EFFECT OF VERTICAL TRAILING ON VEGETATIVE, REPRODUCTIVE AND YIELD OF LUFFA AS INTERCROP IN COCONUT FIELD

Abstract Intercropping trial in coconut (Cocos nucifera L), was carried out for generating more income/yield. The experiment was conducted at Coastal Agricultural Research Station (CARS) Farm, PARC, Karachi. The Tori varieties planted ridge gourd (Luffa acutangulla Roxb.) and sponge gourd (Luffa cylindrica L.) under the trail staked and unstaked Tori were grown satisfactory under coconut plot. The results showed that the staked method compared to unstaked had 30-35% increase in yield and also insect pest protection. The yield data recorded showed that staked gave maximum yield. It was also found that the intercropping did not affect the agronomic trails and yield of the coconut, but increase the yield compared to palms alone

3-(3-Fluoro­benz­yl)isochroman-1-one

In the mol­ecule of the title compound, C16H13FO2, the aromatic rings are oriented at a dihedral angle of 74.46 (4)°. The heterocyclic ring adopts a twisted conformation. In the crystal structure, there is a weak C—H⋯π inter­action

5-(2-Methoxy­benz­yl)-4-(2-methoxy­phen­yl)-4H-1,2,4-triazol-3-ol

In the mol­ecule of the title compound, C17H17N3O3, the triazole ring is oriented at dihedral angles of 88.09 (3) and 83.72 (3)° with respect to the 2-methoxy­benzyl and 2-methoxy­phenyl rings, respectively. The dihedral angle between the 2-methoxy­benzyl and 2-methoxy­phenyl rings is 52.95 (3)°. In the crystal structure, inter­molecular N—H⋯O hydrogen bonds link the mol­ecules into centrosymmetric dimers. There is a π–π contact between the 2-methoxy­phenyl rings [centroid–centroid distance = 3.811 (3) Å]

ANTI-INFLAMMATORY, ANTI-NOCICEPTIVE AND ANTIPYRETIC POTENTIAL OF TERMINALIA CITRINA FRUIT EXTRACTS

Background: Plants and herbs have long been used as remedies without scientific evidences. The objective of the present study was to explore the anti-inflammatory, anti-nociceptive and antipyretic potential of ethanolic and aqueous extracts of Terminalia citrina fruits in mice. Materials and Methods: Extracts of Terminalia citrina fruits were evaluated at doses of 200mg/kg, 400mg/kg and 600mg/kg in albino mice for preventive effect in inflammatory edema, peripheral pain sensation and pyrexia. Carrageenan induced paw edema method was utilized to evaluate anti-inflammatory activity. Analgesic appraisal of extracts was demonstrated using acetic acid induced writhing model of pain. Antipyretic potential was determined by brewer’s yeast induced pyrexia model. Statistical analysis was conducted by ANOVA following post hoc test. Results: Both extracts exhibited significant and dose-dependent anti-inflammatory, analgesic and antipyretic activities. The ethanolic extract was more effective in reducing inflammatory edema, pyrexia and pain sensation than aqueous extracts in all tested doses. Conclusion: It can be concluded that fruit extracts of Terminalia citrina may be effective in reducing inflammation, pyrexia and pain sensation in animals

4-(4-Methoxy­phen­yl)-3-[2-(2-methoxy­phen­yl)eth­yl]-1H-1,2,4-triazol-5(4H)-one

The title compound, C18H19N3O3, is a biologically active triazole derivative. The five-membered ring is oriented with respect to the six-membered rings at dihedral angles of 51.59 (4) and 61.37 (4)°. The crystal structure is stabilized by inter­molecular N—H⋯O hydrogen-bond inter­actions between centrosymmetrically related mol­ecules [the dihedral angle between the benzene rings is 47.44 (5)°]

4-(2-Methoxy­phenyl)-3-(3,4,5-tri­methoxy­phen­ethyl)-2H-1,2,4-triazole-5(4H)-thione

The title compound, C20H23N3O4S, is an important biologically active heterocyclic compound. The five-membered ring is oriented with respect to the six-membered rings at dihedral angles of 78.60 (3) (trimethoxyphenyl ring) and 71.57 (3)° (methoxyphenyl ring). In the crystal structure, inter­molecular N—H⋯O hydrogen bonds link the mol­ecules into infinite chains along the c axis

ADIPONECTIN VERSUS THIAZOLIDINEDIONES AND ANGIOTENSIN RECEPTOR BLOCKERS

Adipose tissue has gained great attention during the last decade. It represents not only a depot for energy stores, but also releases adipocytokines regulating energy disposal and can therefore be considered from therapeutic point of view. Hypoadiponectemia is an independent threat for development of metabolic syndrome. When subjects treated with antidiabetic (Thiazolidinediones) and antihypertensive (angiotensin receptor blocker) agents , the plasma concentration of adiponectin, the only component of adipocytokines, directly proportional to plasma values of these drugs. The prevalance of hypertension and T2DM is mounting with unprecedented degree in both developing and advanced countries, therefore, there is a dire need to find safer and economical therapeutic regimes for the treatment of these ailments, and intensive research is also underway for this purpose. PPARγ serves as a common link in the actions of ADN, TZDs and ARBs when exerting their effects, and it is responsible for stimulation of adiponectin receptors, thus ultimately enhancing the levels of adiponectin in plasma. This review aims to elucidate the role, link and use of ARBs, ADN and TZDs as a safer and convenient approach for the treatment of these co-morbidities as a unanimous or single remedy from comparative point of view

Effects of tranexamic acid on death, disability, vascular occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH-3): a randomised, placebo-controlled trial

Background Tranexamic acid reduces surgical bleeding and decreases mortality in patients with traumatic extracranial bleeding. Intracranial bleeding is common after traumatic brain injury (TBI) and can cause brain herniation and death. We aimed to assess the effects of tranexamic acid in patients with TBI. Methods This randomised, placebo-controlled trial was done in 175 hospitals in 29 countries. Adults with TBI who were within 3 h of injury, had a Glasgow Coma Scale (GCS) score of 12 or lower or any intracranial bleeding on CT scan, and no major extracranial bleeding were eligible. The time window for eligibility was originally 8 h but in 2016 the protocol was changed to limit recruitment to patients within 3 h of injury. This change was made blind to the trial data, in response to external evidence suggesting that delayed treatment is unlikely to be effective. We randomly assigned (1:1) patients to receive tranexamic acid (loading dose 1 g over 10 min then infusion of 1 g over 8 h) or matching placebo. Patients were assigned by selecting a numbered treatment pack from a box containing eight packs that were identical apart from the pack number. Patients, caregivers, and those assessing outcomes were masked to allocation. The primary outcome was head injury-related death in hospital within 28 days of injury in patients treated within 3 h of injury. We prespecified a sensitivity analysis that excluded patients with a GCS score of 3 and those with bilateral unreactive pupils at baseline. All analyses were done by intention to treat. This trial was registered with ISRCTN (ISRCTN15088122), ClinicalTrials.gov (NCT01402882), EudraCT (2011-003669-14), and the Pan African Clinical Trial Registry (PACTR20121000441277). Results Between July 20, 2012, and Jan 31, 2019, we randomly allocated 12 737 patients with TBI to receive tranexamic acid (6406 [50·3%] or placebo [6331 [49·7%], of whom 9202 (72·2%) patients were treated within 3 h of injury. Among patients treated within 3 h of injury, the risk of head injury-related death was 18·5% in the tranexamic acid group versus 19·8% in the placebo group (855 vs 892 events; risk ratio [RR] 0·94 [95% CI 0·86-1·02]). In the prespecified sensitivity analysis that excluded patients with a GCS score of 3 or bilateral unreactive pupils at baseline, the risk of head injury-related death was 12·5% in the tranexamic acid group versus 14·0% in the placebo group (485 vs 525 events; RR 0·89 [95% CI 0·80-1·00]). The risk of head injury-related death reduced with tranexamic acid in patients with mild-to-moderate head injury (RR 0·78 [95% CI 0·64-0·95]) but not in patients with severe head injury (0·99 [95% CI 0·91-1·07]; p value for heterogeneity 0·030). Early treatment was more effective than was later treatment in patients with mild and moderate head injury (p=0·005) but time to treatment had no obvious effect in patients with severe head injury (p=0·73). The risk of vascular occlusive events was similar in the tranexamic acid and placebo groups (RR 0·98 (0·74-1·28). The risk of seizures was also similar between groups (1·09 [95% CI 0·90-1·33]). Interpretation Our results show that tranexamic acid is safe in patients with TBI and that treatment within 3 h of injury reduces head injury-related death. Patients should be treated as soon as possible after injury. Funding National Institute for Health Research Health Technology Assessment, JP Moulton Charitable Trust, Department of Health and Social Care, Department for International Development, Global Challenges Research Fund, Medical Research Council, and Wellcome Trust (Joint Global Health Trials scheme)