Helicobacter pylori-induced REDD1 modulates Th17 cell responses that contribute to gastritis.

OBJECTIVE: Regulated in development and DNA damage responses-1 (REDD1) is a conserved and ubiquitous protein, which is induced in response to multiple stimuli. However, the regulation, function and clinical relevance of REDD1 in Helicobacter pylori-associated gastritis are presently unknown. APPROACH: Immunohistochemistry, real-time PCR and Western blot analyses were performed to examine the levels of REDD1 in gastric samples from H. pylori-infected patients and mice. Gastric tissues from Redd1-/- and wildtype (WT, control) mice were examined for inflammation. Gastric epithelial cells (GECs), monocytes and T cells were isolated, stimulated and/or cultured for REDD1 regulation and functional assays. RESULTS: REDD1 was increased in gastric mucosa of H. pylori-infected patients and mice. H. pylori induced GECs to express REDD1 via the phosphorylated cytotoxin associated gene A (cagA) that activated MAPKp38 pathway to mediate NF-κB directly binding to REDD1 promoter. Human gastric REDD1 increased with the severity of gastritis, and mouse REDD1 from non-marrow chimera-derived cells promoted gastric inflammation that was characterized by the influx of MHCII+ monocytes. Importantly, gastric inflammation, MHCII+ monocyte infiltration, IL-23 and IL-17A were attenuated in Redd1-/- mice. Mechanistically, REDD1 in GECs regulated CXCL1 production, which attracted MHCII+ monocytes migration by CXCL1-CXCR2 axis. Then H. pylori induced MHCII+ monocytes to secrete IL-23, which favored IL-17A-producing CD4+ cell (Th17 cell) polarization, thereby contributing to the development of H. pylori-associated gastritis. CONCLUSIONS: The present study identifies a novel regulatory network involving REDD1, which collectively exert a pro-inflammatory effect within gastric microenvironment. Efforts to inhibit this REDD1-dependent pathway may prove valuable strategies in treating of H. pylori-associated gastritis.

Use of an abdominal obstetric binder in colonoscopy: A randomized, prospective trial.

BACKGROUND AND AIMS: Various methods have been reported as aids to cecal intubation. This study aimed to prospectively investigate whether an abdominal obstetric binder (AOB) used during pregnancy and attached to the patients' abdomen during colonoscopy could facilitate effective colonoscopic insertion. METHODS: This was a prospective study of 451 consecutive outpatient colonoscopies performed by a single experienced endoscopist. The recruited patients were randomly separated into two groups that received colonoscopy either with (Group A) or without an AOB attached (Group B). The cecal intubation time, cecal intubation length of the colonoscope, use of manual pressure, position change of each patient, and the number of patients with abdominal distension were collected for comparison. RESULTS: A total of 451 patients (224 in Group A and 227 in Group B) were ultimately included in this study. In Group A, cecal intubation time and cecal intubation length of colonoscope (CIL) were significantly reduced (P < 0.001). The patients had significantly fewer position changes and manual pressure in Group A (P < 0.001). Significantly less abdominal distension was reported by patients in Group A (P < 0.001). CONCLUSIONS: During colonoscopy, the application of an AOB provided a significantly faster and more effective colonoscope insertion.

Hookworm Infection: A Neglected Cause of Overt Obscure Gastrointestinal Bleeding.

Hookworm infections are widely prevalent in tropical and subtropical areas, especially in low income regions. In the body, hookworms parasitize the proximal small intestine, leading to chronic intestinal hemorrhage and iron deficiency anemia. Occasionally, hookworms can cause overt gastrointestinal bleeding, but this is often ignored in heavily burdened individuals from endemic infectious areas. A total of 424 patients with overt obscure gastrointestinal bleeding were diagnosed by numerous blood tests or stool examinations as well as esophagogastroduodenoscopy, colonoscopy, capsule endoscopy or double-balloon enteroscopy. All of the patients lived in hookworm endemic areas and were not screened for hookworm infection using sensitive tests before the final diagnosis. The patients recovered after albendazole treatment, blood transfusion, and iron replacement, and none of the patients experienced recurrent bleeding in the follow-up. All the 31 patients were diagnosed with hookworm infections without other concomitant bleeding lesions, a rate of 7.3% (31/424). Seventeen out of 227 patients were diagnosed with hookworm infections in the capsule endoscopy (CE), and 14 out of 197 patients were diagnosed with hookworm infections in the double balloon enteroscopy (DBE). Hookworm infections can cause overt gastrointestinal bleeding and should be screened in patients with overt obscure gastrointestinal bleeding (OGIB) in endemic infectious areas with sensitive methods. Specifically, the examination of stool specimens is clinically warranted for most patients, and the proper examination for stool eggs relies on staff's communication.

Rational design of a near-infrared fluorescent probe for monitoring butyrylcholinesterase activity and its application in development of inhibitors.

Butyrylcholinesterase (BChE) is widely expressed in multiple tissues and has a vital role in several key human disorders, such as Alzheimer's disease and tumorigenesis. However, the role of BChE in human disorders has not been investigated. Thus, to quantitatively detect and visualize dynamical variations in BChE activity is essential for exploring the biological roles of BChE in the progression of a number of human disorders. Herein, based on the substrate characteristics of BChE, we customized and synthesized three near-infrared (NIR) fluorescent probe substrates with cyanine-skeleton, and finally selected a NIR fluorescence probe substrate named CYBA. The CYBA demonstrated a significant increase in fluorescence when interacting with BChE, but mainly avoided AChE. Upon the addition of BChE, CYBA could be specifically hydrolyzed to TBO, resulting in a significant NIR fluorescence signal enhancement at 710 nm. Systematic evaluation revealed that CYBA exhibited exceptional chemical stability in complex biosamples and possessed remarkable selectivity and sensitivity towards BChE. Moreover, CYBA was successfully applied for real-time imaging of endogenous BChE activity in two types of nerve-related living cells. Additionally, CYBA demonstrated exceptional stability in the detection of complex biological samples in plasma recovery studies (97.51%-104.01%). Furthermore, CYBA was used to construct a high-throughput screening (HTS) method for BChE inhibitors using human plasma as the enzyme source. We evaluated inhibitory effects of a series of natural products and four flavonoids were identified as potent inhibitors of BChE. Collectively, CYBA can serve as a practical tool to track the changes of BChE activity in complicated biological environments due to its excellent capabilities.

Development and validation of a nomogram for predicting in-hospital mortality of intensive care unit patients with liver cirrhosis.

BACKGROUND: Liver cirrhosis patients admitted to intensive care unit (ICU) have a high mortality rate. AIM: To establish and validate a nomogram for predicting in-hospital mortality of ICU patients with liver cirrhosis. METHODS: We extracted demographic, etiological, vital sign, laboratory test, comorbidity, complication, treatment, and severity score data of liver cirrhosis patients from the Medical Information Mart for Intensive Care IV (MIMIC-IV) and electronic ICU (eICU) collaborative research database (eICU-CRD). Predictor selection and model building were based on the MIMIC-IV dataset. The variables selected through least absolute shrinkage and selection operator analysis were further screened through multivariate regression analysis to obtain final predictors. The final predictors were included in the multivariate logistic regression model, which was used to construct a nomogram. Finally, we conducted external validation using the eICU-CRD. The area under the receiver operating characteristic curve (AUC), decision curve, and calibration curve were used to assess the efficacy of the models. RESULTS: Risk factors, including the mean respiratory rate, mean systolic blood pressure, mean heart rate, white blood cells, international normalized ratio, total bilirubin, age, invasive ventilation, vasopressor use, maximum stage of acute kidney injury, and sequential organ failure assessment score, were included in the multivariate logistic regression. The model achieved AUCs of 0.864 and 0.808 in the MIMIC-IV and eICU-CRD databases, respectively. The calibration curve also confirmed the predictive ability of the model, while the decision curve confirmed its clinical value. CONCLUSION: The nomogram has high accuracy in predicting in-hospital mortality. Improving the included predictors may help improve the prognosis of patients.

HBV infection increases the risk of pancreatic cancer: a meta-analysis.

BACKGROUND: Hepatitis B virus (HBV) infection is reported to be associated with an increased risk of pancreatic cancer (PaC), but it remains controversial whether this is a causal relationship. In addition, it is unclear whether the status of HBV infection also affects PaC risk. Therefore, we conducted a meta-analysis to more closely examine the association between HBV infection and PaC. METHOD: The studies included in the meta-analysis were identified and retrieved from PubMed and several other databases. The literature search was conducted up until August 2012. We adopted the Cochrane Collaboration's RevMan 5.1 in a combined analysis of pooled relative risk (RR) with their corresponding 95 % confidence intervals (CIs) using a random-effects and a fixed-effects model. RESULTS: Nine studies including 6 case-control and 3 cohort studies met eligibility criteria. The meta-analysis showed that the PaC risk was positively correlated with HBV infection when comparing with 'never exposed to HBV' subgroup, the pooled RR was 1.39 (95 % CI 1.22-1.59, p < 0.00001) in chronic HBV carriers, 1.41 (95 % CI 1.06-1.87, p = 0.02) in past exposure to HBV, and 3.83 (95 % CI 1.76-8.36, p = 0.0007) in active HBV infection. Using a stratified analysis, we also found that the risk of PaC was independent of smoking, alcohol drinking, and diabetes. CONCLUSION: Findings from this meta-analysis strongly support that HBV infection is associated with an increased risk of PaC.

Epidemiologic characteristics and risk factors associated with overall survival for patients with mucinous colorectal cancer: A population-based study.

BACKGROUND: Mucinous adenocarcinoma (MC) has attracted much attention as a distinct histologic subtype of colorectal cancer in recent years. However, data about its epidemiologic and prognostic characteristics are limited. Therefore, patient data extracted from the National Cancer Institute's Surveillance, Epidemiology, and End Results Program were collected to analyze the epidemiologic and clinicopathological characteristics of MC. AIM: To determine the epidemiologic and clinicopathological characteristics of MC. METHODS: The incidence trend of MC was calculated through the Joinpoint Regression Program. Cox regression analyses were performed to identify prognostic factors associated with overall survival (OS). A nomogram was established to predict the survival probability of individual patients with MC. RESULTS: We found that rates of MC decreased from 4.50/100000 in 2000 to 1.54/100000 in 2018. Rates of MCs in patients aged ≤ 50 years decreased 2.27%/year during 2000-2018. The incidence of appendiceal MCs increased from 0.14/100000 in 2000 to 0.24/100000 in 2018, while the incidence in other anatomic subsites continued to decrease. On multivariable Cox analyses, age, race, tumor site, T stage, N stage, M stage, surgery, and chemotherapy were associated with OS. A nomogram was developed based on these factors, and the area under the curve for 1-year, 3-year, and 5-year OS in the training cohort was 0.778, 0.778, and 0.768, respectively. CONCLUSION: Our results demonstrated that MC incidence decreased in almost all anatomic subgroups except for the appendix. A nomogram predicting the survival probability of patients with MCs showed good performance.

Antitumor effect of new multiple antigen peptide based on HLA-A0201-restricted CTL epitopes of human telomerase reverse transcriptase (hTERT).

The development of peptide vaccines aimed at enhancing immune responses against tumor cells is becoming a promising area of research. Human telomerase reverse transcriptase (hTERT) is an ideal universal target for novel immunotherapies against cancers. The aim of this work was to verify whether the multiple antigen peptides (MAP) based on HLA-A0201-restricted CTL epitopes of hTERT could trigger a better and more sustained CTL response and kill multiple types of hTERT-positive tumor cells in vitro and ex vivo. Dendritic cells (DC) pulsed with MAP based on HLA-A0201-restricted CTL epitopes of hTERT (hTERT-540, hTERT-865 and hTERT-572Y) were used to evaluate immune responses against various tumors and were compared to the immune responses resulting from the use of corresponding linear epitopes and a recombinant adenovirus-hTERT vector. A 4-h standard (51) Cr-release assay and an ELISPOT assay were used for both in vitro and ex vivo analyses. Results demonstrated that targeting hTERT with an adenovector was the most effective way to stimulate a CD8(+) T cell response. When compared with linear hTERT epitopes, MAP could trigger stronger hTERT-specific CTL responses against tumor cells expressing hTERT and HLA-A0201. In contrast, the activated CTL could neither kill the hTERT-negative tumor cells, such as U2OS cells, nor kill HLA-A0201 negative cells, such as HepG2 cells. We also found that these peptide-specific CTL could not kill autologous lymphocytes and DC with low telomerase activity. Our results indicate that MAP from hTERT can be exploited for cancer immunotherapy.

Noninvasive and real-time monitoring of the therapeutic response of tumors in vivo with an optimized hTERT promoter.

BACKGROUND: Telomerase is commonly recognized as an effective anticancer target. The human telomerase reverse transcriptase (hTERT), the rate-limiting component of telomerase, is expressed in most malignant tumors, but it is not found in most normal somatic cells. Here, we report a real-time and noninvasive method to monitor tumor response to a lentivirus-based hTERT-conditional suicidal gene therapy. METHODS: In this study, we constructed a lentivirus system in which an optimized hTERT promoter was used to drive the expression of the cytosine deaminase (CD) gene, one of the suicide genes, and a green fluorescent protein (GFP) reporter gene (pLenti-CD/GFP). The lentivirus was used to infect telomerase-positive or telomerase-negative cell lines. In vitro and in vivo experiments were conducted to analyze the dynamic processes of exogenous gene expression noninvasively in cell culture and living animals in real time via optical imaging. RESULTS: The lentivirus was able to express the CD gene and GFP in telomerase-positive tumor cells and significantly decrease cell proliferation after the use of prodrug 5-flucytosine. However, it could not express GFP and CD in telomerase-negative cell lines, nor could it induce any suicidal effect in those cells. The in vivo study showed that telomerase-positive tumors can be visualized after intratumor injection of the lentivirus in tumor-bearing nude mice via an optical imaging system. Significant tumor growth suppression was observed in telomerase-positive tumors. CONCLUSIONS: Collectively, this technology provides a valuable, noninvasive method to evaluate the real-time therapeutic response of tumors in vivo.

microRNA-27b suppresses mouse MSC migration to the liver by targeting SDF-1αin vitro.

The SDF-1/CXCR4 axis is critical for inducing stem cell mobilization into the circulation, for homing stem cells to the site of injury, and for stem cell participation in the regeneration of liver tissue. In this study, we have gained insight into the molecular mechanisms involved in regulating the expression of SDF-1α by miRNAs. Using microarray and bioinformatics approaches, we identified six miRNAs with differential expression in damaged liver tissue (21 days after liver injury) compared to normal C57BL/6 murine liver tissue and further confirmed these observations by qPCR; miR-23a, which was identified by other researchers, was also included for comparative purposes. We found that miR-23a, miR-27a and miR-27b expression was significantly lower in the damaged liver than in the normal liver (p<0.05). We further confirmed that miR-27b could directly interact with the 3'UTR of SDF-1α to suppress SDF-1α protein expression using a luciferase reporter assay and Western blot analysis. In addition, we found that the over-expression of miR-27b significantly reduced the directional migration of primary cultured CRCX4-positive murine mesenchymal stem cells (mMSCs) in vitro using a transwell assay. These results suggest that miR-27b may be a unique signature of the stem cell niche in the damaged mouse liver and that mir-27b can suppress the directional migration of mMSCs by down-regulating SDF-1α expression by binding directly to the SDF-1α 3'UTR.

Strategies for enhancing vaccine-induced CTL antitumor immune responses.

Vaccine-induced cytotoxic T lymphocytes (CTLs) play a critical role in adaptive immunity against cancers. An important goal of current vaccine research is to induce durable and long-lasting functional CTLs that can mediate cytotoxic effects on tumor cells. To attain this goal, there are four distinct steps that must be achieved. To initiate a vaccine-induced CTL antitumor immune response, dendritic cells (DCs) must capture antigens derived from exogenous tumor vaccines in vivo or autologous DCs directly loaded in vitro with tumor antigens must be injected. Next, tumor-antigen-loaded DCs must activate CTLs in lymphoid organs. Subsequently, activated CTLs must enter the tumor microenvironment to perform their functions, at which point a variety of negative regulatory signals suppress the immune response. Finally, CTL-mediated cytotoxic effects must overcome the tolerance induced by tumor cells. Each step is a complex process that may be impeded in many ways. However, if these steps happen under appropriate regulation, the vaccine-induced CTL antitumor immune response will be more successful. For this reason, we should gain a better understanding of the basic mechanisms that govern the immune response. This paper, based on the steps necessary to induce an immune response, discusses current strategies for enhancing vaccine-induced CTL antitumor immune responses.

Macrophages in tumor microenvironments and the progression of tumors.

Macrophages are widely distributed innate immune cells that play indispensable roles in the innate and adaptive immune response to pathogens and in-tissue homeostasis. Macrophages can be activated by a variety of stimuli and polarized to functionally different phenotypes. Two distinct subsets of macrophages have been proposed, including classically activated (M1) and alternatively activated (M2) macrophages. M1 macrophages express a series of proinflammatory cytokines, chemokines, and effector molecules, such as IL-12, IL-23, TNF-α, iNOS and MHCI/II. In contrast, M2 macrophages express a wide array of anti-inflammatory molecules, such as IL-10, TGF-ß, and arginase1. In most tumors, the infiltrated macrophages are considered to be of the M2 phenotype, which provides an immunosuppressive microenvironment for tumor growth. Furthermore, tumor-associated macrophages secrete many cytokines, chemokines, and proteases, which promote tumor angiogenesis, growth, metastasis, and immunosuppression. Recently, it was also found that tumor-associated macrophages interact with cancer stem cells. This interaction leads to tumorigenesis, metastasis, and drug resistance. So mediating macrophage to resist tumors is considered to be potential therapy.

The scientific progress and prospects of artificial intelligence in digestive endoscopy: A comprehensive bibliometric analysis.

BACKGROUND: Artificial intelligence (AI) has been used for diagnosis and outcome prediction in clinical practice. Furthermore, AI in digestive endoscopy has attracted much attention and shown promising and stimulating results. This study aimed to determine the development trends and research hotspots of AI in digestive endoscopy by visualizing articles. Publications on AI in digestive endoscopy research were retrieved from the Web of Science Core Collection on April 25, 2022. VOSviewer and CiteSpace were used to assess and plot the research outputs. This analytical research was based on original articles and reviews. A total of 524 records of AI research in digestive endoscopy, published between 2005 and 2022, were retrieved. The number of articles has increased 27-fold from 2017 to 2021. Fifty-one countries and 994 institutions contributed to all publications. Asian countries had the highest number of publications. China, the USA, and Japan were consistently the leading driving forces and mainly contributed (26%, 21%, and 14.31%, respectively). With a solid academic reputation in this area, Japan has the highest number of citations per article. Tada Tomohiro published the most articles and received the most citations.. Gastrointestinal endoscopy published the largest number of publications, and 4 of the top 10 cited papers were published in this journal. "The Classification," "ulcerative colitis," "capsule endoscopy," "polyp detection," and "early gastric cancer" were the leading research hotspots. Our study provides systematic elaboration for researchers to better understand the development of AI in gastrointestinal endoscopy.

[Corrigendum] Downregulation of heparanase by RNA interference inhibits invasion and tumorigenesis of hepatocellular cancer cells in vitro and in vivo.

Following the publication of this article, an interested reader drew to the authors' attention that two images in Fig. 1B (the a and d panels) appeared to represent the same clone, albeit with different intensities and the panels were cropped differently. The authors were able to confirm that Figs. 1B(a) and B(d) were inadvertently selected from the same set of images but with different exposure times: Owing to an error in data handling, a wrong image was chosen during the grouping the figures. The corrected version of Fig. 1 is shown on the next page, featuring the correct image for Fig. 1B(d). The authors regret that this error was not picked up upon before the paper was sent to press, although the error did not affect the major conclusions reported in the paper. The authors thank the Editor of International Journal of Oncology for allowing them the opportunity to publish a Corrigendum. and regret any inconvenience caused to the readership. [the origional article was published on International Journal of Oncology 40: 1601­1609, 2012; DOI: 10.3892/ijo.2012.1338].

Role and mechanisms of action of microRNA­21 as regards the regulation of the WNT/ß­catenin signaling pathway in the pathogenesis of non­alcoholic fatty liver disease.

The aim of the present study was to investigate the role of microRNA­21 (miR­21) in regulating the classical WNT/ß­catenin signaling pathway by targeting low­density lipoprotein­related receptor 6 (LRP6) in non­alcoholic fatty liver disease (NAFLD). For this purpose, we established a NAFLD model by feeding C57BL/6J mice a methionine­choline­â€‹deficient diet. Antagomir­21 was then injected via the tail vein, and the expression levels of WNT/ß­catenin signaling pathway­related proteins, such as LRP6, glycogen synthase kinase­3ß (GSK3ß), p­ß­catenin, ß­catenin and the downstream protein, peroxisome proliferator­activated receptor Î³ (PPAR­Î³), and lipid metabolism­related genes, including sterol regulatory element­binding transcription factor 1c (SREBP1c), fatty acid synthase (FAS), carnitine palmitoyl transferase 1α (CPT1α) and adenosine 5­monophosphate (AMP)­activated protein kinase α (AMPKα), were detected. The results revealed that in the NAFLD model, LRP6 expression was negatively associated with miR­21 expression. After antagonizing the expression of miR­21, the protein level of LRP6 was increased. In addition, the WNT/ß­catenin signaling pathway was activated, and lipid accumulation and inflammation were alleviated in the liver. However, the expression of PPAR­Î³ was not inhibited following the upregulation of the WNT signaling pathway. Taken together, the results of this study demonstrate that the inhibition of miR­21 expression can alleviate NAFLD by targeting LRP6 to activate the WNT/ß­catenin signaling pathway.

The Role of H. pylori CagA in Regulating Hormones of Functional Dyspepsia Patients.

Helicobacter pylori (H. pylori, Hp) colonizes the stomachs of approximately 20%-80% of humans throughout the world. The Word Healthy Organization (WHO) classified H. pylori as a group 1 carcinogenic factor in 1994. Recently, an increasing number of studies has shown an association between H. pylori infection and various extragastric diseases. Functional dyspepsia (FD) is considered a biopsychosocial disorder with multifactorial pathogenesis, and studies have shown that infection with CagA-positive H. pylori strains could explain some of the symptoms of functional dyspepsia. Moreover, CagA-positive H. pylori strains have been shown to affect the secretion of several hormones, including 5-HT, ghrelin, dopamine, and gastrin, and altered levels of these hormones might be the cause of the psychological disorders of functional dyspepsia patients. This review describes the mutual effects of H. pylori and hormones in functional dyspepsia and provides new insight into the pathogenesis of functional dyspepsia.

SDF-1/CXCR4 Axis Promotes MSCs to Repair Liver Injury Partially through Trans-Differentiation and Fusion with Hepatocytes.

MSCs have become a popular target for developing end-stage liver therapies. In this study, two models of bone marrow chimeric mice were used to construct the liver failure models. Then it was found that MSCs can transdifferentiate into hepatocyte-like cells and these hepatocyte-like cells can significantly express albumin. Furthermore it was also found that MSCs can fuse with the hepatocytes and these cells had the proliferation activity. However, the percentage of transdifferentiation was significantly higher than fusion. So it was considered that MSCs which transdifferentiated into hepatocyte-likes cells played important roles for repairing the injuring liver function.

Adipose-derived stem cells: A candidate for liver regeneration.

The scarcity of donor livers and the impracticality of hepatocyte transplantation represent the biggest obstacles for the treatment of liver failure. Adipose-derived stem cells, with their ability to differentiate into the hepatic lineage, provide a reliable alternative cell source with clear ethical and practical advantages. Moreover, adipose-derived stem cells can effectively repair liver damage by the dominant indirect pattern and increase the number of hepatocytes by the secondary direct pattern. In recent years, the development of the indirect pattern, which mainly includes immunomodulatory and trophic effects, has become a hot topic in the field of cell engineering. Therefore, adipose-derived stem cells are considered to be ideal therapeutic stem cells for human liver regeneration. In this article, we reviewed the advantages of adipose-derived stem cells in liver regeneration, and explore their underlying mechanisms.

CD64 expression is increased in patients with severe acute pancreatitis: clinical significance.

BACKGROUND/AIMS: Upregulated CD64 expression on neutrophils is the most useful marker for acute bacterial infections and systemic inflammation. However, it is unknown whether CD64 is involved in the pathogenesis of acute pancreatitis (AP). This study was designed to determine whether CD64 is implicated in severe acute pancreatitis (SAP), and thus, is a suitable marker for SAP. METHODS: SAP was induced in rats with an intraperitoneal injection of L-arginine. CD64 expression in the rat pancreas was determined by quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry. Additionally, the CD64 mRNA expression in peripheral blood leukocytes from 21 patients with mild acute pancreatitis (MAP) and 10 patients with SAP was investigated at the time of admission and during remission by qRT-PCR. RESULTS: CD64 mRNA and protein expression in the pancreas was significantly higher in rats with SAP, compared to the controls. The CD64 expression was higher in the patients with SAP than in the patients with MAP. During remission, CD64 mRNA decreased in both the MAP and SAP patients. The area under the curve of CD64 expression for the detection of SAP was superior to both the Ranson and the Acute Physiology and Chronic Health Evaluation II scores. CONCLUSIONS: The CD64 level was significantly increased in correlation with the disease severity in SAP and may act as a useful marker for predicting the development of SAP.