Hepatitis C, Chronic ; drug therapy ; psychology ; Humans ; Interferons ; therapeutic use ; Quality of Life

Acute Kidney Injury ; etiology ; Adult ; Diagnosis, Differential ; Female ; HELLP Syndrome ; pathology ; Hemolytic-Uremic Syndrome ; complications ; pathology ; therapy ; Humans ; Plasma Exchange ; Postpartum Period ; Pregnancy ; Purpura, Thrombotic Thrombocytopenic ; pathology ; Young Adult

OBJECTIVESTo investigate the histological changes in liver biopsy tissues taken from chronic hepatitis B patients with HBsAg and HBeAg positive and ALT abnormal after lamivudine therapy for one year.

METHODSLamivudine was given orally at the dose of 100 mg once a day for one year. 101 patients were enrolled into this open-label study. Paired liver biopsies from patients with hepatitis B before and after therapy with lamivudine were studied. Blinded biopsies were evaluated by a histopathologist and scored according to Knodell's histology activity index(HAI).

RESULTS53.5% (54/101), 51.5% (52/101) and 31.7% (32/101) patients had a reduction of their total hepatic HAI score, necroinflammation and fibrosis scores by >or=2 points or 1 points at the end of one year of lamivudine therapy, compared with their pretreatment values, respectively. There were significant reduction of HAI score, necroinflammation and fibrosis scores from 8.0+/-4.7 to 5.2+/-3.3 (t=7.358, P<0.01), from 5.9+/-3.8 to 3.6+/-2.5 (t=7.298, P<0.01), and from 2.1+/-1.2 to 1.6+/-1.2 (t=3.827, P<0.01), respectively. The histological improvement was independent on the HBeAg seroconvertion during the therapy.

CONCLUSIONSignificant improvement in liver histology, both necroinflammation and fibrosis, can be obtained in the majority of patients treated with lamivudine for one year.

Adolescent ; Adult ; Antiviral Agents ; therapeutic use ; Child ; Female ; Hepatitis B e Antigens ; analysis ; Hepatitis B, Chronic ; drug therapy ; pathology ; Humans ; Lamivudine ; therapeutic use ; Liver ; pathology ; Liver Cirrhosis ; pathology ; Male

PURPOSE: Cyclooxygenase-2 (COX-2) expression is up-regulated in several types of human cancers and it has been suggested that COX-2 is closely inked to carcinogenesis. The objectives of this study were to investigate COX-2 expression in periampullary cancer and to evaluate the association of the clinicopathological factors with its expression. METHODS: Thirty specimens which were resected from patients with periampullary cancers (13 pancreatic adenocarcinomas, 8 common bile duct cancers, 9 ampulla of vater cancers) were investigated by immunohistochemical staining using Anti COX-2 monoclonal Ab. The 30 specimens were divided into stain-positive and stain-negative groups. The correlation between COX-2 expression and the various clinicopathological factors including the tumor size, nodal metastasis, differentiation, perineural and vascular invasion, were studied. RESULTS: COX-2 was expressed in 69% of pancreatic adenocarcinomas, 100% of common bile duct cancers and 78% of ampulla of vater cancers. However there was no significant correlation between COX-2 expression and the clinicopathological factors. CONCLUSION: COX-2 is highly expressed in periampullary cancer. Even though there was no correlation with the clinicopathological factors, the utility of the COX-2 inhibitors in preventing or treating periampullary cancer remains undetermined but warronts further investigation.
Adenocarcinoma ; Ampulla of Vater ; Carcinogenesis ; Common Bile Duct ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase 2* ; Humans ; Ink ; Neoplasm Metastasis

PURPOSE: Cyclooxygenase (COX) enzymes catalyze the ratelimiting step in arachidonate metabolism. COX-1 is expressed constitutively in many cell types. However COX-2 is an inducible enzyme responsible for prostaglandin production at site of inflammation. Recently, there has been increasing evidence that COX-2 involves in development and progression of human tumors. The aim of the present investigation is to evaluate the antiproliferative effect of NS-398, a selective COX-2 inhibitor, and its mechanism in a papillary thyroid cancer cell line, TPC-1. METHODS: We used TPC-1 cell line, NS-398 and EGF. COX-2 expression was detected by RT-PCR and western blot. We used MTT assay to evaluate antiproliferative effect of NS- 398. The mechanisms of growth inhibition were evaluated by apoptosis assay and cell cycle analysis using flow cytometry. RESULTS: COX-2 expression was identified by both RT-PCR and western blot in TPC-1 cells and it was upregulated by serum, EGF (10 ng/ml), and NS-398 (50 mM). NS-398 induced a dose-dependent inhibition of cell proliferation but did not increases apoptotic cell population significantly in the TPC-1 cell line. EGF treatment (10 ng/ml) for 72 hours did not seem to change the antiproliferative effect of NS-398. The proportion of G0/G1 cell cycle was increased by 10% compared with control after 36 hours of treatment with NS-398. CONCLUSION: TPC-1 cells expressed COX-2 constitutively and its expression was upregulated by serum, EGF, and NS-398. The selective COX-2 inhibitor, NS-398 inhibited cell proliferation in TPC-1 cell line rather by cell cycle arrest at G₀/G₁ phase than by inducing apoptosis.
Apoptosis ; Blotting, Western ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Line* ; Cell Proliferation ; Cyclooxygenase 2 ; Epidermal Growth Factor ; Flow Cytometry ; Humans ; Inflammation ; Metabolism ; Prostaglandin-Endoperoxide Synthases ; Thyroid Gland* ; Thyroid Neoplasms*

AIM To explore the curative effects,adverse events,effects on immunity function and cost-effectiveness of Aiyu Capsules (Cremastrae pseudobulbus,Solanum lyratum,Angelicae sinensis Radix,etc.) or Fufang Banmao Capsules (Mylabris,Ginseng Radix et Rhizoma,Astragali Radix,etc.) combined with icotinib hydrochloride in the treatment of advanced non-small cell lung carcinoma (NSCLC).METHODS One hundred and sixty patients with advanced NSCLC were randomly divided into three groups.The patients in icotinib hydrochloride group (n =80) took icotinib hydrochloride,125 mg each time,three times a day;the patients in Aiyu Capsules + icotinib hydrochloride group or Fufang Banmao Capsules + icotinib hydrochloride group were treated with Aiyu Capsules (40 cases,three pills each time,three times a day) or Fufang Banmao Capsules (40 cases,one pill each time,three times a day) combined with icotinib hydrochloride (125 mg each time,three times a day),respectively.Curative effects,adverse events,serum tumor markers,dendritic cell subsets and cost-effectiveness among the three groups were compared.RESULTS Eight weeks after the treatment,effective rates in the Aiyu Capsules + icotinib hydrochloride group (82.50％) and Fufang Banmao Capsules + icotinib hydrochloride group (97.5％) were significantly higher than that in the icotinib hydrochloride group (73.5％) (P ＜ 0.05).Six-month survival rates in the icotinib hydrochloride group,Aiyu Capsules + icotinib hydrochloride group and Fufang Banmao Capsules + icotinib hydrochloride group were 93.7％,97.5％ and 97.5％,respectively;one-year survival rates in the three groups were 53.7％,72.5％ and 75.0％,respectively;two-year survival rates in the three groups were 20.0％,37.5％ and 40.0％,respectively.One-year,two-year survival rates in the Aiyu Capsules + icotinib hydrochloride group and Fufang Banmao Capsules + icotinib hydrochloride group were significantly higher than those in the icotinib hydrochloride group (P ＜ 0.05).Myeloid dendritic cell (mDC) subsets' increases (d8week-d1) in the Aiyu Capsules + icotinib hydrochloride group and Fufang Banmao Capsules + icotinib hydrochloride group were significantly higher than that in the icotinib hydrochloride group (P ＜ 0.05).There was no statistical significance in plasmacytoid dendritic cell (pDC) subsets' change among the three groups (P ＞ 0.05).Changes of carcinoembryonic antigen (CEA),cytokeratin-19-fragment (CYFRA21-1),neuron-specific enolase (NSE) in the Aiyu Capsules + icotinib hydrochloride group and Fufang Banmao Capsules + icotinib hydrochloride group were higher than those in the icotinib hydrochloride group (P ＜ 0.05).Treatment costs in the Aiyu Capsules + icotinib hydrochloride group and Fufang Banmao Capsules + icotinib hydrochloride group were significantly lower than that in the icotinib hydrochloride group (P ＜ 0.05).No obvious statistical difference in adverse events was found among the three groups (P ＞ 0.05).CONCLUSION The curative effects and cost-effectiveness of Aiyu Capsules or Fufang Banmao Capsules combined with icotinib hydrochloride are better than those of icotinib hydrochloride alone in the treatment of advanced NSCLC.

Objective To study the chest image appearances of penicilliosis marneffei(PSM)in patients with acquired immune deficiency syndrome(AIDS).Methods Chest imaging features of PSM in 36 patients with AIDS were retrospectively analyzed.Results Radiographic features of infiltrative lesions and focal lung consolidation were found in 14 cases(38.89%),in which 2 cases were with single lung disease(5.56%)and 12 cases with bilateral lung involvement(33.33%).Eight cases had diffuse lesions (22.22%),10 cases had reticular image patterns(27.78%),9 cases had nodular patterns(25.00%), 7 cases had ground-glass shadows(19.44%),6 cases had diffuse miliary lesions(16.67%),4 cases had enlarged bilar and enlarged mediastinum lymph nodes(11.11%).Cystic lesions was found in 5 cases (13.89%).Four cases had pleural effusion(11.11%),and 2 cases had nodular bump(5.56%). Pericardial effusion and pneumothorax each appeared in 1 case(2.78%).By HRCT,infiltrative lesion and focal lung consolidation were found in 32 patients(88.89%),in which 4 cases were with single lung lesions (11.11%)and 28 cases were with bilateral lung lesions(77.78%).Thirteen cases had diffuse lesions (36.11%),10 cases had pulmonary interstitial hyperplasia(27.78%),9 cases had nodular patterns (25.00%),8 cases had ground-glass shadows(22.22%),9 cases had diffuse miliary lesions(25.00%), 21 cases had enlarged lymph nodes in the mediastinum(58.33%).Cystic lesions were found in 8 cases (22.22%).Thirteen cases had pleural effusion(36.11%),and 2 cases had nodular bump(5.56%). Pericardial effusion and pneumothorax each appeared in 1 case(2.78%).Conclusion The image appearances of PSM in patients with AIDS include infiltrative lesions or focal lung consolidation,ground- glass shadow,enlarged hilar and mediastinum lymph nodes,pleural effusion,interstitial involvement or reticular image pattern(pulmonary interstitial hyperplasia),diffuse miliary lesion,and cystic lesion.

PURPOSE: Phenylbutyrate is an effective redifferentiating agent in several human cancers. Recently phenylbutyrate has been reported to inhibit histone deacetylase activity. We investigated the effects of sodium 4-henylbutyrate (Na-4-PB) on cell proliferation in a human pancreatic cancer cell line. METHODS: A human pancreatic cancer cell line, Aspc-1 was purchased from Korean Cell Line Bank. Antiproliferative effects of sodium 4-phenylbutyrate were measured by MTT assay and their mechanisms were evaluated by apoptosis assay and cell cycle analysis. RESULTS: After 3 days of treatment with Na-4-PB at the concentration of 2.5, 5, 7.5, and 10 mM, relative growth inhibition compared to control was 21.3+/-8.3% (mean+/-SD), 37.8+/-2.3%, 46.7+/-0.5%, and 56.7+/-1.7% respectively (p < 0.05). Antiproliferative effect of Na-4-PB was also time-dependent. Combination treatment with Na-4-PB and troglitazone, a PPARg agonist, increased antiproliferative effects but was not synergistic. After 48 hour treatment with Na-4-PB, early apoptotic cell population in control, 2.5, and 5 mM of Na-4-PB was 29.6%, 44.2%, and 65.9%, respectively. After 24 hour treatment with Na-4- PB, G0/G1 phase population in control, 2.5, and 5 mM of Na-4-PB was 55.0%, 67.4%, and 65.8%, respectively. CONCLUSION: Na-4-PB inhibited pancreatic cancer cell proliferation by inducing apoptosis and cell cycle arrest at G0/G1 phase in time- and dose-dependent manner. Combination treatment with Na-4-PB and other chemotherapeutic agents such as troglitazone, a PPARg agonist, can enhance antiproliferative effects. Na-4-PB might be a promising potential therapeutic agent for patients with pancreatic cancer.
Apoptosis ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Line* ; Cell Proliferation ; Histone Deacetylases ; Humans ; Pancreatic Neoplasms* ; Sodium

PURPOSE: Selective cyclooxygenase (COX)-2 inhibitors have been reported to inhibit cancer cell proliferation. We investigated the effects of NS-398, a selective COX-2 inhibitor, on cell proliferation in human pancreatic cancer cell lines. METHODS: Human pancreatic cancer cell lines, Aspc-1, Capan-1, and Capan-2 were used. We used western blot and/or RT-PCR to evaluate COX-2 and vascular endothelial growth factor expression. Antiproliferative effects were measured by MTT assay, apoptosis assay and cell cycle analysis. Epidermal growth factor (EGF) and troglitazone were used for combined treatment. RESULTS: COX-2 was relatively overexpressed in Capan-1 and Capan- 2, but minimal in Aspc-1 cell line. COX-2 mRNA expression was upregulated by 50 microM of NS-398 in Aspc-1 cell line but was downregulated at 100 microM in all cell lines. Treatment with NS-398 increased cell population of G0/G1 phase and also induced early apoptotic changes in a dose-dependent manner in all three cell lines. Combined treatment with EGF or troglitazone did not seem to affect antiproliferative effects of NS-398. All three cell lines expressed vascular endothelial growth factor constitutively and its expression was downregulated by treatment with NS-398. Pretreatment with NS-398 prior to radiation exposure increased radiosensitivity in Capan-2 cells. CONCLUSION: COX-2 expression was variable in pancreatic cancer cell lines. NS-398 inhibited pancreatic cancer cell proliferation by inducing apoptosis and cell cycle arrest in a dose-dependent manner. Treatment with NS-398 also inhibited expression of VEGF and enhanced radiosensitivity in pancreatic cancer cell lines. COX-2 inhibitors might be promising potential therapeutic agents for patients with pancreatic cancer.
Apoptosis ; Blotting, Western ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Line* ; Cell Proliferation ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase 2* ; Epidermal Growth Factor ; Humans ; Pancreatic Neoplasms* ; Prostaglandin-Endoperoxide Synthases ; Radiation Tolerance ; RNA, Messenger ; Vascular Endothelial Growth Factor A