Protecting Prostate Cancer Classification From Rectal Artifacts via Targeted Adversarial Training.

Magnetic resonance imaging (MRI)-based deep neural networks (DNN) have been widely developed to perform prostate cancer (PCa) classification. However, in real-world clinical situations, prostate MRIs can be easily impacted by rectal artifacts, which have been found to lead to incorrect PCa classification. Existing DNN-based methods typically do not consider the interference of rectal artifacts on PCa classification, and do not design specific strategy to address this problem. In this study, we proposed a novel Targeted adversarial training with Proprietary Adversarial Samples (TPAS) strategy to defend the PCa classification model against the influence of rectal artifacts. Specifically, based on clinical prior knowledge, we generated proprietary adversarial samples with rectal artifact-pattern adversarial noise, which can severely mislead PCa classification models optimized by the ordinary training strategy. We then jointly exploited the generated proprietary adversarial samples and original samples to train the models. To demonstrate the effectiveness of our strategy, we conducted analytical experiments on multiple PCa classification models. Compared with ordinary training strategy, TPAS can effectively improve the single- and multi-parametric PCa classification at patient, slice and lesion level, and bring substantial gains to recent advanced models. In conclusion, TPAS strategy can be identified as a valuable way to mitigate the influence of rectal artifacts on deep learning models for PCa classification.

Development of crizotinib-associated renal cyst in a non-small cell lung cancer patient with ALK fusion: a case report and review of the literature.

BACKGROUND: Crizotinib, an oral first-generation tyrosine kinase inhibitor (TKI), is superior to systemic chemotherapy for the treatment of non-small cell lung cancer (NSCLC) with positive rearrangement of anaplastic lymphoma kinase (ALK). However, an increased incidence of renal and hepatic cysts has been reported in the patients on crizotinib treatment. CASE PRESENTATION: Here, we describe a case of a 71-year-old Chinese women developed multiple cystic lesions in kidney and liver during crizotinib treatment for the primary and metastatic NSCLC. The renal and hepatic cysts were noted by CT scan 3 months after crizotinib treatment, which were spontaneously and significantly regressed after stopping crizotinib. CONCLUSIONS: Based on literature review and our experience in this case report, we concluded that crizotinib-associated renal cyst (CARCs) has features of malignancy and abscess in radiographic imaging, and thus, pathological confirmation is necessary to avoid inappropriate treatment decision. In addition, to benefit the patients with progress-free survival (PFS), switching from crizotinib to alectinib is recommended for the treatment of NSCLC patients who developed CARCs.

The Chemopreventive Role of ß-Elemene in Cholangiocarcinoma by Restoring PCDH9 Expression.

Background: ß-Elemene, an effective anticancer component isolated from the Chinese herbal medicine Rhizoma Zedoariae, has been proved to have therapeutic potential against multiple cancers by extensive clinical trials and experimental research. However, its preventive role in cholangiocarcinoma (CCA) and the mechanisms of action of ß-elemene on CCA need to be further investigated. Methods: A thioacetamide (TAA)-induced pre-CCA animal model was well-established, and a low dosage of ß-elemene was intragastrically (i.g.) administered for 6 months. Livers were harvested and examined histologically by a deep-learning convolutional neural network (CNN). cDNA array was used to analyze the genetic changes of CCA cells following ß-elemene treatment. Immunohistochemical methods were applied to detect ß-elemene-targeted protein PCDH9 in CCA specimens, and its predictive role was analyzed. ß-Elemene treatment at the cellular or animal level was performed to test the effect of this traditional Chinese medicine on CCA cells. Results: In the rat model of pre-CCA, the ratio of cholangiolar proliferation lesions was 0.98% ± 0.72% in the control group, significantly higher than that of the ß-elemene (0. 47% ± 0.30%) groups (p = 0.0471). Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that the top 10 pathways affected by ß-elemene treatment were associated with energy metabolism, and one was associated with the cell cycle. ß-Elemene inactivated a number of oncogenes and restored the expression of multiple tumor suppressors. PCDH9 is a target of ß-elemene and displays an important role in predicting tumor recurrence in CCA patients. Conclusions: These findings proved that long-term use of ß-elemene has the potential to interrupt the progression of CCA and improve the life quality of rats. Moreover, ß-elemene exerted its anticancer potential partially by restoring the expression of PCDH9.

Dual Skip Connections Minimize the False Positive Rate of Lung Nodule Detection in CT images.

Pulmonary cancer is one of the most commonly diagnosed and fatal cancers and is often diagnosed by incidental findings on computed tomography. Automated pulmonary nodule detection is an essential part of computer-aided diagnosis, which is still facing great challenges and difficulties to quickly and accurately locate the exact nodules' positions. This paper proposes a dual skip connection upsampling strategy based on Dual Path network in a U-Net structure generating multiscale feature maps, which aims to minimize the ratio of false positives and maximize the sensitivity for lesion detection of nodules. The results show that our new upsampling strategy improves the performance by having 85.3% sensitivity at 4 FROC per image compared to 84.2% for the regular upsampling strategy or 81.2% for VGG16-based Faster-R-CNN.

Case Report: Antiangiogenic Therapy Plus Immune Checkpoint Inhibitors Combined With Intratumoral Cryoablation for Hepatocellular Carcinoma.

Background: Hepatocellular carcinoma (HCC) is a common gastrointestinal malignancy with high incidence and poor prognosis. Common treatment methods include surgery, transcatheter arterial chemoembolization (TACE), ablation, and targeted therapy. In recent years, combination treatment with antiangiogenic therapy and immune checkpoint inhibitors has made great progress in the treatment of advanced HCC. Here, we report the case of a patient with HCC who achieved a durable benefit from anti-vascular therapy and immune checkpoint inhibitors combined with intratumoral cryoablation. Main Body: A 38-year-old male patient initially presented with severe abdominal pain that was identified as an HCC rupture and hemorrhage by computed tomography (CT). The patient underwent emergency surgery and postoperative pathology confirmed HCC. The patient received prophylactic TACE after surgery. Unfortunately, three months after surgery, the patient developed multiple liver metastases. Subsequently, he received systemic anti-vascular therapy and immune checkpoint inhibitors combined with intratumoral cryoablation. After treatment, the patient achieved extensive tumor necrosis and the disease was effectively controlled. Conclusions: Anti-angiogenic therapy and immune checkpoint inhibitors combined with cryoablation can induce a powerful and effective systemic anti-tumor immune response, which is worthy of further research.

Sustained Clinical Benefit of Pyrotinib Combined with Capecitabine Rescue Therapy After Trastuzumab Resistance in HER2-Positive Advanced Gastric Cancer: A Case Report.

BACKGROUND: HER2-positive patients with advanced gastric cancer have a poor prognosis, and trastuzumab-resistant patients lack effective treatment. CASE PRESENTATION: We report a 72-year-old male with HER2-positive gastric cancer. The patient had metastatic tumor during adjuvant chemotherapy after surgery, followed by second-line chemotherapy, and achieved a progression-free survival (PFS) of 4.5 months. Subsequent third-line chemotherapy treatment also failed. Fortunately, the patient had a significant tumor response and 8.5 months of PFS on trastuzumab combined with chemotherapy. After trastuzumab resistance, the patient was treated with programmed cell death protein-1 inhibitor combined with apatinib, which selectively inhibited VEGFR2, but the effect was not satisfactory. Finally, the patient was treated with capecitabine combined with pyrotinib, an irreversible TKI, acting on HER2. The tumor shrank significantly after this treatment. CONCLUSION: The mechanism and countermeasures of trastuzumab resistance were discussed in this case. For patients with HER2-positive advanced gastric cancer, pyrotinib can achieve good results after trastuzumab resistance.

Avasimibe Dampens Cholangiocarcinoma Progression by Inhibiting FoxM1-AKR1C1 Signaling.

Avasimibe is a bioavailable acetyl-CoA acetyltransferase (ACAT) inhibitor and shows a good antitumor effect in various human solid tumors, but its therapeutic value in cholangiocarcinoma (CCA) and underlying mechanisms are largely unknown. In the study, we proved that avasimibe retard cell proliferation and tumor growth of CCAs and identified FoxM1/AKR1C1 axis as the potential novel targets of avasimibe. Aldo-keto reductase 1 family member C1 (AKR1C1) is gradually increased along with the disease progression and highly expressed in human CCAs. From survival analysis, AKR1C1 could be a vital predictor of tumor recurrence and prognostic factor. Enforced Forkhead box protein M1 (FoxM1) expression results in the upregulation of AKR1C1, whereas silencing FoxM1 do the opposite. FoxM1 directly binds to promoter of AKR1C1 and triggers its transcription, while FoxM1-binding site mutation decreases AKR1C1 promoter activity. Moreover, over-expressing exogenous FoxM1 reverses the growth retardation of CCA cells induced by avasimibe administration, while silencing AKR1C1 in FoxM1-overexpressing again retard cell growth. Furthermore, FoxM1 expression significantly correlates with the AKR1C1 expression in human CCA specimens. Our study demonstrates a novel positive regulatory between FoxM1 and AKR1C1 contributing cell growth and tumor progression of CCA and avasimibe may be an alternative therapeutic option for CCA by targeting this FoxM1/AKR1C1 signaling pathway.

Identification of Metastasis-Associated MicroRNAs in Metastatic Melanoma by miRNA Expression Profile and Experimental Validation.

It is reported that microRNAs (miRNA) have paramount functions in many cellular biological processes, development, metabolism, differentiation, survival, proliferation, and apoptosis included, some of which are involved in metastasis of tumors, such as melanoma. Here, three metastasis-associated miRNAs, miR-18a-5p (upregulated), miR-155-5p (downregulated), and miR-93-5p (upregulated), were identified from a total of 63 different expression miRNAs (DEMs) in metastatic melanoma compared with primary melanoma. We predicted 262 target genes of miR-18a-5p, 904 miR-155-5p target genes, and 1220 miR-93-5p target genes. They participated in pathways concerning melanoma, such as TNF signaling pathway, pathways in cancer, FoxO signaling pathway, cell cycle, Hippo signaling pathway, and TGF-beta signaling pathway. We identified the top 10 hub nodes whose degrees were higher for each survival-associated miRNA as hub genes through constructing the PPI network. Using the selected miRNA and the hub genes, we constructed the miRNA-hub gene network, and PTEN and CCND1 were found to be regulated by all three miRNAs. Of note, miR-155-5p was obviously downregulated in metastatic melanoma tissues, and miR-18a-5p and miR-93-5p were obviously regulated positively in metastatic melanoma tissues. In validating experiments, miR-155-5p's overexpression inhibited miR-18a-5p's and miR-93-5p's expression, which could all significantly reduce SK-MEL-28 cells' invasive ability. Finally, miR-93-5p and its potential target gene UBC were selected for further validation. We found that miR-93-5p's inhibition could reduce SK-MEL-28 cell's invasive ability through upregulated the expression of UBC, and the anti-invasive effect was reserved by downregulation of UBC. The results show that the selected three metastasis-associated miRNAs participate in the process of melanoma metastasis via regulating their target genes, providing a potential molecular mechanism for this disease.

Accumulated genetic mutations leading to accelerated initiation and progression of colorectal cancer in a patient with Gardner syndrome: A case report.

RATIONALE: Gardner syndrome is a rare autosomal dominant disorder with a high degree of penetrance, which is characterized by intestinal polyposis, osteomas, and dental abnormalities. Majority of patients with Gardner syndrome will develop colorectal cancer by the age of 40 to 50 years. Mutations in the adenomatous polyposis coli gene are supposed to be responsible for the initiation of Gardner syndrome. PATIENT CONCERNS: A 22-year-old Chinese female was admitted to our hospital due to abdominal pain and bloody stool. DIAGNOSIS: The patient presented with multiple intestinal polyposis, desmoid tumors, and dental abnormalities was diagnosed as Gardner syndrome and further examination revealed a colon tumor. INTERVENTIONS AND OUTCOMES: Patients were implanted with stents to alleviate bowel obstruction, and were treated with oxaliplatin combined with 5-Fu for 4 cycles, but the efficacy was not good. We performed next generation sequencing of 390 genes for the tumor specimens. We detected adenomatous polyposis coli E1538Ifs∗5, KRAS G12D, NF1 R652C, loss of SMAD4, TP53 R175H, IRF2 p.R82S, TCF7L2 p.A418Tfs∗14, and SMAD4 p.L43F in this patient. LESSONS: We reported serial mutations in key genes responsible for initiation and progression of colorectal cancer from a patient with Gardner syndrome.

The Expression and Clinical Significance of Aldo-Keto Reductase 1 Member B1 in Gastric Carcinoma.

To study the expression of aldo-keto reductase 1 member B1 (AKR1B1) in gastric carcinoma (GC), the correlation between AKR1B1 and the clinicopathological characteristics of GC patients, and provide reference for the diagnosis and prognosis of GC patients. One hundred thirty-six patients with GC were collected, and the expression level of AKR1B1 in GC and adjacent tissues was detected by immunohistochemistry assays. The clinicopathological features and prognosis of GC patients were collected to analyze the relationship with AKR1B1 expression. The positive expression of AKR1B1 in GC tissues was significantly higher than that of adjacent nontumor tissues. The difference of AKR1B1 expression between GC tissues and paired adjacent nontumor tissues was statistically significant (p < 0.001). AKR1B1 was closely related to tumor size, regional lymph node (N), metastases (M), and tumor-node-metastasis (TNM) stage (p < 0.05). The overall survival of patients with low expression of AKR1B1 was significantly better than that of patients with high expression of AKR1B1 by Kaplan-Meier survival analysis (p < 0.001). AKR1B1 plays an important role in the occurrence and development of GC, and it has a certain reference value for the prognosis of GC patients.

Pancreatic cancer: from bench to bedside.

Pancreatic cancer is recognized as the king of carcinoma, and the gap between basic research and clinical practice is difficult to improve the treatment effect. Translational medicine builds an important bridge between pancreatic cancer basic research and clinical practice from the pathogenesis, early diagnosis of pancreatic carcinoma, drug screening, treatment strategies and metastasis prediction. This article will carry on the concrete elaboration to the above several aspects.

Autoimmunity and dysmetabolism of human acquired immunodeficiency syndrome.

Acquired immunodeficiency syndrome (AIDS) remains ill-defined by lists of symptoms, infections, tumors, and disorders in metabolism and immunity. Low CD4 cell count, severe loss of body weight, pneumocystis pneumonia, and Kaposi's sarcoma are the major disease indicators. Lines of evidence indicate that patients living with AIDS have both immunodeficiency and autoimmunity. Immunodeficiency is attributed to deficits in the skin- and mucosa-defined innate immunity, CD4 T cells and regulatory T cells, presumably relating human immunodeficiency virus (HIV) infection. The autoimmunity in AIDS is evident by: (1) overproduction of autoantibodies, (2) impaired response of CD4 cells and CD8 cells, (3) failure of clinical trials of HIV vaccines, and (4) therapeutic benefits of immunosuppression following solid organ transplantation and bone marrow transplantation in patients at risk of AIDS. Autoantibodies are generated in response to antigens such as debris and molecules de novo released from dead cells, infectious agents, and catabolic events. Disturbances in metabolic homeostasis occur at the interface of immunodeficiency and autoimmunity in the development of AIDS. Optimal treatments favor therapeutics targeting on the regulation of metabolism to restore immune homeostasis.

Efficacy of thalidomide on trinitrobenzene sulfonate-induced colitis in young rats and its mechanism.

BACKGROUND: Thalidomide could relieve clinical symptoms and intestinal mucosal lesions effectively in children with refractory inflammatory bowel disease (IBD) from the pre-clinical study. This study aimed to observe the therapeutic effect of thalidomide by the established animal model of IBD model of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in Sprague-Dawley (SD) rats and to investigate the possible mechanism of action. METHODS: A total of 82 SD rats of about 4-5 weeks were randomly divided into three groups: the control group (25 rats), TNBS-treated group (29 rats), and thalidomide treatment group (28 rats). Daily activities were recorded. At least eight rats from each group were killed on the 4th, 7th, and 14th days. Morphological and histological changes in the colon were individually assessed. Serum was collected and the levels of TNF-α and interleukins (IL-1ß and IL-10) were assayed by ELISA method. The expression of colonic mucosal nuclear factor (NF)-κB was assayed with the immunohistochemical method. RESULTS: (1) In the control group, diarrhea and rectal bleeding recovered rapidly and no death was recorded. In the TNBS-treated group, diarrhea and rectal bleeding persisted for a longer time. The mortality rate was 10.34% during the observation period. In the thalidomide treatment group, diarrhea and rectal bleeding persisted for a significantly shorter time than the TNBS-treated group (P < 0.01). The rats of this group also exhibited faster weight gain on day 7 compared with the TNBS-treated group but still lower than that of the control group. The mortality rate of the thalidomide treatment group was 3.57%. (2) Macroscopic and microscopic scores of the thalidomide-treated group were significantly lower than those of the TNBS model group on the 14th day (P < 0.01). These results suggested faster and better colonic recovery in the thalidomide-treated group. (3) NF-κB expression in the colonic mucosa of the control group was lower than in the others, mainly distributed in the cytoplasm. A large amount of intra-nuclear and cytoplasm staining was observed (more prominently intra-nuclear) in the TNBS model group and the thalidomide treatment group. On the 7th and 14th days, intra-nuclear NF-κB-containing cells in the thalidomide treatment group were still significantly lower than those in the TNBS model group (P < 0.01). (4) In the control group, the cellular inflammatory factors (TNF-α, IL-1ß, and IL-10) were expressed at a low level while in the other two groups they were already expressed at a significantly higher level on day 4. On day 7 the expressions of TNF-α and IL-1ß in the thalidomide treatment group were lower than in the TNBS model group. On day 14, the expressions of TNF-α and IL-1ß in the thalidomide treatment group were significantly lower than in the TNBS model group (P < 0.05). On day 4, the IL-10 levels of the thalidomide treatment group became significantly elevated. The levels gradually decreased but still remained at a higher level. In the TNBS model group, the IL-10 expression peaked later than in the thalidomide treatment group. CONCLUSIONS: Thalidomide was effective in the management of TNBS-induced colitis in young rats. This may be due to the suppression and down-regulation of NF-κB and the expression of the downstream inflammatory mediators (TNF-α and IL-1ß). There is also indication that the expression of the anti-inflammatory cytokine (IL-10) is concomitantly up-regulated as well.

Self assembled temperature responsive surfaces for generation of cell patches for bone tissue engineering.

One of the major challenges in the fabrication of tissue engineered scaffolds is the ability of the scaffold to biologically mimic autograft-like tissues. One of the alternate approaches to achieve this is by the application of cell seeded scaffolds with optimal porosity and mechanical properties. However, the current approaches for seeding cells on scaffolds are not optimal in terms of seeding efficiencies, cell penetration into the scaffold and more importantly uniform distribution of cells on the scaffold. Also, recent developments in scaffold geometries to enhance surface areas, pore sizes and porosities tend to further complicate the scenario. Cell sheet-based approaches for cell seeding have demonstrated a successful approach to generate scaffold-free tissue engineering approaches. However, the method of generating the temperature responsive surface is quite challenging and requires carcinogenic reagents and gamma rays. Therefore, here, we have developed temperature responsive substrates by layer-by-layer self assembly of smart polymers. Multilayer thin films prepared from tannic acid and poly N-isopropylacrylamide were fabricated based on their electrostatic and hydrogen bonding interactions. Cell attachment and proliferation studies on these thin films showed uniform cell attachment on the substrate, matching tissue culture plates. Also, the cells could be harvested as cell patches and sheets from the scaffolds, by reducing the temperature for a short period of time, and seeded onto porous scaffolds for tissue engineering applications. An enhanced cell seeding efficiency on scaffolds was observed using the cell patch-based technique as compared to seeding cells in suspension. Owing to the already pre-existent cell-cell and cell-extracellular matrix interactions, the cell patch showed the ability to reattach rapidly onto scaffolds and showed enhanced ability to proliferate and differentiate into a bone-like matrix.

Treatment of pediatric refractory Crohn's disease with thalidomide.

AIM: To assess the efficacy and tolerability of thalidomide in pediatric Crohn's disease (CD). METHODS: Six patients with refractory CD received thalidomide at an initial dose of 2 mg/kg per day for one month, then increased to 3 mg/kg per day or decreased to 1 mg/kg per day, and again further reduced to 0.5 mg/kg per day, according to the individual patient's response to the drug. RESULTS: Remission was achieved within three months. Dramatic clinical improvement was demonstrated after thalidomide treatment. Endoscopic and pathological improvements were also observed after thalidomide treatment, which was well tolerated by all patients. CONCLUSION: Thalidomide is a useful drug for pediatric refractory CD.

A phase II study of intra-arterial chemotherapy of 5-fluorouracil, cisplatin, and mitomycin C for advanced nonresectable gastric cancer.

The best choice of chemotherapy regimen for patients with advanced gastric cancer (AGC) is still a matter of controversy and requires further investigation. This study was performed to evaluate the efficacy and safety of intra-arterial infusion chemotherapy of 5-fluorouracil 1000 mg/m, cisplatin 50 mg/m, and mitomycin C 10 mg/m (FCM) repeated every 6 weeks, as first-line treatment for AGC. Forty-seven (95.9%) of the 49 patients were assessable for response. Four cases of complete response and 28 cases of partial response were confirmed, giving an overall response rate of 65.3% [95% confidence interval (CI): 52.0-78.6%]. The median time to progression and overall survival for all patients was 8.3 months (95% CI: 6.8-9.8 months) and 14.5 months (95% CI: 12.0-17.0 months). The estimate of overall survival at 12 and 24 months was 55.1% (95% CI: 41.2-69.0%) and 18.4% (95% CI: 7.5-29.2%), respectively. Most patients experienced neutropenia during their course of therapy with 21.3% of patients (n = 10) for grade 3/4 neutropenia. Grade 3 stomatitis, lethargy, and palmar-plantar erythema were observed in two (4.3%), eight (17.0%), and one (2.1%) patients, respectively. Yet, no grade 4 nonhematological toxicity was observed. Intra-arterial infusion chemotherapy of 5-fluorouracil 1000 mg/m, cisplatin 50 mg/m, and mitomycin C 10 mg/m is a tolerated treatment modality with promising activity in patients with previously untreated AGC.

Combination therapy with transarterial chemoembolization and interferon-alpha compared with transarterial chemoembolization alone for hepatitis B virus related unresectable hepatocellular carcinoma.

BACKGROUND AND AIMS: The present study was carried out to test the hypothesis that interferon-alpha (IFN-alpha) treatment would reduce or postpone the recurrence rate and improve the overall survival rate in patients after transarterial chemoembolization (TACE) treatment of hepatitis B virus (HBV) related unresectable hepatocellular carcinoma (HCC). METHODS: 216 patients with unresectable HBV-related HCC were randomized into a TACE group and a TACE-IFN group, each group had 108 patients. In the TACE-IFN group, patients received IFN-alpha1b at a dose of 3 million units (mu) three times a week by intramuscular injection one week after/before TACE treatment, for 48 weeks. RESULTS: The median disease-free survival in the TACE-IFN treatment group was 23.6 months (95% CI: 21.4-25.8) and 20.3 months (95% CI: 15.8-24.8) in the TACE group (P = 0.027). The disease free rate at 24 months in the TACE group was lower than in the TACE-IFN group (39.8% vs 59.3%, P = 0.004). The median overall survival was 29 months (95% CI: 27.5-32.1) in the TACE-IFN group and 26 months (95% CI: 20.1-31.9) in the TACE group (P = 0.003). The 2-year overall survival in the TACE-IFN group was higher than in the TACE group (72.2% vs 52.8%, P = 0.003). CONCLUSIONS: IFN-alpha treatment reduced recurrence and improved the survival of patients after TACE treatment of HBV-related HCC, with acceptable toxicities.

[Long-term outcome of interventional therapy for malignant biliary obstruction: a retrospective analysis of 109 cases].

OBJECTIVE: To evaluate the long-term outcome and its relative influenced factors of interventional therapy in dealing malignant biliary obstruction (MBO). METHOD: 109 MBO patients, 54 males and 55 females, aged (71 +/- 12), underwent interventional therapy: 55 patients received percutaneous transhepatic cholangiography and drainage (PTCD), and 54 underwent bile duct stent implantation. One week later, total bilirubin (TB), direct bilirubin (DB), and alanine transaminase (ALT) were examined, and Child-Pugh scoring was conducted.38 of the patient underwent transcatheter arterial chemo-embolization (TACE). RESULTS: One week after drainage the levels of ALT, TB, and DB of the patients undergoing PTCD and stent implantation all decreased in comparison with those before the treatment, the levels of the stent implantation group being significantly lower than those of the PTCD group (P = 0.019, 0.002, and 0.002 respectively), but there was no significant difference in Child-Pugh scale between these 2 group (P = 0.396). One week after TACE the levels of TB, DB, and Child-Pugh scale of the TACE group were all significantly lower than those of the patients without TACE (P = 0.000, 0.002, and 0.002 respectively), however, there was no significant difference in ALT level between these 2 groups (P = 0.834). The cumulative mean survival time was 26.45 weeks [standard error (SE) 4.07], and the mean survival time of the PTCD group was 28.19 weeks (SE, 6.54), not significantly different from that of the stenting groups were [21.38 weeks (SE, 2.51), P = 0.713]. The mean survival time of the TACE group was 43.71 weeks (SE, 8.32), significantly longer than that of the patients without TACE [14.38 weeks (SE, 2.66), P = 0.000]. CONCLUSION: Stenting is more effective than PTCD on relieving jaundice when the decreasing extent of bilirubin level is concerned. TACE therapy following PTCD and stent implantation will significantly contribute to the survival time of MBO patients.

Characterization and expression of an actin-depolymerizing factor from Eimeria tenella.

Actin-depolymerizing factor (ADF) plays an important role in remodeling the actin cytoskeleton which contributes much to the invasion of host cells by the apicomplexan parasite. The gene encoding for Eimeria tenella ADF with one intron was cloned and identified by the E. tenella genome raw sequence data ( http://www.sanger.ac.uk/projects/E.tenella/ ). The deduced polypeptide sequence was only composed of 118 amino acids (13.14 kDa) without signal peptide and nuclear localization sequence. The amino acid sequence was most similar to the ADF of Toxoplasma gondii, 69.1%. Compared the putative three-dimensional structures between E. tenella and yeast, the actin filament binding sites on the segment from the alpha4-helices to the C-terminal were mostly missed in E. tenella. Real-time RT-PCR and dot blot both revealed that ADF expression was relatively stronger in the sporozoites and merozoites than in sporulated and unsporulated oocysts in both mRNA and protein levels. Northern blot analysis suggested that there was only one form of ADF transcripts in all different life stages of E. tenella. Actin-binding experiment showed that the recombinant fusion ADF protein could bind with actin, which indicated that ADF probably plays an important role in the invasion host of E. tenella.

Effects of lung volume reduction surgery on distribution of ventilation and perfusion.

Lung volume reduction surgery (LVRS) results in functional improvements in most patients. The mechanisms behind the improvements are not clear. We hypothesized that reduced inequalities in ventilation to perfusion ratio (V/Q) may be a contributing explanation. Nine patients who underwent LVRS were investigated by ventilation and perfusion scintigrams before and after surgery. In addition, 8 healthy subjects were investigated once. The relative ventilation, perfusion and V/Q were calculated in 1 x 1 cm lung elements. Normal range of the element count-rate was determined by the corresponding results in the normal subjects. Results of this small study show a significant effect of LVRS on V/Q, with reduction of shunt-like elements. We conclude that the functional improvement after LVRS to some extent may be explained by decreased V/Q inequality.