures of Ta/TaN bilayers have been systematically characterized by X-ray diffraction patterns and cross-sectional transmission electron microscopy. TaN films deposited by SIP system are amorphous. The crystalline behavior of Ta film can be controlled by the N concentration of underlying TaN film. On amorphous TaN film with low N concentration, overdeposited Ta film is the mixture ofα- andβ-phases with amorphous-like structure. Increasing the N concentration of amorphous TaN underlayer successfully leads upper Ta film to form pureα-phase. For the practical application, the electrical property and reliability of Cu interconnection structure have been investigated by utilizing various types of Ta/TaN diffusion barrier. The diffusion barrier fabricated by the combination of crystallizedα-Ta and TaN with high N concentration efficiently reduces the KRc and improves the EM resistance of Cu interconnection structure.

Graves' disease is uncommon in children. The remission rate after antithyroid drugs (ATD) therapy is lower than in adults. We evaluated the clinical course of ATD therapy in children with Graves' disease in southern Taiwan to determine whether their biochemical markers could be used to predict remission in these patients. We retrospectively reviewed the clinical data of 53 children diagnosed with Graves' disease between 2009 and 2019. Clinical and biochemical parameters were analyzed for predictors of remission. About three‐fourths of the patients were female. Their median age at diagnosis was 13 years. No sex differences were found in most clinical characteristics. There was no correlation between thyroid‐stimulating hormone receptor antibody (TRAb) levels at diagnosis and thyroid function or adverse reactions to ATD. Relapse occurred in 62% of patients after discontinuation of first‐course ATD therapy. Three variables—good initial response to ATD, a decrease in TRAb levels during the first year after diagnosis, and a decrease in TRAb levels during the second year after diagnosis—were significant predictors of remission for more than 18 months. In conclusion, children with Graves' disease who had early ATD‐controlled Graves' disease and decreased TRAb levels during the first 2 years are likely to enter remission for more than 18 months.

High-mountain sickness is characterized by brain and pulmonary edema and cognitive deficits. The definition can be fulfilled by a rat model of high-altitude exposure (HAE) used in the present study. This study aimed to investigate the protective effect of hyperbaric oxygen therapy (HBO2T) and to determine the underlying mechanisms. Rats were subjected to an HAE (9.7% O2 at 0.47 absolute atmosphere of 6,000 m for 3 days). Immediately after termination of HAE, rats were treated with HBO2T (100% O2 at 2.0 absolute atmosphere for 1 hour per day for 5 consecutive days) or non-HBO2T (21% O2 at 1.0 absolute atmosphere for 1 hour per day for 5 consecutive days). As compared to non-HAE+non-HBO2T controls, the HAE+non-HBO2T rats exhibited brain edema and resulted in cognitive deficits, reduced food and water consumption, body weight loss, increased cerebral inflammation and oxidative stress, and pulmonary edema. HBO2T increased expression of both hippocampus and lung heat shock protein (HSP-70) and also reversed the HAE-induced brain and pulmonary edema, cognitive deficits, reduced food and water consumption, body weight loss, and brain inflammation and oxidative stress. Decreasing the overexpression of HSP-70 in both hippocampus and lung tissues with HSP-70 antibodies significantly attenuated the beneficial effects exerted by HBO2T in HAE rats. Our data provide in vivo evidence that HBO2T works on a remodeling of brain/lung to exert a protective effect against simulated high-mountain sickness via enhancing HSP-70 expression in HAE rats.

These results suggest that HHP may downgrade both the systemic inflammatory markers and the toxic organ injury indicators in HAE by upregulating tissue HSP70.

Background Dentists may be at a higher risk of developing carpal tunnel syndrome (CTS) because of their use of frequent wrist and vibratory instruments at work; however, this issue remains unclear. Therefore, we conducted this study to clarify it. Methods Taiwan National Health Insurance Research Database was used for this nationwide population-based study. We identified 11,084 dentists, 74,901 non-dentist healthcare professionals (HCPs), and identical number of age- and sex-matched participants from the general population. Participants who had the diagnosis of CTS before 2007 were excluded. Between 2007 and 2011, the risk of developing CTS among dentists, non-dentist HCPs, and the general population was compared by following their medical histories. Results The cumulative incidence rate of CTS among dentists was 0.5% during the 5-year follow-up period. In dentists, the risk was higher in women (women: 0.7%; men: 0.4%) and older individuals (≥60 years: 1.0%; <60 years: 0.4%). After adjusting for age, sex, and underlying comorbidities, dentists had a lower risk of CTS than the general population (adjusted odds ratio [AOR]: 0.65, 95% confidence interval [CI]: 0.45–0.92). Dentists had a higher risk for CTS compared with non-dentist HCPs, although the difference was not statistically significant (AOR: 1.21; 95% CI: 0.90−1.64). Conclusions In CTS, dentists had a lower risk than the general population and a trend of higher risk than non-dentist HCPs. The difference between dentists and non-dentist HCPs suggests that we should pay attention to dentists for potential occupational risk of this disease. However, further studies are warranted to better clarify it.

Background: This study proposed an algorithm to improve resuscitation outcomes in the emergency department (ED) for patients with traumatic out-of-hospital cardiac arrest (TOHCA). We also performed a retrospective chart review of patient outcomes before and after implementing the algorithm and sought to define factors that might influence patient outcomes.Methods: In September 2018, we implemented an algorithm for patients with TOHCA. This algorithm rapidly identifies possible causes of TOHCA and recommends appropriate interventions. We retrospectively reviewed the outcomes of all patients with TOHCA during a five-year period (comprising periods before and after the algorithm) and compared the results before and after the implementation of the algorithm.Results: After this algorithm was implemented, the use of the ED interventions of blood transfusion, placement of a large-bore central venous catheter, and thoracostomy increased significantly. The rate of return of spontaneous circulation (ROSC) also increased (before vs. after: ROSC: 23.6% vs. 41.5%, P = 0.035). Regarding hospital admission and survival to hospital discharge, we observed the trend of increment (hospital admission: 18.2% vs. 24.6%, P = 0.394; survival to hospital discharge: 0.0% vs. 4.6%, P = 0.107). Admitted patients exhibited a higher end-tidal CO 2 level during resuscitation than nonadmitted patients [admitted vs. nonadmitted: 41.5 (33.3-52.0) vs. 12.0 (7.5-18.8), P = 0.001].Conclusion: Our algorithm prioritizes the three major treatable causes of TOHCA: impedance of venous return, hypovolemia, and hypoxia. We found that rate of ROSC increased with the increasing implementation of the ED interventions recommended by the algorithm.