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PubMed1996

Comparing stroke incidence worldwide: what makes studies comparable?

BACKGROUND: Comparing stroke rates in different parts of the world and at different points in time may increase our understanding of the disease. Comparisons are only meaningful if they are based on studies that use similar definitions, methods, and data presentation. SUMMARY OF REVIEW: We discuss the criteria that make such studies comparable, drawing on the experiences of recent studies performed around the world. If only those studies that fulfill the proposed criteria for comparison are considered, comparable data do not exist for vast areas of the world, including Africa, Asia, and South America. The importance of complete, community-based case ascertainment, including strokes managed outside the hospital, is emphasized. An approach for measuring and comparing the incidence of the pathological types of stroke (cerebral infarction, primary intracerebral hemorrhage, and subarachnoid hemorrhage) and subtypes of cerebral infarction is suggested. CONCLUSIONS: The "ideal" stroke incidence study does not exist, but studies closely approaching it will reveal the most reliable and comparable results. There is a need for further studies to fill the gaps in our knowledge of the worldwide incidence of stroke, particularly for developing countries.

Africa↗
PubMed2002

Distinct HLA associations by stroke subtype in children with sickle cell anemia.

Children with sickle cell anemia (SCA) carry a 200-fold increased risk for cerebral infarction. Stroke can be the result of small-vessel (SV) or large-vessel (LV) disease. However, it is unknown whether these subtypes result from the same pathophysiologic processes. Complete HLA genotyping was performed on 231 eligible children previously enrolled in the Cooperative Study of Sickle Cell Disease (CSSCD). Cerebral infarction on magnetic resonance imaging (MRI) was documented in 71 patients, and 160 patients had negative findings on MRI. Based on MRI/magnetic resonance angiography (MRA) findings, infarct size, and location, 36 patients were classified as having LV stroke and 35 as having SV stroke. When comparing the total MRI+ group with the MRI- group, HLA DPB1*0401 was associated with increased stroke risk (P =.01), whereas DPB1*1701 (P =.02) conferred protection from stroke. These DPB1 associations with stroke were attributed to the SV stroke group, in whom DPB1*0401 was associated with susceptibility (P =.003) and DPB1*1701 with protection from stroke (P =.06). In the LV stroke subgroup, HLA-A*0102 (P =.02) and -A*2612 (P =.007) conferred susceptibility, whereas -A*3301(P =.04) protected from stroke. These results suggest that specific HLA alleles influence stroke risk and appear to contribute differently to SV and LV stroke subtypes. The distinct HLA associations with SV and LV stroke suggest that different pathologic processes may be involved in the development of stroke in children with SCA. If these results are confirmed in a larger study, HLA type may serve as a useful marker for the early identification of SCA patients at high risk for stroke.

Adolescent↗
PubMed1999

Expression patterns and regulation of glutamate transporters in the developing and adult nervous system.

Glutamate and aspartate are the primary excitatory neurotransmitters in the mammalian central nervous system and have also been implicated as mediators of excitotoxic neuronal injury and death. The precise control of extracellular glutamate and aspartate is crucial to the maintenance of normal synaptic transmission and the prevention of excitotoxicity following acute insults to the brain, such as stroke or head trauma, or during the progression of neurodegenerative diseases such as amyotrophic lateral sclerosis. The removal of excitatory amino acids (EAAs) from the extracellular space is primarily mediated by a family of sodium-dependent glutamate transporters. These transporters use the sodium electrochemical gradients of the cell to actively concentrate EAAs in both neurons and glia. Five members of this transporter family have been cloned recently and include both 'glial'-specific and 'neuron'-specific subtypes. Although these subtypes share many common functional properties, there are considerable differences in developmental expression, chronic and acute regulation by cellular signaling pathways, and contribution to disease processes among the subtypes. In this review recent studies of glutamate transporter expression, regulation, function, and pathological relevance are summarized, and some of the discrepancies and unexpected results common to any rapidly progressing field are discussed.

Animals↗
PubMed1988

Immunogenetics of collagen-induced arthritis in rats.

CIA can be viewed as a multifactorial animal model of experimentally-induced autoimmunity that is targeted to joint tissues and under multiple gene control. Thus, although induction of CIA requires immune reactivity to type II collagen, a high immune response to type II collagen is not pathognomonic of CIA, indicating that determinant specificity is of crucial importance. Also, both RT1-linked and non-RT1-linked gene directed functions are involved in the final clinical response to immunization with type II collagen. RT1-linked control is likely exerted at the level of Class II (Ia) molecules (as it is in mice) with inherent selectivity of arthritogenic vs non-arthritogenic epitopes for presentation to the immune response system; non-RT1-linked control may reflect genes controlling T-cell receptors, immunoglobulin subtypes or complement components. There is also evidence that the effects of potentially pathological anti-collagen autoimmunity may in some strains be muted or even obviated by other non-RT1 gene controlled traits that are not directly related to the immune system. These general conclusions are in close accord with those of other investigators who have carefully conducted extensive and in-depth studies of the immunogenetics of CIA in mice. CIA is obviously not an exact model of any one of the more common rheumatic diseases, such as rheumatoid arthritis or systemic lupus erythematosus. In fact, it is more closely analogous to polychondritis and some of the other sero-negative connective tissue diseases. However, CIA remains an extremely useful model in attempts to understand the genetic and environmental factors which influence a specific and definable autoimmune process--anti-collagen reactivity. In turn, autoimmunity to collagen, and to other autoantigens, is a contributing or complicating aspect of most of the diverse human rheumatic disease syndromes which have been identified to date. The characteristics of the CIA model in rats which have been discussed in this article, i.e., genetically controlled variations in incidence, severity, rate of progression and expression of clinical disease, are also characteristic of the human rheumatic disease patient population. Likewise, the probable contribution of multiple genes to these syndromes is recognized. Continued investigation of the CIA model can be expected to yield important information that can be used to better understand its human counterparts.

Animals↗
PubMed2000

[Transformation of the fungus ball type pulmonary aspergillosis].

Though the concept of semi-invasive pulmonary aspergillosis was advocated in 1981 by Gefter et al., its histopathological appearance has not yet been reported in detail. Pathological studies on fungus ball type pulmonary aspergillosis (PA) were originally made mainly in regard to related bronchi. Chronic-progressive destructive changes cannot be completely explained from this viewpoint alone. Clinically, since bloody sputum and hemoptysis appeared frequently, further studies on the pulmonary vasculature were considered necessary. In the resected lungs of 3 cases of semi-invasive pulmonary aspergillosis, the pathological features of pulmonary vasculature were characterized by numerous fungal clots within pulmonary arteries and veins, marked destruction of pulmonary blood vessels and extensive intravascular fibrin deposition. Intravascular fibrin deposition causes stasis of blood flow, promotes intravascular proliferation of aspergilli and probably accelerates pulmonary destruction caused by blood stasis. Important pathological findings of fungus ball type pulmonary aspergillosis of the semi-invasive subtype with clinical aspects of chronic-progressive lung destruction caused by severe inflammation, were reported for both the vascular and the bronchial system.

Adult↗
PubMed2004

Bronchoalveolar carcinoma: current treatment and future trends.

Bronchoalveolar carcinoma (BAC) is a subtype of non-small-cell lung cancer (NSCLC) with unique clinical and pathologic characteristics. The most recent classification system defines BAC as a primary lung cancer that tends to be peripheral and grow in a lepedic fashion along the alveolar septae without parenchymal invasion. Most of the clinical information on BAC comes from retrospective institutional reviews; however, recent studies have focused more specifically on BAC. In particular, clinical trials of molecular-targeted anticancer therapies against the epidermal growth factor receptor have led to a deeper understanding of the distinct features of this cancer and suggest that BAC may require a therapeutic paradigm different from that of other NSCLCs.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMed2000

Utility of flow cytometry immunophenotyping for the diagnosis and classification of lymphoma in community hospital clinical needle aspiration/biopsies.

CONTEXT: Flow cytometry immunophenotyping (FC) of needle aspiration/biopsy (NAB) samples has been reported to be useful for the diagnosis and classification of lymphoma in university and cancer center-based settings. Nevertheless, there is no agreement on the utility of these methods. OBJECTIVE: To further define the utility of adjunctive FC of clinical NAB for the diagnosis and classification of lymphoma, and to determine if this approach is practicable in a routine clinical practice setting. SETTING: A community-based hospital. METHODS: Clinical NABs were submitted for adjunctive FC between June 1996 and September 1999 if initial smears were suspicious for lymphoma. Smears and cell block or needle core tissues were routinely processed and paraffin-section immunostains were performed if indicated. The final diagnosis was determined by correlating clinical and pathologic data, and the revised European-American classification criteria were used to subtype lymphomas. RESULTS: Needle aspiration/biopsies from 60 different patients were submitted for FC. Final diagnoses were lymphoma (n = 38), other neoplasm (n = 15), benign (n = 6), or insufficient (n = 1). For 38 lymphomas (20 primary, 18 recurrent), patients ranged in age from 32 to 86 years (mean, 62 years); samples were obtained from the retroperitoneum (n = 11), lymph node (n = 9), abdomen (n = 8), mediastinum (n = 6), or other site (n = 4); and lymphoma subtypes were indolent B-cell (n = 20; 2 small lymphocytic, 14 follicle center, 4 not subtyped), aggressive B-cell (n = 14; 3 mantle cell, 10 large cell, 1 not subtyped), B-cell not further specified (n = 2), or Hodgkin disease (n = 2). For the diagnosis of these lymphomas, FC was necessary in 20 cases, useful in 14 cases, not useful in 2 cases, and misleading in 2 cases. Thirty-two of 36 lymphoma patients with follow-up data received antitumor therapy based on the results of NAB plus FC. CONCLUSIONS: Adjunctive FC of NABs is potentially practicable in a community hospital, is necessary or useful for the diagnosis and subtyping of most B-cell lymphomas, and can help direct lymphoma therapy. Repeated NAB or surgical biopsy is necessary for diagnosis or treatment in some cases.

Adult↗
PubMed1998

Nonpeptide antagonists for vasopressin receptors. Pharmacology of SR 121463A, a new potent and highly selective V2 receptor antagonist.

Involvement of AVP in several pathological states is now established and specific modulation of the different AVP receptor subtypes (V1a, V1b and V2) offers new clinical perspectives for treating major diseases. Recent years have marked a turning point with the design and the use of the first nonpeptide vasopressin receptor antagonists expressing various selectively profile. In that field, we report here the characterization of SR 121463A a highly selective, orally-active antagonist of vasopressin V2 receptors in several models in vitro and in vivo. This compound displayed competitive nanomolar affinity for V2 receptors in various species including man and exhibited a highly selective AVP V2 profile. In vitro, SR 121463A potently antagonized AVP-stimulated adenylyl cyclase activity in human kidney preparations (Ki = 0.26 +/- 0.04 nM) without any intrinsic agonistic effect. In normally-hydrated rats, SR 121463A induced dose-dependent powerful and long-lasting aquaresis after intravenous (0.003 to 0.3 mg/kg) or oral (0.03 to 10 mg/kg) administration. The action of SR 121463A is purely aquaretic with no changes in urine Na+ and K+ excretions unlike that of known diuretic agents such as furosemide or hydrochlorothiazide. In vasopressin-deficient Brattleboro rats, SR 121463A is devoid of any V2 antidiuretic agonist properties. In addition, this compound potently antagonized DDAVP extrarenal V2 effects on hemostasis factor release (FVIII, vW and t-PA) in dogs (ID50 approximately 10 micrograms/kg i.v.). Thus, SR 121463A is the most potent and selective, orally-active V2 antagonist yet described. It is a useful ligand for exploring V2 receptors and the therapeutical usefulness of pure V2 aquaretic agents in several water-retaining diseases and congestive heart failure.

Adenylyl Cyclases↗
PubMed1999

Serologic abnormalities in systemic sclerosis.

Recent evidence has confirmed that sera from most systemic sclerosis (SSc) patients contain one of three mutually exclusive, SSc-associated autoantibodies (anti-RNA polymerase III, anti-topoisomerase I, or anti-centromere antibodies). Each is associated with the presence of particular clinical features and certain human lymphocyte antigen (HLA) alleles. Based on the available data the most likely model is for the existence of three distinct disease processes, each with certain key pathologic features. In turn, each pathologic state is responsible for characteristic symptoms, and leads to the production of a distinctive set of modified autoantigens. Certain cryptic epitopes are consequently produced by antigen-presenting cells, and are effectively presented according to the available HLA molecules, with subsequent HLA-restricted autoantibody production. Thus, while not directly involved in disease pathogenesis, SSc-associated autoantibodies appear to be reliable reporters of disease-specific pathologic phenomena, and may prove valuable pointers toward the etiopathogenesis of the different subtypes of SSc.

Autoantibodies↗
PubMed2001

[Regulation of microglial cell function by ATP].

Accumulated evidence suggests that extracellular ATP functions occur in neurons and glial cells in the nervous systems. Besides well-documented roles as a neurotransmitter or neuromodulator, ATP has also been demonstrated to have effects on glial cells. Reports have shown that ATP stimulates microglia to release various biologically active substances, such as interleukin-1 beta, tumor necrosis factor-alpha, and plasminogen. Microglial cell death was also demonstrated after stimulation with high-dose ATP. Although these responses were known to occur, via P2X7, we have recently found that ATP and ADP induced the formation of membrane ruffles and chemotaxis through Gi/o-coupled P2Y receptors. Taken together, it is suggested that two distinct P2X and P2Y receptor subtypes are involved in the diverse function of microglia in both physiological and pathological states.

Adenosine Triphosphate↗
PubMedDate not supplied

[Classic fowl plague--a review].

Highly pathogenic avian influenza (HPAI) represents a severe form of generalized avian influenza which is characterized by a rapid and severe course of disease and a very high mortality. All poultry species are susceptible. Turkeys and chickens are most vulnerable. There are no pathognomonic symptoms or specific pathological alterations. The disease is caused by avian influenza virus strains of the subtypes H5 or H7. These viruses arise spontaneously from apathogenic progenitors by insertional mutation in the HA gene. Until recently, outbreaks of HPAI were rare events, however, they have been found to cause increasing losses over the past few years. Since 2003, a widespread occurrence of HPAI has been registered in southeast Asia, and some countries are endemically infected with HPAIV strain H5N1. In six countries this virus has also caused fatal human infections. This has sparked fears that this agent may be the progenitor of a new pandemic influenza virus. During summer 2005 the disease has slowly spread westward. Isolated outbreaks have been reported from Kazakhstan, Russia, Romania, Turkey, Croatia and Ukraine. Migratory birds have been tentatively accused for spreading the infection along their flyways.

Animal Migration↗
PubMed2004

Molecular analysis of nicotinic receptor expression in autism.

Autism is a developmental disorder of unknown aetiopathology and lacking any specific pharmacological therapeutic intervention. Neurotransmitters such as serotonin, gamma-aminobutyric acid (GABA) and acetylcholine have been implicated. Abnormalities in nicotinic acetylcholine receptors have been identified including cortical loss of binding to the alpha4/beta2 subtype and increase in cerebellar alpha7 binding. Receptor expression (mRNA) has not so far been systematically examined. This study aims to further explore the role of nicotinic receptors in autism by analysing nicotinic receptor subunit mRNA in conjunction with protein levels and receptor binding in different brain areas. Quantitative RT-PCR for alpha4, alpha7 and beta2 subunit mRNA expression levels; alpha3, alpha4, alpha7 and beta2 subunit protein expression immunochemistry and specific radioligand receptor binding were performed in adult autism and control brain samples from cerebral cortex and cerebellum. Alpha4 and beta2 protein expression and receptor binding density as well as alpha4 mRNA levels were lower in parietal cortex in autism, while alpha7 did not change for any of these parameters. In cerebellum, alpha4 mRNA expression was increased, whereas subunit protein and receptor levels were decreased. Alpha7 receptor binding in cerebellum was increased alongside non-significant elevations in mRNA and protein expression levels. No significant changes were found for beta2 in cerebellum. The data obtained, using complementary measures of receptor expression, indicate that reduced gene expression of the alpha4beta2 nicotinic receptor in the cerebral cortex is a major feature of the neurochemical pathology of autism, whilst post-transcriptional abnormalities of both this and the alpha7 subtype are apparent in the cerebellum. The findings point to dendritic and/or synaptic nicotinic receptor abnormalities that may relate to disruptions in cerebral circuitry development.

Acetylcholine↗
PubMed2001

Neoplasia versus hyperplasia of the retinal pigment epithelium. A comparison of two cases.

PURPOSE: To present the clinical and histopathological characteristics of two different tumor-like lesions of the retinal pigment epithelium (RPE). METHODS: Two cases of tumor-like lesions of the RPE were identified in the files of the Eye Pathology Institute. The clinical characteristics and the light- and electron microscopical morphology of the lesions were compared and the diagnoses were re-evaluated applying modern immunostainings. RESULTS: Clinically, both adenoma and tumor-like hyperplasia of the RPE may present with prominent retinal feeder arterioles. The lesions are hypofluorescent in the filling phases and have multiple hyperfluorescent zones in the late phase in fluorescein angiography. They show high internal reflectivity by A-scan and appear as solid tumors by B-scan ultrasonography. Histologically, the two presented lesions of the RPE are different. The first is an adenoma of the vacuolated subtype. The other lesion is a hyperplasia of the RPE disclosing a tubular morphology. The pathologically active cells in both cases were positive for the reaction with antibodies against: cytokeratin, NSE, vimentin, S-100, HMB-45, desmin and SMA. However, only the adenoma was sporadic melan-A positive. CONCLUSION: Adenomas and tumor-like hyperplastic lesions of the RPE are very rare lesions. They share many morphological and immunohistological characteristics. Of the presented cases only the RPE adenoma is sporadic melan-A positive.

Adenoma↗
PubMed1997

Phospholipase A2 and its role in brain tissue.

Phospholipase A2 (PLA2) is the name for the class of lipolytic enzymes that hydrolyze the acyl group from the sn-2 position of glycerophospholipids, generating free fatty acids and lysophospholipids. The products of the PLA2-catalyzed reaction can potentially act as second messengers themselves, or be further metabolized to eicosanoids, platelet-activating factor, and lysophosphatidic acid. All of these are recognized as bioactive lipids that can potentially alter many ongoing cellular processes. The presence of PLA2 in the central nervous system, accompanied by the relatively large quantity of potential substrate, poses an interesting dilemma as to the role PLA2 has during both physiologic and pathologic states. Several different PLA2 enzymes exist in brain, some of which have been partially characterized. They are classified into two subtypes, Ca2+-dependent and Ca2+-independent, based on their catalytic dependence on Ca2+. Under physiologic conditions, PLA2 may be involved in phospholipid turnover, membrane remodeling, exocytosis, detoxification of phospholipid peroxides, and neurotransmitter release. However, under pathological situations, increased PLA2 activity may result in the loss of essential membrane glycerophospholipids, resulting in altered membrane permeability, ion homeostasis, increased free fatty acid release, and the accumulation of lipid peroxides. These processes, along with loss of ATP, may be responsible for the loss of membrane phospholipid and subsequent neuronal injury found in ischemia, spinal cord injury, and other neurodegenerative diseases. This review outlines the current knowledge of the PLA2 found in the central nervous system and attempts to define the role of PLA2 during both physiologic and pathologic conditions.

Animals↗
PubMed2006

A working group classification of focal prostate atrophy lesions.

Focal atrophy is extremely common in prostate specimens. Although there are distinct histologic variants, the terminology is currently nonstandardized and no formal classification has been tested for interobserver reliability. This lack of standardization hampers the ability to study the biologic and clinical significance of these lesions. After informal and formal meetings by a number of the authors, focal atrophy lesions were categorized into 4 distinct subtypes as follows: (i) simple atrophy, (ii) simple atrophy with cyst formation, (iii) postatrophic hyperplasia, and (iv) partial atrophy. In phase 1 of the study, pathologists with varying levels of experience in prostate pathology were invited to view via the Internet a set of "training" images with associated descriptions of lesions considered typical of each subtype. In phase 2 of the study, each participant provided diagnoses on a series of 140 distinct "test" images that were viewed over the Internet. These test images consisted of the 4 subtypes of atrophy and images of normal epithelium, high grade prostatic intraepithelial neoplasia, and carcinoma. The diagnoses for each image from each pathologist were compared with a set of "standard" diagnoses and the kappa statistic was computed. Thirty-four pathologists completed both phases of the study. The interobserver reliability (median kappa) for classification of lesions as normal, cancer, prostatic intraepithelial neoplasia, or focal atrophy was 0.97. The median kappa for the classification of atrophy lesions into the 4 subtypes was 0.80. The median percent agreement with the standard diagnosis for the atrophy subtypes were: simple 60.6%, simple with cyst formation 100%; postatrophic hyperplasia 87.5%; partial atrophy 93.9%. The lower percentage for simple atrophy reflected a propensity to diagnose some of these as simple atrophy with cyst formation. Seven pathologists completed the phase 2 analysis a second time, and their intraobserver reproducibility was excellent. Three of 4 pathologists with low agreement with the standard diagnosis for simple atrophy improved their scores after repeating the analysis after re-examination of the "training set" of images. In conclusion, these criteria for variants of focal prostate atrophy may facilitate studies to examine the relation between various patterns of prostate atrophy and prostate cancer.

Atrophy↗
PubMed2001

Activation of metabotropic glutamate receptor subtype 1/protein kinase C/mitogen-activated protein kinase pathway is required for postischemic long-term potentiation in the striatum.

Excessive stimulation of glutamate receptors is believed to contribute substantially in determining neuronal vulnerability to ischemia. However, how this pathological event predisposes neurons to excitotoxic insults is still largely unknown. By using electrophysiological recordings from single striatal neurons, we demonstrate in a corticostriatal brain-slice preparation that in vitro ischemia (glucose and oxygen deprivation) activates a complex chain of intracellular events responsible for a dramatic and irreversible increase in the sensitivity of striatal neurons to synaptically released glutamate. This process follows the stimulation of both N-methyl-D-aspartate and metabotropic glutamate receptors and involves the activation of the mitogen-activated protein kinase ERK via protein kinase C. This pathological form of synaptic plasticity might play a role in the cell type-specific neuronal vulnerability in the striatum, because it is selectively expressed in neuronal subtypes that are highly sensitive to both acute and chronic disorders involving this brain area.

Animals↗
PubMed2004

Gene expression profiling of depression and suicide in human prefrontal cortex.

Mood disorders are a major cause of disability. Etiology includes genetic and environmental factors, but the responsible genes have yet to be identified. Using DNA microarrays, we have conducted a large-scale gene expression analysis, in two regions of the human prefrontal cortex from post-mortem matched groups of subjects with major depression who had died by suicide, and control subjects who died from other causes and were free from psychiatric disorders. Bioinformatic analysis was used to investigate molecular and cellular pathways potentially involved in depression and suicidal behavior. We tested several hypotheses of disease pathology and of their putative molecular impact, including changes in single genes, the existence of subgroups of patients or disease subtypes, or the possibility of common biological pathways being affected in the disease process. Within the analytical limits of this relatively large genomic study, we found no evidence for molecular differences that correlated with depression and suicide, suggesting a pathology that is below the detection level of current genomic approaches, or that is either localized to other brain areas, or more associated with post-transcriptional effects and/or changes in protein levels or functions, rather than altered transcriptome in the prefrontal cortex.

Adult↗