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J-H Lim

Publications and source records attributed to J-H Lim.

8 recordsLinked to original sources
PubMed2007

Pharmacokinetics of florfenicol and its major metabolite, florfenicol amine, in rabbits.

The pharmacokinetics of florfenicol and its active metabolite florfenicol amine were investigated in rabbits after a single intravenous (i.v.) and oral (p.o.) administration of florfenicol at 20 mg/kg bodyweight. The plasma concentrations of florfenicol and florfenicol amine were determined simultaneously by an LC/MS method. After i.v. injection, the terminal half-life (t(1/2lambdaz)), steady-state volume of distribution, total body clearance and mean residence time of florfenicol were 0.90 +/- 0.20 h, 0.94 +/- 0.19 L/kg, 0.63 +/- 0.06 L/h/kg and 1.50 +/- 0.34 h respectively. The peak concentrations (C(max)) of florfenicol (7.96 +/- 2.75 microg/mL) after p.o. administration were observed at 0.90 +/- 0.38 h. The t(1/2lambdaz) and p.o. bioavailability of florfenicol were 1.42 +/- 0.56 h and 76.23 +/- 12.02% respectively. Florfenicol amine was detected in all rabbits after i.v. and p.o. administration. After i.v. and p.o. administration of florfenicol, the observed Cmax values of florfenicol amine (5.06 +/- 1.79 and 3.38 +/- 0.97 microg/mL) were reached at 0.88 +/- 0.78 and 2.10 +/- 1.08 h respectively. Florfenicol amine was eliminated with an elimination half-life of 1.84 +/- 0.17 and 2.35 +/- 0.94 h after i.v. and p.o. administration respectively.

Administration, Oral↗
PubMed2006

Pharmacokinetics of florfenicol and its metabolite, florfenicol amine, in the Korean catfish (Silurus asotus).

The pharmacokinetics of florfenicol and its metabolite, florfenicol amine, was investigated after its intravenous (i.v.) and oral (p.o.) administration of 20 mg/kg of body weight in Korean catfish (Silurus asotus). After i.v. florfenicol injection (as a bolus), the terminal half-life (t(1/2)), the volume of distribution at steady state (V(dss)), and total body clearance were 11.12 +/- 1.06 h, 1.09 +/- 0.09 L/kg and 0.07 +/- 0.01 L x kg/h respectively. After p.o. administration of florfenicol, the t(1/2), C(max), t(max) and oral bioavailability (F) were 15.69 +/- 2.59 h, 9.59 +/- 0.36 microg/mL, 8 h and 92.61 +/- 10.1% respectively. Florfenicol amine, an active metabolite of florfenicol, was detected in all fish. After i.v. and p.o. administration of florfenicol, the observed C(max) values of florfenicol amine (3.91 +/- 0.69 and 3.57 +/- 0.65 mg/L) were reached at 0.5 and 7.33 +/- 1.15 h. The mean metabolic rate of florfenicol amine after i.v. and p.o. administration was 0.4 and 0.5 respectively.

Administration, Oral↗
PubMed2006

Pharmacokinetics of enrofloxacin in Korean catfish (Silurus asotus).

The objective of this study was to evaluate the pharmacokinetic profile of enrofloxacin and its active metabolite, ciprofloxacin, in Korean catfish after intravenous and oral administrations. Enrofloxacin was administered to Korean catfish by a single intravenous and oral administrations at the dose of 10 mg/kg body weight. The plasma concentrations from intravenous and oral administrations of enrofloxacin were determined by LC/MS. Pharmacokinetic parameters from both routes were described to have a two-compartmental model. After intravenous and oral administrations of enrofloxacin, the elimination half-lives (t(1/2,beta)), area under the drug concentration-time curves (AUC), oral bioavailability (F) were 17.44 +/- 4.66 h and 34.13 +/- 11.50 h, 48.1 +/- 15.7 microgxh/mL and 27.3 +/- 12.4 microgxh/mL, and 64.59 +/- 4.58% respectively. The 3.44 +/- 0.81 h maximum concentration (C(max)) of 1.2 +/- 0.2 microg/mL. Ciprofloxacin, an active metabolite of enrofloxacin, was detected at all the determined time-points from 0.25 to 72 h, with the C(max) of 0.17 +/- 0.08 microg/mL for intravenous dose. After oral administration, ciprofloxacin was detected at all the time-points except 0.25 h, with the C(max) of 0.03 +/- 0.01 microg/mL at 6.67 +/- 2.31 h. Ciprofloxacin was eliminated with terminal half-life t(1/2,beta) of 52.08 +/- 17.34 h for intravenous administration and 52.43 +/- 22.37 h for oral administration.

Administration, Oral↗
PubMed2006

Pharmacokinetic/pharmacodynamic modelling of roxithromycin for the inhibitory effect of tumour necrosis factor-alpha and interleukin-6 production in dogs.

The objective of the present study was to determine and characterize the relationship between the plasma concentration of roxithromycin, and its inhibitory effect on cytokine production, in order to predict its possible clinical relevance. Six healthy beagle dogs received a single intravenous dose of 20-mg roxithromycin per kg body weight. Blood samples were obtained at different time points. The plasma was analysed with respect to roxithromycin, tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). The concentration-effect relationship was explored by modelling the data using two compartmental model and an indirect response model with an E(max) concentration-effect relationship. The estimated pharmacokinetic parameters (geometric mean) were as follows: V(c) = 2.59 l; k(10) = 0.08/h; k(12) = 0.26/h; k(21) = 0.40/h. The pharmacodynamic parameters (geometric mean) for the inhibitory effect on cytokine production induced by heat-killed Staphylococcus aureus (HKSA) were for TNF-alpha (k(in) = 1.42 microg/h; k(out) = 1.10 microg/h; EC(50) > 5.69 mg/l) and for IL-6 (k(in) = 2.31 microg/h; k(out) = 2.04 microg/h; EC(50) = 21.07 mg/l) production, respectively. The inhibitory effect of roxithromycin on production can be adequately described by the indirect response model with an E(max) concentration-effect relationship.

Animals↗
PubMed2005

Development of in-situ hybridization for the detection of Mycoplasma haemosuis (Eperythrozoon suis) in formalin-fixed, paraffin wax-embedded tissues from experimentally infected splenectomized pigs.

Mycoplasma haemosuis DNA was detected in experimentally infected splenectomized pigs by in-situ hybridization (ISH) with a nonradioactive digoxigenin-labelled DNA probe. An 839 base pair DNA probe targeting a 16S rRNA gene was generated by the polymerase chain reaction. Eight 6-week-old pigs were inoculated intraperitoneally with 6 ml of M. haemosuis-infected pig blood and eight negative control pigs were inoculated intraperitoneally with 6 ml of M. haemosuis-free blood. Two pigs from each group were killed for examination at 3, 7, 15 and 30 days post-inoculation (dpi). Red blood cells infected with M. haemosuis were first detected by light microscopy at 3 to 7 dpi. No M. haemosuis was observed in negative control pigs. Hybridization signals were evident in blood from the infected pigs at 3 dpi. The ISH method developed in this study was useful for the detection of M. haemosuis DNA in formalin-fixed, paraffin wax-embedded tissues and may be valuable for studying the pathogenesis of M. haemosuis infection.

Animals↗
PubMed2003

Monocyte chemotactic protein-1 production in patients with active pulmonary tuberculosis and tuberculous pleurisy.

OBJECTIVE: The role of monocyte chemotactic protein (MCP)-1 in human pulmonary and pleural tuberculosis (TB) was assessed by examining its production in clinical samples from patients with active pulmonary TB and tuberculous pleurisy (TBP). METHODS: Serum was obtained from 26 active pulmonary TB patients [14 early TB (E-TB), and 12 chronic refractory TB (CR-TB)] and 15 healthy tuberculin reactors (HTRs). The monocytes and peripheral blood mononuclear cells (PBMCs) were separated and stimulated with purified protein derivatives (PPD) or the 30-kDa antigen of Mycobacterium tuberculosis. Pleural exudates were isolated from 25 patients with TBP and 24 non-TBP patients [malignancy and congestive heart failure (CHF)]. The MCP-1 levels were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: In sera, the MCP-1 levels of TB patients were similar to those of HTRs. For monocytes, CR-TB patients spontaneously expressed more MCP-1, compared with HTRs and E-TB patients. In addition, MCP-1 production of PPD- or 30-kDa antigen-stimulated monocytes was significantly elevated in CR-TB patients than that from E-TB. Interestingly, the E-TB patients had significantly depressed MCP-1 production by PBMCs in response to PPD or 30-kDa, compared with HTRs and CR-TB patients. In pleural effusions, MCP-1 levels were significantly higher in patients with TBP than in patients with CHF, but lower than in malignant effusions. CONCLUSIONS: The data suggest that MCP-1 production is not uniquely elevated systemically in TB patients, although MCP-1 production might be elevated by monocytes in the chronic phase of TB or with a local pleural infection.

Adult↗
PubMed2003

The production of tumour necrosis factor-alpha is decreased in peripheral blood mononuclear cells from multidrug-resistant tuberculosis patients following stimulation with the 30-kDa antigen of Mycobacterium tuberculosis.

The clearance of intracellular bacteria requires the appropriate induction of proinflammatory cytokines and chemokines to recruit macrophages and T cells to the site of infection. In this study, we investigated the production of tumour necrosis factor (TNF)-alpha, interleukin (IL)-8 and interferon (IFN)-gamma by the peripheral blood mononuclear cells (PBMC) of patients with multidrug-resistant tuberculosis (MDR-TB) in response to in vitro stimulation with the 30-kDa antigen of Mycobacterium tuberculosis. The results were compared with those from cases of newly diagnosed TB (N-TB) and TB with treatment failure (TF-TB), and healthy tuberculin reactors (HTR). The most significantly depressed TNF-alpha levels were found in MDR-TB patients. IFN-gamma production was depressed significantly in all groups of TB patients compared with the HTR group. TNF-alpha secretion in response to the 30-kDa antigen was unchanged by coculturing with recombinant human interferon (rhIFN)-gamma, and was increased dramatically following IL-10 neutralization with an anti-human IL-10 antibody. The IL-8 levels were depressed significantly in MDR-TB patients compared with N-TB patients, but were similar to the IL-8 levels in TF-TB patients. Furthermore, rhTNF-alpha directly increased IL-8 secretion, and neutralizing antibody to TNF-alpha inhibited IL-8 production by the PBMC of MDR-TB patients that were stimulated with the 30-kDa antigen. Taken together, these data suggest that the PBMC of MDR-TB patients typically show TNF-alpha depression in response to the 30-kDa antigen, and this effect is modulated by IL-10. In addition, we highlight the role of TNF-alpha in IL-8 secretion in MDR-TB patients.

Antigens, Bacterial↗