Biomedical subjects

A K Dash

Publications and source records attributed to A K Dash.

21 records · Page 2Linked to original sources

PubMed1991

Solid-state properties of tobramycin.

Tobramycin (I) obtained from two different sources was subjected to powder X-ray diffractometry, thermal analyses, and Karl Fischer titrimetry. It was concluded to be tobramycin monohydrate (C18H37N5O9 . H2O). When heated in the differential scanning calorimeter (DSC), the dehydration of I resulted in the formation of metastable anhydrous tobramycin, which melted at 164 degrees C. This was followed by the crystallization of the stable anhydrous tobramycin, which then melted at 217 degrees C. The polymorphic transition was concluded to be monotropic and the calculated free energy difference between the metastable and the stable forms, at 25 degrees C, was 348 cal.mol-1. Both the heating rate in the DSC and the sample size had a significant influence on the enthalpy values of most of the thermal events. These observations were attributed to the presence of trace amounts of moisture in the sample. No detectable decomposition of I occurred when it was heated up to 224 degrees C.

Chromatography, High Pressure Liquid↗

PubMedDate not supplied

Determination of the physical state of drug in microcapsule and microsphere formulations.

Tolnaftate microcapsules and microspheres were prepared by gelatin-acacia coacervation and emulsion-solvent evaporation methods respectively. The physical state of the drug in these formulations was determined by using scanning electron microscopy (SEM), X-ray powder diffractometry, and differential scanning calorimetry (DSC). High pressure liquid chromatographic (HPLC) method was used for stability determination and polymer-drug interactions were evaluated using FTIR. The pros and cons of each method, in the assessment of the physical state of drug in these formulations, were investigated. SEM was found to be useful in obtaining a direct visual evidence of the presence of crystalline drug in the microspheres, but not for the microcapsule formulation. The DSC method was used to determine the physical state of the drug qualitatively in both these formulations. In the case of the microcapsules, accurate quantitation of the crystalline drug content by DSC was not possible because of the interference of thermal events. Powder X-ray diffractometric method was able to demonstrate the presence of crystalline drug and polymorphic changes, if any, in both these formulations. HPLC data revealed that the drug was stable in these formulations for at least 6 months. The FTIR studies indicated the absence of any drug interaction with the polymeric matrix materials, during preparation of these dosage forms.

Antifungal Agents↗

PubMedDate not supplied

Nitric oxide concentrations and cerebrospinal fluid parameters in an experimental animal model of Streptococcus pneumoniae meningitis.

Streptococcus pneumoniae is a common cause of meningitis. Nitric oxide (NO) has been implicated in causing cerebral edema. Modulating NO production in cerebrospinal fluid (CSF) may have a role in the treatment of bacterial meningitis. Experimental S. pneumoniae meningitis was induced in a rabbit model to determine CSF parameters and NO concentrations. An electrochemical probe in the CSF throughout the 7-hour experiment monitored NO concentrations. The animals had S. pneumoniae (10(5)) injected intracisternally and incubated for 1 hour. Cerebrospinal fluid 200-300 microl was obtained by intracisternal puncture at zero, 2, 4, and 7 hours after drug administration to measure glucose, protein, and lactic acid by standard chemical methods. White blood cell count was measured by hemocytometry. Three groups of five animals were used-control (C), ceftriaxone (CTX), and ceftriaxone plus dexamethasone (CTX+D). Ceftriaxone concentrations in CSF were obtained by microdialysis and analyzed by high-performance liquid chromatography. Mean (+/- SEM) CSF white blood cell count was significantly higher at 2 hours in the C group than in the other two groups (C 7307 +/- 1302, CTX 605 +/- 345, CTX+D 730 +/- 43/mm3, p<0.002). Ceftriaxone induced a significant rise in protein at 4 hours compared with the other groups (C 364 +/- 107, CTX 1158 +/- 797, CTX+D 365 +/- 100 mg/dl, p<0.02). Cerebrospinal fluid lactic acid was significantly different at 4 and 7 hours between C and CTX+D groups (4-hr C 8.0 +/- 2.2, CTX+D 2.0 +/- 0.4 mmol/L, p<0.05; 7-hr C 10.2 +/- 2.4, CTX+D 2.8 +/- 0.8 mmol/L, p<0.01). Median NO concentrations were significantly elevated in the control group compared with the other two groups (C 11.7, CTX 6.8, CTX+D 6.5 micro, p<0.02 C vs CTX, p<0.01 C vs CTX+D). Average (+/- SEM) NO concentrations were significantly higher in the C group at 4 hours (18.1 +/- 0.4, CTX 5.8 +/- 1.8 microM, p<0.05; CTX+D 11.5 +/- 4.0 microM, p>0.05), whereas they did not rise significantly until 7 hours in the CTX group (CTX 18.7 +/- 0.7, C 8.9 +/- 0.4 microM, p=0.055; CTX+D 8.1 +/- 2.2 microM, p<0.05). These results indicate that ceftriaxone with or without dexamethasone significantly decreases lactic acid concentrations and white cell penetration into the CSF in an experimental model of S. pneumoniae meningitis. In addition, ceftriaxone induced a significant elevation in CSF protein. Median NO production in the CSF was significantly attenuated by ceftriaxone.

Animals↗