ABSTRACT
<p><b>OBJECTIVE</b>To study the feasibility of intraoperative radiotherapy (IORT) in primary liver cancer.</p><p><b>METHODS</b>Based on the target of dose curves, the dose-volume histogram (DVH) and cost of radiation equipment and radiation therapy, IORT was compared with protonbeam therapy (PBT) and 3DCRT in 16 patients with primary liver cancer using the therapy plan system (TPS).</p><p><b>RESULTS</b>IORT had significantly better performance than 3DCRT to allow a target region surrounded by 90% of the dose lines. IORT was similar to protonbeam therapy in terms of target region surroundings and absorbed dose in the normal organs, but the cost of IORT was significantly lower.</p><p><b>CONCLUSION</b>The TPS of IORT is better than 3DCRT and similar to protonbeam therapy in the treatment of primary liver cancer with similar cost to 3DCRT. IORT can effectively protect the neighboring sensitive organs and improve the absorbed dose in the tumors and the local control rate.</p>
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Feasibility Studies , Intraoperative Care , Liver Neoplasms , Radiotherapy , General Surgery , Radiotherapy , Methods , Radiotherapy Dosage , Radiotherapy, Adjuvant , MethodsABSTRACT
<p><b>OBJECTIVES</b>To investigate the expression of Survivin in patients with extrahepatic cholangiocarcinoma (EHCC) and its relationship with clinicopathological features of EHCC, and the correlation between the expression of Survivin and lymph node micrometastasis, tumor markers, and the prognosis of EHCC.</p><p><b>METHODS</b>The expression of Survivin protein in paraffin-embedded specimens of 59 patients with EHCC and their 20 para-carcinoma tissues were evaluated by S-P method of immunohistochemical staining. The correlation between the expression of Survivin and the lymph node micrometastasis, clinicopathological features of EHCC and the prognosis of EHCC were analyzed.</p><p><b>RESULTS</b>The positive expression rate of Survivin protein was 67.8% (40/59) in paraffin-embedded specimens of 59 patients with EHCC and was 20.0% (4/20) in para-carcinoma tissues, and difference between carcinoma tissues and para-carcinoma tissues was significant (P<0.01). Histological differentiation in EHCC had a negative correlation with the expression of Survivin protein, while the expression of Survivin protein in EHCC had a positive correlation with TNM of EHCC, lymphatic vessel infiltration, lymph node metastasis and perineural invasion (P<0.05). The serum CA19-9 levels in the positive group with expression of Survivin protein was (290,300+/-55 500) U/L and was obviously higher than that in the negative group [(113,300+/-31,400) U/L, P<0.05]. The mean survival time of the patients with negative expression of Survivin protein was higher than that of the patients with positive expression (43.5 vs. 21.1 months, P<0.01). Screened to significance univariate, the multivariate analysis through Cox proportional hazard model analysis showed that lymph node metastasis, residual tumor margins, and expression of Survivin protein were independent prognosis factors of the patients with EHCC (P<0.05, P<0.01, P<0.01).</p><p><b>CONCLUSIONS</b>The expression of Survivin protein in EHCC has a negative correlation with histological differentiation, while has a positive correlation with lymphatic vessel infiltration and serum CA19-9 concentrations. The expression of Survivin protein maybe an independent prognosis factor of the patients with EHCC.</p>
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Bile Duct Neoplasms , Metabolism , Pathology , Bile Ducts, Extrahepatic , Cholangiocarcinoma , Metabolism , Pathology , Follow-Up Studies , Inhibitor of Apoptosis Proteins , Metabolism , Lymphatic Metastasis , PrognosisABSTRACT
<p><b>OBJECTIVE</b>To identify whether GC-box (-348 to -338) in human insulin gene promoter is a key cis-acting element.</p><p><b>METHODS</b>Human insulin gene promoter was sub-cloned into secreted alkaline phosphatase (SEAP) reporter plasmid. The deletion and mutation of GC-box in insulin gene promoter was performed. The activity of human insulin gene promoter was determined by evaluating the activity of SEAP in the supernatant of cell culture after the reporter plasmids were transfected in beta cell line betaTC3.</p><p><b>RESULT</b>Deletion and mutation of GC box in human insulin gene promoter did not result in significant changes of the activity of the promoter in betaTC3.</p><p><b>CONCLUSION</b>The GC-box is not a key cis-acting element in human insulin gene promoter.</p>
Subject(s)
Humans , Alkaline Phosphatase , Genetics , Metabolism , Base Sequence , Cell Line , Enhancer Elements, Genetic , GC Rich Sequence , Gene Expression Regulation , Insulin , Genetics , Promoter Regions, Genetic , Recombinant Fusion Proteins , Genetics , Metabolism , Sequence Deletion , Transcription, Genetic , TransfectionABSTRACT
<p><b>OBJECTIVE</b>To observe the effect of prostaglandin E(1) (PGE(1)) on the expression of monocyte chemotactic protein-1 (MCP-1) in Kupffer cells (KCs) of rats with hepatic ischemia-reperfusion injury (IRI).</p><p><b>METHODS</b>Seventy-two SD rats were randomized into sham operation group, ischemia-reperfusion group (I/R group) and PGE(1) treatment group (PGE(1) group). Rat models of partial warm ischemia-reperfusion injury of the liver was established, and in PGE(1) group, PGE(1) were given 10 min before the operation. At 1, 6, 12 and 24 h after the reperfusion, blood sample was taken from the inferior vena cava for measuring alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. The KCs were isolated and incubated in vitro, and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in the supernatant were measured by enzyme-linked immunosorbent assay. MCP-1 expression in the KCs was detected by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>ALT and AST levels of the PGE(1) group were significantly lower than I/R group (P<0.01). The mRNA and protein expression of MCP-1 and the TNF-alpha and IL-1beta levels in the I/R group significantly increased in the course of reperfusion and slightly decreased at 24 h, but were still significantly higher than those in the sham operation group (P<0.05). The expression of these factors were markedly decreased after PGE(1) treatment as compared with the I/R group (P<0.05).</p><p><b>CONCLUSION</b>PGE(1) can protect against ischemia-reperfusion injury of the rat liver partially by suppressing KCs activation, reducing excessive release of TNF-alpha and IL-1beta from KCs and decreasing the high expression of MCP-1 protein and mRNA.</p>
Subject(s)
Animals , Male , Rats , Alanine Transaminase , Blood , Alprostadil , Pharmacology , Aspartate Aminotransferases , Blood , Chemokine CCL2 , Genetics , Enzyme-Linked Immunosorbent Assay , Immunohistochemistry , Kupffer Cells , Metabolism , Liver , RNA, Messenger , Genetics , Random Allocation , Rats, Sprague-Dawley , Reperfusion Injury , Blood , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
<p><b>OBJECTIVE</b>To investigate the expression of beta-protein 1 (BP(1)) gene, a novel member of DLX homeobox gene family, in lung cancer tissue and its relationship with clinical features of lung cancer.</p><p><b>METHODS</b>RT-PCR was employed for detecting BP(1) gene expression in the lung cancer tissues, adjacent tissues, non-cancer lung tissues of 46 lung cancer patients.</p><p><b>RESULTS</b>Thirty-six lung cancer tissues and 6 adjacent tissues but none of the normal tissues were found to have BP(1) gene overexpression, showing significant difference in BP(1) expression between the tissues (P<0.01). Significant difference in BP1 gene overexpression was noted between well differentiated cancers (13 of out 21) and poorly differentiated cancers (22 of the 25), but not between cancers of different stages or between squamous carcinoma and adenocarcinoma.</p><p><b>CONCLUSION</b>BP(1) gene expression is up-regulated in human lung cancer in related to the differentiation level of lung cancer but not to the clinical stage.</p>
Subject(s)
Female , Humans , Male , Adenocarcinoma , Genetics , Pathology , Carcinoma, Squamous Cell , Genetics , Pathology , Gene Expression Regulation, Neoplastic , Homeodomain Proteins , Genetics , Lung Neoplasms , Genetics , Pathology , RNA, Messenger , Genetics , Metabolism , Reverse Transcriptase Polymerase Chain Reaction , Transcription Factors , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To study the effect and mechanism of Ganbi decoction (GBD) in treating patients with antituberculotic agent caused liver injury (ATB-LI).</p><p><b>METHODS</b>One hundred and twenty-eight patients with ATB-LI were randomly assigned to the treated group (n = 66) and the control group (n = 62) with the envelop method. Meanwhile, 60 healthy persons were selected as the healthy control group. The treated group was treated by GBD one dose every day with the constituents modified depending on patients' symptoms, and the control group was treated with glucuronolactone tablets and inosine injection. One week was taken as one treatment course. The changes of clinical syndromes, physical signs, T-lymphycyte sub-groups and serum level of nitric oxide (NO) were observed before and after treatment and the recovery time of liver function was recorded. The outcome was compared with that in the healthy control group.</p><p><b>RESULTS</b>In the treated group, 28 patients (42.4%) were cured, 30 (45.5%) improved and 8 (12.1%) ineffectively cured, the total effective rate being 87.9% (58/66). In the control group, 17 patients (27.4%) were cured, 24 (38.7%) improved, and 21 (33.9%) ineffectively cured, the total effective rate being 66.1% (41/62). The total effective rate in the treated group was significantly higher than that in the control group (P < 0.05). Liver function was improved in both groups, recovery time in the treated group was 12.0 +/- 7.0 days, which was significantly shorter than that in the control group (16.0 +/- 8.0 days), showing significant difference between the two groups (P < 0.05). The levels of CD3, CD4 and CD8 were significantly higher and level of NO significantly lower in the two groups of patients than those in the healthy control group (P < 0.05), but these parameters were improved more significantly in the treated group after treatment, when compared with those before treatment or with those in the control group, all showing significant difference (P < 0.05).</p><p><b>CONCLUSION</b>GBD could prevent ATB-LI, and its mechanism could be by way of reducing NO production induced by endotoxin of macrophage and stimulating the proliferation of T-lymphycyte to elevate immunity.</p>