PubMed Health⌕ Search

Biomedical subjects

Jing Lan

Publications and source records attributed to Jing Lan.

15 recordsLinked to original sources
PubMed2007

Mild hypothermia diminishes oxidative DNA damage and pro-death signaling events after cerebral ischemia: a mechanism for neuroprotection.

Mild hypothermia, applied either during or soon after cerebral ischemia, has been shown to confer robust neuroprotection against brain injury in experimental stroke and in patients recovering from cardiac arrest. However, the mechanism underlying hypothermic neuroprotection is not completely understood. In this study, the effect of mild hypothermia on the induction of oxidative DNA damage, an early harmful event during post-ischemic reperfusion that triggers both necrotic and apoptotic cell death in the brain, was studied using the rat model of middle cerebral artery occlusion (MCAO) and reperfusion. Rats were subjected to 2-hr MCAO and reperfusion of various durations up to 3 days. Selective brain hypothermia (33 degrees C) was induced at the onset of ischemia and terminated at the beginning of reperfusion, and this significantly decreased infarct volume 72 hr later. Correlated with this protective effect, intraischemic mild hypothermia markedly attenuated the nuclear accumulations of several oxidative DNA lesions, including 8-oxodG, AP sites, and DNA single-strand breaks, after 2-hr MCAO. Consequently, harmful DNA damage-dependent signaling events, including NAD depletion, p53 activation, and mitochondrial translocation of PUMA and NOXA, were reduced during post-ischemic reperfusion in hypothermia-treated brains. These results suggest that the attenuation of oxidative DNA damage and DNA damage-triggered pro-death signaling events may be an important mechanism underlying the neuroprotective effect of mild hypothermia against ischemic brain injury.

Animals↗
PubMed2006

High efficient degradation of dyes with lignin peroxidase coupled with glucose oxidase.

The H(2)O(2) supply strategy was one of crucial factors for high efficient degradation of pollutants with lignin peroxidase (LiP). In this paper, an attempt was made to couple a H(2)O(2) producing enzymatic reaction to the LiP catalyzed oxidation of dyes. H(2)O(2) needed was generated by glucose oxidase (GOD) and its substrate glucose. The generation rate of H(2)O(2) could be easily controlled by adjusting the pH of the degradation system and the amount of GOD added. Due to the controlled release of H(2)O(2), a sustainable constant activity of LiP was observed. The inhibition of LiP by high level H(2)O(2) supplied externally by a single addition at the beginning of the experiments could be avoided. Degradation of three dyes (xylene cyanol, fuchsine and rhodamine B) with LiP coupled with GOD indicated that the present H(2)O(2) supply strategy was very effective for improvement of the efficiency of the decolourization of dyes.

Benzenesulfonates↗
PubMed2006

Liquid chromatographic/tandem mass spectrometric method for the quantitation of tranilast in human plasma.

An analytical method for the determination of tranilast in human plasma using tramadol as the internal standard has been developed based on liquid chromatography/tandem mass spectrometry. Sample preparation involved protein precipitation with methanol. Separation by reversed-phase high-performance liquid chromatography using methanol/10 mM ammonium acetate (70: 30, v/v) as mobile phase was complete in a run time of 2.4 min. Detection on a Q TRAP system used multiple reaction monitoring. The method was linear in the range 0.06-20 microg/mL with intra- and inter-day precisions (as relative standard deviation) of 2.2-2.6% and 2.3-2.9%, respectively. Accuracy (as relative error) was <-2.5%. The method was applied in a pharmacokinetic study in healthy volunteers treated with a single 80 mg oral dose of tranilast.

Administration, Oral↗
PubMed2006

The effect of combination of recombinant human bone morphogenetic protein-2 and basic fibroblast growth factor or insulin-like growth factor-I on dental implant osseointegration by confocal laser scanning microscopy.

BACKGROUND: The healing period of bone-implant osseointegration usually varies from 3 to 6 months or even longer. Failure may occur during this time. This study aimed to investigate whether osseointegration of dental implants can be enhanced by the combination of growth factors. METHODS: Sixty-four implants were coated with polylactic acid and divided into four groups. Group I was applied with 1.0 mg recombinant human bone morphogenetic protein-2 (rhBMP-2) and 200 microg recombinant human basic fibroblast growth factor (rhbFGF), group II with 1.0 mg rhBMP-2 and 250 mug recombinant human insulin-like growth factor-I (rhIGF-I), group III with 1.0 mg rhBMP-2, and group IV without growth factors as control. In total, 16 rabbits were used, and two osteotomies were drilled on each side of the femur, in which four different groups were randomly placed. Four weeks after implanting, 20 mg calcein green/kg body weight was administered intravenously, and 8 weeks after implanting, 20 mg alizarin/kg body weight was administered intravenously. Twelve weeks after implanting, the animals were sacrificed. The block of bone with implants was embedded in methylmethacrylate and sectioned, and the percentage of new bone surrounding the implant was analyzed by confocal laser scanning microscopy. RESULTS: There was a statistical difference in bone formation between rhBMP-2-applied groups and the non-applied group at 4 or 8 weeks, and no significant difference between groups I and II (although bone formation in group II was greater than that in group I at 4 weeks). The bone formation in group II was greater than that in group III at 4 or 8 weeks. The formed bone in group I was also greater than the one in group III at 8 weeks, but there was no difference at 4 weeks. CONCLUSIONS: rhBMP-2 could increase new bone formation, and it acted synergistically with rhbFGF and rhIGF-I to improve bone-implant osseointegration. The combination of rhBMP-2 and rhbFGF (group 1) showed faster growth of new bone than other groups at 8 months.

Animals↗
PubMed2005

Phase I pharmacokinetic-pharmacodynamic study of 17-(allylamino)-17-demethoxygeldanamycin (17AAG, NSC 330507), a novel inhibitor of heat shock protein 90, in patients with refractory advanced cancers.

PURPOSE: 17-(Allylamino)-17-demethoxygeldanamycin (17AAG), a benzoquinone antibiotic, down-regulates oncoproteins by binding specifically to heat shock protein 90 (HSP90). We did a phase I study of 17AAG to establish the dose-limiting toxicity and maximum tolerated dose and to characterize 17AAG pharmacokinetics and pharmacodynamics. EXPERIMENTAL DESIGN: Escalating doses of 17AAG were given i.v. over 1 or 2 hours on a weekly x 3 schedule every 4 weeks to cohorts of three to six patients. Plasma pharmacokinetics of 17AAG and 17-(amino)-17-demethoxygeldanamycin (17AG) were assessed by high-performance liquid chromatography. Expression of HSP70 and HSP90 in peripheral blood mononuclear cells was measured by Western blot. RESULTS: Forty-five patients were enrolled to 11 dose levels between 10 and 395 mg/m2. The maximum tolerated dose was 295 mg/m2. Dose-limiting toxicity occurred in both patients (grade 3 pancreatitis and grade 3 fatigue) treated with 395 mg/m2. Common drug-related toxicities (grade 1 and 2) were fatigue, anorexia, diarrhea, nausea, and vomiting. Reversible elevations of liver enzymes occurred in 29.5% of patients. Hematologic toxicity was minimal. No objective responses were observed. 17AAG pharmacokinetics was linear. Peak plasma concentration and area under the curve of 17AG, the active major metabolite of 17AAG, increased with 17AAG dose, but the relationships were more variable than with 17AAG. 17AAG and 17AG in plasma were >90% protein bound. There were no consistent changes in peripheral blood mononuclear cell HSP90 or HSP70 content. CONCLUSIONS: 17AAG doses between 10 and 295 mg/m2 are well tolerated. 17AAG pharmacokinetics is linear. Peripheral blood mononuclear cell HSP90 and HSP70 are uninformative pharmacodynamic markers. The dose recommended for future studies is 295 mg/m2 weekly x 3, repeated every 4 weeks.

Adult↗
PubMed2005

[Clinical application of maxillary sinus lifting, bone graft and simultaneous placement of implant].

PURPOSE: To evaluate the results of two kinds of sinus lifting techniques with simultaneous implant placement. METHODS: 31 maxillary sinus underwent two kinds of sinus lifting techniques and simultaneously 42 implants placement. The sinuses were observed 1, 3, 6 months after the surgery. RESULTS: There were no implants loose or lost; X ray examination showed well osseointegration and no maxillary sinusitis. All the patients finished implant prosthesis in 6 months postoperatively. Through 6-36 months' follow-up, clinical results were satisfactory. CONCLUSION: With properly handling of indication and the operation skill, the results of two kinds of maxillary sinus lifting techniques with bone grafting and simultaneously implants placement are both satisfactory.

Bone Transplantation↗
PubMed2004

Pharmacokinetics and pharmacodynamics of 17-demethoxy 17-[[(2-dimethylamino)ethyl]amino]geldanamycin (17DMAG, NSC 707545) in C.B-17 SCID mice bearing MDA-MB-231 human breast cancer xenografts.

PURPOSE: 17-demethoxy 17-[[(2-dimethylamino)ethyl]amino]geldanamycin (17DMAG, NSC 707545) is a water-soluble analogue of 17-(allylamino)-17-demethoxygeldanamycin (17AAG), a compound currently in clinical trials. These preclinical studies: (1) characterized 17DMAG concentrations in plasma, normal tissues, and tumor after i.v. delivery to mice; and (2) correlated tumor and normal tissue 17DMAG concentrations with alterations in heat shock protein 90 (HSP90) and selected HSP90-chaperoned proteins. METHODS: At specified times after i.v. administration of 75 mg/kg 17DMAG, SCID mice bearing s.c. MDA-MB-231 human breast xenografts were killed and plasma and tissues were retained. 17DMAG concentrations were determined by HPLC. Raf-1, heat shock protein 70 (HSP70), and HSP90 in tissues were determined by Western blotting. RESULTS: Peak plasma 17DMAG concentration was 15.4+/-1.4 microg/ml. The area under the plasma 17DMAG concentration versus time curve was 1072 microg/ml min, corresponding to a total body clearance of 70 ml/kg/min. Peak 17DMAG concentrations in liver (118.8+/-5.7 microg/g), kidney (122.9+/-10.6 microg/g), heart (81.3+/-8.1 microg/g), and lung (110.6+/-25.4 microg/g) occurred at 5-10 min, while peak concentrations in spleen (70.6+/-9.6 microg/g) and tumor (9.0+/-1.0 microg/g) occurred at 30-45 min. At 48 h, 17DMAG was detectable in tumor but not in any normal tissue. Raf-1 in tumors of 17DMAG-treated mice killed at 4, 7, 24 and 48 h was about 20% lower than in tumors from vehicle-treated mice. HSP90 and HSP70 in tumors of 17DMAG-treated animals were significantly lower than in tumors of control animals at 4, 7, and 24 h. Hepatic Raf-1 was decreased by more than 60% at all times after 17DMAG treatment; however, hepatic HSP90 was not affected. HSP70 was undetectable in livers of vehicle-treated mice or mice killed at 2 or 4 h after 17DMAG treatment, but was detected in livers at 7, 24 and 48 h. 17DMAG did not affect renal Raf-1. In contrast, renal HSP70 and HSP90 were decreased by more than 50% at 2 and 4 h after 17DMAG treatment. Renal HSP70 increased approximately twofold above that in kidneys from vehicle-treated control mice at 7 and 24 h, while HSP90 relative protein concentration was no different from that in controls. CONCLUSIONS: Plasma pharmacokinetics of 17DMAG in tumor-bearing mice were similar to those previously reported in nontumor-bearing mice. 17DMAG was distributed widely to tissues but was retained for longer in tumors than normal tissues. Raf-1, HSP90, and HSP70 were altered to different degrees in tumors, livers, and kidneys of 17DMAG-treated animals. These data illustrate the complex nature of the biological responses to 17DMAG.

Animals↗
PubMed2004

[The test of metal-ceramic bonding strength among three ceramic alloies].

PURPOSE: To compare the metal-ceramic bonding strength of different ceramic alloies. METHODS: 30 wax sheets were divided into 6 groups at random. Each group included 5 sheets. After being invested conventionally with Bellaves SH,the samples were casted and fused with porcelain.The metal-ceramic bonding strength was evaluated. RESULTS: The highest bonding strength was found in Bio Herador N alloy, and then in TILITE alloy and Heraenium S alloy respectively. Bio Herador N alloy and TILITE alloy all had significant differences of the bonding strength before and after treatment (P<0.05). There was no significant differences in the bonding strength of the Heraenium S alloy after treatment (P>0.05). CONCLUSION: The bonding strength of precious metal-ceramic was higher than that of non-precious metal-ceramic.Pre-oxygen treatment can improve the metal-ceramic bonding strength of Bio Herador N alloy and TILITE alloy,but it had no effect on the metal-ceramic bonding strength of the Heraenium S alloy.

Dental Bonding↗
PubMed2003

Inducible repair of oxidative DNA lesions in the rat brain after transient focal ischemia and reperfusion.

To determine the role of oxidative DNA damage and repair in brain injury after focal ischemia and reperfusion, the authors investigated DNA base damage and DNA base excision repair (BER) capacity, the predominant repair mechanism for oxidative DNA lesions, in the rat model of temporary middle cerebral artery occlusion. Contents of 8-hydroxyl-2'-deoxyguanosine (8-oxodG) and apurinic/apyrimidinic abasic site (AP site), hallmarks of oxidative DNA damage, were quantitatively measured in nuclear DNA extracts from brains 0.25 to 72 hours after 1 hour of middle cerebral artery occlusion. In parallel to the detection of DNA lesions, the capacity for 8-oxodG- or AP site-dependent DNA repair synthesis was measured in nuclear protein extracts using specific in vitro DNA repair assays. After postischemic reperfusion, the levels of 8-oxodG and AP sites were markedly increased in ischemic tissues. In frontal/parietal cortex, regions that survived ischemia, 8-oxodG and AP sites were efficiently repaired during reperfusion. However, in the caudate, a region that was destined to infarct, the DNA lesions were poorly repaired. In consistent with the patterns of endogenous lesion repair, a markedly induced and long-lasting (at least 72 hours) BER activity was detected in the cortex but not in the caudate after ischemia. The induced BER activity in ischemic cortex was attributed to the upregulation of gene expression and activation of selective BER enzymes, particularly DNA polymerase-beta and OGG1. These results strongly suggest that inducible DNA BER constitutes an important endogenous mechanism that protects brain against ischemia-induced oxidative neuronal injury.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2003

Helicobacter pylori infection generated gastric cancer through p53-Rb tumor-suppressor system mutation and telomerase reactivation.

AIM: To investigate the relationship between Helicobacter pylori (H.pylori) infection and the expressions of the p53, Rb, c-myc, bcl-2 and hTERT mRNA in a series of diseases from chronic gastritis (CG), intestinal metaplasia type I or II(IMI-II), intestinal metaplasia type III (IMIII), mild or modest dysplasia (DysI-II), severe dysplasia (DysIII) to gastric cancer(GC) and to elucidate the mechanism of gastric carcinogenesis relating to H.pylori infection. METHODS: 272 cases between 1998 and 2001 were available for the study including 42 cases of CG, 46 cases of IMI-II, 25 cases of IMIII, 48 cases of DysI-II, 27 cases of DysIII, 84 cases of GC. H.pylori infection and the expressions of p53, Rb, c-myc, bcl-2 were detected by means of streptavidin-peroxidase (SP) immunohistochemical method. HTERT mRNA was detected by in situ hybridization (ISH). RESULTS: The expressions of p53, Rb, c-myc, hTERT mRNA and bcl-2 were higher in the GC than in CG, IM, Dys. The expression of c-myc was higher in IMIII with H.pylori infection (10/16) than that without infection (1/9) and the positive rate in DysI-II and DysIII with H.pylori infection was 18/30 and 13/17, respectively, higher than that without infection (4/18 and 3/10, respectively). In our experiment mutated p53 had no association with H.pylori infection, the expression of Rb was associated with H.pylori infection in GC, but the p53-Rb tumor-suppressor system abnormal in DysI-II cases, DysIII and GC cases with H.pylori infection was 21/30, 15/17 and 48/48 respectively, higher than non-infection groups (4/18, 3/10, 28/36). Furthermore the level of hTERT mRNA in GC with H.pylori infection (47/48) was higher than that without infection (30/36), however the relationship between bcl-2 and H.pylori was only in IMIII. C-myc had a close association with hTERT mRNA in DysIII and GC (P=0.0 253,0.0 305 respectively). CONCLUSION: In the gastric carcinogenesis, H.pylori might cause the severe imbalance of proliferation and apoptosis in the precancerous lesions (IMIII and GysIII) first, leading to p53-Rb tumor-suppressor system mutation and telomerase reactivation, and finally causes gastric cancer.

Adult↗
PubMed2003

[Relationship between Helicobacter pylori infection and expression of c-myc, Bcl-2, and Bax protein in different gastric mucosa lesions].

BACKGROUND & OBJECTIVE: Helicobacter pylori (HP) has been believed to be a carcinogen of gastric carcinoma. However, its mechanism was yet not clearly understood. This study was designed to investigate the relationship between HP infection and gastric epithelial cell proliferation as well as apoptosis in different gastric mucosa lesions and elucidate the probable mechanism of gastric carcinogenesis relating with HP infection. METHODS: A total of 272 cases were available for the study including 42 cases of chronic gastritis (CG), 46 cases of intestinal metaplasia I or II (IM I- II), 25 cases of intestinal metaplasia III (IM III), 21 cases of mild dysplasia (Dys I), 54 cases of modest or severe dysplasia (Dys II- III), and 84 cases of gastric cancer (GC). HP infection was detected by Warthin-Starry bacterium staining method and streptavidin-peroxidase (SP) immunohistochemical method. HID-AB(pH2.5)- PAS method was used to define the quality of mucus. The expression of c-myc, Bcl-2, and Bax were detected using SP immunohistochemical method. The chi-square test and the Fisher's exact probability test were used to compare the frequencies. RESULTS: (1)The expression of c-myc and Bcl-2 increased as gastric mucosa lesions developed from CG,IM,Dys to GC,but the expression of Bax decreased. The expression of c-myc was significantly higher in GC than that in Dys II- III and IM III(all P< 0.01), but the expression of Bax was significantly lower in GC than that in Dys II- III and IM III(P< 0.05 or P< 0.01). (2)The expression of c-myc in IM III and Dys II- III with HP infection was 62.50% and 66.67%,respectively, significantly higher than that without infection(11.11%,27.78%,all P< 0.05). The expression of Bax in CG, IM I- II and IM III with HP infection were 87.10%, 81.25%, and 62.50%, respectively, significantly higher than those without infection (54.55%, 42.86%, 11.11%, all P< 0.05). Furthermore HP infection was associated with the expression of Bcl-2 in IM III, Dys II- III and GC (P< 0.05 or P< 0.01). CONCLUSION: HP infection can cause serious imbalance between cell proliferation and apoptosis in the precancerous lesions (IM III and Dys II- III), giving chances for gastric carcinogenesis.

Adult↗
PubMed2003

[Clinical effects of three systems of dental implants].

OBJECTIVE: To evaluate the clinical value of dental implants including Brånemark, Steri-oss and BLB systems. METHODS: The total 384 implants of different materials and shapes were inserted normally. According to the Chinese standard of dental implantation, the success rates of three types were compared. RESULTS: By following-up from one year to five years, the success rates of all implants were above 97%. CONCLUSION: The success rates of routine implants were mainly associated with indication, case selection, operation, rehabilitation and patients maintenance.

Adolescent↗
PubMed2002

[Relationship between Helicobacter pylori infection and expressions of tumor suppressor genes in gastric carcinoma and related lesions].

BACKGROUND & OBJECTIVE: Helicobacter pylori (Hp) are believed to be a carcinogen of gastric carcinoma. However, its mechanism was yet not clearly understood. p53, p21WAF1, and p16 are main negative regulator genes of cell cycle. This study was designed to investigate the relationship between these 3 genes and Hp infection. METHODS: The authors examined the expression of these 3 tumor suppressor genes and Hp infection in 65 cases with chronic atrophic gastritis (CAG), 93 cases with intestinal metaplasia(IM), 94 cases with gastric epithelial dysplasia (GED) and 60 cases with gastric carcinoma (GC) using HID-AB (pH 2.5)-PAS, SP immunohistochemistry staining, and Warthin-Starry staining. RESULTS: For CAC, IM stage I-II, IM stage III, GED stage I, GED stage II-III, and GC, the positive expression rates of p53 were 0, 1.64%, 6.25%, 5.45%, 23.08%, and 70.00%, respectively (increased with pathological process); the positive expression rates of p21WAF1 were 100%, 95.08%, 100%, 100%, 71.79%, and 45.00%, respectively; the positive expression rates of p16 were 83.08%, 81.97%, 78.13%, 89.09%, 69.23%, and 40.00%, respectively. All the expression of these 3 genes showed significant difference between GED stage II-III and GED stage I, GC and GED stage II-III. In the same pathological changes, the positive expression rate of these 3 genes was higher in Hp infection group than in no Hp infection group, while there was no significant difference (P > 0.05). CONCLUSION: The mutation of p53 and inactivation of p21WAF1 and p16 play an important role in carcinogenesis of stomach. However, Hp infection was not associated with the abnormal expression of these 3 genes.

Cyclin-Dependent Kinase Inhibitor p16↗