Keragaman Genetik Dan Pendugaan Jumlah Gen Ketahanan Kacang Panjang (Vigna Sinensis L.) Terhadap Penyakit Kuning

Penyakit kuning pada kacang panjang berdampak pada penurunan produksi. Gejala serangan diawali dari gejala daun keriting serta mengakibatkan polong berwarna kuning. Penelitian ini bertujuan mengetahui nilai heritabilitas dan ragam genetik serta menduga jumlah gen pengendali ketahanan kacang panjang terhadap penyakit kuning. Penelitian dilaksanakan di Kabupaten Kediri pada bulan April sampai Juli 2013. Bahan penelitian adalah populasi UB 715 A (P1), Hitam Putih (P2), populasi F1 dan populasi F2. Berdasarkan hasil penelitian, populasi UB 715 A (P1 ) menunjukkan respon tahan terhadap penyakit kuning, populasi Hitam Putih (P2) menunjukkan respon rentan, dan populasi F1 dan F2 menunjukkan respon sedang. Karakter jumlah polong dan jumlah biji per tanaman memiliki keragaman yang sempit sedangkan karakter panjang polong, bobot segar polong, umur berbunga, dan umur panen memiliki keragaman yang luas. Karakter panjang polong dan jumlah biji per polong memiliki nilai heritabilitas rendah, sedangkan karakter jumlah polong, bobot segar polong, umur berbunga, dan umur panen memiliki nilai heritabilitas tinggi. Rasio sifat ketahanan terhadap penyakit kuning pada populasi F2 adalah 9 tahan : 3 sedang : 4 rentan yang berarti ketahanan terhadap penyakit kuning dikendalikan oleh dua gen dengan aksi gen epistasis resesif

Table_1_Sex differences in atrial remodeling and its relationship with myocardial fibrosis in hypertrophic obstructive cardiomyopathy.DOCX

BackgroundThis study aimed to explore the effect of sex on left atrial (LA) remodeling and its relationship with myocardial fibrosis in patients with hypertrophic obstructive cardiomyopathy (HOCM).Methods and resultsA total of 85 patients with HOCM were enrolled. Myocardial fibrosis was quantified by the collagen volume fraction (CVF) in myocardial samples. The early atrial peak of emptying rate (PER-E) was assessed by LA volume/time (V/t) curves derived from cardiac magnetic resonance (CMR) imaging analysis. The PER-E index was PER-E normalized by left ventricular (LV) filling volume. Patients with HOCM showed a lower PER-E index than healthy controls (P = 0.027). Compared with men, the PER-E (P 0.05). The CVF was correlated with the PER-E and PER-E indexes in both sexes (all P-values were ConclusionPatients with HOCM presented LA reverse remodeling. Impaired LA function was more common in female patients with HOCM due to their susceptibility to myocardial fibrosis.</p

Comparison of results at 1 week and 4 weeks.

<p>Results of scar volume changing between 1 week and 4 weeks on 2D (A) and 3D (B) images, respectively, which shows an reduction trend in infarct volume from week 1 to week 4.</p

Comparison of short-axis MR images with TTC staining.

<p>Example of 3D, 2D images and TTC staining obtained from the same pig 4 weeks post MI. It showed good agreement in depiction of the extent of myocardial scar, and the borders of hyperenhanced regions were much clearer on 3D images (arrows).</p

Relationship between scar volume on 3D and 2D images.

<p>The relation between 3D and 2D images for scar volume was evaluated for 6 animals at both time points. (A) Linear regression plot shows a good correlation between scar volume on 3D PSIR images and 2D PSIR images (r=0.859, <i>P</i><0.001). (B) Bland-Altman analysis showed there was no systematic under- or overestimation of scar volume with 3D PSIR images, and limits of agreement were sufficiently small compared with average scar volume.</p

CMR and gene sequencing.

<p>CMR images from a 25-year-old HCM patient with SRVH. RV outflow tract long-axis views during end-diastole (A) and end-systole (B) demonstrating remarkable thickening of the RV anterior wall and apical region with obstruction. A Holter recording of a non-sustained ventricular tachycardia attack. RV short-axis view (D) demonstrating extreme thickening of the RV free wall and regional transmural LGE of the RV anterior and free walls (red arrow). In the left panels, the red arrows indicate the double-peak at the site of the identified mutations. LA: left atrium; LV: left ventricle; LVOT: left ventricular outflow tract; PA: pulmonary artery; RV: right ventricle; RVAW: RV anterior wall.</p

Histological findings.

<p>(A) Histological section of the RV free wall of an HCM patient with SRVH showing cardiomyocyte enlargement and disarray (hematoxylin-eosin staining, 200×) and (B) extensive interstitial fibrosis (Masson’s trichrome staining, 200×). (C) Histological section of the RV free wall of a patient with a double-chambered right ventricle demonstrating cardiomyocyte hypertrophy without disarray (D) and without interstitial fibrosis (E).</p

The baseline clinical characteristics of HCM patients with SRVH and ApHCM patients.

<p>The baseline clinical characteristics of HCM patients with SRVH and ApHCM patients.</p

Clinical outcomes of HCM patients with SRVH and ApHCM patients during the follow-up period.

<p>Clinical outcomes of HCM patients with SRVH and ApHCM patients during the follow-up period.</p

A summary of the mutations affecting HCM patients with SRVH.

<p>A summary of the mutations affecting HCM patients with SRVH.</p