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Biomedical subjects

L Xie

Publications and source records attributed to L Xie.

At least 55 records · Page 3Linked to original sources
PubMed2001

Post-PRK muscular asthenopia and eccentric ablation.

OBJECTIVE: To investigate the relationship between muscular asthenopia post photorefractive keratectomy (PRK) and eccentric ablation. METHODS: 16 eyes of 8 myopia cases whose muscular asthenopia was corrected by subjectively accepted triangular prism after PRK with vision more than 0.8 were followed up for 6-14 months. On the basis of data provided by the pre-PRK, post-PRK and their difference corneal topography, we calculated the real corrected corneal diopter (D) with the Holladay formula and measured the ablating eccentricity (h) and its direction. According to the formula delta approximately Dh, the prism effective value (delta) caused by the eccentric ablation was computed and compared with objectively accepted triangular prism. RESULTS: The subjectively accepted prism was similar to values calculated from the formula. Their mean difference is 0.10 +/- 0.25. The direction of the subjectively accepted prism was in the direction of ablation deviation. CONCLUSIONS: Eccentric ablation was the chief cause of post-PRK muscular visual asthenopia. The triangular prism effective value from eccentric ablation may be estimated by the formula delta approximately Dh. We must pay attention to the diagnosis, treatment and prevention of post-PRK muscular asthenopia.

Adult↗
PubMed2001

Effect of 60Co irradiation on characteristics of hemorheology in rabbits.

A high-dose (7 Gy) whole-body 60Co irradiation for a short period caused disturbances of hematopoietic function. A decrease in the hematocrit of the circulating blood lasted for about 15 days, thus forming an anemic animal model. We studied the influence of high-dose 60Co irradiation on hemorheologic parameters: percentage of reticulocytes, RBC deformability, sedimentation rate and plasma fibrinogen concentration in the rabbit. It was found that the plasma fibrinogen concentration increased to twice more than control level and that percentage of reticulocytes in circulation disappeared immediately after irradiation. The deformation index of RBCs in shear flow decreased from a value of 58% down to a value of 42% in the first two weeks and gradually returned to control levels about 40 days after 60Co irradiation. Our results showed that a short period of high-dose 60Co irradiation caused severe and relatively long-lasting damage of hematopoietic system in animals' body.

Animals↗
PubMed2001

[Clinical observation of astigmatism induced by corneal incision after phacoemulsification].

OBJECTIVE: To evaluate the changes of astigmatism induced by corneal incision after phacoemulsification. METHODS: Phacoemulsification was performed on 62 cases (78 eyes) without suture for a corneal incision. The changes of corneal astigmatism before and after operation in group A (incision at the superior nasal or superior temporal) and B (incision at the steepest corneal meridian) were compared. RESULTS: Three months after the operation, the surgical induced astigmatism was (0.83 plus minus 0.65) D and (0.72 plus minus 0.55) D in group A and B respectively. There was no significant difference, statistically (P > 0.05). The changes of corneal astigmatism were 0.11 D and 0.39 D in group A and B respectively, the difference being statistically significant (P < 0.05). CONCLUSION: Surgically induced astigmatism is very small after a corneal incision in phacoemulsification without a suture. If the incision is placed on the steepest meridian, the corneal astigmatism can be significantly reduced postoperatively.

Adolescent↗
PubMed2001

[Penetrating keratoplasty in active herpes simplex stromal keratitis].

OBJECTIVE: To evaluate the efficacy of penetrating keratoplasty (PKP) in treating active herpes simplex stromal keratitis. METHODS: PKP was performed on 59 patients with quiescent and 66 patients with active herpes simplex stromal keratitis. The results and complications of herpes simplex keratitis (HSK) in the quiescent group were compared with that of the HSK active group. RESULTS: No clinical or statistical significant differences in visual outcome, graft transparent rate and recurrent rate of HSK after operation were identified between the active and quiescent groups. CONCLUSION: When the pre- and intra-operative managements of PKP are properly performed on active HSK, the same results as that performed on quiescent HSK can be obtained, and it can reduce the complications and shorten the duration of the disease.

Acyclovir↗
PubMed2001

[Pathogen detection in the myocardial lesion using in situ RT-PCR in mice induced by experimental CoxB(3m) virus infection].

OBJECTIVE: To detect the location of pathogens in myocardium using in situ RT-PCR technique in order to study the pathogenetic course of the myocardial lesion induced by CoxB(3m) virus infection in mice. METHODS: (1) Thirty and fifty Balb/c mice were used respectively to establish the acute and chronic CoxB(3m) infected models, with another 25 healthy mice as the controls; (2) KS400 image analysis system (Germany) was used to measure the cardiac chamber area and the left ventricular wall thickness of the chronic infected mice and the controls; (3) CoxB(3m) virus in myocardial tissue was detected using in situ RT-PCR by direct incorporated technique which employed nucleotide labeling by anti-digoxin antibody and bonded with alkaline phosphatase (anti-dig-AKP method). RESULTS: Picture analysis indicated that the left ventricular chamber area was enlarged and the left ventricular wall was thinner in the chronic repeated virus infected models than those of the controls. With in situ RT-PCR, positive signals for Coxsackie virus B(3m) RNA were detected not only in the myocardium of the acute Balb/c mice models but also in the myocardium of the chronic mice models. CONCLUSION: Coxsackie virus B(3m) is able to induce pathologic lesions by exhibiting positive CVB-RNA signals in both acute and chronic models in mice. In the chronic experimental models, the cardiac chamber is enlarged while the ventricular wall is thinned which demonstrates the association with persistent infection of Coxsackie virus B(3m) virus.

Animals↗
PubMed2001

[Sequence analysis of RAN4 of a severe isolate of rice stripe virus in China].

RNA4 segment of a severe isolate of Rice stripe virus, isolated from Liaoning province and designated as PJ isolate, was amplified, cloned and sequenced. RNA4 of PJ isolate had 2157 nucleotide in length. When compared with RNA4 of T and M isolates of Japan and CX isolate of Yunnan province of China that had been previously reported, we found that these four isolates could be divided into two groups. PJ, T and M isolates shared 97.0% and 97.0%-97.5% identities in vORF4 and vcOFR4 at the nucleotide level, respectively and formed one group. The sequences in 5' and 3' terminal non-encoding region were completely identical among these three isolates. In this group, PJ isolate was more closely related to T isolate than to M isolate. The length of intergenic region(IR4) of PJ isolate was as same as that of T isolate, and had 93.0% sequence identity. However, PJ IR4 had an insertion of 19 bp in length compared with isolate M and had only 85.0% sequence identity. CX isolate belonged to another group, which shared only 94.0% and 92.5%-93.5% sequences identities in vORF4 and vcORF4 at the nucleotide level, respectively, even though there were not significant difference between these two group at the amino acid level. There was an insertion of 84 bp in length in the IR4 of CX isolate compared with PJ isolate and the sequence identity between two group reached to 72.0%-75.0%. Even though no base variation occurred in 5' terminal non-coding region, there was two bases substitution in 3' terminal non-coding region. These results showed that the isolates were grouped according to their geographical location. Additionally, highly consensus in 5' and 3' non-encoding region suggested that these regions played an very important role in transcription and replication of viral genome. Finally, the molecular epidemiology and gene functions of Rice stripe virus were discussed in this paper.

Amino Acid Sequence↗
PubMed2000

Characterization of the functionally related sites in the neural inducing gene noggin.

Previously we have shown that blocking bone morphogenetic protein (BMP) receptor signaling by a dominant negative BMP receptor causes neurogenesis in Xenopus animal caps (ACs), whereas the physiological neural inducer noggin acts as a homodimer physically binding to BMP-4 and disrupting its signaling at the ligand level. The present study attempted to elucidate the relationship between the structure and function of noggin. By replacing some cysteine residues with serine residues through a site-directed mutagenesis strategy, we generated three noggin mutants, C145S, C205S, and C(218, 220, 222)S (3CS). Although mRNAs encoded by these mutants were translated as efficiently as wild-type (WT) noggin mRNA, they behaved differently when expressed in vivo. Expression of WT noggin or C205S in Xenopus ACs converted the explants (prospective ectoderm) into neural tissue, indicated by the neural-like morphology and expression of the pan neural marker NCAM in the ACs. In contrast, ACs expressing C145S or 3CS sustained an epidermal fate like the control caps. Similar results were observed in the mesoderm where C205S (but not C145S and 3CS) displayed dorsalizing activity as well as WT noggin. Altogether, our results suggest that Cys145 alone or Cys(218, 220, 222) as a whole in noggin protein is required for the biological activities of noggin, probably participating in the dimerization of noggin with BMP-4 or itself.

Animals↗
PubMed2000

NotI clones in the analysis of the human genome.

Not I linking clones contain sequences flanking Not I recognition sites and were previously shown to be tightly associated with CpG islands and genes. To directly assess the value of Not I clones in genome research, high density grids with 50 000 Not I linking clones originating from six representative Not I linking libraries were constructed. Altogether, these libraries contained nearly 100 times the total number of Not I sites in the human genome. A total of 3437 sequences flanking Not I sites were generated. Analysis of 3265 unique sequences demonstrated that 51% of the clones displayed significant protein similarity to SWISSPROT and TREMBL database proteins based on MSPcrunch filtering with stringent parameters. Of the 3265 sequences, 1868 (57.2%) were new sequences, not present in the EMBL and EST databases (similarity < or =90%). Among these new sequences, 795 (24.3%) showed similarity to known proteins and 712 (21.8%) displayed an identity of >75% at the nucleotide level to sequences from EMBL or EST databases. The remaining 361 (11.1%) sequences were completely new, i.e. <75% identical. The work also showed tight, specific association of Not I sites with the first exon and suggest that the so-called 3' ESTs can actually be generated from 5'-ends of genes that contain Not I sites in their first exon.

Base Sequence↗
PubMed2000

Identification of differentially expressed genes in nasopharyngeal carcinoma by means of the Atlas human cancer cDNA expression array.

PURPOSE: To investigate genes of critical areas, including cell cycle/growth control, apoptosis, oncogene/tumor suppressors and growth factor/cytokines, that are differentially expressed in nasopharyngeal carcinoma. METHODS: The Human Cancer cDNA Atlas, which contains 588 genes relating to tumor biology, was used to screen normal nasopharyngeal tissue, nasopharyngeal cancer (NPC). The reverse transcription/polymerase chain reaction was used to confirm the expression pattern of some genes identified by Atlas hybridization. RESULTS: The differentially expressed cell cycle/growth control regulators in NPC showed a stronger tendency toward cell proliferation with the up-regulation of cyclin D1, cyclin D2 etc. The expression pattern of apoptosis-related genes demonstrated the up-regulation of both anti-apoptotic factors such as the BCL-2-related protein A1, TRAF3, the inhibitor of apoptosis protein A1 (IAPI) and apoptotic pathway elements such as Fas/Apo-1, Apo-2 ligand etc. Among oncogenes/tumor suppressors, MDM2, STAT1 and STAT2 were found to be up-regulated in NPC. The expression profile of growth factors/cytokines showed the up-regulation of many growth-enhancing factors such as EGR1, tumor-derived growth factor 1, platelet-derived growth factor A chain etc. as well as Th1-type cytokines e.g. interleukin-1beta and interferons. A smaller number of genes were down-regulated in nasopharyngeal cancer, such as those encoding ERK1, Raf, secreted apoptosis-related protein 1, CD27BP, transforming growth factor beta2, pre-B-cell-stimulating factor homologue etc. CONCLUSION: The consistent tendency toward cell proliferation, the possibility of a stronger antiapoptotic force that operates on the normal apoptotic pathway, or the autocrine or paracrine growth factors may account for the development of NPC. Some genes are reported for the first time to have changed expression in nasopharyngeal carcinoma. The simple, quick, and high-throughput method of profiling gene expression by cDNA array hybridization provides us with a quick overview of key factors that may be involved in NPC, and may identify genes suitable for further study of carcinogenesis mechanism or targets for possible molecular diagnosis or therapy.

Apoptosis↗
PubMed2000

The preferred source of arginine for high-output nitric oxide synthesis in blood vessels.

L-arginine is the substrate for nitric oxide (NO) production by each of the 3 NO synthase (NOS) isoforms encoded by the mammalian genome. Despite the pivotal roles of NO in mammalian physiology and pathophysiology, the source of arginine for NO synthesis is not clearly defined. In this context, it is notable that cell types that do not have a complete urea cycle often possess the urea cycle enzymes argininosuccinate synthase and argininosuccinate lyase; together, these enzymes confer the ability to regenerate arginine from the NOS product, L-citrulline. Herein, the authors summarize evidence to support the view that argininosuccinate synthase and argininosuccinate lyase function in an arginine-citrulline cycle, providing a ready source of arginine for high-output NO synthesis. The arginine-citrulline cycle is induced in vascular cells by the same cytokines that trigger iNOS expression and provides the preferred source of substrate for NO production. Evidence suggests that argininosuccinate synthase activity is rate-limiting to high-output NO synthesis and, hence, represents a novel target for the treatment of pathophysiological conditions arising from NO overproduction.

Animals↗
PubMed2000

Ribozyme-mediated resistance to rice dwarf virus and the transgene silencing in the progeny of transgenic rice plants.

A hammerhead ribozyme (Rz) with long hybridizing arms targeting the mRNA of rice dwarf virus (RDV) segment 5 and a mutated nonfunctional ribozyme (mRz) were constructed. As predicted, Rz transcribed in vitro cleaved the target mRNA of RDV segment 5 into two fragments of 138 and 238 nucleotides in length. The Rz and mRz genes were each placed under the control of the CaMV 35S promoter and used to transform Japonica rice variety 'Tongling No. 1' via Agrobacterium tumefaciens. A total of 32 independent lines containing Rz or mRz was obtained as demonstrated by Southern blot analysis. Challenge inoculation with RDV viruliferous leafhoppers (Nephotettix cincticeps) showed that T1 plants containing the Rz transgene displayed high resistance or delayed and attenuated viral symptoms. In contrast, transgenic lines expressing mRz showed severe symptoms similar to the control plants transformed with the vector alone. These results suggest that Rz confers RDV resistance in transgenic rice. Genomic DNA PCR analysis confirmed that all of the examined T6 progeny plants contained the Rz transgene. However, accumulation of the Rz transcripts was detectable by RT-PCR only in the plants that were resistant to RDV. This suggested that loss of RDV resistance in progeny plants containing the Rz transgene may result from silencing of the Rz transgene.

Base Sequence↗
PubMed2000

Development and validation of sensitive assays to quantitate gene expression after p53 gene therapy and paclitaxel chemotherapy using in vivo dosing in tumor xenograft models.

SCH58500 (ACN53) is a replication-deficient, type 5 adenovirus (Ad) expressing human wild-type p53 tumor suppressor. It is currently undergoing clinical trials as a cancer therapeutic. Many SCH58500 clinical trials incorporate an arm comparing traditional chemotherapy against chemotherapy combined with SCH58500. Paclitaxel was chosen for combination therapy in the preclinical study reported here due to its extensive use as a first-line therapy in ovarian cancer, its synergy with SCH58500 in preclinical cancer models, and its activation of p53-independent apoptosis, which might result in a "lowered threshold" for tumor cell death. SCID mice bearing human tumor xenografts were dosed with intratumoral vehicle, control Ad vector, or SCH58500, with or without paclitaxel. Real-time quantitative reverse transcriptase polymerase chain reaction assays were developed and validated to quantitate expression of p53, the p53 downstream effector gene p21, and the apoptosis-related genes, bax, bcl-2, and survivin. Protein expression was confirmed using immunohistochemical assays for p53 and p21. Only tumors injected with SCH58500 had detectable levels of exogenous p53 DNA and mRNA. After SCH58500 treatment, 3-11-fold elevations of p21 expression were observed in tumor xenografts containing nonfunctional p53 (MDA-MB-468, MDA-MB-231, MIAPaCa2, DU-145, and SK-OV-3), but no change in p21 mRNA in wild-type p53 PA-1 tumors. Immunohistochemical assays confirmed induction of p21 protein in MDAMB-468 and SK-OV-3 cells, but not in PA-1 cells. Ad vector alone or paclitaxel alone had no effect on p21 mRNA levels in most tumors. However, paclitaxel suppressed p21 expression induced by SCH58500 4-fold in DU-145 and SK-OV-3 tumors. Paclitaxel also affected expression of the housekeeping gene gapdh. There was no consistent pattern to the changes in bax, bcl-2, or survivin after SCH58500 treatment with or without paclitaxel between tumor types, although there were consistent responses within individual tumor lines. The mRNA ratios for bax/bcl-2 and bax/survivin were also not informative across tumor types. Of the genes examined, only p21 gave a predictable response 24 hours after p53 gene therapy and therefore, p21 expression may be useful for confirming SCH58500 activity in human tumor biopsies.

Adenoviridae↗
PubMed2000

Use of green fluorescent protein (GFP) to study the invasion pathways of Edwardsiella tarda in in vivo and in vitro fish models.

Edwardsiella tarda is a fish pathogen that causes systemic infections in many food and ornamental fish. E. tarda PPD130/91 and PPD125/87 were selected as representatives of the virulent and avirulent groups, respectively, from eight fish isolates, and transformed with plasmids encoding either green fluorescent protein (pGFPuv) or blue fluorescent protein (pBFP2). Two host models were used to study the invasion pathway of E. tarda in vitro and in vivo. Epithelioma papillosum of carp (EPC) was used as the first model. Virulent and avirulent E. tarda strains were found to adhere to and invade EPC cells. Interactions between E. tarda and host cells examined under confocal microscopy and intracellular growth were followed at different time points. Bacterial internalization of PPD130/91 and PPD125/87 involved microfilaments and protein tyrosine kinase since cytochalasin D (an inhibitor of microfilament polymerization) and genistein (an inhibitor of protein tyrosine kinase) prevented internalization. Confocal studies revealed co-localization of polymerized actin with bacteria. Staurosporine, a protein kinase C inhibitor, accelerated internalization of PPD125/87, whereas PD098059, a mitogen-activated protein kinase (MAPK) kinase inhibitor prevented internalization of PPD130/91. In the second model, blue gourami were infected with E. tarda intramuscularly. Mortalities were observed in PPD130/91(pGFPuv)-infected fish with high bacterial numbers detectable in all organs. PPD125/87(pBFP2)-infected fish did not die and the bacterial population decreased over time. Mixed infections comprised of both PPD130/91(pGFPuv) and PPD125/87(pBFP2), where inoculum size was similar to the single infections, caused mortalities in fish. High bacterial populations were noted only in the fish body muscle. The PPD125/87(pBFP2) population in the fish decreased after 5 d. The number of PPD130/91(pGFPuv) also decreased in the fish organs, except for continued high growth in the body muscle. Histology revealed necrosis of the tissue (body muscle and liver) and fluorescent bacteria in fish that were infected with PPD130/91(pGFPuv) but not with PPD125/87(pBFP2). This study showed that fluorescent proteins are a useful tool for investigating bacterial host cell infection, and information elucidated here sheds new light on the interactions between E. tarda and its hosts.

Actins↗
PubMed2000

[The relationship of polymorphism of angiotensinogen and angiotensin converting enzyme with essential hypertension].

OBJECTIVE: In order to investigate the candidate genes for essential hypertension(EH), the authors determined the frequencies of M235T allele variation in exon 2 of angiotensinogen(AGT) gene and angiotensin converting enzyme (ACE) gene in 95 normotensives and 87 hypertensives in Chinese. METHODS: Polymerase chain reaction combined with restriction enzyme digestion was used to detect the variation AGT gene while PCR was used to determine ACE gene polymorphism. RESULTS: T235 allele frequency was significantly higher in hypertensive patients than in controls (0.45 vs 0.33, P<0. 05) and it was noticeably higher in male hypertensives. The frequency of ACE D allele in the EH patients with family history was higher than that in controls(0.59 vs 0.41,P<0.05). CONCLUSION: The variation of AGT gene was involved in the pathogenesis of hypertension, especially in male. The ACE D allele was associated with EH with family history.

Alleles↗
PubMed2000

Effects of hepatic artery chemotherapeutic embolization combined with perfusing LAK cells into hepatic artery after radical operation of liver cancer.

OBJECTIVE: To evaluate the effects of hepatic artery chemotherapeutic embolization combined with perfusing LAK cells/interleukin 2 into hepatic artery after radical operation of liver cancer. METHODS: Random divide 42 cases into two groups who had accepted radical operation of liver cancer: 21 cases who accepted hepatic artery chemotherapeutic embolization combined with perfusing LAK cells/interleukin 2 into hepatic artery as observing group, 21 cases accepted simply hepatic artery chemotherapeutic embolization as control group. RESULTS: The intrahepatic recurrence rates of 1, 2, and 3 years were 0, 19.05%, 57.14% in observing group, lower than 28.57%, 47.62%, 85.71% of control group (chi(2)=4.86, 3. 86 and 4.20 respectively, P<0.05). The survival rates of 2 and 3 years were 85.71%, 61.90% in observing group, higher than 57.14%, 28. 57% of control group (chi(2)=4.20 and 4.71, P<0.05). CONCLUSION: Hepatic artery chemotherapeutic embolization combined with perfusing LAK cells/interleukin 2 into hepatic artery is an effective therapeutic method to control intrahepatic recurrence rates and raise the survival rates of the patients.

Adult↗
PubMed2000

Reduction of von Willebrand factor by endothelial cells.

The haemostatic activity of plasma von Willebrand factor (vWF) is a function of multimer size. Only the large vWF multimers are effective in promoting platelet adhesion to a site of vascular injury. We observed that the conditioned medium of cultured human umbilical vein, human microvascular and bovine aortic endothelial cells contained an activity which reduced the average multimer size of plasma or purified vWF. The average multimer size of vWF produced endogenously by human umbilical vein endothelial cells was similarly reduced following secretion. The reducing activity was ablated by pre-treatment with heat or the thiol blocking agents. iodoacetamide, N-ethylmaleimide or E-64, but not by a range of specific serine-, cysteine-, aspartic-, or metalloproteinase inhibitors. Reduction in vWF multimer size was associated with formation of new thiols in vWF and there was no evidence for additional proteolytic processing of vWF. The reducing activity was associated with a protein with an anionic pi that binds heparin and contains reactive thiol(s). These results suggested that the interchain disulfide bonds that link the vWF homodimers near the N-termini were being reduced by a vWF reductase secreted by endothelial cells. In support of this hypothesis, incubation of vWF with the protein reductants, protein disulfide isomerase and thioredoxin, resulted in formation of new thiols in vWF and reduction in the average multimer size of vWF. These findings may have consequences for control of vWF haemostatic activity.

Animals↗
PubMed2000

Influence of neuraminidase on the characteristics of microrheology of red blood cells.

Surface charge was removed from RBC (erythrocyte) membrane to different degrees with biochemical methods, i.e., treatment of RBCs with neuraminidase, either using different doses for the same incubation time (1 hour) or using the same dose (75 milli-unit) for different incubation time. Several rheological properties of the RBCs with surface charge removal were observed, including the deformation index DI (using traditional ektacytometry) orientation index (DI)or and small deformation index (Dl)d (using new ektacytometry), the viscosity at low and high shear rates (using a cone-plate rotating viscosimeter). In addition, photographs of RBCs aggregation under a microscope and the histograms of RBC aggregate size after treatment with neuraminidase were obtained. It is found from these experiments that the decrease of the surface charge of RBCs leads to the decrease in the deformation and orientation indices as well as the increase in blood viscosity.

Animals↗