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OBJECTIVE: To determine factors affecting liver and bile duct contrast enhancement during computed tomographic cholangiography (CTC) in living-donor transplant candidates. METHODS: Forty-four candidates underwent preoperative triphasic CT followed by intravenous infusion of 20 mL of iodipamide for CTC. Body size indices and liver volume were correlated to parenchymal and biliary enhancement. Bile duct visibility was compared to duct enhancement. RESULTS: Poorly visualized first- and second-order bile ducts demonstrated diminished enhancement (P < 0.015). Both CTC parenchymal and biliary enhancement correlated inversely with body surface area, height, and weight (P < 0.001); inverse correlation was also seen between liver volume and parenchymal enhancement (P < 0.001). A moderately positive correlation was noted between CTC biliary and parenchymal portal venous enhancement (r = 0.421; P = 0.004). CONCLUSIONS: Computed tomographic cholangiography parenchymal and biliary enhancement diminishes with increased body size and liver volume, supporting a need for adjustable contrast dosing. Portal venous parenchymal enhancement may serve as a preinfusion indicator.

Purpose To retrospectively evaluate CT findings of xanthogranulomatous cholecystitis (XGC) and to measure diagnostic performance for distinguishing it from gallbladder (GB) cancer. Methods and materials Our institutional review board approved this retrospective study. Three blinded radiologists, first independently and then in consensus, retrospectively evaluated postcontrast CT images of 35 patients with histopathologically proved XGC and GB cancer, all of whom subsequently had cholecystectomy. These included 18 patients with XGC (13 male, 5 female; age range, 35–84, mean 63 years) and 17 with GB cancer (6 male, 11 female; age range, 45–95, mean 69). Differences in CT findings between XGC and GB cancer and diagnostic performances for each CT finding were calculated. Sensitivity, specificity, and accuracy were calculated for each radiologist and observer performance was also determined by receiver-operating-characteristic curve analysis. Results Five CT findings showed significant differences between XGC and GB cancer. Sensitivity, specificity, and accuracy of each finding for the differentiation of XGC were 89%, 65%, 77% with diffuse GB wall thickening, 67%, 82%, 74% with a continuous mucosal line, 61%, 71%, 66% with intra-mural hypo-attenuated nodules, 72%, 77%, 74% with absence of macroscopic hepatic invasion, and 67%, 71%, 69% with absence of intra-hepatic bile duct dilatation, respectively. When at least three of these five CT findings were observed in combination, sensitivity, specificity, and accuracy were 83%, 100% and 91%, respectively. Sensitivities, specificities and Az values for the differentiation of XGC from GB cancer were 83%, 88%, 0.94 for reader 1, 78%, 88%, 0.93 for reader 2, and 78%, 82%, 0.84 for reader 3. Conclusions The combination of three of the five CT findings that are common with XGC can provide excellent accuracy for the differentiation of XGC and GB cancer.

Asthma is one of the most common chronic airway inflammatory diseases. The clinical hallmarks of asthma include elevated serum levels of immunoglobulin E (IgE), eosinophilic inflammation and airway hyper-responsiveness (AHR). Arsenic trioxide (As2O3) is considered a carcinogen; however, it has also been used to treat diseases, such as syphilis, in traditional Chinese and Western medicine. Today, As2O3 is used as one of the standard therapies for acute promyelocytic leukemia (APL). Previous studies have indicated that As2O3 can induce apoptosis in eosinophils. However, the effect of As2O3 on asthma has not been investigated. We used ovalbumin (OVA)-immunized mice as a model for asthma and treated mice with As2O3 at doses of 2.5 and 5 mg/kg. The mice were then monitored for OVA-specific IgE production, airway inflammatory cell infiltration and AHR. We found that administration of As2O3 in OVA-immunized mice abrogated airway eosinophil recruitment by downregulating eotaxin expression but did not alter serum IgE or IL-5 levels in bronchoalveolar lavage fluid (BALF). Furthermore, the development of AHR and cellular infiltration into the airway were reduced by treating mice with As2O3. In vitro data suggested that low concentrations of As2O3 could induce only a small degree of apoptosis in primary pulmonary cells but could significantly inhibit the secretion of eotaxin by these cells. These results indicate that the administration of As2O3 to OVA-immunized mice can suppress lung allergic inflammatory responses. As2O3 might therefore have therapeutic potential in treating allergic airway inflammatory diseases.

The purpose of our study was to evaluate the performance of a computer-aided program that performs automated matching of pulmonary nodules imaged in three serial screening chest MDCT studies.Forty subjects with pulmonary nodules depicted in three annual (T0, T1, T2) low-dose MDCT screening studies for lung cancer were selected from the National Lung Screening Trial database at a single institution. All CT images were reevaluated by two radiologists in consensus. One hundred forty-three nodules were identified and characterized by type (solid parenchymal, juxtavascular, juxtapleural, and ground-glass opacity) and size (or = 4 mm, 4-6 mm, 6-8 mm, and8 mm). Using an automated program, nodules at T0 were matched to nodules at T1, and the same nodules at T1 were matched to nodules at T2. Associations between nodule matching rate (i.e., number of nodules matched by the program divided by the number of nodules determined to match by radiologists) and nodule type or size were analyzed.The combined matching rate of the nodules was 92.7% (T0 vs T1, 91.6%; T1 vs T2, 93.7%). By nodule type, the matching rate was 94.6% (parenchymal), 98.4% (juxtavascular), 85.8% (juxtapleural), and 100% (ground-glass opacity), with the rate significantly lower for juxtapleural nodules (p0.01). Matching rates were not significantly influenced by nodule size (p = 0.67).The automated matching rate for pulmonary nodules in screening MDCT scans was high (92.7%) and was not affected by the nodule size but was slightly lower with nodules at juxtapleural locations.

In-situ analysis the chemical composition of tibial articular cartilage of female Hartley guinea pigs with Fourier transform infrared (FTIR) microspectroscopy was conducted. The infrared spectrum survey consists of three ages (1 months, 2 months and 3 months) and three cartilage layers (surface, middle and deep). The results demonstrated that with ages increasing, the peak positions of main absorbance bands in surface and middle shifted to a lower wavenumber, and in deep they shifted to a lower wavenumber first, then shifted to a higher wavenumber. Infrared spectrum character of collagen, nucleic acid and proteoglycan were compared and analyzed. The ratios of I1 657/I 1 548, I1 074/I1 548 and I1 074/I1 237 tend to decrease with ages increasing in surface and middle. However, the ratios at 2 months are less than other ages in deep. These results are consistent with the regular pattern of cartilage ingredient change in different degradation stage, while the tibial platform images created by microscopic spectral imaging technology is highly compliant with pathology description. The authors' primary result illustrated that FTIR microspectroscopy can be used for in-situ analysis of molecular constituents of different levels cartilages. The molecular information obtained from the study is important for understanding the pathogenesis of cartilage diseases.

In the study, a gene encoding Tat protein N terminal 1- 21 amino acid residues-deleted mutant (Tat22-101) was amplified by PCR from a full length Tat gene of human immunodeficiency virus type 1, and the prokaryotic expression plasmid pET32a-Tat22-101 was constructed. After identification by digestion with endonucleases and sequencing, the recombinant plasmid pET32a-Tat22-101 was transformed into E. coli BL21(DE3) and expressed with IPTG induction. The mutant fusion protein with deleted Tat N terminal was purified by an affinity chromatography column Ni(2+)-NTA and subsequently identified by SDS-PAGE and Western blotting. The results showed that the molecular weight of the mutant protein was approximately 26.9kD. Furthermore, BALB/c mice were immunized with the mutant protein and the anti-sera were collected. ELISA results showed that the mutant protein preserved its immunogenicity, particularly it could improve the production of antibodies to other epitopes in addition to the N terminal epitope of Tat protein, which might provide some valuable information for the study of Tat functions as well as for development of potential novel HIV Tat vaccine.

Protein antigens must be taken up, processed, and displayed on the surface of antigen-presenting cells in association with major histocompatibility complex molecules before they can be recognized by T cells. Whether recognition of the haptens used to study allergic contact hypersensitivity in murine models similarly requires processing has not been determined. We analyzed whether presentation of trinitrophenol to trinitrophenol reactive T-cell hybridomas requires antigen processing by studying the effects of inhibitors of antigen processing and presentation on the ability of a syngeneic B-cell tumor (A20) to present trinitrophenol to a series of interleukin-2 producing, trinitrophenol specific, major histocompatibility complex class II-restricted T-cell hybridomas. The ability of trinitrophenol modified A20 cells to stimulate the hybridomas was completely inhibited by monoclonal, anti-trinitrophenol, or anti-Ia antibodies and was significantly reduced by paraformaldehyde fixation immediately after trinitrophenol modification. Trinitrophenol-modified A20 cultured at 37 °C for 2 h prior to fixation was significantly more effective at stimulating the hybridomas than trinitrophenol-modified A20 fixed immediately. The ability of A20 to present trinitrophenol was inhibited by chloroquine. Paraformaldehyde fixation and chloroquine treatment had similar effects on the ability of trinitrophenol modified lymph node dendritic cells to stimulate the trinitrophenol specific hybridomas. Paraformaldehyde fixation and chloroquine treatment had similar effects on the ability of A20 cells to present ovalbumin to ovalbumin-specific hybridomas as they had on the ability of trinitrophenol modified A20 cells to present trinitrophenol to the trinitrophenol specific hybridomas. One of seven T-cell hybridomas responded to trinitrophenol modified ovalbumin but not other trinitrophenol modified proteins. These results suggest that, at least in part, T cells in the contact hypersensitivity response to trinitrophenol recognize antigens that require processing and that trinitrophenol modified proteins can be recognized.

To observe the morphological change of prominence through CT three-dimensional reconstruction before and after manipulative treatment and in order to investigate biomechanical effect of manipulation in treating lumbar intervertebral disc herniation (LIDH).From December 2009 to May 2010, 24 patients with LIDH (32 herniated discs) with the unilateral typing,which were treated with manipulation (on alternate day one time and every time about 20 min, 3 weeks as a course of treatment). There were 10 males and 14 females, ranging in age from 25 to 54 years with an average of 36.2 years, in course of disease from 2 days to 10 years with an average of 6.9 years. Protrusible 12 discs were in L4,5 and 20 discs were in L5S1. According to typing of distance between prominence and zygapophysial joint or vertebral plate (ligamentum flavum), 5 cases were type I, 13 cases were type II and 6 cases were type III. After a course of treatment,the morphological changes of prominences were analyzed in the same level of CT three-dimensional reconstruction, including contour map of nerve root sheath side distance (TD), the distance between prominence and zygapophysial joint or vertebral plate (ligamentum flavum), the deviated angle of prominence (AN value) and the sagittal index (SI value).From the contour map of TD, 19 patients (79.2% of the total) can be identified morphological changes after the treatment; from the distance between prominence and zygapophysial joint or vertebral plate (ligamentum flavum), 7 cases with type II turned into type I and 2 cases with type III turned into type II after treatment; AN value increased after treatment (P0.05),it showed prominence occurred morphological change toward deviated direction of intervertebral foramina; there was no significant difference in SI value between before and after treatment (P0.05).Standard manipulation can make prominence change, the prominence and nerve roots release, and mutual position improve,which can provide imaging evidence for the study in biomechanical effects.

The purpose of our study was to retrospectively evaluate the effect of body weight and iodine dose on aortic and hepatic contrast enhancement in pediatric patients who underwent 64-MDCT of the abdomen and pelvis.Eighty-seven consecutive pediatric patients (50 boys and 37 girls; median age, 12.1 years; age range, 3.8-17.6 years) underwent standard abdominopelvic CT with a 64-MDCT scanner. Contrast medium (350 mg I/mL) was injected using a power injector at 2 mL/s followed by 15-20 mL of saline flush. According to our CT protocol, the volume of administered contrast medium was approximately 1.8 mL/kg of body weight, up to the maximum volume of 80 mL. CT scanning was initiated 60 seconds after the start of the contrast medium injection. CT attenuations of the aorta and liver were measured. For each patient, the injected contrast medium iodine mass per body weight index (g I/kg) (hereafter, iodine mass body index) was calculated. Linear regression analysis was performed between iodine mass body index and aortic and hepatic attenuations.A wide range of patient weights (19-82 kg; mean, 48.6 kg [95% CI, 45.3-51.9 kg]) and contrast volumes (30-80 mL; median, 80.0 mL) were observed. The median attenuations were 149.0 HU (141.0-160.0 HU) for the aorta and 113.5 HU (109.5-120.0 HU) for the liver. Moderately high correlations were observed between iodine mass body index and aortic (Spearman's rho [r(s)] = 0.60 [0.45-0.72]; p0.001) and hepatic (r(s) = 0.60 [0.42-0.70]; p0.001) attenuations. The regression formulae for aortic attenuation (58.4 + 176.3 x iodine mass body index [p0.001]) and hepatic attenuation (58.7 + 108.5 x iodine mass body index [p0.001]) indicate that 1.5 and 1.8 mL/kg (350 mg I/mL) of contrast media are required to achieve 116 and 127 HU, respectively, of contrast-enhanced attenuation in the liver.In our study, using abdominal 64-MDCT in pediatric patients, we found that approximately 1.5 mL/kg, or 0.525 g I/kg, yields 116 HU of hepatic attenuation or 50-55 HU of hepatic enhancement.

The purpose of our study was to evaluate the correlation between the enhancement parameters of dynamic CT; the carcinoma tissue microvessel density (MVD, a hotspot method to provide a histologic assessment of tumor vascularity); and tumor nuclear grade in renal cell carcinomas.Twenty-four patients with histologically diagnosed renal cell carcinoma underwent dynamic enhanced CT. Enhancement parameters, slope of the time-density curve, the density difference before and after tissue enhancement (deltaH), tissue blood ratio (TBR), and area under the time-density curve (AR), were calculated for all lesions. Pathology slides corresponding to the CT plane were stained using mouse antihuman CD34 monoclonal antibody and H and E. Fuhrman nuclear grade was used. Vascular hot spots of microvessels were recorded. Spearman's rank correlation was performed to determine the strength of the relationship between enhancement parameters, MVD determinations, and tumor nuclear grade.MVD with CD34 staining revealed uneven distribution of positively stained vascular endothelial cells in renal cell carcinoma lesions. Heterogeneous distribution of contrast enhancement was seen among and within individual tumors. The tumors appeared as uneven patterns on time-density curves of renal cell carcinoma lesions. Enhancement parameters of H (median, 21.0 H; range, 2.2-105.8 H), TBR (median, 39%; range, 10.7-154.7%), AR (median, 1.58 H x sec; range, 0.23-3.67 H x sec), and slope (median, 2.76; range, 0.53-6.76) varied greatly. Renal cell carcinoma tissue MVD significantly correlated with all enhancement parameters of dynamic CT. The correlation coefficients (r) were 0.62, 0.54, 0.55, and 0.44, respectively, for delta H, slope, TBR, and AR (p0.0 5). All enhancement parameters did not significantly correlate with tumor nuclear grade. They were not predictive of nuclear grade.Enhancement parameters of dynamic CT may be suited to evaluate tumor vascularity in vivo. Dynamic enhanced CT images may reflect the heterogeneity of tumor angiogenesis on the basis of the correlation between enhancement parameters and MVD of renal cell carcinoma.

To detect the aberrant promoter CpG islands hypermethylation status of GSTP1 gene in hepatocellular carcinomas (HCC) and to assess its significant role in hepatocarcinogenesis.Surgically resected cancerous and non-cancerous liver tissues of 26 hepatocellular carcinoma patients were obtained from West China Hospital, and 11 peripheral blood samples from healthy donors as negative control were collected. Breast cancer cell line MCF-7 with CpG islands hypermethylation of GSTP1 as positive control was obtained from the Cell Bank of Chinese Academy of Sciences in Shanghai. All genomic DNA were extracted using common phenolchloroform approach, and the 5' CpG islands methylation status of GSTP1 gene was studied by methylation-specific polymerase chain reaction (MSP).GSTP1 gene promoter CpG island hyperthylation was detected in 88.5% (23/26) of cancerous tissues and in 69% (18/26) of corresponding non-cancerous tissues from the 26 HCC patients. None of the 11 control samples were methylation positive.The data indicates that the detection of GSTP1 gene methyl-lation may be a valuable biomarker by MSP for HCC early diagnosis and disease monitoring.

Purpose and experimental design: Glutathione S -transferases, enzymes that prevent cells from damage mediated by oxidant and electrophilic carcinogens, may be early critical determinants of carcinogenesis. To explore the aberrant promoter CpG island methylation of the GSTP1 gene as a biomarker for screening hepatocellular carcinoma (HCC) high risk individuals and for the early detection of HCC, we analyzed its methylation in the tumor and non-tumor tissues and serum samples from 26 patients with HCC, as well as serum from 8 liver cirrhosis patients by methylation-specific PCR (MSP). Results: Twenty-three of 26 (88.5%) tumor tissues and 18 of 26 (69%) corresponding non-tumor tissues displayed GSTP1 promoter CpG island hypermethylation. Similarly, GSTP1 promoter hypermethylation was detected for the first time in 16 of 32 (50%) of circulating tumor DNA in the peripheral serum from HCC patients and 4 of 8 (50%) cirrhosis tissues and 3 of 8 (37.5%) corresponding serum DNA from cirrhosis patients. The aberrant methylation of the GSTP1 gene in the serum of patients is in agreement with tumor methylation status ( P = 0.004). None of the 12 normal PBMC samples were methylation positive. Conclusions: These data indicate that the epigenetic aberrance of promoter CpG island hypermethylation of the GSTP1 gene may contribute to the hepatopathogenesis of HCC and is a potential valuable biomarker for noninvasive disease monitoring and HCC early diagnosis.

To study the effect and mechanism of pyronaridine (PND) on the reversal of multidrug resistance (MDR) in K562/A02 and MCF7/ADR cell lines with mdr1+.MTT assay was used to determine the cells growth inhibition after incubation for 72 h in the presence of doxorubicin (DOX) with or without PND. Intracellular accumulation of DOX was analyzed by spectrofluorometry. P-glycoprotein (P-gp) activity was investigated by measuring the extrusion of the cationic dye rhodamine 123 (Rh123). The apoptosis of cells and mdr1 gene expression were detected using flow cytometry and RTPCR, respectively.PND slightly inhibited the growth of MDR human leukemia, breast cancer cells, and their parental cell lines. The IC50 of PND were 5.10 - 18.66 micromol/L depending on the kinds of cell lines. PND at low toxic concentrations enhanced antiproliferative effect of DOX on MDR cells and the apoptosis induced by DOX in a concentration-dependent manner. Intracellular accumulation of DOX and Rh123 in MDR cell lines increased after combination with PND. PND did not down-regulate mdr1 gene expression in MDR cell lines K562/A02 and MCF7/ADR.As the third-generation Pgp inhibitor, PND significantly reversed MDR in MDR cell lines K562/A02 and MCF7/ADR by inhibiting P-gp function.

Development of contact hypersensitivity in mice depends on the migration of Langerhans cells from the epidermis to regional lymph nodes. Since ICAM-1 and LFA-1 play important roles in leukocyte migration, we sought to determine whether in vivo administration of anti-ICAM-1 and anti-LFA-1 antibodies would inhibit contact sensitization-induced migration of epidermal Langerhans cells to regional lymph nodes. Twenty-four hours after contact sensitization of mice with FITC, a brightly FITC-stained Ia+ population of dendritic cells capable of stimulating a FITC-specific Ia-restricted T-cell hybridoma was readily detected in their draining lymph nodes. Animals treated with anti-Ia mAb, which depletes Ia+ cells in lymph nodes and spleen but not Ia+ Langerhans cells in the epidermis, had normal numbers of FITC-bearing Ia+ cells capable of stimulating the T-cell hybridoma. Dendritic lymph node cells from mice treated with anti-ICAM-1 and anti-LFA-1 mAb were devoid of brightly FITC-stained cells and cells capable of stimulating the FITC-specific T-cell hybridoma. The combination of anti-ICAM-1 and anti-LFA-1 mAb completely inhibited the induction of contact hypersensitivity to FITC. Animals treated with anti-ICAM-1 or anti-LFA-1 monoclonal antibodies alone had significantly reduced (by 79 and 36%, respectively) numbers of brightly stained cells capable of stimulating the hybridomas. These data suggest that the adhesion molecules, ICAM-1 and LFA-1, play a significant role in contact hypersensitivity-induced migration of Langerhans cells to regional lymph nodes. The immunomodulatory effects of anti-adhesion molecule antibodies in vivo may be in part due to their effects on antigen-presenting cell migration.