Enzymatic recovery of silver from waste radiographic film: Optimize with response surface methodology

Silver is one of the valuable materials exist freely on earth crust. Worldwide, massive demand in different purpose makes silver very valuable. On information nearly twenty percent of silver were collected from non-ferrous metallurgical industry, locally generated scrap and photographic film. The toxicity of silver directly impact on surface and ground ecosystem. So it's compulsory to treat and recycle silver from waste material. To fulfil the demand of silver from waste, an enzyme from pineapple make of use. The aim of research work is to recover the silver metal from waste X-ray film by bromelain enzyme as biocatalyst. Response surface methodology full factorial design was used to optimize three operating parameters for maximum recovery of silver. The result shows silver recovery increases with increase in protein concentration, 5.4 mg of pure silver can be recovered from 600 mg of waste X-rays film at most favourable condition of protein concentration 0.2857 mg/ml; temperature 45 °C, pH6.5 and stripping time 20 min. At same optimised parameters, papain biocatalyst shows 4.8 mg and sodium hydroxide shows 5.2 mg recovery of pure silver. The obtained silver powder (grain) having 91.12% purity and total silver recovered.     

Scalable Preparation and Differential Pharmacologic and Toxicologic Profiles of Primaquine Enantiomers

Hematotoxicity in individuals genetically deficient in glucose-6-phosphate dehydrogenase (G6PD) activity is the major limitation of primaquine (PQ), the only antimalarial drug in clinical use for treatment of relapsing Plasmodium vivax malaria. PQ is currently clinically used in its racemic form. A scalable procedure was developed to resolve racemic PQ, thus providing pure enantiomers for the first time for detailed preclinical evaluation and potentially for clinical use. These enantiomers were compared for antiparasitic activity using several mouse models and also for general and hematological toxicities in mice and dogs. (+)-(S)-PQ showed better suppressive and causal prophylactic activity than (−)-(R)-PQ in mice infected with Plasmodium berghei. Similarly, (+)-(S)-PQ was a more potent suppressive agent than (−)-(R)-PQ in a mouse model of Pneumocystis carinii pneumonia. However, at higher doses, (+)-(S)-PQ also showed more systemic toxicity for mice. In beagle dogs, (+)-(S)-PQ caused more methemoglobinemia and was toxic at 5 mg/kg of body weight/day given orally for 3 days, while (−)-(R)-PQ was well tolerated. In a novel mouse model of hemolytic anemia associated with human G6PD deficiency, it was also demonstrated that (−)-(R)-PQ was less hemolytic than (+)-(S)-PQ for the G6PD-deficient human red cells engrafted in the NOD-SCID mice. All these data suggest that while (+)-(S)-PQ shows greater potency in terms of antiparasitic efficacy in rodents, it is also more hematotoxic than (−)-(R)-PQ in mice and dogs. Activity and toxicity differences of PQ enantiomers in different species can be attributed to their different pharmacokinetic and metabolic profiles. Taken together, these studies suggest that (−)-(R)-PQ may have a better safety margin than the racemate in human.     

Use of dexmedetomidine as an adjunct in the treatment of paradoxical hypertension after surgical repair of coarctation of the aorta in infants

Severe persistent hypertension is seen infrequently in newborns and infants, but we came across two infants who developed severe paradoxical hypertension after successful coarctation repair. Treatment of systemic hypertension following repair of coarctation of the aorta is always challenging particularly in infants. Dexmedetomidine was used successfully as an adjunct to the established anti-hypertensive drugs in the immediate postoperative period in our cases to treat postoperative paradoxical hypertension.     

Effect of neurotransmitters, Guanosine triphosphate, and divalent ions on the regulation of adenylate cyclase activity in malignant and adenosine cyclic 3':5'-monophosphate-induced "differentiated" neuroblastoma cells.

The effect of acetylcholine, 3,4-dihydroxyphenylethylamine, prostaglandin (PGE1), guanosine triphosphate (GTP), and divalent ions on adenylate cyclase activity in homogenates of "differentiated" and malignant mouse neuroblastoma cells was studied. The sensitivity of adenylate cyclase to acetylcholine and 3,4-dihydroxyphenylethylamine markedly increased in adenosine cyclic 3:5-monophosphate-induced differentiated neuroblastoma cells. Although 3,4-dihydroxyphenylethylamine stimulated adenylate cyclase activity in malignant neuroblastoma cells, it failed to do so in X-irradiation induced differentiated cells. PGE1 and GTP stimulated adenylate cyclase activity in malignant and adenosine cyclic 3:5-monophosphate induced differentiated neuroblastoma cells to about the same level. GTP protentiated the PGE1 effect in differentiated concentrations of magnesium and manganese inhibited adenylate cyclase activity; this effect was more pronounced in differentiated cells than in malignant cells. Calcium stimulated adenylate cyclase activity in malignant and differentiated cells to about the same level. There was no significant difference in the values of Km and Vmax of neuroblastoma cells. This study shows that the sensitivity of adenylate cyclase to neurotransmitters and divalent ions (magnesium and manganese) and the sensitivity of PGE1 stimulated enzyme activity to GTP increase in adenosine cyclic 3:5-monophosphate-induced differentiated neuroblastoma cells. Therefore, we suggest that the reverse may be true during malignant transformation of nerve cells.     

Determination and validation of LJ-2698, a potent human A<Subscript>3</Subscript> adenosine receptor antagonist,in rat plasma by liquid chromatography-tandem mass spectrometry and its application in pharmacokinetic study

LJ-2698, a highly potent human A₃ adenosine receptor antagonist with nucleoside structure, was designed to have a minimal species dependence. For further pre-clinical studies, analytical method for the detection of LJ-2698 in rat plasma was developed by liquid chromatography-tandem mass. Plasma samples were processed by protein precipitation method with acetonitrile, using losartan as the internal standard (IS). Chromatographic separation was carried out using a Kinetex C18 column (100 × 4.6 mm; 100 Å; 2.6 μ) with acetonitrile/water with 0.2% (v/v) formic acid (65:35, v/v) in the isocratic mode at a flow rate of 0.4 mL/min. Mass spectrometric detection in multiple reaction monitoring mode was performed with positive electrospray ionization. The mass transitions of LJ-2698 and IS were m/z 412.3 → 294.1 and m/z 423.1 → 207.2, respectively. The calibration curves were linear in the range 5.00–5000 ng/mL (r ² ≥ 0.998). The lower limit of quantification was established as 5.00 ng/mL. Within- and between-run precisions were <7.01%, as relative standard deviation; and accuracies were in the range 3.37–3.64%, as relative error. The validated method was successfully applied to its pharmacokinetic evaluation after intravenous and oral administration in rats, and the dose-dependent pharmacokinetic behavior of LJ-2698 was elucidated for the first time.