Helicobacter pylori infection in epileptic patients.

It is well known that there might be an epidemiological association between Helicobacter pylori infection and extraintestinal diseases. This study aimed at determining H. pylori infection in epileptic patients. Forty-seven cryptogenic epileptic patients (Group 1) and 35 healthy people (Group 2) participated in this study. Presence of H. pylori infection was examined by H. pylori stool antigen (HpSA), H. pylori IgG, and IgM. HpSA was detected in 21 participants (44.6%) in Group 1 and in 3 participants (8.5%) in Group 2. H. pylori IgM was positive in 27 participants (57.4%) in Group 1 and in 8 participants (22.8%) in Group 2. H. pylori IgG was positive in 37 participants (78.7%) in Group 1 and in 13 participants (38%) in Group 2. The difference of rates of HpSA, H. pylori IgM and IgG in Groups 1 and 2 were found statistically significant (chi2=4.18, p=0.04; chi2=9.18, p=0.0017; chi2=14.58, p<0.001, respectively). We also compared presence of H. pylori infection between the epileptic patients with poor and good prognosis; HpSA positivity was detected in 15 (62.5%) of 24 and 6 (26%) of 23, respectively, and the differences were statistically significant (chi2=6.30, p=0.012). H. pylori IgM positivity was detected in 16 (66%) of 24 patients with poor prognosis and 11 (47.8%) of 23 patients with good prognosis (p>0.05). H. pylori IgG positivity was detected in 18 (75%) of 24 patients with poor prognosis and 19 (82.6%) of 23 patients with good prognosis. The differences of H. pylori IgM and IgG positivity rates in epileptic patients with poor and good prognosis were not found statistically significant (p>0.05). These results suggest a probable association between the acute H. pylori infection and epilepsy, especially with poor prognosis.     

IGF-I signalling in bone growth: inhibitory actions of dexamethasone and IL-1beta.

OBJECTIVE: To determine if glucocorticoids and proinflammatory cytokines inhibit bone growth through a common mechanism involving impaired IGF-I signalling. DESIGN: IGF-I (100 ng/ml), dexamethasone (dex) (10(-6)M) and IL-1beta (10 ng/ml) with inhibitors of the PI3K (LY294002) and Erk 1/2 (PD98059 and UO126) IGF-I pathways (all 10 microM) were studied using the ATDC5 chondrocyte cell line and murine fetal metatarsal cultures. RESULTS: IGF-I stimulated ATDC5 chondrocyte proliferation (322%; P < 0.001 versus control). Addition of PD or LY individually to IGF-I supplemented ATDC5 cultures partially reduced proliferation by 32% (P < 0.001), and 66% (P < 0.001), respectively. PD and LY in combination blocked all IGF-I stimulated ATDC5 proliferation. LY significantly reversed IGF-I stimulatory effects on metatarsal growth (P < 0.001), whereas PD and UO treatment had no effect. IGF-I induced ATDC5 proliferation was further decreased when Dex (24%; P < 0.01) or IL-1beta (33%; P < 0.001) were added to PD but not LY cultures. Metatarsal growth inhibition by LY was unaltered by Dex or IL-1beta addition. CONCLUSIONS: Both the PI3K and Erk 1/2 pathways contributed independently to IGF-I mediated ATDC5 proliferation. However in metatarsal cultures, the Erk 1/2 pathway was not required for IGF-I stimulated growth. Dex and IL-1beta may primarily inhibit IGF-I induced bone growth through the PI3K pathway.     

Application of continent retubularized ileal stoma (Monti procedure) to an ileocecal pouch

We describe the application of a retubularized ileal stoma (Monti procedure) to an ileocecal pouch in a patient with a spinal cord injury who required a continent urinary diversion. When constructing a continent diversion with an ileocecal pouch, this technique seems a good choice, with significant advantages over the other alternatives.     

循证病例报告 原发性脑出血患者是否应该进行抗血小板或抗凝治疗？

原发性脑出血伴有血栓危险因素的患者治疗比较棘手，如以下病例：老年男性，55岁，因右侧肢体无力入院。既往患有难治陛高血压、Ⅱ型糖尿病、心绞痛及高脂血症。约10年前右侧肢体曾有一次轻微卒中。入院时所服药物为：阿司匹林75mg，1次／日；阿托伐他汀10mg，1次／日；苄氟噻嗪2．5mg，1次／日；雷米普利2．5mg，1次／日；氨氯地平5mg，1次／日；     

RNA interference demonstrates a novel role for integrin-linked kinase as a determinant of pancreatic adenocarcinoma cell gemcitabine chemoresistance.

Integrin-linked kinase (ILK) facilitates signal transduction between extracellular events and important intracellular survival pathways involving protein kinase B/Akt. We examined the role of ILK in determining pancreatic adenocarcinoma cellular chemoresistance to the nucleoside analogue gemcitabine. Cellular ILK expression was quantified by Western blot analysis. We examined the effects of overexpression of active ILK and of ILK knockdown induced by RNA interference on gemcitabine chemoresistance. We also examined the effects of modulating ILK expression on gemcitabine-induced caspase 3-mediated apoptosis, phosphorylation status of Akt (Ser473) and glycogen synthase kinase. Overexpression of ILK increased cellular gemcitabine chemoresistance, whereas ILK knockdown induced chemosensitization via increased caspase 3-mediated apoptosis. ILK knockdown attenuated Akt Ser473 and glycogen synthase kinase phosphorylation, whereas overexpression of constitutively active myristoylated Akt was sufficient to induce significant recovery in gemcitabine chemoresistance in the presence of ILK knockdown. Levels of ILK expression affect gemcitabine chemoresistance in pancreatic adenocarcinoma cells. This novel finding suggests that therapies directed against ILK and its downstream signaling targets may have the potential to enhance the efficacy of gemcitabine-based chemotherapy.     

Evaluation of a Thin-film Peripheral Nerve Cuff Electrode

Abstract

This is a study of the reaction of large nerves to implantation using a flexible, thin-film cuff electrode. Cuff electrodes were implanted on the sciatic nerve of three cats. An implantation period of six weeks allowed sufficient time for any injury responses in the nerve and connective tissue sheath around the cuff to develop. The electrode came off the nerve in one of the cats. In the remaining two cats, gross observation following explantation of the electrodes revealed encapsulation of the cuffs without swelling of nerve tissue. Histological evaluation did not demonstrate nerve injury. The nerve cuff electrodes, which are comprised of titanium and iridium coatings on a fluorocarbon polymer substrate, appeared unaffected by the implantation, and connective tissue encapsulation did not adhere to either the polymer substrate or metallization. Evaluation of the electrodes using activated iridium oxide charge injection sites in more extended studies is now being undertaken. (J Spinal Cord Med; 18:28–32)