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T Dao

Publications and source records attributed to T Dao.

At least 19 recordsLinked to original sources
PubMed2006

Risk factors for postoperative chest wound infections due to gram-negative bacteria in cardiac surgery patients.

Gram-negative bacteria account for up to 35% of postoperative sternal wound infections (SWI) in patients undergoing cardiac surgery. Despite this, risk factors for Gram-negative SWI have not been investigated. The objective of this study was to define risk factors associated with Gram-negative SWI in patients undergoing cardiac surgery. 2590 patients undergoing cardiac surgery between 2002-2005 were prospectively monitored for development of SWI. Patient, operative, and post-operative risk factors were compared among patients that developed Gram-negative SWI and Gram-positive SWI to uninfected controls using univariate and multivariate analysis. A p < 0.05 was considered significant. Surgical site infections developed in 152 (5.9%) patients. Isolates were recovered from the sternum for 128 (5.0%) patients, from the leg donor site for 19 (0.73%) patients, and from the sternum and donor site for 5 (0.19%) patients. Gram-positive pathogens were isolated from 83 (3.3%) patients, Gram-negative pathogens from 42 (1.6%) patients, and mixed pathogens from 27 (1.0%) patients. Hospital admission greater than 48 hours before surgery (OR: 2.25; 95% CI: 1.11 - 4.58), ventilator-dependency preoperatively (OR: 5.32 95% CI: 2.22 - 12.75), and thoracentesis procedure postoperatively (OR: 3.71; 95% CI: 1.45 - 9.49) and diabetes (OR: 2.04; 95% CI: 1.17 - 3.55) were identified as significant risk factors for SWI due to Gram-negative bacteria using multivariate logistic regression. Diabetes, increased age, and peripheral vascular disease were identified as significant risk factors for SWI due to Gram-positive bacteria (p < 0.05, each). The risk factors associated with Gram-negative SWI differed significantly from those associated with Gram-positive SWI. Risk factors associated with Gram-negative SWI were identified. Unique interventions may be necessary to prevent Gram-negative SWI in cardiac surgery patients.

Aged↗
PubMed2001

Involvement of CD1 in peripheral deletion of T lymphocytes is independent of NK T cells.

During peripheral T cell deletion, lymphocytes accumulate in nonlymphoid organs including the liver, a tissue that expresses the nonclassical, MHC-like molecule, CD1. Injection of anti-CD3 Ab results in T cell activation, which in normal mice is followed by peripheral T cell deletion. However, in CD1-deficient mice, the deletion of the activated T cells from the lymph nodes was impaired. This defect in peripheral T cell deletion was accompanied by attenuated accumulation of CD8(+) T cells in the liver. In tetra-parental bone marrow chimeras, expression of CD1 on the T cells themselves was not required for T cell deletion, suggesting a role for CD1 on other cells with which the T cells interact. We tested whether this role was dependent on the Ag receptor-invariant, CD1-reactive subset of NK T cells using two other mutant mouse lines that lack most NK T cells, due to deletion of the genes encoding either beta(2)-microglobulin or the TCR element J alpha 281. However, these mice had no abnormality of peripheral T cell deletion. These findings indicate a novel role for CD1 in T cell deletion, and show that CD1 functions in this process through mechanisms that does not involve the major, TCR-invariant set of NK T cells.

Animals↗
PubMed2001

[Patients with alcoholic liver disease hospitalized in gastroenterology. A national multicenter study].

OBJECTIVES: To describe the characteristics of in-patients with alcoholic liver disease in Hepatogastroenterology and to evaluate whether geographic location was a risk factor for cirrhosis. METHODS: A French, national, multicenter, prospective investigation was performed in the last quarter of 1997. To be included in the study, patients had to have drunk at least 50 g of alcohol per day for the past year or to have cirrhosis. RESULTS: Seventeen centers included 802 patients, 20% had histologically proven cirrhosis or probable cirrhosis. Thirty-five percent had undergone liver biopsy. Twenty five percent of these patients had cirrhosis without acute alcoholic hepatitis and 37% had cirrhosis with acute alcoholic hepatitis. After dividing France along a Bordeaux-Strasbourg axis, there was more histologically proven or probable cirrhosis in the North (46%) than in the South (36%) (P<0.005) while daily alcohol intake was greater the South (150 +/- 6 g) than in the North (129 +/- 4 g) (P<0.0001). When the six variables (age, sex, daily consumption of alcohol over the past 5 years, presence of hepatitis B surface antigen and antibodies to hepatitis C virus, total duration of alcohol abuse) were considered together in stepwise logistic regression analysis, geographic location changed the prediction of cirrhosis. The odds ratio for cirrhosis in patients living to the North of the Bordeaux-Strasbourg axis was 1.9 (95% confidence interval range 1.1-3.2) (P<0.02), suggesting the role of nutritional factors.

Age Distribution↗
PubMed2000

CD95/Fas signaling in T lymphocytes induces the cell cycle control protein p21cip-1/WAF-1, which promotes apoptosis.

Ligation of CD95 on T lymphocytes resulted in the up-regulation of a cell cycle control protein, p21cip-1/WAF-1, an inhibitor of cyclin-dependent kinases. This up-regulation was completely blocked by the cysteine protease inhibitor Z-VAD-fmk (benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone), whereas DEVD-CHO (succinyl-Asp-Glu-Val-Asp-aldehyde), a caspase 3 inhibitor, had no effect. In Faslpr-cg mice, a point mutation in the death domain of CD95 results in failure to recruit FADD (Fas-associated death domain), and in the present study this mutation prevented both CD95-mediated apoptosis and p21cip-1/WAF-1 induction. During apoptotic cell death due to irradiation, p21cip-1/WAF-1 is up-regulated by a p53-dependent pathway that responds to DNA damage. However, CD95-induced up-regulation of p21cip-1/WAF-1 in T cells was p53-independent. T cells deficient in p21cip-1/WAF-1 were less susceptible to CD95-induced apoptosis. We conclude that in T cells, ligation of CD95 and activation of caspases cause the induction of p21cip-1/WAF-1, which acts to promote cell death.

3T3 Cells↗
PubMed2000

Prevalence of electrocardiographic and echocardiographic abnormalities in ambulatory ischemic colitis.

The aim of this study was to evaluate the prevalence of cardiac arrhythmia and intracardiac embolic process in ambulatory ischemic colitis. From November 1994 to November 1997, 33 consecutive cases of ambulatory ischemic colitis were detected. This study included 21 women and 12 men with a mean age of 71 years. All patients underwent a cardiovascular investigation including questioning, electrocardiogram, 24-hr ambulatory electrocardiography and transthoracic echocardiography. A prior history of ischemic colitis was found in four cases (12%). Cardiac arrhythmia was detected in eight cases. Transthoracic echocardiography showed an intracardiac process, potentially responsible for a peripheral embolism, in four cases. In conclusion, the aggregate, in 33% of the patients, there was potential cardiac etiology. This suggests that when ambulatory ischemic colitis occurs, it is necessary to perform an exhaustive cardiovascular evaluation similar to those performed in other ischemic diseases.

Aged↗
PubMed2000

The liver as a site of T-cell apoptosis: graveyard, or killing field?

The liver is a site at which apoptotic CD8+ cells accumulate during the clearance phase of peripheral immune responses. Normal mouse liver contains an unusual mixture of lymphocytes in which natural killer (NK) and NK-T cells are abundant and apoptotic T cells are present, and we interpret these cell populations as, respectively, agents and targets of an intrahepatic T-cell trapping and killing mechanism. In support of this idea, direct perfusion of activated lymphocyte populations through the normal liver results in the selective retention of activated CD8+ T cells. T cells trapped in this manner undergo apoptosis in the liver. This mechanism could explain the importance of the liver in oral tolerance, the phenomenon of tolerance induced by portal vein infusion of antigenic cells, the tolerance to allogeneic liver allografts, and the persistence of some liver pathogens including hepatitis C.

Adoptive Transfer↗
PubMed2000

Induction of murine hepatocyte death by membrane-bound CD95 (Fas/APO-1)-ligand: characterization of an in vitro system.

Hepatocytes constitutively express CD95 (also called Fas/APO-1) and are therefore potential targets for CD95-ligand (CD95L)-mediated injury. To study this mechanism of cell death in hepatocytes we developed an in vitro model of liver cell apoptosis using membrane-bound CD95L as the inducing agent. Primary mouse hepatocytes were cocultured with NIH 3T3 fibroblasts, stably transfected with mouse CD95L (F(CD95L+)). Fibroblasts stably transfected with vector only (F(CD95L-)) served as controls. Hepatocytes from mice expressing low levels of CD95 (Fas(lpr) mice) served as controls for effects unrelated to CD95. Morphologic and biochemical studies indicate that CD95 is expressed in cultured mouse hepatocytes. Membrane-bound CD95 from transfected fibroblasts destroyed all cocultured hepatocytes within 24 hours in the absence of protein synthesis inhibitors. Characteristic features of apoptosis were observed in dying hepatocytes and occurred in the following sequence: formation of cytoplasmic blebs and nuclear condensation after 3 hours; nuclear fragmentation and DNA strand breaks after 4 hours. These changes were observed only when normal hepatocytes were cocultured with F(CD95L+) and were not observed with F(CD95L-) or in hepatocytes from Fas(lpr) mice. Anti-CD95 antibody (Jo2) evoked similar changes in hepatocytes, although to a much lesser extent. We conclude that coculture of mouse hepatocytes with F(CD95L+) is a useful in vitro model for CD95-mediated apoptosis induced by CD95L. The high incidence of apoptosis caused by membrane-bound CD95L differs from the much smaller effects induced by the Jo2 antibody. In view of the high sensitivity of hepatocytes towards CD95L we speculate that CD95L-induced liver damage in vivo may be minimized by restricting exposure of hepatocytes to CD95L.

3T3 Cells↗
PubMed2000

Liver adenomatosis: reappraisal, diagnosis, and surgical management: eight new cases and review of the literature.

OBJECTIVE: Liver adenomatosis (LA) is a rare disease originally defined by Flejou et al in 1985 from a series of 13 cases. In 1998, 38 cases were available for analysis, including eight personal cases. The aim of this study was to review and reappraise the characteristics of this rare liver disease and to discuss diagnosis and therapeutic options. BACKGROUND: LA was defined as the presence of >10 adenomas in an otherwise normal parenchyma. Neither female predominance nor a relation with estrogen/progesterone intake has been noted. Natural progression is poorly known. METHODS: The clinical presentation, evolution, histologic characteristics, and therapeutic options and results were analyzed based on a personal series of eight new cases and an updated review of the literature. RESULTS: From a diagnostic standpoint, two forms of liver adenomatosis with different presentations and evolution can be defined: a massive form and a multifocal form. The role of estrogen and progesterone is reevaluated. The risks of hemorrhage and malignant transformation are of major concern. In the authors' series, liver transplantation was indicated in two young women with the massive, aggressive form, and good results were obtained. CONCLUSION: Liver adenomatosis is a rare disease, more common in women, where outcome and evolution vary and are exacerbated by estrogen intake. Most often, conservative surgery is indicated. Liver transplantation is indicated only in highly symptomatic and aggressive forms of the disease.

Adenoma, Liver Cell↗
PubMed1998

Caspase-3 controls both cytoplasmic and nuclear events associated with Fas-mediated apoptosis in vivo.

Both caspase-1- and caspase-3-like activities are required for Fas-mediated apoptosis. However, the role of caspase-1 and caspase-3 in mediating Fas-induced cell death is not clear. We assessed the contributions of these caspases to Fas signaling in hepatocyte cell death in vitro. Although wild-type, caspase-1(-/-), and caspase-3(-/-) hepatocytes were killed at a similar rate when cocultured with FasL expressing NIH 3T3 cells, caspase-3(-/-) hepatocytes displayed drastically different morphological changes as well as significantly delayed DNA fragmentation. For both wild-type and caspase-1(-/-) apoptotic hepatocytes, typical apoptotic features such as cytoplasmic blebbing and nuclear fragmentation were seen within 6 hr, but neither event was observed for caspase-3(-/-) hepatocytes. We extended these studies to thymocytes and found that apoptotic caspase-3(-/-) thymocytes exhibited similar "abnormal" morphological changes and delayed DNA fragmentation observed in hepatocytes. Furthermore, the cleavage of various caspase substrates implicated in mediating apoptotic events, including gelsolin, fodrin, laminB, and DFF45/ICAD, was delayed or absent. The altered cleavage of these key substrates is likely responsible for the aberrant apoptosis observed in both hepatocytes and thymocytes deficient in caspase-3.

3T3 Cells↗
PubMed1998

IL-18 augments perforin-dependent cytotoxicity of liver NK-T cells.

The liver contains abundant cytotoxic cells, including NK-T cells, NK cells, and CTLs. However, the regulation of this cytotoxicity is not fully understood. In this study, we investigated the effect of a recently described cytokine, IL-18, which is present in large quantities in the liver, on the cytotoxicity of intrahepatic lymphocyte subpopulations. This effect of IL-18 was assessed by assaying the in vitro cytotoxicity of purified NK-T, NK, and T cells against a CD95- and perforin-sensitive T cell line, Jurkat. The results show that IL-18 enhances the killing activity of liver NK-T cells by a CD95-independent, perforin-dependent pathway. IL-18 also augments liver NK cell activity, but the exact mechanisms of this killing remain to be elucidated. Finally, the augmentation of the killing activities of liver NK-T and NK cells by IL-18 is not due to soluble TNF-alpha, because none of these cell populations had detectable TNF-alpha production.

Adjuvants, Immunologic↗
PubMed1998

Treatment of unresectable hepatocellular carcinoma with lipiodol chemoembolization: a multicenter randomized trial. Groupe CHC.

BACKGROUND/AIMS: Lipiodol chemoembolization is a widely used method of treatment in patients with unresectable hepatocellular carcinoma, but its efficacy is still debated. The aim of our study was to assess the efficacy of lipiodol chemoembolization in patients with unresectable hepatocellular carcinoma. METHODS: Seventy-three patients with unresectable hepatocellular carcinoma, but without severe liver disease or portal vein occlusion, were randomly assigned to receive either repeated lipiodol chemoembolization (lipiodol, cisplatin (2 mg/kg), lecithin, and gelatin sponge injected into the hepatic artery) plus tamoxifen (40 mg) or tamoxifen alone. The main end-point was survival. RESULTS: The 37 patients in the lipiodol chemoembolization group received 104 courses (median 3 per patient). By 1 September 1996, 58 patients had died: 30 in the lipiodol chemoembolization group and 28 in the tamoxifen group. There was no difference in survival between the two groups (p=0.77). The relative risk of death in the lipiodol chemoembolization plus tamoxifen group as compared to the tamoxifen group was 0.92 (95% confidence interval 0.55 to 1.56). At 1 year, survival was 51% and 55%, respectively. An objective tumoral response was more frequently observed in the lipiodol chemoembolization group than in the tamoxifen group (24 versus 5.5%, respectively, p=0.046). Lipiodol chemoembolization caused two deaths and induced signs of liver failure in 51% of the patients assigned to this treatment. CONCLUSION: In our randomized study, lipiodol chemoembolization did not improve the survival of patients with unresectable hepatocellular carcinoma treated with tamoxifen.

Adult↗
PubMed1998

[Superficial cancer of the stomach in the area of Calvados from 1978 to 1990. Epidemiology and prognostic factors].

AIMS OF THE STUDY: The 5-year survival rate of gastric cancer is less than 20% in cancer registries. The prognosis of early gastric cancer is much better but this diagnosis is rare in Europe. The aim of the study was to evaluate the prognosis and trends in the incidence of early gastric cancer in the area of Calvados (France) during a 13-year period. METHODS: Between 1978 and 1990 the Digestive Cancer Registry of Calvados recorded 1,160 new cases of gastric cancer. The diagnosis of early gastric cancer was defined according to the Japanese Gastroenterological Society criteria. Prognostic factors were determined with univariate and multivariate analysis. RESULTS: One hundred patients had early gastric cancer (8.6%). This rate did not change significantly during the period. The mean age was 64.2 +/- 1.5 in males and 64.8 +/- 2.2 in females and 39% of patients were older than 70. A precancerous condition was present in 56% of cases on the surgical specimen. A total gastrectomy was performed in 23% of cases and a subtotal gastrectomy in 72% of cases. The postoperative mortality was 5% and the 5-year relative survival was 86.8% +/- 4.6. Univariate and multivariate analysis found a better prognosis in patients younger than 75 or in patients with a superficial or excavated gross appearance compared with those older than 75 or with a protruded type. Lymph node metastasis, depth of invasion, size of the tumor and histologic differentiation did not influence significantly the outcome. CONCLUSION: According to the data of the Cancer Registry of Calvados the proportion of Early Gastric Cancer was low and did not change between 1978 and 1990. The prognosis of EGC is good, mainly altered in elderly and in cases with a protruded type.

Adult↗
PubMed1998

[Castleman's disease of the abdomen].

Plasmocytic variants of Castleman's disease are uncommon. We report a new case of abdominal location with a rapidly fatal outcome. Another particularity of that case was the negativity of Kaposi's sarcoma associated herpesvirus, a virus recently implicated in human immunodeficiency virus associated Castleman's disease.

Aged↗
PubMed1997

Specific resistance of T cells to CD95-induced apoptosis during S phase of the cell cycle.

We have examined the susceptibility of mouse thymocytes and Con A-activated mature T cells to CD95 (Fas; APO-1)-induced apoptosis at different phases of the cell cycle. Signaling through CD95, induced by murine CD95 ligand expressed on fibroblasts, resulted in the preferential apoptosis of T cells in G0-G1 phase of the cell cycle. T cells in S phase were selectively protected. CD95-induced apoptosis was inhibited by exogenous IL-2, which increases the percentage of cells in S phase. The inverse relationship between DNA synthesis and apoptosis in CD95-ligated T cells was not observed during the spontaneous death of T cells in culture or during propriocidal apoptosis due to TCR cross-linking, to which cells in S phase were susceptible. These results show that in T cells there is no distinctively apoptosis-vulnerable phase of the cell cycle; instead, apoptosis can occur at different phases of the cycle depending on the apoptotic stimulus.

Animals↗
PubMed1997

[Epidemiology of hepatocellular carcinoma in the department of Calvados].

OBJECTIVES: The aim of this study was to determine the epidemiological characteristics of hepatocellular carcinoma in a non-selected population. METHODS: Between 1984 and 1990, all cases of hepatocellular carcinoma were registered at the Registry of Digestive Tumors of Calvados. Standardized incidence rates were calculated for males and females. Prognostic factors were determined by the Cox multivariate method. RESULTS: 213 patients with hepatocellular carcinoma were registered. Standardized incidence rates were 7.5/100,000 in men and 0.4/100,000 in women. Sex-ratio was 18.3. Mean age was 66.4 years; hepatocellular carcinoma was uncommon (3%) before the age of 50. Cirrhosis was associated in 85.9% of patients. The cause of cirrhosis was known in 150 cases: alcoholic: 73.3%, cryptogenetic: 8.7%, viral B or C: 7.3%, alcoholic and viral B or C: 5.3%, and genetic hemochromatosis: 4.7%. The overall survival rate in 203 patients was 21%, 8% and 3% at 1 year, 3 years and 5 years, respectively. The multivariate study identified 4 prognostic factors: number of tumors < or = 2, lack of ascites, serum alpha-fetoprotein < or = 10 mg/mL, and hepatocellular carcinoma revealing a well-compensated liver disease until the time of diagnosis. CONCLUSION: The occurrence of hepatocellular carcinoma seems to be linked to cirrhosis, male sex, and age > 50, which could be used as the main selection criterias for the screening of hepatocellular carcinoma.

Adult↗