Direct regeneration protocols of five Capsicum annuum L. varieties

The bud induction obtained is a simple and efficient protocol developed for in vitro propagation of five varieties of cultivars. Seeds of Capsicum annuum L. of five varieties red, yellow, green, purple and white were decontaminated and placed in a culture bottle containing a Murashige and Skoog medium, supplemented with 6-benzylaminopurine (BAP, 5 mg/l) and naphthalene acetic acid (NAA, 1 mg/l) or indole-3- acetic acid (IAA, 0.5 mg/l) and then were incubated in the dark for 10 - 12 days for germination. Leaf explants excised from 4 weeks -old aseptic seedlings were cultured on a MS medium supplemented with hormones BAP, kinetin (Kin), the combination of BAP + Kin, BAP with NAA (0.1 or 0.01 mg/l) and BAP with IAA (0.5 mg/l). The 2.0 mg/l BAP with 0.1 mg/l NAA media was observed to be more suitable for callus formation. The highest number of regenerated shoot buds was obtained when shoot explants were cultured on a MS medium supplemented with 2.0 mg/l BAP and 0.5 mg/l IAA. The mean number of shoot per explants was obtained in red (6.3), yellow (3.6), purple (3.3), and white (3.0) variety of C. annuum whereas 3.0 mg/l BAP and 0.5 mg/l IAA were observed to be more suitable for green (6.6) variety of C. annuum. Plantlets were successfully acclimatized in greenhouse.Keywords: Capsicum, auxin, cytokinin, micropropagation, organogenesis, sweet pepperAfrican Journal of Biotechnology, Vol. 13(2), pp. 307-312, 8 January, 201

Mapping the human genetic architecture of COVID-19

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease

The Magpie Trial: A randomised trial comparing magnesium sulphate with placebo for pre-eclampsia. Outcome for children at 18 months

Objective: To assess the long-term effects of in utero exposure to magnesium sulphate for children whose mothers had pre-eclampsia. Design: Assessment at 18 months of age for children whose mothers were recruited to the Magpie Trial (recruitment 1998-2001 ISRCTN 86938761), which compared magnesium sulphate with placebo. Setting: Follow-up of children born at 125 centres in 19 countries across five continents. Population: A total of 6922 children were born to women randomised before delivery at follow-up centres. Of these, 2271 were not included for logistic reasons and 168 were excluded (101 at a centre where <20% were contacted, 40 whose death or disability was due to a problem at conception or embryogenesis and 27 whose parent/s opted out). Therefore, 4483 children were included in follow-up, of whom 3283 (73%) were contacted. Methods: Assessment by questionnaire, with interview and neurodevelopmental testing of selected children. Main outcome measures: Death or neurosensory disability at age of 18 months. Results: Of those allocated magnesium sulphate, 245/1635 (15.0%) were dead or had neurosensory disability at 18 months compared with 233/1648 (14.1%) allocated placebo (relative risk [RR] 1.06, 95% CI 0.90-1.25), and of survivors, 19/1409 (1.3%) had neurosensory disability at 18 months compared with 27/1442 (1.9%) (RR 0.72, 95% CI 0.40-1.29). There were no substantial differences in causes of death or in the risk of individual impairments or disabilities. Conclusions: The lower risk of eclampsia following prophylaxis with magnesium sulphate was not associated with a clear difference in the risk of death or disability for children at 18 months. © RCOG 2006 BJOG An International Journal of Obstetrics and Gynaecology.Articl

The Magpie Trial: A randomised trial comparing magnesium sulphate with placebo for pre-eclampsia. Outcome for women at 2 years

Objective: The aim of this study was to assess long-term effects for women following the use of magnesium sulphate for pre-eclampsia. Design: Assessment at 2-3 years after delivery for women recruited to the Magpie Trial (recruitment in 1998-2001, ISRCTN 86938761), which compared magnesium sulphate with placebo for pre-eclampsia. Setting: Follow up after discharge from hospital at 125 centres in 19 countries across five continents. Population: A total of 7927 women were randomised at the follow-up centres. Of these women, 2544 were not included for logistic reasons and 601 excluded (109 at a centre where <20% of women were contacted, 466 discharged without a surviving child and 26 opted out). Therefore, 4782 women were selected for follow-up, of whom 3375 (71%) were traced. Methods: Questionnaire assessment was administered largely by post or in a dedicated clinic. Interview assessment of selected women was performed. Main outcome measures: Death or serious morbidity potentially related to pre-eclampsia at follow up, other morbidity and use of health service resources. Results: Median time from delivery to follow up was 26 months (interquartile range 19-36). Fifty-eight of 1650 (3.5%) women allocated magnesium sulphate died or had serious morbidity potentially related to pre-eclampsia compared with 72 of 1725 (4.2%) women allocated placebo (relative risk 0.84, 95% CI 0.60-1.18). Conclusions: The reduction in the risk of eclampsia following prophylaxis with magnesium sulphate was not associated with an excess of death or disability for the women after 2 years. © RCOG 2006 BJOG An International Journal of Obstetrics and Gynaecology.Articl

Thrombin-receptor antagonist vorapaxar in acute coronary syndromes

BACKGROUND Vorapaxar is a new oral protease-activated–receptor 1 (PAR-1) antagonist that inhibits thrombin-induced platelet activation. METHODS In this multinational, double-blind, randomized trial, we compared vorapaxar with placebo in 12,944 patients who had acute coronary syndromes without ST-segment elevation. The primary end point was a composite of death from cardiovascular causes, myocardial infarction, stroke, recurrent ischemia with rehospitalization, or urgent coronary revascularization. RESULTS Follow-up in the trial was terminated early after a safety review. After a median follow-up of 502 days (interquartile range, 349 to 667), the primary end point occurred in 1031 of 6473 patients receiving vorapaxar versus 1102 of 6471 patients receiving placebo (Kaplan–Meier 2-year rate, 18.5% vs. 19.9%; hazard ratio, 0.92; 95% confidence interval [CI], 0.85 to 1.01; P = 0.07). A composite of death from cardiovascular causes, myocardial infarction, or stroke occurred in 822 patients in the vorapaxar group versus 910 in the placebo group (14.7% and 16.4%, respectively; hazard ratio, 0.89; 95% CI, 0.81 to 0.98; P = 0.02). Rates of moderate and severe bleeding were 7.2% in the vorapaxar group and 5.2% in the placebo group (hazard ratio, 1.35; 95% CI, 1.16 to 1.58; P<0.001). Intracranial hemorrhage rates were 1.1% and 0.2%, respectively (hazard ratio, 3.39; 95% CI, 1.78 to 6.45; P<0.001). Rates of nonhemorrhagic adverse events were similar in the two groups. CONCLUSIONS In patients with acute coronary syndromes, the addition of vorapaxar to standard therapy did not significantly reduce the primary composite end point but significantly increased the risk of major bleeding, including intracranial hemorrhage

Mapping the human genetic architecture of COVID-19

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3,4,5,6,7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease