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Increased Incidence (increased + incidence)
Selected AbstractsIncreased Incidence of Gastrointestinal Bleeding Following Implantation of the HeartMate II LVADJOURNAL OF CARDIAC SURGERY, Issue 3 2010David R. Stern M.D. To avoid device-related thromboembolic complications, antiplatelet, and anticoagulation therapy are routinely administered. A worrisome frequency of gastrointestinal (GI) bleeding events has been observed. Methods: A retrospective review of all 33 patients undergoing long-term LVAD implantation between June 1, 2006 and July 31, 2008 at our institution for any indication was conducted. Anticoagulation consisted of heparin (intravenous or subcutaneous) followed by transition to Coumadin therapy to a target INR of two to three. Antiplatelet therapy consisted of low-dose aspirin and dipyridamole. Results: Twenty patients received the HMII and 13 patients received other devices. Eight (40%) HMII recipients suffered at least one episode of GI bleeding while no GI bleeding occurred in recipients of other devices (p = 0.012). Of 17 total bleeding episodes, no definitive source could be identified in 11 instances (65%). Conclusions: Although definitive source identification remains elusive, we believe that the majority of bleeding arises in the small bowel, possibly due to angiodysplasias, similar to the pathophysiology encountered in patients with aortic stenosis and GI bleeding. As we move toward wider use of the HMII and other axial continuous-flow devices in both bridge-to-transplant patients and for destination therapy, more studies will be necessary to understand the mechanisms of this obscure GI bleeding and develop treatment strategies to minimize its development.,(J Card Surg 2010;25:352-356) [source] Increased Incidence of Colorectal Malignancies in Renal Transplant Recipients: A Case Control StudyAMERICAN JOURNAL OF TRANSPLANTATION, Issue 9 2010J. M. Park This study was to evaluate the frequency of colorectal neoplasia in renal transplant recipients and to investigate the association with Epstein-Barr virus (EBV) and cytomegalovirus (CMV) infection. We compared the frequency of colorectal neoplasia among renal transplant recipients with that of the healthy subjects. Specimens of colorectal neoplasia were examined for EBV and CMV using in situ hybridization and immunohistochemistry, respectively. Of 796 renal transplantation cohorts, 315 were enrolled. The frequency of colorectal neoplasia among the patients was 22.9%. Compared with the healthy subjects, the odds ratio (OR) for advanced adenoma was 3.32 (95% CI, 1.81,6.10). The frequency of cancer among the patients was 1.9% (OR, 12.0; 95% CI, 1.45,99.7). A long interval between transplantation and colonoscopy was a significant factor in the development of advanced colorectal neoplasia. EBV positivity was detected in 30.6% of colorectal neoplasia specimens from renal transplant recipients, which was higher than that for the controls (p = 0.002). CMV was not detected in any lesions of patients or controls. In conclusion, renal transplant recipients have a significantly increased risk of advanced colorectal neoplasia. EBV was more frequently found in specimens of advanced colorectal neoplasm obtained from the renal transplant recipients. [source] Increased Incidence of Tuberculosis in Immigrant Dialysis PopulationsARTIFICIAL ORGANS, Issue 8 2002R. Vanholder No abstract is available for this article. [source] Increased incidence of saprophytic bacteria, coliforms and E. coli following severe flooding requires risk assessment for human health: results of the River Elbe flood in August 2002JOURNAL OF FLOOD RISK MANAGEMENT, Issue 1 2009B. Karrasch Abstract In August 2002, flooding in the Elbe valley caused severe damage of sewage treatment plants and networks. We investigated the impact of flooding on the bacteriological water quality (colony-forming units of saprophytic bacteria, coliform bacteria and Escherichia coli) compared with levels from previous and subsequent years. The flood introduced organic matter and elevated saprophytic bacteria levels, and a general increase of coliform bacteria. Markedly high loads of coliforms and E. coli were detected in the water column in areas where damage to sewage treatment plants was rife, exceeding the European Commission's Bathing Water Directive. The rapid disappearance from the water column may partly be caused by sedimentation creating deposits on pasture, farmland and in built-up areas, which could represent a health hazard. Future flood risk reduction should therefore be focused on the protection of sewage systems and hygienic monitoring of floodwater and flood sediments. [source] Increased incidence of malignancies in Sweden after the Chernobyl accident,a promoting effect?AMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 3 2006Martin Tondel Abstract Background After the Chernobyl accident in 1986, as much as 5% of the released caesium-137 was deposited in Sweden due to a heavy rainfall 2 days after the event. A study of increased incidence of malignancies was initiated after the accident. Methods The cohort included 1,137,106 inhabitants who were 0,60 years old in 1986 and lived in 8 counties of Sweden with the highest fallout of caesium-137. With the dwelling coordinate, GIS-technique and a digital map on caesium-137, each individual was matched for the exposure. Adjustments were made for several potential confounding factors. During the follow-up 33,851 malignancies was recorded 1988,1999. Results Exposure categories were: 0,8 (reference), 9,23, 24,43, 44,66, 67,84, and ,85 nGy/hr. The corresponding adjusted Mantel-Haenszel incidence rate ratios for total malignancies during follow-up amounted to 1.000, 0.997, 1.072, 1.114, 1.068, 1.125, respectively. The excess relative risk per 100 nGy/hr with the same adjustments and time period was 0.042 95% confidence limit 0.001;0.084. An excess for thyroid cancer or leukemia could not be ruled out. Conclusion Increased incidence of total malignancies possibly related to the fallout from the Chernobyl accident is seen. Am. J. Ind. Med. © 2006 Wiley-Liss, Inc. [source] Increased incidence of autoantibodies to interleukin-1, in rheumatoid arthritis with interstitial lung diseaseRESPIROLOGY, Issue 4 2000Koji Maniwa Objective: To clarify the clinical significance of autoantibodies (auto-Ab) to interleukin-1, (IL-1,) in rheumatoid arthritis (RA) with interstitial lung disease (ILD), we examined the IL-1, auto-Ab level in serum of patients with RA with/without ILD. Methodology: We investigated the level of IL-1, auto-Ab in serum of 70 patients with RA with/without ILD and 40 control patients (CP). Levels of IL-1, auto-Ab were measured by radioimmunoassay, and serum was regarded as IL-1, auto-Ab positive at an auto-Ab level of more than 5 ng/mL. Results: Interleukin-1, auto-Ab was detected in the serum of 30 out of 70 RA patients (42.9%), and six out of 40 CP (15%) (P < 0.05). Interleukin-1, auto-Ab were detected in the serum of 18 out of 32 patients with RA with ILD (56.2%) and 12 out of 38 patients with RA without ILD (31.5%). The positive rate of these autoantibodies in RA with ILD was significantly higher than that in RA without ILD (P < 0.05). Although C-reactive protein, immunoglobulin G, rheumatoid factor and rheumatoid arthritis particle agglutination levels in serum from patients with RA with ILD were not significantly different between the IL-1, auto-Ab-positive and -negative groups, the lactate dehydrogenase level (LDH) and AaDO2 in the IL-1, auto-Ab-positive group were significantly higher than those in the negative group (LDH: P < 0.001, AaDO2: P < 0.05). Conclusion: These results suggest that IL-1, auto-Ab are generated in response to the immuno-inflammatory process of ILD in RA, and these autoantibodies may neutralize and regulate the IL-1, activity. [source] Increased incidence of cardiovascular events in patients with antineutrophil cytoplasmic antibody,associated vasculitides: A matched-pair cohort studyARTHRITIS & RHEUMATISM, Issue 11 2009Matthew D. Morgan Objective To explore the risk of cardiovascular disease in patients with antineutrophil cytoplasmic antibody,associated vasculitides (AAVs) and to assess contributing risk factors. Methods In a retrospective matched-pair cohort study, 113 of 131 patients with AAVs from a vasculitis clinic registry were matched 1:1 for renal function, age at diagnosis, sex, smoking status, and previous history of a cardiovascular disease to patients with noninflammatory chronic kidney disease (CKD). Cardiovascular events were defined as acute coronary syndrome, new-onset angina, symptomatic peripheral vascular disease, stroke, and transient ischemic attack. Results Median followup times were 3.4 years for the AAV patients and 4.2 years for the CKD patients. More cardiovascular events occurred in the AAV group (23 of 113) than in the CKD group (16 of 113). Cox regression survival analysis showed a significantly increased risk of a cardiovascular event for AAV patients, with a hazard ratio (HR) of 2.23 (95% confidence interval [95% CI] 1.1,4.4) (P = 0.017). Within the cohort of AAV patients, the most strongly predictive factors were previous history of cardiovascular disease (HR 4 [95% CI 1.7,9.8]), history of dialysis dependency (HR 4.3 [95% CI 1.5,12.1]), ever having smoked (HR 3.9 [95% CI 1.5,10]), age at diagnosis (HR 1.038 [95% CI 1.006,1.072]), estimated glomerular filtration rate at remission (HR 0.977 [95% CI 0.957,0.998]), and serum cholesterol concentration at presentation (HR 0.637 [95% CI 0.441,0.92]). Conclusion In this retrospective study, patients with AAVs appear at greater risk of cardiovascular disease, with increased risk in those with a previous history of cardiovascular disease, dialysis dependency, poor renal function at remission, or a history of smoking. Measures to reduce the risk of cardiovascular disease should be integral to the management of systemic vasculitis. [source] Increased incidence of symptomatic venous thrombosis in patients with cervical carcinoma treated with concurrent chemotherapy, radiation, and erythropoietinCANCER, Issue 7 2003Ted Wun M.D. Abstract BACKGROUND Because studies have suggested that anemia has an adverse effect on outcome for patients with cervical carcinoma who are treated with radiation, recombinant human erythropoietin (rHuEpo) has been used increasingly to maintain hemoglobin levels in these patients. Erythropoietin may increase the risk of thrombosis. The authors performed a retrospective analysis to determine whether there was an increased rate of symptomatic venous thrombosis associated with the use of rHuEpo in patients with carcinoma of the uterine cervix and vagina. METHODS A retrospective, case,control study was performed on consecutive patients with localized carcinoma of the uterine cervix or vagina who were treated with chemotherapy and radiation (chemoradiotherapy). The primary outcome was symptomatic venous thrombosis. RESULTS One hundred forty-seven patients were reviewed. When they were divided into women who received rHuEpo (n = 75 patients) and women who did not receive rHuEpo (n = 72 patients), there were no significant differences in age, height, weight, disease stage, or body mass index. Fewer patients in the rHuEpo group required transfusions. In the rHuEpo group, 17 of 75 patients had either an upper extremity thrombosis (n = 12 patients) or a lower extremity thrombosis (n = 7 patients): 2 patients had both, and 2 patients had more than 1 event. Two of 72 patients who did not receive rHuEpo had symptomatic thrombosis. Patients who received rHuEpo had an odds ratio (OR) of developing thrombosis of 10.3 (95% confidence interval [95% CI], 2.3,46.2). Multiple logistic regression revealed that only the use of rHuEpo was associated with an increased risk of thrombosis (OR, 15.3; 95% CI, 3.1,76.7). CONCLUSIONS Patients with cervical carcinoma who received chemoradiotherapy and rHuEpo had an increased risk of symptomatic venous thrombosis. Cancer 2003;98:1514,20. © 2003 American Cancer Society. DOI 10.1002/cncr.11700 [source] The effects of low dietary calcium during egg-laying on eggshell formation and skeletal calcium reserves in the Zebra Finch Taeniopygia guttataIBIS, Issue 2 2001S. JAMES REYNOLDS Many small passerines forage intensively for calcium-rich foods during laying. Increased incidences of shell defects in eggs of small passerines have been reported, particularly in western Europe, and these have been explained in terms of declining calcium availability in soils, resulting from prolonged anthropogenic acid deposition. Studies in the field have provided laying birds, nesting in areas of low calcium availability, with calcium supplements. An alternative approach was adopted in this study by allowing captive Zebra Finches Taeniopygia guttata to lay first clutches on ad libitum calcium, switching them to a low calcium diet for 72 hours for the formation of all but the first egg of the second clutch and reinstating ad libitum calcium for the final clutch. Control females had access to ad libitumcalcium for all three clutches. Clutch sizes did not vary significantly between birds on low calcium and controls. The former took over three days longer to lay clutch 3 than did controls but the difference was not statistically significant. Birds on low calcium laid eggs that declined in shell ash mass with laying sequence, indicating that birds may have been calcium-limited. Although not statistically significant, eggshell thickness also declined with laying sequence in clutches laid by females on low calcium. The remaining egg measurements (shell mass, shell surface area and volume] of clutches laid by birds on low calcium did not differ significantly from those of controls. Furthermore, females on low calcium did not resort to skeletal reserves to provide sufficient calcium for egg formation. Dietary calcium appears to be of paramount importance in providing sufficient calcium for clutch formation. [source] Antiandrogenic effects of dibutyl phthalate and its metabolite, monobutyl phthalate, in ratsCONGENITAL ANOMALIES, Issue 4 2002Makoto Ema ABSTRACT, Developmental toxicity following administration of dibutyl phthalate (DBF) and its major metabolite, monobutyl phthalate (MBuP), by gavage was determined in Wistar rats. DBF on days 0,8 of pregnancy induced an increase in the incidence of preimplantation loss at 1250 mg/kg and higher and postimplantation loss at 750 mg/kg and higher. MBuP on days 0,8 of pregnancy produced an increase in the incidence of pre-and postimplantation loss at 1000 mg/kg. DBF on days 7,15 of pregnancy caused an increase in the incidence of fetuses with malformations at 750 mg/kg. MBuP on days 7,15 of pregnancy produced an increased incidence of fetuses with malformations at 500 mg/kg and higher. DBF on days 15,17 of pregnancy resulted in a decrease in the anogenital distance (AGD) of male fetuses and increase in the incidence of fetuses with undescended testes at 500 mg/kg and higher. MBuP on days 15,17 of pregnancy caused a decreased male AGD and increased incidence of fetuses with undescended testes at 250 mg/kg and higher. No effect of DBF and MBuP on the AGD was found in female offspring. The spectrum of fetal malformations, dependence of gestational days of treatment on the manifestation of teratogenicity, and alterations in development of the male reproductive system observed after administration of DBF were in good agreement with those observed after administration of MBuP. These findings suggest that MBuP may be responsible for the induction of developmental toxic effects of DBP. The doses that produced a decrease in the AGD and undescended testes in male offspring were lower than those producing maternal toxicity, fetal malformations after administration during major organogenesis, and embryonic loss. The male reproductive system may be more susceptible than other organ systems to DBP and MBuP toxicity after maternal exposure. [source] Prenatal developmental toxicity studies of 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane (p, p,-DDT) in rats and rabbitsCONGENITAL ANOMALIES, Issue 4 2001Ken L. Takahashi ABSTRACT, The studies were conducted in rats and rabbits to elucidate the potential developmental toxicity of p, p'-DDT in general accordance with the improved Japanese MAFF guidelines (12-Nousan-No. 8147,2,1,18, 2000). p, p'-DDT suspended in 1% aqueous solution of CMC was administered orally to pregnant Jcl:SD rats on gestational days (GD) 6,19 at a dose of 0,5, 25, or 100 mg/kg/day and to pregnant KbI: JW rabbits on GD 6,27 at a dose of 0,5,20, or 80 mg/kg/day. Maternal animals were killed on the day after the last day of administration for morphological examination of their fetuses with special attention to the reproductive organs. Adverse effects on maternal animals were found only at the highest dose in both species; i.e., clonic convulsion (2/24 in rats, 5/22 in rabbits), mortality (1/24 in rats), abortion or premature delivery (4/22 in rabbits), and reduced body weight gains and food consumption. However, the control and treated groups showed comparable values for the numbers of corpora lutea and implants, percent preimplantation losses, number of live fetuses, percent resorptions and fetal deaths, sex ratio, fetal body weights, and placental weights in both species, and anogenital distance and testicular histology in rats. Although fetal examination revealed slightly increased incidence of 27 presacral vertebrae in the highest dose group in rats, there was no treatment-related increase in the incidence of malformations in any of the species. Based on these results, it is concluded that p, p'-DDT causes no malformations, including male reproductive organ abnormalities, in either rats or rabbits, although it results in an increased incidence of skeletal variations in rats at a maternally toxic dose. [source] Cardiac hypertrophy and failure: lessons learned from genetically engineered miceACTA PHYSIOLOGICA, Issue 1 2001Y. Takeishi Congestive heart failure is a major and growing public health problem. Because of improved survival of myocardial infarction patients produced by thrombolytic therapy or per-cutaneous revascularization it represents the only form of cardiovascular disease with significantly increased incidence and prevalence. Clinicians view this clinical syndrome as the final common pathway of diverse pathologies such as myocardial infarction and haemodynamic overload. Insights into mechanisms for heart failure historically derived from physiological and biochemical studies which identified compensatory adaptations for the haemodynamic burden associated with the pathological condition including utilization of the Frank Starling mechanism, augmentation of muscle mass, and neurohormonal activation to increase contractility. Therapy has largely been phenomenological and designed to prevent or limit the deleterious effects of these compensatory processes. More recently insights from molecular and cell biology have contributed to a more mechanistic understanding of potential causes of cardiac hypertrophy and failure. Many different analytical approaches have been employed for this purpose. These include the use of conventional animal models which permit serial observation of the onset and progression of heart failure and a sequential analysis of underlying biochemical and molecular events. Neonatal murine cardiomyocytes have been a powerful tool to examine in vitro subcellular mechanisms devoid of the confounding functional effects of multicellular preparations and heterogeneity of cell type. Finally, significant progress has been made by utilizing tissue from human cardiomyopathic hearts explanted at the time of orthotopic transplantation. Each of these methods has significant advantages and disadvantages. Arguably the greatest advance in our understanding of cardiac hypertrophy and failure over the past decade has been the exploitation of genetically engineered mice as biological reagents to study in vivo the effects of alterations in the murine genome. The power of this approach, in principle, derives from the ability to precisely overexpress or ablate a gene of interest and examine the phenotypic consequences in a cardiac specific post-natal manner. In contrast to conventional animal models of human disease which employ some form of environmental stress, genetic engineering involves a signal known molecular perturbation which produces the phenotype. [source] Pulp revascularization of replanted immature dog teeth after different treatment methodsDENTAL TRAUMATOLOGY, Issue 5 2000K. Yanpiset Abstract , The purpose of the present study was to determine the effect of topical treatment with doxycycline and/or the application of unfilled resin to the anatomical crown on the occurrence of revascularization in reimplanted dog teeth. Ninety-six teeth in 4 young mongrel dogs were used. Eighty one teeth were atraumatically extracted and divided into four groups. Group 1, 17 teeth were kept dry for 5 min and then replanted. Group 2, 21 teeth were soaked with a freshly prepared solution of doxycycline (1 mg/20 mL saline) for 5 min before replantation. Group 3, 23 teeth were soaked with the doxycycline solution for 5 min, and then replanted. The crowns were coated with 2 layers of light cured unfilled resin. Group 4, 20 teeth were kept dry for 5 min, and then replanted. The crowns were treated as with the teeth in Group 3. Three months after surgery, radiographic evaluation revealed that 27 teeth had continued root development and 32 teeth showed arrested root development with periradicular pathosis. The remaining 17 teeth, which had arrested root development but no signs of periradicular pathosis, were all histologically evaluated for final assessment. The occurrence of revascularization according to treatment group was 29.4%, 60%, 60%, 36.8% in Group 1, 2, 3, and 4, respectively. A multiple logistic regression analysis in SAS indicated there was no significant association between vitality and dog (P=0.7564). Soaking for 5 min in doxycycline significantly increased the revascularization rate (P=0.024) while the addition of resin to the crown did not result in an increased incidence of pulp revascularization (P=0.823). [source] Combination Surgical Lifting with Ablative Laser Skin Resurfacing of Facial Skin: A Retrospective AnalysisDERMATOLOGIC SURGERY, Issue 9 2004Tina S. Alster MD Background. Cutaneous aging is manifested by rhytides, dyschromias, and skin laxity. Ablative laser skin resurfacing can effectively improve many signs of skin aging; however, the photoaged patient with facial laxity often requires a surgical lifting procedure in order to obtain optimal results. Concerns with delayed or impaired wound healing has led to reluctance to perform both procedures simultaneously. Objective. To report the clinical results and side effect profiles after concomitant surgical facial lifting procedures and ablative carbon dioxide or erbium:YAG laser resurfacing in a series of patients. Methods. A retrospective analysis and chart review was performed in 34 consecutive patients who underwent combination CO2 or erbium:YAG laser skin resurfacing and surgical lifting procedures, including S-lift rhytidectomy, blepharoplasty, and brow lift. Side effects and complication rates were tabulated. Results. The side effect profile of the combined surgical-laser procedures was similar to that reported after a laser-only procedure. The most common side effect was transient hyperpigmentation which occurred in 20.6% of treated patients. None of the patients experienced delayed reepithelialization, skin necrosis, or prolonged healing times. Conclusions. Concurrent laser skin resurfacing and surgical lifting of facial skin maximizes aesthetic results without increased incidence of adverse effects. Patients benefit from the consolidation of anesthesia and convalescent times as well as enhanced global clinical outcomes. [source] Effectiveness of Microporous Polysaccharide Hemospheres for Achieving Hemostasis in Mohs Micrographic SurgeryDERMATOLOGIC SURGERY, Issue 6 2004FRCPC, Stephen R. Tan MD Background. Microporous polysaccharide hemospheres consist of controlled-porosity spherical particles manufactured from bioinert plant polysaccharide. Microporous polysaccharide hemospheres facilitate hemostasis by rapidly absorbing the fluid component of blood, concentrating platelets and clotting factors to accelerate blood clotting. Objective. The objective was to compare a microporous polysaccharide hemosphere bandage and electrocautery in achieving hemostasis. Methods. Twenty-four patients with a total of 48 stages of Mohs micrographic surgery were included. Patients were stratified by whether or not they were taking anticoagulant medications. Within each group, patients were randomized to receive either the microporous polysaccharide hemosphere bandage or electrocautery. Outcomes included bleeding through the dressing (early time point) and active bleeding upon dressing removal (late time point). Results. Nineteen patients not taking anticoagulants had 40 stages, of which 18 received the study bandage and 22 received electrocautery. The remaining 5 patients on anticoagulants had 8 stages, of which 4 received the study bandage and 4 received electrocautery. In both total and subgroup analysis, there was a higher incidence of bleeding through the dressing with the study bandage (p<0.05), but no increase in the incidence of active bleeding upon dressing removal (p>0.05). Conclusion. The microporous polysaccharide hemosphere study bandage had an increased incidence of bleeding through the dressing compared to electrocautery, but did not have an increased incidence of active bleeding upon dressing removal. [source] Cognitive and neuropsychological outcomes: More than IQ scoresDEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 4 2002Glen P. Aylward Abstract Improved survival in preterm infants has broadened interest in cognitive and neuropsychological outcomes. The incidence of major disabilities (moderate/severe mental retardation, neurosensory disorders, epilepsy, cerebral palsy) has remained consistent, but high prevalence/low severity dysfunctions (learning disabilities, ADHD, borderline mental retardation, specific neuropsychological deficits, behavioral disorders) have increased. The follow-up literature contains methodologic problems that make generalizations regarding outcome difficult, and these are discussed. Although mean IQs of former VLBW infants generally are in the low average range and are 3,9 points below normal birth weight peers, these scores mask subtle deficits in: visual-motor and visual-perceptual abilities, complex language functions, academics (reading, mathematics, spelling and writing), and attentional skills. There is an increased incidence of non-verbal learning disabilities, need for special educational assistance, and behavioral disorders in children born prematurely. Males have more problems, and there is a trend for worsening outcome over time, due to emergence of more subtle deficits in response to increased performance demands. In addition to IQ and achievement testing in follow-up, there should be evaluation of executive functions and attention, language, sensorimotor functions, visuospatial processes, memory and learning, and behavioral adjustment. MRDD Research Reviews 2002;8:234,240. © 2002 Wiley-Liss, Inc. [source] Basolateral junctions are sufficient to suppress epithelial invasion during Drosophila oogenesisDEVELOPMENTAL DYNAMICS, Issue 2 2007Przemyslaw Szafranski Abstract Epithelial junctions play crucial roles during metazoan evolution and development by facilitating tissue formation, maintenance, and function. Little is known about the role of distinct types of junctions in controlling epithelial transformations leading to invasion of neighboring tissues. Discovering the key junction complexes that control these processes and how they function may also provide mechanistic insight into carcinoma cell invasion. Here, using the Drosophila ovary as a model, we show that four proteins of the basolateral junction (BLJ), Fasciclin-2, Neuroglian, Discs-large, and Lethal-giant-larvae, but not proteins of other epithelial junctions, directly suppress epithelial tumorigenesis and invasion. Remarkably, the expression pattern of Fasciclin-2 predicts which cells will invade. We compared the apicobasal polarity of BLJ tumor cells to border cells (BCs), an epithelium-derived cluster that normally migrates during mid-oogenesis. Both tumor cells and BCs differentiate a lateralized membrane pattern that is necessary but not sufficient for invasion. Independent of lateralization, derepression of motility pathways is also necessary, as indicated by a strong linear correlation between faster BC migration and an increased incidence of tumor invasion. However, without membrane lateralization, derepression of motility pathways is also not sufficient for invasion. Our results demonstrate that spatiotemporal patterns of basolateral junction activity directly suppress epithelial invasion by organizing the cooperative activity of distinct polarity and motility pathways. Developmental Dynamics 236:364,373, 2007. © 2006 Wiley-Liss, Inc. [source] Efficacy and safety of sitagliptin when added to insulin therapy in patients with type 2 diabetesDIABETES OBESITY & METABOLISM, Issue 2 2010T. Vilsbøll Objective: To evaluate the efficacy and tolerability of sitagliptin when added to insulin therapy alone or in combination with metformin in patients with type 2 diabetes. Methods: After a 2 week placebo run-in period, eligible patients inadequately controlled on long-acting, intermediate-acting or premixed insulin (HbA1c , 7.5% and , 11%), were randomised 1:1 to the addition of once-daily sitagliptin 100 mg or matching placebo over a 24-week study period. The study capped the proportion of randomised patients on insulin plus metformin at 75%. Further, the study capped the proportion of randomised patients on premixed insulin at 25%. The metformin dose and the insulin dose were to remain stable throughout the study. The primary endpoint was HbA1c change from baseline at week 24. Results: Mean baseline characteristics were similar between the sitagliptin (n = 322) and placebo (n = 319) groups, including HbA1c (8.7 vs. 8.6%), diabetes duration (13 vs. 12 years), body mass index (31.4 vs. 31.4 kg/m2), and total daily insulin dose (51 vs. 52 IU), respectively. At 24 weeks, the addition of sitagliptin significantly (p < 0.001) reduced HbA1c by 0.6% compared with placebo (0.0%). A greater proportion of patients achieved an HbA1c level < 7% while randomised to sitagliptin as compared with placebo (13 vs. 5% respectively; p < 0.001). Similar HbA1c reductions were observed in the patient strata defined by insulin type (long-acting and intermediate-acting insulins or premixed insulins) and by baseline metformin treatment. The addition of sitagliptin significantly (p < 0.001) reduced fasting plasma glucose by 15.0 mg/dl (0.8 mmol/l) and 2-h postmeal glucose by 36.1 mg/dl (2.0 mmol/l) relative to placebo. A higher incidence of adverse experiences was reported with sitagliptin (52%) compared with placebo (43%), due mainly to the increased incidence of hypoglycaemia (sitagliptin, 16% vs. placebo, 8%). The number of hypoglycaemic events meeting the protocol-specified criteria for severity was low with sitagliptin (n = 2) and placebo (n = 1). No significant change from baseline in body weight was observed in either group. Conclusion: In this 24-week study, the addition of sitagliptin to ongoing, stable-dose insulin therapy with or without concomitant metformin improved glycaemic control and was generally well tolerated in patients with type 2 diabetes. [source] Balancing needs and means: the dilemma of the ,-cell in the modern worldDIABETES OBESITY & METABOLISM, Issue 2009G. Leibowitz The insulin resistance of type 2 diabetes mellitus (T2DM), although important for its pathophysiology, is not sufficient to establish the disease unless major deficiency of ,-cell function coexists. This is demonstrated by the fact that near-physiological administration of insulin (CSII) achieved excellent blood glucose control with doses similar to those used in insulin-deficient type 1 diabetics. The normal ,-cell adapts well to the demands of insulin resistance. Also in hyperglycaemic states some degree of adaptation does exist and helps limit the severity of disease. We demonstrate here that the mammalian target of rapamycin (mTOR) system might play an important role in this adaptation, because blocking mTORC1 (complex 1) by rapamycin in the nutritional diabetes model Psammomys obesus caused severe impairment of ,-cell function, increased ,-cell apoptosis and progression of diabetes. On the other hand, under exposure to high glucose and FFA (gluco-lipotoxicity), blocking mTORC1 in vitro reduced endoplasmic reticulum (ER) stress and ,-cell death. Thus, according to the conditions of stress, mTOR may have beneficial or deleterious effects on the ,-cell. ,-Cell function in man can be reduced without T2DM/impaired glucose tolerance (IGT). Prospective studies have shown subjects with reduced insulin response to present, several decades later, an increased incidence of IGT/T2DM. From these and other studies we conclude that T2DM develops on the grounds of ,-cells whose adaptation capacity to increased nutrient intake and/or insulin resistance is in the lower end of the normal variation. Inborn and acquired factors that limit ,-cell function are diabetogenic only in a nutritional/metabolic environment that requires high functional capabilities from the ,-cell. [source] Efficacy and safety of the dipeptidyl peptidase-4 inhibitor alogliptin in patients with type 2 diabetes inadequately controlled by glyburide monotherapyDIABETES OBESITY & METABOLISM, Issue 2 2009R. E. Pratley Aim:, To evaluate the efficacy and safety of alogliptin, a potent and highly selective dipeptidyl peptidase-4 (DPP-4) inhibitor, in combination with glyburide in patients with type 2 diabetes inadequately controlled by sulphonylurea monotherapy. Methods:, After a 2-week screening period, adult patients 18,80 years of age entered a 4-week run-in/stabilization period in which they were switched from their own sulphonylurea medication to an equivalent dose of glyburide (open label) plus placebo (single blind). After the run-in period, patients were randomly assigned to double-blind treatment with alogliptin 12.5 mg (n = 203), alogliptin 25 mg (n = 198), or placebo (n = 99) for 26 weeks. The primary end-point was change from baseline to week 26 in glycosylated haemoglobin (HbA1c). Secondary end-points included clinical response rates and changes in fasting plasma glucose, ,-cell function (fasting proinsulin, insulin, proinsulin/insulin ratio, and C-peptide, and homeostasis model assessment ,-cell function), body weight, and safety end-points [adverse events (AEs), clinical laboratory tests, vital signs and electrocardiographic readings]. Results:, The study population had a mean age of 57 years and a mean disease duration of 8 years; it was well balanced for gender (52% women) and was mainly white (71%). The mean baseline HbA1c was approximately 8.1% in each group. Significantly greater least squares (LS) mean reductions in HbA1c were seen at week 26 with alogliptin 12.5 mg (,0.38%) and 25 mg (,0.52%) vs. placebo (+0.01%; p < 0.001), and more patients in the alogliptin 25-mg group had HbA1c levels ,7.0% at week 26 (34.8%, p = 0.002) vs. placebo (18.2%). Proportionately more patients in the alogliptin 12.5 mg (47.3%) and 25 mg (50.5%) groups had an HbA1c reduction ,0.5% from baseline compared with patients in the placebo group (26.3%; p < 0.001). Minor improvements in individual markers of ,-cell function were seen with alogliptin, but no significant treatment group differences were noted relative to placebo. Minor LS mean changes in body weight were noted across groups (placebo, ,0.20 kg; alogliptin 12.5 mg, +0.60 kg; alogliptin 25 mg, +0.68 kg). AEs were reported for 63,64% of patients receiving alogliptin and 54% of patients receiving placebo. Few AEs were treatment limiting (2.0,2.5% across groups), and serious AEs (2.0,5.6%) were infrequent, similar across groups, and generally considered not related to treatment. The incidences of hypoglycaemia for placebo, alogliptin 12.5 mg and alogliptin 25 mg groups were 11.1, 15.8 and 9.6% respectively. Conclusions:, In patients with type 2 diabetes inadequately controlled by glyburide monotherapy, the addition of alogliptin resulted in clinically significant reductions in HbA1c without increased incidence of hypoglycaemia. [source] Evidence for a vicious cycle of exercise and hypoglycemia in type 1 diabetes mellitusDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2004A. C. Ertl Abstract Exercise is a cornerstone of diabetes management as it aids in glycemic control, weight management, reducing blood pressure, and improving the quality of life of patients. Unfortunately, owing to the complexity and difficulties of regulating exogenous insulin in a physiologic manner during exercise, physical activity often results in hypoglycemia in patients with type 1 diabetes mellitus (type 1 DM). When glucose levels fall below threshold glycemic levels, neuroendocrine, autonomic nervous system (ANS), and metabolic glucose counterregulatory mechanisms are activated. These hypoglycemic counterregulatory mechanisms in type 1 DM can be blunted irreversibly by disease duration or by acute episodes of prior stress. These reduced (or absent) counterregulatory responses result in a threefold increase in severe hypoglycemia when intensive glycemic control is implemented in type 1 DM 1. Much recent work has been focused on determining the in vivo mechanisms responsible for causing the increased incidence of severe hypoglycemia in type 1 DM. Studies from several laboratories have demonstrated the role played by episodes of antecedent hypoglycemia in producing blunted glucose counterregulatory responses during subsequent exposures of hypoglycemia. Until recently, the mechanisms responsible for exercise related hypoglycemia in type 1 DM have been attributed to relative or absolute increases of insulin levels or incomplete glycogen repletion after physical activity. Owing to the qualitative similarity of neuroendocrine, ANS, and metabolic responses to hypoglycemia and exercise, we have hypothesized that neuroendocrine and ANS counterregulatory dysfunction may also play an important role in the pathogenesis of exercise-related hypoglycemia in type 1 DM. Vicious cycles can be created in type 1 DM, where an episode of hypoglycemia or exercise can feed forward to downregulate neuroendocrine and ANS responses to a subsequent episode of either stress, thereby creating further hypoglycemia (Figure 1). This article will review the recent work that has studied the contribution of counterregulatory dysfunction to exercise-induced hypoglycemia in type 1 DM. Copyright © 2004 John Wiley & Sons, Ltd. 1. Reciprocal vicious cycles may be created in type 1 diabetes mellitus (type 1 DM), whereby an episode of hypoglycemia or exercise can feed forward to downregulate neuroendocrine and autonomic nervous system responses to a subsequent episode of either stress, thereby creating further hypoglycemia [source] Epidemiology of gestational diabetes mellitus and its association with Type 2 diabetesDIABETIC MEDICINE, Issue 2 2004A. Ben-Haroush Abstract Gestational diabetes (GDM) is defined as carbohydrate intolerance that begins or is first recognized during pregnancy. Although it is a well-known cause of pregnancy complications, its epidemiology has not been studied systematically. Our aim was to review the recent data on the epidemiology of GDM, and to describe the close relationship of GDM to prediabetic states, in addition to the risk of future deterioration in insulin resistance and development of overt Type 2 diabetes. We found that differences in screening programmes and diagnostic criteria make it difficult to compare frequencies of GDM among various populations. Nevertheless, ethnicity has been proven to be an independent risk factor for GDM, which varies in prevalence in direct proportion to the prevalence of Type 2 diabetes in a given population or ethnic group. There are several identifiable predisposing factors for GDM, and in the absence of risk factors, the incidence of GDM is low. Therefore, some authors suggest that selective screening may be cost-effective. Importantly, women with an early diagnosis of GDM, in the first half of pregnancy, represent a high-risk subgroup, with an increased incidence of obstetric complications, recurrent GDM in subsequent pregnancies, and future development of Type 2 diabetes. Other factors that place women with GDM at increased risk of Type 2 diabetes are obesity and need for insulin for glycaemic control. Furthermore, hypertensive disorders in pregnancy and afterwards may be more prevalent in women with GDM. We conclude that the epidemiological data suggest an association between several high-risk prediabetic states, GDM, and Type 2 diabetes. Insulin resistance is suggested as a pathogenic linkage. It is possible that improving insulin sensitivity with diet, exercise and drugs such as metformin may reduce the risk of diabetes in individuals at high risk, such as women with polycystic ovary syndrome, impaired glucose tolerance, and a history of GDM. Large controlled studies are needed to clarify this issue and to develop appropriate diabetic prevention strategies that address the potentially modifiable risk factors. Diabet. Med. 20, ***,*** (2003) [source] Anal cytology: Is there a role for reflex HPV DNA testing?DIAGNOSTIC CYTOPATHOLOGY, Issue 3 2005A.E. Walts M.D. Abstract There is an increased incidence of anal squamous carcinoma and its precursor lesions (anal intraepithelial neoplasia [AIN]) among persons who engage in anal-receptive sex. Analogous to cervical cancer screening, anal Papanicplaou (Pap) smears currently are used to screen these high-risk populations. Human papilloma virus (HPV) has been implicated in anal carcinoma pathogenesis and this study was performed to assess the potential role of HPV DNA testing as an adjunct to anal cytology. We correlated cytological diagnoses and HPV DNA (Digene Hybrid Capture [HC II] assay) in anal specimens collected in SurePath liquid medium from 118 patients; 54.8% of cases diagnosed as atypical squamous cells of undetermined significance (ASC-US) and 87.8% diagnosed as low-grade squamous intraepithelial lesion (LSIL) or above tested positive for high- risk HPV DNA (B+). High-grade SIL (HSIL) was present in 31 of the 51 patients with follow-up. Although a cytological diagnosis of ASC-US or above was a reliable indicator for AIN, cytology frequently did not accurately predict the grade of SIL in subsequent biopsy. Our findings suggest that reflex HPV DNA testing would be helpful in triaging patients diagnosed with ASC-US. However, patients diagnosed with LSIL or above should go directly to ansocopic biopsy. Diagn. Cytopathol. 2005;33:152,156. © 2005 Wiley-Liss, Inc. [source] Surgery in thoracic esophageal perforation: primary repair is feasibleDISEASES OF THE ESOPHAGUS, Issue 3 2002S. W. Sung SUMMARY. Prompt diagnosis and effective treatment are important for thoracic esophageal perforations. The decision for proper management is difficult especially when diagnosed late. However, there is an increasing consensus that primary repair provides good results for repair of thoracic esophageal perforations, which are not diagnosed on time. Primary repair for thoracic esophageal perforations was applied in 20 out of 25 consecutive patients. The time interval between perforation and repair was less than 24 h in six patients (group I), and more than 24 h in 14 patients (group II). The remaining five patients underwent esophagectomy with simultaneous or staged reconstruction because of incorrectable underlying esophageal pathology. Group I had much more iatrogenic causes (P < 0.05). Preoperative sepsis occurred only in group II (P=0.05) and was highly associated with Boerhaave syndrome (P=0.001). Regional viable tissue was used to reinforce the sites of primary repair (n=15, 75%). All of the postoperative morbidity (n=9, 45%) including esophageal leaks (n=6, 30%) and operative death (n=1, 5%) occurred in group II. In patients with postoperative leaks, five eventually healed, but one became a fistula that required reoperation. Primary healing with preservation of the native esophagus was achieved in all 19 patients except one operative death. In addition, the increased incidence of leak and morbidity did not lead to an increase in mortality. In the esophagectomy group, there was no mortality, but one minor suture leak. Regardless of the time interval between the injury and the operation, primary repair is recommended for non-malignant, thoracic, esophageal perforations, but not for anastomotic leaks. Reinforcement that may change the nature of a possible leak is also useful. For incorrectable underlying esophageal pathology, esophagectomy with simultaneous or staged reconstruction is indicated. [source] Pharmacologic profile of zoledronic acid: A highly potent inhibitor of bone resorptionDRUG DEVELOPMENT RESEARCH, Issue 4 2002Jonathan R. Green Abstract Bisphosphonates are effective in treating benign and malignant skeletal diseases characterized by enhanced osteoclastic bone resorption (i.e., osteoporosis, Paget's disease, tumor-induced osteolysis). The nitrogen-containing bisphosphonate pamidronate is currently the standard treatment for hypercalcemia of malignancy (HCM) and skeletal complications of bone metastases. Zoledronic acid, a novel nitrogen-containing bisphosphonate with an imidazole substituent, has demonstrated more potent inhibition of osteoclast-mediated bone resorption than all other bisphosphonates, including pamidronate, in both in vitro and in vivo preclinical models. Zoledronic acid inhibited ovariectomy-induced bone loss in adult monkeys and rats, and long-term treatment prevented skeletal turnover and subsequent bone loss, reduced cortical porosity, and increased mechanical strength. Zoledronic acid also significantly inhibited bone loss associated with arthritis, bone metastases, and prosthesis loosening. The increased potency of zoledronic acid vs. pamidronate has been demonstrated clinically: zoledronic acid (4 or 8 mg iv) was superior to pamidronate (90 mg iv) in normalizing corrected serum calcium in patients with HCM. In patients with bone metastases, low doses of zoledronic acid (, 2 mg) suppressed bone resorption markers , 50% below baseline, whereas pamidronate 90 mg yielded only 20 to 30% suppression. Importantly, the increased potency of zoledronic acid is not associated with an increased incidence of local (bone) or systemic adverse events. Zoledronic acid does not impair bone mineralization and, compared with pamidronate, has a greater renal and intestinal tolerability therapeutic index. Thus, based on preclinical assays and clinical data, zoledronic acid is the most potent bisphosphonate tested to date. Given its potency and excellent safety profile, zoledronic acid is now poised to become the new standard of treatment for HCM and metastatic bone disease. Drug Dev. Res. 55:210,224, 2002. © 2002 Wiley-Liss, Inc. [source] The Global Diversion of Pharmaceutical DrugsADDICTION, Issue 9 2010Opiate treatment, the diversion of pharmaceutical opiates: a clinician's perspective ABSTRACT Aim To provide a clinician's perspective on the problem of diversion of prescribed pharmaceuticals. Methods The paper provides a personal account of working in a treatment context where diversion from opioid substitution treatment (OST) became a political issue potentially compromising the continued delivery of OST. It summarizes evidence on the impact of diversion, and measures to contain it, from the United Kingdom 1986,2006, Australia 1996,2008 and the United States and France from the mid-1990s. Results Opioid diversion to the black market occurs in proportion to the amount of opioids prescribed to be taken without supervision, and in inverse proportion to the availability of heroin. Diversion for OST programmes using supervision of dosing is less than diversion of opioids prescribed for pain, which is now a growing public health problem. Adverse consequences of diversion include opioid overdose fatalities, an increased incidence of addiction (particularly in jurisdictions where heroin is scarce) and compromising the public acceptance of long-term opioid prescribing. All long-term opioid prescribing requires monitoring of risk and appropriate dispensing arrangements,including dilution of methadone take-aways, supervision of administration for high-risk patients and random urine testing. Clinical guidelines influence practice, although prescribing often deviates from guidelines. Conclusion Clinical guidelines and clinical audit to enhance compliance with guidelines are helpful in maintaining the quality and integrity of the treatment system, and can contribute to keeping diversion within acceptable levels. [source] Is Left Ventricular Diastolic Thickening Documented During Dobutamine and Pacing Stress Echocardiography Related to Myocardial Ischemia?ECHOCARDIOGRAPHY, Issue 1 2002An Animal Model Study Transient increase in diastolic wall thickness (pseudohypertrophy) during pacing stress echocardiography has been reported in normal myocardium. To evaluate the occurrence of pseudohypertrophy and to investigate the contribution of myocardial ischemia on its production during pacing and dobutamine stress echocardiography, we produced a physiologically significant coronary stenosis in 14 open chest dogs. The stenosis in the circumflex artery was measured by quantitative coronary angiography (range: 50% to 89% reduction in luminal diameter), and no resting segmental wallmotion abnormalities were observed by epicardial echocardiography (short-axis, papillary level). In each study, dobutamine (5,40 ,g/kg/min) and pacing (up to 260 beats/min) were performed randomly. Positivity of stress echocardiography tests was quantitatively determined by a significant (P < 0.05) reduction or failure to increase in absolute and percent systolic wall thickening in the myocardial area supplied by the stenotic artery as compared to the left anterior descending (LAD) artery-related areas. Diastolic wall thickness and left ventricular diastolic area were compared before and after each stress test in the circumflex and LAD artery-related regions. Pseudohypertrophy was observed in 57% and 86% of dogs for pacing and dobutamine, respectively, in the circumflex region, and in 50% and 64% in the LAD region. Despite its increased incidence in the circumflex region, the augmented diastolic wall thickness did not correlate with coronary stenosis severity or stress test positivity, but correlated inversely with changes in left ventricular diastolic area. In addition, it correlated directly with changes in heart rate only for pacing. In conclusion, pseudohypertrophy was a frequent finding during pacing and dobutamine stress echocardiography tests but was not related to myocardial ischemia in this animal model. [source] Incidence and impact of axial malformations in larval bullfrogs (Rana catesbeiana) developing in sites polluted by a coal-burning power plantENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 4 2000William A. Hopkins Abstract Amphibian malformations have recently received much attention from the scientific community, but few studies have provided evidence linking environmental pollution to larval amphibian malformations in the field. We document an increased incidence of axial malformations in bullfrog larvae (Rana catesbeiana) inhabiting two sites contaminated with coal combustion wastes. In the polluted sites, 18 and 37% of larvae exhibited lateral curvatures of the spine, whereas zero and 4% of larvae from two reference sites had similar malformations. Larvae from the most heavily polluted site had significantly higher tissue concentrations of potentially toxic trace elements, including As, Cd, Se, Cu, Cr, and V, compared with conspecifics from the reference sites. In addition, malformed larvae from the most contaminated site had decreased swimming speeds compared with those of normal larvae from the same site. We hypothesize that the complex mixture of contaminants produced by coal combustion is responsible for the high incidence of malformations and associated effects on swimming performance. [source] Electroconvulsive seizure thresholds and kindling acquisition rates are altered in mouse models of human KCNQ2 and KCNQ3 mutations for benign familial neonatal convulsionsEPILEPSIA, Issue 7 2009James F. Otto Summary Purpose:, Benign familial neonatal convulsions (BFNC) is caused by mutations in the KCNQ2 and KCNQ3 genes, which encode subunits of the M-type potassium channel. The purpose of this study was to examine the effects of orthologous BFNC-causing mutations on seizure thresholds and the acquisition of corneal kindling in mice with heterozygous expression of the mutations. Methods:, The effects of the Kcnq2 gene A306T mutation and the Kcnq3 gene G311V mutation were determined for minimal clonic, minimal tonic hindlimb extension, and partial psychomotor seizures. The rate of corneal kindling acquisition was also determined for Kcnq2 A306T and Kcnq3 G311V mice. Results:, Seizure thresholds were significantly altered relative to wild-type animals in the minimal clonic, minimal tonic hindlimb extension, and partial psychomotor seizure models. Differences in seizure threshold were found to be dependent on the mutation expressed, the seizure testing paradigm, the genetic background strain, and the gender of the animal. Mutations in Kcnq2 and Kcnq3 were associated with an increased rate of corneal kindling. In the Kcnq2 A306T mice, an increased incidence of death occurred during and immediately following the conclusion of the kindling acquisition period. Conclusions:, These results suggest that genetic alterations in the subunits that underlie the M-current and cause BFNC alter seizure susceptibility in a sex-, mouse strain-, and seizure-test dependent manner. Although the heterozygous mice do not appear to have spontaneous seizures, the increased seizure susceptibility and incidence of death during and after kindling suggests that these mutations lead to altered excitability in these animals. [source] Audiogenic kindling in Wistar and WAG/Rij rats: Kindling-prone and kindling-resistant subpopulationsEPILEPSIA, Issue 10 2008Lyudmila V. Vinogradova Summary Purpose:, Audiogenic kindling (AK) is a model of naturally occurring epileptogenesis triggered by repeated sound stimulation of rats genetically prone to audiogenic seizures. It is accepted that limbic seizure networks underlie progressive changes in behavioral seizure pattern during AK. The present study investigated AK progression in rats susceptible and unsusceptible to absence seizures. Methods:, Progression of AK as indicated by an appearance and intensification of limbic clonus was examined in Wistar Albino Glaxo/Rijswijk (WAG/Rij) rats with genetic absence epilepsy and in Wistar rats. Results:, Subpopulations of kindling-prone and kindling-resistant rats were found in both Wistar and WAG/Rij strains. Despite identical seizure responses to the first sound stimulation, AK progression dramatically differed between the two subpopulations. AK-prone rats exhibited rapid kindling development up to maximal stage-5 severity. In AK-resistant rats, limbic clonus did not appear after 30 stimulations or if it appeared, it did not progress beyond stage 2. The proportions of AK-prone and AK-resistant animals within Wistar and WAG/Rij strains were similar. Comparison of Wistar and WAG/Rij rats within the kindling-prone and kindling-resistant groups did not reveal a significant strain effect on AK progression. However, within the WAG/Rij strain, a significantly higher incidence of absence seizures was found in AK-resistant rats compared to AK-prone rats. Conclusions:, The present study demonstrates that sensitivity to sound-induced epileptogenesis differs dramatically within Wistar and WAG/Rij strains, whereas genetic susceptibility to absence seizures does not change AK progression significantly. It is supposed that an increased incidence of nonconvulsive seizures and resistance to kindling result from a common seizure modulating mechanism. [source] | ||||||||||||||||||||||||||||||||||||||||