The effects of sodium hypochlorite dipping, temperature and duration of storage on the quality of fresh taro corms destined for overseas markets.

A study to determine conditions that promote the longevity of stored taro corms (Colocasia esculenta (L). Schott var. esculenta) following harvest was carried out in Samoa in 2001in response to rotting and weight loss problems. The study investigated the possibility that storage of corms at 5oC causes chilling damage, thus enhancing corm rot, and to confirm the beneficial effects of sodium hypochlorite as a rot control dip. 320 freshly harvested 8 months old mature corms were randomly divided into two groups. One group was dipped in a 0.1% solution of sodium hypochlorite (NaOCl) and the other in water, for 2 minutes and packed into perforated plastic bags so that each contained 40 corms. The bags were then randomly selected into 4 groups so that each dip treatment was represented in every group. The four groups were cool stored for 2 weeks at temperatures of 5oC, 10oC, 15oC and ambient.(25oC) respectively. After 2 weeks, the bags were removed from the coolers, stored at ambient and sampled every 7 days for weight and corm loss. Results showed that over the two weeks of on shelf display following removal from cool storage, corms that were stored at 5oC sustained the least corm rot at 15.8%, followed by 10oC at 16.5% with the highest at 50.5% for 15oC. These results show that chilling damage did not occur at the storage temperature of 5oC and that the best temperature range to store taro corms in order to minimise corm rot when removed to ambient for on-shelf display is 5 to 10oC. Dipping in a 0.1% solution of sodium hypochlorite significantly reduced corm rot from 34.2% to 26.0% and weight loss from 4.0% to 3.7%. However the chemical dip had no significant effect on the number or weight of rootlets that sprouted from the stored corms

Agricultural tools and machinery used by Samoan subsistence farmers

This paper discusses the findings of the research carried out on agricultural tools and machinery used by Samoan subsistence farmers to cultivate and harvest crops like taro (Colocasia esculents var. esculenta), banana (musa spp.), ta’amu ( Alocasia macrorhiza) breadfruit (Artocarpus altilis), yam (Discorea spp.) and coconut (Cocosnucifera). The research was conducted by interviewing farmers chosen by field officers who work directly with them on behalf of the Ministry of Agriculture in Samoa. The information collected focused on the type of tool, implement or machine that the farmer owned or has access to, its effectiveness, susceptibility to breakdowns, maintenance issues, ease of repair and availability of spare parts. In general the level of engineering inputs employed in the production of these crops is low and confined mainly to the bushknife, metal tip for planting stick, spade, the lower – operated knapsack sprayer and the mist blower

Asymmetric dimethylarginine causes hypertension and cardiac dysfunction in humans and is actively metabolized by dimethylarginine dimethylaminohydrolase

OBJECTIVE Plasma levels of an endogenous nitric oxide (NO) synthase inhibitor, asymmetric dimethylarginine (ADMA), are elevated in chronic renal failure, hypertension, and chronic heart failure. In patients with renal failure, plasma ADMA levels are an independent correlate of left ventricular ejection fraction. However, the cardiovascular effects of a systemic increase in ADMA in humans are not known. METHODS AND RESULTS In a randomized, double-blind, placebo-controlled study in 12 healthy male volunteers, we compared the effects of intravenous low-dose ADMA and placebo on heart rate, blood pressure, cardiac output, and systemic vascular resistance at rest and during exercise. We also tested the hypothesis that ADMA is metabolized in humans in vivo by dimethylarginine dimethylaminohydrolase (DDAH) enzymes. Low-dose ADMA reduced heart rate by 9.2+/-1.4% from 58.9+/-2.0 bpm (P<0.001) and cardiac output by 14.8+/-1.2% from 4.4+/-0.3 L/min (P<0.001). ADMA also increased mean blood pressure by 6.0+/-1.2% from 88.6+/-3.4 mm Hg (P<0.005) and SVR by 23.7+/-2.1% from 1639.0+/-91.6 dyne. s. cm-5 (P<0.001). Handgrip exercise increased cardiac output in control subjects by 96.8+/-23.3%, but in subjects given ADMA, cardiac output increased by only 35.3+/-10.6% (P<0.05). DDAHs metabolize ADMA to citrulline and dimethylamine. Urinary dimethylamine to creatinine ratios significantly increased from 1.26+/-0.32 to 2.73+/-0.59 after ADMA injection (P<0.01). We estimate that humans generate approximately 300 micromol of ADMA per day, of which approximately 250 micromol is metabolized by DDAHs. CONCLUSIONS This study defines the cardiovascular effects of a systemic increase in ADMA in humans. These are similar to changes seen in diseases associated with ADMA accumulation. Finally, our data also indicate that ADMA is metabolized by DDAHs extensively in humans in vivo

Immunolocalisation and activity of DDAH I and II in the heart and modification post-myocardial infarctioN

Summary: Asymmetric dimethylarginine (ADMA) and NG monomethyl-l-arginine (l-NMMA) are endogenous inhibitors of nitric oxide synthases (NOS) and their local concentration is determined by the activity of dimethylarginine dimethylaminohydrolases (DDAHs). The current study in male Wistar rats was designed to immunolocalise DDAH I and II in relation to NOS and to investigate changes in distribution, activity and ADMA content in the acute period following myocardial infarction (MI) resulting from coronary artery ligation. Seven days after the coronary artery ligation, l-Arg and methylated arginine content, as well as DDAH activity were determined in homogenates of left ventricular (LV) infarct and border. The distribution of immunoreactive DDAH I, DDAH II, eNOS and iNOS were determined in sections of LV. In healthy hearts, DDAH I was absent, however, DDAH II was localized to endothelium and endocardium with a similar distribution to that of eNOS. Following MI, LV DDAH activity was increased (to 210±19% of control, P<0.05). Both DDAH I and DDAH II proteins were detected in peri-infarct cardiomyocytes, while DDAH II immunoreactivity was additionally localized to infiltrating inflammatory cells and blood vessels in the healing infarct. Both plasma and LV concentrations of the DDAH substrate, ADMA, were increased post-MI, although the ratio of Arg:ADMA was retained in the LV post-MI relative to sham operated controls. In conclusion, DDAH II has a distribution similar to eNOS in healthy myocardium. The increased levels and activity of DDAH I and DDAH II enzymes following myocardial infarction suggest a potential role for them in local protection of NOS enzymes from inhibition by methylated arginines during infarct healing

Increasing dimethylarginine levels are associated with adverse clinical outcome in severe alcoholic hepatitis

Previous studies suggest reduced hepatic endothelial nitric oxide synthase activity contributes to increased intrahepatic resistance. Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, undergoes hepatic metabolism via dimethylarginine-dimethylamino-hydrolase, and is derived by the action of protein-arginine-methyltransferases. Our study assessed whether ADMA, and its stereo-isomer symmetric dimethylarginine (SDMA), are increased in alcoholic hepatitis patients, and determined any relationship with severity of portal hypertension (hepatic venous pressure gradient measurement) and outcome. Fifty-two patients with decompensated alcoholic cirrhosis were studied, 27 with acute alcoholic hepatitis and cirrhosis, in whom hepatic venous pressure gradient was higher (P = 0.001) than cirrhosis alone, and correlated with ADMA measurement. Plasma ADMA and SDMA were significantly higher in alcoholic hepatitis patients and in nonsurvivors. Dimethylarginine-dimethylamino-hydrolase protein expression was reduced and protein-arginine-methyltransferase-1 increased in alcoholic hepatitis livers. ADMA, SDMA and their combined sum, which we termed a dimethylarginine score, were better predictors of outcome compared with Pugh score, MELD and Maddrey's discriminant-function. Conclusion: Alcoholic hepatitis patients have higher portal pressures associated with increased ADMA, which may result from both decreased breakdown (decreased hepatic dimethylarginine-dimethylamino-hydrolase) and/or increased production. Elevated dimethylarginines may serve as important biological markers of deleterious outcome in alcoholic hepatitis

Disruption of methylarginine metabolism impairs vascular homeostasis.

Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA) are endogenously produced amino acids that inhibit all three isoforms of nitric oxide synthase (NOS). ADMA accumulates in various disease states, including renal failure, diabetes and pulmonary hypertension, and its concentration in plasma is strongly predictive of premature cardiovascular disease and death. Both L-NMMA and ADMA are eliminated largely through active metabolism by dimethylarginine dimethylaminohydrolase (DDAH) and thus DDAH dysfunction may be a crucial unifying feature of increased cardiovascular risk. However, despite considerable interest in this pathway and in the role of ADMA as a cardiovascular risk factor, there is little evidence to support a causal role of ADMA in pathophysiology. Here we reveal the structure of human DDAH-1 and probe the function of DDAH-1 both by deleting the DDAH1 gene in mice and by using DDAH-specific inhibitors which, as we demonstrate by crystallography, bind to the active site of human DDAH-1. We show that loss of DDAH-1 activity leads to accumulation of ADMA and reduction in NO signaling. This in turn causes vascular pathophysiology, including endothelial dysfunction, increased systemic vascular resistance and elevated systemic and pulmonary blood pressure. Our results also suggest that DDAH inhibition could be harnessed therapeutically to reduce the vascular collapse associated with sepsis