Coronavirus variant COVID-19 pandemic: a report to seafarers.

We report the current situation regarding the COVID-19 pandemic with particular regard to seafarers and with the indications drawn up by the Centro Internazionale Radio Medico (C.I.R.M.) in this regard.

Tumor necrosis factor-related apoptosis-inducing ligand cooperates with anticancer drugs to overcome chemoresistance in antiapoptotic Bcl-2 family members expressing jurkat cells.

PURPOSE: Overexpression of antiapoptotic Bcl-2 family members has recently been related to resistance to chemo/radiotherapy in several human malignancies, particularly lymphomas. Hence, innovative approaches bypassing this resistance mechanism are required in the therapeutic approach. This study evaluated whether chemoresistance associated with Bcl-2 and Bcl-x(L) overexpression would be overcome by activating the death receptor pathway by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in the Jurkat cell model EXPERIMENTAL DESIGN: We made use of genetically modified Jurkat cells to evaluate the effect of Bcl-2 or Bcl-x(L) overexpression on the cytotoxic effect produced by the anticancer drugs doxorubicin, etoposide, and oxaliplatin and TRAIL. Caspase activation was detected by cleavage of caspase-8 and -3. The mitochondrial transmambrane potential was assessed by staining with DiOC(6) and flow cytometry. Caspase activity was blocked by the broad-spectrum caspase inhibitor zVAD-fmk. RESULTS: Bcl-2 and Bcl-x(L) overexpression but not lack of caspase-8 protects the Jurkat cells from the anticancer drug-induced cytolysis. However, Bcl-2/Bcl-x(L) Jurkat cells retained some susceptibility to TRAIL-induced cytolysis. A highly synergistic cytotoxic effect of the combination of TRAIL with any of the antiblastic used in this study was detected in the chemoresistant cells. This effect was associated with mitochondrial disassemblage and dependent on caspase activation CONCLUSIONS: The combination of TRAIL with conventional anticancer drugs may prove to be useful in the treatment of antiapoptotic Bcl-2 family proteins-expressing malignancies.

Impairment in cardiac autonomic regulation preceding arterial hypertension in humans: insights from spectral analysis of beat-by-beat cardiovascular variability.

BACKGROUND: Subjects in the upper-normal range of arterial pressure have an excess cardiovascular risk, which suggests that other factors, such as impaired autonomic regulation, might be implicated. This study was designed to assess whether noninvasive markers of cardiac and vascular autonomic regulation might already be altered in subjects with high-normal arterial pressure levels. METHODS AND RESULTS: We performed an observational study on a population comprising 300 subjects of both sexes with arterial pressure ranging from 90/60 to 210/120 mm Hg, who were divided into 3 groups (each n=100) with average systolic pressures of 103, 133, and 163 mm Hg. Autonomic regulation was inferred from spectral analysis of RR interval and systolic arterial pressure variability, considering rest and stand-induced changes, to account for sympathetic excitatory components. Significant alterations in markers of sinoatrial regulation (increased low-frequency normalized units, reduced high-frequency normalized units, and alpha-index) were already apparent in subjects in the second tertile, ie, those with arterial pressure within normal limits. Markers of vascular regulation instead showed significant alterations in the third (hypertensive) tertile. In response to standing, changes in markers of sinoatrial modulations were gradually reduced, whereas those of vascular regulation were increased. A tight link between progression of arterial pressure and the continuum of changes in autonomic markers as shown by simple correlation analysis appeared strongly affected by age and was spread across many spectral analysis-derived variables. Hypertensive autonomic dysregulation was particularly apparent in the youngest group. CONCLUSIONS: RR-variability parameters might prove useful to assess, with longitudinal studies, the mechanistic role of autonomic impairment in the increased risk of prehypertensive conditions.

Neurological research in Europe, as assessed with a four-year overview of neurological science international journals.

This paper analyses all the peer-reviewed articles published by European authors in 161 neurological journals screened by ISI in accordance with Current Contents/Life Science and Current Contents/Clinical Medicine in the period 1995-1998. Our aim was to report the amount and quality of neurological research in the different countries of the European Union (EU), the USA and the world. The number of papers, the impact factors (IF), the population of the source country and gross domestic product (GDP), were downloaded. Data show that in the EU there is a progressive increase in the number of published papers from 1995 to 1998 and that large countries such as Germany, the United Kingdom, France and Italy rank at the top four places for absolute number of papers. The gap in the number of papers between the USA and the EU significantly diminished in the examined period, from a difference of 14 % to 6 %. However, when the IF is considered, the USA performed better than EU, although excellent results have been obtained by the United Kingdom, Ireland, Netherlands and Sweden. When the number and quality of papers are plotted against the number of inhabitants or GDP, Sweden, the Netherlands and Finland are the leading countries in Europe. The present study demonstrates that neurological research in the EU is active and productive, is steadily increasing and is now a relevant part of all biomedical world research.

Once-Daily Bedtime Dose of Roxatidine and Ranitidine in Acute Duodenal Ulcer: A Combined Assessment of Acid Inhibitory Activity and Healing Rate.

This study was carried out in order to compare the antisecretory effect of a single bedtime dose of roxatidine 150 mg and ranitidine 300 mg and to assess the relationship between the degree and the duration of acid suppression and the healing rates obtained in duodenal ulcer patients treated with the above regimens. Sixty-three patients with endoscopically proven ulcer underwent 24-h gastric pH-metry on day 0, day 1, and day 28 of treatment with both roxatidine and ranitidine. Ulcer healing was checked endoscopically after 4 weeks of therapy. RESULTS: Eight patients did not complete the study, leaving 55 patients eligible for final analysis, 28 in the roxatidine group and 27 in the ranitidine group. Duodenal ulcers were healed in 24--28 (85%) patients of the former and in 22--27 (81%) patients of the latter group (p minus sign NS). Gastric pH was significantly higher (p < 0.001) than basal values on days 1 and 28 with both H2-antagonists. The 24-h pH levels did not differ between day 1 and day 28 with both roxatidine and ranitidine. There was also do difference between the two active treatments. The pattern of gastric acidity significantly differed (p < 0.01) between responder (n = 46) and nonresponder (n = 9) patients to both H2-blockers, and this difference was mainly sustained by nocturnal pH. CONCLUSIONS: A bedtime close of roxatidine 150 mg and ranitidine 300 mg was able to heal more than 80% of duodenal ulcers within 4 weeks of treatment. The lack of tolerance to H2-blockers in duodenal ulcer patients contributes to this good result. The antisecretory effect of H2-antagonists is reduced in nonresponder patients with respect to responder patients and this is mainly due to an impaired control of nocturnal acidity.