蜂胶酊治疗鸡白痢的试验

根据笔者1985年对河南省唐河县源潭镇40个村庄的鸡群调查结果,全年养鸡280000只,发生白痢病89000只(占31.8％),死亡37000只(占41.6％)。为了探讨一种治疗该病的有效药物,1985年8月～1986年7月,我们使用了蜂胶酊各种制剂和治疗鸡白痢病常用药,进行治疗对比试验;1986年8月～1988年12月,又以20％蜂胶酊临床治疗鸡白痢19300只,效果比较理想,治愈数为17100只(占88.6％),死亡2200只(占11.4％)。取得了明显的效益。(一)

Assessment of natural and interleukin-2-induced production of interferon-gamma in patients with liver diseases

AIMS To clarify whether the lower interferon gamma (IFNγ) production by lymphocytes in patients with liver diseases is due to defects of lymphocytes themselves or of other cofactors such as interleukin-2(IL-2). METHODS Peripheral blood mononuclear cells (PBMCs) from patients with various liver diseases were cultured with or without PHA and IL-2. The cells were harvested and counted and the su- pernatants were tested for IFNγ by a sensitive and quantitative ABC-ELISA. RESULTS IFNγ was not round in serum samples from patients as well as normal individuals. However,in supernatants of non-in- duced and induced PBMCs,IFN7 was detected by ABC-ELISA. In non-induced PBMCs (group 1),the content of IFNγ in super- natants from control,CAH,CPH and HCC was 8.72 μg/L, 5.03 μg/L,6.02 μg/L and 4.91 μg/L respectively. The pro- duction of IFNγ in liver disease was significantly decreased,com- pared to control. In group 2 in which PBMCs were stimulated with PHA,the content of IFNγ was 22.71,17.12,14.54 and 17.63 μg/L respectively. In group 3 in which PBMCs were in- duced by IL-2,the amount of IFN7 in supernatant from control (60.67 μg/L) was much larger than those from CAH (21.70 μg/ L),CPH (24.00 μg/L) and HCC (19.15 μg/L) (P<0.01). Comparing the amount of IFNγ in group 3 (IL-2-induced) with that in group 1 (non-induced),we found that IFNγ production was en- hanced by nearly 4 folds in liver diseases and by over 7 folds in control,Whereas the number of PBMCs,whether from liver dis- eases or from control,was increased by only approximately 3 folds. CONCLUSIONS The decreased production of IFNγ in liver dis- eases including HCC is mainly due to endogenous defects of lym- phocytes though the defects of stimulating cofactors such as IL-2 may also be involved.

Pin1 overexpression in colorectal cancer and its correlation with aberrant β-catenin expression

AIM： To investigate clinical significance of Pin1 and β-catenin expression in colorectal cancers and to demonstrate the relationship of their expression. METHODS： The role of Pin1 and β-catenin protein in colorectal tumorigenesis and their clinicopathologic significance were analyzed by immunohistochemistry, and correlation between Pin1 and β-catenin protein expressions was also studied in 124 patients with colorectal cancer who were surgically treated. RESULTS： Normal colonic epithelium either failed to express or showed focal and weak expression of Pin1 and β-catenin. Overexpression of Pin1 and β-catenin protein was found in 23 （18.54%） and 50 （40.3%） of 124 colorectal cancers, respectively. Overexpression of both proteins was not related to the lymph node metastasis, tumor stage and survival period after excision. Survival analysis results indicated that tumor stage was a valuable predictor of survival. Interestingly, a significant correlation was found between Pin1 and β-catenin protein expression. CONCLUSION： Overexpression of Pin1 and β-catenin may be closely related with the development and/or progression of colorectal carcinoma and further supports that Pin1 overexpression might contribute to the upregulation of β-catenin.

Elevated plasma cryofibrinogen in patients with active inflammatory bowel disease is morbigenous

AIM： To investigate the role of cryofibrinogen （CF） in active inflammatory bowel disease （IBD）. METHODS： CF was assayed in 284 subjects： 61 with active and 63 with inactive ulcerative colitis （UC）, 45 who had proctocolectomy, 35 with active and 20 with inactive Crohn＇s disease （CD）, 40 with other diseases and 20 healthy controls. Trypsin inhibitor （TI） and TI antibody （TI-Ab） were measured in plasma and CF complex by ELISA. RESULTS： CF in active UC was strikingly high compared with all other groups （x^2〈0.001）. Similarly, CF was significantly higher in active CD than in inactive CD or in controls （x^2〈0.01）. In UC, high CF and TI-Ab were associated with the need for operations. Further, high CF, CF/fibrinogen ratio, low TI and high TI-Ab in plasma were associated with disease activity or refractoriness to medication. Elevated CF was not associated with acute reactants like C-reactive protein and white blood cell counts except for erythrocyte sedimentation rate, suggesting that elevated CF was not a consequence of acute inflammation. CONCLUSION： Elevated CF in active IBD appears to be morbigenous. CF promotes IBD via two main mechanisms, quenching of TI （an anti-inflammatory substance） and impairing microvascular perfusion by forming protein aggregates. CF may also serve as a biomarker of chronic IBD. Additional studies are warranted to fully evaluate the role of CF in IBD and the outcome should contribute to a better understanding of the pathogenesis of IBD.

Multidrug resistance 1 gene in inflammatory bowel disease: A meta-analysis

The MDR1 gene is an attractive candidate gene for the pathogenesis of inflammatory bowel disease （IBD） and perhaps response to therapy, with evidences at both functional and genetic levels. Its product, the P-glycoprotein （P-gp） functions as a transmembrane efflux pump thus influencing disposition and response of many drugs, some of whom （i.e. glucocorticoids） central to IBD therapy. In addition P-gp is highly expressed in many epithelial surfaces, included gastrointestinal tract （G-I） with a putative role in decreasing the absorption of endogenous or exogenous toxins, and perhaps host-bacteria interaction. Many genetic variations of MDR1 gene has been described and in some instances evidences for different P-gp expression as well drugs metabolism have been provided. However data are often conflicting due to genetic heterogeneity and different methodologies employed. Perhaps the greatest piece of evidence of the physiological importance of P-gp in the G-I tract has come from the description of the mdrl knock-out mice model, which develops a spontaneous colitis in a specific pathogen-free environment. Studies investigating MDR1 gene polymorphism and predisposition to IBD have also shown conflicting results, owing to the known difficulties in complex diseases, especially when the supposed genetic contribution is weak. In this study we have undertaken a metaanalysis of the available findings obtained with two SNPs polymorphism （C3435T and G2677T/A） in IBD; a significant association of 3435T allele and 3435TT genotype has been found with UC （OR = 1.17, P = 0.003 and OR = 1.36, P = 0.017, respectively）. In contrast no association with CD and the G2677T/A polymorphism could be demonstrated.

Neutrophil depletion-but not prevention of Kupffer cell activation-decreases the severity of cerulein-induced acute pancreatitis

AIM： To determine whether neutrophil depletion and Kupffer cell inhibition might combine their protective effects to decrease the severity of acute pancreatitis. METHODS： Nice had cerulein administration to induce acute pancreatitis and were pretreated with either anti-mouse neutrophil serum or gadolinium chloride （GdCh） to prevent Kupffer cell activation, or both treatments. Injury was assessed in pancreas and lungs. Myeloperoxidases （MPO） assessed neutrophil infiltration. Interleukin-6 （IL-6） and IL-10 were measured in serum, pancreas, lungs and liver. RESULTS： In mice with acute pancreatitis, neutrophil depletion reduced the severity of pancreatitis and pancreatitis-associated lung injury. Kupffer cell inactivation by GdCh had less protective effect, although IL-6 and IL-10 concentrations were significantly decreased. The protective treatment brought by neutrophil depletion was not enhanced by Kupffer cell inactivation and both treatments did not combine their protective effects. CONCLUSION： Our results confirm the role of activated neutrophils in aggravating organ injury in acute pancreatitis while the role of Kupffer cell activation is less obvious.

Anti-inflammatory activity of probiotic Bifidobacterium: Enhancement of IL-10 production in peripheral blood mononuclear cells from ulcerative colitis patients and inhibition of IL-8 secretion in HT-29 cells

AIM: To determine the anti-inflammatory activity of probiotic Bifidobacteria in Bifidobacteria-fermented milk (BFM) which is effective against active ulcerative colitis (UC) and exacerbations of UC, and to explore the immunoregulatory mechanisms. METHODS: Peripheral blood mononuclear cells (PBMNC) from UC patients or HT-29 cells were co-cultured with heat-killed probiotic bacteria or culture supernatant of Bifidobacterium breve strain Yakult (BbrY) or Bifidobacterium bifidum strain Yakult (BbiY) to estimate the amount of IL-10 or IL-8 secreted. RESULTS: Both strains of probiotic Bifidobacteria contained in the BFM induced IL-10 production in PBMNC from UC patients, though BbrY was more effective than BbiY. Conditioned medium (CM) and DNA of both strains inhibited IL-8 secretion in HT-29 cells stimulated with TNF-α, whereas no such effect was observed with heat- killed bacteria. The inhibitory effect of CM derived from BbiY was greater than that of CM derived from BbrY. DNAs of the two strains had a comparable inhibitory activity against the secretion of IL-8. CM of BbiY induced a repression of IL-8 gene expression with a higher expression of IκB-ζ mRNA 4 h after culture of HT-29 cells compared to that in the absence of CM.CONCLUSION: Probiotic Bifidobacterium strains in BFM enhance IL-10 production in PBMNC and inhibit IL-8 secretion in intestinal epithelial cells, suggesting that BFM has anti-inflammatory effects against ulcerative colitis.

Milk protein IgG and IgA:The association with milk-induced gastrointestinal symptoms in adults

AIM:To study the association between serum levels of milk protein IgG and IgA antibodies and milk-related gastrointestinal symptoms in adults.METHODS:Milk protein IgG and IgA antibodies were determined in serum samples of 400 subjects from five outpatient clinics in Southern Finland.Subjects were randomly selected from a total of 1900 adults undergoing laboratory investigations in primary care.All 400 participants had completed a questionnaire on abdominal symptoms and dairy consumption while waiting for the laboratory visit.The questionnaire covered the nature and frequency of gastrointestinal problems,the provoking food items,family history and allergies.Twelve serum samples were disqualifi ed due to insuff icient amount of sera.The levels of specif ic milk protein IgG and IgA were measured by using the ELISA technique.The association of the milk protein-specific antibody level was studied in relation to the milk-related gastrointestinal symptoms and dairy consumption.RESULTS:Subjects drinking milk(n=265) had higher levels of milk protein IgG in their sera than non-milk drinkers(n=123,P<0.001).Subjects with gastrointestinal problems related to milk drinking(n=119) consumed less milk but had higher milk protein IgG levels than those with no milk-related gastrointestinal symptoms(n=198,P=0.02).Among the symptomatic subjects,those reporting dyspeptic symptoms had lower milk protein IgG levels than non-dyspeptics(P<0.05).However,dyspepsia was not associated with milk drinking(P=0.5).The association of high milk protein IgG levels with constipation was close to the level of statistical signif icance.Diarrhea had no association with milk protein IgG level(P=0.5).With regard to minor symptoms,flatulence and bloating(P=0.8),were not associated with milk protein IgG level.Milk protein IgA levels did not show any association with milk drinking or abdominal symptoms.The levels of milk protein IgA and IgG declined as the age of the subjects increased(P<0.004).CONCLUSION:Milk protein IgG but not milk IgA seems to be associated with self-reported milk-induced gastrointestinal symptoms.

Expression of macrophage inflammatory protein-1αin Kupffer cells following liver ischemia or reperfusion injury in rats

AIM： To explore the expression of macrophage inflammatory protein-1α （MIP-1α） in Kupffer cells （KCs） following liver ischemia/reperfusion injury IRI in rats. METHODS： Forty male SD rats were divided randomly into five groups. A model of partial warm ischemia/ reperfusion injury in the rat liver was established. KCs were isolated and incubated one hour, six hours, 12 h, and 24 h after the reperfusion. Tumor necrosis factor alpha （TNF-α） and interleukin-lbeta （IL-1β） in the supernatants were measured by ELISA. MIP-1α in KCs was detected by immunocytochemical and RT-PCR. RESULTS： No or few MIP-1α protein and mRNA were expressed in the KCs of the control group. Its expression in the IRI group had a significant increase after the reperfusion （P 〈 0.05）, which was contrary to the control group. CONCLUSION： The active behavior of the MIP-1α gene in KCs following liver ischemia/reperfusion injury is assumed to be one of the major causes for the hepatic ischemia/reperfusion injury.

Comparison in effect of different metal ions, pH and reducing agent on the protease activity in human hyper mature and mature cataract

This study was undertaken to isolate and characterize the protease activity of human eye lens sample of mature and hyper mature cataract. Samples were collected just after surgery of the cataract lens and were stored at -20 ℃. The total protein extract was isolated from 5 samples in each case （mature and hyper mature cataract） and clear supernatant obtained after centrifugation was used as an enzyme source. The optimum pH for the proteases of mature cataract was 7.5 while the proteases of hyper mature cataract were recorded for maximum activity at pH 5.5 and 7.5. The optimum temperature for both enzyme sources was 50 ℃. Effect of different metal ions such as potassium, lead, silver, zinc and borate was studied. In each case protease activity was increased. Reducing agent e.g. β mercaptoethanol also caused an increase in activity indicating the involvement of sulfhydryl groups. Protease activity was also located on agar plates.

Analysis of the human Atox 1 homologue in Wilson patients

AIM: To analyze the metallochaperone antioxidant-1 (Atox1) gene sequence in Wilson disease patients. METHODS: Mutation analysis of the four exons of the Atox1 gene including the intron- exon boundaries was performed in 63 Wilson disease patients by direct sequencing. RESULTS: From 63 selected patients no mutations were identified after the entire coding region including the intron- exon boundaries of Atox1 were sequenced. One known polymorphism within the Atox1 gene (5’UTR -99 T>C) in 31 (49%) of the Wilson patients as well as one previously undescribed variation (5’UTR -68 C>T) in 2 of the Wilson patients could be detected. Statistical analyses revealed that the existence of a variation within the Atox1- gene showed a tendency towards an earlier onset of the disease. CONCLUSION: Based on the data of this study, no major role can be attributed to Atox1 in the pathophysiology or clinical variation of Wilson disease.

The Prognostic Significance of a Combined Determination of Cathepsin D and Estrogen Receptors in Breast Carcinomas with Positive Axillary Lymph Nodes

OBJECTIVE The aim of this study was to investigate the correlation between cathepsin D （Cath-D） and estrogen receptor （ER）expression in breast cancer tissue and to explore the prognostic significance of their combined determination in breast carcinoma patients with positive axillary lymph nodes. METHODS One hundred and thirty-eight cases of breast carcinoma were examined by immunohistochemistry （IHC） and the results relating to patient follow-up analyzed. RESULTS The overall 5-year disease-free survival rate （DFS） was 60.9% （84/138） in the series. The positive rate of Cath-D expression in the tumor cells was 55.07% and the positive ER staining was 51.4%. A definite significant negative correlation was found between the positive rates for Cath-D and ER （r=-0.294, P=0.001） The Cath-D expression for the cases in clinical Stage Ⅱ, ≥10 positive-node and recurrence or distant metastasis, was higher than that those cases in clinical Stage II with fewer node-metastasis and with 5 year DFS （X^2=13.926, P=0.000; X^2=13.070, P=0.001; X^2=10.545, P=0.001）. However, there was no significant difference of Cath-D expression between 2 groups of patients with different ages or among the different histopathologic types of the nonspecific invasive carcinoma. In the combined examination of Cath-D and ER, the cases that were ER （＋） and Cath-D （-） had the highest 5-year DFS compared to other situations. In contrast, the cases that were reversed in expression, ie, ER（-） and Cath-D（＋）, had a lower 5-year DFS. There was a significant difference between the 2 conditions （X2=18.675, P=0.000）. CONCLUSION A combined determination and analysis of Cath-D and ER expression may be more useful to establish a prognosis than the biological characteristics of carcinomas with positive lymph nodes.

The roles of MAPKs in disease

MAP kinases transduce signals that are involved in a multitude of cellular pathways and functions in response to a variety of ligands and cell stimuli. Aberrant or inappropriate functions of MAPKs have now been identified in diseases ranging from cancer to inflammatory disease to obesity and diabetes. In many cell types, the MAPKs ERK1/2 are linked to cell proliferation. ERK1/2 are thought to play a role in some cancers, because mutations in Ras and B-Raf, which can activate the ERK1/2 cascade, are found in many human tumors. Abnormal ERK1/2 signaling has also been found in polycystic kidney disease, and serious developmental disorders such as cardio-facio-cutaneous syndrome arise from mutations in components of the ERK1/2 cascade. ERK1/2 are essential in well-differentiated cells and have been linked to long-term potentiation in neurons and in maintenance of epithelial polarity. Additionally, ERK1/2 are important for insulin gene transcription in pancreatic beta cells, which produce insulin in response to increases in circulating glucose to permit efficient glucose utilization and storage in the organism. Nutrients and hormones that induce or repress insulin secretion activate and/or inhibit ERK1/2 in a manner that reflects the secretory demand on beta cells. Disturbances in this and other regulatory pathways may result in the contribution of ERK1/2 to the etiology of certain human disorders.

Concurrent systemic AA amyloidosis can discriminate primary sclerosing cholangitis from IgG4-associated cholangitis

Chronic hepatobiliary inflammatory diseases are not widely acknowledged as underlying disorders of systemic AA amyloidosis,except epidemic schistosomiasis.Among them,primary sclerosing cholangitis (PSC) might initiate amyloid A protein deposition in diverse tissues,giving rise to systemic amyloidosis,due to a progressive and unresolved inflammatory process,and its possible association with inflammatory bowel diseases.Nevertheless,only one such case has been reported in the literature to date.We report a 69-year-old Japanese woman with cirrhosis who was diagnosed with PSC complicated with systemic AA amyloidosis,without any evidence of other inflammatory disorders.As a result of cholestasis in conjunction with biliary strictures and increased serum IgG4,the presence of IgG4 + plasma cells was examined systemically,resulting in unexpected documentation of Congo-red-positive amyloid deposits,but not IgG4 + plasma cells,in the liver,stomach and salivary glands.Elevated serum IgG4 is the hallmark of IgG4-related disease,including IgG4-associated cholangitis,but it has also been demonstrated in certain patients with PSC.Amyloid A deposits in multiple organs associated with an indolent clinical course that progresses over many years might have a diagnostic value in discriminating PSC from IgG4-associated cholangitis.

Gastric cancer in a Caucasian population: Role of pepsinogen C genetic variants

AIM： To study the role of an insertion/deletion polymorphism in the pepsinogen C （PGC） gene, an effective marker for terminal differentiation of the stomach mucosa, in the susceptibility to the development of gastric lesions. METHODS： The study was performed with 99 samples of known gastric lesions and 127 samples without evidence of neoplastic disease. PCR was employed and the 6 polymorphic alleles were amplified： Allele 1 （510 bp）, Allele 2 （480 bp）, Allele 3/4 （450/460 bp）, Allele 5 （400 bp） and Allele 6 （310 bp）. RESULTS： Our results revealed that Allele 6 carriers seemed to have protection against the development of any gastric lesion （OR = 0.34; P 〈 0.001）, non-dysplastic lesions associated with gastric adenocarcinoma such as atrophy or intestinal metaplasia （OR = 0.28; P 〈 0.001） or invasive GC （OR = 0.39; P = 0.004）. CONCLUSION： Our study reveals that the Allele 6 carrier status has a protective role in the development of gastric lesions, probably due to its association with higher expression of PGC. Moreover, the frequency of Allele 6 carriers in the control group is far higher than that obtained in Asian populations, which might represent a genetic gap between Caucasian and Asian populations.

Albumin liver dialysis as pregnancy-saving procedure in cholestatic liver disease and intractable pruritus

Progressive familial intrahepatic cholestasis type 3 (PFIC3) is a rare cholestatic liver disease. Such liver disease can get worse by female hormone disorder. Albumin dialysis or Molecular Adsorbent Recirculating System (MARS) has been reported to reverse severe cholestasis-linked pruritus. Here, we report the first use of MARS during a spontaneous pregnancy and its successful outcome in a patient with PFIC3 and intractable pruritus. Albumin dialysis could be considered as a pregnancy-saving procedure in pregnant women with severe cholestasis and refractory pruritus.

Common genetic variations in CLOCK transcription factor are associated with nonalcoholic fatty liver disease

To investigate the role of gene variants and derived haplotypes of the CLOCK transcription factor in nonalcoholic fatty liver disease （NAFID） and their relation with the disease severity.METHODS： A total of 136 patients with NAFLD and 64 healthy individuals were studied. Liver biopsy was performed in 91 patients. Six tag SNPs showing a minor allele frequency 〉 10% （rs1554483 C/G; rs11932595 A/G; rs4580704 C/G; rs6843722 A/C; rs6850524 C/G and rs4864548 A/G） encompassing 117 kb of chromosome 4 and representing 115 polymorphic sites （P 〉 0.8） were genotyped. RESULTS： rs11932595 and rs6843722 showed significant associations with NAFLD （empiric P = 0.0449 and 0.023, respectively）. A significant association was also observed between clinical or histologic spectrum of NAFLD and rs1554483 （empiric P = 0.0399）, rs6843722 （empiric P = 0.0229） and rs6850524 （empiric P = 0.00899） and between fibrosis score and rs1554483 （empiric P = 0.02697）, rs6843722 （empiric P = 0.01898） and rs4864548 （empiric P = 0.02697）. Test of haplotypic association showed that CLOCK gene variant haplotypes frequencies in NAFLD individuals significantly differed from those in controls （empiric P = 0.0097）.CONCLUSION： Our study suggests a potential role of the CLOCK polymorphisms and their haplotypes insusceptibility to NAFLD and disease severity.

A novel computational method for protein-protein interaction networks prediction of alpha-synuclein

Alpha-synuclein plays an important role in Parkinson's disease(PD).The current study of alpha-synuclein mainly concentrates at the gene level.However, it is found that the study at the protein level has special significance.Meanwhile, there is free information on the Internet, such as databases and algorithms of protein-protein interactions(PPIs).In this paper, a novel method which integrates distributed heterogeneous data sources and algorithms to predict PPIs for alpha-synuclein in silico is proposed.The PPIs generated by the method take advantage of various experimental data, and indicate new information about PPIs for alpha-synuclein.In the end of this paper, the result illustrates that the method is practical.It is hoped that the prediction result obtained by this method can provide guidance for biological experiments of PPIs for alpha-synuclein to reveal possible mechanisms of PD.

INTERLEUKIN-6 PROTECTS ANNULUS FIBROSUS CELL FROM APOPTOSIS INDUCED BY INTERLEUKIN-1β IN VITRO

Objective To investigate the effect of interleukin-6 （ IL-6 ） on the apoptosis of annulus fibrosus （AF） cell induced by intedeukin-1β （IL-1β）. Methods Cultured AF cells were divided into 6 groups and treated with no drug, 10 ng/mL IL-6, 10 ng/mL IL-1β, 10 ng/mL IL-1β and Z-VAD-FMK （ a caspase-9 inhibitor）, 10 ng/mL IL-1β and 10 ng/mL IL-6, 10 ng/mL IL-1β and 100 ng/mL IL-6, respectively. After three days of culture, the apoptosis rate, the positive rates of caspase-3, -8, and -9 of AF cells were detected with flow cytometry. Results The apoptosis rates of cells in group 1 to 6 were 2.67% ± 1.08%, 2.71% ± 0.53%, 20. 37% ± 1.57 %, 11.34% ± 0.67 %, 18.17 % ± 0.74%, and 9.42 % ± 1.08 %, respectively. There was no significant difference between group 1 and 2, while the apoptosis rates of group 4, 5, and 6 were significantly lower than group 3 （ P = 0. 001, P =0. 172, and P =0. 001, respectively）. Positive rates of caspase-3 in group 5 （ 12. 35% ±0.64% ） and 6 （9.26% ±0. 36% ） were significantly lower than group 3 （ 17.14% ±0. 72% ; P =0. 001 and P 〈0.001, respectively）. And positive rates of caspase-9 in group 5 （ 15.13% ± 1.45% ） and 6 （ 10.17% ± 2.50% ） were significantly lower than group 3 （ 19.4% ±0.98% ; P =0. 014 and P =0. 004, respectively）. But there was not obvious change of caspase-8 activity after IL-6 was added. Conclusion IL-6 is capable of protecting AF cells from IL-1β induced apoptosis in vitro. Mechanism of the protection is related with the inhibition of caspase-3 and -9 activities.

Expression of interferon inducible protein-10 in pancreas of mice

AIM: To investigate the expression of interferon inducible protein-10 (IP-10) in pancreas of mice and to discuss its possible role in the pathogenesis of type 1 diabetes.METHODS: Non-obese diabetic (NOD) mice were used as experiment group and BALB/c mice as non-diabetic prone model. Immunohistochemistry method was used to evaluate the expression of IP-10 in the pancreas of NOD mice and BALB/c mice. Immunoelectron microscope was used to show the location of IP-10 in pancreatic islet β cells.RESULTS: Pancreatic islets were positively stained in all the NOD mice. Insulitis could be found in mice at the age of 4 wk. The weakly positive results were found in control group with no insulitis. Immunoelectron microscopy further demonstrated that IP-10 was produced by pancreatic β cells and stored in cytoplasm of the cells.CONCLUSION: IP-10 can be largely produced in pancreatic islets of NOD mice at the age of 2 wk when there is no significant insulitis, and may play an important part in the pathogenesis of type 1 diabetes by attracting immune cells to infiltrate the pancreatic islets.