bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased frequency of arousal parasomnias in families with nocturnal frontal lobe epilepsy: A common mechanism?
Authors: Bisulli Francesca , Vignatelli Luca , Naldi Ilaria , Licchetta Laura , Provini Federica , Plazzi Giuseppe , Di Vito Lidia , Ferioli Simona , Montagna Pasquale , Tinuper Paolo 
Published: May 2010

SummaryPurpose:  Retrospective observations disclosed an overlap between parasomnias and nocturnal frontal lobe epilepsy (NFLE) not only in patients but also in their relatives, suggesting a possible common pathogenetic mechanism. This study aimed to verify whether relatives of patients with NFLE have a higher frequency of parasomnias, namely arousal disorders, and thereby shed light on the still unknown pathophysiologic mechanisms underlying NFLE.Methods:  We undertook a case–control family study in which we recruited NFLE probands and healthy controls, matched for age, sex, education, and geographic origin. At least four relatives were included for each proband and control. Each subject underwent a standardized interview, with application of the International Classification of Sleep Disorders–Revised (ICSD‐R 2001) minimal criteria to diagnose the lifetime prevalence of the main parasomnias.Results:  Four hundred fifty‐eight individuals were recruited: 33 NFLE probands, 200 relatives of probands, 31 controls, and 194 control relatives. All NFLE probands but one have sporadic NFLE. The lifetime prevalence of the following parasomnias differed in proband relatives versus control relatives: arousal disorders [odds ratio (OR) 4.7, 95% confidence interval (CI) 2.0–11.6; p < 0.001] and nightmares (OR 2.6, 95% CI 1.6–4.2; p < 0.001) were more frequent among NFLE proband relatives. In the secondary analysis comparing NFLE probands to controls, arousal disorders (OR 6.3, 95% CI 1.3–31.7; p = 0.023) and bruxism (OR 5.4, 95% CI 1.3–21.7; p = 0.017) were more frequent among NFLE probands.Discussion:  The higher frequency of arousal disorders in NFLE families suggests an intrinsic link between parasomnias and NFLE and an abnormal (possibly cholinergic) arousal system as a common pathophysiologic mechanism.
Anxiety disorders, subsyndromic depressive episodes, and major depressive episodes: Do they differ on their impact on the quality of life of patients with epilepsy?
Authors: Kanner Andres M. , Barry John J. , Gilliam Frank , Hermann Bruce , Meador Kimford J. 
Published: May 2010

SummaryAims of the study:  To compare the impact of anxiety disorders, major depressive episodes (MDEs), and subsyndromic depressive episodes (SSDEs) on the quality of life of patients with epilepsy (PWEs), and to identify the variables predictive of poor quality of life.Methods:  A psychiatric diagnosis according to DSM‐IV‐TR criteria was established in 188 consecutive PWEs with the MINI International Neuropsychiatric Interview. Patients also completed the Beck Depression Inventory‐II (BDI‐II), the Centers for Epidemiologic Studies‐Depression (CES‐D), and the Quality of Life in Epilepsy‐89 (QOLIE‐89). A diagnosis of SSDE was made in any patient with total scores of the BDI‐II >12 or CES‐D >16 in the absence of any DSM‐IV diagnosis of mood disorder according to the MINI.Results:  Patients with SSDEs (n = 26) had a worse quality of life than asymptomatic patients (n = 103). This finding was also observed among patients with MDEs only (n = 10), anxiety disorders only (n = 21), or mixed MDEs/anxiety disorders (n = 28). Furthermore, having mixed SSDEs/anxiety disorders yielded a worse quality of life than having only SSDEs. Independent predictors of poor quality of life included having a psychiatric disorder and persistent epileptic seizures in the last 6 months.Conclusions:  Although isolated mood and anxiety disorders, including SSDE, have a comparable negative impact on the quality of life of PWEs; the comorbid occurrence of mood and anxiety disorders yields a worse impact. In addition, seizure freedom in the previous 6 months predicts a better quality of life.
Densities of glutamatergic and GABAergic presynaptic terminals are altered in experimental cortical dysplasia
Authors: Zhou Fu‐Wen , Roper Steven N. 
Published: May 2010

SummaryPurpose:  Cortical dysplasia (CD) is a major cause of epilepsy in children and adults, but underlying mechanisms of epileptogenesis in this disorder are poorly understood. We have utilized the irradiated rat model to study an injury‐based form of diffuse CD in rats. Prior studies in this model have shown reduced numbers of γ‐aminobutyric acid (GABA)ergic interneurons and reduced inhibitory synaptic currents in pyramidal cells in CD. We analyzed the number of excitatory and inhibitory presynaptic terminals in the neocortex of irradiated rats to better characterize altered connectivity in experimental CD.Methods:  Antibodies to vesicular glutamate transporter 1 (VGLUT1), vesicular glutamate transporter 2 (VGLUT2), vesicular GABA transporter (VGAT), and parvalbumin (PV) were used to quantify glutamatergic and GABAergic presynaptic terminals in control and dysplastic cortex.Results:  We found that the density of VGLUT1 terminals was increased in CD in comparison to layers IV, V, and VI in control cortex. VGLUT2 terminals were increased in CD compared to layers IV and VI. VGAT terminals were reduced in CD compared to layers II/III, IV, and V in controls as were PV‐immunoreactive somata and terminals.Discussion:  These findings suggest an overall increase in excitatory synaptic connectivity and decrease in inhibitory synaptic connectivity in CD in irradiated rat. We propose that these changes contribute to hyperexcitability in these animals and may contribute to epileptogenicity in some forms of human CD.
Modulating P‐glycoprotein regulation: Future perspectives for pharmacoresistant epilepsies?
Authors: Potschka Heidrun 
Published: May 2010

SummaryEnhanced brain efflux of antiepileptic drugs by the blood–brain barrier transporter P‐glycoprotein is discussed as one mechanism contributing to pharmacoresistance of epilepsies. P‐glycoprotein overexpression has been proven to occur as a consequence of seizure activity. Therefore, blocking respective signaling events should help to improve brain penetration and efficacy of P‐glycoprotein substrates. A series of recent studies revealed key signaling factors involved in seizure‐associated transcriptional activation of P‐glycoprotein. These data suggested several interesting targets, including theN‐methyl‐d‐aspartate (NMDA) receptor, the inflammatory enzyme cyclooxygenase‐2, and the prostaglandin E2 EP1 receptor. These targets have been further evaluated in rodent models, demonstrating that targeting these factors can control P‐glycoprotein expression, improve antiepileptic drug brain penetration, and help to overcome pharmacoresistance. In general, the approach offers particular advantages over transporter inhibition as it preserves basal transporter function. In this review the different strategies for blocking P‐glycoprotein upregulation, including their therapeutic promise and drawbacks are discussed. Moreover, pros and cons of the approach are compared to those of alternative strategies to overcome transporter‐associated resistance. Regarding future perspectives of the novel approach, there is an obvious need to more clearly define the clinical relevance of transporter overexpression. In this context current efforts are discussed, including the development of imaging tools that allow an evaluation of P‐glycoprotein function in individual patients.
Infantile spasms treated with the ketogenic diet: Prospective single‐center experience in 104 consecutive infants
Authors: Hong Amanda M. , Turner Zahava , Hamdy Rana F. , Kossoff Eric H. 
Published: May 2010

SummaryPurpose:  In 2002, we reported our preliminary experience using the ketogenic diet (KD) for predominantly intractable infantile spasms (IS) in 23 infants. Since that time, we have increased our use of the KD for this condition including those with new‐onset IS.Methods:  Infants were referred and prospectively started on the traditional KD from 1996 to 2009 at our institution. Included subjects had documented clinical IS, hypsarrhythmia on electroencephalography (EEG), and parental consent to start the KD. Efficacy was assessed through phone communication, clinic visits, and EEG every 3 months.Results:  One hundred four infants, mean age 1.2 years, were started on the KD for IS, of which 74 (71%) had a symptomatic etiology. Previous therapy for this patients included a mean of 3.6 anticonvulsants; 71% including corticosteroids or vigabatrin. Using an intent‐to‐treat analysis, >50% spasm improvement occurred in 64% at 6 months and 77% after 1–2 years. Thirty‐eight (37%) became spasm‐free for at least a 6‐month period within a median 2.4 months of starting the KD. In addition, 62% reported improvement in development, 35% had EEG improvement, and 29% were able to reduce concurrent anticonvulsants. Adverse effects were noted in 33%, of which 6% had diminished linear growth. Older age at onset of IS and fewer prior anticonvulsants were more likely to be associated with >90% spasm improvement at 6 months.Discussion:  The KD is an efficacious therapy for IS in approximately two‐thirds of patients treated, and it should be considered strongly after failure of corticosteroids and vigabatrin.
Failure to detect association between polymorphisms of the sodium channel gene SCN1A and febrile seizures in Chinese patients with epilepsy
Authors: Zhang Chunbo , Wong Virgina , Ng Ping Wing , Lui Colin Hiu Tung , Sin Ngai Chuen , Wong Ka Sing , Baum Larry , Kwan Patrick 
Published: May 2010

SummaryA recent study in Caucasians found an association between the single nucleotide polymorphism (SNP) of SCN1A, IVS5N +5 G>A (rs3812718), and febrile seizures (FS). We examined whether this and other tagging SNPs of SCN1A were associated with an increased risk of FS in Han Chinese. A total of 728 Han Chinese patients with focal epilepsy were recruited: 97 had a history of FS (58% male, mean age 35 ± 12 years) and 631 did not (50% male, mean age 40 ± 15 years). Genotyping was performed for IVS5N +5 G>A and seven other tagging SNPs selected from the HapMap database. Genotyping was also performed in 848 ethnically matched population controls (50% male, mean age 37 ± 17 years). There was no statistically significant difference in either allele or genotype frequency of any of the SNPs studied between epilepsy patients with and without FS, and between epilepsy patients with FS and controls. The results do not suggest that SCN1A SNPs are susceptibility factors for FS in Han Chinese.
Effective reduction of transfusion‐related acute lung injury risk with male‐predominant plasma strategy in the American Red Cross (2006‐2008)
Authors: Eder Anne F. , Herron Jr Ross M. , Strupp Annie , Dy Beth , White Jenni , Notari Edward P. , Dodd Roger Y. , Benjamin Richard J. 
Published: May 2010

BACKGROUND:Plasma components from female donors were responsible for most cases of transfusion‐related acute lung injury (TRALI) reported to the American Red Cross (ARC) between 2003 and 2005. Consequently, we began preferentially distributing plasma from male donors for transfusion in 2006 and evaluated the effect on reported TRALI cases in the ensuing 2 years.STUDY DESIGN AND METHODS:Suspected TRALI cases reported to the ARC Hemovigilance Program in calendar years (CY) 2006, 2007, and 2008 are described. Any case involving a fatality was also independently reviewed by three ARC physicians and classified as probable TRALI or not TRALI.RESULTS:The percentage of plasma collected from male donors and distributed for transfusion increased each year from 55% in CY2006 to 79% in CY2007 and 95% in CY2008. Independent medical review of the 77 reported TRALI cases involving a fatality identified 38 cases as probable TRALI. Plasma was the only component transfused in six of these cases in 2006, five in 2007, and zero in 2008. Overall, the analysis of reported fatalities and nonfatal cases demonstrates that TRALI involving only plasma transfusion was significantly reduced in 2008 compared to 2006 (32 vs. 7 cases; odds ratio [OR] = 0.21; 95% confidence interval [CI] = 0.08‐0.45), to a level that was no longer different from the rate of TRALI observed for RBC transfusion (4.0 vs. 2.3 per 106distributed components; OR = 1.78; 95% CI = 0.67‐4.36).CONCLUSIONS:Reported TRALI cases from plasma transfusion decreased in 2008 compared to the prior 2 years simultaneously with the conversion to male‐predominant plasma for transfusion.
Association between length of storage of transfused red blood cells and multiple organ dysfunction syndrome in pediatric intensive care patients
Authors: Gauvin France , Spinella Philip C. , Lacroix Jacques , Choker Ghassan , Ducruet Thierry , Karam Oliver , Hébert Paul C. , Hutchison James S. , Hume Heather A. , Tucci Marisa ,   on behalf of the Canadian Critical Care Trials Group and the Pediatric Acute Lung Injury and Sepsis Investigators (PALISI) Network
Published: May 2010

BACKGROUND: The objective was to determine if there is an association between red blood cell (RBC) storage time and development of new or progressive multiple organ dysfunction syndrome (MODS) in critically ill children.STUDY DESIGN AND METHODS: This was an analytic cohort analysis of patients enrolled in a randomized controlled trial, TRIPICU (Transfusion Requirements in Pediatric Intensive Care Units; ISRCTN37246456), in which stable critically ill children were randomly assigned to a restrictive or liberal strategy. Transfused patients were analyzed using three different sliding time cutoffs (7, 14, and 21 days). Storage time for multiply transfused patients was defined according to the oldest unit transfused.RESULTS: A total of 455 patients were retained (liberal, 310; restrictive, 145). Multivariate logistic regression was performed to determine independent associations. In the restrictive group, a maximum RBC storage time of more than 21 days was independently associated with new or progressive MODS (adjusted odds ratio [OR], 3.29; 95% confidence interval [CI], 1.21‐9.04). The same association was found in the liberal group for a storage time of more than 14 days (adjusted OR, 2.50; 95% CI, 1.12‐5.58). When the two groups were combined in a meta‐analysis, a storage time of more than 14 days was independently associated with increased MODS (adjusted OR, 2.23; 95% CI, 1.20‐4.15) and more than 21 days was associated with increased Pediatric Logistic Organ Dysfunction (PELOD) scores (adjusted mean difference, 4.26; 95% CI, 1.99‐6.53) and higher mortality (9.2% vs. 3.8%).CONCLUSION: Stable critically ill children who receive RBC units with storage times longer than 2 to 3 weeks may be at greater risk of developing new or progressive MODS.
Successful desensitization to immunoglobulin A in a case of transfusion‐related anaphylaxis
Authors: Kiani‐Alikhan Sorena , Yong Patrick F.K. , Grosse‐Kreul Dorothea , Height Susan E. , Mijovic Aleksandar , Suddle Abid R. , Ibrahim Mohammad A.A. 
Published: May 2010

BACKGROUND: A history of anaphylaxis after transfusion of immunoglobulin A (IgA)‐containing blood products in selective IgA‐deficient (sIgAD) patients can be a major problem, particularly in emergencies, when large quantities of blood products are required.CASE REPORT: A 19‐year‐old woman with end‐stage Type 2 autoimmune hepatitis required liver transplantation as her only remaining treatment option. However, she also had sIgAD, anti‐IgA antibodies, and episodes of anaphylaxis after receiving IgA‐containing blood products. Liver transplantation would have been extremely challenging due to the difficulty of obtaining sufficient blood products from suitable IgA‐deficient donors. Hence, it became imperative to devise a protocol to desensitize her to IgA‐containing blood products.RESULTS: Using a continuous infusion of an IgA‐enriched (6 mg/mL IgA) immunoglobulin preparation with gradual increases in concentration, she was successfully desensitized to IgA. Consequently, she was able to receive standard platelets, fresh‐frozen plasma, and red blood cells with no complications.CONCLUSION: This approach could prove very useful in similar cases that may require administration of large quantities of blood products particularly in emergency lifesaving circumstances.
Complement C1q enhances homing‐related responses of hematopoietic stem/progenitor cells
Authors: Jalili Ali , Marquez‐Curtis Leah , Shirvaikar Neeta , Wysoczynski Marcin , Ratajczak Mariusz , Janowska‐Wieczorek Anna 
Published: May 2010

BACKGROUND: Previously, we reported that the complement cleavage fragments C3a and C5a are important modulators of trafficking of hematopoietic stem/progenitor cells (HSPCs). The aim of this study was to examine a possible role for complement component 1, subcomponent q (C1q) in HSPC migration.STUDY DESIGN AND METHODS: CD34+ HSPCs isolated from cord blood (CB), bone marrow (BM), and granulocyte–colony‐stimulating factor (G‐CSF)‐mobilized peripheral blood (mPB) were evaluated for the expression of C1q and its receptor for phagocytosis (C1qRp) using reverse transcription–polymerase chain reaction, Western blotting, and fluorescence‐activated cell sorting. Chemotactic responses and chemoinvasiveness toward stromal cell–derived factor (SDF)‐1 and expression of matrix metalloproteinase (MMP)‐9 were also examined after C1q stimulation. Moreover, G‐CSF– and zymosan‐induced mobilization was evaluated in C1q‐deficient mice.RESULTS: C1q was expressed in CD34+ cells from mPB, but not from CB or steady‐state BM; however, stimulation of the latter with G‐CSF induced C1q expression. C1qRp receptor was found on BM, CB, and mPB CD34+ cells and more mature ex vivo expanded myeloid and megakaryocytic precursors. Although C1q itself was not a chemoattractant for HSPCs, it primed/enhanced the chemotactic response of CD34+ cells to a low SDF‐1 gradient and their chemoinvasion across the reconstituted basement membrane Matrigel and increased secretion of MMP‐9 by these cells. Moreover, in in vivo studies C1q‐deficient mice were found to be easy G‐CSF mobilizers compared to wild‐type mice and normal zymosan mobilizers.CONCLUSION: We demonstrated that C1q primes the responses of CD34+ HSPCs to an SDF‐1 gradient, which may enhance their ability to stay within BM niches, suggesting that the C1q/C1qRp axis contributes to HSPC homing/retention in BM.
Limited prognostic value of tissue protein expression levels of BCl‐2 in Danish ovarian cancer patients: from the Danish ‘MALOVA’ ovarian cancer study
Authors: Høgdall ESTRID V.S. , Christensen Lise , Kjaer Susanne K. , Blaakaer Jan , Christensen Ib Jarle , Høgdall Claus K. 
Published: May 2010

Høgdall EVS, Christensen L, Kjaer SK, Blaakaer J, Christensen IJ, Høgdall CK. Limited prognostic value of tissue protein expression levels of BCl‐2 in Danish ovarian cancer patients. APMIS 2010; 118: 557–64.The purpose of the study was to determine the expression of BCl‐2 in epithelial ovarian tumors and to correlate expression levels with selected clinicopathologic parameters, time to progression and prognosis of the disease. Using tissue arrays (TA), we analyzed BCl‐2 expression in tissues from 191 women diagnosed with low malignant potential ovarian tumors (LMP) and from 582 patients diagnosed with ovarian cancer (OC). Using 30% as cutoff level for BCl‐2 overexpression, 5% of LMPs were positive with a higher proportion of serous ovarian tumor of LMP, compared to mucinous ovarian tumor of LMP (p = 0.02). Women with a BCl‐2‐positive LMP tumor were older than women with a BCl‐2 negative tumor (p = 0.02). Ten percent of OCs were positive for BCl‐2 expression (≥30%). No significant association was found between BCl‐2 expression levels and histologic type of tumors (serous vs mucinous, p = 0.19). A 30% cutoff value or a percentage scale showed that BCl‐2 expression had no prognostic value, both in univariate and in multivariate survival analyses. No difference in time to progression was observed between patients with BCl‐2‐positive and negative tumors. These data suggest that BCl‐2 expression may not be of important clinical value in the treatment of Danish OC patients.
Resistin Concentration is Increased in the Peritoneal Fluid of Women with Endometriosis
Authors: Yi Kyong Wook , Shin Jung‐Ho , Park Hyun Tae , Kim Tak , Kim Sun Haeng , Hur Jun‐Young 
Published: May 2010

Citation Yi KW, Shin J‐H, Park HT, Kim T, Kim SH, Hur J‐Y. Resistin concentration is increased in the peritoneal fluid of women with endometriosis. Am J Reprod Immunol 2010Problem  The aim of this study was to investigate the concentration of resistin and adiponectin in the peritoneal fluid (PF) of patients with endometriosis.Method of study  PF sampling was obtained from women with (n = 48) and without endometriosis (n = 36), and the anthropometric indices of the patients were measured. Resistin and adiponectin concentrations in the PF were determined using the enzyme‐linked immunosorbent assay.Results  The mean concentration of PF resistin was significantly higher in women with endometriosis compared to the controls. PF resistin concentrations were not associated with any of the anthropometric indices. The PF adiponectin did not differ between the two groups, but showed a significant association with the weight, body mass index, and hip circumference. After adjusting for these factors, PF adiponectin expression was not associated with endometriosis.Conclusion  The findings of this study suggest a potent role for resistin in endometriosis. Further studies are needed to elucidate the biological implications of resistin in endometriosis.
Keratinocyte Growth Factor Stimulates Macrophage Inflammatory Protein 3α and Keratinocyte‐derived Chemokine Secretion by Mouse Uterine Epithelial Cells
Authors: Haddad Severina N. , Wira Charles R. 
Published: May 2010

Citation Haddad SN, Wira CR. Keratinocyte growth factor stimulates macrophage inflammatory protein 3α and keratinocyte‐derived chemokine secretion by mouse uterine epithelial cells. Am J Reprod Immunol 2010; 64: 197–211Problem  Communication between uterine epithelial cells and the underlying stromal fibroblasts is critical for proper endometrial function. Stromal fibroblast‐derived growth factors have been shown to regulate epithelial immune functions. The purpose of this study was to determine whether keratinocyte growth factor (KGF) regulates uterine epithelial cell chemokine and antimicrobial secretion.Method of study  Uterine epithelial cells were isolated from Balb/c mice and cultured in either 96‐well plates or transwell inserts. Epithelial cells were treated with KGF, epidermal growth factor (EGF), or hepatocyte growth factor (HGF). Macrophage inflammatory protein 3α (MIP3α) and keratinocyte‐derived chemokine (KC) levels were measured by ELISA.Results  Keratinocyte growth factor stimulated the secretion of MIP3α and KC. The effects on MIP3α by KGF were specific because EGF and HGF had no effect. In contrast, KGF, EGF, and HGF had similar effects on KC. Furthermore, KGF administered to the apical side of epithelial cells had no effect on MIP3α or KC secretion, indicating that the KGF receptor is located on the basolateral surface of uterine epithelial cells.Conclusion  We demonstrate that KGF plays a role in uterine epithelial cell secretion of MIP3α and KC, key immune mediators involved in the protection of mucosal surfaces in the female reproductive tract.