Biomedical subjects

Jie Li

Publications and source records attributed to Jie Li.

At least 289 records · Page 16Linked to original sources

PubMed2003

[Expression of PTEN protein in oromaxillofacial tumor cell lines].

AIM: To investigate expression of PTEN protein in oromaxillofacial tumor cell lines and to compare the difference of PTEN protein expression between highly metastatic cancer cell lines and their parent cell lines. METHODS: ABC immunohistochemical staining was applied for detecting expression of PTEN protein in 8 kinds of cancer cell lines, including tongue cancer cell lines Tca8113 and HSC-3,oral bottom cancer cell line HSC-2, buccal cancer cell line BcaCD885, mucoepidermoid carcinoma cell line MEC-1, adenoid cystic carcinoma cell line SACC83, highly metastatic tongue cancer cell line Tb-TLP and highly metastatic mucoepidermoid carcinoma cell line M3SP2. RESULTS: Of the 8 kinds of cancer cell lines, 5 kinds of cancer cell lines were positive for PTEN protein expression. PTEN protein was located in cytoplasm around nucleus. 3 kinds of cancer cell lines, BcaCD885, Tb-TLP and M3SP2, lacked expression of PTEN protein. CONCLUSION: Deficiency of PTEN protein expression may play a certain role in cancer cell metastasis.

Animals↗

PubMed2003

[Using of selective marker gene in transgenic plants and its removal].

Selective marker gene is usually used to select transformed cells or tissue during gene transfer. However,the use of selective marker gene,especially antibiotic-resistant gene, is harmful to environment, plant development and affects multi-transformation. A new strategy that offers a approach for the elimination of those disadvantages caused by the selectable marker gene is developed. We summarized correlative marker genes used in transgenic plants and some methods of its removal.

English Abstract↗

PubMed2002

[Effect of corticosteroids on the balance of Th cytokines in patients with systemic lupus erythematosus].

OBJECTIVE: To investigate the levels of Th cell-derived cytokines and the effect of corticosteroids on the balance of Th1/Th2 cytokines in patients with systemic lupus erythematosus (SLE). METHODS: Fifty-eight SLE patients were treated with corticosteroids. Their IFN-gamma, IL-4 and IL-10 levels were detected by ELISA before and after the treatment with corticosteroids respectively; and the SLEDAI scores of the patients were compared before and after the treatment. RESULTS: Before the treatment, the serum levels of IFN-gamma, IL-4 and IL-10 were higher than those of the healthy controls (P < 0.05). After the treatment with corticosteroids, the elevated levels of IFN-gamma, IL-4 and IL-10 in the SLE patients were all significantly reduced than those before the treatment (P < 0.05). At the same time, the SLEDAI scores were significantly lower than those before the treatment (P < 0.01). The serum level of IFN-gamma was significantly decreased in the patients with SLE compared with the healthy controls (P < 0.05). By contrast, the levels of IL-4 and IL-10 of the patients with SLE were significantly increased compared with the healthy controls (P < 0.05). CONCLUSION: Corticosteroids may induce a shift from the Th1 to Th2 profile of cytokine secretion. This may be one aspect of the mechanisms for corticosteroids treatment.

Adolescent↗

PubMed2002

Pyranmycins, a novel class of aminoglycosides with improved acid stability: the SAR of D-pyranoses on ring III of pyranmycin.

[reaction: see text] The synthesis of a novel class of aminoglycosides, pyranmycins, is reported along with the structure activity relationship (SAR) of their antibacterial activity against Escherichia coli. Two pyranmycins show prominent activity (9 microM). Pyranmycins also manifest superior stability in acidic media. The SAR information will lead to the future designs of pyranmycin against drug resistant bacteria.

Aminoglycosides↗

PubMed2002

The destruction box of the cyclin Clb2 binds the anaphase-promoting complex/cyclosome subunit Cdc23.

Properly regulated cyclin proteolysis is critical for normal cell cycle progression. A nine-amino acid peptide motif called the destruction box (D box) is present at the N terminus of the yeast mitotic cyclins. This short sequence is required for cyclin ubiquitination and subsequent proteolysis. The anaphase-promoting complex/cyclosome (APC/C) is a multisubunit E3 required for cyclin ubiquitination. We have tested the D box of five mitotic cyclins for interaction with six APC/C subunits. The APC/C subunit Cdc23, but not five other subunits tested, interacted by two-hybrid analysis with the N terminus of wild-type Clb2. None of these subunits interacted with the N termini of the cyclins Clb1, Clb3, or Clb5. Mutations in the D box sequences of Clb2 inhibited interaction with Cdc23 both in vivo and in vitro. Our results provide the first evidence for a direct interaction between an APC/C substrate (Clb2) and an APC/C subunit (Cdc23).

Amino Acid Motifs↗

PubMed2002

The Synthesis of L-aminosugar and the studies of L-pyranoses on the ring III of pyranmycins.

The synthesis of a novel class of aminoglycoside, pyranmycin, and a convenient method for the preparation of 6-amino-L-idopyranosides were reported. One of the members in the reported pyranmycin families, TC010, has prominent activity against Escherichia coli, Staphylococcus aureus, and Bacillus megaterium. We also discovered that the (4)C(1) chair conformation on ring III of pyranmycin is essential for the antibacterial activity. [reaction: see text]

Amino Sugars↗

PubMed2002

Exposure to schistosome eggs protects mice from TNBS-induced colitis.

Crohn's disease results from dysregulated T helper (Th)1-type mucosal inflammation. Crohn's disease is rare in tropical countries but prevalent in developed countries with temperate climates, in which its incidence rose after 1940. In contrast, exposure to helminthic parasites is common in tropical countries but is rare in developed countries. Helminthic parasites induce immunomodulatory T cell responses in the host. We hypothesize that immunomodulatory responses due to helminths may attenuate excessive Th1-type inflammation. To test that hypothesis, mice were exposed to eggs of the helminth Schistosoma mansoni and then challenged rectally with trinitrobenzesulfonic acid (TNBS) to induce colitis. Schistosome egg exposure attenuated TNBS colitis and protected mice from lethal inflammation. Schistosome egg exposure diminished IFN-gamma and enhanced IL-4 production from alphaCD3-stimulated spleen and mesenteric lymph node cells of TNBS-treated mice. Schistosome egg exposure decreased colonic IFN-gamma but increased IL-10 mRNA expression in TNBS-treated mice. Intact signal transducer and activator of transcription 6 was required for attenuation of colitis. Exposure to helminths can decrease murine colonic inflammation.

Animals↗

PubMed2002

Serine repeat antigen (SERA5) is predominantly expressed among the SERA multigene family of Plasmodium falciparum, and the acquired antibody titers correlate with serum inhibition of the parasite growth.

The Plasmodium falciparum serine repeat antigen (SERA) is one of the blood stage malaria vaccine candidates. The malaria genome project has revealed that SERA is a member of the SERA multigene family consisting of eight SERA homologues clustered on chromosome 2 and one SERA homologue on chromosome 9. Northern blotting and real time quantitative reverse transcription-PCR with five independent parasite strains, including three allelic representative forms of the SERA gene, have shown that all of the SERA homologues are transcribed most actively at trophozoite and schizont stages and that SERA5 (SERA/SERP) is transcribed predominantly among the family. Polyclonal antibodies were raised against recombinant proteins representing the N-terminal portions of four significantly transcribed SERA homologues (SERA3 to -6) in the center of the cluster on chromosome 2. Using these antibodies, indirect immunofluorescence microscopy detected the expression of SERA3 to -6, with similar localization, in all trophozoite- and schizont-infected erythrocytes. We have examined 40 sera from Ugandan adults for their antibody reactivity and found that enzyme-linked immunosorbent assay titer against SERA5 N-terminal domain, but not against other SERA proteins, is positively correlated with the inhibition of in vitro parasite growth by individual sera. Our data confirm the usefulness of the N-terminal domain of SERA5 as a promising malaria candidate vaccine.

Adult↗

PubMed2002

Progesterone's role in mammary gland development and tumorigenesis as disclosed by experimental mouse genetics.

The progesterone receptor knockout mouse demonstrated progesterone's importance to parity-induced mammary tertiary branching and lobuloalveologenesis. Because early parity provides significant protection against breast cancer whereas prolonged exposure to premenopausal ovarian progesterone (or to postmenopausal supplementations thereof) has been linked to breast cancer risk, this steroid can be considered to exhibit contrasting roles in breast cancer etiology. This review describes the important mouse models that have contributed to our understanding of progesterone's role in mammary gland development and neoplasia. We conclude by emphasising the urgent need to identify the molecular targets of the progesterone receptor, and to determine whether these targets are modulated differently by the progesterone receptor isoforms (A and B) during mammary morphogenesis and tumorigenesis.

Animals↗

PubMed2002

p53 transgenic mice are highly susceptible to 1, 2-dimethylhydrazine-induced uterine sarcomas.

p53 Transgenic mice were crossed with C57BL/6J mice to investigate whether a germ-line mutation in the p53 gene predisposes for tumorigenesis in mice. (C57BL/6J x UL53-3) F(1) mice were treated with 1,2-dimethylhydrazine (DMH), a colon carcinogen. The presence of a mutant p53 led to an increased incidence or multiplicity of uterine sarcomas, colon carcinomas, lung adenomas, and hepatomas in DMH-treated mice. The most significant effect of mutant p53 was the increased incidence of uterine sarcomas, which were found in approximately 90% of p53(val135/wt) mice but only seen in approximately 10% of p53(wt/wt) mice. After examination of 15 known p53 downstream target genes in uterine sarcomas and normal uteri, we found that expression of the Reprimo gene was significantly increased in normal uteri of p53(wt/wt) mice but not in either normal uterus or uterine sarcomas of p53(val135/wt) mice. In DMH-treated animals, long-term treatment with this chemopreventive agent, piroxicam, reduced colon carcinoma incidence and multiplicity in both p53(val135/wt) or p53(wt/wt) mice but did not affect the formation of uterine sarcomas, lung adenomas, or hepatomas. These results demonstrate a tissue-specific enhancement of tumorigenesis in multiple organs by the mutant p53 transgene and additionally support the utility of (C57BL/6J x UL53-3) F(1) mice for chemoprevention studies.

1,2-Dimethylhydrazine↗

PubMed2002

[The UCSNP44 variation of calpain 10 gene on NIDDM1 locus and its impact on plasma glucose levels in type 2 diabetic patients].

OBJECTIVE: To study the contribution of single nucleotide polymorphism-UCSNP44 at calpain-10 gene (CAPN-10) on NIDDM1 locus to type 2 diabetes mellitus (T2DM) in Chinese. METHODS: 276 Chinese living in Shanghai, 148 with normal glucose tolerance (NGT) and 128 with T2DM were given 75 g glucose. O, 30, 60, 120, and 180 minutes later their plasma glucose (PG), insulin (INS), C-peptide (CP), and free fatty acids (FFA) were measured and the areas under curve (AUC) were calculated. The islet beta-cell insulin secretion and tissue insulin sensitivity were estimated by formulae of homeostasis model assessment and increment ratio of insulin to glucose levels 30 minutes after glucose challenge. The CAPN-10 UCSNP44 as well as UCSNP43 were genotyped by automated DNA direct sequencing. RESULTS: (1) The major genotype of CAPN-10 UCSNP44 in persons with NGT was TT (with a frequency of 0.82); the major allele was T (0.91). The most frequent genotype combination between UCSNP44 and UCSNP43 was TT-GG (corresponding to haplotype combination TG/TG) (0.64). The most frequent haplotype was TG (0.80). The D value for linkage disequilibrium between UCSNP44 and UCSNP43 was -0.11. (2) The frequencies of UCSNP44 and UCSNP44/UCSNP43 haplotype combination did not differ significantly between subjects with NGT and those with T2DM. (3) The PG levels in T2DM subjects with UCSNP44 TT genotype both at fasting and after glucose challenge were statistically significantly higher than those in subjects with non-TT (TC + CC) genotype, especially the PG levels 0, 60, 120, and 180 minutes after glucose challenge (P = 0.036, 0.040, 0.020, and 0.017) and the PG-AUC (P = 0.013). The PG levels and PG-AUC 0 and 120 minutes after glucose challenge were still significant after adjusted with age, sex, and body mass index and waist circumference. Similar results were observed in comparison between the TG/TG and TG/CG subgroups of UCSNP44/UCSNP43 haplotype combination. In addition, T2DM subjects with UCSNP44 TT genotype had lower CP levels after glucose challenge than those with non-TT genotype. However, the difference became not statistically significant after adjusted with above-mentioned variables. CONCLUSION: The variation of CAPN-10 UCSNP44 has an impact on plasma glucose levels at fasting and after glucose challenge in subjects with type 2 diabetes. The relevant mechanism remains to be elucidated.

Blood Glucose↗

PubMed2002

Impaired motor activity and motor learning function in rat with middle cerebral artery occlusion.

The poor quality of life after a stroke is largely attributed to deficits in cognitive-motor functioning. The goals of this study were to detect if damaged motor learning function were attributed to motor deficits in rats following a transient middle cerebral artery (MCA) occlusion. Stroke was induced by a 2-h occlusion of the MCA using an intraluminal filament. Motor functions were evaluated from 5 up to 28 days after reperfusion in ischemic and control rats. Motor function was detected by a series of motor tests (runway traversing and beam balancing, as well as foot fault placing, parallel bar crossing, rope and ladder climbing), and motor learning behavior was determined by analyzing the rate of improvement of impaired function during performance of the motor tasks. Significant (P<0.001) motor deficits were detected in the stroke group (n=10) while performing motor tasks that involve extensive coordination, in comparison to the controls (n=12). Although motor behavior was improved with repeated behavior testing, unparalleled rate of improvement of motor performance on rope and ladder climbing tests was found between the two groups, suggesting an impaired motor learning function. Brain tissue damage was detected in the ischemic animals 28 days after surgery, demonstrated by 40% infarct volume of contralateral hemisphere. Both motor learning and motor function were impaired in ischemic rats. The motor tests used in this study are sensitive, semi-quantitative, and reproducible measurements of functional impairment in rats following an ischemic stroke.

Animals↗

PubMed2002

An analysis of T cell intrinsic roles of E2A by conditional gene disruption in the thymus.

The importance of E2A transcription factors in T cell development has been demonstrated in studies of E2A-deficient mice, which display abnormal T cell development and a high frequency of T cell lymphomas. Because E2A expression is not restricted to the T cell lineage, the primary cause of the T cell phenotype in E2A-deficient mice was not fully determined. To further investigate the role of E2A in T cell lineage, we generated mice with the E2A gene disrupted exclusively during thymocyte development using the Cre-lox system. We show that this system allows E2A gene disruption to occur throughout the double-negative stage of thymocyte development. E2A deletion appears to be completed before development reaches the double-positive stage. Consistent with the gene disruption, these mice reveal a T cell intrinsic role for E2A during the transition from the double-negative stage to the double-positive stage of thymocyte development. In contrast to germline E2A knockout mice, conditional E2A knockout mice do not develop T cell lymphoma. This work establishes a new model for further investigating E2A function in T cell development and leukemiogenesis.

Adoptive Transfer↗

PubMed2002

[Histopathology of congenital pseudarthrosis of tibia].

OBJECTIVE: To investigate the histopathology, origin, and etiology of congenital pseudarthrosis (CPT). METHODS: Specimens of periosteum from 28 CPT cases, 20 cases of traumatic pseudarthrosis (TP), 10 cases of fibromatosis, and 10 normal controls were examined. The pathological changes were observed by electron microscopy and confocal microscopy. The expression of alpha-smooth muscle (SM) actin, vimentin, desmin, bone morphogenic protein (BMP), interleukin (IL)-1, IL-6, tumor necrosis factor-alpha (TNF-alpha) and base fibroblast growth factor (b-FGF) were detected by histochemistry and immunofluorescence chemical staining. Chromosomal karyotype was examined among 11 cases of CPT. RESULTS: (1) Electron microscopy showed that the periosteum and soft tissue between the broken ends in CPT were all dense fibrous connective tissue abundant in cells, including fibroblasts, myofibroblasts, etc. (2) The chief collagen element was type I collagen in normal periosteum and was type III collagen in periosteum of patients with CPT and fibromatosis (P < 0.025). (3) Vimentin was positive and desmin was negative in all specimens. The expression of alpha-SM actin was higher in specimens from CPT and fibromatosis than in specimens from normal control and TP (P < 0.01). The expression of BMP was higher in normal periosteum and TP than in the periosteum of CPT and fibromatosis (P < 0.05). The expression of IL-1, IL-6, TNF-alpha, b-FGF was higher in the periosteum of CPT and TP (P < 0.01). (4) The chromosomal karyotype of all CPT patients was normal 46XY or 46XX. CONCLUSION: (1) Neurofibromatosis is probably not the etiological factor of CPT. (2) CPT is a kind of invasive fibromatosis located in periosteum. (3) Abnormal expression of many kinds of cytokine and high expression of type III collagen play an important role in the pathogenesis of CPT. (4) The main pathology of CPT is hyperplasia of fibroblasts, thus causing thickening of periosteum, contractible circinate coarctation, and compression of tibia and surrounding tissues. (5) The chromosomal karyotype of patients with CPT is normal.

Adolescent↗

PubMed2002

Characterization of proteases involved in the processing of Plasmodium falciparum serine repeat antigen (SERA).

The Plasmodium falciparum serine repeat antigen (SERA), a malaria vaccine candidate, is processed into several fragments (P73, P47, P56, P50, and P18) at the late schizont stage prior to schizont rupture in the erythrocytic cycle of the parasite. We have established an in vitro cell-free system using a baculovirus-expressed recombinant SERA (bvSERA) that mimics the SERA processing that occurs in parasitized erythrocytes. SERA processing was mediated by parasite-derived trans-acting proteases, but not an autocatalytic event. The processing activities appeared at late schizont stage. The proteases are membrane associated, correlating with the secretion and accumulation of SERA within the parasitophorous vacuole membrane (PVM). The activity responsible for the primary processing step of SERA to P47 and P73 was inhibited by serine protease inhibitor DFP. In contrast, the activity responsible for the conversion of P56 into P50 was inhibited by each of the cysteine protease inhibitors E-64, leupeptin and iodoacetoamide. Moreover, addition of DFP, E-64 or leupeptin to the cultures of schizont-stage parasites blocked schizont rupture and release of merozoites from PVM. These results indicate that SERA processing correlates to schizont rupture and the processing is mediated by at least three distinct proteases.

Animals↗

PubMed2002

Accelerated alpha-synuclein fibrillation in crowded milieu.

Parkinson's disease is the second most common age-related neurodegenerative disease, resulting from loss of dopaminergic neurons in the substantia nigra. The aggregation and fibrillation of alpha-synuclein has been implicated as a causative factor in the disease, and the process of fibril formation has been intensively studied in vitro with dilute protein solutions. However, the intracellular environment of proteins is crowded with other macromolecules, whose concentration can reach 400 g/l. To address this discrepancy, the effect of molecular crowding on alpha-synuclein fibrillation has being studied. The addition of high concentrations of different polymers (proteins, polysaccharides and polyethylene glycols) dramatically accelerated alpha-synuclein fibrillation in vitro. The magnitude of the accelerating effect depended on the nature of the polymer, its length and concentration. Our results suggest that the major factor responsible for the accelerated fibrillation under crowded conditions is the excluded volume.

Chemical Phenomena↗

PubMed2002

Heparin and other glycosaminoglycans stimulate the formation of amyloid fibrils from alpha-synuclein in vitro.

Parkinson's disease is the second most common neurodegenerative disease and results from loss of dopaminergic neurons in the substantia nigra. The aggregation and fibrillation of alpha-synuclein have been implicated as a causative factor in the disease. Glycosaminoglycans (GAGs) are routinely found associated with amyloid deposits in most amyloidosis diseases, and there is evidence to support an active role of GAGs in amyloid fibril formation in some cases. In contrast to the extracellular amyloid deposits, the alpha-synuclein deposits in Lewy body diseases are intracellular, and thus it is less clear whether GAGs may be involved. To determine whether the presence of GAGs does affect the fibrillation of alpha-synuclein, the kinetics of fibril formation were investigated in the presence of a number of GAGs and other charged polymers. Certain GAGs (heparin, heparan sulfate) and other highly sulfated polymers (dextran sulfate) were found to significantly stimulate the formation of alpha-synuclein fibrils. Interestingly, the interaction of GAGs with alpha-synuclein is quite specific, since some GAGs, e.g., keratan sulfate, had negligible effect. Heparin not only increased the rate of fibrillation but also apparently increased the yield of fibrils. The molar ratio of heparin to alpha-synuclein and the incorporation of fluorescein-labeled heparin into the fibrils demonstrate that the heparin is integrated into the fibrils and is not just a catalyst for fibrillation. The apparent dissociation constant for heparin in stimulating alpha-synuclein fibrillation was 0.19 microM, indicating a strong affinity. Similar effects of heparin were observed with the A53T and A30P mutants of alpha-synuclein. Since there is some evidence that Lewy bodies may contain GAGs, these observations may be very relevant in the context of the etiology of Parkinson's disease.

Amino Acid Substitution↗

PubMed2002

Biophysical properties of the synucleins and their propensities to fibrillate: inhibition of alpha-synuclein assembly by beta- and gamma-synucleins.

The pathological hallmark of Parkinson's disease is the presence of intracellular inclusions, Lewy bodies, and Lewy neurites, in the dopaminergic neurons of the substantia nigra and several other brain regions. Filamentous alpha-synuclein is the major component of these deposits and its aggregation is believed to play an important role in Parkinson's disease and several other neurodegenerative diseases. Two homologous proteins, beta- and gamma-synucleins, are also abundant in the brain. The synucleins are natively unfolded proteins. beta-Synuclein, which lacks 11 central hydrophobic residues compared with its homologs, exhibited the properties of a random coil, whereas alpha- and gamma-synucleins were slightly more compact and structured. gamma-Synuclein, unlike its homologs, formed a soluble oligomer at relatively low concentrations, which appears to be an off-fibrillation pathway species. Here we show that, although they have similar biophysical properties to alpha-synuclein, beta- And gamma-synucleins inhibit alpha-synuclein fibril formation. Complete inhibition of alpha-synuclein fibrillation was observed at 4:1 molar excess of beta- and gamma-synucleins. No significant incorporation of beta-synuclein into the fibrils was detected. The lack of fibrils formed by beta-synuclein is most readily explained by the absence of a stretch of hydrophobic residues from the middle region of the protein. A model for the inhibition is proposed.

Amino Acid Sequence↗