Background: Hypomagnesemia is the most under-diagnosed electrolyte abnormality in critically ill patients. Many studies have been done previously showing varied prevalence and increased association with mortality and morbidity in these patients.

AIMS AND OBJECTIVES:To find out the prevalence of hypomagnesemia in critically ill medical patients and to relate the serum magnesium levels with patients mortality and morbidityoutcome considering the length of ICU stay, need for ventilatory support, durationof ventilatory support, APACHE 2 and SOFA score, primary medical conditions and other electrolyte abnormalities associated with if any in critically ill patients admitted in a medical intensivecare unit.

 

Keywords:Hypomagnesemia, Critically ill patients, Ventilatory support

[1] Al-Ghamdi SM, Cameron EC, Sutton RA: Magnesium deficiency: Pathophysiologic andclinical overview. Am J Kidney Dis; 24:737-752, 1994.
[2] Paul Marino: Fluid and electrolyte disorders– Magnesium. The ICU Book, 2nd ed., Philadelphia, Lippincott, Williams and Wilkins 2004;660-672.
[3] Sanders GT, Huijgen HJ, Sanders R: Magnesium in disease: A review with special emphasison the serum ionized magnesium. ClinChem Lab Med; 37:1011-1033, 1999.
[4] Fawcett WJ, Haxby EJ, Male DA: Magnesium: Physiology and pharmacology. Br J Anaesth;83:302-320, 1999.
[5] Whang R, Oei TO, Aikawa JK, et al: Predictors of clinical hypomagnesemia: Hypokalemia,hypophosphatemia, and hypocalcemia. Arch Intern Med; 144:1794-1796, 1984.

INTRODUCTION: Some studies have linked serum uric acid with stroke in diabetes mellitus. But it is debated. Therefore, we propose to evaluate hyperuricemia as a risk factor for stroke in patients with diabetes mellitus.

METHODS:In this cross-sectional observational study we studied 100 patients of stroke (both ischemic and hemorrhagic) with diabetes mellitus and compared with 50 controls of stroke (both ischemic and hemorrhagic) without diabetes mellitus and 50 patients of diabetes mellitus without stroke, serum uric acid levels were measured and compared using chi-square test, ANOVA, regression analysis by standard biomedical software (SPSS version 20).

RESULT: In this age and sex matched study the mean uric acid level was highest in diabetic stroke patients (7.98±1.77mg/dl) compared to non-diabetic stroke patients (6.34±1.51mg/dl) and it was lowest in only diabetic patients (5.96±1.50mg/dl; p value <0.001). And, the serum level of uric acid is significantly correlated with FBS, PPBS, glycated haemoglobin, and with duration of diabetes (p value <0.05).

Keywords: serum uric acid, hyperuricemia, stroke, diabetes mellitus

[1] To¨yry JP, Niskanen LK, La¨nsimies EA, Partanen KP, Uusitupa MIJ Autonomic neuropathy predicts the development of stroke in patients with non–insulin-dependent diabetes mellitus. Stroke. 1996;27:1316 –1318.
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[5] Selby JV, Friedman GD, Quesenberry CPJ. Precursors of essential hypertension: pulmonary function, heart rate, uric acid, serum cholesterol, and other serum chemistries. Am J Epidemiol. 1990;131:1017–1027.

Brunner's gland adenoma (also referred to as Brunner's gland hamartoma or Brunerroma) is a rare benign tumor of the duodenum. We report a 58-year-old man presenting with recurrent upper abdominal pain of variable intensity with occasional vomiting for three years. Duodenoscopy revealed a large pedunculated polyp with along stalk arising from the posterior wall of the duodenal bulb and extending into the second part of the duodenum. Endoscopic polypectomy was performed. Histological examination revealed a Brunner's gland adenoma (hamartoma).

1. Chattopadhyay P, Kundu A K, Bhattacharyya S, et al.Diffuse nodular hyperplasia of Brunner's gland presenting as upper gastrointestinal haemorrhage. Singapore Med J 2008; 49 (1) : 81.
2. Janes SEJ, Zaitoun AM1, Catton JA, et al. Brunner's gland hyperplasia at the ampulla of Vater.J Postgrad Med March 2006 Vol 52 Issue 1.
3. Helio B. coutinho', Tania I. robalinho', Vera B. coutinho', et al. Immunocytochemical demonstration that human duodenal Brunner's glands may participate in intestinal defence. J. Anat. (1996) 189, pp. 193-197.
4. J.M. Jansen, W.N.H.M. Stuifbergen, A.W.M. van Milligen de Wit. Endoscopic resection of a large Brunner's gland adenoma. The Netherlands journal of medicine. JULY 2002, VOL. 60, NO. 6 253.
5. Kovacevic I, Ljubicic N, Cupic H, et al. Helicobacter pylori infection in patients with Brunner's gland adenoma. Acta Med Croatica 2001; 55:157-60.
6. Henken EM, Forouhar F. Hamartoma of Brunner's gland causing partial obstruction of the ileum. J Can Assoc Radiol 1983; 34:73-4.
7. Fuller JW, Maj MC Cruse CW, Williams JW. Hyperplasia of Brunner's glands of the duodenum. Am Surg 1997; 43:246-50.

Non-protein coding RNAs (npcRNA) have been recently recognized in bacterial pathogens as a new group to regulate multi-drug resistance. Among several pathogenic bacterial spcecices, Salmonella enterica serovar Typhi (S. typhi) one of the focusing target in order to prevent severe impact in human health and it pose a problem by causing high fever. we report the characterization of StyR-234, a small antisense npcRNA, discovered from Salmonella typhi. StyR-234 is located on positive strand and antisense to, bacA gene. Since bacA is known to participate in MDR, we hypothesis StyR-234 is involve in bacA regulation thus could have role in drug resistance in S. typhi. Overexperssion analysis show that S. typhi became more susceptible to six antibiotics (Amikacin, Cefepime, Trimethoprim Sulphamethoxazole, Imipenem, Meropenem, Piperacillin Tazobactam) while more resistance to two antibiotics (Ampicillin and Cefotaxime). And no changes in sensitivity for three antibiotics (Ciprofloxacin, Clindamycin and Ceftazidime). The results indicated that StyR-234 increasing susceptibility to many antibiotics could be by down regulating antibiotic resistant gene bacA.

 

KEYWORDS: StyR-234; overexpression; drug resistance; S. Typhi

[1]. Zhang XL, Jeza VT and Pan Q. Salmonella typhi: from a human pathogen to a vaccine vector. Cell Mol Immunol, 2008, 5, 91-7.
[2]. Bhan MK, Bahl R and Bhatnagar S. Typhoid and paratyphoid fever. Lancet, 366, 2005, 749-62.
[3]. House D, Bishop A, Parry C, Dougan G. and Wain, J.Typhoid fever: pathogenesis and disease. Curr Opin Infect Dis, 2001, 14, 573-8.
[4]. Cooke FJ andWain J. The emergence of antibiotic resistance in typhoid fever. Travel Med Infect Dis, 2004, 2, 67-74.
[5]. Parry CM. and Threlfall EJ. Antimicrobial resistance in typhoidal and nontyphoidal salmonellae. Curr Opin Infect Dis, 2008, 21, 531-8.

A simple, precise and accurate HPTLC method has been developed for the simultaneous analysis of Metolazone and Spironolactone in bulk drugs and tablet formulation. Chromatographic separation was carried out on Merck HPTLC aluminium plates of Silica gel 60 F254, using n-propanol : triethylamine (7:3 v/v) as the mobile phase. HPTLC separation of the two drugs followed by densitometric measurement was performed in the absorbance mode at 240 nm. The drugs were resolved with Rf values of 0.60 and 0.69 for Metolazone and Spironolactone respectively. The linear regression analysis data for the calibration plots showed good linear relationship with r2 value 0.99886 and 0.99862 for Metolazone and Spironolactone, respectively in the concentration range of 300 -700 ng/spot for Metolazone and 300-700 ng/spot for Spironolactone. The method was validated following the ICH guidelines in terms of accuracy, precision, specificity and robustness. The limit of detection and quantitation were 200 and 600 ng/spot respectively for Metolazone and 200 and 600 ng/spot for Spironolactone. The proposed developed and validated HPTLC method can be utilised for identification and quantitative analysis of Metolazone and Spironolactone in bulk drugs and pharmaceutical dosage form.

 

Keywords: HPTLC, Metolazone, Spironolactone, Validation.

[1] M.J. O'Neil, The Merck Index (fifteenth ed., RSC publishing, 2013), pp. 6222, 8885

[2] United States Pharmacopoeia (Vol III, thirty fourth ed., , Rockville, MD: The United States Pharmacopeial Convention, 2011), 3506, 4267-4268.

[3] British Pharmacopoeia (Vol II, The Stationary Office on behalf of MHRA, 151 Buckingham Palace Road, London, 2012), 1458-1459, 2030-2032.

[4] M.C. Anthony, M. David Osselton, Clark's analysis of drugs and poison (Vol II, third ed.), 313, 1273-1568.

[5] K.D. Tripathi , Essentials of Medical Pharmacology (sixth ed., Jaypee Brothers Medical Publishers (P) ltd. 2008), 561-578.

[6] Indian Pharmacopoeia (Vol III, The Indian Pharmacopoeia Commission, Ghaziabad, Govt. of India Ministry of Health and Family Welfare, 2010), 2147-2148.

6-chloro-5-((4-chlorophenyl) diazenyl) pyrimidine-2, 4-diamine and 4-chloro-6-methoxy-N,N-dimethylpyrimidin-2-amine has been used as precursors for the synthesis of new pyrimidine derivatives, employing Suzuki cross-coupling reaction. Thus, treatment of pyrimidine derivative with various arylboronic acids in the presence of palladium tetraacetate, PhP3 and Na2CO3 in refluxing n-propanol afforded the target compounds. The synthesis was supported by spectroanalytical techniques. The synthesized compounds have been screened for their inhibitory activity against some microbial, the results were showed that among gram positive isolates only (1/10) isolates of S. aureus and (3/10) isolates of S. saprophyticaus were sensitive for compound 13, while (1/10) isolates of S. aureus and (1/10) isolates of S.saprophyticaus were sensitive for compound 4. All isolates of S. pyogenes were resisting to all compounds, among gram negative bacterial isolates only (2/10) isolates of E. coli and (1/10) isolates of K. pneumoniae were sensitive to compound 4. Concerning the antifungal effects of compounds 3, 4, 5, 13, 14, 15 the results revealed that, all C. albicans and C. glabrata isolate were resist these compounds.

 

Keywords: Pyrimidine, arylboronic acid, synthesis, Suzuki, gram positive

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[2.] Kappe. C. O. Tetrahedron 1993, 49, 6937-6963 (review).
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[4.] Kidwai. M.; Saxena. S.; Rastogi. S.; Venkataramanan. R. Curr. Med. Chem.-Anti-Infect. Agents 2003, 24, 269-286.
[5.] Jain. M. K.; Sharnevsas. S. C. organic chemistry, III edition, 2008, 997-999.
[6.] Heidelberger. C.; Chaudhuri. N. K.; Danneberg.P.; Mooren. D.; Griesbach. L.; R., Duschinsky. R.; Schnitzer. J.; Pleven. E.; Scheiner. J. Nature 1957, 179, 663-666

Type 1 diabetes is associated with damage to the liver, kidney and pancreas of patients. The damage varies in proportion and susceptibility among diabetic patients of type 1 class. This study assessed the hypoglycemic, hepatoprotective and nephroprotective activities of whole methanolic leaf extract of Heinsia crinita (HC) in alloxan-induced diabetic albino Wistar rats. Twenty four (24) rats weighing 140-180g were divided into 4 groups of 6 rats each. Group 1 served as normal control (NC), while Group 2 served as diabetic control (DC) and both received placebo treatment consisting of 0.2ml of 50% DMSO respectively. Group 3 was treated with standard insulin (5iu/kg b.w) and Group 4 was treated with 400mg/kg b.w of the methanol extract of Heinsia crinita (HC) twice daily via oral gastric intubation. After 14 days, the animals were sacrificed and serum was analyzed for glucose, oxidative stress biomarkers and electrolyte profile. The results showed that HC reduced serum glucose level by 15% within 14 days, while the DC showed no reduction. The results further showed significant (p<0.05) decrease in ALT, AST and ALP activity in groups 4 and 3, when compared with group 2 (DC) which gave high values of these enzymes. Group 4 showed high values of K+ (10.93+0.10 Mmol/l) and Cl- (353.23+0.34 Mmol/l) but lower Na+ (71.06+12.94 Mmol/l) and urea (66.04+6.06Mmol/l) values when compared to DC with low values of K+ (3.83+0.82 Mmol/l) and Cl- (127.09+14.43 Mmol/l) but high values of Na+(203.00+14.47 Mmol/l) and urea (86.00+14.13 Mmol/l) respectively. Electrolyte modulation by the plant extract was shown in this study to be better than insulin. These findings showed that Heinsia crinita may possess antidiabetic properties and beneficial in the management of Type 1 diabetes and its attendant liver and kidney complications.

 

Key word. Hencia crinita, Alloxan, Type 1 Diabetes, Hepatoprotective, Nephroprotective

[1.] Lorke, D. (1983). A new approach to practical acute toxicity testing. Archives of toxicology, 53:275-287.
[2.] Prince P S M, and Menon V.P (2000). Hypoglycaemic and other related actions of tinospora cardifolia roots in alloxan - induced diabetic rats. J. Ethnopharmacol. 70: 9-15.
[3.] Kang J, Dai X S, Yu T B, Wen B, and Yang Z W, (2005). Glycogen accumulation in renal tubules, a key morphological change in the diabetic rat kidney. Acta. Diabetol, 42: 110-116.
[4.] Enyi-idoh K H, Ikpeme E M, Iwuh G. C (2012). Antibacterial activity of gnetum africanum and heinsia crinita on diarrhoeagenic bacteria stool isolates from children in Calabar south Lga, cross river state, Nigeria. Transnational journal of science and technology march 2013 edition vol.3, no.3
[5.] Edet, E.E; I.J. Atangwho, M.I. Akpanabiatu, T. E. Edet, F.E. Uboh, E, David-Oku (2011). Effect of gongronema latifolium leaf extract on some liver enzymes and protein levels in diabetic and non diabetic rats. J. Pharm. Biomed. Sci., 1(5) 104-107.

Two olenane triterpenes, 18β-glycyrrhetinic acid-3-O-β-D-glucuronide and 18β-glycyrrhetinic acid were obtained from the acid hydrolysis of 18β-glycyrrhetinic acid-3-O-β-D-glucuronopyranosyl-(1→2)-β-D-glucuronide (Glycyrrhizic acid or Glycyrrhizin), a triterpene glucuronide isolated from the commercial extract of the roots of Glycyrrhia glabra. The complete 1H and 13C NMR assignments of the two triterpenes 18β-glycyrrhetinic acid-3-O-β-D-glucuronide and 18β-glycyrrhetinic acid were achieved on the basis of extensive 1D and 2D NMR (1H and 13C, COSY, HSQC, and HMBC) as well as mass spectral data.

 

Keywords: Glycyrrhiza glabra, Fabaceae, Glycyrrhizin, Triterpene glucuronide, Hydrolysis products, 1D and 2D NMR spectral data, Structure characterization.

[1.] Biondi, D.M., Rocco, C., Ruberto, G. Dihydrostilbene derivatives from Glycyrrhiza glabra leaves, Journal of Natural Products, 2005, 68, 1099-1102.
[2.] El-Refai, A.M.H., Sallam, A.R., El-Menoufy, H., Amin, H.A.S. Physiological and chemical studies on the bioconversion of glycyrrhizin by Aspergillus niger NRRL595, Malaysian Journal of Microbiology, 2012, 8, 75-82.
[3.] Nomura, T., Fukai, T., Akiyama, T. Chemistry of phenolic compounds of licorice (Glycyrrhiza species) and their estrogenic and cytotoxic activities. Pure and Applied Chemistry, 2002, 74, 1199-1206.
[4.] Akao, T. Effects of glycyrrhizin and glycyrrhetic acid on the growth, glycyrrhizin β-D-glucuronidase and 3β-hydroxysteroid dehydrogenase of human intestinal bacteria, Biological and Pharmaceutical Bulletin, 2000, 23, 104-107
[5.] Chaturvedula, V.S.P., Yu, O., Mao, G. (2013). NMR analysis and hydrolysis studies of glycyrrhizic acid, a major constituent of Glycyrrhia glabra, European Chemical Bulletin, 2014, 3, 104-107.
[6.] Chaturvedula, V.S.P., Chen, S., Yu, O., Mao, G. NMR spectral analysis and hydrolysis studies of rebaudioside N, a minor steviol glycoside of Stevia rebaudiana Bertoni. Food and Nutrition Sciences, 2013, 4, 1004-1008.