A CLINICAL STUDY TO EVALUATE THE EFFECT OF SPHATIKAYUKTHA RASA SINDOORA WITH LODHRA KASHAYA IN DYSFUNCTIONAL UTERINE BLEEDING

Dysfunctional Uterine Bleeding is defined as a state of abnormal uterine bleeding without any clinically detectable organic, systemic and iatrogenic cause. The prevalence varies widely but an incidence of 10% amongst new patients attending the outpatient seems logical. Along with increased susceptibility to iron deficiency, heavy menstrual bleeding can negatively impact physical, emotional and social quality of life and reduce work capacity of females. Objective: A clinical study was conducted to evaluate the effect of Sphatikayuktha Rasa Sindoora with Lodhra Kashaya in Dysfunctional Uterine Bleeding. Design: This pre-post interventional study was conducted among 20 females in the age group 20-45 years who had the symptoms of Dysfunctional Uterine Bleeding for the past 3 cycles. Drug administration started on the 3rd day of menstruation and was continued till bleeding stopped or upto a maximum of 7 days for 3 consecutive cycles. Follow up was done in the next cycle. The condition of the patient after drug administration in the first, second and third months were separately compared with the condition of the patient before treatment. Outcome measures: Outcome variables were change in the amount, duration and frequency of bleeding. Results and Discussion: Results were analysed statistically using Wilcoxon signed rank test and Paired t-test. The treatment was effective in reducing the amount of bleeding during treatment period and the follow up period. It was effective in reducing the duration of bleeding during the treatment period as compared to the follow up period and in controlling the cycle interval during the treatment period

In vitro studies indicate that acid catalysed generation of N-nitrosocompounds from dietary nitrate will be maximal at the gastro-oesophageal junction and cardia

Background: Dietary nitrate increases saliva nitrite levels and swallowed saliva is the main source of nitrite entering the acidic stomach. In acidic gastric juice, this nitrite can generate potentially carcinogenic N-nitrosocompounds. However, ascorbic acid secreted by the gastric mucosa can prevent nitrosation by converting the nitrite to nitric oxide. Methods: To study the potential for N-nitrosocompound formation in a model simulating salivary nitrite entering the acidic stomach and the ability of ascorbic acid to inhibit the process. Concentrations of ascorbic acid, total vitamin C, nitrite, nitrosomorpholine, oxygen and nitric oxide were monitored during the experiments. Results: The delivery of nitrite into HCl containing thiocyanate resulted in nitrosation of morpholine, with the rate of nitrosation being greatest at pH 2.5. Under anaerobic conditions, ascorbic acid converted the nitrite to nitric oxide and prevented nitrosation. However, in the presence of dissolved air, the ascorbic acid was ineffective at preventing nitrosation. This was due to the nitric oxide combining with oxygen to reform nitrite and this recycling of nitrite depleting the available ascorbic acid. Further studies indicated that the rate of consumption of ascorbic acid by nitrite added to natural human gastric juice (pH 1.5) was extremely rapid with 200 μmol/l nitrite consumed 500 μmol/l ascorbic acid within 10 s. Conclusions: The rapid consumption of ascorbic acid in acidic gastric juice by nitrite in swallowed saliva indicates that the potential for acid nitrosation will be maximal at the GO junction and cardia where nitrite first encounters acidic gastric juice. The high incidence of mutagenesis and neoplasia at this anatomical location may be due to acid nitrosation arising from dietary nitrate

Role of Guanidyl Moiety in the Insertion of Arginine and Nα-Benzoyl-l-argininate Ethyl Ester Chloride in Lipid Membranes

Role of Guanidyl Moiety in the Insertion of Arginine and Nα-Benzoyl-l-argininate Ethyl Ester Chloride in Lipid Membranes AbstractFull Text HTMLHi-Res PDF[1247 KB]PDF w/ Links[216 KB]FiguresReferencesA. C. Fonseca‡, M. A. Frías†, A. M. Bouchet†, S. Jarmelo‡§, P. N. Simões‡, R. Fausto§, M. H. Gil‡, F. Lairion† and E. A. Disalvo*† Laboratory of Physical Chemistry of Lipid Membranes, Department of Analytical Chemistry and Physical Chemistry, Pharmacy and Biochemistry, University of Buenos Aires Junín 956 2° piso (1113), Buenos Aires, Argentina, Department of Chemical Engineering, University of Coimbra, Polo II, Pinhal de Marrocos, 3030-790 Coimbra, Portugal, and Department of Chemistry, University of Coimbra, 3004-535 Coimbra, Portugal J. Phys. Chem. B, 2010, 114 (17), pp 5946–5952 DOI: 10.1021/jp101007b Publication Date (Web): April 13, 2010 Copyright © 2010 American Chemical Society * Corresponding author. Phone: 54 11 39648249. Fax: 54 11 45083645. E-mail: [email protected]., † Department of Analytical Chemistry and Physical Chemistry, Pharmacy and Biochemistry, University of Buenos Aires Junín 956 2° piso (1113). , ‡ Department of Chemical Engineering, University of Coimbra. , § Department of Chemistry, University of Coimbra. AbstractGuanidyl moieties of both arginine (Arg) and Nα-benzoyl-l-argininate ethyl ester chloride (BAEE) are protonated in all environments studied, i.e., dry solid state, D2O solutions, and dry and hydrated lipids as suggested by DFT(B3LYP)/6-31+G(d,p) calculations. Arg and BAEE are able to insert in the lipid interphase of both DMPC and DOPC monolayers as revealed by the observed decrease in the membrane dipole potential they induce. The larger decrease in the dipole potential induced by BAEE, compared to Arg, can be explained partially by the higher affinity of the hydrophobic benzoyl and ethyl groups for the membrane phase, which allows an easier insertion of this molecule. FTIR studies indicate that the guanidyl moiety of Arg is with all probability facing the hydrophobic part of the lipids, whereas in BAEE this group is facing the water phase. Zeta potential measurements provide a direct evidence that Arg orients in the lipid interphase of phosphatidylcholine (PC) bilayers with the negative charged carboxylate group (−COO−) toward the aqueous phase