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Biomedical subjects

S H Jin

Publications and source records attributed to S H Jin.

At least 19 recordsLinked to original sources
PubMed2006

Effect of basiliximab on renal allograft rejection within 1 year after transplantation.

Basiliximab is widely used in clinical practice for initial immunosuppressive treatment of renal transplant recipients, seeking to reduce the incidence of acute rejection episodes without adverse events. This retrospective study included 123 renal allograft recipients transplanted at a single center. All were followed for longer than 1 year after transplantation and treated with calcineurin inhibitor and steroid (methylprednisolone) for prophylactic immunosuppression, but basiliximab and mycophenolate mofetil were optional. We compared the outcomes of renal transplant recipients who were versus treated were not with basiliximab as initial immunosuppressive therapy. Basiliximab was used for initial immunosuppression in 42 patients. Their maintenance immunosuppressive treatment included triple (n = 44) or double (n = 79) regimens, including a calcineurin inhibitor (cyclosporine [n = 87] or tacrolimus [n = 36]), methylprednisolone with or without mycophenolate mofetil. Twenty-six (21.1%) patients had a rejection episode within 1 year after transplantation and 22 (17.9%) had infections. Within the first year after transplantation the patients who were treated with basiliximab showed fewer rejection episodes (n = 6, 14.3%) than the patients without this therapy (n = 20, 24.7%), which was not statistically significant (P = .245). However, basiliximab significantly affected the occurrence of rejection episodes among the double immunosuppressive regimen group (P = .006), but not the triple regimen group (P = .098) without an impact on infection episodes (P value of double, triple = .291, .414) within 1 year after transplantation. We concluded that basiliximab was more useful for the recipients treated with double immunosuppression with a calcineurin inhibitor and steroid than for those on a triple regimen including mycophenolate mofetil.

Adult↗
PubMed2004

Characteristics of electrically evoked potentials in patients with auditory neuropathy/auditory dys-synchrony.

The primary goal of this study was to compare the characteristics of the post-implant evoked potentials with preimplant evoked potentials in patients with auditory neuropathy (AN) or dys-synchrony. AN is typically characterized by sensorineural hearing loss, reduced speech perception, abnormal temporal processing, and unusual patterns of results with various objective audiological tests. In some cases, these patients may be appropriate candidates for a cochlear implant. In this article, we highlight evoked potential findings in two children diagnosed with AN who were provided with multichannel cochlear implants. Preoperative, interoperative and postoperative evoked potential measures show that the restoration of neural synchrony may occur at multiple levels of the auditory pathways in patients with AN when appropriate diagnostic tests, cochlear implantation and rehabilitation are provided.

Acoustic Impedance Tests↗
PubMed2001

Prolonged activation of mitogen-activated protein kinases during NSAID-induced apoptosis in HT-29 colon cancer cells.

The mechanisms of the antineoplastic effect of nonsteroidal anti-inflammatory drugs (NSAIDs) still are unknown, but the induction of apoptosis is one of the possible mechanisms. We attempted to demonstrate the role of mitogen-activated protein (MAP) kinases, generally considered to be important mediators of proliferative and apoptotic signals, in NSAID-induced colon cancer cell apoptosis. Apoptosis was detected by demonstration of DNA fragmentation in agarose gel electrophoresis. Cell death was assessed by trypan blue dye exclusion method. MAP kinase activation was assessed by Western blot using phosphospecific antibodies to MAP kinases. Kinase assay using activating transcription factor-2 (ATF-2) fusion protein as a substrate was also performed for measuring p38 MAP kinase activity. For the inhibition of p38 MAP kinase, pyridinylimidazole compound (SB203580) was utilized. Caspase-3 activity was measured using the tetrapeptide fluorogenic substrate Ac-DEVD-AMC. Treatment of HT-29 cells with NSAIDs results in time- and dose-dependent induction of apoptosis, accompanied by sustained activation of all three MAP kinase subfamilies. The SB203580, a p38 MAP kinase inhibitor, reduced indomethacin-induced cell death by 43%, while PD098059, a MAPK/ERK kinase (MEK)1 inhibitor, did not affect cell death. p38 MAP kinase and caspase-3 activation were not significantly interlinked in indomethacin-induced apoptosis. From these results, we conclude that NSAIDs can induce prolonged activation of MAP kinases in colon cancer cells and that, of these, p38 MAP kinase may play a partial but significant role in indomethacin-induced apoptosis.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2001

Use of dopamine-beta-hydroxylase-deficient mice to determine the role of norepinephrine in the mechanism of action of antidepressant drugs.

Norepinephrine (NE) is thought to play an important role in the pathophysiology of depression, and in the mechanism of action of antidepressant compounds. Previously, we created mice that are unable to synthesize NE and epinephrine due to targeted disruption of the dopamine-beta-hydroxylase gene (Dbh). To specifically test the role of NE in mediating behavioral changes elicited by antidepressants, these mice were examined in the forced swim test. There was no difference in baseline immobility scores in the forced swim test between Dbh(+/-) mice, which have normal levels of NE, and Dbh(-/-) mice. However, the Dbh(-/-) mice failed to demonstrate antidepressant-like behavioral effects following the administration of several classes of antidepressants. These included the NE reuptake inhibitors desipramine and reboxetine, the monoamine oxidase inhibitor pargyline, and the atypical antidepressant bupropion. In addition, desipramine significantly reduced immobility in the Dbh(-/-) mice following pretreatment with the synthetic NE precursor L-threo-3,4-dihydroxyphenylserine, but not saline. Biochemical studies showed that there was no significant difference in the regional brain levels of NE transporter immunoreactivity or monoamine oxidase activity, the primary targets for most of the compounds examined. Taken together, these data show that the use of mice that lack endogenous NE may be an important strategy for unraveling the role of NE in tests sensitive to the effects of various psychotherapeutic agents.

Animals↗
PubMed2000

Differential expression of protein kinase C subtypes during ginsenoside Rh2-lnduced apoptosis in SK-N-BE(2) and C6Bu-1 cells.

We examined the modulation of protein kinase C (PKC) subtypes during apoptosis induced by ginsenoside Rh2 (G-Rh2) in human neuroblastoma SK-N-BE(2) and rat glioma C6Bu-1 cells. Apoptosis induced by G-Rh2 in both cell lines was confirmed, as indicated by DNA fragmentation and in situ strand breaks, and characteristic morphological changes. During apoptosis induced by G-Rh2 in SK-N-BE(2) cells, PKC subtypes alpha, beta and gamma were progressively increased with prolonged treatment, whereas PKC delta increased transiently at 3 and 6 h and PKC epsilon was gradually down-regulated after 6 h following the treatment. On the other hand, PKC subtype zeta markedly increased at 24 h when maximal apoptosis was achieved. In C6Bu-1 cells, no significant changes in PKC subtypes alpha, gamma, delta, epsilon and zeta were observed during apoptosis induced by G-Rh2. These results suggest the evidence for a possible role of PKC subtype in apoptosis induced by G-Rh2 in SK-N-BE(2) cells but not in C6Bu-1 cells, and raise the possibility that G-Rh2 may induce apoptosis via different pathways interacting with or without PKC in different cell types.

Animals↗
PubMed1999

Ginsenoside Rh2 induces apoptosis independently of Bcl-2, Bcl-xL, or Bax in C6Bu-1 cells.

In ginsenoside Rh2-treated rat glioma C6Bu-1 cells, apoptotic morphological changes, such as cell shrinkage, chromatin condensation and pyknosis were confirmed by means of electron microscopy. To evaluate whether induction of apoptosis by ginsenoside Rh2 is mediated by the members of Bcl-2 family, we first established C6Bu-1 cells overexpressing Bcl-2. It was demonstrated that the expression of Bcl-2, Bcl-xL and Bax was not altered in ginsenoside Rh2-treated C6Bu-1 cells. Bcl-2 overexpressing C6Bu-1 cells failed to prevent from ginsenoside Rh2-induced cell death. These results suggest the existence of other apoptotic pathway that requires induction of apoptosis by ginsenoside Rh2 rather than the pathway through Bcl-2, Bcl-xL or Bax in C6Bu-1 cells.

Animals↗
PubMed1999

Korean red ginseng saponins with low ratios of protopanaxadiol and protopanaxatriol saponin improve scopolamine-induced learning disability and spatial working memory in mice.

The effects of two ginseng saponins having a different ratio of protopanaxadiol (PD) and protopanaxatriol saponins (PT) on the learning impairment induced by scopolamine, and learning and memory in mice were investigated in a passive avoidance task and a Morris water maze task. The ratio of PD and PT was 1.24 and 1.46, respectively. Before training, the ginseng saponins were administered intraperitoneally at doses of 50 and 100 mg/kg. The two saponins improved the scopolamine-induced learning impairment at different dosages in mice, 50 and 100 mg/kg, respectively. However, the two saponins did not show a favorable effect on learning and memory in normal mice. Korean red ginseng saponin with a low PD/PT ratio had an improving effect on spatial working memory, but the saponin with a high PD/PT ratio did not. This finding suggests that the PD/PT ratio of the ginseng saponins may be an important factor in the pharmacological role of red ginseng as a medicinal herb.

Animals↗
PubMed1997

New scoring system using tumor markers in diagnosing patients with moderate pericardial effusions.

We performed diagnostic and therapeutic pericardiostomy with drainage and biopsy in 51 patients with moderate to large pericardial effusions of different etiologies from August 1991 to July 1995. Patients were divided into 4 groups (group 1, tuberculous pericarditis; group 2, suspected tuberculous pericarditis; group 3, acute pericarditis; group 4, malignancy). The pericardial fluid adenosine deaminase level in tuberculosis (87 +/- 10 U/l) was significantly higher than that in malignancy or acute pericarditis (21 +/- 4 U/l, 23 +/- 7 U/l, respectively) (P = 0.0001). The mean pericardial fluid carcinoembryonic antigen level (1.8 +/- 0.3 ng/ml) in benign disease was significantly lower than that (170.7 +/- 46.4 ng/ml) in malignant disease (P = 0.0001). Follow-up study has been done. With a new scoring system (each score 1 for adenosine deaminase > or = 40 U/l, or carcinoembryonic antigen < or = 5 ng/ml) in 25 patients since November 1993, we could diagnose 5 among 7 patients (71%) with tuberculosis, 11 among 13 patients (85%) with malignancy (adenosine deaminase < or = 40 U/l, or carcinoembryonic antigen > or = 5 ng/ml) and 5 among 5 patients (100%) with acute pericarditis (adenosine deaminase < or = 40 U/l, or carcinoembryonic antigen < or = 5 ng/ml), respectively. Our long-term follow-up study suggests that with the new scoring system we can decrease complications or avoid unnecessary procedures or treatments of patients.

Adenosine Deaminase↗
PubMed1997

[Studies on sultamicillin hydrolysis].

Sultamicillin is an oral mutual pro-drug composed of double esters of formaldehyde hydrate in which one of the hydroxyl groups is esterified with ampicillin and the other with sulbactam. It is hydrolyzed fast in neutral or weakly alkaline condition. When hydrolyzed, it forms ampicillin and hydroxylmethyl sulbactam or sulbactam and hydroxylmethyl ampicillin by different routes. Usually, the former has priority as the two ester bonds have different activities. The ratio of ampicillin to sulbactam in the products is about 3:1. Both the hydroxylmethyl sulbactam and the hydroxylmethyl ampicillin can be further catalyzed by esterase to produce formaldehyde.

Ampicillin↗
PubMed1995

Antigenic properties and immunoelectron microscopic localization of Mycobacterium fortuitum beta-lactamase.

Mycobacterium fortuitum is a fast-growing Mycobacterium species which produces a beta-lactamase involved in the intrinsic resistance of the microorganism to beta-lactam antibiotics. An anti-beta-lactamase serum against the purified enzyme was raised in rabbits. Antibody binding was specific for native beta-lactamase, and enzyme activity was partially inhibited by the serum; furthermore, cross-reactions with denatured class A beta-lactamases were observed. This serum was used as a probe in immunogold labeling for the localization of the cell-bound beta-lactamase in both the low-level producer ATCC 19542 (parental strain) and the overproducer mutant D316. By the combination of preembedding immunogold labeling and replica technique, it was shown that the beta-lactamase was uniformly distributed on the whole external cell surface, where it appeared to be associated with a Tween 80-removable capsule-like material. Compared with the parental strain, a much higher level of expression of surface enzyme was observed in strain D316. Surface labeling was more intense in the stationary phase of growth than in exponentially growing cells. The data obtained are interpreted in the context of the intrinsic resistance of M. fortuitum to beta-lactam antibiotics.

Antigens, Bacterial↗
PubMed1994

Ruptured aneurysm of the sinus of Valsalva in a patient with Behçet's disease.

The vast majority of sinus of Valsalva aneurysm originated from a localized congenital defect of the aortic media and less frequently from infections or degenerative processes affecting the aortic wall. But aneurysm of sinus of Valsalva has not been reported up to the present in a patient with Behçet's disease. We report a 39-year-old woman presenting ruptured aneurysm of the sinus of Valsalva and Behçet's disease.

Adult↗
PubMed1994

Adenosine deaminase and carcinoembryonic antigen in pericardial effusion diagnosis, especially in suspected tuberculous pericarditis.

BACKGROUND: Adenosine deaminase (ADA) and carcinoembryonic antigen (CEA) have been measured in pleural fluid to help distinguish malignant from benign effusions, especially in tuberculous pleurisy. We investigated ADA and CEA levels in patients with moderate to large pericardial effusions of different etiologies. METHODS AND RESULTS: We performed diagnostic and therapeutic pericardiostomy with drainage and biopsy. We measured ADA and CEA levels in the pericardial fluid in 26 patients with moderate to large pericardial effusion and 19 control patients. Patients were included in a prospective protocol from August 1991 to August 1993. Patients were grouped as follows: group 1, 9 patients with tuberculous pericarditis (TP) confirmed by bacteriologic culture or histology of pericardial biopsy; group 2, 5 patients with clinically strongly suspected TP; group 3, 12 patients with malignancy (8) and acute pericarditis (4); group 4, 19 control patients without pericardial disease. We treated patients with TP with isoniazid, rifampin, and either streptomycin or ethambutol for 12 months and pyrazinamide for 2 months. We observed for symptoms and signs of recurrent pericarditis or constrictive pericarditis on follow-up. In group 1 the ADA activity was significantly higher (101 +/- 14 U/L) than that in group 3 (22 +/- 5 U/L) or that in group 4 (17 +/- 2 U/L) (P < .05). There was no significant difference between ADA activity in group 1 (101 +/- 14 U/L) and that in group 2 (100 +/- 26 U/L). With a cutoff value for ADA activity of 40 U/L, sensitivity was 93% and specificity 97% in the diagnosis of TP. In benign diseases, the CEA level was significantly lower (1.0 +/- 0.3 ng/mL) than that in malignant diseases (135.1 +/- 79.7 ng/mL) (P < .05). With a cutoff value for CEA level of 5 ng/mL, sensitivity was 75% and specificity 100% in the diagnosis of malignant pericarditis. Follow-up study (mean, 12.9, 19.8, and 11.8 months in groups 1, 2, and 3, respectively, showed no symptoms or signs of constrictive pericarditis, except for 1 patient. CONCLUSIONS: Pericardial fluid ADA and CEA are useful for the differential diagnosis of pericardial effusion of various causes. They also have great value in early diagnosis of TP, particularly when the results of other clinical and laboratory tests are negative.

Adenosine Deaminase↗
PubMed1994

Detection of dystrophin gene deletion in Chinese Duchenne/Becker muscular dystrophy patients utilizing multiplex polymerase chain reaction.

Multiplex PCR was utilized to detect deletions at the hot spot regions of dystrophin gene. Thirty-four cases of DMD and 7 cases of BMD, based on their clinical manifestations, were examined. Eight normal male adults were included as control. Eleven DNA fragments coding the exons 1, 3, 6, 8, 13, 17, 43, 47, 50, 52 and 60 were chosen and primers were prepared with oligonucleotide synthesizer. Multiplex PCR was performed under the condition of 94 degrees C 1 minute for denaturation, 65 degrees C 3 minutes for annealing, 72 degrees C 3 minutes for extension. Thirty cycles were followed by a last cycle with 7 minutes extension. Clinically, there were no significant differences between Chinese patients and those reported in other areas except the low rate of positive family history (32%). The results from multiplex PCR showed that 15 cases (37%), 11 DMD and 4 BMD, proved to have deletions in the exons studied; 1 located at exons 6 and 8, 1 at exon 8, 1 at exons 8, 13 and 17, 1 at exons 13 and 17, 1 at exon 17, 3 at exon 43, 1 at exon 50, and 3 at exons 50 and 52, after false negatives were excluded. No difference in size or location was noticed between DMD and BMD in the sample-limited result.

Adult↗
PubMed1992

Resistance to beta-lactams in Mycobacterium fortuitum.

It is widely assumed that the high level of intrinsic resistance to beta-lactam antibiotics exhibited by mycobacteria results from the combination of factors including permeability to the drugs, beta-lactamase production, and affinity for penicillin-binding proteins (PBPs). We conducted an evaluation of the second and third factors by isolating nitrosoguanidine-induced mutants from the beta-lactamase-producing strain Mycobacterium fortuitum ATCC 19542 that displayed either elevated or reduced resistance to various beta-lactam antibiotics. The mutants studied included D1 (a beta-lactamase producer with high penicillin resistance), gamma 27 (a low-level beta-lactamase producer with low penicillin resistance), and D316 (a high-level beta-lactamase producer with high penicillin resistance). In all strains examined, four major PBPs, named 1, 2a, 2b, and 3, with apparent molecular weights of 102,000, 90,000, 87,000, and 50,000, respectively, were found. The MICs of various beta-lactams toward ATCC 19542 and its mutants were considered in the context of beta-lactamase production, the quantity of PBPs synthesized, and their affinities for beta-lactam antibiotics. The data obtained show that beta-lactamase production is likely to be an important factor in the expression of resistance by clinical isolates and that PBP alterations can contribute to resistance at least in laboratory-derived mutants.

Anti-Bacterial Agents↗
PubMed1992

Activity of antimicrobial agents against Mycobacterium avium-intracellulare complex (MAC) strains isolated in Italy from AIDS-patients.

Twenty-five strains of Mycobacterium avium-intracellulare (MAC) isolated from acquired immunodeficiency syndrome (AIDS) patients in three medical centres in Italy have been studied. Serotyping performed on eighteen strains showed various serovars within either M. avium or M. intracellulare serotypes and with serovars 1 and 21 being the most prevalent (four strains for each serovar). Among fourteen drugs used for testing the antibiotic sensitivity, rifapentine, rifabutin and clofazimine showed to have the best in vitro activity. In an ex vivo model of infection using peritoneal resting macrophages from the C57BL/6 mouse, the intracellular viability of a strain of M. avium (strain 489, serovar 3) was reduced by clofazimine, amikacin, ciprofloxacin, rifabutin and clarithromycin (99, 98, 93, 89 and 69%, respectively), thus indicating for clofazimine a good correlation between in vitro and ex vivo activity.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Beta-lactamase of Mycobacterium fortuitum: kinetics of production and relationship with resistance to beta-lactam antibiotics.

The kinetics of both intracellular and extracellular beta-lactamase production and the relationship between extracellular enzyme and in vitro susceptibility of Mycobacterium fortuitum to beta-lactam antibiotics have been studied. To this end we used a panel of stable nitrosoguanidine-induced mutants of M. fortuitum derived from the parental strain ATCC 19542 and differing in beta-lactamase production from 0.0001 to 278 U/liter in Mueller-Hinton broth. For overproducers of beta-lactamase (mutants A188, B180, C207, D316, and E31), MICs of benzylpenicillin, amoxicillin, ampicillin, and cephaloridine progressively increased with the amount of enzyme released into the medium, whereas MICs of imipenem and cefoxitin did not. The resistance of the mutants to amoxicillin was reduced up to 32-fold by clavulanic acid, whereas that to ampicillin was reduced 8-fold by sulbactam. These data suggest that the enzyme participated in the mechanisms of resistance to the beta-lactam antibiotics. However, for a mutant of M. fortuitum (gamma 27) with virtually nonexistent beta-lactamase production, the antibiotics still had relatively high MICs (for instance, benzylpenicillin and cephaloridine had MICs of 64 and 32 micrograms/ml, respectively). This suggests that, aside from beta-lactamase production, other mechanisms such as cell wall permeability and/or affinity for penicillin-binding proteins could coexist in M. fortuitum and explain its natural resistance to beta-lactam antibiotics.

Anti-Bacterial Agents↗