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Biomedical subjects

S Xie

Publications and source records attributed to S Xie.

At least 19 recordsLinked to original sources
PubMed2006

Voxel-based detection of white matter abnormalities in mild Alzheimer disease.

OBJECTIVE: To detect white matter abnormalities in patients with mild Alzheimer disease (AD) by diffusion tensor imaging and to determine their topographic relationship with gray matter atrophy. METHODS: Thirteen patients with mild AD and 16 normal age-matched volunteers underwent diffusion tensor imaging and three-dimensional spoiled gradient-recalled sequence scanning. Voxel-based morphometry was conducted to detect regions of gray matter atrophy in the AD group relative to the control group. Fractional anisotropy (FA) maps were processed using SPM2 to make voxel-wise comparison of anisotropy in whole brain between the two groups. The relationship between locations of abnormalities in the white and gray matter was examined. RESULTS: Significant reductions in anisotropy were found in the white matter of both medial temporal lobes, bilateral temporal stems, bilateral superior longitudinal fasciculi, bilateral internal capsules, and cerebral peduncles, as well as the white matter of left middle temporal gyrus and right superior parietal lobule, the body and genu of the corpus callosum, and the right lateral capsule in patients with AD. Although the decrease in FA was consistent with cortical volumetric reduction in both temporal lobes, the widespread involvement of bilateral superior longitudinal fasciculi was dominant in these white matter findings. CONCLUSIONS: Voxel-wise comparison of whole-brain anisotropy revealed widely distributed disintegration of white matter in mild Alzheimer disease (AD). The white matter shows a different pattern of degeneration from gray matter and may be an independent factor in the progress of AD.

Aged↗
PubMed2006

Co-transplantation of bone marrow stromal cells transduced with IL-7 gene enhances immune reconstitution after allogeneic bone marrow transplantation in mice.

Allogeneic bone marrow transplantation (allo-BMT) is followed by a period of profound immune deficiency, which results in significant susceptibility to infections and limits the extensive application of this approach in clinic. Here, we transduced human interleukin-7 (IL-7) gene into donor-derived bone marrow stromal cells (MSCs) using adenovirus vector, and transplanted this gene-engineered MSCs (MSC-IL-7) into lethally irradiated C57BL/6 mice to investigate their effects on immune reconstitution following allo-BMT. Recipient mice receiving MSC-IL-7 cells plus T-cell-depleted bone marrow cells of BALB/c mice showed a significant increase in thymopoiesis and homeostatic expansion of peripheral T lymphocytes. Furthermore, injection of MSC-IL-7 cells following allo-BMT protected the host from the lethality caused by acute graft-versus-host disease (GVHD) and prevented the occurrence of GVHD induced by transplanted T cells. Thus, the use of MSC-IL-7 cells may be therapeutically useful for enhancing immune reconstitution without aggravating GVHD in allo-BMT mice.

Adenoviridae↗
PubMed2006

Softening caused by profuse shear banding in a bulk metallic glass.

By controlling the specimen aspect ratio and strain rate, compressive strains as high as 80% were obtained in an otherwise brittle metallic glass. Physical and mechanical properties were measured after deformation, and a systematic strain-induced softening was observed which contrasts sharply with the hardening typically observed in crystalline metals. If the deformed glass is treated as a composite of hard amorphous grains surrounded by soft shear-band boundaries, analogous to nanocrystalline materials that exhibit inverse Hall-Petch behavior, the correct functional form for the dependence of hardness on shear-band spacing is obtained. Deformation-induced softening leads naturally to shear localization and brittle fracture.

Journal Article↗
PubMed2005

Transforming growth factor beta1-modified donor cell transfusion induced allo-heart tolerance.

The therapeutic value of the transforming growth factor beta 1 (TGF-beta1) in transplantation has been reported; however, cell-mediated gene therapy using TGF-beta1 is not a widespread application in organ transplantation. This study was performed to evaluate whether TGF-beta1-modified donor spleen cell-specific transfusion could induce tolerogenicity and prolong allograft survival in rat heterotopic heart transplantation. Stable TGF-beta1-transduced spleen cells were established. Wistar rat splenic T-cell responses to donor spleen cells that received TGF-beta1-transduced were severely impaired. Survival of Sprague-Dawley cardiac allografts in Wistar rats given TGF-beta1-modified donor spleen cells (5 x 10(6), 7 days before transplantation), was extended modestly but significantly. Liposome transduction of donor spleen cells to overexpress TGF-beta1 is associated with marked impairment of their T-cell allostimulatory activity but only modest prolongation of allo-heart survival.

Animals↗
PubMed2005

Gender-specific association between pulse pressure and C-reactive protein in a Chinese population.

There is growing evidence that low-grade chronic inflammation, as reflected by the raised serum concentration of C-reactive protein, might be a risk factor for hypertension, in particular in women. We therefore investigated gender-specific associations of systolic and diastolic blood pressure and pulse pressure with serum C-reactive protein concentration in a Chinese population sample. In 463 participants, we measured serum C-reactive protein concentration using a high-sensitivity immunonephelometric latex-enhanced assay. We performed single and multiple linear regression analyses. The 224 male and 239 female subjects were of similar age (51.0 years) and had similar levels of systolic blood pressure (124.7 mmHg) and pulse pressure (47.1 mmHg), but men, compared with women, had higher diastolic blood pressure (79.6 vs 75.8 mmHg; P<0.0001) and body mass index (24.3 vs 23.4 kg/m2; P=0.003). Both before and after adjustment for age, age2, body mass index, current smoking, alcohol intake, and use of antihypertensive drugs, pulse pressure was significantly associated with serum C-reactive protein concentration in women (P< or =0.002) but not in men (P>0.10; P=0.02 for interaction between gender and serum C-reactive protein). In women, with one-fold increase in serum C-reactive protein concentration, pulse pressure was 1.94 mmHg higher. The categorical analyses confirmed our findings. With similar adjustments applied, women in the fourth quartile, compared with those in the lowest quartile, had a 7.6 mmHg higher pulse pressure (95% confidence interval 3.5-11.7 mmHg; P=0.0003). Furthermore, when women were analysed according to menopausal status, the association between pulse pressure and C-reactive protein was only significant in postmenopausal (P< or =0.04), but not in premenopausal, subjects (P> or =0.21). In conclusion, taken together with the previous gender-specific observations on carotid lesions and hypertension, our finding suggests that chronic low-grade inflammation might play a role in the widening of pulse pressure in Chinese women. This cross-sectional observation warrants further investigation in prospective studies.

Biomarkers↗
PubMed2004

Simultaneous stimulation of Fas-mediated apoptosis and blockade of costimulation prevent autoimmune diabetes in mice induced by multiple low-dose streptozotocin.

Type I diabetes is the result of a selective destruction of insulin-producing beta cells in pancreatic islets by autoreactive T cells. Depletion of autoreactive T cells through apoptosis may be a potential strategy for the prevention of autoimmune diabetes. Simultaneous stimulation of the Fas-mediated pathway and blockade of costimulation by a CTLA4-Fas ligand (FasL) fusion protein has been reported to lead to enhanced in vitro apoptosis of peripheral lymphocytes. To test the feasibility of CTLA4-FasL-based gene therapy to prevent autoimmune diabetes, we developed a recombinant adenovirus containing the human CTLA4-FasL gene (AdCTLA4-FasL). A single injection of 2 x 10(8) plaque-forming units of AdCTLA4-FasL via the tail vein of mice greatly reduced the incidence of autoimmune diabetes (13%, n=15) induced by multiple low-dose streptozotocin. AdCTLA4-FasL administration abrogated pancreatic insulitis, significantly increased apoptosis of pancreatic T-lymphocytes, and altered splenocyte response to mitogenic and antigenic stimulation. These results indicate the therapeutic potential of simultaneous stimulation of the Fas-mediated pathway and blockade of costimulation by adenovirus-mediated CTLA4-FasL gene transfer in the prevention of autoimmune diabetes.

Adoptive Transfer↗
PubMed2002

Dominant NZB contributions to lupus in the (SWR x NZB)F1 model.

(SWR x NZB)F1 (or SNF1) mice succumb to lupus nephritis. Analysis of NZB x SNF1 backcross mice has recently revealed the existence of four dominant SWR loci (H2 on Chr 17, Swrl-1 on Chr 1, Swrl-2 on Chr 14 and Swrl-3 on Chr 18), and two NZB loci (Nba1 and Lbw2/Sbw2, both on Chr 4) conferring lupus susceptibility. The present study focusing on a panel of 88 SWR x SNF1 backcross mice reveals the existence of five suggestive loci for antinuclear antibody formation, consisting of three dominant NZB contributions (Nba4 on Chr 5, Lbw4 on Chr 6, and Nba5 on Chr 7), and two recessive SWR contributions (Swrl-1 on Chr 1, and Swrl-4 on Chr 10). In addition, this study reveals a dominant NZB locus for GN (Nba3 on Chr 7, peak at 31 cM), and a dominant NZB locus linked to early mortality, on Chr 10 (peak at 4 cM). Collectively, these studies suggest that lupus in the SNF1 strain is the epistatic end-product of four dominant SWR loci and four dominant NZB loci. The immunological functions and molecular identities of these loci await elucidation.

Animals↗
PubMed2001

Genetic contributions of nonautoimmune SWR mice toward lupus nephritis.

(SWR x New Zealand Black (NZB))F(1) (or SNF(1)) mice succumb to lupus nephritis. Although several NZB lupus susceptibility loci have been identified in other crosses, the potential genetic contributions of SWR to lupus remain unknown. To ascertain this, a panel of 86 NZB x F(1) backcross mice was immunophenotyped and genome scanned. Linkage analysis revealed four dominant SWR susceptibility loci (H2, Swrl-1, Swrl-2, and Swrl-3) and a recessive NZB locus, Nba1. Early mortality was most strongly linked to the H2 locus on chromosome (Chr) 17 (log likelihood of the odds (LOD) = 4.59 - 5.38). Susceptibility to glomerulonephritis was linked to H2 (Chr 17, LOD = 2.37 - 2.70), Swrl-2 (Chr 14, 36 cM, LOD = 2.48 - 2.71), and Nba1 (Chr 4, 75 cM, LOD = 2.15 - 2.23). IgG antinuclear autoantibody development was linked to H2 (Chr 17, LOD = 4.92 - 5.48), Swrl-1 (Chr 1, 86 cM, colocalizing with Sle1 and Nba2, LOD = 2.89 - 2.91), and Swrl-3 (Chr 18, 14 cM, LOD = 2.07 - 2.13). For each phenotype, epistatic interaction of two to three susceptibility loci was required to attain the high penetrance levels seen in the SNF(1) strain. Although the SWR contributions H2, Swrl-1, and Swrl-2 map to loci previously mapped in other strains, often linked to very similar phenotypes, Swrl-3 appears to be a novel locus. In conclusion, lupus in the SNF(1) strain is truly polygenic, with at least four dominant contributions from the SWR strain. The immunological functions and molecular identities of these loci await elucidation.

Animals↗
PubMed2001

Involvement of Jak2 tyrosine phosphorylation in Bcr-Abl transformation.

We have previously reported that the Jak2 tyrosine kinase but not Jak1 is tyrosine phosphorylated in the absence of IL-3 in Bcr-Abl positive M3.16 cells, which are rendered IL-3 independent by BCR-ABL gene expression. We have explored the involvement of Jak2 tyrosine phosphorylation in Bcr-Abl oncogenic effects. Our results indicate that Jak2 became tyrosine-phosphorylated in a number of cell lines expressing Bcr-Abl, when maintained in medium lacking IL-3, whereas Bcr-Abl negative cells lacked Jak2 tyrosine phosphorylation. Jak2 was poorly tyrosine-phosphorylated in cells expressing the SH2 deletion mutant of Bcr-Abl compared to either wild-type Bcr-Abl or its SH3 deletion mutant. Moreover, tyrosine phosphorylation of Jak2 by Bcr-Abl was inhibited by the Abl tyrosine kinase inhibitor, STI 571, in a dose-dependent manner. This inhibition of Bcr-Abl kinase by the drug did not interfere with the ability of Jak2 and Bcr-Abl to form a complex. Studies with deletion mutants of Bcr-Abl indicated that the C-terminal domain of Abl within Bcr-Abl was involved in complex formation with Jak2. Similarly, GST-Abl pull-down assays confirmed the strong binding to Jak2 by the C-terminus of Abl. Jak2 peptide substrate studies indicated that the Bcr-Abl and Abl tyrosine kinases specifically phosphorylated Y1007 of Jak2 but only poorly phosphorylated Y1008. Phosphorylation of Y1007 of Jak2 is known to be critical for its tyrosine kinase activation. Tyrosine residue 1007 of Jak2 was phosphorylated in 32Dp210 cells as measured by Western blotting with a phosphotyrosine 1007 sequence-specific antibody. A kinase-inactive Jak2 mutant blocked the colony forming ability of K562 cells. Tumor formation of K562 cells in nude mice was similarly inhibited by this kinase-inactive Jak2 mutant. This inhibition was independent of Stat5 tyrosine phosphorylation. Furthermore, tyrosine-phosphorylated Jak2 was detected in blood cells from CML patients in blast crisis but not in a normal marrow sample. In summary, these findings provide strong evidence that the Jak2 tyrosine kinase is a critical factor in Bcr-Abl malignant transformation.

Animals↗
PubMed2001

Plk3 functionally links DNA damage to cell cycle arrest and apoptosis at least in part via the p53 pathway.

Polo-like kinase 3 (Plk3, previously termed Prk) contributes to regulation of M phase of the cell cycle (Ouyang, B., Pan, H., Lu, L., Li, J., Stambrook, P., Li, B., and Dai, W. (1997) J. Biol. Chem. 272, 28646-28651). Plk3 physically interacts with Cdc25C and phosphorylates this protein phosphatase predominantly on serine 216 (Ouyang, B., Li, W., Pan, H., Meadows, J., Hoffmann, I., and Dai, W. (1999) Oncogene 18, 6029-6036), suggesting that the role of Plk3 in mitosis is mediated, at least in part, through direct regulation of Cdc25C. Here we show that ectopic expression of a kinase-active Plk3 (Plk3-A) induced apoptosis. In response to DNA damage, the kinase activity of Plk3 was rapidly increased in an ATM-dependent manner, whereas that of Plk1 was markedly inhibited. Recombinant Plk3 phosphorylated in vitro a glutathione S-transferase fusion protein containing p53, but not glutathione S-transferase alone. Recombinant Plk1 also phosphorylated p53 but on residues that differed from those targeted by Plk3. Co-immunoprecipitation and pull-down assays demonstrated that Plk3 physically interacted with p53 and that this interaction was enhanced upon DNA damage. In vitro kinase assays followed by immunoblotting showed that serine 20 of p53 was a target of Plk3. Furthermore, expression of a kinase-defective Plk3 mutant (Plk3(K52R)) resulted in significant reduction of p53 phosphorylation on serine 20, which was correlated with a decrease in the expression of p21 and with a concomitant increase in cell proliferation. These results strongly suggest that Plk3 functionally links DNA damage to cell cycle arrest and apoptosis via the p53 pathway.

Apoptosis↗
PubMed2001

Reactive oxygen species-induced phosphorylation of p53 on serine 20 is mediated in part by polo-like kinase-3.

Upon exposure of cells to hydrogen peroxide (H(2)O(2)) phosphorylation of p53 was rapidly induced in human fibroblast GM00637, and this phosphorylation occurred on serine 9, serine 15, serine 20, but not on serine 392. In addition, H(2)O(2)-induced phosphorylation of p53 was followed by induction of p21, suggesting functional activation of p53. Induction of phosphorylation of p53 on multiple serine residues by H(2)O(2) was caffeine-sensitive and blocked in ATM(-/-) cells. Polo-like kinase-3 (Plk3) activity was also activated upon H(2)O(2) treatment, and this activation was ATM-dependent. Recombinant His(6)-Plk3 phosphorylated glutathione S-transferase (GST)-p53 fusion protein but not GST alone. When phoshorylated in vitro by His(6)-Plk3, but not by the kinase-defective mutant His6-Plk3(K52R), GST-p53 was recognized by an antibody specifically to serine 20-phosphorylated p53, indicating that serine 20 is an in vitro target of Plk3. Also serine 20-phosphorylated p53 was coimmunoprecipitated with Plk3 in cells treated with H(2)O(2). Furthermore, although H(2)O(2) strongly induced serine 15 phosphorylation of p53, it failed to induce serine 20 phosphorylation in Plk3-dificient Daudi cells. Ectopic expression of a Plk3 dominant negative mutant, Plk3(K52R), in GM00637 cells suppressed H(2)O(2)-induced serine 20 phosphorylation. Taken together, our studies strongly suggest that the oxidative stress-induced activation of p53 is at least in part mediated by Plk3.

Cell Cycle Proteins↗
PubMed2001

[Study on the improved effect of anti-TCR alpha beta monoclonal antibody on the induction of transplantation tolerance to the allogeneic skin graft in mice and its mechanisms].

OBJECTIVE: To study skin allograft tolerance induced by intravenous injection of allogeneic spleen cells and intraperitoneal injection of cyclophosphamide (CP), followed by anti-TCR monoclonal antibody injections in adult recipient mice and its mechanisms. METHODS: Injecting the spleen cells of BALB/c mice (H-2(d)) were injected to C57BL/6 mice (H-2(b), B6) via the tail vein. Two days later an intraperioneal injection of cyclophosphamide was given to the B6 mice, and followed by anti-TCR alpha beta monoclonal antibody injection via the tail vein, after which skin of BALB/c mice were grafted to the tolerance-induced B6 mice. The control groups were: (1) normal B6 mice grafted with BABL/c skin; (2) normal B6 mice grafted with KM skin; (3) B6 mice treated with SC + CP + anti-TCR alpha beta monoclonal antibody administration and grafted with BALB/c skin allograft; (4) B6 mice treated as group 3, and grafted with KM skin instead of BALB/c skin. Detection of chimerism, adoptive transfer assay and the effect of exogenous IL-2 on MLR were performed to explore tolerance mechanisms. Group data in each experiment were compared with Group's t-test. RESULTS: The survival of BALB/c skin allograft in recipient B6 mice was 66.3 days, P < 0.001 compared with the other three groups. The results of FACS analysis showed that a mixed microchimerism was developed in the thymus and spleen of tolerant mice. The percentage of cells of BALB/c origin in the thymus on day 15, 35, and 70 after induction of tolerance was 2.67%, 1.61%, and 0.47%, and in the spleen is 7.66%, 5.99%, and 3.87%, respectively. No suppressive activity in the spleen cells of tolerant mice was observed by in vivo and in vitro cell transfer experiments. MLR of spleen cells in the tolerant B6 mice to spleen cells of BALB/c origin was specifically suppressed, which was 4 725 +/- 406 cpm by (3)H-TdR incorporation. However, the specific inhibition of MLR of tolerant B6 mice could be partially reversed (P < 0.01), the (3)H-TdR incorporation reached 18 175 +/- 3 642 cpm by adding exogenous IL-2. CONCLUSION: Chimerism and clonal anergy are the main mechanisms of the tolerance.

Animals↗
PubMed2001

The relationship of health-related quality of life to prevalent and incident vertebral fractures in postmenopausal women with osteoporosis: results from the Multiple Outcomes of Raloxifene Evaluation Study.

OBJECTIVE: To examine the effect of both prevalent and incident vertebral fractures on health-related quality of life (HRQOL) in postmenopausal women with osteoporosis and to characterize the effect of prevalent vertebral fractures on HRQOL with respect to number, location, severity, and adjacency. METHODS: Participants were a subset of women (n = 1,395, mean age 68.5 years) from the Multiple Outcomes of Raloxifene Evaluation trial who had low bone mineral density and/or prevalent vertebral fractures. Vertebral fractures were measured by radiography at baseline, 2 years, and 3 years. HRQOL was assessed using the Osteoporosis Assessment Questionnaire (OPAQ), a validated disease-targeted instrument, at baseline and annually for 3 years. RESULTS: Both prevalent and incident radiographic vertebral fractures were associated with decreased HRQOL. At baseline, women with a prevalent vertebral fracture had significantly lower OPAQ scores on physical function, emotional status, clinical symptoms, and overall HRQOL compared with women without a prevalent fracture (all P < 0.01). HRQOL scores were lower with each subsequent fracture. The effect of prevalent vertebral fracture was dependent on the location within the spine and was strongest in the lumbar region (L1-L4). Incident vertebral fractures significantly decreased OPAQ scores on physical function, emotional status, clinical symptoms, and overall HRQOL (all P < 0.001). CONCLUSION: Our findings demonstrate the importance of treating postmenopausal women who have prevalent vertebral fractures to prevent further decreases in HRQOL associated with subsequent incident vertebral fracture.

Aged↗
PubMed2001

Gene for porcine pregnancy-associated glycoprotein 2 (poPAG2): its structural organization and analysis of its promoter.

The pregnancy-associated glycoproteins (PAG) are abundant secretory products of the placental trophectoderm of ungulate species. They are structurally related to pepsin, having the capability to bind peptides. However, many cannot function as enzymes due to amino acid substitutions in and around the catalytic site. Here, we demonstrate that pigs, like cattle and sheep, but unlike equids, have multiple PAG genes. One of the transcribed porcine PAG (poPAG) genes, the one for poPAG2, was cloned. It had a nine-exon organization similar to that of other mammalian aspartic proteinase genes with an atypical TATA sequence. A total of 1.2 kbp upstream from exon 1 was sequenced. This region shared identity (> 65%) with the promoter regions of the bovine (bo) PAG1, boPAG2 and equine (eq) PAG genes, but not with other aspartyl proteinase genes, including that of pepsinogen A. Nor were there clear similarities to the promoters of other genes with trophoblast-specific expression. Of the different poPAG2 promoter constructs tested in transfection experiments in two human (JAr and JEG3) and one rat (Rcho) choriocarcinoma cell lines, only the shortest (-149 bp) was required to provide full expression of a luciferase reporter. Although this short promoter was not active in Cos-1 and L-929 cells, it was active in CHO cells, a transformed non-trophoblast hamster ovarian cell line. Co-transfection of Ets2 elevated the activity of this short promoter approximately six-fold in JAr cells, but, disruption of the two putative Ets sites did not alter the ability of Ets2 to transactivate the promoter. In the non-trophoblast cell lines, Ets2 failed to elicit any response. Ets2 responsiveness may be a common feature of most or all trophoblast-expressed genes, although in the case of poPAG2, the effect may be indirect.

5' Untranslated Regions↗
PubMed2001

Steroidal saponins from Tribulus terrestris.

Three new steroidal saponins were isolated from the fruits of Tribulus terrestris, and their structures were elucidated as (25R,S)-5 alpha-spirostane-12-one-3 beta-ol-3-O-beta-xylopyranosyl(1-->2)- [beta-xylopyranosyl(1-->3)]-beta-glucopyranosyl(1-->4)-[alpha-rhamno- pyranosyl(1-->2)]-beta-galactopyranoside; 26-O-beta-glucopyranosyl-(25S)-5 alpha-furostane-12-one-3 beta,22 alpha,26-triol-3-O-beta-glucopyranosyl(1-->2)-beta-galactopyranoside; 26-O-beta-glucopyranosyl-(25S)-5 alpha-furostane-12-one-3 beta,22 alpha,26-triol-3-O-beta-glucopyranosyl(1-->4)-[alpha- rhamnopyranosyl(1-->2)]-beta-galactopyranoside, respectively, by spectroscopic analysis and color reaction.

Carbohydrate Sequence↗
PubMed2001

[Accurate diagnosis of stages of hepatic fibrosis by measuring levels of serum hyaluronic acid, procollagen type III, and collagen type IV].

OBJECTIVE: To study the accurate diagnosis of various stages of hepatic fibrosis by measuring serum hyaluronic acid (HA), procollagen type III (PC III), and collagen type IV (CIV). METHODS: The concentrations of serum HA, PC III, CIV in 253 patients with chronic liver disease were measured by radioimmunoassay. Liver biopsies were performed in all of the patients at the same time. According to the results of liver pathological diagnosis, we assessed the ability of serum HA, PC III and CIV to identify correctly patients with hepatic fibrosis (staging >or=S(2)) or cirrhosis (S(4)). RESULTS: The cutoff value of HA, PC III and C IV to identify correctly patients with hepatic fibrosis was 90 microg/L, 90 microg/L, 75 microg/L respectively. The sensitivity (Se) was 80.4%, 82%, 63.1%; the specificity (Spe) was 70.2%, 60.8%, 83.8%; the positive prediction value (PPV) was 86.7%, 83.5%, 90.4%; the negative prediction value (NPV) was 59.8%, 58.4%, 48.4%, respectively. The cutoff value to identify patients with cirrhosis was: HA 210 microg/L, Se 96.2%, Spe 85.3%, PPV 65.4%, NPV 98.8%; PC III 150 microg/L, Se 76.4%, Spe 68.7%, PPV 40.4%, NPV 91.3%; C IV 90 microg/L, Se 80%, Spe 75.8%, PPV 47.8%, NPV 93.2%, respectively. CONCLUSIONS: The determination of serum HA, PC III and C IV can make relatively accurate diagnosis to various stages of hepatic fibrosis. HA is the best for diagnosis of liver cirrhosis.

Biopsy↗
PubMed2001

[Mycobacterium tuberculosis L forms in patients with pulmonary silicotuberculosis and silicosis].

OBJECTIVE: To evaluate significance of Mycobacterium tuberculosis L forms in pathogenesis of silicotuberculosis and silicosis. METHODS: Sputum culture for Mycobacterium tuberculosis and its L forms was conducted from both silicotuberculosis and silicosis groups, and the results were compared. RESULTS: Among 60 silicotuberculosis patients, 6 (10%) were sputum Mycobacterium tuberculosis culture positive, of which 5 (83%) were Mycobacterium tuberculosis L forms culture positive; 28 were sputum Mycobacterium tuberculosis L forms culture positive (positive rates in the patients with silicosis stage I, stage II, stage III were 33%, 67%, 100% respectively), with a positive rate of 47%, and a significant difference was found comparing with the frequency of detecting Mycobacterium tuberculosis (P < 0.01). All of the 30 cases with silicosis were Mycobacterium tuberculosis culture negative, however, 3 of them were sputum Mycobacterium tuberculosis L forms culture positive, accounting for 10 percent. CONCLUSIONS: Sputum culture for Mycobacterium tuberculosis L forms is a convenient and rapid way to improve the detection rate of Mycobacterium tuberculosis, with a positive value in early diagnosis of silicotuberculosis by reducing misdiagnosis and underdiagnosis of this disease. Detection rate of Mycobacterium tuberculosis L forms significantly increases with deterioration of silicosis.

Aged↗