Numerical modeling of rogue waves in coastal waters

Spatio-temporal evolution of rogue waves measured in Taiwanese coastal waters is reconstructed by means of numerical simulations. Their lifetimes are up to 100 s. The time series used for reconstructions were measured at dimensionless depths within the range of <i>kh</i> = 1.3&ndash;4.0, where <i>k</i> is the wave number and <i>h</i> is the depth. All identified rogue waves are surprisingly weakly nonlinear. The variable-coefficient approximate evolution equations, which take into account the shoaling effect, allow us to analyze the abnormal wave evolution over non-uniform real coastal bathymetry. The shallowest simulated point is characterized by <i>kh</i> &approx; 0.7. The reconstruction reveals an interesting peculiarity of the coastal rogue events: though the mean wave amplitudes increase as waves travel onshore, rogue waves are likely to occur at deeper locations, but not closer to the coast

Monstrous ocean waves during typhoon Krosa

This paper presents a set of ocean wave time series data recorded from a discus buoy deployed near northeast Taiwan in western Pacific that was operating during the passage of Typhoon Krosa on 6 October 2007. The maximum trough-to-crest wave height was measured to be 32.3 m, which could be the largest &lt;I&gt;H&lt;/I&gt;&lt;sub&gt;max&lt;/sub&gt; ever recorded

Field investigations of coastal sea surface temperature drop after typhoon passages

Sea surface temperature (SST) variability affects marine ecosystems, fisheries, ocean primary productivity and human activities and is the primary influence on typhoon intensity. SST drops of a few degrees in the open ocean after typhoon passages have been widely documented; however, few studies have focused on coastal SST variability. The purpose of this study is to determine typhoon-induced SST drops in the near-coastal area (within 1&thinsp;km of the coast) and understand the possible mechanism. The results of this study were based on extensive field data analysis. Significant SST drop phenomena were observed at the Longdong Buoy in northeastern Taiwan during 43 typhoons over the past 20 years (1998–2017). The mean SST drop (ΔSST) after a typhoon passage was 6.1&thinsp;∘C, and the maximum drop was 12.5&thinsp;∘C (Typhoon Fungwong in 2008). The magnitude of the SST drop was larger than most of the observations in the open ocean. The mean duration of the SST drop was 24&thinsp;h, and on average, 26.1&thinsp;h were required for the SST to recover to the original temperature. The coastal SST drops at Longdong were correlated with the moving tracks of typhoons. When a typhoon passes south of Longdong, the strong and persistent longshore winds induce coastal upwelling and pump cold water up to the surface, which is the dominant cause of the SST drops along the coast. In this study, it was determined that cold water mainly intruded from the Kuroshio subsurface into the Okinawa Trough, which is approximately 50&thinsp;km from the observation site. The magnitude of coastal SST drops depends on the area of overlap between typhoons generating strong winds and the Kuroshio. The dataset used in this study can be accessed from https://doi.org/10.1594/PANGAEA.895002.</p

Changes in bone turnover and bone loss in HIV-infected patients changing treatment to tenofovir-emtricitabine or abacavir-lamivudine

BACKGROUND: Those receiving tenofovir/emtricitabine (TDF-FTC) had greater bone loss compared with abacavir/lamivudine (ABC-3TC) in a randomized simplification trial (STEAL study). Previous studies associated increased bone turnover and bone loss with initiation of antiretroviral treatment, however it is unclear whether change in bone mineral density (BMD) was a result of specific drugs, from immune reconstitution or from suppression of HIV replication. This analysis determined predictors of BMD change in the hip and spine by dual-energy x-ray absorptiometry in virologically suppressed participants through week 96. METHODOLOGY/PRINCIPAL FINDINGS: Bone turnover markers (BTMS) tested were: formation [bone alkaline phosphatase, procollagen type 1 N-terminal propeptide (P1NP)]; resorption (C-terminal cross-linking telopeptide of type 1 collagen [CTx]); and bone cytokine-signalling (osteoprotegerin, RANK ligand). Independent predictors of BMD change were determined using forward, stepwise, linear regression. BTM changes and fracture risk (FRAX®) at week 96 were compared by t-test. Baseline characteristics (n = 301) were: 98% male, mean age 45 years, current protease-inhibitor (PI) 23%, tenofovir/abacavir-naïve 52%. Independent baseline predictors of greater hip and spine bone loss were TDF-FTC randomisation (p ≤ 0.013), lower fat mass (p-trend ≤ 0.009), lower P1NP (p = 0.015), and higher hip T score/spine BMD (p-trend ≤ 0.006). Baseline PI use was associated with greater spine bone loss (p = 0.004). TDF-FTC increased P1NP and CTx through Wk96 (p<0.01). Early changes in BTM did not predict bone loss at week 96. No significant between-group difference was found in fracture risk. CONCLUSIONS/SIGNIFICANCE: Tenofovir/emtricitabine treatment, lower bone formation and lower fat mass predicted subsequent bone loss. There was no association between TDF-FTC and fracture risk.Hila Haskelberg, Jennifer F. Hoy, Janaki Amin, Peter R. Ebeling, Sean Emery, Andrew Carr, STEAL Study Grou

Hsp70 chaperones: Cellular functions and molecular mechanism

Hsp70 proteins are central components of the cellular network of molecular chaperones and folding catalysts. They assist a large variety of protein folding processes in the cell by transient association of their substrate binding domain with short hydrophobic peptide segments within their substrate proteins. The substrate binding and release cycle is driven by the switching of Hsp70 between the low-affinity ATP bound state and the high-affinity ADP bound state. Thus, ATP binding and hydrolysis are essential in vitro and in vivo for the chaperone activity of Hsp70 proteins. This ATPase cycle is controlled by co-chaperones of the family of J-domain proteins, which target Hsp70s to their substrates, and by nucleotide exchange factors, which determine the lifetime of the Hsp70-substrate complex. Additional co-chaperones fine-tune this chaperone cycle. For specific tasks the Hsp70 cycle is coupled to the action of other chaperones, such as Hsp90 and Hsp100

Lack of efficacy of troglitazone at clinically achievable concentrations, with or without 9-cis retinoic acid or cytotoxic agents, for hepatocellular carcinoma cell lines

[[abstract]]Although the PPARgamma agonist troglitazone has been shown to induce growth inhibition of hepatocellular carcinoma (HCC) cells at high concentration, this study indicates troglitazone does not significantly inhibit the growth of HCC cells at clinically achievable concentrations (1-10 muM), and this lack of activity could not be improved by the addition of 9-cis-retinoic acid. Furthermore, no synergistic effect was found between troglitazone and cytotoxic anticancer agents

BAG3: a multifaceted protein that regulates major cell pathways

Bcl2-associated athanogene 3 (BAG3) protein is a member of BAG family of co-chaperones that interacts with the ATPase domain of the heat shock protein (Hsp) 70 through BAG domain (110–124 amino acids). BAG3 is the only member of the family to be induced by stressful stimuli, mainly through the activity of heat shock factor 1 on bag3 gene promoter. In addition to the BAG domain, BAG3 contains also a WW domain and a proline-rich (PXXP) repeat, that mediate binding to partners different from Hsp70. These multifaceted interactions underlie BAG3 ability to modulate major biological processes, that is, apoptosis, development, cytoskeleton organization and autophagy, thereby mediating cell adaptive responses to stressful stimuli. In normal cells, BAG3 is constitutively present in a very few cell types, including cardiomyocytes and skeletal muscle cells, in which the protein appears to contribute to cell resistance to mechanical stress. A growing body of evidence indicate that BAG3 is instead expressed in several tumor types. In different tumor contexts, BAG3 protein was reported to sustain cell survival, resistance to therapy, and/or motility and metastatization. In some tumor types, down-modulation of BAG3 levels was shown, as a proof-of-principle, to inhibit neoplastic cell growth in animal models. This review attempts to outline the emerging mechanisms that can underlie some of the biological activities of the protein, focusing on implications in tumor progression