Mucins,a family of heavily glycosylated proteins,present mainly in epithelial cells.They function as essential barriers for epithelium and play important roles in cellular physiological processes.Aberrant expression and glycosylation of mucins in gastric epithelium occur at pathological conditions,such as Helicobacter pylori infection,chronic atrophic gastritis,intestinal metastasis,dysplasia,and gastric cancer.This review addresses the major roles played by mucins and associated O-glycan structures in normal gastric epithelium.Further,we expound the alterations of expression patterns and glycan signatures of mucins at those pathological conditions.
Gastric Mucosa/pathology* ; Glycosylation ; Helicobacter Infections/pathology* ; Helicobacter pylori/metabolism* ; Humans ; Mucins/metabolism* ; Stomach Neoplasms/pathology*

Animals ; Chickens ; Cold Temperature ; adverse effects ; Gastric Mucosa ; metabolism ; pathology ; physiopathology ; Intestinal Mucosa ; metabolism ; pathology ; physiopathology ; Male ; Serum ; metabolism

OBJECTIVEThe aim of this study was to investigate the clinicopathological features of different histological types of primary gastric neuroendocrine neoplasms (including the esophagogastric junction), and to analyze the characteristics and difficulties in diagnosis of all the subtypes of this disease.

METHODS75 cases of primary gastric neuroendocrine neoplasms (including the esophagogastric junction) were included in this study. The expressions of several markers including somatostatin, synaptophysin, chromogranin A, CD56, S-100, neuron-specific enolase and CD57 were assayed in all the specimens by immunohistochemical staining, and their significance in the diagnosis and prognosis of gastric neuroendocrine neoplasms were assessed. In addition, the relationship between various clinical parameters such as tumor location, histological types, depth of invasion and metastasis was also analyzed.

RESULTSThe incidence of gastric neuroendocrine neoplasms accounted for 1.5% of gastric cancer in the same period, and the proportion of each subtype was 53.3% (40/75) in G3, 29.3% (22/75) in MANEC, 16.0% in G1(12/75), and 1.3% (1/75) in G2, respectively. 41.7% (5/12) of the G1 showed multifocal lesions, accompanyied with neuroendocrine cell hyperplasia in the gastric mucosa. 54.67% (41/75) of the NEN located in the esophagogastric junction. The lymph node metastasis of MANEC is unique. The coincidence rate in diagnosis of preoperative biopsies and postoperative specimen was 75.0% (9/12) in G1, 72.7% (16/22) in MANEC, and 25.0% (10/40) in G3, respectively.

CONCLUSIONSGastric neuroendocrine neoplasms occur mainly in the esophagogastric junction, and most of them were highly malignant. The coincidence rate of preoperative and postoperative pathological diagnosis for primary gastric neuroendocrine neoplasms is low. Therefore, it should be very cautious when diagnosis of this disease is made in a preoperative biopsy.

Chromogranin A ; metabolism ; Esophagogastric Junction ; metabolism ; Gastric Mucosa ; metabolism ; pathology ; Humans ; Lymphatic Metastasis ; pathology ; Neuroendocrine Tumors ; pathology ; Phosphopyruvate Hydratase ; metabolism ; Prognosis ; Stomach Neoplasms ; pathology ; Synaptophysin ; metabolism

AIMTo observe the degree of gastric mucosal injury following limb ischemia/reperfusion (LI/R), and to investigate the mechanism of gastric mucosal injury and the protection of ischemic preconditioning (IPC) on gastric mucosal injury.

METHODSThe model rats which underwent 4 hours of ischemia and 4 hours of reperfusion of hind limbs were made. Then we respectively observed and determined the histologic lesion score after I/R and IPC + I/R. The gastric barrier mucus in mucus were measured in different groups. The values of MPO, SOD, MDA and XOD in gastric mucosa and the values of MDA, XOD, SOD, LDH in plasma were detected.

RESULTSIn the LI/R group, the histologic lesion score increased significantly. The content of gastric barrier mucus in mucus decreased significantly. The value of MPO, MDA, XOD in gastric mucosa and the values of MDA, XOD, LDH in plasma increased remarkably and SOD activity in gastric mucosa and in plasma decreased. However in the IPC group, the histologic lesion score decreased significantly and the content of gastric barrier mucus in mucus increased significantly and the value of MPO MDA XOD LDH in gastric mucosa or in plasma decreased remarkably and the SOD activity increased compared to LI/R group.

CONCLUSIONLI/R will lead to the development of stress ulcer, oxygen free radicals play an important role in it. IPC can alleviate the damage of gastric mucosa following ischemia/reperfusion of hind limbs. The decrease of OFR is one of the protection mechanism of IPC.

Animals ; Extremities ; blood supply ; Gastric Mucosa ; metabolism ; pathology ; Ischemic Preconditioning ; Male ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism ; pathology

AIMTo demonstrate the protective effect of nitric oxide (NO) on gastric mucosa and its relationship to the acid secretion of parietal cells under stress in rats.

METHODSWater immersion-restraint stress (WRS) model in SD rats was performed. The gastric mucosal ulcer index (UI), NO contents in gastric mucosa and H+, K(+) -ATPase activity of parietal cells were measured. The effects of N(G)-nitro-L-arginine methyl ester(L-NAME) and L-arginine (L-Arg) on the H+, K(+)-ATPase activity of parietal cells and stress-induced gastric mucosal lesion were observed.

RESULTSL-NAME pretreatment decreased NO contents in gastric mucosa, activated H+, K(+) -ATPase activity of parietal cells and aggravated gastric mucosal lesion, whereas L-Arg pretreatment increased NO contents, inhibited H+, K(+) -ATPase activity and significantly ameliorated stress-induced gastric mucosal lesion.

CONCLUSIONEndogenous nitric oxide plays an important role in protecting gastric mucosa from stress-induced lesion by inhibiting H+, K(+) -ATPase activity of parietal cells.

Animals ; Arginine ; metabolism ; Gastric Acid ; secretion ; Gastric Mucosa ; metabolism ; H(+)-K(+)-Exchanging ATPase ; metabolism ; Male ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Oxidative Stress ; Parietal Cells, Gastric ; metabolism ; Rats ; Rats, Sprague-Dawley ; Stomach Ulcer ; metabolism ; pathology ; Stress, Physiological

BACKGROUND/AIMS: Oxidative stress may contribute to gastric epithelial damage and mutagenesis caused by Helicobacter pylori (H. pylori). H. pylori induces recruitment and activation of inflammatory cells, which produces reactive oxygen species. H. pylori extract directly induces the synthesis of reactive oxygen species in gastric epithelial cells and causes DNA damage. The aim of this study was to investigate the association between the levels of glutathione (GSH) and H. pylori density, histological findings, endoscopic findings, clinical variables, and virulence factors. METHODS: Gastric biopsy specimens were obtained from 73 consecutive patients. The 5,5'-dithiobis-(2-nitrobenzoic acid) reaction was used to determine GSH levels. RESULTS: The infection rate of H. pylori was 68.5%. The GSH level was not related to age, sex, alcohol intake, and endoscopic findings. The GSH level was lower in patients infected with H. pylori. GSH levels were not correlated significantly with the grades of neutrophil, intestinal metaplasia, and atrophy. However, the GSH levels were significantly correlated with H. pylori density (r=-0.296, p=0.01) and monocyte grade (r=-0.257, p=0.02). The GSH levels were not related to CagA, VacA, and UreA. CONCLUSIONS: This study suggests that H. pylori causes oxidative stresses which deplete GSH in gastric mucosa of patients infected with H. pylori.
Adolescent ; Adult ; Aged ; Female ; Gastric Mucosa/*metabolism/pathology ; Glutathione/*metabolism ; Helicobacter Infections/*metabolism/pathology ; *Helicobacter pylori ; Humans ; Male ; Middle Aged ; Oxidative Stress ; Stomach Diseases/*metabolism/microbiology/pathology

BACKGROUND/AIMS: Oxidative stress may contribute to gastric epithelial damage and mutagenesis caused by Helicobacter pylori (H. pylori). H. pylori induces recruitment and activation of inflammatory cells, which produces reactive oxygen species. H. pylori extract directly induces the synthesis of reactive oxygen species in gastric epithelial cells and causes DNA damage. The aim of this study was to investigate the association between the levels of glutathione (GSH) and H. pylori density, histological findings, endoscopic findings, clinical variables, and virulence factors. METHODS: Gastric biopsy specimens were obtained from 73 consecutive patients. The 5,5'-dithiobis-(2-nitrobenzoic acid) reaction was used to determine GSH levels. RESULTS: The infection rate of H. pylori was 68.5%. The GSH level was not related to age, sex, alcohol intake, and endoscopic findings. The GSH level was lower in patients infected with H. pylori. GSH levels were not correlated significantly with the grades of neutrophil, intestinal metaplasia, and atrophy. However, the GSH levels were significantly correlated with H. pylori density (r=-0.296, p=0.01) and monocyte grade (r=-0.257, p=0.02). The GSH levels were not related to CagA, VacA, and UreA. CONCLUSIONS: This study suggests that H. pylori causes oxidative stresses which deplete GSH in gastric mucosa of patients infected with H. pylori.
Adolescent ; Adult ; Aged ; Female ; Gastric Mucosa/*metabolism/pathology ; Glutathione/*metabolism ; Helicobacter Infections/*metabolism/pathology ; *Helicobacter pylori ; Humans ; Male ; Middle Aged ; Oxidative Stress ; Stomach Diseases/*metabolism/microbiology/pathology

OBJECTIVETo study the syndrome evolution law of Chinese medicine (CM) in the patients with gastric mucosal dysplasia.

METHODSThree hundred and twenty four gastric mucosal dysplasia patients with deficiency and excess correlation syndromes were enrolled by a multi-center collaboration for two years' clinical follow-up to detect the levels of tumor supplied group of factors (TSGF) and carcino-embryonic antigen (CEA).

RESULTSAmong the 324 cases, 29 cases turned cancer in the two years, and the canceration rate was 9.0%. The three syndromes with higher canceration rate were the damp-heat accumulating Wei syndrome concurring or combining with asthenia-cold in Pi and Wei syndrome for 16.7%; stagnation in Wei collaterals syndrome concurring or combining with asthenia of both qi and yin syndrome for 13.2%; stagnation of Gan and Wei qi syndrome concurring or combining with asthenia-cold in Pi and Wei syndrome for 8.0%, respectively. Among the three syndromes, the highest level of TSGF occurred in the former two syndromes. In the half year before carcinogenesis, the syndromes of the patients took on deficiency and excess concurrent syndromes, and the deficiency syndromes involving the qi and blood deficiency syndrome and the Shen deficiency syndrome accounting for 48.0%.

CONCLUSIONSGastric mucosal dyspalsia canceration syndromes took on the polymorphism of excess and deficiency concurrent syndromes and had the characteristics of deficiency syndromes involving qi and blood deficiency syndrome and Shen-yin-yang deficiency syndrome.

Biomarkers, Tumor ; metabolism ; Carcinoembryonic Antigen ; metabolism ; Gastric Mucosa ; metabolism ; pathology ; Gastroscopy ; Humans ; Hyperplasia ; Medicine, Chinese Traditional ; Precancerous Conditions ; metabolism ; pathology ; Stomach Neoplasms ; diagnosis ; pathology ; Syndrome

OBJECTIVETo study the relationship between hRad17 mRNA expression and clinicopathologic factors and lymph node metastasis of gastric cancer, and to assess the significance of predicting the extent of lymph node metastasis and prognosis.

METHODShRad17 mRNA expression was examined in matched primary lesions, normal gastric mucosa and lymph node metastatic lesions among 52 gastric cancer patients by reverse transcription polymerase chain reaction (RT-PCR), polyacrylamide gel electrophoresis (PAGE) and silver stain with the relation between hRad17 mRNA expression and clinicopathologic factors analyzed. At the same time, hRad17 mRNA expressions in 5 gastric benign lesions and SGC7901 gastric carcinoma cell lines were also examined.

RESULTSThe primary tumor samples (88.4% positive) showed a significantly higher level of hRad17 expression compared with matched normal tissue (76.9% positive) (P = 0.014), so did the lymph node metastatic samples (94.2% positive) (P = 0.001). The hRad17 mRNA expression showed a low level in benign lesions, but very high in SGC7901 cell line. The hRad17 mRNA expression showed a higher level in patients with the number of lymph node metastasis above 15 than below 15 (P = 0.02), so did the diffused growth than the mass-like growth (P = 0.04).

CONCLUSIONThe method of PAGE and silver stain can improve the sensitivity of RT-PCR. The degree of lymph node metastasis and invasiveness of carcinoma cells are more serious in cases with hRad17 mRNA overexpression, and extensive lymph node dissection should be carried out for these patients. Examination of hRad17 expression by RT-PCR before surgery is indicated to arrive at an optimum treatment scheme and to estimate the prognosis.

Cell Cycle Proteins ; genetics ; Gastric Mucosa ; metabolism ; Humans ; Lymphatic Metastasis ; RNA, Messenger ; analysis ; Stomach Neoplasms ; metabolism ; pathology

The effects of electrical and chemical stimulation and electrolytic lesion of lateral hypothalamic area (LHA) on gastric ischemia-reperfusion injury (GI-RI) were investigated in rats whose celiac arteries were clamped for 30 min and reperfused for 60 min by removal of the clamp. The results are as follows. (1) Electrical stimulation of LHA could aggravate GI-RI in an intensity-dependent manner by using 0.2, 0.4 or 0.6 mA current respectively. Microinjection of L-glutamic acid into LHA resulted in a similar effect to that of electrical stimulation of LHA on GI-RI. After electrolytic lesion of bilateral LHA, the area of gastric mucosal injury induced by gastric ischemia-reperfusion (GI-R) was smaller than that by electrical stimulation of LHA plus GI-R. (2) Dorsal vagal complex (DVC) lesion or vagotomy could eliminate the effect of electrical stimulation of LHA on GI-RI. (3) Electrical stimulation of LHA increased the content of malondialdehyde (MDA) but decreased the activity of superoxide dismutase (SOD) of ischemia-reperfusion (I-R) gastric mucosa. (4) Electrical stimulation of LHA plus gastric I-R increased gastric juice volume and total acid output, but there were no significant changes in acidity, pepsin activity and gastric barrier mucus. These results indicate that the LHA is an area in the CNS exerting aggravate effects on GI-RI. The DVC and vagus may be involved in the regulative effects of LHA on GI-RI. These effects are associated with increases in gastric mucosal MDA content, gastric juice volume, and total acid output, and a decrease in SOD activity.Acidity, pepsin activity and gastric barrier mucus do not seem to play an important role.
Animals ; Electric Stimulation ; Gastric Mucosa ; blood supply ; metabolism ; pathology ; Hypothalamic Area, Lateral ; metabolism ; Male ; Malondialdehyde ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; pathology ; Superoxide Dismutase ; metabolism