objective To investigate the clinicopathological features of mini-cancer of the stomach. Method In this study,out of 296 early gastric cancer cases there were 34 cases of early gastric cancer in which tumor diameter was≤10 mm,among those there were 5 cases with tumor size≤2 mm and 29 cases of the size 2～10 mm. Result Mini-cancer accunted for 2% of all early gastric cancers in this series:All these mini-cancers were of intramucosal cancer(100%),while that took up to 45%in control group in which tumors were between≥2 mm and≤10 mm:Tumors were high or moderately differentiated pathologically in 100%of mini-cancers and 55%in control group.None of mini-cancer patients had lymph node metastasis,however,1 of 29 patients in control group had lymph node metastasis.Both groups had no blood vessel and lymphatic vessel invasion:The differentiation concordance rate between superficial lesions and invasive fronts in mini-cancer was 100%,higher than 86%in control group. Conclusion Gastric mini-cancer is usually of high differentiation,low tumor invasion and low rate of lympy node metastasis than control group.Endoscopic therapy is applicable for most gastric mini-cancers.

Objective To investigate the expression and correlation of hypoxia-inducible factor-1?(HIF-1?),vascular endothelial growth factor(VEGF)and sFlt-1 in the preeclampsia placenta,and discuss their significance in the pathogenesis of preeclampsia.Methods Placentas were collected from 20 pregnant women with preeclampsia as study group and 15 normal pregnant women as control group.The expressions of HIF-1?,VEGF and sFlt-1 protein were semi-quantitatively analyzed with immunohistochemical assay and mRNA level was determined using reverse transcription polymerasc chain reaction(RT-PCR)technique. Results(1)the expression of HIF-1?and sFlt-1 protein in preeclampsia group obviously increased.Strong (+++)positive expression was observed in 9 and 11 cases respectively,significantly higher than in control group(2 and 3 cases)(P＜0.05),however,VEGF expression obviously reduced in preeclampsia group(P＜0.01).(2)the level of HIF-1?and sFlt-1 mRNA in preeclamptic placenta was 0.604?0.013, 0.898?0.041,significantly higher than 0.208?0.007 and 0.559?0.244 in normal placenta(P＜0.05). Although the level of VEGF mRNA increased in preeclampsia placenta,it was not significantly different from that in normal placenta(P＞0.05).The ratio of VEGF mRNA/sFlt-1 mRNA obviously reduced in preeclampsia group and was significantly lower than in control group(P＜0.05).(3)in preeclampsia group,HIF-1?mRNA expression was positively correlated with the expression of sFlt-1 mRNA(r=0.577, P＜0.05),and negatively correlated with the ratio of VEGF mRNA/sFlt-1 mRNA(r=-0.376,P＜0.05).Conclusion Abnormal high HIF-1?expression in preeclampsia placenta indicates that HIF-1?might play an important role in the pathogenesis of preeclampsia,possibly through affecting the cytotrophoblastic invasion and placental vascular reconstruction via the modulation of VEGF and sFlt-1 gene transcription.

Objective To explore the clinical characteristics and treatment of nodular panniculitis disease in children. Methods Clinical data of 13 cases with nodular panniculitis disease were reviewed retrospectively. Their etiology,clinical manifestation,misdiagnosis cause,pathologic characteristics, treatment and outcome were analyzed. Results Its clinical manifestation was multiform and showed mainly as fever and hypodermic nodule. Concomitant damages to digestive, respiratory, circulatory and renal system might occur in those children with the system type of this disorder. Conclusion Pediatric nodular panniculitis disease can be easily misdiagnosed and lack of specificity in the early stage, and complicates multiple organs damage.

The aim of this study is to develop monoclonal antibody against human hepatocyte growth factor activator inhibitor 1 (HAI-1) for future study of HAI-1. The cDNA fragments of human hepatocyte growth factor activator inhibitor 1 (HAI-1) were subcloned to construct GST-HAI-1 fusion protein expression vectors. The vectors were transformed into E. coli and fusion protein expression was induced by IPTG. The GST-HAI-1 fusion proteins were separated on preparative SDS-PAGE and recovered by electroelution, and used to immunize BALB/c mice. Hybridomas producing monoclonal antibodies against human HAI-1 were prepared by cell fusion technique and characterized by ELISA, Western Blot and immunohistochemical staining. One hybridoma cell line, ZMC6, was obtained, which produces specific antibody against the expressed GST-HAI-1 fusion protein. The monoclonal antibody recognizes both the membrane-type and secretory-type HAI-1 proteins of colorectal tissue. The successful development of anti-HAI-1 antibody provides a powerful tool for further investigation on HAI-1's function.
Animals ; Antibodies, Monoclonal ; immunology ; Blotting, Western ; Glutathione Transferase ; genetics ; Immunohistochemistry ; Mice ; Mice, Inbred BALB C ; Proteinase Inhibitory Proteins, Secretory ; analysis ; genetics ; immunology ; Recombinant Fusion Proteins ; biosynthesis ; immunology

Objective To investigate the endoscopic and pathological characteristics of Barrett's esophagus (BE).Methods Data of 152 patients who were diagnosed as having BE with endoscopy and pathology were retrospectively analyzed.Results BE was most commonly seen in patients of 40-60 years old.The clinical manifestations overlapped in different patients,including regurgitation and heartburn in 78 (51.32%),dysphagia in 9 (5.92%),retrosternal pain in 12 (7.89%),upper abdominal pain or discomfort in 67 (44.08%),and asymptomatic in 8 (5.26%).Long segment BE (LSBE) was determined in 7 patients (4.61%),and short segment BE (SSBE) in 145 (95.39%).The metaplasia pattern under endoscopy included island like in 98 (64.47%),tongue like in 39 (25.66%) and circumferential in 15 (9.87%).Stratified squamous epithelia in the lower part of the esophagus were replaced by columnar epithelia in all cases,and intestinal metaplasia occurred in 68 cases (44.74 %).Conclusion BE is most frequently seen in the middle-aged and can be diagnosed by endoscopy and pathology without special clinical manifestations.Island pattern occurs in most cases and is with lowest rate of intestinal metaplasia,which is associated with age.Patients with specialized intestinal metaplasia and dysplasia should be followed up for surveillance of cancer.

OBJECTIVETo analyze the mutational features of adenomatous polyposis coli (APC) gene and to explore the effect of mismatch repair (MMR) deficiency on its mutations in hereditary non-polyposis colorectal cancers (HNPCC).

METHODSPCR-based in vitro synthesized protein test (IVSP) assay and sequencing analysis were used to confirm somatic mutations of whole APC gene in 19 HNPCC patients.

RESULTSEleven cases with thirteen mutations were determined. The frequency of APC mutation was 58%(11/19). The exhibiting mutations consisted of 9 frameshift mutations and 4 nonsense ones, indicating the existence of more frameshift mutations (69%). All of frameshift mutations were deletion or insertion of 1-2 bp and most of them (7/9) happened at simple nucleotide repeat sequences, particularly within (A) n tracts (5/9). All of four nonsense mutations resulted from C to T transitions at CpG sites.

CONCLUSIONMutational inactivations of APC gene were detected in more than half of HNPCC patients in this study, indicating that APC mutation is a common molecular event in the tumorigenesis of HNPCC. According to the location of frameshift mutations at simple nucleotide repeat sequences and point mutations at CpG sites, it was suggested that endogenous mechanisms like MMR deficiency might exert an effect on the nature of APC mutations in most HNPCC.

Adenomatous Polyposis Coli ; genetics ; Adenomatous Polyposis Coli Protein ; genetics ; metabolism ; Carcinoma ; genetics ; Colorectal Neoplasms ; genetics ; pathology ; Colorectal Neoplasms, Hereditary Nonpolyposis ; genetics ; Genes, APC ; physiology ; Humans

BACKGROUNDThe peripheral enhancement of small hepatocellular carcinoma (SHCC) is a rare appearance in dual phase images by helical computed tomography (CT). This study discusses this phenomenon and its correlative histopathology.

METHODSThe helical CT dual phase appearance of peripheral enhancement in SHCC was analyzed in 21 cases (22 lesions). All lesions were confirmed as SHCC by histopathological examination.

RESULTSIn these 22 lesions, enhanced peripheral ring in 20 lesions was incomplete, the thickness of enhanced peripheral ring varied and mural node could be found in hepatic arterial phase; only 2 lesions had complete peripheral ring enhancement and ring of uniform thickness in hepatic arterial phase. The enhancement of some peripheral rings and mural nodes dropped to very low density in portal venous phase. The tumour cells were grade I in 3 lesions, II in 16, III in 2 and IV in 1. The vascular supply was more abundant at the border than in the centre of 15 lesions and the vascular supply was deficient in both centre and border of the remaining 7 lesions. In 3 lesions, the pseudocapsule showed in the border of the lesion. In 12 lesions, flecks of necrosis were found in the border and/or centre of the lesion.

CONCLUSIONSThe characteristic peripheral enhancement in helical CT dual phase images of small hepatocellular carcinoma correlates with different vascular supplies, fibrous capsule and necrosis of the lesion.

Adolescent ; Adult ; Aged ; Carcinoma, Hepatocellular ; diagnostic imaging ; pathology ; Humans ; Liver Neoplasms ; diagnostic imaging ; pathology ; Male ; Middle Aged ; Tomography, Spiral Computed

OBJECTIVETo clone and screen genes related to multidrug resistance (MDR) in leukemia.

METHODSSuppression subtractive hybridization (SSH) was performed to profile differentially expressed genes between a MDR leukemia cell line (K562/DOX, as tester) and its parent cell line (K562, as driver). Reverse Northern dot blot was carried out to further screen the subtracted cDNA library. The overexpressed cDNA fragments in K562/DOX cells were sequenced and compared with known genes in Genbank. RT-PCR and Northern blot were employed to confirm the differential expression of some identified genes.

RESULTSEleven genes were identified being overexpressed in K562/DOX, including S3 ribosomal protein (S3rp) gene, NADH dehydrogenase subunit 2 (ND2) gene and My023 gene, which have not been reported to be related to MDR in cancer.

CONCLUSIONSeveral genes, which might be involved in MDR were identified, indicating novel mechanisms of MDR in leukemia.

Blotting, Northern ; Drug Resistance, Multiple ; genetics ; Drug Resistance, Neoplasm ; genetics ; Gene Library ; Genes, MDR ; genetics ; Humans ; K562 Cells ; Leukemia ; genetics ; NADH Dehydrogenase ; genetics ; Nucleic Acid Hybridization ; methods ; Reverse Transcriptase Polymerase Chain Reaction ; Ribosomal Proteins ; genetics

OBJECTIVETo investigate the effects of immunization with fusions of dendritic cells and H22 cells on tumor-bearing mice and their possible mechanisms.

METHODSFusion cells of DC and H22 cells were prepared with polyethylene glycol (PEG). Expression of MHC and costimulatory molecules by dendritomas were determined by FACs. To study the antitumor immune preventative and therapeutic effects, fusions were subcutaneously injected into tumor-bearing mice. The cytotoxic T lymphocyte (CTL) activity was determined by LDH method, the expression of TNF-a and IFN-g in tumors were assayed by RT-PCR.

RESULTSThe data showed that the hybridomas of DC and H22 cells acquired both DC and H22 cell phenotypes. Immunization of BALB/C mice with DC/H22 fusions induced potent CTL activity (mean CTL activity=0.624+/-0.024, compared with DC + H22, DC, H22 groups, F = 65.46) and a protective immunity against a high dose of H22 tumor challenge. After treatment with hybridomas, the survival time of tumor-bearing mice was greatly extended (x2=18.45). The expression levels of TNF-a and IFN-g mRNA were remarkably increased (TNF-a, F = 47.84; IFN-g, F = 37.23).

CONCLUSIONSThe hybridomas of DC and H22 cells could induce effective antitumor immune responses and may have a useful potential in prevention and management of the recurrences and metastases of HCC.

Animals ; Cancer Vaccines ; immunology ; Carcinoma, Hepatocellular ; genetics ; immunology ; Cell Fusion ; Dendritic Cells ; immunology ; Female ; Hybridomas ; Immunization ; Interferon-gamma ; biosynthesis ; genetics ; Liver Neoplasms, Experimental ; genetics ; immunology ; prevention & control ; Mice ; Mice, Inbred BALB C ; Polyethylene Glycols ; T-Lymphocytes, Cytotoxic ; immunology ; Tumor Necrosis Factor-alpha ; biosynthesis ; genetics ; Vaccination

OBJECTIVETo explore the effect and mechanism of dexamethasone (DEX) in the prevention of central pontine myelinolysis (CPM) in rats.

METHODSHyponatremia was induced in rat by subcutaneous injection of Vasopressin Tannate and intraperitoneal injection of 2.5% dextrose in water for 3 d, the rats of Group A received a bolus of 1 mol/L NaCl (2 ml/kg) and DEX (5 mg/kg) simultaneously at the 4th day; the rats of Group B were treated with DEX after 24 h of the injection of 1 mol/L NaCl; the rats in Group C received a bolus of 1 mol/L NaCl and saline simultaneously; Group D was the control group. The demyelinative lesions were evaluated by myelin staining. The Evans blue (EB) contents of brain were detected to evaluate the blood-brain-barrier permeability after rapid correction of hyponatremia. The expression of inducible nitric oxide synthase (iNOS) in brains was evaluated by Western blotting.

RESULTCPM was induced successfully in rats. The EB contents of Group A, B and C had no significant difference at 0 h after injection of hypertonic saline compared with Group D. The EB contents of Group C began to increase significantly at 6 h after injection of hypertonic saline, peaked at 24 h; the expression of iNOS in brains began to increase after 3 h after the rapid correction of hyponatremia. The rate of morbidity in Group C was 66.7%. The demyelinative lesions were rarely seen in Group A, the EB contents of brain decreased significantly compared with Group C at the same time point (P<0.05), the iNOS expression was also inhibited. DEX could not prevent the attack of CPM at Group B, the rate of morbidity (75%) had no significant difference compared with Group C (P>0.05).

CONCLUSIONEarly treatment with DEX can protect blood-brain-barrier and inhibit the expression of iNOS to prevent the attack of CPM.

Animals ; Arginine Vasopressin ; Blood-Brain Barrier ; drug effects ; physiopathology ; Dexamethasone ; therapeutic use ; Glucocorticoids ; therapeutic use ; Glucose ; Male ; Myelinolysis, Central Pontine ; chemically induced ; physiopathology ; prevention & control ; Nitric Oxide Synthase Type II ; metabolism ; Rats ; Rats, Sprague-Dawley ; Time Factors ; Vasopressins