ST8SIA6-AS1 contributes to hepatocellular carcinoma progression by targeting miR-142-3p/HMGA1 axis.

Hepatocellular carcinoma (LIHC) accounts for 90% of all liver cancers and is a serious health concern worldwide. Long noncoding RNAs (lncRNAs) have been observed to sponge microRNAs (miRNAs) and participate in the biological processes of LIHC. This study aimed to evaluate the role of the ST8SIA6-AS1-miR-142-3p-HMGA1 axis in regulating LIHC progression. RT-qPCR and western blotting were performed to determine the levels of ST8SIA6-AS1, miR-142-3p, and HMGA1 in LIHC. The relationship between ST8SIA6-AS1, miR-142-3p, and HMGA1 was assessed using luciferase assay. The role of the ST8SIA6-AS1-miR-142-3p-HMGA1 axis was evaluated in vitro using LIHC cells. Expression of ST8SIA6-AS1 and HMGA1 was significantly upregulated, whereas that of miR-142-3p was markedly lowered in LIHC specimens and cells. ST8SIA6-AS1 accelerated cell growth, invasion, and migration and suppressed apoptosis in LIHC. Notably, ST8SIA6-AS1 inhibited HMGA1 expression by sponging miR-142-3p in LIHC cells. In conclusion, sponging of miR-142-3p by ST8SIA6-AS1 accelerated the growth of cells while preventing cell apoptosis in LIHC cells, and the inhibitory effect of miR-142-3p was abrogated by elevating HMGA1 expression. The ST8SIA6-AS1-miR-142-3p-HMGA1 axis represents a potential target for the treatment of patients with LIHC.

Umbilical cord blood-derived mesenchymal stem cells transplantation decreases incidence of liver cancer in end-stage liver disease patients: a retrospective analysis over 5 years.

OBJECTIVE: To investigate effects of umbilical cord blood-derived mesenchymal stem cells (UC-MSCs) transplantation on the risks of liver cancers in end-stage liver disease (ESLD) patients. METHODS: Data of 45 ESLD patients received UC-MSCs transplantation (UC-MSCs group) and 50 ESLD patients received non-UC-MSCs transplantation (non-UC-MSCs group) were retrospectively analyzed, and they were followed up for 5 years. RESULTS: The incidence of liver cancer was much lower in UC-MSCs group than that in the non-UC-MSCs group (12% vs 2.2%, P=0.008). The survival rate of patients was significantly higher in the UC-MSCs group than that in the non-UC-MSCs group during the five years follow-up (P=0.043). The inflammation and fibrosis scores were lower in the UC-MSCs group than those in the non-UC-MSCs group (P<0.036). Compared with the non-UC-MSCs group, the UC-MSCs group showed largely improved liver cirrhosis degree and lower Child-Pugh scores (P<0.05). CONCLUSIONS: UC-MSCs transplantation is able to decrease the risks of liver cancers in ESLD patients, which might work by inhibiting inflammation.

Efficacy and safety of drug-eluting beads bronchial arterial chemoembolization versus conventional bronchial arterial chemoembolization in lung cancer patients with hemoptysis.

Background: This study aimed to explore the efficacy and safety of drug-eluting beads bronchial arterial chemoembolization (DEB-BACE) compared with conventional bronchial arterial chemoembolization (cBACE) in lung cancer patients with hemoptysis. Materials & methods: Thirty-six lung cancer patients with hemoptysis treated by DEB-BACE or cBACE were retrospectively analyzed. Results: Technical success of BACE and clinical success of hemoptysis treatment were no different between DEB-BACE and cBACE (both p > 0.050), whereas DEB-BACE achieved increased total clinical response (p = 0.021), objective response rate (p = 0.035) and prolonged hemoptysis relapse-free survival (p = 0.013) compared with cBACE. The adverse event rates were similar between these two groups (all p > 0.05). Conclusion: DEB-BACE presents with higher tumor treatment response, prolonged hemoptysis relapse-free survival and comparable safety profiles compared with cBACE in lung cancer patients with hemoptysis.

The expression of m6A regulators correlated with the immune microenvironment plays an important role in the prognosis of pancreatic ductal adenocarcinoma.

BACKGROUND: The relationship between N6-methyladenosine (m6A) RNA methylation regulators and the tumor immune microenvironment has been extensively studied. Nevertheless, the potential function of m6A regulators in the tumor immune landscape of pancreatic ductal adenocarcinoma (PDAC) remains to be fully elucidated. METHODS: Here, we systematically evaluated the expression of 19 m6A regulators in PDAC patients from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) database. Utilizing consensus clustering, the PDAC patients were segmented into two subgroups according to the expression of 19 m6A regulators. A prognostic risk signature of 5 m6A methylation regulators (ALKBH5, IGF2BP2, IGF2BP3, LRPPRC, and KIAA1429) was then built, and the PDAC patients were divided into high-risk and low-risk groups. Subsequently, differences in independent prognostic parameters, risk score distribution, survival, and cluster analysis between high-risk and low-risk groups were analyzed. RESULTS: We found two subgroups with dramatically different immune landscapes and prognoses. Subsequently, differences in independent prognostic parameters, risk score distribution, survival, and cluster analysis between the high-risk and low-risk groups were found. Moreover, these gene signatures displayed good discriminative performances in the GEO datasets. We also found that the risk score was positively correlated with the tumor mutation burden (TMB), and the TMB value was higher in the high-risk scoring group. The low-risk scoring group was linked by a stronger response to anti-programmed cell death ligand 1 (anti-PD-L1) immunotherapy and clinical advantages in the immunotherapeutic advanced urothelial cancer (IMvigor210) cohort. Ultimately, we found that these 5 m6A regulators had a fatal regulatory role on the tumor immune microenvironment in PDAC patients. CONCLUSIONS: The construction signature based on the m6A regulators may be crucial regulators of the tumor immune microenvironment in PDAC, providing a new approach to improving the immunotherapy strategy for PDAC patients.

Repression of MicroRNA-124-3p Alleviates High-Fat Diet-Induced Hepatosteatosis by Targeting Pref-1.

Nonalcoholic fatty liver disease (NAFLD) is the common disease in the liver, which is associated with metabolic syndrome and hepatocellular carcinoma. Accumulated evidence establishes that small non-coding microRNAs (miRNAs) contribute to the initiation and progression of NAFLD. However, the molecular repertoire of miRNA in NAFLD is still largely unknown. Here, using an integrative approach spanning bioinformatic analysis and functional approaches, we demonstrate that miR-124-3p participates in the development of NAFLD by directly targeting preadipocyte factor-1 (Pref-1). In response to high-fat diet (HFD), expression of miR-124-3p was increased in the liver. Inhibition of miR-124-3p expression led to a dramatic reduction of triglyceride contents in hepatocytes, in parallel with decreased inflammatory factors. Mechanistically, miR-124-3p directly controls the transcription of Pref-1, a secretory factor that has been proved to resist metabolic syndrome. Our work identifies a novel molecular axis in hepatosteatosis, and highlights miR-124-3p/Pref-1 as potential targets for clinical interventions of NAFLD.

The Effect of Vascular Endothelial Growth Factor on Bone Marrow Mesenchymal Stem Cell Engraftment in Rat Fibrotic Liver upon Transplantation.

BACKGROUND: According to existing related experiments and research reports, stem cell transplantation therapy has been shown to have a positive effect on the recovery of liver fibrosis/cirrhosis, but for some reason, this therapy still cannot be widely used in clinical work. One of the reasons that cannot be ignored is the low quantity of exogenous stem cells transplanted into the liver in vivo. Thus, we investigated whether the use of the vascular endothelial growth factor (VEGF) can increase the number of stem cell transplants and improve the efficacy of stem cell transplantation therapy. METHODS: Using a Sprague-Dawley rat liver fibrosis model, we transplanted into fibrosis liver allograft bone marrow mesenchymal stem cells (BMSCs) which were labelled with chlormethylbenzamido-1,1-dioctadecyl-3,3,3'3'-tetramethylin-docarbocyamine (CM-DiI) or injected VEGF adenovirus solution through the tail vein or conducted the above two operations simultaneously. The cell surface receptor profile of BMSC was examined by flow cytometry and immunofluorescence staining. Hepatic sinusoidal vascular leakage was measured with Evan's blue dye assay. Paraffin section staining, immunofluorescent staining, RT-qPCR (quantitative reverse transcription polymerase chain reaction), and Western blot were used to evaluate hepatic pathological changes and physiology function. RESULT: The in vivo study indicated that, comparing with other groups of rats, the rats with combined treatment of BMSC transplantation and VEGF injection exhibited obvious reduction in liver fibrosis. Evan's blue dye assay suggests that after injecting with VEGF adenovirus solution, the rat's hepatic sinusoidal permeability would be increased. We confirmed the expression of very late antigen-4 (VLA4, integrin α 4 ß 1) on rat BMSCs and the elevated expression of vascular adhesion molecule-1 (VCAM-1) in the hepatic sinusoidal endothelial cells. In addition, the analysis of CM-DiI-labeled BMSCs showed that the BMSC+VEGF group exhibited better cell engraftment and that the engrafted cells were mainly distributed in the hepatic parenchyma. Furthermore, compared with the other situation, it is best to reconstitute the liver secretion and regeneration function of rats after combined application of VEGF and BMSC. CONCLUSION: We showed that VEGF promotes the engraftment of BMSCs in liver fibrosis, enhances liver regeneration, and improves liver function. These outcomes may be related to the increasing hepatic sinusoidal endothelium permeability and VCAM-1-increased expression.

Development and validation of a primate model for liver fibrosis.

INTRODUCTION: Many liver diseases involve liver fibrosis. Most preclinical studies of liver fibrosis are carried out in small animals such as rodents, and thus lack direct potential for extrapolation to human diseases. The aim of the current study was to develop a primate model for liver fibrosis with greater relevance to translational research. METHODS: Liver fibrosis was induced in adult male healthy rhesus monkeys using repeated CCl4 treatment (40% in olive oil, 1.5 ml/kg once every 3 days via peritoneal injection, subcutaneous injection or gastric gavage). Liver biopsy was conducted at various time points for histologic examination. Blood samples were taken for standard liver function test. RESULTS: Gastric gavage was the optimal approach for establishing stably liver fibrosis without animal loss due to toxicity. The progression of fibrosis appeared to involve epithelial to mesenchymal transition and hepatic ductular reaction. CONCLUSION: Repeated CCl4 gavage in rhesus monkeys results in stable liver fibrosis. Such a model may be an effective platform for future studies of human liver fibrosis.

Hsa_circ_0101432 promotes the development of hepatocellular carcinoma (HCC) by adsorbing miR-1258 and miR-622.

The present research was major in investigating the regulation association among hsa_circ_0101432 (has_circ_RPPH1), miR-1258, miR-622 and MAPK1 in hepatocellular carcinoma (HCC), and we explored the mechanism underlying pathogenesis of HCC. Microarray analysis was employed to detect hsa_circ_0101432 expression in HCC. Hsa_circ_0101432 was verified as a circRNA by testing divergent primers and RNase R. And qRT-PCR was performed to determine the expression of hsa_circ_0101432, miR-1258, miR-622 and MAPK1 mRNA. Furthermore, miRanda predicted that mRNAs targeted miR-1258 and miR-622. CCK-8 assay, colony formation assay, flow cytometry as well as transwell assay were performed to detect cell viability, proliferation, apoptosis and invasive ability, respectively. Xenograft in nude mice was applied to observe tumor growth in vivo. Up-regulated hsa_circ_0101432 and down-regulated miR-1258 and miR-622 were detected in HCC while Hsa_circ_0101432 enhanced expression of MAPK1 mRNA by targeting miR-1258 and miR-622. Knocking down hsa_circ_0101432 or overexpressing miR-1258 and miR-622 inhibited proliferation and invasive ability of HCC cell and promoted cell apoptosis. Hsa_circ_0101432 was confirmed to promote tumor growth via inhibiting miR-1258 and miR-622 expression and promoting MAPK1 mRNA expression by in vivo experiment. Hsa_circ_0101432 inhibited HCC cell apoptosis, promoted cell proliferation, invasive ability and HCC tumor growth by targeting miR-1258 and miR-622 and upregulating MAPK1 mRNA expression.

Radiation resistance of the lung adenocarcinoma is related to the AKT-Onzin-POU5F1 axis.

Non-small cell lung carcinoma is the predominant type of lung cancer, and shows an easily developable tolerance to radiotherapy. Cancer stem cells are suggested to be involved in the resistance against therapies. Onzin might be accumulated during the process tumor overcoming the radiation stress. To address the relationship between Onzin, stemness and radiation resistance, we treated the lung cancer tumor bearing mice with radiaotherapy and observed the differences between radiation sensitive (RS) and resistant (RR) tumors. Immunohistochemistry and HE staining were used to observe Onzin and POU5F1 expression in tumor tissues. Quantitative realtime-PCR and Western blot were applied for Onzin and POU5F1 in tumors and cells. In-vitro cellular viability was assessed by CCK8 methods for tumor derived cells. The stably transfected A549 cell lines overexpressing Onzin were generated through lentivirus transfection. After radiotherapy, those RR adenocarcinoma tumors and cells derived from them showed an increased Onzin expression. Further, RR cells were found upregulated stemness, indicated by increased sphericity and proliferation, as well as POU5F1 expression. Next, we overexpressed Onzin in the A549 cells and found an elevated POU5F1 expression, increased proliferation, and enhanced sphericity. Moreover, this could be suppressed by the AKT inhibitor MK-2260. In vivo, the A549 cells overexpressing Onzin showed not only higher tumor formation capability and growth, but also a significant resistance to radiation. Taken together, RR tumors have upregulated Onzin and POU5F1 expression. Ectopic expression of Onzin promotes the POU5F1 expression as well as stemness functions, and confers adenocarcinomas the resistance to radiotherapy.

Preliminary experience in laparoscopic resection of hepatic hydatidectocyst with the Da Vinci Surgical System (DVSS): a case report.

BACKGROUND: At present, Da Vinci robotic assisted hepatectomy has been routinely carried out in conditional units. But there is no report concerning the use of Da Vinci robots for hepatic hydatid cystectomy and experience on this aspect is seldom mentioned before. This study was to summarize the preliminary experience in laparoscopic resection of hepatic hydatidectocyst with the Da Vinci Surgical System (DVSS). CASE PRESENTATION: A 29-year-old female diagnosed as hepatic hydatid in the right anterior lobe of liver was treated with laparoscopic resection by the DVSS under general anesthesia. Appropriate disposal of tumor cell in vascular system and disinfection of surgical field with hypertonic saline were conducted. The hepatic hydatidectocyst was resected completely with an operation time of 130 min, an intraoperative blood loss of 200 ml and a length of hospital stay for five days. The vital signs of patient were stable and no cyst fluid allergy occurred after operation. CONCLUSIONS: Our result showed that laparoscopic resection of hepatic hydatidectocyst by using the DVSS is safe and feasible on the basis of hospitals have rich experience in treatment of cystic echinococcosisliver, resection with DVSS and laparoscopic excision.

Effectiveness and safety of diagnostic flexi-rigid thoracoscopy in differentiating exudative pleural effusion of unknown etiology: a retrospective study of 215 patients.

BACKGROUND: The aim of this study was to evaluate the effectiveness and safety of diagnostic flexi-rigid thoracoscopy in differentiating exudative pleural effusion of unknown etiology. METHODS: A total of 215 patients with undiagnosed exudative pleural effusion were consecutively recruited between January 2011 and February 2013. Thoracoscopy was carried out under local anesthesia, and multisite pleural biopsies were performed using a flexi-rigid thoracoscope. The tolerance of the patients, surgical complications and postoperative pathological diagnosis rate were used to evaluate the effectiveness and safety of the thoracoscopy procedures. RESULTS: All patients, Karnofsky performance status (KPS) >70, could tolerate both the thoracoscopic surgery and pleural biopsy; there were no severe complications. Thoracoscopic findings included pleural hyperaemia, fibrinous adhesion, nodular bulge and fester. The pathological biopsy confirmed diagnoses of malignant tumor (97 cases), tuberculous pleuritis (91 cases), tuberculous empyema (one case), pulmonary schistosomiasis (one case) and unknown etiology (25 cases). The total diagnosis rate was 88.4%. Subcutaneous emphysema occurred in ten cases and fever in six cases, all of which recovered completely with conservative treatment. CONCLUSIONS: Flexi-rigid thoracoscopy had a high diagnosis rate, differentiating exudative pleural effusion of unknown etiology with satisfactory effectiveness and safety. There was high degree of relationship between thoracoscopic appearance and primary disease or tumor classification.

Deleted in liver cancer-1 inhibits cell growth and tumorigenicity in human pancreatic cancer.

Deleted in liver cancer-1 (DLC-1) has been isolated from primary hepatocellular carcinoma and demonstrated to be a potential tumor suppressor gene. The aim of the present study was to observe the effect of the DLC-1 gene on pancreatic cancer cell growth and evaluate the feasibility of using the DLC-1 gene in gene therapy for pancreatic cancer. A recombinant plasmid (pcDNA3.1/DLC-1) was transfected into PANC-1 cells by liposomes and then the pre-established human PANC-1 pancreatic carcinoma cells were injected into athymic nude mice via the tail vein. The results showed that the overexpression of DLC-1 in the PANC-1 cells inhibited cell proliferation in vitro, while the act of introducing DLC-1 reduced tumorigenicity in the nude mice. The findings suggest that DLC-1 may have an effect on the pathogenesis of pancreatic cancer. The DLC-1 gene may be a promising target in gene therapy for pancreatic cancer.

Standard versus extended pancreaticoduodenectomy in treating adenocarcinoma of the head of the pancreas.

OBJECTIVES: To compare the postoperative complications and survival of standard pancreatoduodenectomy (SPD) and extended pancreatoduodenectomy (EPD) in patients with resectable adenocarcinoma of the head of the pancreas. METHODS: Between January 1994 and December 2011, 165 patients with biopsy-proven adenocarcinoma of the pancreatic head were treated in West China Hospital, among whom 93 underwent SPD and 72 had EPD. Complications and survival after the surgery were analyzed retrospectively. RESULTS: The median operation time of the EPD group was longer compared with the SPD group (375 minutes vs.310 minutes, P<0.01), the volume of blood transfusion was larger (700 mL vs.400 mL, P<0.05), while the median hospital stay (13.5 days vs.12 days, P=0.79) and the total complication rates were comparable (34.7% vs.32.4%, P=0.93). The total recurrence rates of the SPD and EPD groups were not significantly different (52.7% vs. 43.1%, P=0.83). No significant differences were found between the SPD and EPD groups in 1-year (81.7% vs. 86.1%), 3-year (38.7% vs. 43.1%), 5-year (16.7% vs. 19.4%), and median survivals (19.8 months vs. 23.2 months, P= 0.52). CONCLUSION: The postoperative complications and survival donot differ significantly between SPD and EPD.

Central pancreatectomy for benign or borderline lesions of the pancreatic neck: a single centre experience and literature review.

BACKGROUND/AIMS: To investigate the effectiveness and safety of central pancreatectomy. METHODOLOGY: We retrospectively studied 44 cases that underwent central pancreatectomy (CP), 55 patients who underwent distal pancreatectomy (DP), and 62 patients who underwent pancreatoduodenectomy (PD) for their benign or borderline pancreatic lesions; as well as the different management styles for pancreatic stumps in CP. RESULTS: The duration of surgery and length of hospital stay were shorter in the CP group than that of PD group, and blood loss was also less in CP group. There were no differences between the CP and DP groups in duration of surgery, length of hospital stay, and blood loss. The incidence of common surgical complications was higher in the PD group. There were more pancreatic fistulas (grade B/C) in CP and PD groups compared to that of the DP group. New onset or worsening of diabetes occurred only in the CP and PD groups at 4.8% and 10.9%, respectively. A pancreaticogastrostomy for distal pancreatic stumps reduced the incidence of pancreatic fistula (p=0.038). Duct-to-mucosa anastomosis had less pancreatic fistula than invagination anastomosis (p=0.017). There was no difference in incidence of pancreatic fistula between pancreaticojejunostomy and oversewing of proximal pancreatic stumps (p=0.601). CONCLUSIONS: CP is an available and safe operation for benign or borderline lesions located in the pancreatic neck. A pancreaticogastrostomy for distal pancreatic stumps or duct-to-mucosa anastomosis may reduce the risk of pancreatic fistula.

Coexistence of pancreatic carcinoma and pancreatic tuberculosis: case report.

Pancreatic tuberculosis (TB) is extremely rare and mimics pancreatic carcinoma both clinically and radiologically. This paper discusses the occurrence of 2 heterogeneous masses located in the head and tail of the pancreas in an adult male. In this patient, laparotomy was performed because of the high suspicion of pancreatic carcinoma. Intraoperative fine needle aspiration biopsy revealed the coexistence of pancreatic carcinoma with pancreatic TB, and a combined resection of the distal pancreas and spleen was successfully performed. Following surgery, the patient received standard chemotherapy for TB. At 7-month follow-up, computed tomography showed resolution of the mass in the pancreatic head. Clinicians must maintain a high index of suspicion for pancreatic TB in patients with pancreatic masses. The coexistence of malignancy and TB should be considered when patients present with multiple pancreatic masses.

[Diagnosis and surgical interventions for the chronic obstructive pancreatitis due to the inflammatory lesions at the opening of the pancreatic duct].

OBJECTIVE: To explore the diagnostic methods and reasonable surgical interventions for the chronic obstructive pancreatitis due to the inflammatory lesions at the opening of the pancreatic duct. METHODS: From January 2002 to November 2010 the data of 28 patients who were diagnosed as the chronic obstructive pancreatitis (COP) was retrospectively reviewed. Out of the 28 patients, it was analyzed that the clinical manifestations, diagnostic methods, surgical finding and surgical interventions of the 13 patients who were diagnosed as COP due to the inflammatory lesions at the opening of the pancreatic duct in the exploratory operation accompanying recurrent acute abdominal pain with increased serum amylase and lipase, dilation of entire pancreatic duct on imaging before surgery. The conditions included pain recrudescence, quality of life, pancreatic changes on imaging and the serum amylase and lipase after surgery were recorded. RESULTS: All the 13 patients had clinical manifestations of COP. However, 12 patients had different manifestations on imaging from those chronic pancreatitis imaging due to tumors at the duodenal papilla, ampulla or inner pancreatic duct. Via exploratory operation and magnetic resonance cholangiopancreatography (MRCP), there were short pancreaticobiliary common channel or pancreas divisum existing in most patients. There was no acute abdominal pain with the increased serum amylase and lipase in the 12 patients who receiving the transduodenal mastoid, ampulla and pancreatic ductal opening incision and plasty, the paramastoideus incision and plasty in the visit. CONCLUSIONS: The imaging character of COP due to the inflammatory lesions at the opening of the pancreatic duct is the dilation of the pancreatic duct without the chronic obstruction in the bile duct. The patients with short pancreaticobiliary common channel or pancreas divisum easily suffer COP due to the stenosis of the pancreatic ductal opening caused by the duodenal mastoiditis or paramastoiditis. The local plasty surgery to correct the stenosis at the pancreatic ductal opening and improve the drainage of the pancreatic duct is an easy and effective management.

Cordyceps sinensis extract suppresses hypoxia-induced proliferation of rat pulmonary artery smooth muscle cells.

OBJECTIVE: To investigate the effects of a Chinese herb Cordyceps sinensis (C. sinensis) extract on hypoxia-induced proliferation and the underlying mechanisms involved. METHODS: This prospective study was carried out at the Central Laboratory of Yichang Central People's Hospital, Yichang, China from March 2008 to April 2010. The C. sinensis was extracted from the Chinese herb C. sinensis using aqueous alcohol extraction techniques. Forty healthy adult male Sprague Dawley rats were used in the study. The proliferation of pulmonary artery smooth muscle cells (PASMCs) was measured using 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and cell viability was determined by trypan blue exclusion. Cell cycles were analyzed using FACSort flow cytometric analysis. The expression of proliferating cell nuclear antigen (PCNA), c-jun, and c-fos in rat PASMCs was determined by immunohistochemistry. RESULTS: We found an increased proliferation of PASMCs and increased expression of transcription factors, c-jun and c-fos in PASMCs cultured under hypoxic conditions. The C. sinensis extract significantly inhibited hypoxia-induced cell proliferation in a dose-dependent manner. In addition, C. sinensis extract also significantly inhibited the expression of PCNA, c-jun, and c-fos in these PASMCs. CONCLUSION: Our results indicated that C. sinensis extract inhibits hypoxia-induced proliferation of rat PASMCs, probably by suppressing the expression of PCNA, c-fos, c-jun, and decreasing the percentage of cells in synthesis phase, second gap phase, and mitotic phase in cell cycle (S+G2/M) phase. Our results therefore, provided novel evidence that C. sinensis extract may be used as a therapeutic reagent in the treatment of hypoxic pulmonary hypertension.

[Clinical study of 34 patients with extranodal NK/T cell lymphoma-nasal type].

OBJECTIVE: To explore the clinical feature, the reason of misdiagnosis and mistreatment, influential factor of prognosis in patients with extranodal NK/T cell lymphoma-nasal type. METHOD: A retrospective study was made on the clinical data of 34 patients with extranodal NK/T cell lymphoma-nasal type. Among them, 10 cases were staged I(E) intra-cavity, 15 cases were I(E) ex-cavity, 6 cases were II(E) and 3 cases were IV(E). Among them, 29 cases were in nasal cavity, 5 cases were outside nasal cavity; 14 cases were treated with single chemotherapy or radiation therapy, 20 cases were treated with radiation therapy add chemotherapy. RESULT: The total rate of misdiagnosis and mistreatment were 58.8% (20/34), 52.3% (18/34), respectively. The 5-year survival rate of the I(E) intra-cavity group were 60.0% (6/10), and those of I(E) ex-cavity group were 26.7% (4/15), and those of II(E) group and IV(E) group were 16.7% (1/6), 0% (0/3), respectively There was significant difference between 3 groups by statistical analysis (P < 0.01). The 5-year survival rate of I(E) ex-cavity group treated with single therapy were 0% (0/6), and those of I(E)-cavity group treated with combined therapy were 50% (1/2). CONCLUSION: The early clinical manifestation of extranodal NK/T tell lymphoma-nasal type is atypical and which is hard to diagnose and treat. Diagnosis depends on pathologic biopsy and immunohistochemistry, there are many factors that influence the prognosis of this disease, in which the clinical stage is a major factor. It is crucial for diagnosing and treating early.