Vascular Disturbances Research Articles

Blast induced brain injuries – a grand challenge in TBI research

Blast induced brain injuries – a grand challenge in TBI research

THE CASE OF THE SUPERVISION OF PATIENT SUFFERRING MIXED DEMENTIA WITH ALZHEIMER’S DISEASE

The article is presented the supervision of the authors of case mixed (atypical) dementia with Alzheimer's disease. The evaluation of patient is carried out with using modern functional, neurointrascopic and psychometric methods of diagnostics. This research detected as Alzheimer’s nature of disease, so and vascular disturbance, that lead to clinical picture of mixed dementia with Alzheimer's disease.

Spontaneous infarction of pleomorphic adenoma: Report of a case simulating malignancy on fine‐needle cytology sample

Ischemic or hemorrhagic infarction has been described as an uncommon but possible complication of fine-needle cytology sampling in numerous organs, more frequently the thyroid, the salivary glands, the breast, the lymph node, and the kidney. In these situations, infarction appears to be directly related to the vascular disturbances caused by needle sampling, though fine this latter might be. One case of a spontaneous infarction of a parotid pleomorphic adenoma in a 46-year-old lady is here described in which the cytopathologic findings, which were related to ischemic infarction, preceded fine-needle cytology sampling and mimicked malignancy. The cytopathologic picture showed a quizzical mixture of necrosis and inflammation coupled to hyperplastic changes of the acinar cells, oncocytic metaplasia, and atypical squamous metaplasia of extreme degree simulating high-grade epidermoid- or mucoepidermoid carcinoma. Due to the cytologically suggestive changes, a nerve-sparing radical parotidectomy was performed. The differential diagnostic problems encountered in this case are discussed together to the possible medical-legal implications originating from such striking atypias as to closely simulate malignancy.

Hemodynamic and Histological Effects of Traumatic Brain Injury in eNOS-Deficient Mice

Microvascular dysfunction in the brain, characterized by vasoconstriction, vascular occlusion, and disruption of the blood brain barrier, may adversely affect outcome following traumatic brain injury (TBI). Because of its vasodilating and antiaggregative properties, nitric oxide (NO) produced by nitric oxide synthase in the endothelium (eNOS) is a key regulator of vascular homeostasis. The objective of the present study was to evaluate the role of eNOS in vascular disturbances and histological outcome in the brain following TBI. Cortical blood flow ([(14)C]-iodoantipyrine technique), number of perfused capillaries (FITC-dextran technique), brain water content (wet vs. dry weight), and the transfer constant (K(i)) for [(51)Cr]-EDTA, reflecting permeability, were analyzed 3 h and 24 h after a controlled cortical impact injury (CCI) in eNOS-deficient (eNOS-KO) and wild-type (WT) mice. Cortical contusion volume and cell count in the hippocampus were evaluated 3 weeks after injury. Blood flow in the injured cortex decreased in both groups following trauma. There were no significant differences between the groups at 3 h, but blood flow was lower in eNOS-KO mice than in WT mice 24 h after trauma. Brain water content was higher in the WT mice than in eNOS-KO mice at 24 h. Number of perfused capillaries, K(i), and histological outcome were similar in both groups. We conclude that eNOS is important for maintenance of cerebral blood flow after trauma and that eNOS promotes edema formation by mechanisms other than increased permeability. The vascular effects of eNOS do not, however, influence histological outcome.

Budd-Chiari Syndrome Complicating Hepatic Sarcoidosis: Definitive Treatment by Liver Transplantation: A Case Report

Sarcoidotic involvement of the liver is frequent, albeit uncommonly symptomatic. Severe complications are rare, but may seldom require liver transplantation. Budd-Chiari syndrome has been described in a few patients with hepatic sarcoidosis. Herein we have reported the case of a young woman suffering from hepatic sarcoidosis who developed severe cholestasis and chronic Budd-Chiari syndrome. She successfully underwent orthotopic liver transplantation (OLT) and is asymptomatic with normal liver function at 3 years follow-up. Histopathological assessment of the liver explant demonstrated a florid granulomatous process, with involvement of the large intrahepatic veins, providing an anatomical basis for the vascular flow disturbances. This case adds further evidence that liver transplantation may be the curative treatment for complicated sarcoidotic liver disease.

Altered metabolisms of mediators controlling vascular function and enhanced oxidative stress in asymptomatic children with congenital portosystemic venous shunt

Children with congenital portosystemic venous shunt (PSVS) are at risk for developing pulmonary hypertension, irrespective of the severity of portal hypertension or liver damage. Altered metabolisms of nitric oxide (NO) and endothelin-1 (ET-1), which are linked with oxidative stress and control vascular tone, might contribute to the vascular disturbance. This study examined 14 children (aged 1-5 years) with congenital PSVS lacking major liver damage and portal hypertension. Serum levels of nitrite/nitrate (NOx) as stable metabolites of NO, and of asymmetric dimethylarginine (ADMA) as an endogenous NO synthase inhibitor were determined, along with the plasma level of ET-1. Oxidative stress, which might affect the production of such mediators, was also examined using specific urinary and blood markers. The NOx levels were significantly lower in affected children than in the age-matched control group, although ET-1 levels were significantly higher than the control levels. In the affected children, the ADMA levels and ADMA/NOx ratios were higher, respectively, by 30% and 130% and showed significant positive correlations with the shunt ratios. Oxidative stress markers, including plasma thiobarbiturate reactive substances and urinary acrolein-lysine and 8-hydroxy-2′-deoxyguanosine, were significantly higher in affected children than in the control group, consistent with them being subjected to enhanced oxidative stress. These results suggest the presence of altered metabolisms of vascular mediators and enhanced oxidative stress in asymptomatic preschool children with congenital PSVS.

Rapeseed Protein in a High-Fat Mixed Meal Alleviates Postprandial Systemic and Vascular Oxidative Stress and Prevents Vascular Endothelial Dysfunction in Healthy Rats

High-saturated fat and high-sucrose meals induce vascular endothelial dysfunction, the early hallmark of atherogenesis. The impact of dietary protein on vascular homeostasis remains misunderstood. In this study, we investigated whether rapeseed protein, an emergent arginine- and cysteine-rich protein, can acutely modulate the onset of adverse effects induced by a high-saturated fat meal (HFM). In a series of crossover experiments, healthy rats received 3 HFM (saturated fat: 60%; sucrose: 20%; protein: 20% energy) with the protein source being either total milk protein (MP; control), rapeseed protein (RP), or MP supplemented with cysteine and arginine to the same level as in RP (MP+AA). Endothelium-related vascular reactivity, measured as an acetylcholine-induced transient decrease in blood pressure, and plasma triglycerides, hydroperoxides, cyclic GMP (cGMP), and free 3-nitrotyrosine were measured before and 2, 4, and 6 h after meals. Superoxide anion production, expressed as ethidine fluorescence, was measured in the aorta 6 h after meals. Whereas plasma triglycerides rose similarly in all meals, the decrease in vascular reactivity after MP was attenuated after MP+AA and entirely prevented after RP. The type of meal had no consistent effect on plasma cGMP and free 3-nitrotyrosine over the postprandial period. The postprandial increase in plasma hydroperoxides differed according to the meal, and concentrations were 43% lower 6 h after MP+AA and RP than after MP. Aortic superoxide anion production was 36% lower 6 h after RP than MP. These results show that substituting rapeseed protein for milk protein markedly reduces vascular and oxidative disturbances induced by an HFM and this may be mediated in part by cysteine and arginine.

Disease mechanisms leading to impaired blood flow in glaucoma

Abstract Purpose SIS lecture Methods Literature search Results Although primary open‐angle glaucoma (POAG), is associated more closely with elevated intraocular pressure (IOP), other risk factors already implicated in the aetiology of this disease and especially in the aetiology of normal‐tension glaucoma are: abnormal ocular circulation, ocular and systemic vascular dysregulation, as well as systemic blood pressure (BP) alterations. Oxidative stress, which occurs as a result of an imbalance between generation of reactive oxygen species (ROS) and antioxidant defence mechanisms and is implicated in the pathogenesis of disorders ranging from atherosclerosis to neurodegenerative disorders, diabetes and aging, may also contribute to the general vascular disturbances observed in glaucoma. Moreover, increasing evidence shoes that oxidative stress plays a role in promoting endothelial dysfunction, which is a key factor in progression of vascular diseases. Indeed, glaucomatous optic nerve damage has been related to endothelial damage/dysfunction. This presentation explores the role of various ocular and systemic circulatory factors in the pathogenesis of glaucomatous neuropathy.

Arterial Stiffness and Other Vasculatures Impairments That Cause in Hypertensive Older Patients and Smoking Cognitive Impairments Are Not Linked to Gender

HomeStrokeVol. 40, No. 9Arterial Stiffness and Other Vasculatures Impairments That Cause in Hypertensive Older Patients and Smoking Cognitive Impairments Are Not Linked to Gender Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBArterial Stiffness and Other Vasculatures Impairments That Cause in Hypertensive Older Patients and Smoking Cognitive Impairments Are Not Linked to Gender Karim Hnid Karim HnidKarim Hnid Mitochondrial Interest Group (MIG), Zemamra, Morocco Search for more papers by this author Originally published6 Aug 2009https://doi.org/10.1161/STROKEAHA.109.557181Stroke. 2009;40:e539Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: August 6, 2009: Previous Version 1 To the Editor:The article by Kearney-Schwartz et al1 explains the mechanism by which cognitive impairments in the elderly can happen in hypertensive patients.They suggest that memory impairment was only observed in men and explain this fact by possible differential effects of gender in hypertensive patients at an early stage of cognitive impairment.They omitted to tell us in their paragraph discussion, that only 15% of women were smokers or exsmokers versus 66% of men.Hill2 has done a study in which he concluded that the residual effects of current cigarette smoking negatively influenced speeded cognitive capabilities in older adults, and exsmokers did not differ from smokers in their performance on any of the cognitive tasks. Moreover, Reitz et al3 found that current smokers aged >75 years had cognitive and memory impairment than their peers who do not smoke. Finally, the Rotterdam Study4 demonstrates that current smoking increases the risk of dementia and Alzheimer disease.On the other hand, Mahmud et al5 in their study found that hemodynamic consequences of chronic smoking increase arterial stiffness and arterial wave reflection, which leads to increased aortic systolic blood pressure, and chronic smoking females are not protective from such vascular effects.This finding about smoking and genesis of arterial stiffness is comforted by Jatoi et al,6 Polonia et al,7 and Liang et al8 in their respective studies. They all demonstrate, after a long period of smoking cessation, a clear improvement of pulse wave velocity, central pressure, and vascular stiffness.Smoking has a central role in the genesis of vascular disturbances in this particular study, and gender is not the cause of the difference noted in the study.DisclosuresNone.1 Kearney-Schwartz A, Rossignol P, Bracard S, Felblinger J, Fay R, Boivin J-M, Lecompte T, Lacolley P, Benetos A, Zannad F. Vascular structure and function is correlated to cognitive performance and white matter hyperintensities in older hypertensive patients with subjective memory complaints. Stroke. 2009; 40: 1229–1236.LinkGoogle Scholar2 Hill RD. Residual effects of cigarette smoking on cognitive performance in normal aging. Psychol Aging. 1989; 4: 251–254.CrossrefMedlineGoogle Scholar3 Reitz C, Luchsinger J, Tang M-X, Mayeux R. Effect of smoking and time on cognitive function in the elderly without dementia. Neurology. 2005; 65: 870–875.CrossrefMedlineGoogle Scholar4 Reitz C, den Heijer T, van Duijn C, Hofman A, Breteler MMB. Relation between smoking and risk of dementia and Alzheimer disease: the Rotterdam Study. Neurology. 2007: 69: 998–1005.CrossrefMedlineGoogle Scholar5 Mahmud A, Feely J. Effect of smoking on arterial stiffness and pulse pressure amplification. Hypertension. 2003; 41: 183–918.LinkGoogle Scholar6 Jatoi NA, Jerrard-Dunne P, Feely J, Mahmud A. Impact of smoking and smoking cessation on arterial stiffness and aortic wave reflection in hypertension. Hypertension. 2007; 49: 981–985.LinkGoogle Scholar7 Polonia J, Barbosa L, Silva JA, Rosas M. Improvement of aortic reflection wave responses 6 months after stopping smoking: a prospective study. Blood Pressure Monitoring. 2009; 14: 69–75.CrossrefMedlineGoogle Scholar8 Liang Y-L, Shiel LM, Teede H, Kotsopoulos D, McNeil J, Cameron JD, McGrath BP. Effects of blood pressure, smoking, and their interaction on carotid artery structure and function. Hypertension. 2001; 37: 6–11.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Li J, Bao J, Gao C, Wei Z, Tan L, Liu P, Wang Z and Tian S (2021) Increased Serum E-Selectin Levels Were Associated with Cognitive Decline in Patients with Stroke, International Journal of General Medicine, 10.2147/IJGM.S292171, Volume 14, (733-739) September 2009Vol 40, Issue 9 Advertisement Article InformationMetrics https://doi.org/10.1161/STROKEAHA.109.557181PMID: 19661473 Originally publishedAugust 6, 2009 PDF download Advertisement

Alpha-1 adrenoceptor stimulation triggers axon-reflex vasodilatation in human skin

The aim of this study was to determine whether pre-treatment of human skin with the α 1-adrenoceptor antagonist terazosin would block vasoconstrictor responses and axon-reflex vasodilatation to the α 1-adrenoceptor agonist methoxamine. Drugs were administered by iontophoresis into the skin of the forearm of 15 healthy participants, and skin blood flow was monitored with a laser Doppler flow probe at the site of methoxamine iontophoresis (to monitor direct vasoconstrictor responses) or 5–10 mm from the site of methoxamine iontophoresis (to monitor axon-reflex vasodilatation). Experimental sites were pre-treated with terazosin (administered by iontophoresis for 10 min at 200 µA), and the same current intensity was passed through 0.9% saline to control for the nonspecific effects of iontophoresis. Pre-treatment with terazosin blocked vasoconstrictor responses to increasing doses of methoxamine, and also blocked vasodilatation several mm from the site of terazosin and methoxamine administration. These findings support the view that α 1-adrenoceptors play a role in generating axon-reflex vasodilatation, and thus might contribute to local vascular disturbances in acute and chronic inflammation.

Morphological aspects used of semisynthetic antioxidant dibornol in treatment of rats OXYS with involutional central chorioretinal degeneration

Retina of rats OXYS 6 months of age by treatment of 4-methyl-2,6-diisobornylphenol (dibornol) was researched. Mainly, rats OXYS have of vascular disturbances such as reduction open functional vasculars of choroidea, destruction of retinal pigmental epithelium and retinal neurons. Dibornol was protected of retina increased area of open vascular and safety of retinal neurons. Besides dibornol was prevented thrombosis in retinal vasculars.

Cytopathological and histopathological diagnosis of canine splenic disorders

To determine (1) the common types of canine splenic disorders, and the breeds affected, that are diagnosed by cytopathological and histopathological examination in Sydney, Australia and (2) the accuracy of cytopathological examination compared with histopathological examination for the diagnosis of canine splenic disorders. 69 cytopathological and 51 histopathological diagnoses of canine splenic disorders presented to the Veterinary Pathology Diagnostic Services, The University of Sydney during 2006 and 2007 were tabulated and analysed; 17 cases examined both cytopathologically and histopathologically during 2001-07 were also analysed. The most common cytopathological diagnoses were benign disorders of growth, vascular disturbances and necrosis (29%), followed by no abnormalities detectable (28%), malignant neoplasms (20%), equivocal diagnoses (20%) and inflammatory disorders (3%). The most common breeds were Kelpie crosses and mixed breeds. The most common histopathological diagnoses were benign disorders of growth, vascular disturbances and necrosis (49%), followed by malignant neoplasms (43%) and inflammatory disorders (8%). The most common breeds were German Shepherd Dogs, Boxers and Maltese Terriers. Cytopathological and histopathological diagnoses were in complete agreement in 59% of cases, partial agreement in 29% and disagreement in 12%. Benign disorders of growth, vascular disturbances and necrosis were the most commonly diagnosed canine splenic disorders, both cytopathologically and histopathologically. Kelpie crosses presented most frequently for cytopathological examination. German Shepherd Dogs were the most common breed diagnosed histopathologically with haemangiosarcoma. Although cytopathological and histopathological splenic examinations are complementary for diagnosis, this study has shown a high correlation for complete and partial agreement between the two.

Erectile dysfunction and cardiovascular disease: efficacy and safety of phosphodiesterase type 5 inhibitors in men with both conditions.

Risk factors for cardiovascular disease and erectile dysfunction (ED) are similar, as might be expected given their shared etiologic and pathophysiologic origins. It is now generally accepted that most cases of ED result from a vascular disturbance of the endothelium. Recent epidemiological studies have documented a strong association between ED and comorbid conditions such as hypertension, diabetes mellitus, and dyslipidemia. Phosphodiesterase type 5 (PDE5) inhibitors are recommended as first-line therapy for erection problems of all etiologies and severities. The efficacy and safety of PDE5 inhibitors in the general ED population is well documented and has been extensively reviewed. To examine the association between ED and vascular disorders in the context of current knowledge regarding PDE5 inhibitors, an electronic search was performed of articles published from January 2002 through April 2008 using the PubMed, EMBASE, and MEDLINE databases. Although preference was given to randomized, blinded, controlled clinical trials, data from retrospective studies were also reviewed when appropriate. This analysis revealed that the clinical evidence linking ED to future cardiovascular events is compelling, presenting physicians with a unique interventional opportunity to address underlying cardiovascular health concerns in men presenting with ED. In most studies, PDE5 inhibitors were shown to effectively and safely improve erectile function regardless of cause, severity, or presence of comorbid conditions, including hypertension, diabetes mellitus, and dyslipidemia.

035. THE ROLE OF THE SERTOLI CELL IN REGULATING SPERMATOGENESIS, IMMUNE RESPONSES AND INFLAMMATORY DISEASE: MULTIPLE FUNCTIONS, COMMON MECHANISMS?

There is increasing evidence that the Sertoli cell, in addition to modulating responses to direct antigenic challenges (eg. intratesticular allografts), is central to the response of the testis to inflammation and infection. Systemic inflammation exerts an inhibitory effect on spermatogenesis, which has been attributed to the effects of fever, vascular disturbances, or loss of androgenic support. However, recent studies point to more direct effects of inflammation on spermatogenesis. The discovery that Sertoli cells express Toll-like receptors (TLR), and react to TLR ligands by producing inflammatory cytokines and other mediators, provides a mechanism to account for this direct inhibition. Moreover, the pattern of cytokines produced by the Sertoli cell during inflammation is highly characteristic. For example, when stimulated with TLR ligands the Sertoli cell produces the pro-inflammatory cytokines, interleukin-1α (IL1α) and IL6, and the regulatory cytokine, activin A, but does not produce IL1β and tumour necrosis factor-α, which are major pro-inflammatory products of activated macrophages. The disruptive effects of inflammation on spermatogenesis may be attributed to the elevated production of these cytokines, all of which have stimulatory or inhibitory effects on germ cell mitosis, meiosis and apoptosis and Sertoli cell tight junction formation, In addition, activation of TLR/IL1 mediated inflammatory pathways in the Sertoli cell inhibits its ability to respond to its principal trophic hormone, follicle-stimulating hormone. Studies on the regulation of these interactions will further establish the role of the Sertoli cell in inflammation and infection. However, such studies also have important implications for normal Sertoli cell function, as TLRs can respond to endogenous ligands as well. Consequently, the Sertoli cell may be viewed as a sentinel cell, supporting and protecting spermatogenesis when conditions are optimal, but rapidly shutting down spermatogenesis in the presence of infection or illness. Intriguingly, these apparently disparate roles appear to involve common inflammation-related mechanisms.

The Retrocapital Osteotomy (“Chevron”) for Correction of Splayfoot with Hallux Valgus

Surgical treatment of hallux valgus deformity with a distal osteotomy of the first metatarsal to address an increased intermetatarsal angle (IMA) I-II. This procedure is combined with a soft-tissue procedure at the first metatarsophalangeal joint: realignment of the first ray, lateral displacement of the first metatarsal head above the sesamoids, rebalancing of the soft tissues at the metatarsophalangeal joint. Pain and soft-tissue inflammation at the bunion, impaired function of the metatarsophalangeal joint, and lateral deviation of the hallux. IMA I-II <or= 15 degrees, hallux valgus angle (HVA) <or= 40 degrees, distal metatarsal articular angle (DMAA) > 10 degrees. Symptomatic osteoarthritis of the first metatarsophalangeal joint, assessed clinically or radiographically. Acute inflammation of the forefoot, osteoporosis of the first metatarsal. Vascular disturbance. Cosmetic indication only. Relative: hypermobility of the first ray, valgus malalignment of the hindfoot, previous retrocapital osteotomy. Lateral soft-tissue release. Resection of the medial pseudoexostosis. V-shaped osteotomy of the distal metatarsal I. Exostosectomy. Lateral displacement of the first metatarsal head. Screw fixation. Realignment of the metatarsophalangeal joint by tightening of the medial soft tissues. Postoperative shoe with full weight bearing. Active exercises of the foot and hallux. Physiotherapy. Prophylaxis of deep vein thrombosis depending on the degree of mobility. Radiographic control after 6 weeks. Bandage or orthosis to maintain toe alignment. IMA I-II was reduced from 13.6 degrees preoperatively to 6.6 degrees postoperatively. HVA decreased from 29.8 degrees to 8.2 degrees postoperatively.

Angiogenesis in systemic sclerosis: Impaired expression of vascular endothelial growth factor receptor 1 in endothelial progenitor–derived cells under hypoxic conditions

To assess angiogenesis and explore the expression and regulation of vascular endothelial growth factor (VEGF), VEGF receptor 1 (VEGFR-1), and VEGFR-2, the leading mediators of angiogenesis, in SSc patients and controls. Late-outgrowth endothelial progenitor cells (EPCs), isolated from the peripheral blood of systemic sclerosis (SSc) patients and controls, and human umbilical vein endothelial cells (HUVECs) were assessed under normal and hypoxic conditions. Genomic background was evaluated in a large case-control study (including 659 patients with SSc and 511 controls) using tag single-nucleotide polymorphisms on VEGFR1 and VEGFR2 genes. EPCs from SSc patients had the phenotype of genuine endothelial cells and displayed in vitro angiogenic properties similar to those of HUVECs and control EPCs under basal conditions, as determined by flow cytometry, tube formation, and migration assay. However, after 6 hours of hypoxic exposure, EPCs from SSc patients exhibited lower induced expression of VEGFR-1 at the messenger RNA and protein levels, but similar VEGF and VEGFR-2 expression, compared with HUVECs or EPCs from healthy controls. There was no evidence of defective expression of hypoxia-inducible factor 1alpha. These results were supported by the lower serum levels of soluble VEGFR-1 found in SSc patients (n = 187) compared with healthy controls (n = 48) (mean +/- SD 163.7 +/- 98.5 versus 210.4 +/- 109.5 pg/ml; P = 0.0042). These abnormalities did not seem to be related to genomic background. Our findings shed new light on the possible role of VEGFR-1 in the main vascular disturbances that occur in SSc and lead to more severe disease.

2008 Sol Sherry Distinguished Lecture in Thrombosis—Platelet Adhesion in Acute Arterial Thrombosis

Platelet adhesion is an essential function in response to vascular injury, through which single platelets bind to specific membrane receptors onto cellular and extracellular matrix constituents of the vessel wall and tissues initiating thrombus formation that arrests hemorrhage and permits wound healing. Pathological conditions that cause vascular alterations and blood flow disturbances may turn this defense process into a disease mechanism resulting in arterial occlusion, mostly in atherosclerotic vessels of the heart and brain. Besides their relevant role in hemostasis and thrombosis, platelet adhesive properties are central to a variety of pathophysiological processes that extend from inflammation to immune-mediated host defense and pathogenic mechanisms as well as cancer metastasis. All these activities depend on the ability of platelets to circulate in blood as sentinels of vascular integrity, adhere where alterations are detected, and signal the abnormality to other platelets and blood cells. In this respect, therefore, platelet adhesion to vascular wall structures, to one another (aggregation), or to other blood cells represents different aspects of the same fundamental biological process. Novel concepts and tools are being developed to advance our knowledge of the mechanisms through which platelets respond to vascular injury. Of particular interest are specific microparticles endowed with selective targeting properties conferred by recombinant adhesive domains that may be used for targeting areas of the vasculature with thrombogenic potential and for diagnostic purposes. Particles with such specific adhesive properties may also be used for the local delivery of anti-thrombotic drugs.

A Histological and Ultrastructural Study of the Iliac Crest Apophysis in Legg-Calve-Perthes Disease

Legg-Calve-Perthes disease (LCPD) is a common hip disorder in children characterized by avascular necrosis of the proximal capital femoral epiphysis. The underlying etiology of the vascular disturbance is still unknown, but it is suggested that LCPD may be a part of a generalized constitutional disorder associated with growth disturbance of bone and cartilage tissue. In this study, the biopsy specimens of the iliac crest apophysis from LCPD patients were examined histologically and ultrastructurally to determine preexisting generalized abnormalities of endochondral ossification. Iliac crest apophysis cartilage was taken during Salter innominate osteotomy from 11 children (8 boys and 3 girls) with LCPD at an average age of 7.8 years. As controls, the samples were also obtained from 10 children (2 boys and 8 girls) at an average age of 6.3 years undergoing Salter osteotomy due to residual acetabular dysplasia after reduction of developmental dysplasia of the hip. Each iliac crest apophysis specimen was examined histologically (Toluidine blue staining and Sudan III staining) and ultrastructurally. Although there were no obvious differences in Toluidine blue-stained sections of the iliac crest cartilage between LCPD and control patients, the Sudan III-positive chondrocytes in the resting cartilage were more prominent in the LCPD specimens than in the control specimens. These sudanophilic granules were confirmed to be lipid droplets by electron microscopic examinations. Ultrastructural examinations of the resting chondrocytes from 3 LCPD patients demonstrated numerous cytoplasmic inclusion bodies with electron dense materials, which were similar to those seen in some of the mucopolysaccharidoses. Increased lipid droplets and numerous cytoplasmic inclusions filled with fibrillar materials were suggestive of the initial metabolic changes of the chondrocytes, which may have a pivotal role in degenerating matrix and lead to vulnerability of the cartilage tissue. Our results indicated that generalized insufficiency in growth cartilage metabolism may be related to the onset of the disease in some LCPD patients.

Cardiometabolic syndrome: How important is PPARy receptor activation for clinical practice?

Resume Interaction of genetic and environmental factors, metabolic and vascular disturbances increases the risk of total mortality, renal dysfunction, cardiovascular complications. Insulin resistance plays the key role in metabolic syndrome development. Connection of renin-angiotensin-aldosterone system (RAAS) and metabolic risk factors has been carefully studied. Peroxisome proliferator-activated receptors г (PPARг) role in fatty and carbohydrate metabolism is being studied intensively nowadays. Thiazolidinediones impact on cardio-vascular prognosis is controversial, and needs subsequent research. Pleiotropic effects of RAAS-blockers play important role in treatment of high risk patients. Telmisartan, being a partial PPARг-agonist, extends perspective rational pharmacotherapy of hypertension in patients with metabolic syndrome.

Kreislaufstörungen der Milz

Splenic vascular disturbances mainly affect the red pulp and can involve the venous or arterial blood flow. The venous blood flow may be impaired by congestion and morphologically shows dilated splenic sinuses. Disturbances of the arterial blood flow may occur in connection with anomalies of the erythrocyte membrane or in immune haemolysis and usually are characterized by narrow splenic sinuses. Infarction of the spleen is usually caused by arterial embolism.