In Vitro Culture of Seaweed Kappaphycus alvarezii under Different Formulation of Growth Stimulating Substances and Culture Media

This study aims at obtaining a sustainably superior seed stock following the characteristics of the parent plant, determining the best formulation of the growth stimulating substance. In general, cytokinin and auxin combination was used, but this study also added with the combination of cytokinin and giberelin and cytokinin and abscisic acid (AA).Parameters measured were bud length, number of buds, and survival rate. Bacterial Vibrio sp test was also done as a cause of the explant mortality. Results showed that the longest bud was recorded in treatment C (S+A 1:2.5) cultured in a jar, 1.343 mm long, 38% of survival, while the highest number of buds was found in treatment B (S+A 1 : 2) 8.86. The shortest bud was recorded in treatment J (S + AA 1:2.5) cultured in a jar, 0.093 mm long, 2.64 buds, 10% of survival, while the explant cultured in the bottle had a length of 0.051 mm long, 1.50 buds, 4% of survival. As conclusion, the best growth stimulating substance was found in the treatment C for the bud length and the survival rate, while the best number of bud was recorded in the treatment B. The best culture tank was topless bottle (aerated). In vitro culture could also use S + G formulation. The explant mortality was caused by Vibrio charchariae. The use of S + AA formulation had lower growth than that of control treatment.Keywords :in vitro, growth stimulating substance, culture media, Kappaphycus alvarezii, Vibrio charchariae ABSTRAKPenelitian ini bertujuan untuk memperoleh benih unggul secara berkelanjutan yang mengikuti karakteristik dari tanaman induk, menentukan formulasi terbaik dari substansi pertumbuhan merangsang. Secara umum, kombinasi sitokinin dan auksin digunakan, tetapi penelitian ini juga menambahkankombinasi sitokinin, giberelin, sitokinin dan asam absisat (AA). Parameter yang diukur adalah panjang tunas, jumlah tunas, dan tingkat kelangsungan hidup. Bakteri Vibrio Uji sp juga dilakukan sebagai penyebab kematian eksplan . Hasil penelitian menunjukkan bahwa tunas terpanjang terdapat pada perlakuan C (S + A 1: 2,5)  kultur dalam toples, 1,343 mm, 38% hidup, sementara jumlah tertinggi tunas ditemukan pada perlakuan B (S + A 1: 2) 8.86 . Jumlah tunas paling sedikit terdapat pada perlakuan J (S + AA 1: 2,5) yang dikultur dalam toples, 0,093 mm, 2,64 tunas, 10% hidup, sedangkan eksplan yang dikultur dalam botol memiliki panjang 0.051 mm, 1. 50 tunas , 4% bertahan hidup. Sebagai kesimpulan, pertumbuhan terbaik merangsang zat ditemukan dalam perlakuan C untuk panjang tunas dan tingkat kelangsungan hidup, sementara jumlah tunas terbanyak ditemukan pada perlakuan B. Penggunaan wadah budaya terbaik adalah topless yang diaerasi. Kultur in vitro juga dapat menggunakan formulasi S + G. Kematian eksplan disebabkan oleh Vibrio charchariae . Penggunaan formulasi S + AA memiliki pertumbuhan yang lebih rendah dari pada pengobatan kontrol .Kata kunci : in vitro, zat perangsang tumbuh, media kultur, Kappaphycus alvarezii, Vibrio charcharia

Leptogenesis in Neutrino Textures with Two Zeros

The leptogenesis is studied in the neutrino textures with two zeros, which reduce the number of independent phases of the CP violation. The phenomenological favored neutrino textures with two zeros are decomposed into the Dirac neutrino mass matrix and the right-handed Majorana one in the see-saw mechanism. Putting the condition to suppress the $\mu \to e\gamma$ decay enough, the texture zeros of the Dirac neutrino mass matrix are fixed in the framework of the MSSM with right-handed neutrinos. These textures have only one CP violatig phase. The magnitude of each entry of the Dirac mass matrix is determined in order to explain the baryon asymmetry of the universe by solving the Boltzman equations. The relation between the leptogenesis and the low energy CP violation is presented in these textures.Comment: Latex file with 20 pages, 6 eps figure

Pharmacogenetics of Bleeding and Thromboembolic Events in Direct Oral Anticoagulant Users

Publisher Copyright: © 2021 The Authors. Clinical Pharmacology & Therapeutics published by Wiley Periodicals LLC on behalf of American Society for Clinical Pharmacology and TherapeuticsThis study aimed to analyze associations between genetic variants and the occurrence of clinical outcomes in dabigatran, apixaban, and rivaroxaban users. This was a retrospective real-world study linking genotype data of three Finnish biobanks with national register data on drug dispensations and healthcare encounters. We investigated several single-nucleotide variants (SNVs) in the ABCG2, ABCB1, CES1, and CYP3A5 genes potentially associated with bleeding or thromboembolic events in direct oral anticoagulant (DOAC) users based on earlier research. We used Cox regression models to compare the incidence of clinical outcomes between carriers and noncarriers of the SNVs or haplotypes. In total, 1,806 patients on apixaban, dabigatran, or rivaroxaban were studied. The ABCB1 c.3435C>T (p.Ile1145=, rs1045642) SNV (hazard ratio (HR) 0.42, 95% confidence interval (CI), 0.18-0.98, P = 0.044) and 1236T-2677T-3435T (rs1128503-rs2032582-rs1045642) haplotype (HR 0.44, 95% CI, 0.20-0.95, P = 0.036) were associated with a reduced risk for thromboembolic outcomes, and the 1236C-2677G-3435C (HR 2.55, 95% CI, 1.03-6.36, P = 0.044) and 1236T-2677G-3435C (HR 5.88, 95% CI, 2.35-14.72, P A (rs4148738) SNV associated with a lower risk for bleeding events (HR 0.37, 95% CI, 0.16-0.89, P = 0.025) in apixaban users. ABCB1 variants are potential factors affecting thromboembolic events in rivaroxaban users and bleeding events in apixaban users. Studies with larger numbers of patients are warranted for comprehensive assessment of the pharmacogenetic associations of DOACs and their relevance for clinical practice.Peer reviewe

Age at symptom onset and death and disease duration in genetic frontotemporal dementia : an international retrospective cohort study

Background: Frontotemporal dementia is a heterogenous neurodegenerative disorder, with about a third of cases being genetic. Most of this genetic component is accounted for by mutations in GRN, MAPT, and C9orf72. In this study, we aimed to complement previous phenotypic studies by doing an international study of age at symptom onset, age at death, and disease duration in individuals with mutations in GRN, MAPT, and C9orf72. Methods: In this international, retrospective cohort study, we collected data on age at symptom onset, age at death, and disease duration for patients with pathogenic mutations in the GRN and MAPT genes and pathological expansions in the C9orf72 gene through the Frontotemporal Dementia Prevention Initiative and from published papers. We used mixed effects models to explore differences in age at onset, age at death, and disease duration between genetic groups and individual mutations. We also assessed correlations between the age at onset and at death of each individual and the age at onset and at death of their parents and the mean age at onset and at death of their family members. Lastly, we used mixed effects models to investigate the extent to which variability in age at onset and at death could be accounted for by family membership and the specific mutation carried. Findings: Data were available from 3403 individuals from 1492 families: 1433 with C9orf72 expansions (755 families), 1179 with GRN mutations (483 families, 130 different mutations), and 791 with MAPT mutations (254 families, 67 different mutations). Mean age at symptom onset and at death was 49\ub75 years (SD 10\ub70; onset) and 58\ub75 years (11\ub73; death) in the MAPT group, 58\ub72 years (9\ub78; onset) and 65\ub73 years (10\ub79; death) in the C9orf72 group, and 61\ub73 years (8\ub78; onset) and 68\ub78 years (9\ub77; death) in the GRN group. Mean disease duration was 6\ub74 years (SD 4\ub79) in the C9orf72 group, 7\ub71 years (3\ub79) in the GRN group, and 9\ub73 years (6\ub74) in the MAPT group. Individual age at onset and at death was significantly correlated with both parental age at onset and at death and with mean family age at onset and at death in all three groups, with a stronger correlation observed in the MAPT group (r=0\ub745 between individual and parental age at onset, r=0\ub763 between individual and mean family age at onset, r=0\ub758 between individual and parental age at death, and r=0\ub769 between individual and mean family age at death) than in either the C9orf72 group (r=0\ub732 individual and parental age at onset, r=0\ub736 individual and mean family age at onset, r=0\ub738 individual and parental age at death, and r=0\ub740 individual and mean family age at death) or the GRN group (r=0\ub722 individual and parental age at onset, r=0\ub718 individual and mean family age at onset, r=0\ub722 individual and parental age at death, and r=0\ub732 individual and mean family age at death). Modelling showed that the variability in age at onset and at death in the MAPT group was explained partly by the specific mutation (48%, 95% CI 35\u201362, for age at onset; 61%, 47\u201373, for age at death), and even more by family membership (66%, 56\u201375, for age at onset; 74%, 65\u201382, for age at death). In the GRN group, only 2% (0\u201310) of the variability of age at onset and 9% (3\u201321) of that of age of death was explained by the specific mutation, whereas 14% (9\u201322) of the variability of age at onset and 20% (12\u201330) of that of age at death was explained by family membership. In the C9orf72 group, family membership explained 17% (11\u201326) of the variability of age at onset and 19% (12\u201329) of that of age at death. Interpretation: Our study showed that age at symptom onset and at death of people with genetic frontotemporal dementia is influenced by genetic group and, particularly for MAPT mutations, by the specific mutation carried and by family membership. Although estimation of age at onset will be an important factor in future pre-symptomatic therapeutic trials for all three genetic groups, our study suggests that data from other members of the family will be particularly helpful only for individuals with MAPT mutations. Further work in identifying both genetic and environmental factors that modify phenotype in all groups will be important to improve such estimates. Funding: UK Medical Research Council, National Institute for Health Research, and Alzheimer's Society

AHA 2012: The 85th Scientific Sessions of American Heart Association

Therapeutic Research342131-145THRE