Biomedical subjects

K Jin

Publications and source records attributed to K Jin.

At least 37 records · Page 2Linked to original sources

PubMed2001

[Human telomerase RNA (hTR) expression in lung cancer in the Gejiu and Xuanwei regions of Yunnan].

OBJECTIVE: To investigate the correlation between the expression of hTR in and the pathogenesis of lung cancer in Gejiu and Xuanwei regions of Yunnan province. METHODS: By use of in situ hybridization, the expression of hTR gene was observed in 81 cases of lung cancer tissues including 24 cases of Gejiu Tin miners (GTM), 36 cases of Xuanwei farmers (XF) and 21 cases of other regions. RESULTS: hTR was detected in 65.4% (53/81) of the lung cancer cases. The positive rate of hTR in GTM, XF and other regions was 66.7% (16/24), 58.3% (21/36) and 76.2% (16/21) respectively. Positive hTR expression was not found in normal bronchial and alveolar epithelia, but was found in highly proliferating type II alveolar epithelial cells adjacent to the carcinoma (12.3%, 10/81). No significant difference was observed with regard to the positive rate of hTR expression among three different regions. There was no statistically significant correlation between the expression of hTR, the patients' sex, age and the differentiation degree of the tumor, but the expression of hTR was correlated with histological type and lymph node metastasis (P < 0.05). CONCLUSION: The expression of hTR is a prevailing event in lung cancer and therefore can be used as an indicator of lung malignancy.

Adult↗

PubMed2001

[p53 mutation in lung cancer in Gejiu and Xuanwei regions of Yunnan Province].

OBJECTIVE: To incidence rates of lung cancer among tin miners in Gejiu and among peasants in Xuanwei are higher than the average incidence rate in Yunnan Province, and the causes of the disease in these two regions have been preliminarily clarified. This study was directed to the molecular biological basis of its pathogenesis. METHODS: Twenty-six specimens of the lung cancers of Gejiu tin miners(GTM) and 15 ones of Xuanwei peasants (XP) were examined by single-strand conformation polymorphism analysis of polymerase chain reaction products. RESULTS: Using PCR primers for the most highly conserved region of the p53 including exons 5-8, we have identified p53 mutations in 13 lung cancer tumor DNA samples of GTM and in 4 ones of XP. Nucleotide sequencing of one of the exon 5 mutations of GTM indicated that there was a C to T transition, which resulted in substitution of Val for Ala at amino acid 135, and there was an AAC to TTC transertion in the exon 7 of XP, which resulted in substitution of Phe for Asn at amino acid 247. CONCLUSION: p53 mutation is a frequent incident in lung cancer of GTM and XP, and two new mutation sites were found in p53 gene, which have not been reported before now. There was no statistically significant correlation between the detection of p53 mutation and the patient's age, sex, mining history and histologic type of the cancer.

China↗

PubMed2001

[A study on the state of cell proliferation and apoptosis in human middle ear cholesteatoma].

OBJECTIVE: To study the state of proliferation and apoptotic cell death in cholesteatoma. METHOD: 20 cholesteatoma samples and 10 normal external ear canal skin samples were studied with immunohistochemical SABC technique and TUNEL technique. RESULT: Immunohistochemical analysis using a monoclonal antibody to proliferation cell nuclear antigen (PCNA) demonstrated the presence of proliferating cell in the basal cell layer of normal external ear canal skin, whereas in the cholesteatoma tissue samples larger numbers of proliferation cell nuclear antigen-positive cells were also observed in the prickle and granular cell layers. The PCNA labeling index and the mean optical density were (10.52 +/- 2.65)% and (0.1340 +/- 0.0363) in normal external ear canal skin samples and (36.91 +/- 22.77)% and (0.2427 +/- 0.0586) in cholesteatoma tissue samples. In cholesteatoma tissue samples and normal external ear canal skin samples, apoptotic cell were observed in the prickle and granular cell layers. The apoptotic indexers were (27.50 +/- 12.50)% in cholesteatoma tissue samples and (9.96 +/- 3.86)% in skin samples. CONCLUSION: The results demonstrate the rates of apoptotic cell death and cell proliferation in cholesteatoma are higher than those in normal skin. Increased cell proliferation and cell death will contribute to increased keratous debris.

Adult↗

PubMed2001

[The study of TNF-alpha destructive action to the bone in human middle cholesteatoma].

OBJECTIVE: To study the expression of TNF-alpha in the cholesteatoma and elucidate the role of TNF-alpha in the destruction of bone. METHOD: All samples (5 microns paraffin sections) from 25 cholesteatoma cases and 10 normal cases were examined by immunohistochemical SABC method and analysed by computer image. RESULT: In 25 cholesteatoma cases, TNF-alpha expressed in the cytoplasm of the full epithelial tissue cells, subcutaneous inflammatory cells and fibroblast. In contrast, the normal cases, there were 6 cases week positive, 4 cases negative. The results of the computer image quantitative analysis system showed that the mean optical density of TNF-alpha was 0.1326 +/- 0.0022 in the cholesteatoma epithelial tissue and 0.0868 +/- 0.0014 in normal skin epithelial tissue respectively, both of which had significantly differentiation (P < 0.05). CONCLUSION: TNF-alpha may be a factor of the destruction of bone of cholesteatoma.

Adolescent↗

PubMed2000

Expression of the RNA-binding protein TIAR is increased in neurons after ischemic cerebral injury.

T-cell restricted intracellular antigen-related protein (TIAR) is an RNA recognition motif-type RNA-binding protein that has been implicated in the apoptotic death of T-lymphocytes and retinal pigment epithelial cells. Western blots prepared with a monoclonal antibody against TIAR showed expression in normal rat hippocampus, and induction by 15 min of global cerebral ischemia. This increased expression was evident at 8 hr after ischemia and maximal at 24 hr, whereas expression at 72 hr was reduced below basal levels. Expression of TIAR protein was also increased in parietal cortex 6 and 24 hr after 90 min of focal cerebral ischemia induced by middle cerebral artery (MCA) occlusion, as well as in cultured cortical neurons and astroglia after exposure to hypoxia in vitro. Immunocytochemistry showed that increased expression of TIAR occurred mainly in the CA1 sector of hippocampus 24 hr after global ischemia, and in cortical and striatal neurons 24 hr after 20 or 90 min of focal ischemia. Double-labeling studies showed that TIAR protein expression was co-localized with DNA damage in neuronal cells. The findings suggest that TIAR may be involved in neuronal cell death after cerebral ischemic injury.

Animals↗

PubMed2000

Increased expression of apoptosis-linked gene 2 (ALG2) in the rat brain after temporary focal cerebral ischemia.

Calcium is an important mediator of programmed cell death induced by transient cerebral ischemia, and calcium-binding proteins have been implicated in calcium-regulated signal transduction. Apoptosis-linked gene 2 is a calcium-binding protein required for cell death induced by different apoptotic stimuli. By Western blot analysis, we found that apoptosis-linked gene 2 protein was expressed in normal brains, and that expression increased in ischemic brains after 20 or 90 min of transient focal cerebral ischemia. Immunocytochemistry showed increased apoptosis-linked gene 2 protein expression in frontal cortex, a region where neurons underwent ischemic stress but still survived, after 20 or 90 min of focal cerebral ischemia. Apoptosis-linked gene 2 protein was also up-regulated in the ischemic border-zone of parietal cortex 24h after 20 min of focal ischemia, and was remarkably over-expressed in the caudate-putamen and parietal cortex, (where cells are destined to die) 24h after 90 min of ischemia. The expression pattern of apoptosis-linked gene 2 protein was similar to that of deoxyribonucleic acid damage detected by Klenow labeling assay. Our results suggest that apoptosis-linked gene 2 may be involved in the regulation of cell death after transient focal cerebral ischemia.

Animals↗

PubMed2000

[Diffuse Lewy body disease searched out from 114 patients with parkinsonism].

From 114 patients who had been previously diagnosed as Parkinson's disease, we diagnosed six cases as clinically definite "diffuse Lewy body disease (DLBD)" according to McKeith's criteria with more strict modifications. Besides a central feature, dementia, and core features including parkinsonism, fluctuating cognition, and recurrent visual hallucinations, the patients presented some of supportive features, that is, repeated falls (4 cases), syncope (5 cases), and transient loss of consciousness (all cases). Autopsy, which was performed in 2 of the cases, revealed Lewy bodies in various nervous tissues including autonomic nervous systems in both cases. 7 cases of probable DLBD and 8 cases of possible DLBD, which lacked fluctuating cognition and/or visual hallucinations, demonstrated neither of repeated falls, syncope, nor transient loss of consciousness. Episodes of these supportive features, which seem to be associated with autonomic dysfunctions and/or fluctuating cognition, should be important in the differential diagnosis of DLBD.

Adult↗

PubMed1999

Cannabinoids and neuroprotection in global and focal cerebral ischemia and in neuronal cultures.

Marijuana and related drugs (cannabinoids) have been proposed as treatments for a widening spectrum of medical disorders. R(+)-[2, 3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1, 4-benzoxazin-yl]-(1-naphthalenyl)methanone mesylate (R(+)-WIN 55212-2), a synthetic cannabinoid agonist, decreased hippocampal neuronal loss after transient global cerebral ischemia and reduced infarct volume after permanent focal cerebral ischemia induced by middle cerebral artery occlusion in rats. The less active enantiomer S(-)-WIN 55212-3 was ineffective, and the protective effect of R(+)-WIN 55212-2 was blocked by the specific central cannabinoid (CB1) cannabinoid receptor antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2, 4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide-hydrochloride. R(+)-WIN 55212-2 also protected cultured cerebral cortical neurons from in vitro hypoxia and glucose deprivation, but in contrast to the receptor-mediated neuroprotection observed in vivo, this in vitro effect was not stereoselective and was insensitive to CB1 and CB2 receptor antagonists. Cannabinoids may have therapeutic potential in disorders resulting from cerebral ischemia, including stroke, and may protect neurons from injury through a variety of mechanisms.

Animals↗

PubMed1999

In situ detection of neuronal DNA strand breaks using the Klenow fragment of DNA polymerase I reveals different mechanisms of neuron death after global cerebral ischemia.

Ischemic cell injury in the brain may involve a cascade of programmed cell death. DNA damage may be either a catalyst or a consequence of this cascade. Therefore, the induction of DNA strand breaks in the rat brain following transient global ischemia was examined using (a) the Klenow labeling assay, identifying DNA single-strand breaks (SSBs) or double-strand breaks (DSBs) with protruding 5' termini, and (b) terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL), detecting DNA DSBs with protruding 3' termini or blunt ends. Klenow-positive staining occurred within 2 h of reperfusion and increased with increasing durations of reperfusion. DNA damage detected with the Klenow labeling assay preceded that of TUNEL expression in the caudate putamen, reticular thalamus, thalamus, and cortex. However, in CA1, DNA SSBs were not detected until 72 h of reperfusion and occurred simultaneously with DSBs. Thus, the time course and fragmentation characteristics of DNA damage differ between the hippocampal CA1 and other selectively vulnerable brain regions. This distinct pattern suggests that the delayed neuronal death in CA1 following transient global ischemia may occur via an apoptotic mechanism different from that of other brain regions.

Animals↗

PubMed1999

Molecular cloning of a cell cycle regulation gene cyclin H from ischemic rat brain: expression in neurons after global cerebral ischemia.

Gene expression plays an important role in determining the fate of neurons after ischemia. To identify additional genes that promote survival or execute programmed cell death in ischemic neurons, a subtractive cDNA library was constructed from hippocampus of rats subjected to global ischemia. With use of a differential screening technique, a cDNA was identified that was up-regulated after ischemia. The cDNA was found to have high homology with human cyclin H at both the nucleotide level (89%) and the amino acid level (93%). Northern blotting detected cyclin H mRNA in nonischemic and ischemic brains. In situ hybridization studies revealed that cyclin H message was found in hippocampal neurons in nonischemic brain. After ischemia, expression was increased primarily in the dentate gyrus and CA3 regions of hippocampus. Expression of cyclin H protein, detected by western blotting of hippocampal tissue, was increased after global ischemia, but expression of cyclins B1 and D1 and other related cell cycle genes (Cdk7 and Cdc2) was not increased. Cyclin H immunoreactivity was found exclusively within neurons. After ischemia, there was increased immunoreactivity within neurons in dentate gyrus, CA3, and cortex. Thus, cyclin H is expressed in normal postmitotic neurons and expression is increased in neurons that are ischemic yet survive. These results suggest that cyclin H may have functions in neurons other than cell cycle regulation, including other known functions such as DNA repair.

Amino Acid Sequence↗

PubMed1999

AIDS-related perceptions and condom use of prostitutes in Korea.

The purpose of this study was to assess the impact of AIDS-related knowledge and attitudes of prostitutes on condom use from diverse 'sex markers' in Korea. The data were collected by interviewers at five different 'sex markets'. During March 1993, research assistants at the Institute of Health Services Research interviewed 371 prostitutes visiting sexually transmitted disease (STD) clinics. Multiple regression method was used in identifying the determinants of condom use. The level of condom use was regressed on personal characteristics of prostitutes, AIDS-related perceptions, and market type. Prostitutes' level of condom use turned out to be different across the markets featuring diverse types of services and fees. Neither perceived vulnerability nor perceived seriousness of AIDS had significant effects on condom use. Our findings suggested that the many AIDS-preventive educational efforts by STD clinics are ineffective. Hence, individual STD clinics need to develop AIDS-preventive education programs which are suitable for the unique circumstances of their respective 'sex markets'.

Acquired Immunodeficiency Syndrome↗

PubMed1999

[The expression of Ras protein in human middle ear cholesteatoma].

OBJECTIVE: To evaluate the possible role of Ras protein in acquired middle ear cholesteatoma. METHODS: The specimens from the acquired middle ear cholesteatoma tissue of 22 cases and the normal external ear skin of 10 cases were examined by immunohistochemical S-P method and computer image analysis. RESULTS: All epithelial layers of cholesteatoma revealed a relatively abundant expression of Ras protein, among which 15 cases showed an inner plasma membrane expression, 5 cases a cytoplasm and membrane expression, and 2 cases cytoplasm expression only. In contrast, the normal external ear skin revealed a sparse distribution of Ras protein in the inner plasma membrane of epithelial cells with a more intensely staining in the basal layer. The integral absorbency of Ras protein in the two types of tissues were 0.870 and 0.463 respectively with a significant difference between them. CONCLUSION: There is an aberrant regulation of Ras protein in cholesteatoma. Ras protein plays a pivotal role during the aberrant growth and the differentiation of cholesteatoma.

Adolescent↗

PubMed1998

Induction of caspase-3-like protease may mediate delayed neuronal death in the hippocampus after transient cerebral ischemia.

Delayed neuronal death after transient cerebral ischemia may be mediated, in part, by the induction of apoptosis-regulatory gene products. Caspase-3 is a newly characterized mammalian cysteine protease that promotes cell death during brain development, in neuronal cultures, and in other cell types under many different conditions. To determine whether caspase-3 serves to regulate neuronal death after cerebral ischemia, we have (1) cloned a cDNA encoding the rat brain caspase-3; (2) examined caspase-3 mRNA and protein expression in the brain using in situ hybridization, Northern and Western blot analyses, and double-labeled immunohistochemistry; (3) determined caspase-3-like activity in brain cell extracts; and (4) studied the effect of caspase-3 inhibition on cell survival and DNA fragmentation in the hippocampus in a rat model of transient global ischemia. At 8-72 hr after ischemia, caspase-3 mRNA and protein were induced in the hippocampus and caudate-putamen (CPu), accompanied by increased caspase-3-like protease activity. In the hippocampus, caspase-3 mRNA and protein were predominantly increased in degenerating CA1 pyramidal neurons. Proteolytic activation of the caspase-3 precursor was detected in hippocampus and CPu but not in cortex at 4-72 hr after ischemia. Double-label experiments detected DNA fragmentation in the majority of CA1 neurons and selective CPu neurons that overexpressed caspase-3. Furthermore, ventricular infusion of Z-DEVD-FMK, a caspase-3 inhibitor, decreased caspase-3 activity in the hippocampus and significantly reduced cell death and DNA fragmentation in the CA1 sector up to 7 d after ischemia. These data strongly suggest that caspase-3 activity contributes to delayed neuronal death after transient ischemia.

Amino Acid Sequence↗

PubMed1998

Transient global ischemia triggers expression of the DNA damage-inducible gene GADD45 in the rat brain.

Using in situ hybridization, Northern blot analysis, Western blot analysis, and immunocytochemistry, mRNA and protein expression of the novel DNA damage-inducible gene GADD45 was examined in the rat brain at 0.5, 2, 4, 8, 16, 24, 48, and 72 hours after 15 minutes of transient global ischemia. Transient ischemia produced by the four-vessel occlusion method resulted in DNA double-strand breaks and delayed neuronal cell death in vulnerable neurons of the hippocampal CA1 sector, the hilus, dorsal caudate-putamen, and thalamus, as shown by in situ DNA nick end-labeling and histologic staining. GADD45 mRNA was transiently increased in less-vulnerable regions such as the parietal cortex (up to 8 hours after ischemia) and dentate granule cells (up to 24 hours after ischemia) but was persistently increased in vulnerable neurons such as CA1 pyramidal neurons (up to 48 hours). GADD45 immunoreactivity was increased in both vulnerable and less-vulnerable regions at earlier reperfusion periods (4 to 16 hours), but thereafter immunoreactivity was decreased below control levels in most vulnerable regions before delayed cell death and DNA double-strand breaks. At 72 hours after transient ischemia, a moderate increase in GADD45 immunoreactivity was still detectable in some CA3 neurons and in a few surviving neurons in the CA1 region. Double staining performed at 16 to 72 hours after ischemia revealed that GADD45 immunoreactivity was persistently increased in neurons that did not develop DNA damage. Because GADD45 protein may participate in the DNA excision repair process and because it has been shown that this protein is also overexpressed in neurons that survive focal ischemia and kainate-induced epileptic seizures, the results reported here support the hypothesis that GADD45 could have a protective role in neuronal injury.

Animals↗

PubMed1998

[Study on expression of nm23-H1 protein/NDPK-A in laryngeal carcinoma].

To investigate the expression of nm23-H1 gene in laryngeal squamous cell carcinoma, immunohistochemistry was carried out with a monoclonal antibody against nm23-H1. Of 48 cancer tissues tested, 35(72.9%) showed a positive immuno-reaction for nm23-H1. The percentage of nm23-H1 positivity was significantly lower (P < 0.01) in the tumors with cervical lymph node metastasis than in those without metastasis. Moreover, the percentage of nm23-H1 positivity was significantly lower (P < 0.05) in tumors of stages III-IV than in those of stages I-II. No significant correlation was found between nm23-H1 expression and tumor sites or histopathological grades. Analyzed with following up date, we found that the overall survival was better (P < 0.01) in patients with nm23-H1 expression than in those without expression. These results suggest that nm23-H1 gene may play a role in the suppression of lymph node metastasis and tumor progression in laryngeal carcinoma, and the expression of nm23-H1 gene is a useful predictor of prognosis.

Adult↗

PubMed1998

How do HMOs achieve savings? The effectiveness of one organization's strategies.

OBJECTIVE: To examine how a group practice used organizational strategies rather than provider-level incentives to achieve savings for health maintenance organization (HMO) compared to fee-for-service (FFS) patients. DATA SOURCES/STUDY SETTING: A large group practice with a group model HMO also treating FFS patients. Data sources were all patient encounter records, demographic files, and clinic records covering 3.5 years (1986-1989). The clinic's procedures to record services and charges were identical for FFS and HMO patients. All FFS and HMO patients under age 65 who received any outpatient services during approximately 100,000 episodes of the seven study illnesses were eligible. STUDY DESIGN: Using an explanatory case design, we first compared HMO and FFS rates of resource utilization, in standardized dollars, which measured the impact of organizational strategies to influence patient and provider behavior. We then examined the effect of HMO insurance and organizational measures to explain total outpatient use. Key variables were standardized charges for all outpatient services and the HMO's strategies. PRINCIPAL FINDINGS: Patient and provider behavior responded to organizational strategies designed to achieve savings for HMO patients; for instance, HMO patients used midlevel providers and generalists more often and ER and specialists less often. Overall HMO savings, adjusted for case mix, were explained by the specialty of the physicians the patients first visited and appeared to affect patients with average health more than others. CONCLUSION: Organizational strategies, without resort to differential financial incentives to each provider, resulted in lower rates of outpatient services for HMO patients. Savings from outpatient use, especially for common diseases that rarely require hospitalization, can be substantial.

Adult↗

PubMed1997

A Bcl-2 antisense oligonucleotide increases alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) toxicity in cortical cultures.

Both alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor-mediated neurotoxicity and the induction of death-regulatory genes have been implicated in the pathophysiology of delayed ischemic neuronal injury. To assess the role of the antiapoptotic gene Bcl-2 in the modulation of AMPA toxicity, we exposed neuron-enriched cultures from rat cerebral cortex to AMPA, in the absence or presence of an antisense oligodeoxynucleotide (ODN) directed against Bcl-2. AMPA produced concentration-dependent toxicity detected by a decrease in fluorescence of the redox indicator Alamar blue and by an increase in lactic acid dehydrogenase release. This effect was accompanied by the induction of Bcl-2 protein expression, with maximal induction at 100 microM AMPA. A phosphorothioate antisense ODN against Bcl-2 reduced the AMPA-stimulated induction of Bcl-2 protein levels, detected by western blotting, by about 70%. In the presence of the antisense ODN, but not sense or scrambled ODNs, the toxicity of 100 microM AMPA was increased by about 60%. These findings suggest that induction of Bcl-2 expression by AMPA may have a protective role to limit AMPA receptor-mediated neuronal damage and that modifying Bcl-2 expression could have therapeutic potential in ischemia.

Animals↗

PubMed1997

Early detection of DNA strand breaks in the brain after transient focal ischemia: implications for the role of DNA damage in apoptosis and neuronal cell death.

Using in situ DNA polymerase I-mediated biotin-dATP nick-translation (PANT) and terminal deoxynucleotidyl-transferase-mediated dUTP nick end-labeling (TUNEL), we investigated the evolution of DNA strand breaks, a marker of DNA damage, in rat brain after 1 h of middle cerebral artery occlusion and various durations of reperfusion. DNA single-strand breaks (SSBs) detected by PANT were present in neurons after as little as 1 min of reperfusion. Numbers of neurons containing an SSB increased progressively in the ischemic core but decreased in the ischemic penumbra after 1 h of reperfusion. DNA double-strand breaks (DSBs) detected by TUNEL were first seen in neurons after 1 h of reperfusion, and their numbers then increased progressively in the ischemic core, with a regional distribution similar to that of SSBs. However, the number of SSB-containing cells was greater than that of DSB-containing cells at all time points tested. SSB-containing cells detected within the first hour of reperfusion were exclusively neuronal and exhibited normal nuclear morphology. At 16-72 h of reperfusion, many SSB- and DSB-containing cells, including both neurons and astrocytes, showed morphological changes consistent with apoptosis. Gel electrophoresis of DNA isolated from the ischemic core showed DNA fragmentation at 24 h, when both SSBs and DSBs were present, but not at 1 h, when few DSBs were detected. These results suggest that damage to nuclear DNA is an early event after neuronal ischemia and that the accumulation of unrepaired DNA SSBs may contribute to delayed ischemic neuronal death, perhaps by triggering apoptosis.

Animals↗