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This survey may be a potentially reliable and valid instrument to assess risk and protection in different cultures and populations. However, there is still a gap in the instrument's cross-cultural adaptation processes.

This survey may be a potentially reliable and valid instrument to assess risk and protection in different cultures and populations. However, there is still a gap in the instrument's cross-cultural adaptation processes.

We use massive transfusion in various clinical conditions and it is associated with high mortality. Although some massive transfusion protocols improve patient outcomes, the clinical circumstances requiring it are not well defined.

MATRA-A is a multicenter retrospective study. Six University and Training Research Hospitals in Ankara participated in the study. We collected clinical data on patients (>18years) who received massive transfusions (≥10 units/24h) from 2017 through 2019.

Overall, 167 (0·27% of transfused patients) received a massive transfusion of 2586 units of red blood cells (1·5% of total RBCs transfused). The median interquartile range values for RBCs, fresh frozen plasma (FFP) and platelets were 13 (11-176), 16 (9-33) and 4 (0-11), respectively. Surgical patients received 90% of massive transfusions. The most common clinical indications for massive transfusion were cardiovascular diseases (42·6%), trauma (20·3%) and malignancies (11%). FFP RBC Platelets ratio was 1·910·5. The overall ato define the areas that need improvement on a national scale.

Transfusion reactions (TRs) may cause or contribute to death. Cardiopulmonary TRs are distressing, and collectively account for most transfusion fatalities, though the degree to which they alter survival more broadly is unclear. Deaths (and their timing) after TRs may provide further insights.

Adult (tri-hospital network) haemovigilance data (2013-2016) recorded referrals with conclusions ranging from unrelated to transfusion (UTR) to entities such as septic TRs, serologic/haemolytic reactions, transfusion-associated circulatory overload (TACO), transfusion-associated dyspnoea (TAD), transfusion-related acute lung injury (TRALI), allergic transfusion reaction (ATR), and others. For (in- or out-patient) visits involving suspected TRs (VISTRs), all-cause mortalities (% [95% confidence interval]) and associated time-to-death (TTD) (median days, [interquartile range]) were compared. Diagnoses were defined inclusively (possible-to-definite) or strictly (probable-to-definite).

Of 1144 events, rank order VISTRrked higher VISTR mortality with shorter TTDs. Short ( less then 1 week) TTDs in TAD, BaCon or TRALI imply either contributing roles in death, treatment refractoriness and/or applicable TR susceptibilities in the dying.

Iron overload in thalassaemia is a crucial prognostic factor and a major cause of death due to heart failure or arrhythmia. Therefore, previous research has recommended amlodipine as an auxiliary treatment to current chelating agents for reducing iron overload in thalassaemia patients.

A systematic review and meta-analysis of the results of three randomized clinical trials evaluating the use of amlodipine in thalassaemia patients through 12 databases were carried out.

Our final cohort included 130 patients. Insignificant difference in decreasing liver iron concentrations was found between amlodipine and control groups weighted mean difference=-0·2, [95% confidence interval=(-0·55-0·15), P=0·26]. As regards serum ferritin, our analysis also showed no significant difference in serum ferritin between amlodipine and control groups weighted mean difference [95% confidence interval=-0·16 (-0·51-0·19), P=0·36]. Similarly, there was insignificant difference in cardiac T2* between amlodipine and control groups weighted mean difference [95% confidence interval=0·34 (-0·01-0·69), P=0·06].

Despite the growing evidence supporting the role of amlodipine in reducing iron overload in thalassaemia patients, our meta-analysis did not find that evidence collectively significant. The results of our simulation suggest that when more data are available, a meta-analysis with more randomized clinical trials could provide more conclusive insights.

Despite the growing evidence supporting the role of amlodipine in reducing iron overload in thalassaemia patients, our meta-analysis did not find that evidence collectively significant. The results of our simulation suggest that when more data are available, a meta-analysis with more randomized clinical trials could provide more conclusive insights.To explore the largely unknown etiology of small intestine cancer, we examined metabolic factors and risk of small intestine cancer overall and by subtypes. Among 404 220 women and 403 265 men in six European cohorts, we applied Cox regression with adjustment for smoking and body mass index (BMI), to calculate sex-specific hazard ratios (HRs) of small intestine cancer by levels of BMI, mean arterial pressure (MAP) and plasma total cholesterol, triglycerides and glucose. We also calculated HRs for these factors combined (metabolic score; MetS) and used Wald test statistics to investigate pairwise interactions between metabolic factors on risk. We also performed analyses separately per subtype (neuroendocrine tumors [NETs] and adenocarcinomas). During a median follow-up of 16.9 years, 144 women and 195 men were diagnosed with small intestine cancer, including 184 NETs and 99 adenocarcinomas. OICR9429 Among men, no main associations or interactions between metabolic factors were observed in relation to the risk of small intestine cancer. Among women, triglycerides were positively and linearly associated with risk (HR per standard deviation [SD] 1.23, 95% confidence interval [CI] 1.04-1.46), and a positive association was also observed for the MetS (HR per SD 1.25, 95% CI 1.02-1.52). Positive interactions were observed among women between triglycerides and cholesterol (P = .0005), and between MAP and glucose (P = .009), on risk. Glucose was positively associated with adenocarcinomas among women. This large, prospective study suggests that elevated triglycerides, and metabolic factors in interaction, confer an increased risk of small intestine cancer among women, but not among men.