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Therapeutic Points (therapeutic + point)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Prevalence of Anti-cardiolipin, Anti-,2 Glycoprotein I, and Anti-prothrombin Antibodies in Young Patients with Epilepsy

EPILEPSIA, Issue 1 2002
R. Cimaz
Summary: ,Purpose: To measure anti-cardiolipin (aCL), anti-,2 glycoprotein I (anti-,2GPI), and anti-prothrombin (aPT) antibodies in young patients with epilepsy, and to correlate their presence with demographic data, clinical diagnoses, laboratory and neuroradiologic findings, and antiepileptic drugs (AEDs). Methods: Sera from one hundred forty-two consecutive patients with epilepsy with a median age of 10 years were tested for aCL and anti-,2GPI autoantibodies by solid-phase assays. aPT antibodies also were assayed in sera from 90 patients. Positive results were confirmed after a minimum of 6 weeks. Antinuclear antibodies (ANAs) and antibodies against extractable nuclear antigens (ENAs) also were tested. Results: An overall positivity of 41 (28.8%) of 142 sera was found. Fifteen patients were positive for aCL, 25 for anti-,2GPI, and 18 for aPT antibodies. Several patients (12%) displayed more than one specificity in their serum. Only one of these patients had a concurrent positivity for ANAs and ENAs. A predominance of younger patients was found in the antibody-positive group. All types of epilepsy were represented in the positive group. No relation between antibody positivity and AEDs was found. Diffuse ischemic lesions at computed tomography (CT)/magnetic resonance imaging (MRI) scans were present in higher percentages in patients who were antibody positive. No positive patient had a history of previous thrombosis or other features related to systemic lupus erythematosus (SLE), and no patient was born of a mother with SLE. Conclusions: Our study suggests a relation between epilepsy and aPL in young patients. A pathogenetic role for these autoantibodies cannot be excluded, and their determination might prove useful even from a therapeutic point of view. [source]

TOWARD THE GLOBAL STANDARDIZATION OF ENDOSCOPIC SUBMUCOSAL DISSECTION PROPOSAL FOR 10 YEARS FROM NOW , PRESENT AND FUTURE VIEW OF KOREA

DIGESTIVE ENDOSCOPY, Issue 2009
Joo Young Cho
Endoscopic submucosal dissection (ESD) is the main treatment of early gastric cancer in Korea. The Korean Society of Gastrointestinal Endoscopy (KSGE) has organized an ESD research group and made several plans to standardize pathologic and therapeutic points of view. This article is to introduce the present and future view of ESD in Korea. [source]

Sphincter of Oddi dysfunction: role of sphincterotomy

DIGESTIVE ENDOSCOPY, Issue 4 2001
Choichi Sugawa
Sphincter of Oddi dysfunction (SOD) is one of the causes of post-cholecystectomy syndrome and biliary pain and is a challenge from both the diagnostic and therapeutic points of view. Sphincter of Oddi dysfunction is typically diagnosed months to years after cholecystectomy. Continued biliary type pain after cholecystectomy may occur in as many as 10,20% of patients. Ten percent or more of these patients may eventually be shown to have SOD. The syndrome is often associated with a variety of other gastrointestinal disorders thought to be caused by dysmotility. According to the Milwaukee classification, patients with biliary pain can be divided into three types. Type I patients show all the objective signs suggestive of a disturbed bile outflow (i.e. elevated liver function tests, dilated common bile duct and delayed contrast drainage during endoscopic retrograde cholangiopancreatography). Type II patients have biliary type pain along with one or two of the criteria from type I. Type III patients have biliary pain only, with no other abnormalities. The present paper will focus primarily on SOD syn-drome, papillary stenosis and the diagnostic and therapeutic approaches, in particular endoscopic sphincterotomy. [source]

Prevention of spinal motor neuron death by insulin-like growth factor-1 associating with the signal transduction systems in SODG93A transgenic mice

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 4 2005
Hisashi Narai
Abstract The role of insulin-like growth factor-1 (IGF-1) in amyotrophic lateral sclerosis (ALS) and its mechanism of action are important from both pathogenic and therapeutic points of view. The present study investigated the changes of IGF-1R, and the key intracellular downstream protein insulin receptor substrate-1 (IRS-1) by using SOD1G93A transgenic mice with continuous intrathecal IGF-1 treatment. The number of lumbar spinal motor neurons was preserved with IGF-1 treatment in a dose-dependent manner. The numbers of immunopositive motor neurons for IGF-1R, and IRS-1 were not significantly different between wild-type and Tg mice with vehicle treatment, whereas treatment of Tg mice with IGF-1 decreased the numbers of immunopositive motor neurons in a dose-dependent manner. On the other hand, the ratio of immunopositive motor neurons per total living motor neurons in vehicle-treated mice was greatly increased in Tg mice with vehicle treatment compared with wild-type mice. With IGF-1 treatment, the ratio was dramatically decreased in a dose-dependent manner. These results suggest that IGF-1 treatment prevents motor neuron loss by affecting the signal transduction system through IGF-1R and the main downstream signal, IRS-1. © 2005 Wiley-Liss, Inc. [source]