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The impact of tropical cyclones (TCs) on the CO2partial pressure at the sea surface (pCO2sea) and air‐sea CO2flux (FCO2) in the Bay of Bengal (BoB) was quantified based on satellite data and in situ observations between November 2013 and January 2017. The in situ observations were made at the BoB Ocean Acidification mooring buoy. A weak time‐mean net source of 55.78 ± 11.16 mmol CO2m−2year−1at the BoB Ocean Acidification site was estimated during this period. A wide range in increases of pCO2sea(1.0–14.8 μatm) induced by TCs occurred in postmonsoon (October–December), and large decreases of pCO2sea(−14.0 μatm) occurred in premonsoon (March–May). Large vertical differences in the ratio of dissolved inorganic carbon (DIC) to total alkalinity (TA) in the upper layer (ΔDIC/TA) were responsible for increasing pCO2seain postmonsoon. Relatively small values of ΔDIC/TA were responsible for decreasing pCO2seain premonsoon. Five TCs (Hudhud, Five, Kyant, Vardah, and Roanu) were considered. Hudhud significantly enhanced CO2efflux (18.49 ± 3.70 mmol CO2/m2) in oversaturated areas due to the wind effect during the storm and wind‐pumpeffects after the storm. Vardah insignificantly changed FCO2(1.22 ± 0.24 mmol CO2/m2) in undersaturated areas because of the counteraction of these two effects. Roanu significantly enhanced CO2efflux (19.08 ± 3.82 mmol CO2/m2) in highly oversaturated conditions (ΔpCO2> 20 μatm) since the wind effect greatly exceeded the wind‐pump effects. These five TCs were estimated to account for 55 ± 23% of the annual‐mean CO2annual efflux, suggesting that TCs have significant impacts on the carbon cycle in the BoB. We examined the impact by five tropical cyclones on the sea surface pCO2and air‐sea CO2exchange using Bay of Bengal Ocean Acidification moored buoy measurements over the Bay of Bengal. To our knowledge, this is the first study on the different effects of tropical cyclones and vertical differences in the ratio of dissolved inorganic carbon to total alkalinity in the upper layer on the sea surface pCO2and local air‐sea CO2flux. TCs tended to increase the pCO2seain the postmonsoon and to decrease the pCO2seain the premonsoon in the Bay of BengalLarge vertical differences in the ratio of DIC to TA in the upper layer were responsible for increasing pCO2seainduced by TCsTCs were estimated to account for 55 ± 23% of the annual‐mean CO2annual efflux

N-myc downstream-regulated gene 3 (NDRG3), which belongs to the NDRG family, is believed to play important roles in human cancer. In this present study, one-step quantitative reverse transcription-polymerase chain reaction (qPCR) and western blotting tests with 10 fresh-frozen laryngeal squamous cell carcinoma (LSCC) samples and immunohistochemistry (IHC) analysis in 109 LSCC cases were performed to investigate the relationship between NDRG3 expression and the clinicopathological characteristics of LSCC. Results demonstrated that NDRG3 mRNA and protein expression levels were statistically higher in LSCC tissues than that in non-cancerous tissues (all p<0.05). IHC data showed that the NDRG3 protein expression was remarkably correlated with lymph node metastasis (p=0.043). Univariate and multivariate survival analysis implied that high NDRG3 expression (p=0.004), lymph node metastasis (p=0.044) and TNM stage (p=0.020) were independently associated with the unfavourable overall survival of patients with LSCC. The above findings suggested that NDRG3 may be identified as a novel biomarker predicting the prognosis of LSCC.

Mutations in the cardiac ryanodine receptor gene (RyR2) have been recently identified in victims of sudden infant death syndrome. The aim of this study was to determine whether a gain-of-function mutation in RyR2increases the propensity to cardiac arrhythmias and sudden death in young mice.

In unexcitable, noncardiac cells, ultrashort (nanosecond) high-voltage (megavolt-per-meter) pulsed electrical fields (nsPEF) can mobilize intracellular Ca2+ and create transient nanopores in the plasmalemma. We studied Ca2+ responses to nsPEF in cardiac cells. Fluorescent Ca2+ or voltage signals were recorded from isolated adult rat ventricular myocytes deposited in an electrode microchamber and stimulated with conventional pulses (CPs; 0.5–2.4 kV/cm, 1 ms) or nsPEF (10–80 kV/cm, 4 ns). nsPEF induced Ca2+ transients in 68/104 cells. Repeating nsPEF increased the likelihood of Ca2+ transient induction (61.8% for <10 nsPEF vs. 80.6% for ≥10 nsPEF). Repetitive Ca2+ waves arising at the anodal side and Ca2+ destabilization occurred after repeated nsPEF (12/29) or during steady-state single nsPEF delivery at 2 Hz. Removing extracellular Ca2+ abolished responses to nsPEF. Verapamil did not affect nsPEF-induced Ca2+ transients, but decreased responses to CP. Tetrodotoxin and KB-R7943 increased the repetition threshold in response to nsPEF: 1–20 nsPEF caused local anodal Ca2+ waves without Ca2+ transients, and ≥20 nsPEF caused normal transients. Ryanodine-thapsigargin and caffeine protected against nsPEF-induced Ca2+ waves and showed less recovery of diastolic Ca2+ levels than CP. Voltage recordings demonstrated action potentials triggered by nsPEF, even in the presence of tetrodotoxin. nsPEF can mobilize intracellular Ca2+ in cardiac myocytes by inducing action potentials. Anodal Ca2+ waves and resistance to Na+ and Ca2+ channel blockade suggest nonselective ion channel transport via sarcolemmal nanopores as a triggering mechanism.

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