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Vascular Pathology (vascular + pathology)
Selected AbstractsNeuropathological correlates to clinically defined dementia with Lewy bodiesINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 7 2001E. Londos Abstract Objectives To analyse the neuropathological changes behind clinically defined dementia with Lewy bodies (clinDLB) compared with clinically diagnosed Alzheimer's disease (clinAD). Methods The prevalence of neuropathological findings in 48 clinDLB and 45 clinAD cases was compared. Sixteen clinDLB and 10 clinAD cases were reassessed with ,-synuclein staining for Lewy bodies (LB). Results Alzheimer pathology was found in 81% of the clinDLB and 93% of the clinAD cases. The clinDLB group had a higher prevalence of frontal white matter pathology, mostly of ischemic type, and a more severe degeneration of the substantia nigra compared with the clinAD group. In hematoxylin,eosin staining, LBs were identified in seven (15%) of the clinDLB and in four (9%) of the clinAD group. In ,-synuclein staining, 38% of the clinDLB and 40% of the clinAD cases exhibited LBs. The cases without LBs, in the clinDLB group, had AD pathology in combination with frontal white matter disease. Vascular pathology of significant degree was prevalent in more than 40% of all the cases with verified LBs regardless of clinical diagnosis. Conclusion Consecutive dementia cases, fulfilling the clinical consensus criteria for DLB, may exhibit combinations of neuropathological changes which in themselves can explain the clinical picture of DLB even when LBs are absent. Copyright © 2001 John Wiley & Sons, Ltd. [source] Vascular pathology in dermatomyositis and anatomic relations to myopathologyMUSCLE AND NERVE, Issue 1 2010Alan Pestronk MD Abstract The causes of perifascicular myofiber atrophy and capillary pathology in dermatomyositis are incompletely understood. We studied 11 dermatomyositis muscles by histochemistry, immunohistochemistry, and ultrastructure. We found that endomysial capillaries within regions of perifascicular atrophy are not entirely lost, but they have reduced size, endothelial loss, C5b9 complement deposits, and relatively preserved connective tissue molecules and pericytes. In all muscles, the perimysium varies regionally. Some areas contain intermediate-sized vessels. Others are avascular. In dermatomyositis, vascular perimysium contains abnormal vessel fragments, perivascular inflammation, and increased PECAM-1. Perifascicular myofiber atrophy and capillary pathology are concentrated near the avascular perimysium. We conclude that both perimysial intermediate-sized vessels and endomysial capillaries within regions of perifascicular myofiber atrophy are abnormal in dermatomyositis. Capillary damage and myofiber atrophy are concentrated in regions distant from intermediate-sized perimysial vessels. Chronic immune vascular damage and insufficiency in dermatomyositis may cause ischemia, myofiber atrophy, and capillary damage in "watershed" regions of muscle near the avascular perimysium. Muscle Nerve, 2010 [source] Risk Factors for Erectile Dysfunction in Patients with Urethral Strictures Secondary to Blunt TraumaTHE JOURNAL OF SEXUAL MEDICINE, Issue 11 2008Chao Feng PhD ABSTRACT Introduction., Erectile dysfunction (ED) is a well-known consequence of pelvic fracture, particularly in cases involving urethral injury. There are several risk factors that may be related to ED. However, no systemic approach is used to assess erectile function secondary to urethral trauma. Aim., To investigate ED associated with urethral injury secondary to pelvic fracture and perineal trauma. Methods., Forty patients with traumatic urethral strictures secondary to blunt traumatic impact episode to the pelvis or perineum were included in our study. Pelvic fractures and urethral strictures were categorized according to injury types and radiological findings. All patients underwent nocturnal penile tumescence (NPT) monitoring, dynamic color-duplex Doppler ultrasonography (D-CDDU) before surgery. NPT monitoring was conducted again after surgery. Main Outcome Measures., The events of NPT and D-CDDU were recorded. Results., In all patients, 11 had organic ED demonstrated by NPT. Vascular pathology was identified in three of 11 patients (27%). The peak systolic velocity of cavernosal artery was lower in patients with pubic diastasis in comparison to those without diastasis (P < 0.05). Significant changes in penile length and circumference were noted in posterior urethral injury compared with anterior urethral injury during erection (P < 0.05). The erectile duration time has a similar statistical difference in two groups mentioned above. However, no significant difference could be observed in the end-to-end anatomosis procedure before and after surgery (P > 0.05). Conclusions., The pelvic fracture type, especially pubic diastasis, is a risk factor for ED following urethral injury. Location of the stricture is also a risk factor for subsequent erectile dysfunction. Feng C, Xu Y-M, Yu J-J, Fei X-F, and Chen L. Risk factors for erectile dysfunction in patients with urethral strictures secondary to blunt trauma. J Sex Med 2008;5:2656,2661. [source] Human First-Trimester Decidua Vascular Density: An Immunohistochemical Study Using VE-Cadherin and Endoglin as Endothelial Cell MarkersAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 1 2000BRUNO VAILHÉ PROBLEM: Angiogenesis and vasculogenesis appear to be of critical importance for the success of pregnancy. Recent data have emphasized that pregnancy complications, such as abortion or pre-eclampsia, are linked with vascular pathologies. The aim of this study was to quantify human first-trimester decidua microvascular density, using two novel, highly specific endothelial cell markers, VE-cadherin and endoglin. METHOD OF STUDY: We collected decidua from women undergoing termination of normal pregnancies. VE-cadherin and endoglin were localized by immunohistochemistry. The blood vessel densities detected by VE-cadherin or endoglin-stainings were microscopically quantified per mm2. RESULTS: Endothelial cells in first-trimester human decidua both express VE-cadherin and endoglin. The microvascular density detected by VE-cadherin-staining varied from 32.2±1.7 in decidua basalis, to 30±0.6 in decidua parietalis. For the endoglin-staining, the values varied from 37.5±3 in decidua basalis, and 26.7±1.2 in decidua parietalis. CONCLUSIONS: Our data shows that both VE-cadherin and endoglin are good candidates to highlight the decidual endothelial cells, and to quantify the blood vessels density of endometrium. [source] Whole-body MR angiography using a novel 32-receiving-channel MR system with surface coil technology: First clinical experienceJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 5 2005Michael Fenchel MD Abstract Purpose To demonstrate the feasibility of detecting atherosclerotic vascular disease using an innovative magnetic resonance angiography (MRA) protocol in combination with a dedicated whole-body MR scanner with new surface coil technology. Materials and Methods A total of 10 volunteers and eight patients with peripheral arterial occlusive disease (PAOD) were examined at 1.5 T. Conventional digital subtraction angiography (DSA) of the symptomatic region was available as a reference standard in all eight patients. Depending on subjects' size, four to five three-dimensional data sets were acquired using an adapted injection protocol. Images were assessed independently by two readers for vascular pathology. Additionally, signal-to-noise ratios (SNRs) and contrast-to-noise ratios (CNRs) were measured. Results Whole-body MRA yielded excellent sensitivity and specificity of more than 95% for both readers with high interobserver agreement (k = 0.93). Surface coil signal reception rendered a high SNR (mean 151.28 ± 54.04) and CNR (mean 120.75 ± 46.47). Despite lower SNR and CNR of the cranial and cervical vessels, a two-step injection protocol exhibited less venous superposition and therefore proved to be superior compared to single-bolus injection. Conclusion Our approach provides accurate noninvasive high-resolution imaging of systemic atherosclerotic disease, covering the arterial vasculature from intracranial arteries to distal runoff vessels. The recently introduced MR scanner and coil technology is feasible to significantly increase the performance of whole-body MRA. J. Magn. Reson. Imaging 2005;21:596,603. © 2005 Wiley-Liss, Inc. [source] Involvement of the contact phase and intrinsic pathway in herpes simplex virus-initiated plasma coagulationJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 5 2010E. S. GERSHOM Summary.,Background:,A hemostatic response to vascular injury is initiated by the extrinsic pathway of coagulation and amplified by the intrinsic pathway. We previously reported that purified herpes simplex virus type-1 (HSV1) has constitutive extrinsic pathway tissue factor (TF) and anionic phospholipid on its surface derived from the host cell, and can consequently bypass strict cellular control of coagulation. Objective:,The current work addresses the hypothesis that HSV1-induced plasma coagulation also involves intrinsic pathway, factor VIII (FVIII), and upstream contact activation pathway, factor XII (FXII). Results:,HSV1-initiated clotting was accelerated when purified FVIII was added to FVIII-deficient plasma and in normal plasma attenuated by an inhibitory anti-FVIII antibody (Ab). High HSV1 concentrations predictably reduced the effect of FVIII due to the availability of excess viral TF. To further define TF-independent clotting mechanisms initiated by HSV1, the extrinsic pathway was disabled using factor VII-deficient plasma. The intrinsic pathway is triggered by activation of FXII associated with surface-bound kallikrein, which subsequently activates factor XI. Here we found that an inhibitor of activated FXII, corn trypsin inhibitor, and anti-FXII, anti-kallikrein and anti-FXI Abs inhibited HSV1-initiated clotting. HSV1-enhanced activation of purified FXII was confirmed by Western blot, but required prekallikrein. Conclusion:,The current work shows that HSV1 can trigger and amplify coagulation through the contact phase and intrinsic pathway, and suggests an additional mechanism that may contribute to vascular pathology. [source] Neuropathological changes in vibration injury: An experimental studyMICROSURGERY, Issue 1 2005Hani S. Matloub M.D. Vibration syndrome, a clinical condition arising from chronic use of vibrating tools, is associated with a spectrum of neurovascular symptoms. To date, only its vascular pathology has been extensively studied; we sought to determine what direct neurologic injury, if any, is caused by vibration. Hindlimbs of anesthetized rats were affixed to a vibrating platform 4 h a day for 7 days. Study animals were vibrated with set parameters for frequency, acceleration, velocity, and amplitude; control animals were not vibrated. On day 7, nerves were studied by light and electron microscopy. While light microscopy showed minimal histologic differences between vibrated (n = 12) and control (n = 12) nerves, electron microscopic changes were dramatic. Splitting of the myelin sheath and axonal damage (e.g., myelin balls and "finger ring") were consistently seen in both myelinated and nonmyelinated axons. Despite relatively short vibration, definite pathology was demonstrated, suggesting that vibration syndrome has a direct neurologic component. © 2005 Wiley-Liss, Inc. Microsurgery 25:71,75, 2005. [source] Mild Parkinsonian signs: An overview of an emerging conceptMOVEMENT DISORDERS, Issue 12 2007Elan D. Louis MD Abstract Mild Parkinsonian signs (MPS) include gait and balance changes, rigidity, bradykinesia, and tremor. MPS can occur commonly during the clinical examination of older people who do not have known neurological disease, with prevalence estimates for MPS as a whole ranging from 15% to 95%. MPS are generally progressive and they are coupled with functional difficulties, impaired gait and balance, and increased risks of mild cognitive impairment, dementia, and mortality. The mechanistic basis for these signs is unclear, but is likely to be multifactorial, with possible factors including an age-associated decline in dopaminergic nigrostriatal activity, the early development of neurodegenerative (Lewy body or Alzheimer's type) pathologies in the basal ganglia, or the accumulation of vascular pathology in the brain. It would be valuable to identify those individuals with MPS who are at increased risk for the development of future Alzheimer's disease, full-blown Parkinson's disease, or strokes, and to develop therapeutic strategies to intervene to lessen the likelihood of MPS-related morbidity and mortality. © 2007 Movement Disorder Society [source] Kidney Transplantation Using Elderly Non-Heart-Beating Donors: A Single-Center ExperienceAMERICAN JOURNAL OF TRANSPLANTATION, Issue 5p1 2006M. G. J. Snoeijs Although acceptable outcomes have been reported in both non-heart-beating (NHB) and elderly donors individually, the large pool of elderly NHB donors has not yet been fully utilized. In 1994, we expanded our transplant protocol to include NHB donors aged over 65 years and this study compares the clinical outcomes with regular NHB transplantations. Up to June 2005, 24 patients were transplanted at our center with kidneys from NHB donors aged 65 years or more, whereas 176 patients received grafts from conventional NHB donors during the same period. Grafts from older donors were associated with inferior glomerular filtration rates (29 vs. 44 mL/min after 1 year, p = 0.01) and graft survival (52% vs. 68% after 5 years, p = 0.19) compared to younger NHB donor grafts, although the difference in graft survival was not statistically significant. Exclusion of older NHB donor kidneys with severe vascular pathology resulted in similar graft survival of older and younger NHB donor kidneys. We conclude that the use of elderly NHB donors in order to expand the donor pool was associated with unacceptable clinical outcomes and cannot be justified without further refinement in their selection, for example, by histological assessment of pretransplant biopsies. [source] Circulating endothelial microparticles as a marker of cerebrovascular disease,ANNALS OF NEUROLOGY, Issue 2 2009Keun-Hwa Jung MD Objective Circulating endothelial microparticles (EMPs) have been reported to reflect vascular damage. Detailed profiling of these blood endothelial markers may adumbrate the pathogenesis of stroke or enable determination of the risk for stroke. We investigated EMP profiles in patients at risk for cerebrovascular disease. Methods We prospectively examined 348 consecutive patients: 73 patients with acute stroke and 275 patients with vascular risk factors but no stroke events. We quantified various types of EMPs by flow cytometry using CD31, CD42b, annexin V (AV), and CD62E antibodies in the peripheral blood of patients. This method allowed fractionation of CD31+/CD42b,, CD31+/AV+, and CD62E+ EMPs. Clinical and laboratory factors associated with EMPs were assessed. Results Recent ischemic episodes were found to be more strongly associated with greater CD62E+ EMP levels than with levels of other phenotypes. Increased National Institutes of Health Stroke Scale scores and infarct volumes in acute stroke patients were significantly associated with greater CD62E+ EMP levels. In the risk factor group, patients with extracranial arterial stenosis had greater CD62E+ EMP levels, whereas those with intracranial arterial stenosis had greater CD31+/CD42b, and CD31+/AV+ EMP levels. The ratio of CD62E+ to CD31+/CD42b, or CD31+/AV+ EMP level significantly discriminated extracranial and intracranial arterial stenosis. Interpretation Circulating EMP phenotypic profiles reflect distinct phenotypes of cerebrovascular disease and are markers of vascular pathology and an increased risk for ischemic stroke. Ann Neurol 2009;66:191,199 [source] Imaging appearance of the symptomatic perforating artery in patients with lacunar infarction: Occlusion or other vascular pathology?ANNALS OF NEUROLOGY, Issue 2 2001Joanna M. Wardlaw FRCR Lacunar infarction is associated with distinct clinical features. It is thought to result from occlusion of a deep perforating artery in the basal ganglia, centrum semiovale, or brainstem. However, occluded perforating arteries have only rarely been observed at postmortem in patients with lacunar stroke and have not been noted previously on imaging despite the increasing sophistication of the techniques. We observed nine patients with lacunar stroke imaged with computed tomography and magnetic resonance imaging in whom we observed a linear structure with density or signal features consistent with an occluded (or at least abnormal) perforating artery associated with the relevant lacunar infarct. The appearance might also have been caused by a leak of blood and fluid into the perivascular space around the artery, as in several patients the width of the tubular vessel-like structure (>1mm in diameter) was greater than the expected width of a perforating artery (<0.8mm in diameter). This interpretation is supported by the fact that the area of infarction was usually around the abnormal vessel, not at the end of it. We describe the patients' clinical and imaging features, and discuss alternative explanations for the imaging appearance and the implications for gaining insights into the cause of lacunar infarction. [source] Apolipoprotein E,deficient mice are resistant to the development of collagen-induced arthritisARTHRITIS & RHEUMATISM, Issue 2 2010Darren L. Asquith Objective To determine whether elevated serum lipid levels resulting from feeding animals a high-fat diet can affect the inflammatory process in C57BL/6 (B6) wild-type (WT) and B6 ApoE,/, mouse models of collagen-induced arthritis (CIA). Methods Male B6 WT or ApoE,/, mice were fed either a normal chow diet or a high-fat diet. CIA was induced in mice at 12 weeks of age using type II chicken collagen, Freund's complete adjuvant, and, on occasion, a lipopolysaccharide boost. Expression levels of autoantibodies and cytokines were measured using enzyme-linked immunosorbent assay and multiplex assay, respectively. Results Whereas B6 WT mice developed severe articular inflammation after collagen immunization, ApoE,/, mice developed no clinical or histologic evidence of disease regardless of whether they had been fed a high-fat diet or a normal chow diet. The fact that arthritis was not present in ApoE,/, mice did not result from inadequate production of serum IgG2a collagen antibodies, since levels observed in ApoE,/, mice were similar to those observed in arthritic B6 WT control mice. Critically, development of atherosclerosis in ApoE,/, mice was not affected by the CIA protocol. Conclusion Our findings suggest that ApoE,/, mice are resistant to the development of CIA. Intriguingly, induction of host autoimmunity in the absence of articular inflammation had no effect on atherosclerosis progression, suggesting that articular inflammatory load may be a critical risk factor in vascular pathology. [source] The role of tyrosine kinase-mediated pathways in diabetes-induced alterations in responsiveness of rat carotid arteryAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 2 2005M. H. M. Yousif Summary 1 G-protein-coupled receptor signalling, including transactivation of receptor tyrosine kinases (RTKs), has been implicated in vascular pathology. However, the role of specific RTKs in the development of diabetes-induced cardiovascular complications is not known. 2 We investigated the ability of a chronic administration of genistein, a broad-spectrum inhibitor of tyrosine kinases (TKs), AG1478, a specific inhibitor of epidermal growth factor receptor (EGFR) TK activity, and AG825, a specific inhibitor of Erb2, to modulate the altered vasoreactivity of isolated carotid artery ring segments to common vasoconstrictors and vasodilators in streptozotocin (STZ)-induced diabetes. 3 In diabetic carotid artery, the vasoconstrictor responses induced by noradrenaline (NE), endothelin-1 (ET-1), and angiotensin II (Ang II), were significantly increased whereas vasodilator responses to carbachol and histamine were significantly reduced. Inhibition of TKs, EGFR or Erb2 pathway did not affect the body weight or agonist-induced vasoconstrictor and vasodilator responses in the non-diabetic control animals. However, inhibition of TKs by genistein, EGFR TK by AG1478 or Erb2 by AG825 treatment produced a significant normalization of the altered agonist-induced vasoconstrictor responses without affecting blood glucose levels. Treatment with diadzein, an inactive analogue of genistein, did not affect the vasoconstrictor and vasodilator responses in the diabetic animals. 4 Treatment with genistein, AG1478 or AG825 resulted in a significant improvement in diabetes-induced impairment in endothelium-dependent relaxation to carbachol and histamine. 5 These data suggest that activation of TK-mediated pathways, including EGFR TK signalling and Erb2 pathway, are involved in the development of diabetic vascular dysfunction in the carotid artery. [source] Antagonism of AT2 receptors augments Angiotensin II-induced abdominal aortic aneurysms and atherosclerosisBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2001Alan Daugherty We have recently demonstrated that chronic infusion of Angiotensin II into apoE,/, mice promotes the development of abdominal aortic aneurysms. To determine the involvement of specific Angiotensin II receptors in this response, we co-infused Angiotensin II (1000 ng kg,1 min,1 for 28 days) with losartan (30 mg kg,1 day,1) or PD123319 (3 mg kg,1 day,1) to antagonize AT1 and AT2 receptors, respectively. Infusion of Angiotensin II promoted the development of abdominal aortic aneurysms in 70% of mature female apoE,/, mice. The formation of aortic aneurysms was totally inhibited by co-infusion of Angiotensin II with losartan (30 mg kg,1 day,1; P=0.003). In contrast, the co-infusion of Angiotensin II with PD123319 resulted in a marked increase in the incidence and severity of aortic aneurysms. To determine whether AT2 antagonism also promoted Angiotensin II-induced atherosclerosis, Angiotensin II was infused into young female apoE,/, mice that had little spontaneous atherosclerosis. In these mice, co-infusion of PD123319 led to a dramatic increase in the extent of atherosclerosis. This increase was associated with no change in plasma lipid concentrations and only transient and modest increases in blood pressure during co-infusion with PD123319. While antagonism of AT1 receptors totally prevented the formation of aneurysms, antagonism of AT2 receptors promoted a large increase in the severity of Angiotensin II-induced vascular pathology. British Journal of Pharmacology (2001) 134, 865,870; doi:10.1038/sj.bjp.0704331 [source] White matter disorders with autosomal dominant heredity: a review with personal clinical case studies and their MRI findingsACTA NEUROLOGICA SCANDINAVICA, Issue 5 2010C. Sundal Sundal C, Ekholm S, Andersen O. White matter disorders with autosomal dominant heredity: a review with personal clinical case studies and their MRI findings. Acta Neurol Scand: 2010: 121: 328,337. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Background,,, Leukoencephalopathies are a heterogeneous group of severe encephalopathy syndromes with myelin, axonal or vascular pathology, typically with extensive white matter lesions on MRI T2-FSE and/or -FLAIR sequences. Objectives,,, This review is restricted to leukoencephalopathies with onset in adult age and a dominant inheritance. These diseases are generally severe and often lethal and present with an exacerbating or insidiously progressive course. Material and methods,,, The focus is on four syndromes with pure leukoencephalopathies, however, leukoencephalopathies with associated clinical features are included. Results,,, T2 weighted MR imaging often show features common for leukoencephalopathies, yet shows distinguishing features in transthyretin amyloidosis. Conclusion,,, The diagnosis within the group of leukoencephalopathies thus characterized by MRI relies mainly upon clinical and genetic analysis. The differential diagnosis against treatable leukoencephalopathies is increasingly relevant. [source] Cardiac complications in Behçet's diseaseCLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 8 2002Ü. Türsen Summary Behçet's disease (BD) is a multisystem disease of unknown aetiology characterized by chronic relapsing oro-genital ulcers, uveitis, and systemic involvement including articular, gastrointestinal, cardiopulmonary, neurologic and vascular pathology. Vascular involvement is observed in 30% of cases. Although the pathogenic mechanisms underlying the thrombotic disposition in BD are not well known, prothrombin (PT) gene mutations may be one factor that contributes to the development of vascular involvement in this disorder. We report a case of BD with a PT gene mutation, presenting with cardiovascular involvement. [source] | ||||||||||||||||||||||