Conclusion: Localized gastric amyloidosis, being rare in incidence, should be considered in the differentiation of gastric tumors, in which biopsy is the only means to confirm the diagnosis. Key Word(s): 1. Gastric amyloidosis diagnosis Presenting Author: SHIGENAGA MATSUI Additional Authors: HIROSHI see more KASHIDA, MASANORI KAWASAKI, YUTAKA ASAKUMA, TOSHIHARU SAKURAI,

MASATOSHI KUDO Corresponding Author: SHIGENAGA MATSUI Affiliations: Kinki University Faculty of Medicine, Kinki University Faculty of Medicine, Kinki University Faculty of Medicine, Kinki University Faculty of Medicine, Kinki University Faculty of Medicine Objective: Eosinophilic esophagitis (EoE) is a chronic inflammatory condition characterized by esophageal dysfunction and eosinophilic infiltrate in the esophageal epithelium in the absence of other potential causes of eosinophilia. In this study, we investigated the clinical characteristics, endoscopic appearances, and treatments for patients with EoE. Methods: Three patients with EoE (3 women; mean age, 27.3 years) were diagnosed with EoE based on typical symptoms, endoscopic abnormalities and infiltration of the esophageal epithelium with >15 eosinophils/high-power field. The average endoscopic follow-up period was 19.2 months. Results: Two patients had dysphagia symptoms and 1 patitent had epigastralgia symptoms, which not improved in 3 patients who were treated with proton pump inhibitor. Three patients

had the history of the allergy disease of asthma, atopic dermatitis, and a food allergy. The endoscopic features were linear furrows in 2 patients, and was white papules in 1 patient. CX-5461 chemical structure Three patients had a mean peak eosinophil count of 94.7 eos/hpf in the esophageal biopsy specimens.

All the patients had an average of 9.13% of peripheral eosinophilia. All the patients were given with the corticosteroid administration of 30 mg of introduction, and the quantity of it was decreased gradually. As a result, the improvement of symptoms and endoscopic Ribociclib price features had in all the patients. However, the one patient was permitted recurrence of symptom when corticosteroid was 5 mg. Conclusion: Endoscopic features of EOE is should be known. New evidence from ongoing research on EoE should thus seek to define a common treatment algorithm to optimize EoE patient management. Key Word(s): 1. Eosinophilic esophagitis treatment Presenting Author: HEE SEOK MOON Additional Authors: JAE KYU SEONG, HYUN YOUNG JEONG Corresponding Author: HEE SEOK MOON Affiliations: Chungnam National University School of Medicine, Chungnam National University School of Medicine Objective: Palliation of malignant esophageal obstruction endoscopically placed stent has been shown to improve patient quality of life by allowing restoration of oral alimentation. But complications and failures have not been well described in stomach cancer with esophageal invasion as well as esophageal and lung cancer.

05). Perceptible ΔE between manual and mechanical mixing techniques were 5.93 and 5.18 for both unpigmented and pigmented specimens, respectively. Under sebum storage, manually mixed unpigmented

specimens showed lower ΔE (p < 0.05) than those that were mechanically mixed; however, pigmented silicone specimens showed the same ΔE (p > 0.05). After light aging, mixing method had no effect on ΔE of unpigmented specimens (p > 0.05). Furthermore, mechanically mixed pigmented specimens showed lower ΔE (p < 0.05). Conclusions: Within silicone elastomers (whether pigmented or unpigmented), mechanical mixing under vacuum reduced pore numbers Selleck JNK inhibitor and percentages in comparison to manual mixing. For selected skin shade, pores affected the resultant color of prosthesis (color reproducibility). Additionally, silicone pores affected silicone color stability upon service. Clinical significance: In fabricating maxillofacial prostheses, mechanically mixing silicone under vacuum produces pore-free prostheses, tending to enhance their color production and stability. “
“This report describes the case of a patient who underwent osseointegrated dental implant ICG-001 price placement. The implants were misplaced inside the nasal fossae and in the right maxillary sinus, causing

chronic purulent sinusitis. CT scan without contrast showed signs of right maxillary sinusitis and confirmed OSBPL9 the misplacement of four dental implants that surfaced into the nasal cavities. The imaging also revealed the

presence of another implant that emerged inside the maxillary sinus. The patient underwent functional endoscopic sinus surgery with complete symptom remission at the long-term follow-up. We propose that sinusitis caused by protrusion of implants and by sinus floor lift procedures could share common physiopathological patterns and predisposing factors. “
“Purpose: Selective infiltration etching (SIE) is a newly developed surface treatment used to modify the surface of zirconia-based materials, rendering them ready for bonding to resin cements. The aim of this study was to evaluate the zirconia/resin bond strength and durability using the proposed technique. Materials and Methods: Fifty-four zirconia discs were fabricated and divided into three groups (n = 18) according to their surface treatment: as-sintered surface (control group), airborne-particle abrasion (50-μm aluminum oxide), and SIE group. The zirconia discs were bonded to preaged composite resin discs using a light-polymerized adhesive resin (Panavia F 2.0). The zirconia/resin bond strength was evaluated using microtensile bond strength test (MTBS), and the test was repeated after each of the following intervals of accelerated artificial aging (AA): thermocycling (10,000 cycles between 5 and 55°C), 4 weeks of water storage (37°C), and finally 26 weeks of water storage (37°C).

7,8 This review focuses on the relationships between the 3 classes of drugs known to be involved in severe SS, and the relative degrees of toxicity they characteristically precipitate. A key point to be emphasized is the spectrum concept of SS. SS is a synaptic serotonin (5-HT) concentration-related phenomenon.9 Readers are referred to recent selected reviews of SS for a broader perspective. There have been advances in the quantification of the frequency

and severity of SS with different drugs,9-14 in the definition of SS in animals and humans,15-17 in the pathophysiology,15 in the clinical presentation,18 and in its management and treatment.19-21 Serotonin syndrome can be diagnosed with accuracy and confidence, but few reports classify it using recognized diagnostic criteria, hence diminishing their value. It is not, as far as Talazoparib cost current human and animal evidence indicates, an idiosyncratic response, but a predictable and inevitable selleck chemicals result of

toxicity (mediated via the final common pathway of elevated intra-synaptic serotonin). If a case history were to appear reporting SS following an overdose of vitamin C, it would be parsimonious to assume that there had been a failure to ascertain or recognize the simultaneous ingestion of a potently serotonergic drug, cf. the Stanford case report.22 It would not be logical to make an initial assumption that vitamin C had previously unknown serotonergic properties, especially as we have good reasons to predict that it does not affect serotonin. That is Bayesian reasoning, ie, considering the prior probability when

estimating the likelihood of an outcome. Without such frameworks of knowledge and understanding of SS, case reports are often difficult to interpret, and the type of information they can yield reliably requires cautious consideration.23 The uncertainty and debate surrounding triptans demonstrates this problem clearly. The FDA alert was based on case reports, most of them informal, or “second-hand” and not peer-reviewed, and interpreted with an imperfect notion of Inositol oxygenase the symptoms and pathophysiology of SS, and without using validated criteria to establish diagnoses (eg, the Hunter Serotonin Toxicity Criteria [HSTC]17,20). The HSTC demonstrate unequivocally that clonus is the single most important sign required to diagnose SS, a fact that has now been established for many years, yet case reports of SS rarely, if ever, document the presence, or absence, of this sign. When such key information is lacking, little credence can be given to many reports. Case reports constitute a low grade of evidence, but they command undue attention and are repeatedly cited, even when they have been firmly rebutted (for just such an error that occurs in the FDA case reports, see24,25). The 3 classes of therapeutic drugs that, in certain combinations at usual doses, have been reliably documented to be capable of precipitating severe SS are: monoamine oxidase inhibitors (MAOIs), SRIs, and releasers.

Therefore, physicians treating AHC have investigated the use of viral kinetics in determining treatment duration. The European multicentre cohort study in HCV/HIV-infected patients showed that in those who achieved an RVR, 93% achieved an SVR [125]. Sub-analysis demonstrated that after a first undetectable HCV RNA, those who received at least 20 weeks of treatment achieved SVR of 96% compared with only 20%

in those who Selleckchem Antiinfection Compound Library received less than 20 weeks of therapy. Together, these findings suggest that 24 weeks of therapy may be sufficient in HIV-infected individuals with AHC who achieve an RVR. This has been supported by a number of other studies. In the Australian Trial in Acute Hepatitis C, where 24 weeks of combination therapy was used, RVR yielded a positive predictive value (PPV) for SVR of 75% and negative Buparlisib chemical structure predictive value (NPV) of 13% [116,126]. The high PPV supports 24 week treatment duration for those who achieve an RVR, while the low NPV suggests that 24 weeks of therapy may also be sufficient in those who do not achieve an RVR. However, not all studies demonstrate similarly low levels of relapse in non-RVR subjects treated for only 24 weeks. A recent Spanish study investigated 24 weeks of combination

therapy with a low overall SVR of 47%. While 92% of those who achieved an RVR also achieved an SVR, only 20% of non-RVR individuals did, suggesting that 24 weeks of therapy may have been insufficient [133]. Few studies have compared short and long treatment durations. Observational cohort data are difficult to interpret as it is unclear how to deal with ‘null responders’ whose therapy is discontinued early [134]. Results exist from a prospective study where individuals were treated for either 24 or 48 weeks with combination therapy: SVRs were achieved in 71% and 79%, respectively, with PPV of RVR for SVR also similar (81% and 89%). However, those without RVR in the 24-week group only achieved a 40% (2/5) SVR, compared to a 64% (7/11) SVR Lck in the 48-week group [117]. A 48-week therapy duration may thus be necessary

to achieve acceptable SVR rates in those who do not achieve an RVR. Due to these results, a treatment strategy where RVR is used to determine duration of therapy (24 weeks if RVR is achieved and 48 weeks if it is not) has been suggested. Data from a London cohort have demonstrated that this strategy can lead to an SVR of 91%, similar to that observed in the HCV-monoinfected population [135]. In chronic HCV, week-12 HCV RNA levels are routinely used to determine the likely futility of therapy and thus the need to discontinue treatment. Interpreting week-12 data within the available AHC cohort studies is difficult as it is not always transparent whether failure to achieve an EVR has been used as a stopping rule, thus heavily biasing its NPV.

Transverse strengths of white and pink acetal resin could not be calculated in this study, as white and pink acetal resin specimens did not break at the maximum applied force in the three-point bending test. Flexural strength of acetal resin was found to be within the ISO specification limits. As the water storage time increased, the deflection values of PMMA showed no significant difference (p > 0.05). Both the white and pink acetal resin

showed significant increase in deflection as the water storage time was increased from 50 hours to 180 days (p < 0.05). Conclusion: The results of this study indicated that transverse strength values of PMMA were within the ISO specification limit. Water storage time (50 hours, 30, 60,

and 180 days) had no statistically significant effect on the transverse strength and deflection of PMMA. Acetal resin suffered from permanent deformation, but did not break in the three-point bending test. Acetal check details resin showed significant increase in deflection as the water storage time was increased from 50 hours to 180 days. All materials tested demonstrated deflection values in compliance with ISO specification No 1567. “
“The aim of this study was to investigate the effect of accelerated light aging on bond strength of a silicone elastomer to three types of denture resin. A total of 60 single lap joint specimens were fabricated with auto-, heat-, and photopolymerized (n = 20) resins. EGFR targets An addition-type silicone elastomer (Episil-E) was bonded to resins treated with the ioxilan same primer (A330-G). Thirty specimens served as controls and were tested after 24 hours, and the remaining were aged under accelerated exposure to daylight for 546 hours (irradiance 765 W/m2). Lap shear joint tests were performed to evaluate bond strength at 50 mm/min crosshead speed. Two-way ANOVA and Tukey’s test were carried out to detect statistical significance (p < 0.05). ANOVA showed that the main effect of light aging was the most important factor determining the shear bond strength. The mean bond strength values ranged from 0.096 to 0.136 MPa. The highest

values were recorded for auto- (0.131 MPa) and photopolymerized (0.136 MPa) resins after aging. Accelerated light aging for 546 hours affects the bond strength of an addition-type silicone elastomer to three different denture resins. The bond strength significantly increased after aging for photo- and autopolymerized resins. All the bonds failed adhesively. “
“The CAD/CAM technology associated with rapid prototyping (RP) is already widely used in the fabrication of all-ceramic fixed prostheses and in the biomedical area; however, the use of this technology for the manufacture of metal frames for removable dentures is new. This work reports the results of a literature review conducted on the use of CAD/CAM and RP in the manufacture of removable partial dentures.

CXCR4 concentrated at the tumor border and perivascular areas, suggesting its potential involvement in tumor cell dissemination. Conclusion: A crosstalk exists among the TGF-β and CXCR4 pathways in liver tumors, reflecting a novel molecular mechanism that explains the protumorigenic effects of TGF-β and opens new perspectives for tumor therapy. (Hepatology 2013; 58:2032–2044) Transforming growth factor-beta (TGF-β) is an important regulatory suppressor factor; however, paradoxically, it also modulates other processes that contribute to tumorigenesis, such as fibrosis, immune regulation, microenvironment modification, and cell invasion.[1] Indeed,

in addition to its suppressor effects, TGF-β induces antiapoptotic signals in fetal hepatocytes Trichostatin A supplier and hepatoma cells,[2, 3] through activation of the epidermal growth factor receptor (EGFR) pathway.[4] Cells that survive to TGF-β-induced apoptotic signals undergo epithelial-mesenchymal

transition (EMT).[3, Neratinib solubility dmso 5, 6] Upon progression of liver cancer, EMT is considered a key process that may drive intrahepatic metastasis.[7] TGF-β levels are increased in hepatocellular carcinoma (HCC) tissue, plasma, and urine and decreased in patients who underwent effective therapy for HCC.[8] Liver tumors expressing late TGF-β-responsive genes (antiapoptotic and EMT-related genes) display a higher invasive phenotype and increased tumor recurrence when compared to those that show an early TGF-β signature (suppressor genes).[9] Interestingly, blocking TGF-β up-regulates E-cadherin and reduces migration and invasion of HCC cells.[10] Recent studies place chemokines and their receptors

at the center not only of physiological cell migration, but also of pathological processes, such as metastasis in cancer.[11] In particular, CXCR4 and its ligand, stromal cell-derived factor 1α (SDF-1α) / chemokine (C-X-C motif) ligand 12 (CXCL12), have been revealed as important molecules check details involved in the spreading and progression of a variety of tumors.[12] Different data suggest that molecular strategies to inhibit the CXCR4/CXCL12 pathway could be of therapeutic use for the treatment of HCC.[13] CXCR4 is up-regulated in human HCC,[14] correlating with progression of the disease.[15] Its ligand CXCL12 stimulates human hepatoma cell growth, migration, and invasion.[14] We have recently described that TGF-β up-regulates CXCR4 in rat hepatoma cells[16] and sensitizes cells to respond to CXCL12, which mediates cell scattering and survival. These results suggest a crosstalk between the increased protumorigenic response to TGF-β and the establishment of a functional CXCR4/CXCL12 axis. Nothing is known about whether a similar situation occurs in human liver tumorigenesis.

We have reported recently that mig-6 is a negative regulator of epidermal growth factor receptor (EGFR)-dependent skin morphogenesis and tumor formation in vivo. In the liver, ablation of mig-6 leads to an increase in EGFR protein levels, suggesting that mig-6 is a negative regulator of EGFR function. In line with this observation, primary hepatocytes isolated from mig-6 knockout and wild-type control mice display sustained mitogenic signaling in response to EGF. In Selleck MK-1775 order to explore the role of mig-6 in the liver in vivo, we

analyzed liver regeneration in mig-6 knockout and wild-type control mice. Interestingly, mig-6 knockout mice display enhanced hepatocyte proliferation in the initial phases after partial hepatectomy. This phenotype correlates with activation of endogenous EGFR signaling, predominantly through the protein kinase B pathway. In addition, mig-6 is an endogenous inhibitor of EGFR signaling and EGF-induced tumor cell migration in human liver cancer cell lines. Moreover, mig-6 is down-regulated in human hepatocellular carcinoma and this correlates BMS-777607 solubility dmso with increased EGFR expression. Conclusion: Our data implicate mig-6 as a regulator of EGFR activity in hepatocytes and as a suppressor of EGFR signaling in human liver cancer. (HEPATOLOGY 2009.) In rodents,

the liver has a tremendous capacity to regenerate. Normally, hepatocytes are in a quiescent state and rarely divide. In response to two-thirds partial hepatectomy (PH), however, 95% of all hepatocytes synchronously re-enter the cell cycle and restore the liver to its full size.1 This rapid growth provides an excellent model to study the molecular mechanisms of cell proliferation in vivo. Importantly, defects in liver regeneration can contribute to the development of severe diseases such as liver cirrhosis and

liver cancer.2 Teicoplanin The process of liver regeneration is dependent on various growth factors, cytokines, and metabolic processes. Cytokines, like tumor necrosis factor-α or interleukin-6, act as the priming factors of liver regeneration, driving quiescent hepatocytes into the cell cycle.3 Several growth factors and receptor tyrosine kinases control cell cycle progression by stimulating the S-phase entry of hepatocytes. The epidermal growth factor receptor (EGFR), heparin-binding EGF-like growth factor (HB-EGF), transforming growth factor-α (TGFα), amphiregulin, and the MET receptor have been described to be potent regulators of liver regeneration.4–8 Mitogen-inducible gene-6 (mig-6)—also known as RALT, gene33, or Errfi1—is an adaptor protein implicated in the regulation of receptor tyrosine kinases.9, 10 Mig-6 can be induced by a variety of external stimuli including growth factors, hypoxia, and stress.11 Overexpression or small interfering RNA (siRNA)-mediated knockdown studies have shown that mig-6 is a negative regulator of EGF receptor signaling.

[78] It was reported that platelets were recruited to the liver, delaying virus elimination and promoting immunopathological liver cell damage after viral infection.[38] Viral hepatitis in human is a disease arising from destruction of virus-infected hepatocytes caused by immune-mediated mechanisms.[79, 80] It is generally recognized that T cell-mediated cellular immunity is responsible for the liver damage. Lang et al. reported that lack of platelet-derived serotonin in serotonin-deficient mice normalized hepatic microcirculatory dysfunction, accelerated virus clearance in the liver, and reduced CD8+ T cell-dependent acute liver injury.[38] Iannacone et al. also revealed a harmful role of

find more activated platelets in mediating cytotoxic T lymphocyte-induced liver damage in mouse models with acute viral hepatitis.[36] In drug-induced hepatitis model, inhibition of platelet activation resulted in the reduction of hepatic platelet accumulation and liver necrosis.[81] Furthermore, it was reported that platelet activation and subsequent adherence to liver sinusoidal selleck chemicals endothelial cells (LSECs) promote the accumulation of neutrophils, which mediates hepatic injury after ischemia-reperfusion.[15, 82] Sindram et al. reported

that platelets caused the apoptosis of LSECs upon reperfusion of the cold ischemic rat liver.[37] On the other hand, it is well known that platelets immediately accumulate at injured tissue, where they release key mediators of hemostasis and promote healing.[21] Recently it was reported that tissue repair is delayed in platelet-depleted tuclazepam animals after postischemic liver injury, suggesting that platelets could have a protective effect against acute liver injury.[83] Hepatocytes are very sensitive to Fas-mediated apoptosis because the Fas antigen is constitutively expressed on hepatocytes.[84] Hepatocytic upregulation of Fas has been observed in hepatitis B and C, suggesting that the Fas/Fas Ligand system plays important roles in the trigger of hepatitis and other liver diseases.[85-87] In addition, because severe damage to LSECs and the disruption of the sinusoidal

lining are known to be major causes of acute liver injury, the protection of LSECs is very important for preventing acute liver injury, just like the proliferation of LSECs is a crucial requirement for liver regeneration.[37, 88-90] Hisakura et al. reported that platelets have a potent role in protecting against acute liver injuries.[31] The increment of platelets ameliorated Fas-induced hepatitis by preventing both the apoptosis of hepatocytes through the activation of the Akt signaling pathway, which is known to suppress apoptosis and promote cell survival, and the disruption of the sinusoidal lining.[31] The result suggested that platelets could play pivotal roles in preventing acute liver injury through the protection of non-parenchymal cells in addition to hepatocytes.

The primary outcome was the modified Rankin score (mRS) at 90-days with a good outcome defined by mRS of 0-2.000. There were 114 (50.7%) patients in the LVO and 111 (49.3%) in the No-LVO group. A good outcome was seen in 28 (24.6%) patients in the LVO and 77 (69.4%) patients in the No-LVO

group (OR .14; 95% CI: .08-.26; P < .0001). Mortality was observed in 13 (11.7%) patients in the No-LVO group and 48 (42.1%) patients in the LVO group (OR .18; 95% CI: .09-.36; P < .0001). Significant www.selleckchem.com/products/jq1.html hemorrhage was seen in 14 (12.5%) patients in the LVO and 0 (0%) patients in the No-LVO group (P < .0001). Older age (OR .96; 95% CI: .93-.98; P = .002) and presence of LVO (OR .29; 95% CI: .12-.68; P = .004) were significant independent predictors of poor outcome. CTA identification of proximal occlusions is associated with significantly poor outcomes in patients receiving

intravenous stroke thrombolysis. “
“To reveal the characteristics of susceptibility-weighted imaging (SWI) under low cerebral blood flow (CBF) induced by hyperventilation (HV). This study was approved by the institutional review board. Informed consent was obtained. Six healthy volunteers (5 men, 1 woman; mean age, 29 years; range, 24-33 years) underwent SWI and arterial spin labeling perfusion imaging under normal ventilation (NV) and HV at 3.0 T. Regions of interest (ROIs)

were placed on gray matter (GM) and white matter LY294002 molecular weight (WM) of the frontal lobe (FL) and occipital lobe (OL). Intensities of ROIs were compared between NV and HV. Contrast of veins compared with adjacent 17-DMAG (Alvespimycin) HCl cerebral parenchyma (CV) was also compared between NV and HV. CBF during HV (CBFHV) was decreased compared with CBF during NV (CBFNV) (29.1 ± 4.6%). FL-GMHV and OL-GMHV showed significant signal decreases compared with FL-GMNV and OL-GMNV, respectively (P= .018, .017). CVHV was significantly increased compared with CVNV (164.1 ± 29.9%) (P= .00019). SWI sensitively reflects HV-induced decreases in CBF. The present results might assist in the interpretation of SWI in clinical practice, since CBF decreases might also influence signal changes on SWI. “
“Various anastomosis and aberrant origins of the middle meningeal artery (MMA) have been documented in literature. However, there has been no report of its origin from the posterior inferior cerebellar artery (PICA) or its branches. In this report, we discuss an anomalous origin of the MMA from the PICA. Also, we discuss the embryological and anatomical development of the MMA. Imaging identification of the origin of the MMA is important while planning surgical and endovascular interventions in the region of the skull base.

Infliximab; 3. Follow-up study; Presenting Author: MAJUN FANG Additional Authors: KONG CHAO-MEIKONG CHAO-MEI KONG CHAO-MEI, ZHANGYU SHU, ZHANGZHEN YU Corresponding Author: KONG CHAO-MEIKONG CHAO-MEI KONG CHAO-MEI Affiliations: Nanjing Medical University Objective: To observe the expression of Corticotrophin Releasing Factor Receptor 2 (CRFR2) in Ulcerative Colitis (UC) and the relationship between CRFR2 and ICAM-1, NF-κB P65, IL-6, and to study the role of CRFR2 in UC pathogenesis. Methods: CRFR2, ICAM-1 and NF-κB P65 in colonic mucosal biopsy samples collected from 30 patients with active UC, 30 patients with remittent UC and 30 healthy people were studied by immunohistochemistry.

IL-6 in serum KU-57788 supplier was studied by ELISA. Results: Colon

tissues from patients with UC had significant increases in expression to CRFR2 compared with the remittent group and the control group (all P < 0.05), but there was remarkable statistical significance between the remittent group and the control group (P > 0.05). There was significant correlation between CRFR2 and ICAM-1, NF-κB P65, IL-6.(all P < 0.05). Conclusion: significantly increased in active UC patients, compared with the remittent group and a control group, our results and the present study showed that CRFR2 may act as a possible local pro-inflammatory mediator in UC. Key Word(s): 1. CRFR2; 2. Ulcerative Colitis; 3. NF-κB P65; 4. IL-6; Presenting Author: NAIZHONG HU Additional Authors: ZHONGJU YANG Corresponding Author: NAIZHONG HU Affiliations: he First Affiliated Hospital NVP-LDE225 ic50 of Anhui Medical University; the Third Affiliated Hospital of Anhui Medical University Objective: To O-methylated flavonoid analyze the clinical efficacy, safety and appropriate dose of azathioprine in treatment of chronic corticosteroid-dependent ulcerative colitis. Methods: Selected the hospitalized patients and outpatients of chronic corticosteroid-dependent ulcerative colitis (UC), who continued to use azathioprine (AZA) for more than 6 months and had a regular follow-up, at the department of gastroenterology, the first

affiliated hospital of Anhui Medical University from 2000 to 2011. Observed and contrasted the clinical manifestations of stool frequency, hematochezia, colonoscopy, laboratory indicators of CRP, ESR, blood routine, liver and kidney function with AZA of different doses before and after treatment. Used unified standard to evaluate clinical efficacy of AZA, recorded adverse reactions, and analysed therapeutic effect, safety and proper dose of AZA in management of chronic refractory UC. Results: Collected 30 cases of patients with chronic refractory UC, eliminated 3 cases of irregular or initialized taking AZA, 3 cases of stopping AZA with a reduced white blood cells in 6 months, and finally included 24 cases of chronic corticosteroid-dependent UC which met the inclusion criteria. There were 18 cases (75%) of males and 8 cases (25%) of females.