Exercise intervention and health checks for middle-aged men with elevated cardiovascular risk : A randomized controlled trial

Peer reviewe

Penekanan Klorosis dengan Pseudomonas fluorescens dan Belerang untuk Peningkatan Hasil Kacang Tanah di Tanah Alkalin

Klorosis pada tanaman kacang tanah di tanah alkalin dapat menurunkan hasil hingga 60%, karena tanaman mengalami kahat Fe dan S. Penekanan klorosis tersebut di antaranya dapat dilakukan dengan aplikasi belerang dan pupuk hayati berbahan baku Pseudomonasfluorescens. Penelitian bertujuan untuk menentukan keefektifan belerang dan P. fluorescens dalam menekan klorosis dan meningkatkan hasil kacang tanah di tanah alkalin. Penelitian dilaksanakan di Rumah Kaca Balai Penelitian Tanaman Aneka Kacang dan Umbi Malangpada bulan Januari–Mei 2015, menggunakan rancangan acak kelompok dengan dua faktor perlakuan, tiga ulangan. Faktor pertama adalah 3 konsentrasi P. fluorescens (cfu/mL), terdiri dari: 1) P0=0, 2) P1=107, 3) P2=109 cfu/mL. Faktor kedua adalah 4 dosispemberian serbuk belerang (g/kg tanah) terdiri dari: 1) S0=0, 2) S1=1, 3) S2=2, 4) S3=3. Penelitian menggunakan tanah Alfisol dari Lamongan Jawa Timur dengan pH 9,5. Hasil penelitian menunjukkan tidak terdapat interaksi nyata antara pengaruh penggunaan P. fluorescens dengan belerang terhadap penekanan klorosis dan peningkatan hasil kacang tanah. P. fluorescens mampu meningkatkan kadar Fe tersedia dalam tanah hingga 35%tetapi tidak mampu menekan klorosis dan meningkatkan hasil kacang tanah. Pemberian belerang dapat meningkatkan kadar SO4 2– di tanah, menurunkan pH tanah, menekan klorosis dan meningkatkan hasil 81% pada dosis 3 g/kg tanah di tanah alkalin ber-pH 9,5. Penekanan klorosis, peningkatan hasil polong dan indeks panen kacang tanah berkorelasi positif dengan peningkatan kadar SO4 2– di tanah dan penurunan pH tanah

Effectiveness of exercise intervention and health promotion on cardiovascular risk factors in middle-aged men: a protocol of a randomized controlled trial

Peer reviewe

Response to letter on use of functional imaging by 11C-metomidate PET for primary aldosteronism subtyping

Non peer reviewe

The Finnish genetic heritage in 2022 - from diagnosis to translational research

Publisher Copyright: © 2022. Published by The Company of Biologists Ltd.Isolated populations have been valuable for the discovery of rare monogenic diseases and their causative genetic variants. Finnish disease heritage (FDH) is an example of a group of hereditary monogenic disorders caused by single major, usually autosomal-recessive, variants enriched in the population due to several past genetic drift events. Interestingly, distinct subpopulations have remained in Finland and have maintained their unique genetic repertoire. Thus, FDH diseases have persisted, facilitating vigorous research on the underlying molecular mechanisms and development of treatment options. This Review summarizes the current status of FDH, including the most recently discovered FDH disorders, and introduces a set of other recently identified diseases that share common features with the traditional FDH diseases. The Review also discusses a new era for population-based studies, which combine various forms of big data to identify novel genotype-phenotype associations behind more complex conditions, as exemplified here by the FinnGen project. In addition to the pathogenic variants with an unequivocal causative role in the disease phenotype, several risk alleles that correlate with certain phenotypic features have been identified among the Finns, further emphasizing the broad value of studying genetically isolated populations.Peer reviewe

The Finnish genetic heritage in 2022 - from diagnosis to translational research

Isolated populations have been valuable for the discovery of rare monogenic diseases and their causative genetic variants. Finnish disease heritage (FDH) is an example of a group of hereditary monogenic disorders caused by single major, usually autosomal-recessive, variants enriched in the population due to several past genetic drift events. Interestingly, distinct subpopulations have remained in Finland and have maintained their unique genetic repertoire. Thus, FDH diseases have persisted, facilitating vigorous research on the underlying molecular mechanisms and development of treatment options. This Review summarizes the current status of FDH, including the most recently discovered FDH disorders, and introduces a set of other recently identified diseases that share common features with the traditional FDH diseases. The Review also discusses a new era for population-based studies, which combine various forms of big data to identify novel genotype-phenotype associations behind more complex conditions, as exemplified here by the FinnGen project. In addition to the pathogenic variants with an unequivocal causative role in the disease phenotype, several risk alleles that correlate with certain phenotypic features have been identified among the Finns, further emphasizing the broad value of studying genetically isolated populations

Understanding the genetic complexity of puberty timing across the allele frequency spectrum

Pubertal timing varies considerably and is associated with later health outcomes. We performed multi-ancestry genetic analyses on ~800,000 women, identifying 1,080 signals for age at menarche. Collectively, these explained 11% of trait variance in an independent sample. Women at the top and bottom 1% of polygenic risk exhibited ~11 and ~14-fold higher risks of delayed and precocious puberty, respectively. We identified several genes harboring rare loss-of-function variants in ~200,000 women, including variants in ZNF483, which abolished the impact of polygenic risk. Variant-to-gene mapping approaches and mouse gonadotropin-releasing hormone neuron RNA sequencing implicated 665 genes, including an uncharacterized G-protein-coupled receptor, GPR83, which amplified the signaling of MC3R, a key nutritional sensor. Shared signals with menopause timing at genes involved in DNA damage response suggest that the ovarian reserve might signal centrally to trigger puberty. We also highlight body size-dependent and independent mechanisms that potentially link reproductive timing to later life disease