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Functional Loss (functional + loss)
Selected AbstractsNational Political Parties and European Integration: Mapping Functional LossPOLITICS, Issue 1 2000Gijs Berends This article specifically examines the role of national political parties in the light of European integration. It introduces the functions that are normally associated with parties, which allows for a systematic evaluation of the performance of national parties in the European Union. Probing these functions that parties are reputed to implement, it arrives at the conclusion that national parties are fairly unsuccessful in fulfilling their core tasks at the European level. [source] Reducing the duration of untreated first-episode psychosis , effects on baseline social functioning and quality of lifeACTA PSYCHIATRICA SCANDINAVICA, Issue 6 2005I. Melle Objective:, Long duration of untreated psychosis (DUP) is associated with poorer outcome. The TIPS study demonstrated that DUP can be reduced through early detection (ED). As quality of life (QoL) is associated with DUP it is expected that reduction of DUP leads to better QoL. Method:, Consecutive first-episode patients with a DSM-IV diagnosis of non-organic, non-affective psychosis were included, 281 patients gave informed consent and 263 completed a full evaluation of QoL. Results:, There were no differences in subjective QoL between ED and No-ED groups attributable to reduction in DUP. There were significant bivariate differences in frequency of family and social contacts in favor of the ED group, but multivariate analyses indicated that these differences were based on differences in sample characteristics. Conclusion:, Deterioration in QoL may precede overt symptom formation. Focus on functional loss in ED educational campaigns may identify risk subjects earlier in the course of the disorder. [source] Hereditary neuropathy with liability to pressure palsies associated with central nervous system myelin lesionsEUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2001J. Dac Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant disorder most commonly caused by a 1.5-Mb deletion in chromosome 17p11.2 which contains the peripheral myelin protein-22 (PMP22) gene. Mutations resulting in functional loss of one PMP22 gene copy are less frequent. We present a 51-year-old patient with a l.5-Mb deletion in chromosome 17p11.2 who exhibited signs of peripheral as well as central nervous system lesions. He gave a history of recurrent episodes of limb numbness and weakness with spontaneous but incomplete recovery since age 20. His father and two brothers had similar symptoms. Neurological examination revealed signs of multiple mononeuropathy associated with frontal lobe, corticospinal tract and cerebellar dysfunction, as well as signs of initial cognitive impairment. Electrophysiological investigations showed a demyelinating peripheral nerve disease with multiple conduction blocks and conduction disturbances in both optic nerves. Magnetic resonance imaging of the brain revealed multiple subcortical and periventricular foci of myelin lesions. The association of central and peripheral nervous system lesions in this patient indicates a possible role of PMP22 not only in peripheral but also in central nervous system myelin structure. [source] Microcell-mediated transfer of chromosome 4 into HeLa cells suppresses telomerase activityGENES, CHROMOSOMES AND CANCER, Issue 2 2001Claudia Backsch Telomerase activity can be detected in most human cancers and immortal cell lines. In contrast, the lack of telomerase activity in normal diploid fibroblasts has been correlated with progressive reduction of telomere lengths to critically short sizes followed by the cessation of cell division and the onset of senescence. Several investigators have provided evidence for the localization of a telomerase suppressor gene on chromosome 3. The aim of our study was to determine whether other chromosomes are involved in telomerase repression. Beside human chromosome 3 (serving as positive control), chromosomes 4, 6, and 11 were introduced into HeLa cells via microcell-mediated chromosome transfer. Telomerase activity from different hybrid cell lysates was determined at an early time point after fusion using a Telomerase ELISA kit. Strong repression of telomerase activity was only found in a subset of HeLa hybrids in which chromosome 3 or chromosome 4 had been introduced. Telomerase suppression induced by chromosome 3 or 4 transfer was paralleled by a high frequency (30% or 43%, respectively) of a senescent-like phenotype. Chromosomes 6 and 11, the functional loss of which is also implicated in cervical cancer, had no effect. These results indicate that normal human chromosomes 3 and 4 carry a gene or genes that suppress telomerase activity and induce cellular senescence in HeLa cells.©2001 Wiley-Liss, Inc. [source] The TLR3 ligand polyI:C downregulates connexin 43 expression and function in astrocytes by a mechanism involving the NF-,B and PI3 kinase pathwaysGLIA, Issue 8 2006Yongmei Zhao Abstract Toll-like receptor 3 (TLR3) is a component of the innate immune response that responds to dsRNA viruses and virus replication intermediates. In this study we show that activation of astrocytes with the dsRNA mimetic polyinosinic-cytidylic acid (pI:C) results in loss of expression of connexin43 (Cx43) mRNA and protein while upregulating the expression of the ionotropic P2 receptor P2X4R. Analysis of the signaling pathways involved failed to demonstrate a role for the p38 MAP kinase, ERK, or JNK signaling pathways whereas an inhibitor of the PI3 kinase/Akt pathway effectively blocked the action of pI:C. Using adenoviral vectors containing a super-repressor of NF-,B (NF-,B SR) construct or a dominant negative interferon regulatory factor 3 (dnIRF3) construct showed that inhibition of both transcription factors also blocked the effects of pI:C. To explore the functional consequences of pI:C activation we used a pore-forming assay for P2X4R activity and a scrape loading assay for gap junction intercellular communication (GJIC). No pore-forming activity consistent with functional P2X4R expression was detected in either control or activated astrocytes. In contrast, robust Lucifer yellow transfer indicative of GJIC was detected in resting cells that was lost following pI:C activation. The dnIRF3 construct failed to restore GJIC whereas the NF-,B SR or the NF-,B inhibitor BAY11-7082 and the PI3K inhibitor LY294002 all significantly reversed the effect of pI:C on GJ connectivity. We conclude that activation of the innate immune response in astrocytes is associated with functional loss of GJIC through a pathway involving NF-,B and PI3 kinase. © 2006 Wiley-Liss, Inc. [source] Pediatric Short Bowel Syndrome: Pathophysiology, Nursing Care, and Management IssuesJOURNAL FOR SPECIALISTS IN PEDIATRIC NURSING, Issue 3 2000Louise D. Jakubik ISSUES AND PURPOSE. A comprehensive overview of the etiology, pathophysiology, nursing care, and medical and surgical management of the child with short bowel syndrome (SBS), which follows massive anatomical or functional loss of the small intestine. CONCLUSIONS. The outlook for children with SBS has improved due to recent advances in parenteral and enteral nutrition, pharmacologic interventions, and surgical options. PRACTICE IMPLICATIONS. Nurses whose practice reflects an in-depth knowledge of the etiology, pathophysiology, medical and surgical management, nursing interventions, and complications of SBS will be equipped to provide quality care for children and families affected by SBS. [source] Expression of survivin protein in pterygium and relationship with oxidative DNA damageJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 6a 2008C. Maxia Abstract Ultraviolet radiation is known to cause oxidative DNA damage and is thought to be a major factor implicated in the pathogenesis of pterygium. Among all the photo-oxidative DNA products, the 8-hydroxydeoxyguanosine (8-OHdG) is regarded a sensitive and stable biomarker for evaluating the degree of DNA damage. The protein p53 is a major cell stress regulator that acts to integrate signals from a wide range of cellular stresses. UV radiation has a carcinogenic effect resulting in DNA damaged cells with loss of normal growth control. This assumption is supported by the association between UV-B exposure and activation of survivin, a member of the inhibitor of apoptosis protein family (IAP), highly up-regulated in almost all types of human malignancy. In this study we demonstrate, for the first time in pterygium, the immunohistochemical presence of survivin, and investigate the correlation between survivin, p53 and 8-OHdG. Our results demonstrate that oxidative stress could lead to a significant activation of survivin expression, suggesting that this might be an important event in the development of pterygium, inducing and supporting a hyperproliferative condition. Survivin expression in pterygium would counteract UV-B-induced apoptosis and would cooperate with loss of p53. The co-operation between survivin and functional loss of p53 might provide a general mechanism for aberrant inhibition of apoptosis that could be responsible for the development of pterygium and its possible progression to neoplasia. [source] Minocycline neuroprotects, reduces microgliosis, and inhibits caspase protease expression early after spinal cord injuryJOURNAL OF NEUROCHEMISTRY, Issue 5 2006Barry W. Festoff Abstract Minocycline, a clinically used tetracycline for over 40 years, crosses the blood,brain barrier and prevents caspase up-regulation. It reduces apoptosis in mouse models of Huntington's disease and familial amyotrophic lateral sclerosis (ALS) and is in clinical trial for sporadic ALS. Because apoptosis also occurs after brain and spinal cord (SCI) injury, its prevention may be useful in improving recovery. We analyzed minocycline's neuroprotective effects over 28 days following contusion SCI and found significant functional recovery compared to tetracycline. Histology, immunocytochemistry, and image analysis indicated statistically significant tissue sparing, reduced apoptosis and microgliosis, and less activated caspase-3 and substrate cleavage. Since our original report in abstract form, others have published both positive and negative effects of minocycline in various rodent models of SCI and with various routes of administration. We have since found decreased tumor necrosis factor-,, as well as caspase-3 mRNA expression, as possible mechanisms of action for minocycline's ameliorative action. These results support reports that modulating apoptosis, caspases, and microglia provide promising therapeutic targets for prevention and/or limiting the degree of functional loss after CNS trauma. Minocycline, and more potent chemically synthesized tetracyclines, may find a place in the therapeutic arsenal to promote recovery early after SCI in humans. [source] Plasma Clearance of Exogenous Creatinine, Exo-Iohexol, and Endo-Iohexol in Hyperthyroid Cats before and after Treatment with RadioiodineJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 4 2008I. Van Hoek Background: Glomerular filtration rate (GFR) can be measured by clearance methods of different markers showing discrepancies and different reproducibility in healthy cats. Studies comparing different methods of GFR measurement in hyperthyroid cats have not yet been performed. Hypothesis: Plasma clearance of exogenous creatinine (PECCT), exo-iohexol (PexICT), and endo-iohexol (PenICT) could lead to differences in GFR measurement and the need to use the same clearance method when comparing GFR before and after radioiodine treatment in hyperthyroid cats. Animals: Fifteen client-owned hyperthyroid cats. Methods: GFR was measured 1 day before and 1, 4, 12, and 24 weeks after treatment. Intravenous injection of iohexol was followed immediately by IV injection of creatinine. Plasma creatinine was measured by an enzymatic method. Plasma endo- and exo-iohexol were measured by high-performance liquid chromatography coupled to ultraviolet detection. Results: Globally, the 3 GFR methods resulted in significantly different (P < .001) GFR results. GFR results among the different methods were the same (P= .999) at all time points. All 3 techniques indicated decreasing GFR after 131I treatment. For each GFR technique, a significant decrease in GFR was observed between time point 0 and all other time points. This decrease stabilized 4 weeks after treatment, with very little decline afterward. Conclusion and Clinical Importance: It is mandatory to use the same GFR technique in follow-up studies. GFR testing at 4 weeks posttreatment could allow assessment of the final renal functional loss after treatment in hyperthyroid cats. [source] Measuring contrast sensitivity with inappropriate optical correction*OPHTHALMIC AND PHYSIOLOGICAL OPTICS, Issue 6 2000Russell L. Woods Summary Spatial frequency-selective minima (notches) in the contrast sensitivity function (CSF) because of defocus can mimic those that occur with ocular disease. We examined the influence of measurement conditions on CSF shape in simulated clinical testing. CSF notches occurred with almost all levels of defocus for all subjects. Multiple notches were found under some conditions. Notches were found with defocus as small as 0.50 D. Effects of induced astigmatism depended on the orientation of the target. Notches were apparent in defocus conditions after stimulus size and room illuminance were modified and when subjects had insufficient accommodation to compensate for hypermetropic defocus. The equivalent of notches was not noted with the Pelli-Robson chart. As defocus-induced CSF notches may be mistaken for functional loss, careful refractive correction should be conducted prior to clinical or experimental CSF measurement, even at low spatial frequencies. [source] TLR4 Mediates Early Graft Failure After Intraportal Islet TransplantationAMERICAN JOURNAL OF TRANSPLANTATION, Issue 7 2010Q. Gao We have previously shown that islet emboli in the portal vein block blood flow and induce local inflammatory reaction, resulting in functional loss of islet grafts following intraportal transplantation. This study was designed to test whether Toll-like receptor (TLR) activation mediates early islet graft failure. Syngeneic islet grafts were transplanted into chemically induced diabetic mice, and TLR deficient mice were used as donors and/or recipients of islet grafts. Islet viability, proinflammatory cytokines, high-mobility group box-1 (HMGB1) and NF-,B activation were analyzed by bioluminesce imaging (BLI), quantitative RT-PCR (qRT-PCR) and histology. Early islet graft failure was observed in mice with intraportal islet engrafts with increased proinflammatory cytokines, HMGB1 expression, NF-,B activation, caspase-3 and TUNEL positive cells. Deficiency of TLR4 in donor, but not in recipient, inhibited NF-,B activation, reduced proinflammatory cytokines and improved viability of islet grafts. Blockade of HMGB1 with anti-HMGB1 monoclonal antibody (mAb, 2g7) inhibited inflammatory reactions, as evidenced by reduced TNF, and IL-1ß production, and improved islet viability. We conclude that TLR4 activation mediates early graft failure following intraportal islet transplantation. Inhibition of TLR4 activation represents a novel strategy to attenuate early graft failure following intraportal islet transplantation. [source] Assessment of Changes in Kidney Allograft Function Using Creatinine-Based Estimates of Glomerular Filtration RateAMERICAN JOURNAL OF TRANSPLANTATION, Issue 4 2007M. Gera These analyses assessed whether creatinine based estimates of glomerular filtration rate (eGFR) accurately represent (1) graft function at different times post-transplant and (2) changes in function over time. These analyses compared iothalamate GFR to eGFR in 684 kidney allograft recipients. Changes in graft function over time (GFR slope) were measured in 360 of 459 recipients (78%) who were followed for at least 3 years. Ninety-five percent of the patients were Caucasians and 72% received kidneys from living donors. All eGFR calculations correlated significantly with GFR at all time points. However, eGFR were less precise and less accurate during the first-year post-transplant than thereafter. The average rate of GFR change (slope) was ,2.93 ± 11.3%/year (,1.06 ± 5.3 mL/min/1.73m2/year). Fifty-four percent of patients had stable or positive GFR slopes. The GFR and eGFR slopes were highly correlated. However, eGFR slope, particularly when calculated by MDRD, significantly underestimated the number of patients with declining graft function. For example, 165 out of 360 patients (46%) lost GFR faster than ,1 mL/min/1.73m2/year. eMDRD identified only 83 of these patients (50%) while the eMayo formula identified 134 (81%). In conclusion, eGFR correlate with GFR but they have relatively low precision and accuracy particularly early post-transplant. eGFR slopes underestimate graft functional loss although some formulas are significantly better than others for this calculation. [source] Tailoring the Type of Donor Hepatectomy for Adult Living Donor Liver TransplantationAMERICAN JOURNAL OF TRANSPLANTATION, Issue 7 2005Norihiro Kokudo Donor hepatectomies for adult living donor liver transplantations were performed in 200 consecutive donors to harvest a left liver (LL) graft (n = 5), a LL plus caudate lobe (LL + CL) graft (n = 63), a right liver (RL) graft (n = 86), a RL and middle hepatic vein (RL + MHV) graft (n = 28) or a right lateral sector (RLS) graft (n = 18). The graft type was selected so that at least 40% of the recipient's standard liver volume was harvested. No donor deaths occurred, and no significant differences in the morbidity rates among either donors or recipients were observed when the outcomes were stratified according to the graft type. Donors who donated RL exhibited higher values of serum total bilirubin and prothrombin time than those who donated non-RL (LL, LL + CL, RLS) grafts. The time taken for hilar dissection and parenchymal transection increased in the following order: RLS graft, LL graft and RL graft harvesting. In conclusion, non-RL grafting was more time consuming, but the hepatic functional loss in the donors was smaller. Our graft selection criteria were useful for reducing the use of RL grafts with acceptable morbidity in both donors and recipients. [source] Axonal loss and myelin in early ON loss in postacute optic neuritisANNALS OF NEUROLOGY, Issue 3 2008Alexander Klistorner PhD Objective To investigate the relation between retinal nerve fiber layer (RNFL) thickness and latency and amplitude of multifocal visual-evoked potentials (mfVEPs) in the postacute stage of optic neuritis in patients with early or possible multiple sclerosis. Method Thirty-two patients with clinical diagnosis of unilateral optic neuritis and magnetic resonance imaging lesions typical of demyelination and 25 control subjects underwent mfVEP and optical coherence tomography imaging. Results Although there was significant reduction of RNFL thickness in the affected eyes (18.7%), a considerably larger decrease was observed for the amplitude of the mfVEPs (39.8%). Latency of the mfVEPs was also significantly delayed in optic neuritis eyes. In fellow eyes, the amplitude of mfVEPs was significantly reduced and the latency prolonged, but RNFL thickness remained unaltered. RNFL thickness correlated highly with the mfVEP amplitude (r = 0.90). There was also strong correlation between optical coherence tomography measure of axonal loss and mfVEP latency (r = ,0.66). Interpretation Although our findings demonstrate strong associations between structural and functional measures of optic nerve integrity, the functional loss was more marked. This fact, together with amplitude and latency changes of the mfVEPs observed in clinically normal fellow eyes, may indicate greater sensitivity of mfVEPs in detecting optic nerve abnormality or the presence of widespread inflammation in the central nervous system, or both. The significant correlation of the mfVEP latency with RNFL thickness suggests a role for demyelination in promoting axonal loss. Ann Neurol 2008 [source] The Role of Myocardial KATP -Channel Blockade in the Protective Effects of Glibenclamide against Ischaemia in the Rat HeartBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2002Roger J. Legtenberg This study addresses the possible involvement of KATP channels in this beneficial action of glibenclamide. We hypothesized that if glibenclamide improved postischaemic cardiac function by blocking of KATP channels, opening of these KATP channels should result in the opposite, namely detrimental effects on postischaemic heart function. Postischaemic functional loss and coronary blood flow were recorded during treatment with glibenclamide (4 ,mol.l,1; n=5), the KATP channel openers pinacidil (1 ,mol.l,1; n=5) and diazoxide (30 ,mol.l,1; n=5), the combination of glibenclamide with pinacidil (n=5) and glibenclamide with diazoxide (n=5), and vehicle (n=8). Both pinacidil and diazoxide significantly increased coronary blood flow 2,3 times, which was abolished by glibenclamide pre- and postischaemically. This confirms that under both flow conditions glibenclamide significantly blocks KATP channels in the coronary vasculature. The 12 min. global ischaemic incident resulted in a cardiac functional loss of 22.2±2.9% during vehicle. Glibenclamide reduced the cardiac functional loss to 4.3±1.2% (P<0.01). Interestingly, both pinacidil and diazoxide reduced the cardiac functional loss to 4.0±1.5% (P<0.01) and 2.9±1.4% (P<0.001), respectively. The combination pinacidil+glibenclamide resulted in additional protection compared with the individual components (0.6±0.1 versus 4.0±1.5%, P<0.05). Thus, in contrast to its effect on coronary vascular tone, the glibenclamide-induced improvement of postischaemic cardiac function may not be mediated through blockade of the KATP channel. Alternative mechanisms may be operative, such as uncoupling of the mitochondrial respiratory chain, thereby preconditioning the hearts against stunning. [source] Psoriatic skin expresses the transcription factor Gli1: possible contribution of decreased neurofibromin expressionBRITISH JOURNAL OF DERMATOLOGY, Issue 4 2006H. Endo Summary Background, Psoriasis is a chronic inflammatory disorder of skin characterized by hyperproliferation of keratinocytes. Intracellular signalling pathways inducing the hyperproliferation of keratinocytes remain to be elucidated. An inhibitor of Hedgehog (Hh) signalling, cyclopamine, was recently reported to clear psoriatic skin lesions, suggesting involvement of the Hh signalling pathway in the hyperproliferation of lesional keratinocytes. We have previously observed activation of the Hh signalling pathway in Schwann cells of plexiform neurofibroma in neurofibromatosis type 1 (NF1), which results from functional loss of the NF1 encoding protein, neurofibromin. In psoriasis, deficiency of neurofibromin expression has been observed in lesional keratinocytes. Objectives, To investigate whether the Hh signalling pathway would be activated in psoriasis and whether inhibition of neurofibromin expression would enhance the activation of the Hh signalling pathway. Methods, Activation of the Hh signalling pathway was examined by protein expression of one of the target genes, GLI1, coding for the transcription factor Gli1. Immunohistochemical studies were performed on seven psoriatic skin samples and seven control normal skin samples with a standard immunoperoxidase technique. mRNA expression of GLI1 was analysed by reverse transcriptase,polymerase chain reaction in HaCaT cells transfected with double-strand small interfering RNA for NF1. Results, Our results showed Gli1 expression in psoriatic skin but not in control normal skin. Inhibition of neurofibromin expression in HaCaT cells upregulated mRNA expression of GLI1. Conclusions, Our findings indicate that the Hh signalling pathway is activated in psoriasis and that neurofibromin deficiency may upregulate the pathway. [source] CpG methylation at promoter site ,140 inactivates TGF,2 receptor gene in prostate cancerCANCER, Issue 1 2005Hong Zhao M.D. Abstract BACKGROUND The action of transforming growth factor , (TGF-,) is mediated through type 1 (T,RI) and type 2 (T,RII) receptors. Prostate cancer cells are often resistant to TGF-, signaling due to loss of T,RII expression. The authors of the current study hypothesized that CpG methylation of the T,RII promoter at the Sp1 binding site ,140 mediates this loss of T,RII expression in prostate cancer. METHODS Sixty-seven prostate cancer (PC) samples, 8 benign prostatic hyperplasia (BPH) samples, and 4 prostate cancer cell lines (DUPro, LNCaP, ND-1 and PC-3) were analyzed for 1) T,RII mRNA expression by semiquantitative RT-PCR, 2) T,RII protein expression by immunohistochemistry, and 3) TGF,RII promoter methylation at CpG site ,140 by methylation specific PCR and bisulfite DNA sequencing. Prostate cancer cell lines were treated with the demethylating agent 5aza2,deoxycytidine to determine if T,RII gene expression could be increased by blocking promoter methylation. RESULTS mRNA and protein expression of T,RII was lower in the PC samples than in the BPH samples. CpG methylation at site ,140 was higher in PC than in BPH (P < 0.01). Promoter methylation was inversely correlated with T,RII mRNA expression in the PC and BPH samples (P < 0.0001). PC3, ND1, and DUPro T,RII mRNA expression increased following treatment of cells with 5-aza-2,-deoxycytidine. CONCLUSION CpG methylation of the T,RII promoter at CPG site ,140 leads to functional loss of the T,RII gene in prostate cancer. Treatment with 5-aza-2, deoxycytidine can restore gene expression. The current study results report the first association between prostate cancer and loss of the TGF- , signaling pathway by T,RII DNA promoter methylation. Cancer 2005;. © 2005 American Cancer Society. [source] Multiple sclerosis siblings with cerebrospinal fluid immunopathy but without any indication of neuronal damageACTA NEUROLOGICA SCANDINAVICA, Issue 5 2003S. Haghighi Objective , In a previous study, we found that nine of the 47 siblings to multiple sclerosis (MS) patients with a normal neurologic examination carry an intrathecal oligoclonal immunopathy with limited specificity, a condition we termed MS immunopathic trait. Here we searched for neurological dysfunction with increased sensitivity. Method , We used high-pass resolution perimetry, which reveals visual pathway lesions by their impaired neural effective capacity (EC) in early MS cases even without optic neuritis. Results , These nine individuals with MS immunopathic trait did not differ from nine healthy controls with normal cerebrospinal fluid regarding their EC. Conclusion , This is further evidence that a group of MS immunopathic trait individuals, siblings to MS patients, are essentially free from the central nervous system functional loss typically found in MS. [source] Subtle myelin defects in PLP-null mice ,GLIA, Issue 3 2006Jack Rosenbluth Abstract This study explores subtle defects in the myelin of proteolipid protein (PLP)-null mice that could potentially underlie the functional losses and axon damage known to occur in this mutant and in myelin diseases including multiple sclerosis. We have compared PLP-null central nervous system (CNS) myelin with normal myelin using ultrastructural methods designed to emphasize fine differences. In the PLP-null CNS, axons large enough to be myelinated often lack myelin entirely or are surrounded by abnormally thin sheaths. Short stretches of cytoplasm persist in many myelin lamellae. Most strikingly, compaction is incomplete in this mutant as shown by the widespread presence of patent interlamellar spaces of variable width that can be labeled with ferricyanide, acting as an aqueous extracellular tracer. In thinly myelinated fibers, interlamellar spaces are filled across the full width of the sheaths. In thick myelin sheaths, they appear filled irregularly but diffusely. These patent spaces constitute a spiral pathway through which ions and other extracellular agents may penetrate gradually, possibly contributing to the axon damage known to occur in this mutant, especially in thinly myelinated fibers, where the spiral path length is shortest and most consistently labeled. We show also that the "radial component" of myelin is distorted in the mutant ("diagonal component"), extending across the sheaths at 45° instead of 90°. These observations indicate a direct or indirect role for PLP in maintaining myelin compaction along the external surfaces of the lamellae and to a limited extent, along the cytoplasmic surfaces as well and also in maintaining the normal alignment of the radial component. © 2006 Wiley-Liss, Inc. [source] Depressive symptoms among poststroke patients in Japan: frequency distribution and factor structure of the GDSINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 10 2001Andrea S. Schreiner Abstract Objective The present study examined the nature, prevalence, and covariates of depressive symptoms among home-dwelling poststroke patients in Japan using the Geriatric Depression Scale Short Form (GDS-1). Poststroke results were compared with those of elderly with affective disorders and with those of healthy nonstroke elderly. Methods Poststroke patients (n,=,101) who did not also have a diagnosis of Alzheimer's dementia, were identified from patient records at seven randomly selected hospitals with outpatient rehabilitation clinics in a metropolitan area in western Japan and invited to participate in the study. All instruments were interview-administered. Results GDS scores did not correlate with age, sex, education, functional dependence, aphasia, paralysis or presence of other chronic illnesses. However, GDS scores did correlate significantly with self-rated general health and poststroke duration. Compared with the frequency distribution in a psychiatric sample, poststroke patients had higher positive affect and lower depressed mood but similar social withdrawal scores. The factor structure of the poststroke sample differed from that of nonstroke elderly in that depressed mood items loaded with items for energy loss and memory problems. Conclusion Despite the fact that 62% of subjects scored ,,6 on the GDS, none were currently receiving assessment and/or treatment for their depressive symptoms. The frequency distribution and factor structure suggest that poststroke GDS scores reflect endorsement of functional losses such as decreased energy and impaired memory and subsequent feelings of helplessness, boredom and social withdrawal rather than decreased positive affect. Treatment should focus on dealing with these issues. Copyright © 2001 John Wiley & Sons, Ltd. [source] Composite estimates of physiological stress, age, and diabetes in American SamoansAMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY, Issue 3 2007Douglas E. Crews Abstract Composite estimates of physiological stress such as allostatic load (AL) were developed to help assess cumulative impacts of psychosocial and physical stressors on the body. Physiological responses to stress generally accelerate somatic wear-and-tear and chronic degenerative conditions (CDCs). Following McEwen (Neuropsychopharmacology 22 (1999) 108,124) and others, primary physiological mediators of somatic stress responses include glucocorticoids (cortisol), catecholamines (adrenaline and noradrenaline), and serum dihydroepiandosterone-sulfate (DHEA-S). Conversely, blood pressure (BP), serum HDL and total cholesterol, glycated hemoglobin (HbA1c), and waist/hip (w/h) ratio are modulated by such hormones, thereby acting as secondary mediators of stress response. When these risk factors are aggregated into a composite score, higher stress loads are associated with increased risks for days of school/work missed, functional losses, morbidity, and mortality in US samples. To examine stress loads in American Samoans, data on all 6 secondary mediators along with estimates of body habitus (i.e. height, weight, circumferences, skinfolds) and physiology (i.e. fasting insulin, LDLc, triglycerides, fasting glucose) were measured on 273 individuals residing on Tutuila Island in 1992. Four combinations of these physiological factors were used to determine composite estimates of stress. These were then assessed by sex for associations with age and the presence of diabetes. Composite estimates of stress load were higher in Samoan women than men. Associations with age tended to be low and negative in men, but positive in women, appearing to reflect cultural circumstances and population history. Stress load scores also were higher among those with diabetes than those without among both men and women. These results suggest that composite estimates of stress may be useful for assessing future risks of CDC's and the senescent processes that may underlie them in cross-cultural research. Am J Phys Anthropol, 2007. © 2007 Wiley-Liss, Inc. [source] | |||||||||||||||||||||||||