Rheumatoid arthritis (RA) is a common systemic inflammatory disease which DMARDS have been widely used as a treatment modality both as monotherapy and combination therapy Bucillamine, one of newer DMARDS, has recently proven its efficacy as monotherapy in the treatment of RA. The objective of this study was to compare the efficacy and the safety of bucillamine monotherapy and bucillamine plus methotrexate combination therapy in the treatment of rheumatoid arthritis. Forty-nine mild RA patients were enrolled in this prospective, open-trial and were assigned to receive bucillamine 200 mg/day (n=18) or bucillamine 200 mg/day and methotrexate 7.5-15 mg/week (n=31) orally for 16 weeks. Concomitant use of NSAID and prednisolone <5 mg/day or equivalent dose of steroid were allowed. Both monotherapy group and combination therapy group have shown significant improvement in disease activities (Ritchie index, painful joints, swollen joints, morning stiffness, grip strength, ESR, RF, CRP, patient's self assessment of pain, physician's global assessment of disease activity) from the baseline. However, there was no statistically significant difference between two groups. The adverse effects were more frequently shown in combination therapy group than monotherapy group. In conclusion, in patients with mild RA monotherapy has shown to be equally efficacious as combination therapy with less side effects.

The purpose of this study was to determine pharmacokinetic parameters of vancomycin using the compartment model dependent and compartment model independent analysis in 6 Korean normal volunteers and 8 ovarian cancer patients. Vancomycin was administered 1.0 g bolus by IV infusion over 60 minutes. The elimination rate constant ($\beta$), volume of distribution (Vd), total body clearance (CLt), and area under the plasma level-time curve (AUC) of vancomycin in normal volunteers using the compartment model dependent analysis were $0.150\pm0.030\;hr^{-1},\;32.9\pm2.81\;L/kg,\;5.36\pm0.63\;L/hr,\;and\;186.5\pm20.5\;{\mu}g/ml{\cdot}hr$, respectively. The $\beta$, Vd, CLt, and AUC of vancomycin in ovarian cancer patients using the compartment model dependent analysis were $0.109\;0.008\;hr^{-1},\;41.5\pm3.01\;L/kg,\;4.58\pm0.57\;L/hr\;and\;218.3\pm22.9\;{\mu}g/ml{\cdot}hr$, respectively. There were significant differences (p<0.05,\;p<0.01) in $\beta$, Vd, CLt, and AUC between normal volunteers and ovarian cancer patients. The elimination rate constant (Kel), CLt, and AUC of vancomycin in normal volunteers using the compartment model independent analysis were $0.152\pm0.022\;hr^{-1},\;5.77\pm0.75\;L/hr,\;and\;173.2\pm22.5;{\mu}g/ml{\cdot}hr$, respectively. The Kel, CLt, and AUC of vancomycin in ovarian cancer patients using the compartment model independent analysis were $0.126\pm0.012\;hr^{-1},\;4.96\pm0.55\;L/hr,\;and\;201.7\pm25.6;{\mu}g/ml{\cdot}hr$, respectively. There were significant differences (p<0.05, p<0.01) in Kel, CLt, and AUC between normal volunteers and ovarian cancer patients. And also, there was significant difference (p<0.05) in Kel of vancomycin in ovarian cancer patients between the compartment model dependent and independen analysis. It is necessary for effective dosage regimen of vancomycin in ovarian cancer patient to use these population parameters.

Cefixime is an orally absorbed 3rd generation cephalosporin with a broad spectrum of activity against Gram-positive and Gram-negative bacteria and is highly resistant to $\beta-lactamase$ degradation. This study was carried out to evaluate the bioavailability of a new test drug of cefixime (100 mg/capsule) relative to the reference drug. The bioavailability was conducted on 20 healthy volunteers who received a single dose (400 mg) of the test and the reference drugs in the fasting state, in a randomized balanced 2-way crossover design. After dosing, serial blood samples were collected for a period of 12 hours. Plasma was analyzed for cefixime by a sensitive and validated HPLC assay. The major pharmacokinetic parameters $(AUC_{0-12hr},\;C_{max},\;T_{max})$ were calculated from the plasma concentration-time data of each volunteer. The $AUC_{0-12hr},\;C_{max}\;and\;T_{max}$ of the test drug were $36.91\pm11.85\;{\mu}g{\cdot}hr/ml,\;5.47\pm1.61\;{\mu}g/ml,\;and\;4.00\pm0.65\;hr,$ respectively, and those of the reference drug were $34.08\pm8.81\;{\mu}g{\cdot}hr/ml,\;5.25\pm1.40\;{\mu}g/ml,\;and\;4.20\pm0.62\;hr$, respectively. Mean differences of those parameters were 8.32, 4.29, and $4.76\%$, respectively, and the least significant differences at $\alpha$=0.05 for $AUC_{0-12hr},\;C_{max},\;T_{max}$ were 16.02, 13.78, and $11.76\%$, respectively. In conclusion, the test drug was bioequivalent with the reference drug.

The pharmacokinetics of atenolol (25 mg/kg, i.v.) in the folate-induced renal failure rabbits was studied. Renal failure was induced by the i.v. injection of folate (50, 100, and 200 mg/kg). At folate dose of 100 and 200 mg/kg, the serum creatinine concentration (Scr) and blood urea nitrogen (BUN) increased significantly compared with control rabbits. Plasma concentrations and AUC of atenolol increased significantly at folate dose of 100 and 200 mg/kg. The elimination rate constant $(K_{el})$ and total body clearance $(CL_t)$ of atenolol decreased significantly, and half-life ($t_{1/2}$) and mean residence time (MRT) of atenolol increased significantly at folate dose of 100 and 200 mg/kg. The serum creatinine concentration $(S_{cr})$ correlated well (p<0.05) with half-life $(t_{1/2})$ and elimination rate constant $(K_{el})$ of atenolol, as well as BUN with AUC and total body clearance $(CL_t)$ of atenolol.

Murine CD38 is a 42 kDa type II glycoprotein expressed on cell surface of both B and T lymphocytes. CD38 is a multifunctional enzyme that catalyzes the formation and hydrolysis of cyclic adenosine diphosphoribose (cADPR): ADP-ribosyl cyclase activity of CD38 catalyzes the formation of cADPR from NAD and cADPR hydrolase activity of CD38 catalyzes the hydrolysis of cADPR to ADP-ribose (ADPR). And also, CD38 has the catalytic activity of NAD glycohydrolase (NADase) which catalyzes the hydrolysis of catalyzes the formation and hydrolysis of cyclic adenosine diphosphoribose (cADPR): ADP-ribosyl cyclase activity of CD38 catalyzes the formation of cADPR from NAD to ADPR. In this study, we attempted to purify CD38 from mouse lymphocytes by using the immobilized anti-CD38 monoclonal antibody. The single step immuno-affinity column chromatography resulted in homogeneous purification, showing a single protein of 42 kDa on a SDS polyacrylamide gel. We have investigated the effects of various inhibitors on the enzyme activities of the purified CD38. Cibacron blue (0.5 mM) inhibited all three enzyme activities of CD38, NADase, ADP-ribosyl cyclase and cADPR hydrolase activities. ADPR (2 mM) showed inhibitory effect on both cADPR hydrolase activity and NADase, but not on ADP-ribosyl cyclase activity. However, ATP (2 mM) inhibited only cADPR hydrolase activity. $Zn^{2+}$ (1 mM) showed similar inhibitory effect as that of ADPR, but activated cyclase activity These results suggest that CD38 has three different catalytic activity domains which might be differentially regulated by their specific inhibitors.

A retrospective study was conducted to evaluate the appropriateness of total parenteral nutrition (TPN) for 200 hospitalized adult patients in Samsung Medical Center from January 1st in 1995 to June 31st in 1997. Standard criteria were modified and determined from those stated by AJHP (American Journal of Health System Pharmacy) and ASPEN (American Society of Parenteral and Enteral Nutrition). The justification for indications was appropriate in $35\%,\;44\%,\;and\;32\%$ of the patient's in 1995, 1996, and 1997, respectively, without significant improvement over the last two and half years. Before and during the administration of TPN, several monitoring indicators were well documented, and monitoring frequencies were increased over two and half years period. However, the majority of the monitoring indicators were not found in the standard criteria range of $90\%$. The monitoring indicators for electrolyte balance, $PO_4$ and Mg, were not measured appropriately and resulted in the complications which could have been prevented. The indicator for lipid tolerance, triglyceride and the indicator for hemorrhagic incidence, prothrombin time (PT), were not well documented in comparison with other indicators. The indicators for the improvement in nutritional status, albumin and total protein, were appropriate in $90\%$ of the patients. Determination of TPN formula was based on the laboratory data and chart reviews, and it was appropriate in $98\%$. But the administration of lipid and vitamin K for the prevention of essential fatty acid deficiency and hemorrhage, respectively, was not carried out appropriately when the administration of TPN was prolonged, lasting more than 7 days. When a patient returned to oral or enteral feeding, TPN was terminated. However, increase in albumin level or weight was rarely observed. In conclusion, healthcare professionals should all work as a team and active participation to provide optimized nutrition support for partners.

This study intended to investigate the pediatric drug dispensing practice at hospital pharmacies in order to provide the children with proper pharmaceutical care services. According to the study results, the most significant problem in dispensing pediatric drugs was that only a few pediatric drugs were supplied by the pharmaceutical companies in Korea. It was found that pediatric drugs like rifampicin, phenobarbital and theophylline should be produced in the form of syrup or powder, for the children to swallow drugs with ease. The study results also showed that only $35.5\%$ of the hospital pharmacists reviewed all the prescriptions issued by doctors. In most cases $(65.3\%)$ drug information was only provided when the patients asked to the pharmacists. The lack of working time and clinical information on the patients were found as major barriers. Thus in order to provide better pharmaceutical care services for the children, not only the pharmaceutical companies should pay attention to the production of pediatric drugs, but pharmacists should make every efforts on playing patient-oriented roles.

The stability of ceftriaxone sodium 100 mg/ml in the water for injection was tested at two temperature conditions (refrigerator and room temperature) and two storage containers (vitro and syringe). The stability of each sample was determined by high-performance liquid chromatography while storing for 5 days at room temperature and 27 days at refrigerator. The concentration of ceftriaxone sodium was 100 mg/ml which the hospital usually use as a filling preparation for I.V. push or Y-site injection. There was no significant difference between the storage in vials and syringes. There was no significant difference in the change of concentration until storing the reconstituted ceftriaxone sodium injection for 2 days at room temperature and 14 days at refrigerator. In conclusion, the ceftriaxone sodium 100 mg/ml in the water for injection can be stored in vial or syringe for 2 days at room temperature and 14 days at refrigerator after preparation.

The stability of cytarabine (manufactured by two pharmaceutical companies) in intravenous admixture and in plastic syringe was investigated. The admixures containing cytarabine 0.35, 8.6, and 17.1 mg/ml in $0.9\%\;NaCl\;or\;5\%$ D5W were placed in PVC bags or glass bottles, and the reconstituted cytarabine (50 mg/ml) was placed in plastic syringe. One ml aliquots were withdrawn immediately after each preparation and stored at $4^{\circ}C\;or\;24^{\circ}C$ for 1, 2, 4, 6, 8, 10, and 14 days unprotected from light. Each sample was tested for pH and visually inspected for precipitation and change in color. Cytarabine concentrations were measured using high-performance liquid chromatography. Neither precipitation nor change in color was noted, and there were no change in pH during 14 days of testing. The changes in cytarabine concentrations were less than $10\%$. In conclusion, cytarabine in IV admixture or plastic syringe was stable for at least 14 days at $4^{\circ}C\;and\;24^{\circ}C.$(Kor. J. Clin. Pharm. 1998; 8(1): 59-67)