Objective To determine the changes in brain dopamine transporter and serotonin transporter in mice receiving propofol anesthesia, 125I-?-CIT binding was studied.Methods Twenty-seven Kunming mice ,weighing 18-22g ,were randomly assigned to receive either intraperitoneal propofol 100 mg/kg (n=9) or 200 mg/kg(n=9) or 10% intralipid (used as control,n=9) in equal liquid volume respectively. 10 min after intraperitoneal administration, 0.1ml 2?Ci 125I-?-CIT was given intravenously via the tail vein. Two hours later animals were decapitated. Brains were rapidly removed and dissected on ice and cerebellum, hypothalamus, striatum and cerebral cortex were separated. Brain tissues were weighed and the radioactivity of 125I-?-CIT in different brain regions was measured.Results 125I-?-CIT binding to dopamine transporter or serotonin transporter decreased significantly in propofol groups as compared with that in control group. The decrease in binding was greater in 200 mg/kg propofol group (P

Objective To investigate the effects of propofol on learning and amnesia in the old miceMethods The normal Kunming mice were trained in a one-trial, step-through, light-dark passive avoidance paradigm Propofol (50 or 100 mg/kg) was administered intraperitoneally 15 min before training ,and propofol (100 or 200 mg/kg) separately 30 min and 6 h in the immediate post-training period The latency of escaping into a darkened chamber and the wrong number of entering darkened chamber were recorded Animals were tested for recall at 24th h post-training time The activity of acetyltransferase was determined with radiommunoassay in the brain 3h after administrationResults All control animals were liable to learn the task as judged by their increased latencies to enter the darkened chamber at 24th h post-training time After administration with propofol 50 mg/kg or 100 mg/kg, the latencies were reduced (246 and 208,repectively), compared with control (P

Objective To determine if propofol can affect uptake of dopamine ( DA) by dopamine transporter (DAT) . Methods Chinese hamster ovary (CHO) cells in which DAT was highly expressed were incubated with H-dopamine in the presence or absence of propofol. Uptake of H-DA was measured. The kinetic parameters Vmax and Km were calculated. Results Propofol significantly inhibited uptake of DA by DAT in CHO cells as compared with the control ( P

Objective To study the effects of propofol exposure during pregnancy on space cognitive and exploration abilities and expression of phosphorylated tau protein ( P-tau) and beta-amyloid protein[ Aβ(1-42) ] in hippocampus of the offspring. Methods Sprague-Dawley female (n=24) and male rats (n=8) of three months old were mated at the same cage at the ratio of 3:1. Pregnant rats were randomly divided into early group (group E), medium group (group M), late group (group L) and control group ( group C) , with 6 rats in each group. Groups E, M and L received propofol 80 mg · kg-1 · d-1 for 7 consecutive days. Propofol was replaced with equal volume of physiological saline in group C. Learning and memory of the 30-day offspring rats were assessed by using Morris water maze test. Then offspring rats were sacrificed to determine the expression of P-tau and Aβ(1-42) in the hippocampus by ELISA and immunohistochemistry. Results The learning and memory abilities were declined significantly in group E (51. 20±8. 11) s, group M (36. 00±6. 44) s and group L (47. 20±12. 30) s, as compared with group C (65. 60± 7. 23) s (all P<0. 05). The result of immunohistochemistry and ELISA showed that expression of Aβ(1-42) and P-tau in hippocampus was significantly higher in group M than in groups E, L and C[(immunohistochemistry: Aβ(1-42), (27. 38±5. 90) vs. (12. 65± 2. 08), (13. 79±3. 37), and (65. 60±7. 23); P-tau, (26. 35±5. 83) vs. (13. 65±3. 46), (14. 56±3. 82), and (8. 49±1. 20);ELISA:Aβ(1-42) , (88. 6±7. 43) vs. (71. 60±6. 79), (13. 79±3. 37), and (65. 80±6. 28);P-tau, (230. 13±8. 22) vs. (210. 42± 2.20), (210.95±1. 75), and (200. 65±1. 57)] (all P<0.05). Conclusion Multiple propofol injections may impair rat offspring’ s space cognitive abilities and exploration abilities, and the impairment is especially obvious in second trimester of pregnancy, which may be associated with over-expression of P-tau and Aβ(1-42) .

Objective To evaluate the relationship of preoperative neutrophil-lymphocyte ratio (NLR) with clinicopathological features and prognosis of colorectal cancer in middle-aged and elderly patients.Methods A retrospective analysis was performed in 212 patients with colorectal cancer in the First Affiliated Hospital of Nanjing Medical University from January 2011 to June 2013.All patients were divided into middle-aged group (46-65 year old,n=130) and old-aged group (66-89 year old,n=82),The optimal cut-off point of NLR was identified by the area under receiver operating characteristic curve,while NLR ＞ 3.13 and NLR≤3.13 were classified as high and low NLR group.The clinicopathological features and prognosis between the two groups were compared.Results There was no difference in gender,tumor growth site,depth of invasion,tumor embolus,lymphatic metastasis,distant metastasis,TNM stage between low and high NLR group (allP＞ 0.05).However,the difference between high NLR group and low NLR group in old-aged group with diabetes mellitus was statistically significant (P＜0.05).The 1-,2-,and 3-year survival rate of the overall 212 patients were 96.2％ (204/212),87.7％ (186/212) and 74.5％ (158/212) In middle-aged group,the 1-,2-,and 3-year survival rates were 98.8％ (85/86),90.7％ (78/86) and 84.9％ (73/86) respectively in low NLR group,but 95.5％ (42/44),84.1％ (37/44) and 72.7％ (32/44) respectively in high NLR group,(allP＜0.05).In old-aged group,the 1-,2-,and 3-year survival rates were 95.7％ (44/46),89.1％ (41/46) and 73.9％ (34/46) respectively in low NLR group,but 91.7％ (33/ 36),83.3％ (30/36) and 52.8％ (19/36) respectively in high NLR group (all P＜0.05).Cox regression showed that TNM stage and NLR were independent risk factors for the prognosis of the middle-aged and elderly patients with colorectal cancer (P＜0.05 or P＜0.01).Conclusions Preoperative NLR ＞ 3.13 suggest that the prognosis is poor in middle-aged and elderly patients with colorectal cancer.

Aim Our previous study has found that ur-solic acid( UA) increased intracellular reactive oxygen species ( ROS ) production and adenosine monophos-phate-activated protein kinase ( AMPK ) phosphoryla-tion, inhibited signal transducer and activator of tran-scription 3 ( STAT3 ) phosphorylation and cyclooxygen-ase-2 ( COX-2 ) expression in gastric cancer cells . However , the molecular mechanism by which UA in-hibits COX-2 expression in gastric cancer cells has not been fully clarified .In this study we aimed to further clarify the signal transduction pathways involved in the UA-mediated inhibition of COX-2 expression in gastric cancer cells .Methods Human gastric cancer cell lines SGC-7901 and MKN-45 were routinely cultured in RPMI-1640 medium supplemented with 10% heat-in-activated fetal calf serum .Sub-confluent cell cultures were pre-treated with antioxidant N-acetylcysteine ( NAC) , AMPK activator 5-amino-4-imida-zolecarbox-amide-riboside ( AICAR ) , AMPK inhibitor compound C, or STAT3 inhibitor WP1066 and then treated with or without UA for 24 h.The expression of AMPK and phosphorylated AMPK ( p-AMPK ) , STAT3 and phos-phorylated STAT3 ( p-STAT3 ) , as well as COX-2 was detected by Western blot analysis .Results Antioxi-dant NAC and AMPK inhibitor compound C blocked UA-induced inhibition of STAT 3 phosphorylation and down-regulation of COX-2 expression in gastric cancer cells.Both AMPK activator AICAR and UA inhibited STAT3 phosphorylation and COX-2 expression; the combination of two drugs resulted in further reduction . STAT3 inhibitor WP1066 did not affect UA-induced AMPK phosphorylation , whereas it inhibited STAT3 phosphorylation and COX-2 expression .The inhibitory effects on the STAT3 phosphorylation and COX-2 ex-pression were significantly enhanced when SGC-7901 and MKN-45 cells were treated simultaneously with WP1066 plus UA.Conclusion UA inhibits COX-2 expression in gastric cancer cells , which may be medi-ated through ROS/AMPK/STAT3 signal transduction pathway .

Objective To study how to improve velopharyngeal ring ligafion procedure by using ring ligator in velopharyngeal ring ligatian procedure and settle the problem that there is no standard to measure the interspace of the cavity of pharynx.Methods Select some deft palate patients who were between 3 to 17 ages.Then made five groups according to age (3 to 5,6 to 8,9 to 11,12 to 14,15 to 17).Then made five different types of ring ligators accrding to the normal size of the cavity of pharynx of different ages.Results The ring ligators were easily used and all the patients were repaired satisfied.Conclusion The application of ring ligator in velopharyngeal ring ligation procedure is simple and feasible.

The process of diagnosis and nursing of a case with human granulocytic anaplasmosis who was confirmed by etiological diagnosis and molecular biology analysis was analyzed.The matters needing attention in nursing and nosocomial infection control were discussed and analyzed.To avoid misdiagnosis and mistreatment,cross infection,reduce pain and economic burden of the patients,to provide references for future diagnosis and treatment of human granulocytic anaplasmosis.

OBJECTIVE: To explore the curative effect and origin of antrochoanal polyp (ACP) with various approaches. METHOD: Fifty-seven patients with ACP were included in the study. All the ACP patients were examined by preoperative endoscopy and computer tomographic (CT) scans. The patients were treated by various endoscopic approaches including endoscopic middle meatus antrostomy, inferior meatus antrostomy combined with endoscopic middle meatus antrostomy or endoscopic medial maxillectomy combined with endoscopic middle meatus antrostomy respectively. The relationship between polyp location in middle meatus and lesions in the antrum was explored during the surgery. Pathological examination was carried out and patients were regularly followed up after operation. RESULT: Fifty-seven ACP develops from antral cyst. In 22 cases of endoscopic middle meatus antrostomy, two patients relapsed. In 17 cases of inferior meatus antrostomy combined with endoscopic middle meatus antrostomy, one patients relapsed. In 18 cases of endoscopic medial maxillectomy combined with endoscopic middle meatus antrostomy, no one relapsed. CONCLUSION Our data indicated that the ACP mainly originates in antral cyst, and capsule wall herniates to middle meatus through the antral ostium. ACP are common in unilateral, rare in both sides. The endoscopic approaches of middle meatus antrostomy and inferior meatus antrostomy combined with endoscopic middle meatus antrostomy might guarantee good prognosis. If the cyst is on the anterior wall of maxillary sinus, the approach of endoscopic medial maxillectomy can obtain a better vision and completely remove the lesions.
Cysts ; surgery ; Endoscopy ; Humans ; Maxillary Sinus ; surgery ; Nasal Polyps ; surgery ; Nasal Surgical Procedures ; methods ; Tomography, X-Ray Computed

Background: Previous study has found that ursolic acid (UA) inhibited the proliferation of gastric cancer cells by the down-regulation of cyclooxygenase-2 (COX-2) expression.However,its molecular mechanism is not fully clear.Aims: To investigate the role of adenosine monophosphate-activated protein kinase (AMPK)/signal transducer and activator of transcription 3 (STAT3)/COX-2 signaling pathway in UA-mediated inhibition of gastric cancer cells proliferation.Methods: AMPK-pLVX,AMPK-shRNA,STAT3-pLVX,STAT3-shRNA plasmids were constructed,and then were transfected into human gastric cancer cell lines SGC-7901 and MKN-45,respectively.Gastric cancer cells were cultured with different concentrations of UA for different times.The expressions of phosphorylated AMPK (p-AMPK),phosphorylated STAT3 (p-STAT3) and COX-2 were measured by Western blotting,and cell proliferation was detected by CCK-8 assay.Results: UA dose-and time-dependently increased p-AMPK expression,inhibited p-STAT3 and COX-2 expressions in SGC-7901 and MKN-45 cells.Knockdown of AMPK blocked UA-induced inhibition of STAT3 phosphorylation and COX-2 expression.Overexpression of STAT3 blocked UA-induced down-regulation of COX-2 expression.Knockdown of AMPK and overexpression of STAT3 blocked UA-induced inhibition of proliferation of gastric cancer cells.Conclusions: UA may inhibit the proliferation of gastric cancer cells via down-regulation of COX-2 expression through AMPK/STAT3 pathway.