Adenocarcinoma ; diagnostic imaging ; metabolism ; pathology ; surgery ; Carcinoembryonic Antigen ; metabolism ; Diagnosis, Differential ; Follow-Up Studies ; Humans ; Keratin-20 ; metabolism ; Male ; Microfilament Proteins ; metabolism ; Middle Aged ; Phosphopyruvate Hydratase ; metabolism ; Thymus Neoplasms ; diagnostic imaging ; metabolism ; pathology ; surgery ; Tomography, X-Ray Computed

Objective To analyze and compare the imaging features of chromophobe cell renal carcinoma(CCRC)with pathologic findings in order to improve the diagnostic accuracy.Methods The data of CT and MRI of 12 patients with CCRC were reviewed retrospectively.Ten patients underwent CT examination,including precontrast scan,the contrast eortieomedullary phase scan and the parenchymal phase scan(one patient without corticomedullary phase scan).Two patients underwent MR examination including precontrast T_1WI,T_2WI and enhanced T_1WI of the corticomedullary phase and the parenchymal phase.Results Four lesions located in left kidney and eight in right kidney.Maximum diameter of lesions ranged from 24 mm to 125 mm,average 56.7 ram.Homogenous density was observed in six lesions of ten on unenhanced CT scan and five lesions had homogenous enhancement on enhanced CT scan,which was due to the less incidence of necrosis,liquefaction and hemorrhage on pathologic findings.Nine Lesions showed hyperdense compared with renal medulla but the density was lower than renal cortex on the corticomedullary phase.The enhanced degree was positively correlated with microvessel density(MVD).All ten lesions became hypodense compared with renal medulla on the parenchymal phase scan.Central stellate scar was found in two big lesions and psudocapsula were observed in four lesions confirmed by pathology.Two patients underwent MRI examination.Compared with medulla,the two lesions showed hyperintense on unenhanced T_1WI and obviously hypointense on unenhaneed T_2WI.The enhancement pattern of them was similar to CT. Conclusion The imaging features of CCRC,such as homogeneity,special enhancement pattern and distinct hypointensity on T_2WI,help to differentiate CCRC from other renal tumors.

OBJECTIVETo screen the candidate TSGs on 22q13 involved in sporadic colorectal cancer.

METHODSThe DNA samples of 83 cases with colorectal carcinoma and normal tissues were analyzed using eight fluorescent labeled polymorphic microsatellite markers by PCR. PCR products were electrophoresed on an ABI 377 DNA sequencer. Genescan 3.7 and Genotype 3.7 software was used for LOH scanning and analysis. Comparison between LOH frequency and clinicopathological factors were performed by chia2 test.

RESULTSThe prevalence of LOH was 35.58%, and the average hereditary distance was 1.9 cM. The highest frequency of LOH (D22S1160 locus) and the lowest (D22S1170 locus) were 64.71% and 20%, respectively. Two obvious LOH regions were detected: One between D22S1171 locus and D22S274 locus (about 2.7 cM); another between D22S1160 and D22S1149 locus (about 1.8 cM). Furthermore,significant differences were observed between the frequency of LOH on D22S1171 locus and tumors location (P=0.020), the frequency of LOH on D22S114 locus and liver metastasis (P=0.008), the frequency of LOH on D22S1160 locus and lymph node metastasis (P=0.016). No significant differences were found between LOH on other loci and those factors above. Gene function screening revealed that ARHGAP8 and PPARA gene were involved in carcinogenesis.

CONCLUSIONSTwo obvious high frequency LOH regions are detected by refined deletion mapping. One locates between D22S1171 locus and D22S274 locus (about 2.7 cM); another locates between D22S1160 and D22S1149 locus (about 1.8cM), ARHGAP8 and PPARA gene may be TSGs which contribute to carcinogenesis and progression of sporadic CRC on 22q13 region.

Adult ; Aged ; Aged, 80 and over ; Chromosomes, Human, Pair 22 ; Colorectal Neoplasms ; genetics ; pathology ; Female ; Genes, Tumor Suppressor ; Humans ; Loss of Heterozygosity ; Male ; Middle Aged ; Polymerase Chain Reaction ; Sequence Deletion

Drug Design ; Genomics ; methods ; Oligonucleotide Array Sequence Analysis ; Protein Array Analysis ; Proteomics ; Technology, Pharmaceutical

OBJECTIVETo analyse the video-oculographic findings of positional tests and evaluate the efficacy of canalith repositioning procedure (CRP) in patients with paroxysmal positional vertigo ( BPPV) of the anterior semicircular canal (ASC).

METHODSA retrospective study of 31 patients with ASC BPPV. Then the CRP was performed.

RESULTSTwenty-two individuals (70.97%) presented a unilateral positional nystagmus during the Dix-Hallpike test, in 17 individuals had torsional nystagmus component, 5 individuals only had pure positional down beat nystagmus. Nine patients presented bilateral positional nystagmus, 7 individuals had torsional component positional nystagmus, in 2 patients the direction of the torsional component were the same during right and left Dix-Hallpike test, in 4 patients the torsional component were concurrent with positional down beat nystagmus but the direction could not be ascertained clinically, in 2 patients had pure positional down beat nystagmus. Nineteen patients (61.29%) had unilateral lesion, 11 patients had the left ASC BPPV, 8 patients had right ASC BPPV. Eleven patients had with both ASC and PSC BPPV in the ipsilateral. Twenty-one patients (67.74%) were cured, 29 patients (93.55%) were improved, 2 (6.45%) patients were inefficacy. CRP effectively resolved the nystagmus and vertigo in 14 patients (45.16%) when applied only once, The average number of CRP was 1.7 times, there were 5 patients recurrence during the follow-up.

CONCLUSIONSASC BPPV was not a common condition. The torsional nystagmus component of ASC BPPV might be weak during the Dix-Hallpike test. The positional nystagmus of ASC BPPV was triggered bilaterally. Based on these findings, CRP could be one of the most effective treatment methods for ASC BPPV.

Adult ; Aged ; Benign Paroxysmal Positional Vertigo ; Female ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Semicircular Canals ; Vertigo ; diagnosis ; therapy

Acute Disease ; Animals ; Astrocytes ; metabolism ; pathology ; Cats ; Dimethoate ; analogs & derivatives ; poisoning ; Female ; Glial Fibrillary Acidic Protein ; metabolism ; Male ; Poisoning ; metabolism ; pathology

AIMTo prepare liposomes of nosiheptide and study its ability to inhibit hepatitis B virus HBsAg and HBeAg secreted.

METHODSLiposomes of nosiheptide was prepared by sodium deoxycholate dialysis and sonication. Nosheptide was determined by HPLC and partical size was determined by using laser light scattering instrument. Transmission electron microscopy (TEM) was used to examine the morphology of liposomes. Its actions to inhibit hepatitis B virus HBsAg and HBeAg secreted was studied by a HBV-transfectted cell line (HepG2 2. 2. 15 ).

RESULTSEncapsulation efficiency of liposomes by chloroform:methanol (2:1, v/v) was higher than that by dioxane. With the increase of the ratio of nosiheptide: PC (W/W), the encapsulation efficiency of liposomes decreased with the increase of ratio of sodium deoxycholate: PC, the liposomes partical size decreased. The liposomes kept stable at -20 degrees C after 2 years. The drug concentrations of liposomes that inhibit HBsAg secreted by (46.9 +/- 2. 6) %, (55.4 +/- 1.2) %, (65 +/- 3) % and HBeAg secreted by (15.1 +/- 2.3) %, (36.2 +/- 1.7) %, (36.8 +/- 2.5) % were 1.25, 2.5, 5.0 microg x mL(-1), respectively.

CONCLUSIONLiposomes of nosheptide can be prepared by sodium deoxycholate dialysis and sonication, which ability to inhibit hepatitis B virus HBsAg and HBeAg secreted is better than nosheptide.

Antiviral Agents ; administration & dosage ; pharmacology ; Cell Line, Tumor ; Drug Carriers ; Drug Compounding ; Drug Delivery Systems ; Drug Stability ; Hepatitis B Surface Antigens ; drug effects ; Hepatitis B e Antigens ; drug effects ; Hepatitis B virus ; drug effects ; immunology ; Hepatoblastoma ; virology ; Humans ; Liposomes ; Liver Neoplasms ; virology ; Particle Size ; Thiazoles ; administration & dosage ; pharmacology

OBJECTIVETo investigate osthole effect on femoral tissue resorption activity of rat in vitro.

METHODSSix SD rats weighted (80 ± 5) g were used to isolate and culture femoral tissue (diaphyses and metaphysis) in vitro. The cultured tissue were devided into control group, estradiol group and osthole group. The femoral tissue was treated with final concentration of 1 x 10(-5) mol/L osthole and 1 x 10(-8) mol/L estradiol culture in vitro at 48 hours after cultured. Tartrate-resistant acid phosphatase (StrACP) activity, glucose and Lactic acid content, StrACP, MCSF (Macrophage colony stimulating factor) and CTSK (Cathepsin K) mRNA was detected by Real-Time RT-PCR were detected.

RESULTSConcetration of Alkaline phosphatase activity were 2226 and 2498 in 1 x 10(-5) mol/L osthole and 1 x 10(-8) mol/L estradiol respectively. As compared with control group, the activity of StrACP of 1 x 10(-5) mol/L osthole and 1 x 10(-8) mol/L estradiol were inhibited at 6, 9, 12 days (P < 0.05); under treatment of in l x 10(-5) mol/L osthole, the content of Lactic acid were increased and the content of glucose were decreased at 3, 6, 9 days (P < 0.05); StrACP, MCSF and CTSK mRNA expression level were inhibited at 6, 9 days (P < 0.05).

CONCLUSIONOsthole can inhibit bone resorption and raise the level of nutrition metabolism of femurs tissue.

Acid Phosphatase ; metabolism ; Animals ; Bone Resorption ; prevention & control ; Coumarins ; pharmacology ; Estradiol ; pharmacology ; Femur ; drug effects ; Glucose ; analysis ; Lactic Acid ; analysis ; Male ; Rats ; Rats, Sprague-Dawley

BACKGROUND: The effect of pituitary adenylate cyclase activating polypeptide (PACAP) during traumatic brain injury (TBI) and whether it can modulate secondary injury has not been reported previously. The present study evaluated the potential protective effects of ventricular infusion of PACAP in a rat model of TBI. METHODS: Male Sprague Dawley rats were randomly divided into 3 treatment groups (n=6, each): sham-operated, vehicle (normal saline)+TBI, and PACAP+TBI. Normal saline or PACAP (1g/5L) was administered intracerebroventricularly 20 minutes before TBI. Right parietal cortical contusion was produced via a weight-dropping method. Brains were extracted 24 hours after trauma. Histological changes in brains were examined by HE staining. The numbers of CD4+ and CD8+ T cells in blood and the spleen were detected via flow cytometry. RESULTS: In injured brain regions, edema, hemorrhage, inflammatory cell infiltration, and swollen and degenerated neurons were observed under a light microscope, and the neurons were disorderly arrayed in the hippocampi. Compared to the sham group, average CD4+ CD8– lymphocyte counts in blood and the spleen were significantly decreased in rats that received TBI+vehicle, and CD4– CD8+ were increased. In rats administered PACAP prior to TBI, damage was attenuated as evidenced by significantly increased CD4+, and decreased CD8+, T lymphocytes in blood and the spleen. CONCLUSION: Pretreatment with PACAP may protect against TBI by influencing periphery T cellular immune function.

OBJECTIVETo explore the roles of NF-κB in factor VIIa-induced proliferation and migration of a colon cancer cell line (SW620) in vitro and its possible mechanism.

METHODSThe expression levels of NF-κB (p65), inhibitory protein of NF-κB (IκB-α), caspase-7, interleukin 8 (IL-8) and tissue factor (TF) in SW620 cells treated with factor VIIa, PDTC (an inhibitor of NF-κB) and other factors were measured by Western-blotting and real-time PCR. Proliferation and migration of the cells were analyzed by flow cytometry and Transwell assay, respectively.

RESULTSFactor VIIa down-regulated the IκB-α level in SW620 cells and increased the intranuclear level of NF-κB. Those effects of factor VIIa were blocked by anti-TF or anti-PAR2 antibodies. The effects of factor VIIa on proliferation and migration of SW620 cells, expression of IL-8, TF as well as caspase-7, were interfered by PDTC (the inhibitor of NF-κB).

CONCLUSIONSTF/VIIa complex activates NF-κB pathway via PAR2, thereby up-regulates IL-8 and down-regulates caspase-7 expression in SW620 cells, finally promotes proliferation and migration of colon cancer cells. In addition, TF/VIIa/PAR2/NF-κB pathway also upregulates TF expression, thus to create a positive feedback loop of TF/VIIa/PAR2/NF-κB/TF.

Antineoplastic Agents ; pharmacology ; Caspase 7 ; genetics ; metabolism ; Cell Line, Tumor ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Colonic Neoplasms ; metabolism ; pathology ; Factor VIIa ; pharmacology ; Humans ; I-kappa B Proteins ; metabolism ; Interleukin-8 ; genetics ; metabolism ; NF-KappaB Inhibitor alpha ; Proline ; analogs & derivatives ; pharmacology ; RNA, Messenger ; metabolism ; Receptor, PAR-2 ; metabolism ; Thiocarbamates ; pharmacology ; Thromboplastin ; genetics ; metabolism ; Transcription Factor RelA ; antagonists & inhibitors ; metabolism