To study the correlation between the spatial cognitive impairment and different subtypes of estrogen receptor α (ERα) of hippocampus in diabetic mice, we used alloxan (intraperitoneal injection) to induce type 1 diabetes in male Kunming mice and compared the spatial cognitive ability of the model mice with that of control mice through Morris water maze test. Meanwhile, using Western blot, we detected the protein expressions of ER-α36, ER-α66, caveolin-1, PKCα, cAMP-response element binding protein 2 (CREB2), and synaptophysin (Syn) in the hippocampus of the mice. The results showed that on the 3rd and 5th days of training, the ability of spatial learning and memory in the diabetic mice was significantly inferior to that of the control mice (P < 0.05). In the diabetic mice, the protein expressions of caveolin-1 and PKCα were decreased (P < 0.05), but ER-α66 expression was unaffected, while ER-α36 and CREB2 expressions were significantly increased (P < 0.05) compared with those of the control mice. The results suggest that abnormal expression of ER-α36 and related signal molecules may be important factors for diabetes-induced spatial cognitive impairment.
Animals ; Caveolin 1 ; metabolism ; Cognitive Dysfunction ; Cyclic AMP Response Element-Binding Protein ; metabolism ; Diabetes Mellitus, Experimental ; physiopathology ; Estrogen Receptor alpha ; metabolism ; Hippocampus ; metabolism ; physiopathology ; Male ; Maze Learning ; Memory ; Mice ; Protein Kinase C-alpha ; metabolism ; Synaptophysin ; metabolism

OBJECTIVETo investigate the association of neuroendocrine differentiation with progression and prognosis of gastric adenocarcinoma.

METHODSClinicopathological data of 240 patients with gastric adenocarcinomas were retrospectively analyzed. The expression of chromogranin A, synaptophysin and secrectagogin in cancer tissue was assessed by immunohistochemistry. The association of neuoroendocrine differentiation parameters with disease progression and survival of patients was analyzed.

RESULTSThe expression of synaptophysin was positively correlated with depth of invasion and secretagogin more often expressed in cases with lymph node metastasis. In Lauren diffuse type of cancer, expression of chromogranin A and secretagogin was unfavorable prognostic predictor. In TNM stage II adenocarcinoma, expression of chromogranin A and synaptophysin related to poor survival, and multivariate Cox proportional hazard model showed that synaptophysin was an independent predictor for poor survival.

CONCLUSIONNeuroendocrine differentiation predicts deeper depth of invasion, more possibility of lymph node metastasis and poor survival in gastric adenocarcinoma.

Adenocarcinoma ; diagnosis ; pathology ; Biomarkers, Tumor ; metabolism ; Chromogranin A ; metabolism ; Disease Progression ; Humans ; Immunohistochemistry ; Lymphatic Metastasis ; Neoplasm Staging ; Neuroendocrine Tumors ; diagnosis ; pathology ; Prognosis ; Proportional Hazards Models ; Retrospective Studies ; Secretagogins ; metabolism ; Stomach Neoplasms ; diagnosis ; pathology ; Synaptophysin ; metabolism

OBJECTIVETo study the expression of squamous cell markers p63, p40 and CK5/6 in small cell carcinoma of lung (SCLC).

METHODSImmunohistochemical study for squamous cell markers (p63, p40 and CK5/6), neuroendocrine markers (chromogranin A, synaptophysin and CD56) and TTF1 was carried out in 283 cases of SCLC. The diagnostic value of these markers was evaluated.

RESULTSThe expression rate of p63, p40 and CK5/6 were 20.7% (54/261), 7.9% (5/63) and 0.5% (1/221), respectively in the cases of SCLC studied. Amongst the squamous cell markers, CK5/6 had the lowest rate of positivity (P < 0.01). On the other hand, chromogranin A, synaptophysin and CD56 were positive in 61.8% (170/275), 85.5% (242/283) and 89.2% (248/278), respectively. The positivity rate for chromogranin A was lower than that for synaptophysin and CD56 (P < 0.01). TTF1 was expressed in 77.2% (217/281).

CONCLUSIONSp63 and p40 are expressed in a subset of SCLC. In contrast, CK5/6 is rarely positive in SCLC. An immunohistochemical panel of CK5/6, synaptophysin and CD56 is recommended for differential diagnosis of SCLC.

CD56 Antigen ; genetics ; metabolism ; Chromogranin A ; genetics ; metabolism ; DNA-Binding Proteins ; genetics ; metabolism ; Diagnosis, Differential ; Humans ; Keratin-5 ; genetics ; metabolism ; Keratin-6 ; genetics ; metabolism ; Lung Neoplasms ; genetics ; metabolism ; Small Cell Lung Carcinoma ; genetics ; metabolism ; Synaptophysin ; genetics ; metabolism ; Transcription Factors ; genetics ; metabolism ; Tumor Suppressor Proteins ; genetics ; metabolism

OBJECTIVETo explore the protective effects of rutin against learning and memory impairment induced by trimethyltin (TMT) and investigate the possible mechanism.

METHODSForty 6- to 9-week-old male BALB/c mice were randomized equally into saline group (control), TMT group, TMT+rutin group, and rutin group. Mouse models of learning and memory impairment were establish by acute TMT (2.25 mg/kg) exposure. In TMT+rutin and rutin treatment groups, the mice received intraperitioneal injection of rutin (10 mg/kg) for 1 week before TMT exposure. Twenty-four hours after TMT exposure, Morris water maze test was employed to test the escape latency of the mice, and the synaptophysin expression in the hippocampus and cortex were analyzed by Western blotting.

RESULTSCompared that in TMT group, the escape latency of the mice in water maze test was significantly shorter in the other 3 groups (P<0.05); the escape latency in TMT +rutin group was similar with that in the control and rutin groups (P>0.05). Western blotting showed significantly decreased synaptophysin expression in the hippocampus and cortex in TMT group (P<0.05); synaptophysin expression in TMT +rutin group increased significantly compared with that in TMT group (P<0.05) but showed no statistical significance from that in rutin and control groups (P>0.05).

CONCLUSIONRutin pretreatment offers protective effect against TMT-induced learning and memory impairment in mice possibly by antagonizing decreased synaptophysin in the hippocampus and cortex.

Animals ; Cerebral Cortex ; drug effects ; metabolism ; Hippocampus ; drug effects ; metabolism ; Learning ; drug effects ; Male ; Memory Disorders ; chemically induced ; drug therapy ; Mice ; Mice, Inbred BALB C ; Neuroprotective Agents ; pharmacology ; Rutin ; pharmacology ; Synaptophysin ; metabolism ; Trimethyltin Compounds ; adverse effects

OBJECTIVETo explore the mechanisms of acupuncture treatment promoting the motor function recovery of neonate rats with cerebral palsy.

METHODSThe improved hypoxic-ischemic encephalopathy (HIE) means was performed to establish the model of neonate rats with cerebral palsy. All neonate rats were randomly divided into 3 groups: sham group, model group and acupuncture group (n = 20). We observed and scored motor function of rats, measured the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in serum, and also measured the expression of synaptophysin (SYP) and growth associated protein-43 (GAP-43) in the diseased region of cerebral tissue.

RESULTSThe motor function scores (11.3 +/- 0.29) and the serum level of SOD (147.1 +/- 12.7) U/ml in acupuncture treatment group were higher than those of model group ( P < 0.05). The serum level of MDA was lower in acupuncture treatment group than that of model group (P < 0.05). The expression of SYP and GAP-43 in the diseased region of cerebral tissue of acupuncture treatment group were higher than those of model group ( P < 0.05) .

CONCLUSIONAcupuncture-therapy could improve the motor function of neonate rats with cerebral palsy by decreasing the content of MDA in serum, increasing the contents of SOD in serum, and prolonging the upregulation of SYP and GAP-43 expressions in hmin tissue.

Acupuncture Therapy ; Animals ; Animals, Newborn ; Cerebral Palsy ; therapy ; Disease Models, Animal ; GAP-43 Protein ; metabolism ; Hypoxia-Ischemia, Brain ; therapy ; Malondialdehyde ; metabolism ; Rats ; Superoxide Dismutase ; metabolism ; Synaptophysin ; metabolism

OBJECTIVETo investigate the expression of neuron-specific enolase (NSE) and synaptophysin(SYN) proteins in different developmental stages of human embryonic esophagus.

METHODSImmunohistochemistry was used to detect the expressions of NSE and SYN proteins in embryonic esophagus tissues of fetuses of 2, 3 and 4 month gestational age (n=16). One-way ANOVA and LSD-t test were employed to compare the staining intensity and number of positive expression cells in embryonic esophageal tissues of different gestational age.

RESULTSIn fetuses with 2, 3 and 4 months of gestation, the number of NSE-positive nerve cells in the myenteric nerve plexus and submucosa of human embryonic esophageal tissues were 18.38 ± 8.37, 25.00 ± 11.54 and 38.00 ± 15.09, respectively; the staining intensity of NSE-positive nerve cells and nerve fibers in myenteric nerve plexus and submucosa of embryonic esophageal tissues were 74.38 ± 14.93, 62.25 ± 18.59 and 56.44 ± 14.70, respectively. NSE-positive cells were detected in the esophageal epithelium only at the third month. In the fetuses at 2, 3 and 4 months of gestation, SYN in all layers of esophageal tissue were positively or strong positively expressed, especially in the myenteric plexus and submucosal plexus. The staining intensity of SYN-positive cells in embryonic esophagus tissues of 2, 3 and 4 month gestation were 54.69 ± 9.34, 51.84 ± 6.10 and 46.41 ± 6.44, respectively.

CONCLUSIONSYN and NSE may be involved in the regulation of nerve system of esophageal tissues during the human embryonic development.

Esophagus ; embryology ; Female ; Fetus ; Gestational Age ; Humans ; Immunohistochemistry ; Phosphopyruvate Hydratase ; metabolism ; Pregnancy ; Synaptophysin ; metabolism

OBJECTIVETo analyze the clinicopathological features of pancreatic neuroendocrine neoplasms (P-NENs).

METHODSFrom January 2006 to December 2010, 64 patients with P-NENs were diagnosed in the Department of Pathology, West China Hospital, Sichuan University. Immunohistochemical staining of neuroendocrine markers, synaptophysin (Syn) and chromogranin A (CgA), were first made to determine whether the tumor had neuroendocrine properties, then the P-NENs were classified as neuroendocrine tumor (NET), neuroendocrine carcinoma (NEC) and mixed adenoneuroendocrine carcinoma (MANEC, G3) according to the morphological changes and proliferative activity (Ki 67 expression).

RESULTSOf all the 64 cases detected, 60 were NETs and four were NEC. Most of the tumors were single solitary masses, and more than half of the tumors arose in the head of the pancreas, while about one third in the tail. The positive rates of CgA and Syn immunostaining were 96.9% and 95.3%, respectively. The tumor stages of the 64 patients were as follows: stage I, 44 cases; stage II, 11 cases; stage III, one case; and stage IV, 8 cases. The median age of patients in the study was 45.56 years. Of all the P-NENs, 38 cases were functional ones, presenting with characteristic clinical syndrome owing to hormone hypersecretion, while 26 cases were nonfunctional ones with no distinct clinical syndrome. 58 patients underwent surgical operation. The 5-year progression-free survival rate was 91.4%.

CONCLUSIONSP-NENs may occur anywhere in the pancreas, and the clinical manifestations may not be easy to distinguish from other diseases. Diagnosis depends on pathological examination. Surgery is the major approach option, and the clinical prognosis is rather good. The tumor histological grade and distant metastasis are independent prognostic factors in P-NENs.

Adult ; Aged ; Carcinoma, Neuroendocrine ; metabolism ; pathology ; secondary ; surgery ; therapy ; Chemoembolization, Therapeutic ; Chromogranin A ; metabolism ; Disease-Free Survival ; Female ; Humans ; Liver Neoplasms ; secondary ; Lymphatic Metastasis ; Male ; Middle Aged ; Neoplasm Staging ; Neuroendocrine Tumors ; metabolism ; pathology ; secondary ; surgery ; therapy ; Pancreatic Neoplasms ; metabolism ; pathology ; surgery ; therapy ; Retrospective Studies ; Survival Rate ; Synaptophysin ; metabolism ; Young Adult

Adult ; CD56 Antigen ; metabolism ; Carcinoma, Neuroendocrine ; metabolism ; pathology ; surgery ; Humans ; Ki-67 Antigen ; metabolism ; Male ; Mediastinal Neoplasms ; metabolism ; pathology ; surgery ; Mediastinum ; pathology ; surgery ; Phosphopyruvate Hydratase ; metabolism ; Synaptophysin ; metabolism

Adenocarcinoma ; genetics ; metabolism ; pathology ; Biopsy ; CD56 Antigen ; metabolism ; DNA-Binding Proteins ; metabolism ; Gene Deletion ; Humans ; Keratin-7 ; metabolism ; Lung Neoplasms ; genetics ; metabolism ; pathology ; Male ; Middle Aged ; Receptor, Epidermal Growth Factor ; genetics ; metabolism ; Small Cell Lung Carcinoma ; genetics ; metabolism ; pathology ; Synaptophysin ; metabolism ; Transcription Factors

Autoimmune Diseases ; metabolism ; pathology ; surgery ; Chromogranin A ; metabolism ; Female ; Gastrectomy ; Gastric Mucosa ; pathology ; Gastrin-Secreting Cells ; metabolism ; pathology ; Gastrins ; metabolism ; Gastritis, Atrophic ; metabolism ; pathology ; surgery ; Humans ; Hyperplasia ; Middle Aged ; Mucin-6 ; metabolism ; Neuroendocrine Tumors ; metabolism ; pathology ; surgery ; Stomach ; pathology ; surgery ; Stomach Neoplasms ; metabolism ; pathology ; surgery ; Synaptophysin ; metabolism