Skinning Injury Responses in Sweetpotato

In sweetpotatoes (Ipomoea batatas L. Lamb), the loss of skin from the surface of the storage roots is known as skinning injury. It is responsible for significant postharvest loss resulting from moisture increase and weight reduction, wrinkling, and susceptibility to pathogen attack. Reduced root weight by water loss is associated with a higher rate of rot predominantly occurred in the developing and underdeveloped countries which can count of 8-20% of postharvest loss. Plants have different adaptation to protect themselves against skinning injury. Lignification, suberization, and increased sugar at the wound site have been shown to be correlated with wound healing. Changing in gene expressions have been associated with skinning injury. Genes associated in the biosynthesis of lignin and suberin, protein fate, cell-wall modification, transcription and protein synthesis, and stress responses and defense have been associated with skinning injury responses in plants. Understanding the skinning injury responses and how to regulate them can be used to produce a more desirable plant resistant to skinning injury. This paper especially reviews and discusses skinning injury responses in sweetpotato, a root crop which product may severely be affected by skinning injury. Keywords: gene expression, Ipomoea batatas, lignification, postharvest loss, wounding   ABSTRAK Pada ubi jalar (Ipomoea batatas L. Lamb), cedera kulit adalah hilangnya kulit dari permukaan umbi. Cedera kulit ini bertanggung jawab atas kerugian pascapanen yang signifikan akibat peningkatan laju kelembaban dan penurunan berat umbi, pengerutan, dan kerentanan terhadap serangan patogen. Berat umbi yang berkurang karena kehilangan air dikaitkan dengan tingkat pembusukan yang lebih tinggi, terutama terjadi di negara-negara berkembang dan yang kurang berkembang dengan kehilangan hasil panen umbi 8-20%. Tanaman memiliki adaptasi yang berbeda untuk melindungi diri dari cedera kulit. Lignifikasi, suberisasi, dan peningkatan gula di lokasi pelukaan telah terbukti berkorelasi dengan penyembuhan luka. Perubahan ekspresi gen telah dikaitkan dengan cedera kulit. Gen-gen yang terlibat dalam jalur biosintesis lignin dan suberin, protein tujuan akhir, modifikasi dinding sel, transkripsi dan sintesis protein, serta respons stres dan pertahanan telah dikaitkan dengan respons cedera kulit pada tanaman. Memahami respons cedera kulit dan bagimana cara mengaturnya dapat digunakan untuk menghasilkan tanaman yang diinginkan yang tahan terhadap cedera kulit umbi. Paper ini secara khusus mengulas dan membahas respon cedera kulit pada ubi jalar, suatu tanaman umbian yang hasilnya sangat terpengaruh oleh cedera kulit. Kata kunci: ekspresi gen, Ipomoea batatas, lignifikasi, kehilangan pascapanen, pelukaa

Impaired Sleep Quality in COPD Is Associated With Exacerbations The CanCOLD Cohort Study

BackgroundCOPD increases susceptibility to sleep disturbances, which may in turn predispose to increased respiratory symptoms. The objective of this study was to evaluate, in a population-based sample, the relationship between subjective sleep quality and risk of COPD exacerbations.MethodsData were obtained from the Canadian Cohort Obstructive Lung Disease (CanCOLD) study. Participants with COPD who had completed 18 months of follow-up were included. Sleep quality was measured with the Pittsburgh Sleep Quality Index (PSQI) and a three-factor analysis. Symptom-based (dyspnea or sputum change ≥ 48 h) and event-based (symptoms plus medication or unscheduled health services use) exacerbations were assessed. Association of PSQI with exacerbation rate was assessed by using negative binomial regression. Exacerbation-free survival was also assessed.ResultsA total of 480 participants with COPD were studied, including 185 with one or more exacerbations during follow-up and 203 with poor baseline sleep quality (PSQI score > 5). Participants with subsequent symptom-based exacerbations had higher median baseline PSQI scores than those without (6.0 [interquartile range, 3.0-8.0] vs 5.0 [interquartile range, 2.0-7.0]; P = .01), and they were more likely to have baseline PSQI scores > 5 (50.3% vs 37.3%; P = .01). Higher PSQI scores were associated with increased symptom-based exacerbation risk (adjusted rate ratio, 1.09; 95% CI, 1.01-1.18; P = .02) and event-based exacerbation risk (adjusted rate ratio, 1.10; 95% CI, 1.00-1.21; P = .048). The association occurred mainly in those with undiagnosed COPD. Strongest associations were with Factor 3 (sleep disturbances and daytime dysfunction). Time to symptom-based exacerbation was shorter in participants with poor sleep quality (adjusted hazard ratio, 1.49; 95% CI, 1.09-2.03).ConclusionsHigher baseline PSQI scores were associated with increased risk of COPD exacerbation over 18 months' prospective follow-up

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)