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Progressive Loss (progressive + loss)
Selected AbstractsDecreased lymphatic vessel counts in patients with systemic sclerosis: Association with fingertip ulcersARTHRITIS & RHEUMATISM, Issue 5 2010Alfiya Akhmetshina Objective Systemic sclerosis (SSc) is a connective tissue disease that is characterized by microvascular disease and tissue fibrosis. Progressive loss and irregular architecture of the small blood vessels are well characterized, but the potential involvement of the lymphatic vessel system has not been analyzed directly in SSc. This study was undertaken to assess whether the lymphatic vascular system is affected in SSc, and whether changes to the lymphatic vessels are associated with dystrophic changes and tissue damage in patients with SSc. Methods Lymphatic endothelial cells in skin biopsy samples from patients with SSc and age- and sex-matched healthy volunteers were identified by staining for podoplanin and prox-1, both of which are specifically expressed in lymphatic endothelial cells but not in blood vascular endothelial cells. CD31 was used as a pan,endothelial cell marker. Statistical analyses were performed using Kruskal-Wallis, Mann-Whitney U, and Spearman's rank correlation tests. Results The numbers of podoplanin- and prox-1,positive lymphatic vessels were significantly reduced in patients with SSc as compared with healthy individuals. The number of podoplanin-positive lymphatic precollector vessels was significantly lower in SSc patients with fingertip ulcers than in SSc patients without ulcers. Moreover, the number of lymphatic vessels correlated inversely with the number of fingertip ulcers at the time of biopsy and with the number of fingertip ulcers per year. The inverse correlation between lymphatic precollector vessel counts and fingertip ulcers remained significant after statistical adjustment for the blood vessel count, age, and modified Rodnan skin thickness score. Conclusion These results demonstrate a severe reduction in the number of lymphatic capillaries and lymphatic precollector vessels in patients with SSc. Patients with decreased lymphatic vessel counts may be at particularly high risk of developing fingertip ulcers. [source] Longterm visual prognosis in Usher syndrome types 1 and 2ACTA OPHTHALMOLOGICA, Issue 4 2006André M. Sadeghi Abstract. Purpose:, To estimate the age at diagnosis of retinitis pigmentosa and to determine visual acuity deterioration, visual field impairment and the frequency of cataracts in Usher syndrome types 1 and 2. Methods:, We carried out a retrospective study of 328 affected subjects with Usher syndrome types 1 and 2. Study subjects were divided into seven different age groups by decade. Data were analysed using descriptive statistics, general linear model anova and survival analysis. Results:, Retinitis pigmentosa was diagnosed significantly earlier in subjects with Usher syndrome type 1 than in those with type 2. Visual acuity was significantly more impaired in affected subjects with Usher syndrome type 1 than in those with type 2 from 50 years of age onwards. Survival analysis revealed a significant difference in visual field loss (, 10 degrees) between the two groups, with type 2 subjects tending to be more impaired, while comparison indicated no significant differences between the groups in any of the other visual field categories. Cataract was found to be generally more common in Usher syndrome type 1 than type 2. Conclusions:, Progressive loss of visual acuity and visual field begins to be substantial between the second and third decades of life in both Usher types. The rate of degeneration varies between individuals in both groups. The data are useful for the counselling of affected subjects with Usher syndrome types 1 and 2. [source] Forearm and leg amino acid metabolism in the basal state and during combined insulin and amino acid stimulation after a 3-day fastACTA PHYSIOLOGICA, Issue 3 2009J. Gjedsted Abstract Aim:, Fasting is characterized by a progressive loss of protein, but data on protein kinetics are unclear and few have studied the effects of re-feeding. The present study was designed to test the hypothesis that a combined infusion of insulin and amino acids after fasting would induce compensatory increases in protein synthesis and reductions in protein breakdown at the whole body level and in muscle. Methods:, We included 10 healthy male volunteers and studied them twice: (1) in the post-absorptive state and (2) after 72 h of fasting. Amino acid kinetics was measured using labelled phenylalanine and tyrosine, whole body energy expenditure was assessed and urea nitrogen synthesis rates were calculated. Results:, After fasting we observed an increase in arterial blood concentration of branched chain amino acids and a decrease in gluconeogenic amino acids (P < 0.05). Isotopically determined whole body, forearm and leg phenylalanine fluxes were unaltered apart from a 30% decrease in phenylalanine-to-tyrosine conversion (2.0 vs. 1.4 ,mol kg,1 h,1, P < 0.01). During infusion of insulin and amino acids, amino acid concentrations increased. Conclusion:, Our data indicate that after a 72-h fast basal and insulin/amino acid-stimulated regional phenylalanine fluxes in leg and forearm muscle are unaltered. During fasting concentrations of gluconeogenic amino acids decrease and hepatic and/or renal phenylalanine-to-tyrosine conversion decreases. Thus, as opposed to glucose and lipid metabolism, fasting does not induce insulin resistance as regards amino acid metabolism. [source] Why insulin sensitizers but not secretagogues should be retained when initiating insulin in type 2 diabetesDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 1 2008Philip Raskin Abstract The stringent targets set for HbA1c levels in type 2 diabetes are currently achieved by fewer than half the patients in the United States. Failure to manage hyperglycaemia in the early stages of disease results in progressive loss of ,-cell function, which ultimately necessitates the initiation of insulin therapy. At this point, choices have to be made on whether to continue oral anti-diabetic drug therapy and, if so, with which agent(s). Historically, sulfonylureas have been the mainstay of oral anti-diabetic drug therapy; however, their long-term efficacy in patients with depleted ,-cell capacity is doubtful, and other classes of oral anti-diabetic drugs, notably the insulin sensitizers, may prove more reliable. These agents (metformin and thiazolidinediones) appear to provide various benefits over and above sustained glycaemic control, which may variably include reduced loss of ,-cell function as well as improvements to cardiovascular risk factors, morbidity, and mortality. Metformin also limits weight gain associated with insulin therapy. This manuscript presents the case that when insulin therapy is initiated it should be tailored to individual needs through combination with one or more insulin sensitizers rather than a secretagogue. Copyright © 2007 John Wiley & Sons, Ltd. [source] Immunohistochemical expression of E-cadherin in sclerosing adenosis, ductal carcinoma in situ and invasive ductal carcinoma of the breastDIAGNOSTIC CYTOPATHOLOGY, Issue 4 2010Gil Facina M.D., Ph.D. Abstract E-cadherin (EC) is an important glycoprotein cell-adhesion molecule that appears to play a significant role in the progression of breast lesions. The objective of this study was to evaluate EC expression in sclerosing adenosis, ductal carcinoma in situ and invasive ductal carcinoma. Samples of breast lesions from 44 women were used in this study, comprising cases of sclerosing adenosis (n = 11), ductal carcinoma in situ (DCIS) (n = 10) and invasive ductal carcinoma (n = 23). Immunohistochemical evaluation of EC expression was assessed semiquantitatively and considered negative (<10% of cells with stained cytoplasmic membranes), positive+ (10,50% of cells stained) or positive++ (> 50% of cells stained). Fisher's exact test was used to compare the distribution of staining intensity in the lesions (P< 0.05). There was a progressive loss of EC expression from benign to malignant lesions. This difference was statistically significant when sclerosing adenosis was compared with DCIS (P < 0.0002), when sclerosing adenosis was compared with invasive ductal carcinoma (P < 0.008) and when DCIS was compared with invasive ductal carcinoma (P < 0.007). The present findings point to a significant association between reduced EC expression and the progression and aggressivity of breast lesions. Diagn. Cytopathol. 2010. © 2009 Wiley-Liss, Inc. [source] Persistent inhibition of human natural killer cell function by ziram and pentachlorophenolENVIRONMENTAL TOXICOLOGY, Issue 4 2005Thyneice R. Taylor Abstract Ziram is a currently used agricultural fungicide. It is also used as an additive in the production of latex gloves. Because of these uses, there is a potential for human exposure to this compound. Pentachlorophenol (PCP) has been used as an insecticide, fungicide, disinfectant, and ingredient in antifouling paints. Currently, it is used as a wood preservative for power-line poles and fence posts. Measurable levels of PCP have been detected in human blood and urine. In previous studies we demonstrated that both these compounds could cause very significant inhibition of the tumor-killing function of human natural killer (NK) cells. NK lymphocytes play a central role in immune defense against viral infection and the formation of primary tumors. So interference with their function could increase the risk of tumor development. In the present study we examined the effects of exposure to ziram or PCP of brief duration (1 h) on the ability of NK cells to destroy tumor cells. NK cells were exposed to either ziram (5,0.5 ,M) or PCP (10,5 ,M) for 1 h followed by 0 h, 24 h, 48 h, or 6 days in compound-free media and then were tested for the ability to lyse as well as to bind tumor cells. A 1-h exposure to as little as 2.5 ,M ziram decreased the ability of NK cells to lyse target tumor cells, which persisted up to 6 days following exposure. The loss of lytic function for from 24 h to 6 days following exposure was accompanied by a comparable loss of NK capacity to bind tumor cells. Exposure to 10 ,M PCP for 1 h caused a progressive loss (greater than 80%) of lytic function within 6 days of exposure. In contrast to ziram, PCP exposure caused no accompanying loss of binding function. © 2005 Wiley Periodicals, Inc. Environ Toxicol 20: 418,424, 2005. [source] Long-term survey of laryngoplasty and ventriculocordectomy in an older, mixed-breed population of 200 horses.EQUINE VETERINARY JOURNAL, Issue 4 2003Part 1: Maintenance of surgical arytenoid abduction, complications of surgery Summary Reasons for performing study: Laryngoplasty (LP) is currently the most common surgical treatment for equine laryngeal paralysis, however, there have been no reports quantifying the degree of retention of arytenoid abduction following L P. ADitionally, the complications of LP have been poorly documented. Objectives: To record the degree of arytenoid abduction retention following LP and to accurately document all complications of surgery. Methods: A study (1986,1998) of 200 horses of mixed breed and workload, median age 6 years (prospective 136 cases and retrospective 64 cases) undergoing LP (using 2 stainless steel wires) and combined ventriculocordectomy was undertaken; 198 owners completed questionnaires, a median of 19 months following surgery. The degree of arytenoid abduction achieved was endoscopically, semi-quantitatively evaluated using a 5-grade system, at 1 day, 7 days, and 6 weeks after surgery. Results: On the day following LP, 62% of horses had good (median grade 2) arytenoid abduction, 10% had excessive (grade 1), and 5% had minimal (grade 4) abduction (overall - median grade 2). Due to progressive loss of abduction, moderate (median grade 3, range 1,5) abduction was present overall at 1 and 6 weeks after LP. Further surgery was required to re-tighten prostheses in 10% of cases with excessive loss of abduction, or to loosen prostheses in 7% of horses which had continuing high levels of LP abduction and significant post operative dysphagia. LP wound problems (mainly seromas and suture abscesses) were reported to last <2 weeks in 9% of cases, <4 weeks in 4% and >4 weeks in 4%. The (partially sutured) laryngotomy wounds discharged post operatively for <2 weeks in 22% of cases, <4 weeks in 7% and for >4 weeks in 2%. Coughing occurred at some stage post operatively in 43% of cases and its presence correlated significantly with the degree of surgical arytenoid abduction. This coughing occurred during eating in 24% of cases and was not associated with eating (or dysphagia) in the other 19% of cases. Chronic (>6 months duration) coughing occurred in 14% of cases, but appeared to be due to intercurrent pulmonary disease in half of these horses. Conclusions: Suturing the cricotracheal membrane allows most laryngotomy wounds to heal quickly. Laryngoplasty wound problems were of little long-term consequence when stainless steel wire prostheses were used. Potential relevance: A significant loss of LP abduction occurs in most horses in the 6 weeks following surgery and efforts should be made to find ways to prevent such loss. However, excessive LP abduction is associated with post operative dysphagia and coughing. [source] Clinical and imaging characterization of a patient with idiopathic progressive ataxia and palatal tremorEUROPEAN JOURNAL OF NEUROLOGY, Issue 8 2007R. Cilia We describe clinical and imaging features of a patient with sporadic progressive ataxia and palatal tremor (PAPT) of unknown etiology. There was hypertrophy of bilateral inferior olivary nuclei with hyperintense T2-weighted signal and mild cerebellar atrophy at brain magnetic resonance imaging. 18F-fluoro-2-desoxy- d -glucose positron emission tomography scanning (FDG-PET) showed hypometabolism in the red nucleus, external globus pallidus and precuneus while FP-CIT-SPECT imaging revealed mild and progressive loss of striatal dopaminergic terminals. Our findings suggest that in idiopathic PAPT involvement of the dentato-rubro-olivary pathway occurs along with some dopaminergic dysfunction. [source] Examination of intravenous and intra-CSF protein delivery for treatment of neurological diseaseEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2009Kim M. Hemsley Abstract Mucopolysaccharidosis type IIIA is a neurodegenerative lysosomal storage disorder characterized by progressive loss of learned skills, sleep disturbance and behavioural problems. Absent or greatly reduced activity of sulphamidase, a lysosomal protein, results in intracellular accumulation of heparan sulphate. Subsequent neuroinflammation and neurodegeneration typify this and many other lysosomal storage disorders. We propose that intra-cerebrospinal fluid protein delivery represents a potential therapeutic avenue for treatment of this and other neurodegenerative conditions; however, technical restraints restrict examination of its use prior to adulthood in mice. We have used a naturally-occurring Mucopolysaccharidosis type IIIA mouse model to determine the effectiveness of combining intravenous protein replacement (1 mg/kg) from birth to 6 weeks of age with intra-cerebrospinal fluid sulphamidase delivery (100 ,g, fortnightly from 6 weeks) on behaviour, the level of heparan sulphate-oligosaccharide storage and other neuropathology. Mice receiving combination treatment exhibited similar clinical improvement and reduction in heparan sulphate storage to those only receiving intra-cerebrospinal fluid enzyme. Reductions in micro- and astrogliosis and delayed development of ubiquitin-positive lesions were seen in both groups. A third group of intravenous-only treated mice did not exhibit clinical or neuropathological improvements. Intra-cerebrospinal fluid injection of sulphamidase effectively, but dose-dependently, treats neurological pathology in Mucopolysaccharidosis type IIIA, even when treatment begins in mice with established disease. [source] The mouse MPTP model: gene expression changes in dopaminergic neuronsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2003Kati Kühn Abstract Parkinson's disease (PD) is a common neurodegenerative disorder, characterized by the progressive loss of dopaminergic neurons in the substantia nigra. Although valuable animal models have been developed, our knowledge of the aetiology and pathogenic factors implicated in PD is still insufficient to develop causal therapeutic strategies aimed at halting its progression. The neurotoxicity induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is one of the most valuable models for analysing pathological aspects of PD. In this paper we studied the gene expression patterns underlying the pathogenesis of MPTP-induced neurodegeneration. We treated young and old C57BL/6 mice with different schedules of MPTP to induce degenerative processes that vary in intensity and time-course. During the first week after intoxication we used nonradioactive in situ -hybridization to investigate the expression patterns of genes associated with (i) dopamine metabolism and signalling; (ii) familial forms of PD; (iii) protein folding and (iv) energy metabolism. MPTP injections induced different severities of neuronal injury depending on the age of the animals and the schedule of administration as well as a significant degeneration in the striatum. In situ hybridization showed that MPTP intoxication initiated a number of gene expression changes that (i) were restricted to the neurons of the substantia nigra pars compacta; (ii) were correlated in intensity and number of changes with the age of the animals and the severity of histopathological disturbances; (iii) displayed in each a significant down-regulation by the end of one week after the last MPTP injection, but (iv) varied within one MPTP regimen in expression levels during the observation period. The subacute injection of MPTP into one-year-old mice induced the most severe changes in gene expression. All genes investigated were affected. However, ,-synuclein was the only gene that was exclusively up-regulated in MPTP-treated animals displaying cell death. [source] Deposition of chromatin-IgG complexes in skin of nephritic MRL-lpr/lpr mice is associated with increased local matrix metalloprotease activitiesEXPERIMENTAL DERMATOLOGY, Issue 8 2010Annica Hedberg Please cite this paper as: Deposition of chromatin-IgG complexes in skin of nephritic MRL-lpr/lpr mice is associated with increased local matrix metalloprotease activities. Experimental Dermatology 2010; 19: e265,e274. Abstract:, Chromatin-IgG complexes appear as electron dense structures (EDS) in glomerular basement membranes in lupus nephritis. Here, we present results of comparative analyses of the composition of EDS in murine lupus dermatitis and nephritis. One focus was to perform an analytical approach to understand why such complex structures bind skin basement membrane components. Transcription of skin membrane-encoding genes was analysed to see if expression of such genes was increased, eventually indicating that binding capacity of immune complexes increased when dermatitis developed. Variations in matrix metalloprotease 2 (MMP2), MMP9 and Dnase1 mRNA levels and enzymatic activities were correlated with circulatory chromatin-IgG complexes and deposition in skin. We also examined if glomerular deposits of EDS predicted similar deposits in skin of (NZB × NZW)F1 or MRL-lpr/lpr mice, as we observed chromatin-IgG complexes in capillary lumina in skin and glomeruli in both strains. EDS consisting of chromatin fragments and IgG were found sub-epidermally in skin with LE-like lesions of end-stage nephritic MRL-lpr/lpr mice. Dermal MMP-encoding genes were up-regulated during disease progression, and gelatinolytic activity was increased in affected skin. Dnase1 mRNA level and total nuclease activity remained stable in skin during the disease, in contrast to progressive loss of renal Dnase1 mRNA and total renal nuclease activity during development of nephritis. Loss of renal Dnase1 may explain release of chromatin fragments, while increased MMP activity may disrupt membranes making them accessible for chromatin fragment-IgG complexes. Circulatory chromatin-IgG complexes, and up-regulated intradermal MMP activity may be crucial for deposition of immune complexes in skin of lupus-prone mice. [source] Canopy recovery after drought dieback in holm-oak Mediterranean forests of Catalonia (NE Spain)GLOBAL CHANGE BIOLOGY, Issue 12 2004Francisco Lloret Abstract Climate change is likely to produce more frequent and longer droughts in the Mediterranean region, like that of 1994, which produced important changes in the Quercus ilex forests, with up to 76% of the trees showing complete canopy dieback. At the landscape level, a mosaic of responses to the drought was observed, linked to the distribution of lithological substrates. Damage to the dominant tree species (Q. ilex) and the most common understorey shrub (Erica arborea) was more noticeable on the compact substrates (breccia) than on the fissured ones (schist). This result was consistent with observations documenting deeper root penetration in schist than in breccia materials, allowing the plants growing on fissured substrates to use water from deeper soil levels. Smaller plants were more vulnerable to drought than larger plants in the trees, but not in the shrubs. Overall, Q. ilex was more affected than E. arborea. The resilience of the system was evaluated from the canopy recovery 1 year after the episode. Stump and crown resprouting was fairly extensive, but the damage pattern in relation to substrate, plant size, and species remained similar. The effect of recurrent drought episodes was studied on vegetation patches of Q. ilex located on mountain slopes and surrounded by bare rock. We observed that plants that resprouted weakly after a previous drought in 1985 were more likely to die or to produce poor regeneration in 1995 than plants that had resprouted vigorously. Vegetation patches located on the lower part of the slope were also less damaged than patches situated uphill. The study provides evidence of relevant changes in forest canopy as a consequence of extreme climate events. The distribution of this effect across the landscape is mediated by lithological substrate, causing patchy patterns. The results also support the hypothesis that recurrent droughts can produce a progressive loss of resilience, by depleting the ability of surviving plants to regenerate. [source] Disrupted B-lymphocyte development and survival in interleukin-2-deficient miceIMMUNOLOGY, Issue 2 2001Michael Schultz Summary Interleukin-2-deficient (IL-2,/,) mice develop a spontaneous, progressive, CD4+ T-cell-mediated colitis with an age-related decrease in the number of B lymphocytes. The aim of this study was to determine the mechanisms of B-cell loss in IL-2,/, mice. Serum immunoglobulin G1 (IgG1) levels in 8-week-old IL-2,/, mice were above normal but then decreased dramatically with advancing age. Between 8 and 11 weeks of age, the number of B-cell progenitors (B220+ IgM,) in the bone marrow of IL-2,/, mice was less than half of those in IL-2+/+ littermates. By 22 weeks of age, very few progenitor cells remained in the bone marrow of most mice, and spleens were almost devoid of B cells. Likewise, B1 cells were not present in the peritoneal cavity of aged IL-2,/, mice. Flow cytometry analysis of B-cell differentiation in the bone marrow suggested a progressive loss of B cells from the most mature to the least mature stages, which was not dependent on IL-2 receptor-, (IL-2R,) expression. B cells transferred from normal animals had similar survival rates in IL-2,/, and wild-type mice. We conclude that conventional B cells in older IL-2,/, mice are lost by attrition owing to a derangement in B-cell development. Because B1 cells are less dependent on the bone marrow, a separate mechanism for their loss is suggested. [source] The transitional object in dementia: clinical implicationsINTERNATIONAL JOURNAL OF APPLIED PSYCHOANALYTIC STUDIES, Issue 2 2007Sheila LoboPrabhu Abstract The concept of the transitional object in human development was first proposed by Winnicott, and it has been extensively discussed in the child psychoanalytic literature. However, there are very few empirical studies on the transitional object in adult development. The transitional object has been discussed in relation to medical illness, medication, aggression, dreams, spirituality and religion, borderline personality disorder, anxiety disorder, fetishes, medication, and body image. There is very little literature on the transitional object in dementia. Dementia is a process of transition from a healthy, active state to a dependent state with progressive loss of memory, functional skills, and independence. Patients and families experience grief, loss, fear, anxiety, guilt, and anger. In this article, we address the role of the transitional object in dementia. We discuss the concepts of the transitional object and precursor object, and their possible role in interventions with patients and caregivers. We discuss various aspects of the therapeutic process and treatment setting, which may serve as transitional objects in various stages of dementia. The therapeutic relationship serves as the "holding environment" in which various transitions may be safely accomplished. Copyright © 2007 John Wiley & Sons, Ltd. [source] High tumor tissue concentration of urokinase plasminogen activator receptor is associated with good prognosis in patients with ovarian cancerINTERNATIONAL JOURNAL OF CANCER, Issue 4 2003Christer Borgfeldt Abstract The urokinase plasminogen activator (uPA) system is involved in tumor growth and metastasis. We assayed the components of the uPA system in homogenates of 64 primary epithelial ovarian tumors and 5 metastases and evaluated the association of these parameters to prognosis in the 51 malignant cases. The levels of uPA, PAI-2 and the uPA:PAI-1 complex increased with progressive loss of histological differentiation (ptrend <0.001, <0.05 and <0.001). The level of PAI-1 was higher in poorly than in well/moderately differentiated tumors (p = 0.03). The content of uPAR was lower in benign tumors as compared to borderline malignancies (p = 0.002), invasive primary tumors (p < 0.001), and metastases (p = 0.002). Surprisingly, the level of uPAR was lower in poorly differentiated as compared to both borderline (p = 0.01) and well differentiated malignant tumors (p = 0.005). Also, the level of uPAR was lower in advanced as compared to early stages of the disease (ptrend = 0.002). The median follow-up time for patients was 5.8 years. High tumor tissue levels of uPAR were associated with longer postoperative survival (HR = 0.4, 95% CI = 0.2,0.8, p = 0.01). In contrast, shorter survival was evident in patients with high tumor levels of uPA from 2 years on after operation (HR = 4.6, 95% CI = 1.2,17, p = 0.02). High tPA levels tended to be associated with shorter overall survival after 2 years (HR = 2.9, 95% 95% CI = 0.9,9.8, p = 0.08). Although high tumor tissue content of uPAR was associated with a less aggressive phenotype characterized by well differentiated histology and longer survival, low content of uPAR in the poorly differentiated tumors and metastases presumably results from increased elimination of uPAR. © 2003 Wiley-Liss, Inc. [source] Analysis of hair lipids and tensile properties as a function of distance from scalpINTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 4 2005L. Duvel Synopsis Cuticle cells form the outer covering surrounding and protecting the cortex. The cuticle cells are thin, flat and overlap, and intercellular lipid lamellae are found in the gaps between the cell boundaries. The lipid lamellae are also found within the cortex in the cell boundaries between the long fribrous corticle cells. In addition, the outer surfaces of the cuticle cells are covered by a monolayer of covalently bound fatty acids, a major component of which is 18-methyleicosanoic acid. The fatty acids are thought to be attached through thio-ester linkages. Together these lipids are thought to be major determinants of the physical properties of the hair. The present study tested the hypothesis that both free and covalently bound lipids are progressively lost during normal environmental exposures. This progressive loss within the cuticle layers may, in part, lead to an increased susceptibility of the protein and lipid lamellae in the cortex to degradation. This degradation, in turn, would contribute to a progressive decrease in the tensile properties of the hair. Research grade hair was cut into five segments from the root to the distal end. Lipids from each segment were extracted and analyzed by thin-layer chromatography in conjunction with photodensitometry. The major free polar lipid classes in the hair included ceramides, glucosylceramides and cholesterol sulfate. The concentrations of all of the free polar lipids as well as the covalently bound fatty acids decreased in going from the root to the distal end of the hair. In addition, there was a significant reduction in tensile properties of the hair from the root to distal end. In conclusion, the progressive loss of endogenous free and covalently bound lipids from hair, which are probably related to normal weathering of the hair and grooming practices, may help contribute to a marked decrease in tensile properties to the hair. Résumé Les cellules de la cuticule forment le revêtement externe qui protège le cortex des cheveux. Les cellules de la cuticule sont minces, plates et se chevauchent. De fines couches de lipides sont présentes dans le matériau assurant la jonction entre les cellules cuticulaires. D'autres fines couches de lipides sont également présentes dans les espaces intercellulaires du cortex, entre les longues cellules corticales fibreuses. De plus, les surfaces externes des cellules de la cuticule sont recouvertes d'une couche monomoléculaire d'acides gras liés par covalence, un des composants majoritaires étant l'acide 18-méthyleicosanoique. On pense que ces acides gras sont fixés par liaisons thioesters. On pense également que l'ensemble de ces lipides joue un rôle important sur les propriétés physiques du cheveu. L'hypothèse testée dans cette étude est que les lipides libres et ceux liés par covalence sont progressivement éliminés lors de l'exposition normale des cheveux à l'environnement extérieur. Cette délipidation progressive de la cuticule pourrait, en partie, entraîner une plus grande sensibilité des constituants lipidiques et protéiniques du cortex aux agressions externes et accroître leur dégradation. Cette dégradation, à son tour, contribuerait à une diminution progressive des propriétés mécaniques en extension des cheveux. Des cheveux de provenance commerciale ont été coupés en cinq segments de leur racine à leur extrémité distale. Les lipides de chaque segment ont été extraits, séparés par chromatographie couche mince et dosés par densitométrie photographique. Les classes majoritaires de lipides polaires libres sont constituées de céramides, de glucosylcéramides et de sulfate de cholestérol. Les teneurs de tous les lipides polaires libres ainsi que des acides gras liés par covalence diminuent de la racine à l'extrémité distale du cheveu. De plus, on constate une réduction considérable des propriétés mécaniques en extension des cheveux de la racine à l'extrémité distale.-.En conclusion, la perte progressive des lipides endogènes libres et liés par covalence, probablement attribuables aux expositions à l'environnement et au stress des traitements capillaires peut aider à contribuer à une baisse marquée des propriétés mécaniques en extension des cheveux. [source] Therapeutic effects of long-term administration of an oral adsorbent in patients with chronic renal failure: two-year studyINTERNATIONAL JOURNAL OF UROLOGY, Issue 1 2005NOBUYOSHI TAKAHASHI Abstract Background:, Kremezin is an oral adsorbent that attenuates the progression of chronic renal failure by removing uremic toxins and their precursors from the gastrointestinal tract. Previously two clinical studies based on reciprocal serum creatinine levels (1/Scr) have confirmed the efficacy of Kremezin (Kureha Chemical, Tokyo, Japan) in undialyzed patients who had been followed up for 6 months or 1 year. This is the first report to evaluate the therapeutic effects of long-term administration (2 years.) of Kremezin in undialyzed patients. Methods:, Kremezin was given to 48 enrolled undialyzed patients with a median Scr level of 4.3 mg/dL. Rates of decline of 1/Scr, as well as the time for Scr level to reach 10 mg/dL, the critical value requiring dialysis, were compared before and after administration of Kremezin. Results:, During the 2-year therapeutic period, 1/Scr gradients were significantly attenuated (P = 0.0083), and the estimated time to dialysis was prolonged from 16.3 ± 16.3 months to 29.8 ± 24.1 months (P = 0.002). When the patients were divided into two groups, based on of systolic blood pressure (SBP), defined by the World Health Organization (WHO) classification, a significantly smaller number of patients in the low blood pressure group (SBP < 160 mmHg) were introduced to dialysis (P = 0.0005), and the estimated time to dialysis was significantly extended in the low blood pressure group (P = 0.0125). Conclusion:, In addition to the control of blood pressure in undialyzed patients, Kremezin has additive salutary effects to halt the progressive loss of renal function, resulting in the delay of dialysis. [source] The Assembly and Remodeling of the Extracellular Matrix in the Growth Plate in Relationship to Mineral Deposition and Cellular Hypertrophy: An In Situ Study of Collagens II and IX and Proteoglycan,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 2 2002Fackson Mwale Abstract The recent development of new specific immunoassays has provided an opportunity to study the assembly and resorption of type II and IX collagens of the extracellular matrix in relationship to endochondral calcification in situ. Here, we describe how in the bovine fetal physis prehypertrophic chondrocytes deposit an extensive extracellular matrix that, initially, is rich in both type II and type IX collagens and proteoglycan (PG; principally, aggrecan). The majority of the ,1(IX)-chains lack the NC4 domain consistent with our previous studies with cultured chondrocytes. During assembly, the molar ratio of type II/COL2 domain of the ,1(IX)-chain varied from 8:1 to 25:1. An increase in the content of Ca2+ and inorganic phosphate (Pi) was initiated in the prehypertrophic zone when the NC4 domain was removed selectively from the ,1(IX)-chain. This was followed by the progressive loss of the ,1(IX) COL2 domain and type II collagen. In the hypertrophic zone, the Ca2+/Pi molar ratio ranged from 1.56 to a maximum of 1.74, closely corresponding to that of mature hydroxyapatite (1.67). The prehypertrophic zone had an average ratio Ca2+/Pi ranging from 0.25 to 1, suggesting a phase transformation. At hypertrophy, when mineral content was maximal, type II collagen was reduced maximally in content coincident with a peak of cleavage of this molecule by collagenase when matrix metalloproteinase 13 (MMP-13) expression was maximal. In contrast, PG (principally aggrecan) was retained when hydroxyapatite was formed consistent with the view that this PG does not inhibit and might promote calcification in vivo. Taken together with earlier studies, these findings show that matrix remodeling after assembly is linked closely to initial changes in Ca2+ and Pi to subsequent cellular hypertrophy and mineralization. These changes involve a progressive and selective removal of types II and IX collagens with the retention of the PG aggrecan. [source] Lack of inhibitory effects of the anti-fibrotic drug imatinib on endothelial cell functions in vitro and in vivoJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 10 2009Paulius Venalis Abstract Systemic sclerosis (SSc) is a systemic autoimmune disease that is characterized by microangiopathy with progressive loss of capillaries and tissue fibrosis. Imatinib exerts potent anti-fibrotic effects and is currently evaluated in clinical trials. The aim of the present study was to exclude that the anti-fibrotic effects of imatinib are complicated by inhibitory effects on endothelial cell functions, which might augment vascular disease in SSc. Endothelial cells and mice were treated with pharmacologically relevant concentrations of imatinib. The expression of markers of vascular activation was assessed with real-time PCR. Proliferation was analysed with the cell counting experiments and the MTT assay. Apoptosis was quantified with caspase 3 assays, annexin V in vitro and with TUNEL staining in vivo. Migration was studied with scratch and transwell assays. Tube forming was investigated with the matrigel assay. Imatinib did not alter the expression of markers of vascular activation. Imatinib did not increase the percentage of annexin V positive cells or the activity of caspase 3. No reduction in proliferation or metabolic activity of endothelial cells was observed. Imatinib did not affect migration of endothelial cells and did not reduce the formation of capillary tubes. Consistent with the in vitro data, no difference in the number of apoptotic endothelial cells was observed in vivo in mice treated with imatinib. Imatinib does not inhibit activation, viability, proliferation, migration or tube forming of endothelial cells in vitro and in vivo. Thus, treatment with imatinib might not augment further endothelial cell damage in SSc. [source] Src promotes delta opioid receptor (DOR) desensitization by interfering with receptor recyclingJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 1 2009Elodie Archer-Lahlou Abstract An important limitation in the clinical use of opiates is progressive loss of analgesic efficacy over time. Development of analgesic tolerance is tightly linked to receptor desensitization. In the case of delta opioid receptors (DOR), desensitization is especially swift because receptors are rapidly internalized and are poorly recycled to the membrane. In the present study, we investigated whether Src activity contributed to this sorting pattern and to functional desensitization of DORs. A first series of experiments demonstrated that agonist binding activates Src and destabilizes a constitutive complex formed by the spontaneous association of DORs with the kinase. Src contribution to DOR desensitization was then established by showing that pre-treatment with Src inhibitor PP2 (20 ,M; 1 hr) or transfection of a dominant negative Src mutant preserved DOR signalling following sustained exposure to an agonist. This protection was afforded without interfering with endocytosis, but suboptimal internalization interfered with PP2 ability to preserve DOR signalling, suggesting a post-endocytic site of action for the kinase. This assumption was confirmed by demonstrating that Src inhibition by PP2 or its silencing by siRNA increased membrane recovery of internalized DORs and was further corroborated by showing that inhibition of recycling by monensin or dominant negative Rab11 (Rab11S25N) abolished the ability of Src blockers to prevent desensitization. Finally, Src inhibitors accelerated recovery of DOR-G,l3 coupling after desensitization. Taken together, these results indicate that Src dynamically regulates DOR recycling and by doing so contributes to desensitization of these receptors. [source] Submerged healing following surgical treatment of peri-implantitis: a case seriesJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 8 2007Ann-Marie Roos-Jansåker Abstract Objectives: The aim was to study a regenerative surgical treatment modality for peri-implantitis employing submerged healing. Material and Methods: Twelve patients, having a minimum of one osseointegrated implant with peri-implantitis, with a progressive loss of 3 threads (1.8 mm) following the first year of healing were involved in the study. After surgical exposure of the defect, granulomatous tissue was removed and the implant surface was treated using 3% hydrogen peroxide. The bone defects were filled with a bone substitute (Algipore®), a resorbable membrane (Osseoquest®) was placed over the grafted defect and a cover screw was connected to the fixture. The implant was then covered by flaps and submerged healing was allowed for 6 months. After 6 months the abutment was re-connected to the supra-structure. Results: A 1-year follow-up demonstrated clinical and radiographic improvements. Probing depth was reduced by 4.2 mm and a mean defect fill of 2.3 mm was obtained. Conclusion: Treatment of peri-implant defects using a bone graft substitute combined with a resorbable membrane and submerged healing results in defect fill and clinical healthier situations. [source] Surgical treatment of peri-implantitis using a bone substitute with or without a resorbable membrane: a prospective cohort studyJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 7 2007Ann-Marie Roos-Jansåker Abstract Objectives: The aim of this prospective cohort study was to compare two regenerative surgical treatment modalities for peri-implantitis. Material and Methods: Thirty-six patients having a minimum of one osseointegrated implant, with a progressive loss of bone amounting to 3 threads (1.8 mm) following the first year of healing, combined with bleeding and/or pus on probing, were involved in this study. The patients were assigned to two different treatment strategies. After surgical exposure of the defect, granulomatous tissue was removed and the infected implant surface was treated using 3% hydrogen peroxide. The bone defects were filled with a bone substitute (Algipore®). In 17 patients (Group 1), a resorbable membrane (Osseoquest®) was placed over the grafted defect before suturing. In 19 patients (Group 2), the graft was used alone. Results: One-year follow-up demonstrated clinical and radiographic improvements. Probing depths were reduced by 2.9 mm in Group 1 and by 3.4 mm in Group 2. Defect fill amounted to 1.5 and 1.4 mm, respectively. There was no significant difference between the groups. Conclusion: It is possible to treat peri-implant defects with a bone substitute, with or without a resorbable membrane. [source] Increasing Expression of the Retinoic X Receptor-B During Malignant Melanoma ProgressionJOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2005S.J. McAlhany Retinoic X receptor-b (RXR-b) is a heterodimerization partner for vitamin D receptor (VDR). 1,25-dihydroxyvitamin D3 activation of VDR leads to growth inhibition in numerous cell lines, including some melanoma lines. Evaluation of VDR and RXR-b expression in vivo in melanocytic neoplasms will increase our understanding of this pathways potential role in growth control. Previous studies in our laboratory showed decreased VDR expression in superficially invasive melanoma, and progressive loss of expression in deeply invasive melanomas and metastatic melanomas (MET). We next sought to evaluate RXR-b expression. Twenty-eight melanocytic neoplasms including 8 melanomas in situ (MIS), 9 primary invasive melanomas (PIM), and 11 MET were evaluated for RXR-b expression by immunohistochemistry. Nuclear labeling was assessed as 0 (0%), 1+(<5%), 2+(>5% but <50%), or 3+(>=50%). A significant increase in RXR-b expression from low (0,1+) to high (>1+) was found when comparing MIS to PIM and MET (chi2 p < 0.05). These data suggest: 1) potential loss of 1,25-dihydroxyvitamin D3 induced growth inhibition during melanoma progression may be due to decreased VDR expression without concomitant loss of RXR-b; and 2) increased RXR-b expression during melanoma progression may offer selective advantage through alternative signaling pathways. [source] Declining expression of a single epithelial cell-autonomous gene accelerates age-related thymic involutionAGING CELL, Issue 3 2010Liguang Sun Summary Age-related thymic involution may be triggered by gene expression changes in lymphohematopoietic and/or nonhematopoietic thymic epithelial cells (TECs). The role of epithelial cell-autonomous gene FoxN1 may be involved in the process, but it is still a puzzle because of the shortage of evidence from gradual loss-of-function and exogenous gain-of-function studies. Using our recently generated loxP -floxed- FoxN1(fx) mouse carrying the ubiquitous CreERT (uCreERT) transgene with a low dose of spontaneous activation, which causes gradual FoxN1 deletion with age, we found that the uCreERT -fx/fx mice showed an accelerated age-related thymic involution owing to progressive loss of FoxN1+ TECs. The thymic aging phenotypes were clearly observable as early as at 3,6 months of age, resembling the naturally aged (18,22-month-old) murine thymus. By intrathymically supplying aged wild-type mice with exogenous FoxN1-cDNA, thymic involution and defective peripheral CD4+ T-cell function could be partially rescued. The results support the notion that decline of a single epithelial cell-autonomous gene FoxN1 levels with age causes primary deterioration in TECs followed by impairment of the total postnatal thymic microenvironment, and potentially triggers age-related thymic involution in mice. [source] Neuroprotective effects of hydrogen sulfide on Parkinson's disease rat modelsAGING CELL, Issue 2 2010Li-Fang Hu Summary Parkinson's disease (PD) is a neurodegenerative disorder characterized by a progressive loss of dopaminergic neurons in the substantia nigra (SN). The present study was designed to examine the therapeutic effect of hydrogen sulfide (H2S, a novel biological gas) on PD. The endogenous H2S level was markedly reduced in the SN in a 6-hydroxydopamine (6-OHDA)-induced PD rat model. Systemic administration of NaHS (an H2S donor) dramatically reversed the progression of movement dysfunction, loss of tyrosine-hydroxylase positive neurons in the SN and the elevated malondialdehyde level in injured striatum in the 6-OHDA-induced PD model. H2S specifically inhibited 6-OHDA evoked NADPH oxidase activation and oxygen consumption. Similarly, administration of NaHS also prevented the development of PD induced by rotenone. NaHS treatment inhibited microglial activation in the SN and accumulation of pro-inflammatory factors (e.g. TNF-, and nitric oxide) in the striatum via NF-,B pathway. Moreover, significantly less neurotoxicity was found in neurons treated with the conditioned medium from microglia incubated with both NaHS and rotenone compared to that with rotenone only, suggesting that the therapeutic effect of NaHS was, at least partially, secondary to its suppression of microglial activation. In summary, we demonstrate for the first time that H2S may serve as a neuroprotectant to treat and prevent neurotoxin-induced neurodegeneration via multiple mechanisms including anti-oxidative stress, anti-inflammation and metabolic inhibition and therefore has potential therapeutic value for treatment of PD. [source] PPAR: a therapeutic target in Parkinson's diseaseJOURNAL OF NEUROCHEMISTRY, Issue 2 2008Rajnish K. Chaturvedi Abstract Parkinson's disease (PD) is a progressive and chronic neurodegenerative disorder, characterized by progressive loss of dopaminergic neurons in substantia nigra. The etiology and pathogenesis of PD is still elusive, however, a large body of evidence suggests a prominent role of oxidative stress, inflammation, apoptosis, mitochondrial dysfunction and proteosomal dysfunction in the pathogenesis of PD. Due to multifactorial nature of the disease, currently available drug therapy cannot halt / slow down the disease progression, and only provides symptomatic relief. Peroxisome proliferator-activated receptor (PPAR), a member of nuclear receptor superfamily, regulates development, tissue differentiation, inflammation, mitochondrial function, wound healing, lipid metabolism and glucose metabolism. Recently, several PPAR agonists were shown to exert neuroprotective activity against oxidative damage, inflammation and apoptosis in several neurodegenerative disorders including Alzheimer's, Parkinson's, Huntington's, amyotrophic lateral sclerosis and multiple sclerosis. Similarly, regular intake of PPAR activating non-steroidal anti-inflammatory drugs such as indomethacin and ibuprofen was associated with reduced incidence and progression of neurodegenerative disorders in several epidemiological studies. In this article, we review studies relating to the neuroprotective effect of PPAR agonists in in vitro and in vivo models of PD. Similarly, the pharmacological mechanism in neuroprotective actions of PPAR agonists is also reviewed. In conclusion, PPAR agonists exert neuroprotective actions by regulating the expression of a set of genes involved in cell survival processes, and could be a therapeutic target in debilitating neurodegenerative illnesses such as PD. [source] Metabolic changes detected by proton magnetic resonance spectroscopy in vivo and in vitro in a murin model of Parkinson's disease, the MPTP-intoxicated mouseJOURNAL OF NEUROCHEMISTRY, Issue 3 2008Carine Chassain Abstract Parkinson's disease is a neurodegenerative disorder characterized by the progressive loss of the dopaminergic neurons in the substantia nigra pars compacta, which project to the striatum. The aim of this study was to analyze in vivo and in vitro consequences of dopamine depletion on amount of metabolites in a mouse model of Parkinson's disease using proton 1H magnetic resonance spectroscopy (MRS). The study was performed on control mice (n = 7) and MPTP-intoxicated mice (n = 7). All the experiments were performed at 9.4 T. For in vivo MRS acquisitions, mice were anesthetized and carefully placed on an animal handling system with the head centered in birdcage coil used for both excitation and signal reception. Spectra were acquired in a voxel (8 ,L) centered in the striatum, applying a point-resolved spectroscopy sequence (TR = 4000 ms, TE = 8.8 ms). After in vivo MRS acquisitions, mice were killed; successful lesion verified by tyrosine hydroxylase immunolabeling on the substantia nigra pars compacta and in vitro MRS acquisitions performed on perchloric extracts of anterior part of mice brains. In vitro spectra were acquired using a standard one-pulse experiment. The absolute concentrations of metabolites were determined using jmrui (Lyon, France) from 1H spectra obtained in vivo on striatum and in vitro on perchloric extracts. Glutamate (Glu), glutamine (Gln), and GABA concentrations obtained in vivo were significantly increased in striatum of MPTP-lesioned mice (Glu: 15.5 ± 2.5 vs. 12.9 ± 1.0 mmol/L, p < 0.05; Gln: 2.3 ± 0.9 vs. 1.8 ± 0.6 mmol/L, p < 0.05; GABA: 2.3 ± 0.9 vs. 1.3 ± 0.6 mmol/L, p < 0.05). The in vitro results confirmed these results, Glu (10.9 ± 2.5 vs. 7.9 ± 1.7 ,mol/g, p < 0.05), Gln (6.8 ± 2.9 vs. 4.3 ± 1.0 ,mol/g, p < 0.05), and GABA (2.9 ± 0.9 vs. 1.5 ± 0.4 ,mol/g, p < 0.01). The present study strongly supports a hyperactivity of the glutamatergic cortico-striatal pathway hypothesis after dopaminergic denervation in association with an increase of striatal GABA levels. It further shows an increased of striatal Gln concentrations, perhaps as a strategy to protect neurons from Glu excitotoxic injury after striatal dopamine depletion. [source] Progressive depletion of complexin II in a transgenic mouse model of Huntington's diseaseJOURNAL OF NEUROCHEMISTRY, Issue 1 2001A. J. Morton Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by motor, emotional and cognitive dysfunction. There is no treatment or cure for this disease, and after the onset of symptoms, usually in the fourth decade of life, there is an inexorable decline to death. In many patients there is a complex deterioration of function before the onset of neuronal loss and, at least in mouse models, abnormalities in neurotransmission represent early events in the development of the disease. Here we describe the specific and progressive loss of complexin II from the brains of mice carrying the HD mutation (R6/2 line), and the later appearance of this protein in a subpopulation of neuronal intranuclear inclusions. Although the precise role of complexin II is still unclear, it is known to bind to the SNARE complex, and is therefore likely to be involved in the control of exocytosis. Our results suggest that changes in neurotransmitter release might contribute to the neuronal dysfunction seen in these mice. [source] Hexokinase II gene transfer protects against neurodegeneration in the rotenone and MPTP mouse models of Parkinson's disease,JOURNAL OF NEUROSCIENCE RESEARCH, Issue 9 2010Juan Carlos Corona Abstract A typical feature of Parkinson's disease is the progressive loss of dopaminergic neurons in the substantia nigra, in which inhibition of mitochondrial complex I activity may play an important role. Rotenone or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) inhibit the mitochondrial complex I and they cause the death of substantia nigra dopaminergic neurons, thereby providing acute murine models of Parkinson's disease. We have found that increasing mitochondrial hexokinase II activity can prevent cell death in neuronal cultures treated with rotenone. As a result, we have studied the effects of hexokinase II gene transfer in vivo using a herpes simplex virus type 1 (HSV-1) amplicon vector. The placHK2 amplicon vector was injected into substantia nigra of mice that were subsequently administered rotenone or MPTP. Overexpression of hexokinase II prevented both rotenone and MPTP-induced dopaminergic neuronal cell death, as well as reducing the associated motor defects. Our results provide the first proof-of-principle that hexokinase II protects against dopaminergic neurodegeneration in vivo, emphasizing the role of this enzyme in promoting neuronal survival. Thus, the increase of hexokinase II expression by gene transfer or other means represents a promising approach to treat Parkinson's and other neurodegenerative diseases. © 2010 Wiley-Liss, Inc. [source] Cytoarchitectonics and afferent/efferent reorganization of neurons in layers II and III of the lateral entorhinal cortex in the mouse pilocarpine model of temporal lobe epilepsyJOURNAL OF NEUROSCIENCE RESEARCH, Issue 6 2008Dong Liang Ma Abstract With the mouse pilocarpine model of temporal lobe epilepsy (TLE), we showed a progressive loss of both principal cells and calbindin (CB)-, calretinin (CR)-, and parvalbumin (PV)-immunopositive interneurons in layers II,III of lateral entorhinal cortex (LEnt) from 2 months to 1 year after pilocarpine-induced status epilepticus (PISE). In the efferent pathway of LEnt, more Phaseolus vulgaris leucoagglutinin (PHA-L)-labelled en passant and terminal boutons with larger diameters were shown in the hippocampus and subiculum; in the prefrontal, piriform, and perirhinal cortices; and in the amygdaloid complex in experimental mice at the two time points compared with the control after iontophoretical injection of an anterograde tracer PHA-L into the LEnt. Furthermore, the numbers of CB- or CR-immunopositive neurons contacted by PHA-L-labelled en passant and terminal boutons decreased in most of these areas at 2 months or 1 year after PISE. In the afferent pathway of LEnt, the numbers of retrogradely labelled neurons were reduced significantly in the ipsilateral piriform cortex and endopiriform nucleus at 2 months and 1 year and in the reuniens thalamic nucleus only at 1 year after injection of a retrograde tracer cholera toxin B subunit (CTB) into the LEnt. The percentages of the number of CTB and CB or CR double-labelled neurons of all the retrogradely labelled neurons were also decreased in the reunions thalamic nucleus at 1 year after PISE. It is concluded that both cytoarchitectonic change and reorganization of afferent and efferent pathways in LEnt may be involved in the occurrence of TLE. © 2007 Wiley-Liss, Inc. [source] | ||||||||||||||||||||||||||||||||||||||||