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

Mid-term outcomes of biventricular obstruction and left ventricular outflow tract obstruction after surgery correction in child and adolescent patients with hypertrophic cardiomyopathy - Fig 2

<p>Fig 2a. Preoperative two-dimensional transthoracic echocardiography (tte) parasternal long axis (PLAX) views in a 16-year-old hypertrophic cardiomyopathy patient with BVOTO. (A) PLAX view demonstrating the massive septal hypertrophy and the thickening of the ventricular septum bulging into the LVOT and RVOT resulting in biventricular obstructions (the colour flows). (B) Colour Doppler flow imaging of PLAX view during systole showing high velocity jet flow simultaneously in both LVOT and RVOT. Postoperative PLAX views showing a substantial decrease in the ventricular septum thickness and an increase in the RV and LV cavity sizes during diastole (C) and the LV and RV colour flows showing laminar without evidence of significant residual obstructions during systole (D).RV: right ventricle; RVOT: right ventricular outflow tract; IVS: interventricular septum; LV: left ventricle; LA: left atrium; LVOT: left ventricular outflow tract.AO: aorta. Fig 2b. Preoperational cardiovascular magnetic resonance (CMR) image 3-chamber views during diastole (A) and systole (B) showing remarkable myocardial hypertrophy at the base ventricular level with LVOT and RVOT obstruction. The postoperative CMR images (C, D) showing thinner IVS, wider LVOT and RVOT diameter and larger LV and RV cavity without the projection of septum into RVOT or LVOT after biventricular resection. LA: left atrial; LV: left ventricular.</p

Baseline characteristics.

<p>Baseline characteristics.</p

Middle-Term results in the three groups.

<p>Middle-Term results in the three groups.</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

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

Transthoracic echocardiography and gene sequencing.

<p>An apical 4-chamber view of an 18-year-old patient with HCM demonstrating pronounced hypertrophy of the RV free wall during end-diastole (A) and RV cavity obliteration in the mid-ventricular region, as well as in the apical cavity (B). (C) Modified parasternal short-axis views with color Doppler flow mapping demonstrating striking hypertrophy of the RV anterior wall and narrowing of the RV outflow tract. (D) Color Doppler mapping demonstrating turbulent flow from the RV outflow tract to the PA (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; RA: right atrium; RV: right ventricle.</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

A summary of the mutations affecting HCM patients with SRVH.

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