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Selected AbstractsPrediabetes and the big baby,DIABETIC MEDICINE, Issue 1 2008D. R. Hadden Abstract The concept of prediabetes has come to the fore again with the worldwide epidemic of Type 2 diabetes. The careful observations of W. P. U. Jackson and his colleagues in Cape Town, South Africa 50 years ago still deserve attention. Maternal hyperglycaemia cannot be the only cause of fetal macrosomia, and the pathophysiological reason for the unexplained stillbirth in late diabetic pregnancy still eludes us. The biochemical concepts of ,facilitated anabolism' and ,accelerated starvation' were developed by Freinkel as explanations of the protective mechanisms for the baby during the stresses of pregnancy. Some of these nutritional stresses may also occur in the particular form of early childhood malnutrition known in Africa as kwashiorkor, where subcutaneous fat deposition, carbohydrate intolerance, islet hyperplasia and sudden death may follow a period of excess carbohydrate and deficient protein intake. Different feeding practices in different parts of the world make comparisons uncertain, but there is evidence for insulin resistance in both the macrosomic fetus of the hyperglycaemic mother and in the child with established kwashiorkor. These adaptive changes in early development may play both a physiological and a pathological role. Worldwide studies of hyperglycaemia in pregnancy are gradually establishing acceptable diagnostic criteria, appropriate screening procedures and an evidence base for treatment. Nevertheless the challenge of prediabetes and the big baby is still with us,in Jackson's words,,diabetes mellitus is a fascinating condition,the more we know about it the less we understand it'. [source] Recurrent spreading depolarizations after subarachnoid hemorrhage decreases oxygen availability in human cerebral cortexANNALS OF NEUROLOGY, Issue 5 2010Bert Bosche MD Objective Delayed ischemic neurological deficit (DIND) contributes to poor outcome in subarachnoid hemorrhage (SAH) patients. Because there is continuing uncertainty as to whether proximal cerebral artery vasospasm is the only cause of DIND, other processes should be considered. A potential candidate is cortical spreading depolarization (CSD)-induced hypoxia. We hypothesized that recurrent CSDs influence cortical oxygen availability. Methods Centers in the Cooperative Study of Brain Injury Depolarizations (COSBID) recruited 9 patients with severe SAH, who underwent open neurosurgery. We used simultaneous, colocalized recordings of electrocorticography and tissue oxygen pressure (ptiO2) in human cerebral cortex. We screened for delayed cortical infarcts by using sequential brain imaging and investigated cerebral vasospasm by angiography or time-of-flight magnetic resonance imaging. Results In a total recording time of 850 hours, 120 CSDs were found in 8 of 9 patients. Fifty-five CSDs (,46%) were found in only 2 of 9 patients, who later developed DIND. Eighty-nine (,75%) of all CSDs occurred between the 5th and 7th day after SAH, and 96 (80%) arose within temporal clusters of recurrent CSD. Clusters of CSD occurred simultaneously, with mainly biphasic CSD-associated ptiO2 responses comprising a primary hypoxic and a secondary hyperoxic phase. The frequency of CSD correlated positively with the duration of the hypoxic phase and negatively with that of the hyperoxic phase. Hypoxic phases significantly increased stepwise within CSD clusters; particularly in DIND patients, biphasic ptiO2 responses changed to monophasic ptiO2 decreases within these clusters. Monophasic hypoxic ptiO2 responses to CSD were found predominantly in DIND patients. Interpretation We attribute these clinical ptiO2 findings mainly to changes in local blood flow in the cortical microcirculation but also to augmented metabolism. Besides classical contributors like proximal cerebral vasospasm, CSD clusters may reduce O2 supply and increase O2 consumption, and thereby promote DIND. ANN NEUROL 2010;67:607,617 [source] Optimal Pressure Regulation of the Pneumatic Ventricular Assist Device With Bellows-Type DriverARTIFICIAL ORGANS, Issue 8 2009Jung Joo Lee Abstract The bellows-type pneumatic ventricular assist device (VAD) generates pneumatic pressure with compression of bellows instead of using an air compressor. This VAD driver has a small volume that is suitable for portable devices. However, improper pneumatic pressure setup can not only cause a lack of adequate flow generation, but also cause durability problems. In this study, a pneumatic pressure regulation system for optimal operation of the bellows-type VAD has been developed. The optimal pneumatic pressure conditions according to various afterload conditions aiming for optimal flow rates were investigated, and an afterload estimation algorithm was developed. The developed regulation system, which consists of a pressure sensor and a two-way solenoid valve, estimates the current afterload and regulates the pneumatic pressure to the optimal point for the current afterload condition. Experiments were performed in a mock circulation system. The afterload estimation algorithm showed sufficient performance with the standard deviation of error, 8.8 mm Hg. The flow rate could be stably regulated with a developed system under various afterload conditions. The shortcoming of a bellows-type VAD could be handled with this simple pressure regulation system. [source] The Influence of Molecular Orientation on the Yield and Post-Yield Response of Injection-Molded PolycarbonateMACROMOLECULAR MATERIALS & ENGINEERING, Issue 12 2009Tom A. P. Engels Abstract The influence of the flow history experienced during injection molding on the mechanical properties of amorphous polymers is investigated. It is demonstrated that flow-induced molecular orientation only causes a small anisotropic effect on the yield stress, which can be regarded as insignificant with respect to its absolute value. Its influence on the post-yield strain-hardening response is also shown to be imperceptible, in contrast to a orientation which is applied during deformation below the glas transition. [source] Urodynamic findings in female diabetic patients with and without overactive bladder symptoms,,NEUROUROLOGY AND URODYNAMICS, Issue 3 2010Chen-Hsun Ho Abstract Aims The purpose was to analyze urodynamic findings in female diabetic patients with OAB symptoms. Methods Data from 94 female diabetic patients who underwent urodynamic studies in evaluation of various LUTS were retrospectively reviewed. Urodynamic findings, demographic data, and clinical symptoms were compared between patients with and without OAB. Results Among the 94 subjects analyzed, 34 (36.2%) were diagnosed as OAB. Demographic data were similar between the patients with and without OAB. In the OAB group, patients had significantly higher storage symptom scores and marginally higher voiding symptom scores. On cystometry, the OAB group had a higher percentage of increased bladder sensation (41.2% vs 11.7%, P,=,0.001) and detrusor overactivity (29.4% vs 10.0%, P,=,0.023). The OAB group had lower peak flow rate (16.2,±,5.9 vs 19.3,±,6.3 ml/s, P,=,0.023), greater PVR volume (60.3,±,29.4 vs 45.0,±,25.1 ml, P,=,0.009), and lower bladder voiding efficiency (BVE, 75.2,±,2.8 vs 81.5,±,2.9%, P,<,0.001). On pressure-flow studies, the OAB group had a higher percentage of BOO (26.5% vs 6.7%, P,=,0.008). Conclusions Our study shows that the most frequent urodynamic finding of OAB in female diabetic patients is increased bladder sensation, followed by detrusor overactivity. Compared to those without OAB, female diabetic patients with OAB are more likely to have impaired voiding function, characterized by lower peak flow rate, greater PVR volume, lower BVE, and a higher percentage of BOO. In these patients, BOO not only causes voiding difficulty but may also contribute to the development of OAB. Neurourol. Urodynam. 29:424,427, 2010. © 2009 Wiley-Liss, Inc. [source] NF-,B2/p52 enhances androgen-independent growth of human LNCaP cells via protection from apoptotic cell death and cell cycle arrest induced by androgen-deprivationTHE PROSTATE, Issue 16 2008Nagalakshmi Nadiminty Abstract PURPOSE Androgen-deprivation therapy only causes a temporary regression of prostate cancer, as all tumors will eventually progress to refractory to hormonal therapy after 1,3 years of treatment. The underlying mechanisms of prostate cancer androgen refractory progression are incompletely understood. In this study, we employed in vitro as well as in vivo models to examine the role of NF-,B2/p52 in prostate cancer growth and androgen independent progression. EXPERIMENTAL DESIGN The effects of NF-,B2/p52 on cell growth, androgen responsiveness, cell cycle and apoptosis were examined in androgen sensitive LNCaP cells. The effect of NF-,B2/p52 on tumor growth was examined in intact and castrated male mice. RESULTS Overexpression of NF-,B2/p52 enhances androgen-sensitive LNCaP human prostate cancer cell growth and clonogenic ability in androgen-deprived condition in vitro. NF-,B2/p52 induced androgen-independent growth is through protecting LNCaP cells from apoptotic cell death and cell cycle arrest induced by androgen-deprivation. In addition, NF-,B2/p52 stimulates Cyclin D1 expression and knock down of Cyclin D1 expression by siRNA abolished NF-,B2/p52-induced cell growth in vitro. Adenoviral mediated NF-,B2/p52 expression in LNCaP cells enhances tumor growth in intact male nude mice and induces tumor growth in castrated male nude mice, suggesting that overexpression of NF-,B2/p52 induces androgen-independent growth of androgen-sensitive LNCaP cells. CONCLUSIONS Overexpression of NF-,B2/p52 protects androgen sensitive LNCaP cells from apoptotic cell death and cell cycle arrest induced by androgen-deprivation. NF-,B2/p52 activation induces androgen-independent growth in vitro and in vivo. Prostate © 2008 Wiley-Liss, Inc. [source] | ||||||||||