bluuebunny/crossref_metadata_2025 huggingface dataset:
Advances in salivary gland pathology
Authors: Cheuk W , Chan J K C
Published: June 2007

This review summarizes the new findings on salivary gland pathology under the following categories: immunohistochemistry; molecular genetics; newly recognized tumour types; known tumour entities with new findings; and progression of salivary gland tumours. In the application of immunohistochemistry, CD117 can aid in highlighting the luminal cell component of various salivary gland tumours, whereas p63 or maspin can aid in highlighting the abluminal cell component. A high Ki67 index remains the most useful marker to predict adverse outcome in salivary gland carcinoma. Specific chromosomal translocations are recognized in pleomorphic adenoma (with translocation involving PLGA1 or HMGA2 gene) and mucoepidermoid carcinoma (with MECT1–MAML2 gene fusion). Newly recognized entities include: sclerosing polycystic adenosis (with recent molecular evidence supporting its neoplastic nature), sclerosing mucoepidermoid carcinoma with eosinophilia, keratocystoma, adenoma with additional stromal component (lymphadenoma, lipoadenoma and adenofibroma), cribriform adenocarcinoma of the tongue and signet ring adenocarcinoma of minor salivary gland. Known tumour entities with new findings include: salivary duct carcinoma (with newly recognized mucinous, micropapillary and sarcomatoid variants), intraductal carcinoma (with controversies in terminology), mucoepidermoid carcinoma (with newly proposed grading parameters and oncocytic variant), epithelial–myoepithelial carcinoma (with newly recognized morphological variants), small cell carcinoma (with most cases being related to Merkel cell carcinoma), extranodal marginal zone B‐cell lymphoma (with specific chromosomal translocation) and chronic sclerosing sialadenitis (being a component of IgG4‐related sclerosing disease). Progression of salivary gland tumours can take the form of malignant transformation of a benign tumour, progression from low‐grade to high‐grade carcinoma, dedifferentiation, or stromal invasion of an in situ carcinoma.
Prospective comparison of subjective arousal during the pre‐sleep period in primary sleep‐onset insomnia and normal sleepers
Authors: ROBERTSON JENNIFER A. , BROOMFIELD NIALL M. , ESPIE COLIN A.
Published: June 2007

Psychophysiological insomnia (PI) is the most common insomnia subtype, representing 12–15% of all sleep centre referrals. Diagnostic guidelines describe PI as an intrinsic sleep disorder involving both hyperarousal and learned sleep‐preventing associations. Whilst evidence for the first component is reasonably compelling, evidence for learned (conditioned) sleep effects is markedly lacking. Indeed, to date no study has attempted to capture directly the conditioned arousal effect assumed to characterize the disorder. Accordingly, the present study explored variations in subjective arousal over time in 15 PI participants (sleep onset type) and 15 normal sleepers (NS). Self‐report measures of cognitive arousal, somatic arousal and sleepiness were taken at three time points: 3 h before bedtime (early to mid‐evening); 1 h before bedtime (late evening); and in the bedroom at lights out (bedtime) across four, 24‐h cycles. Fluctuations in mean arousal and sleepiness values, and in day‐to‐day variation were examined using analyses of variance. Participants with PI were significantly more cognitive aroused and significantly less sleepy relative to NS, within the bedroom environment. These results support the tenet of conditioned mental arousal to the bedroom, although competing explanations cannot be ruled out. Results are discussed with reference to extant insomnia models.
Amygdala dysfunction in narcolepsy‐cataplexy
Authors: KHATAMI RAMIN , BIRKMANN STEFFEN , BASSETTI CLAUDIO L.
Published: June 2007

The blink reflex of acoustic startle reflex (ASR) is modulated by emotions and a loss of physiological aversive ASR potentiation is reported in humans following amygdala lesions. Patients with narcolepsy‐cataplexy (NC) were found to have normal ASR, but they failed to exhibit startle potentiation during unpleasant stimuli. This absence of aversive ASR potentiation gives support to the hypothesis of an amygdala dysfunction in human NC.
The effect of short‐term withdrawal from continuous positive airway pressure therapy on sympathetic activity and markers of vascular inflammation in subjects with obstructive sleep apnoea
Authors: PHILLIPS CRAIG L. , YANG QIAO , WILLIAMS ANDREW , ROTH MICHAEL , YEE BRENDON J. , HEDNER JAN A. , BEREND NORBERT , GRUNSTEIN RONALD R.
Published: June 2007

Obstructive sleep apnoea (OSA) is commonly associated with cardiovascular disease and sympathetic activation. However, it is unclear whether this association is independent of obesity and to what extent treatment with nasal continuous positive airway pressure (CPAP) alleviates the vascular inflammation that underpins cardiovascular disease. We therefore evaluated whether short‐term withdrawal from CPAP therapy in subjects with moderate–severe OSA would result in increased levels of sympathetic activity and circulating inflammatory cytokines independent of weight. Vascular inflammatory markers (hsCRP, hsIL‐6 and hsTNF‐α) were assessed in 20 subjects after one and seven nights of withdrawal from CPAP together with the hypoxia‐responsive angiogenic marker VEGF and urinary catecholamines. Compared with baseline on CPAP, withdrawal from therapy resulted in an immediate return of OSA with an increase in RDI to 26.7 ± 5.2 and 39.0 ± 5.9 events per hour after one and seven nights without CPAP, respectively (both P < 0.0001). This was accompanied by a concomitant rise in daytime urinary noradrenaline (P < 0.0001) after seven nights CPAP withdrawal that was positively associated with the severity of hypoxaemia. In contrast, withdrawal from CPAP therapy was not accompanied by any change in measured cytokines or VEGF (all P > 0.1). In conclusion, 1 week of CPAP withdrawal was associated with a return of OSA and a marked increase in sympathetic activity without a concomitant elevation of vascular inflammatory markers.
Plasma Surfactant Protein D Levels and the Relation to Body Mass Index in a Chinese Population
Authors: Zhao X. M. , Wu Y. P. , Wei R. , Cai H. X. , Tornoe I. , Han J. J. , Wang Y. , De Groot P. G. , Holmskov U. , Xia Z. L. , Sorensen G. L.
Published: June 2007

Surfactant protein D (SP‐D) is a member of the collectin family and is an important component of the pulmonary innate host defence. The protein has a widespread distribution in the human body and is present in multiple epithelia, in endothelium and in blood. Various studies have looked at the relationship between serum SP‐D levels and pulmonary inflammatory diseases. The SP‐D distribution has been most thoroughly described in European populations and appears with a broad range of serum values highly influenced by genetic factors. In the present study, we investigated the plasma SP‐D distribution in a Chinese population from the Tai An region comprising 268 individuals. We found that (i) plasma SP‐D in the Chinese population was distributed with a median value of 380.2 ng/ml (324.9; 418.7) and a range from 79.4 to 3965.3 ng/ml, (ii) significantly higher plasma SP‐D in men than in women, and no significant effect of age, and (iii) a significant inverse association between serum SP‐D and body mass index (BMI) (P = 0.012). The data indicate that racial differences in SP‐D expression exist as the median plasma SP‐D in the Chinese population was approximately two times lower than the median serum SP‐D previously measured in a Danish population using the same immuno‐assay. The inverse association between serum SP‐D and BMI found in the Chinese population indicates that serum SP‐D is related to obesity in similar ways in Chinese and Danes.
Immunodeficiency and Autoimmunity in 22q11.2 Deletion Syndrome
Authors: McLean‐Tooke A. , Spickett G. P. , Gennery A. R.
Published: June 2007

22q11.2 deletion syndrome is the commonest chromosome deletion syndrome. 22q11.2 deletion may result in variable clinical phenotypes which may differ even between patients with identical deletions. Abnormal pharyngeal arch development results in defects in the development of the parathyroid glands, thymus and conotruncal region of the heart. Defective thymic development is associated with impaired immune function. ‘Complete’ DiGeorge syndrome with total absence of the thymus and a severe T‐cell immunodeficiency accounts for <0.5% of patients. The majority of patients with 22q11.2 deletion syndromes have ‘partial’ defects with impaired thymic development rather than complete absence with variable defects in T‐cell numbers. Immunodeficiency in these patients is not solely due to T‐cell deficiency and abnormalities of T‐cell clonality or impairment of proliferative responses may play a role. Humoral deficiencies including defects in the B‐cell compartment have also been identified in these patients. 22q11.2 deletion syndrome patients are at increased risk of a variety of autoimmune diseases. A number of immune defects may predispose to the development of autoimmunity in these patients including increased infection, impaired development of natural T‐regulatory cells and impaired thymic central tolerance.
Subclinical Neuromuscular Transmission Abnormality Detected by Single-Fibre EMG is More Pronounced in Cluster Headache Than in Migraine With Aura
Authors: Coban A , Baslo MB , Baykan B , Tutkavul K , Orhan EK , Ertas M
Published: June 2007

The aim was to investigate neuromuscular transmission (NMT) by single-fibre EMG (SFEMG) in a large series of patients having migraine with aura (MA) or cluster headache (CH). Recent studies using SFEMG have shown subclinical dysfunction of NMT in MA and CH. Forty-three patients having MA, 51 with CH and 38 healthy control subjects underwent nerve conduction studies, EMG and SFEMG during voluntary contraction of the extensor digitorum communis muscle. Twenty different potential pairs were recorded and individual, mean and total abnormal individual jitter values were calculated. The results obtained from MA patients were compared with those from CH patients. In MA patients, 32 of 860 jitters were abnormally high, whereas 73 of 1020 of the jitters showed this abnormality in CH patients. None of the control subjects, five MA patients (11.6%) and 11 CH patients (21.6%) were designated as having subclinical NMT abnormality. Thus, patients having junction dysfunction were significantly more common in the CH group. The subclinical NMT abnormality shown by SFEMG is more common in CH than in MA. These two primary headache syndromes may have some shared functional abnormality of NMT constituents which is more evident in CH.
Family-Based Analysis of Serotonin Transporter Gene Polymorphisms in Migraine With and Without Aura
Authors: Karwautz AFK , Sousa S Campos de , Wöber C , Wagner G , Li T , Konrad A , Zesch HE , Zormann A , Berger G , Wanner C , Wöber-Bingöl Ç , Collier DA
Published: June 2007

Genetic epidemiological twin studies have demonstrated a significant heritability for migraine, with >60% of liability to migraine either with or without aura coming from additive genetic factors. Because of the essential role of serotonin in the pathophysiology and treatment of migraine, genes of the serotonin system are candidates for involvement in migraine. Consequently, we examined two functional VNTR polymorphisms in the serotonin transporter gene, the 5-HTTLPR and the intron 2 VNTR, in a sample of 212 family trios each with a proband with childhood migraine, 153 with migraine without aura (MoA) and 59 with migraine with aura (MA). For the first time, we used transmission disequilibrium test analysis with the program TDTPHASE to examine the transmission of these two markers and their haplotypes to offspring affected by migraine. We found no significant transmission distortion of any marker, with the common L allele of the 5-HTTLPR transmitted 170 times and not transmitted 178 times, and the S allele 130 vs. 122 times. Likewise, the common 12 allele of the intron 2 VNTR was transmitted 201 times and not transmitted 188 times, and the 10 allele 107 vs. 120 times. The markers were not associated with MoA and MA and none of the haplotypes was associated with overall migraine, MoA or MA. The 5-HTTLPR and the intron 2 VNTRs do not play a major role in susceptibility to migraine.
Cervical Musculoskeletal Impairment in Frequent Intermittent Headache. Part 1: Subjects With Single Headaches
Authors: Jull G , Amiri M , Bullock-Saxton J , Darnell R , Lander C
Published: June 2007

Musculoskeletal disorders are considered the underlying cause of cervicogenic headache, but neck pain is commonly associated with migraine and tension-type headaches. This study tested musculoskeletal function in these headache types. From a group of 196 community-based volunteers with headache, 73 had a single headache classifiable as migraine ( n = 22), tension-type ( n = 33) or cervicogenic headache ( n = 18); 57 subjects acted as controls. Range of movement, manual examination of cervical segments, cervical flexor and extensor strength, the cranio-cervical flexion test (CCFT), cross-sectional area of selected extensor muscles at C2 (ultrasound imaging) and cervical kinaesthetic sense were measured by a blinded examiner. In all but one measure (kinaesthetic sense), the cervicogenic headache group were significantly different from the migraine, tension-type headache and control groups (all P < 0.001). A dicriminant function analysis revealed that collectively, restricted movement, in association with palpable upper cervical joint dysfunction and impairment in the CCFT, had 100% sensitivity and 94% specificity to identify cervicogenic headache. There was no evidence that the cervical musculoskeletal impairments assessed in this study were present in the migraine and tension-type headache groups. Further research is required to validate the predictive capacity of this pattern of impairment to differentially diagnose cervicogenic headache.
Theories of Embodied Knowledge: New Directions for Cultural and Cognitive Sociology?
Authors: IGNATOW GABRIEL
Published: June 2007

Sociological propositions about the workings of cognition are rarely specified or tested, but are of central relevance to studies of culture, social judgment, and social movements. This paper draws out lessons of recent work from sociological theory, cognitive science, psychology, and neuroscience on the embodied nature of knowledge and thought, and develops implications of these lessons for cultural and cognitive sociology. Knowledge ought to be conceived of as fundamentally embodied, because sensory information is a fundamental component of experience as it is stored in long‐term memory, and because bodily responses and intuitions often precede reflexive or strategic thought. I argue that the challenge of embodied knowledge for cultural sociology is threefold: to develop cultural theories of motivation; to specify the ways in which the body structures discourses endogenously; and to specify how embodied motivations and embodied discourses interact.
Radical Interactionism: Going Beyond Mead*
Authors: ATHENS LONNIE
Published: June 2007

George Herbert Mead argues that human society is comprised of six basic institutions—language, family, economics, religion, polity, and science. I do not believe that he can be criticized for making institutions the cornerstones of a society, but he can definitely be criticized for his explanation of how our basic institutions originate, how these institutions operate in society after their inception, and how they later change, modifying society in the process. The problem with Mead's explanation of these three critical matters is that he based them on his principle of “sociality” rather than on the principle of “domination.” If Mead's principle of sociality is replaced by the principle of domination and his notion of the “generalized other” is replaced by the notion of the “phantom community,” then most of these problems can be largely solved. Thus, in this paper, I will not only point out the key problems in Mead's theory of society, but I will also offer solutions to them based on the notions of domination and the “phantom community.” The end product is a “radical interactionism” that surpasses Mead's original interactionism in identifying the part that both domination and the composite “other” play in every known human society—big and small, and past and present.
Towards a Dynamic Model of the Psychological Contract
Authors: SCHALK RENÉ , ROE ROBERT E.
Published: June 2007

This paper presents a dynamic perspective in which the psychological contract is treated as a structured set of beliefs that are held by individual employees about the mutual obligations of the organization as employer and themselves as employees. This set of beliefs is assumed to produce a state of commitment to the organization in which the employee is willing to accept work roles and tasks offered by the organization, and to carry them out in accordance with certain standards. The dynamic model that is presented can help to explain why the commitment of employees remains relatively stable over time, and why it may suddenly decrease or increase under circumstances that are perceived as critical by the employee. The model assumes that the employee's evaluation of the organization's behavior changes over time, but that the structure of the psychological contract and the associated commitment change only when certain limits are overstepped. This perspective on changes in the psychological contract transforms the concept into a powerful construct that may lead to fruitful research on the dynamics of organization‐employee relationships. Implications for future research are discussed.
Understanding Procrastination
Authors: ANDREOU CHRISOULA
Published: June 2007

Procrastination is frustrating. Because the procrastinator's frustration is self‐imposed, procrastination can also be quite puzzling. I consider attempts at explaining, or explaining away, what appear to be genuine cases of procrastination. According to the position that I propose and defend, genuine procrastination exists and is supported by preference loops, which can be either stable or evanescent.
Elder‐Vass's Move and Giddens's Call
Authors: VARELA CHARLES
Published: June 2007

David Elder‐Vass's “For Emergence: refining Archer's account of social structure,” is the latest of a number of papers which together constitute a family quarrel in the cognitive space After Postmodernism among realist social scientists. In the case under examination here in “Elder‐Vass's Move and Giddens's Call”, the concern is the structure and agency problem in the social sciences. The debate continuing in Elder‐Vass's paper represents the proponents of the resurrection of Durkheim's social realism under the auspices of Bhaskar's Transcendental Realism; the debate that continues here as a response to the Elder‐Vass paper, opposes the latter's attempt to advance the argument for social realism under the canopy of Harre's Immanental realism. The theme of this response is this: Elder‐Vass fails to realize the promise of reconciling social structural realism and social relational realism.
An in vitro model of aneurysmal subarachnoid hemorrhage: oxidation of unconjugated bilirubin by cytochrome oxidase
Authors: Loftspring Matthew C. , Wurster William L. , Pyne‐Geithman Gail J. , Clark Joseph F.
Published: June 2007

Aneurysmal subarachnoid hemorrhage is a stroke subtype with high rates of mortality and morbidity. Cerebral vasospasm can lead to ischemic injury or death and is a common complication of aneurysmal subarachnoid hemorrhage, usually occurring 3–9 days afterwards. The cause of vasospasm is not known. Recently, there has been strong evidence that vasoactive oxidation products of bilirubin may be involved. Currently, the factors that lead to bilirubin oxidation are poorly characterized. In this study, we have designed an in vitro model of hemorrhagic stroke in order to investigate conditions that promote the oxidation of bilirubin to form vasoactive compounds. Using our model, we created a basic hematoma system of blood, CSF, and hemeoxygenase‐1. We manipulated this system in various ways, incubated it and determined the concentration of vasoactive bilirubin oxidation products that resulted. Conditions where cytochrome oxidase was stimulated caused an increase bilirubin oxidation products (292.6 ± 39.9 μmol/L respectively, vs. 79.3 ± 1.3 μmol/L for the basic reaction, p < 0.05), which was attenuated by cyanide. Our data suggest that bilirubin oxidation products may be produced by oxidation(s) requiring an oxygen‐utilizing enzyme like cytochrome oxidase.
COX‐2 oxidative metabolite of endocannabinoid 2‐AG enhances excitatory glutamatergic synaptic transmission and induces neurotoxicity
Authors: Sang Nan , Zhang Jian , Chen Chu
Published: June 2007

Neuroinflammation has been implicated in the pathogenesis of neurodegenerative diseases. Cyclooxygenase‐2 (COX‐2), an inducible enzyme converting arachidonic acid (AA) to prostaglandins, is the key player in neuroinflammation. It has been long thought that the COX‐2‐mediated neuronal injury/degeneration is attributed to the increased production of AA‐derived prostaglandins. Recent studies show that endogenous cannabinoid 2‐arachidonoylglycerol (2‐AG) is a natural substrate for COX‐2, and it can be oxygenated by COX‐2 to form prostaglandin glyceryl esters. In this study, we demonstrate that prostaglandin E2glyceryl ester (PGE2‐G), a major COX‐2 oxidative metabolite of 2‐arachidonoylglycerol, enhanced hippocampal glutamatergic synaptic transmission indicated by the increased frequency of miniature excitatory post‐synaptic currents, and induced neuronal injury/death revealed by the terminal transferase dUTP nick end labeling staining and caspase 3 activation. The actions of PGE2‐G are not mediated via a cannabinoid receptor 1, but mediated through ERK, p38 mitogen‐activated protein kinase, IP3, and NF‐κB signal transduction pathways. In addition, the PGE2‐G‐induced neurotoxicity is attenuated by blockade of the NMDA receptors. Our results suggest that the COX‐2 oxidative metabolism of endocannabinoids is an important mechanism contributing to the inflammation‐induced neurodegeneration.
Blood Pressure Management in Acute Ischemic Stroke
Authors: Lakshminarayan Kamakshi , Anderson David C. , Borbas Catherine , Duval Sue , Luepker Russell V.
Published: June 2007

Data from the Project for Improvement of Stroke Care Management in Minnesota were used to characterize provider practice in the management of hypertension in hospitalized acute ischemic stroke patients in relation to guidelines from the American Stroke Association (ASA) and the European Stroke Initiative (EUSI). Among 1181 patients, 129 received as‐needed medication in direct response to elevated blood pressure in the first 24 hours after admission. Of these 129, 56% were overtreated according to ASA guidelines and 24% by EUSI guidelines. Of the 1052 patients not treated, 16% were undertreated by ASA guidelines and 3% by EUSI guidelines. In contrast, discharge hypertension was well treated, with 93% (424 of 454) of patients likely to have chronic hypertension appropriately treated with antihypertensive medication on discharge. These findings support the need for more research to fill identified gaps in evidence, improve treatment guidelines, and reduce variability in patient management.
The Management of Hypertension in the African American Patient
Authors: Wright Jackson T. , Jamerson Kenneth A. , Ferdinand Keith C.
Published: June 2007

A panel was convened to discuss the topic of the management of hypertension in the African American patient. Jackson T. Wright, MD, PhD, Professor of Medicine, Case Western Reserve University, Cleveland, OH, moderated the panel. Kenneth A. Jamerson, MD, Professor of Medicine, University of Michigan, Ann Arbor, MI, and Keith C. Ferdinand, MD, Association of Black Cardiologists, Inc, and Emory University, Atlanta, GA, participated in the discussion. This expert panel discussion was supported by Novartis and each author received an honorarium from Novartis for time and effort spent participating in the discussion and reviewing the transcript for important intellectual content prior to publication. The authors maintained full control of the discussion and the resulting content of this article; Novartis had no input in the choice of topic, speakers, or content.
Elevated Serum Cardiac Markers Predict Coronary Artery Disease in Patients With a History of Heart Failure Who Present With Chest Pain: Insights From the i*trACS Registry
Authors: Glauser Jonathan , Erickson James , Bhatt Deepak , Lindsell Christopher , Gibler Brian , Hoekstra James , Pollack Charles , Hollander Judd , Peacock W. Franklin
Published: June 2007

The significance of a history of heart failure (HF) in patients presenting with acute coronary syndromes and elevated cardiac markers is unclear. The authors performed an analysis of patients enrolled in the Internet Tracking Registry of Acute Coronary Syndromes (i*trACS). Cardiac marker measurement and cardiac catheterization were performed in 1174 patients. Of these, 116 (9.9%) had heart failure (HF). Coronary artery disease (CAD) was found in 61 (52.6%) patients in the HF group and 581 (54.9%) in the group without HF. In the non‐HF cohort, positive markers occurred in 306 patients, in whom 217 (70.9%) had CAD at catheterization. In the HF subset, 24 patients had positive biomarkers and 15 (62.5%) had CAD. A history of HF did not lessen the likelihood of CAD as evidenced by angiography and does not diminish the utility of cardiac markers in diagnosing acute coronary syndromes.
Clinical Findings, Natriuretic Peptides, and Echocardiography: Integrating Tools to Optimize Heart Failure Management
Authors: Beck‐da‐Silva Luis , Rohde Luis E. , Goldraich Livia , Clausell Nadine
Published: June 2007

The hemodynamic profile of heart failure (HF) patients may be critical to their clinical outcome, whereby congestion emerges as a particularly important aspect to define therapeutic goals, optimize HF treatment, and determine prognosis. Accordingly, individualized HF management must include several strategies to detect congestion, which might easily be underestimated in chronic HF patients. Therefore, it is important to recognize the true reliability of traditional HF signs and symptoms. The contemporary understanding of HF has brought new value to some aspects of physical examination. Natriuretic peptides have emerged as potential new tools in the diagnosis of congestion in patients with HF, and echocardiography has gained renewed importance in HF management when it is used to investigate hemodynamic profile. The aim of this article is to review and integrate these 3 ways of assessing and monitoring HF patients: clinical findings, natriuretic peptides, and echocardiography.
Right Ventricular Failure in Patients With Preserved Ejection Fraction and Diastolic Dysfunction: An Underrecognized Clinical Entity
Authors: Zakir Ramzan M. , Al‐Dehneh Anthony , Maher James , Saric Muhamed , Berkowitz Robert L.
Published: June 2007

It is well recognized that patients with severe left ventricular (LV) systolic dysfunction develop pulmonary venous hypertension or postcapillary pulmonary hypertension, which leads to an increase in pulmonary vascular resistance (PVR) and right ventricular (RV) systolic failure. It is often underrecognized, however, that patients with heart failure with preserved LV ejection fraction and diastolic dysfunction may also develop postcapillary pulmonary hypertension with elevated PVR leading to RV systolic failure. This form of biventricular failure is a result of diastolic failure on the left in patients with preserved LV ejection fraction and systolic failure on the right. At this time, there are no randomized trials or guidelines addressing the management of patients with diastolic heart failure with and without resultant RV failure. The authors review the pathophysiology, clinical presentation, and suggested treatment of this underrecognized clinical entity.
Factors Determining Extreme Brain Natriuretic Peptide Elevation
Authors: Guglin Maya , Hourani Rayan , Pitta Sridevi
Published: June 2007

Brain natriuretic peptide (BNP) level is elevated in heart failure and reflects its severity. It is unknown why some patients have extremely high BNP levels. The authors retrospectively reviewed data on 179 consecutive patients whose BNP levels fell within one of several predetermined ranges: mild elevation, 500 to 1000 pg/mL (n=82); moderate elevation, 2000 to 3000 pg/mL (n=48); and high elevation, 4000 to 20,000 pg/mL (n=49). The statistical analysis was conducted with the unpaired t test and Pearson's correlation coefficient. Adjustments were made for age, sex, and serum creatinine level. Patients with moderate BNP elevation were more symptomatic and had more advanced structural and hemodynamic changes than did patients with lower BNP elevation. Characteristics of the high BNP level group did not differ from those of the moderate BNP level group. Serum creatinine level correlated with BNP level, but neither age nor sex did. High BNP level (4000–20,000 pg/mL) is determined more by renal dysfunction than by the severity of heart failure.
Molecular Neuropathology of Temporal Lobe Epilepsy: Complementary Approaches in Animal Models and Human Disease Tissue
Authors: Majores Michael , Schoch Susanne , Lie Ailing , Becker Albert J.
Published: June 2007

Summary: Patients with temporal lobe epilepsies (TLE) frequently develop pharmacoresistance to antiepileptic treatment. In individuals with drug‐refractory TLE, neurosurgical removal of the epileptogenic focus provides a therapy option with high potential for seizure control. Biopsy specimens from TLE patients constitute unique tissue resources to gain insights in neuropathological and molecular alterations involved in human TLE. Compared to human tissue specimens in most neurological diseases, where only autopsy material is available, the bioptic tissue samples from pharmacoresistant TLE patients open rather exceptional preconditions for molecular biological, electrophysiological as well as biochemical experimental approaches in human brain tissue, which cannot be carried out in postmortem material. Pathological changes in human TLE tissue are multiple and relate to structural and cellular reorganization of the hippocampal formation, selective neurodegeneration, and acquired changes of expression and distribution of neurotransmitter receptors and ion channels, underlying modified neuronal excitability. Nevertheless, human TLE tissue specimens have some limitations. For obvious reasons, human TLE tissue samples are only available from advanced, drug‐resistant stages of the disease. However, in many patients, a transient episode of status epilepticus (SE) or febrile seizures in childhood can induce multiple structural and functional alterations that after a latency period result in a chronic epileptic condition. This latency period, also referred to as epileptogenesis, cannot be studied in human TLE specimens. TLE animal models may be particularly helpful in order to shed characterize new molecular pathomechanisms related to epileptogenesis and open novel therapeutic strategies for TLE. Here, we will discuss experimental approaches to unravel molecular–neuropathological aspects of TLE and highlight characteristics and potential of molecular studies in human and/or experimental TLE.
Relevance of Seizure‐Induced Neurogenesis in Animal Models of Epilepsy to the Etiology of Temporal Lobe Epilepsy
Authors: Scharfman Helen E. , Gray William P.
Published: June 2007

Summary:  Seizure induction in laboratory animals is followed by many changes in structure and function, and one of these is an increase in neurogenesis—the birth of new neurons. This phenomenon may be relevant to temporal lobe epilepsy (TLE), because one of the regions of the brain where seizure‐induced neurogenesis is most robust is the dentate gyrus—an area of the brain that has been implicated in the pathophysiology of TLE. Although initial studies predicted that neurogenesis in the dentate gyrus would be important to normal functions, such as learning and memory, the new neurons that are born after seizures may not necessarily promote normal function. There appears to be a complex functional and structural relationship between the new dentate gyrus neurons and preexisting cells, both in the animal models of TLE and in tissue resected from patients with intractable TLE. These studies provide new insights into the mechanisms of TLE, and suggest novel strategies for intervention that could be used to prevent or treat TLE.
Gene Expression, Genetics, and Genomics in Epilepsy: Some Answers, More Questions
Authors: Crino Peter B.
Published: June 2007

Summary:  The rapid technical progress made in molecular genetics has provided new strategies to study the molecular pathogenesis of human epilepsy. In particular, the abilities to assay the expression of many thousands of genes simultaneously with cDNA or oligonucleotide arrays and to rapidly screen thousands of DNA basepairs permits exciting insights into how human epilepsy may result from alterations in gene transcription and sequence. These approaches can show how monogenic and even complex genetic disorders lead to network alterations and seizures. Most recently, investigation of single nucleotide polymorphisms (SNPs) has shown that even subtle alterations in gene sequence across the genome can raise or lower seizure threshold. Clearly, there is a complex interplay between gene expression, genetics, and genomics which ultimately leads to seizure onset and epilepsy. Identifying the contribution that each plays in epileptogenesis may help define new therapeutic targets.
The Relevance of Kindling for Human Epilepsy
Authors: Bertram Edward
Published: June 2007

Summary:  Kindling is one of the most widely used models of seizures and epilepsy, and it has been used in its more than three decade history to provide many key insights into seizures and epilepsy. It remains a mainstay of epilepsy related research, but the question remains how the results from kindling experiments further our understanding of the underlying neurobiology of human epilepsy. In this article we compare the basic features of kindling and human epilepsy, especially human limbic or temporal lobe epilepsy. In this review we focus on a limited number of topics that may show areas in which kindling has been often cited as a tool for better understanding of human epilepsy. These areas include the underlying circuits, the importance of seizure spontaneity, the associated neuropathology, the contribution of genetics, seizure susceptibility, and the underlying pathophysiology of epilepsy. In the course of this article we will show that there are many features that kindling can teach us by direct comparison or implication about human temporal epilepsy. We will also see that not all findings associated with kindling may be applicable to the human condition. Ultimately we wish to encourage critical thinking about kindling and the similarities that it shares and does not share with the human epilepsy so the results from studies using this model are applied rationally to further our insights the mechanisms of human epilepsy.
Age‐Dependent Consequences of Status Epilepticus: Animal Models
Authors: Scantlebury Morris H. , Heida James G. , Hasson Henry J. , Velíšková Jana , Velíšek Libor , Galanopoulou Aristea S. , Moshé Solomon L.
Published: June 2007

Summary:  Status epilepticus (SE) is a significant neurological emergency that occurs most commonly in children. Although SE has been associated with an elevated risk of brain injury, it is unclear from clinical studies in whom and under what circumstances brain injury will occur. The purpose of this review is to evaluate the effects of age on the consequences of SE. In this review, we focus mainly on the animal data that describe the consequences of a single episode of SE induced in the adult and immature rat brain. The experimental data suggest that the risk of developing SE‐induced brain damage, subsequent epilepsy and cognitive deficits in large part depends on the age in which the SE occurs. Younger rats are more resistant to seizure‐induced brain damage than older rats; however, when SE occurs in immature rats with abnormal brains, there is an increase in the severity of seizure‐induced brain injury. Better understanding of the pathophysiologic mechanisms underlying the age‐specific alterations to the brain induced by SE will lead to the development of novel and effective strategies to improve the deleterious consequences.
Neonatal Seizures: Gaps Between the Laboratory and the Clinic
Authors: Lombroso Cesare T.
Published: June 2007

Summary:  Seizures in neonates (NBs) remain the most frequent neurological problem in the nursery. Considerable debate about their consequences exists between data and deductions reached through animal experimentations and those obtained through clinical investigations. The main conflicting issues are whether seizures in NBs can plant the roots for epileptogenesis and cause long‐term deficits. The purpose of this chapter is to evaluate both laboratory and clinical results.

Methods: Clinical data will be presented, including a 20‐year‐long cohort of NBs. This will be followed by the main seminal discoveries obtained in neonatal models. The phenomenon of transient or persistent dysmaturity following NB seizures will be discussed in relation to etiological factors.

Results: The findings and deductions from animal models support the notions that epileptogenesis and cognitive deficits result from NB seizures. These conclusions contrast with clinical investigations maintaining that NB seizures, per se, are symptomatic markers of preexisting or of ongoing morbidities. The reasons for contrasting views will be discussed. Suggestions will be advanced for more animal models whose seizures are consistent with the etiologies and the phenotypes of human NB seizures.
Neuroprotective Strategies to Avert Seizure‐Induced Neurodegeneration in Epilepsy
Authors: Naegele Janice R.
Published: June 2007

Summary:  Neurodegeneration in limbic circuits is a hallmark feature of chronic temporal lobe epilepsy (TLE). Studies in experimental animal models and human patients indicate that seizure‐induced neuronal injury involves some active, as well as passive cell death processes. Experimental approaches that inhibit active steps in cell death programs have been shown to reduce neuronal cell death and sclerosis, but not to prevent epileptogenesis in animal models of TLE. These findings suggest that we need additional research using both animal models and brain slices from human patients to understand the pathological mechanisms underlying seizure generation. Such comparative studies will also aid in evaluating the potential therapeutic value of inhibiting cell death in seizure disorders.
The Emotional Climate of Nations and Their Culture of Peace
Authors: De Rivera Joseph , Kurrien Rahael , Olsen Nina
Published: June 2007

Societies seem to have emotional climates that affect how people feel and act in public situations. Unlike the emotions experienced in an individual's personal life, these modal feelings reflect a collective response to the socio‐economic‐political situation of the society and influence how most people behave toward one another and their government. A government may foster a climate of fear to ensure social control, or it may encourage the formation of heterogeneous social groups to facilitate a climate of trust between people from different groups. On one hand, emotional climates may be viewed as reflecting the relative peacefulness or violence of a society. Thus, an assessment of emotional climate may provide a subjective index of human security to complement objective measures of democracy, human rights, equality, and other factors that we presume are beneficial to human welfare. On the other hand, we may view emotional climates as influences that act to further or to impede the development of the culture of peace advocated by the General Assembly of the United Nations. Thus, their assessment may have predictive power, and measuring a society's emotional climate may help us to create desirable policy. In this article we show that it is possible to measure some important aspects of the emotional climates of three nations that have different degrees of a culture of peace: Norway, the United States, and India. We show that estimates of the collective emotions that constitute climate can be distinguished from reports of personal emotions in that the former are more influenced by nation and the latter by social class. It is the subjective experience of national emotional climate, rather than personal emotional experience, that appears most related to objective indices for the culture of peace in the different nations.
The Social Sharing of Emotion as an Interface Between Individual and Collective Processes in the Construction of Emotional Climates
Authors: Rimé Bernard
Published: June 2007

The study of private emotional experiences reveals that an emotion is typically followed by social sharing. Additionally, the target's responses stimulate the sharing person's emotional expression. The reciprocal stimulation of interactants favors empathy and emotional communion. Consequences are two‐fold: (1) the sharing process reactivates emotional arousal in both agent and target, and (2) it strengthens social bonds. Sharing targets also share what they heard with others, who then experience a similar need. Social sharing also develops when an emotional event strikes collectively. In this case, however, the propagation consequences are geared up in a spectacular manner both because there are as many sharing sources as there are members in the community and because every sharing reactivates felt emotions among interactants, thus reloading the propagation flow. It is argued that such chain reactions contribute to construct an emotional climate in the concerned community. It is predicted that emotion sharing would impact (1) on emotional climate in general; (2) on group cohesion and solidarity, with positive consequences for emotional climate; and (3) on collective memory, with potential consequences for emotional climate in the long run. Each of these predictions is detailed and illustrated with available empirical evidence.
Social Sharing, Participation in Demonstrations, Emotional Climate, and Coping with Collective Violence After the March 11th Madrid Bombings1
Authors: Páez Darío , Basabe Nekane , Ubillos Silvia , González‐Castro José Luis
Published: June 2007

This study examined how social sharing and participating in secular political rituals regarding the March‐Eleven (M‐11) 2004 train bombings in Madrid, Spain, helps to cope with the wounds of trauma and enhances the reconstruction of a positive emotional climate. A questionnaire was completed by college students (63% of sample) and their relatives (37%) (N = 661) from five Spanish regions and eight universities at 1, 3, and 8 weeks after the bombing. Participating in demonstrations and experiencing a positive emotional climate, as reported a week after M‐11, predicted the degree of social support and positive affect as well as the amount of posttraumatic growth reported at the 3‐week period. Demonstrations (indirectly) and social sharing (directly) predict positive emotional climate 2 months after the attack. Participation in protest rituals or demonstrations, coupled with elections and changes in government office, helps overcome the effects of collective trauma and leads to an improvement of the emotional climate in the aftermath of a terrorist attack. Participating in ceremonies and rituals reinforces social cohesion and can be conceived of as a communal form of coping, which enhances a culture of peace.
Emotional Climate as Emotion Accessibility: How Countries Prime Emotions
Authors: Fernández‐Dols José‐Miguel , Carrera Pilar , De Mendoza Alejandra Hurtado , Oceja Luis
Published: June 2007

Many everyday collective emotions are shared emotional conventions, that is, social practices with an attributed emotional meaning (e.g., complimenting as a sign of conventional love). Emotional conventions lead to a collective priming of some categories of emotion. For example, New Year Eve's emotional conventions prime words such as “happy.” We define emotional atmosphere and emotional climate as emotion accessibility caused by the priming of specific categories of emotion linked to emotional conventions. We report two sets of data in support of this approach: (1) the accessibility of categories of emotion in relation to unusual historical events (the 1992 World Expo in Seville and the March–April 2004 terrorist attacks in Madrid), and (2) the differential priming of specific categories of emotion on the Internet in different countries. We discuss the theoretical and practical implications of this approach to “emotional climate.”
Collective Emotions in Conflict Situations: Societal Implications
Authors: Bar‐Tal Daniel , Halperin Eran , De Rivera Joseph
Published: June 2007

It is well established today that emotions are an important part of most societal dynamics. The current article focuses on the role of different collective emotional elements in creating, preserving, and resolving conflicts. The main premise is that collective emotions play a pivotal role in shaping individual and societal responses to conflicting events and in contributing to the evolvement of a social context that maintains the emotional climate and collective emotional orientation that have developed. The first part of the article provides a conceptual framework to discuss the relations between conflict, context, and collective emotions. The second part uses the conceptual framework to discuss the societal implications of the articles presented in this issue. Taken together, the parts create a platform for future research on the role of collective emotions in conflict resolution and the construction of cultures of peace.
Albuminuria and Chronic Kidney Disease in Association With the Metabolic Syndrome
Authors: Ninomiya Toshiharu , Kiyohara Yutaka
Published: June 2007

Chronic kidney disease is a worldwide public health problem because it is an important risk factor for cardiovascular disease and premature death. The metabolic syndrome, which is characterized by abdominal obesity, high blood pressure, impaired glucose tolerance, and dyslipidemia, is also an increasingly common disorder and a major risk factor for diabetes and cardiovascular disease. A close association has been found between the metabolic syndrome and the risk for developing renal impairment, clinically expressed in the form of microalbuminuria or chronic kidney disease. Several potential mechanisms, including insulin resistance, renal atherosclerosis, and inflammation, induce the deterioration of renal function. Despite the close association between the metabolic syndrome and renal impairment, it is still unclear whether and to what extent treating the metabolic syndrome will prevent renal impairment. A clinical trial is needed to clarify whether the effect of preventing and treating metabolic syndrome components will result in improved renal prognosis.
C‐Reactive Protein in Cardiovascular Risk Assessment: A Review of the Evidence
Authors: Abraham Jacob , Campbell Catherine Y. , Cheema Aamir , Gluckman Ty J. , Blumenthal Roger S. , Danyi Peter
Published: June 2007

C‐reactive protein (CRP) is an inflammatory biomarker that is strongly associated with coronary heart disease, inflammation, and the metabolic syndrome. Large‐scale prospective cohort trials have shown that measurement of CRP may add predictive accuracy to the Framingham risk score, but interpretation of these data are conflicting. In the primary prevention setting, CRP can be used to reclassify patients in low or intermediate Framingham risk score groups to a higher risk category, thus making them eligible for more intensive pharmacologic interventions.