14 results
Transcriptome profiling in depression with and without loss of appetite
- J. Pawlak, A. Szczepankiewicz, K. Bilska, P. Kapelski, P. Zakowicz, E. Paszynska, M. Dmitrzak-Weglarz
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- Journal:
- European Psychiatry / Volume 66 / Issue S1 / March 2023
- Published online by Cambridge University Press:
- 19 July 2023, p. S423
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Introduction
Depression has been described very comprehensively and is a highly prevalent mental condition. However, how its features develop and clinical course shape remains not fully understood.
ObjectivesThe study aimed to compare mRNA characteristics between specific symptoms and identification of differently expressed genes (DEGs) in patients with depression with specifiers such as loss of appetite, loss of weight, sleep disturbances and psychomotor retardation.
MethodsMaterial and method we used was transcriptome profiling of peripheral blood mononuclear cells in 30 patients diagnosed with depressive episode in course bipolar or unipolar affective disorder. The blood samples were drawn during acute depressive episode with at least moderate severity. The diagnosis and specific symptoms were described according to ICD-10 and DSM5 criteria using SCID-I, OPCRIT, and HDRS. Agilent microarrays were used for transcriptome profiling and GeneSpring software was applied. Minimal fold change 2 and significant p-value <0.05 were assumed. DAVID and KEGG databases were searched.
ResultsComparing depressed patients with and without decreased appetite or weight loss revealed 718 DEGs. When compared depressed patients with and without psychomotor retardation, 95 genes were up- or down regulated. In both comparisons DEGs were not identified as significant according to DAVID and KEGG database. When considering weight loss of more than 2 kg per month, 418 DEGs were identified. According to searched databases only one, characterized with phosphoserine phosphatase activity, was indicated as having a significant role in molecular functioning. The most numerous list of DEGs (n=855) was found when compared depressed patients with and without insomnia. Among these genes, several were indicated as significant for biological processes and cellular components: those linked with response to oxygen-compound, cytoplasmic and secretory vesicles and granules and circulatory system.
ConclusionsNumerous genes are differently expressed in depression with specific clinical features, such as appetite and sleeping disturbances, but their role in pathology remains unclear. One might expect that secretory and circulation activity is involved.
This research was funded by the National Science Center, Poland (Grant No: 2016/23/B/NZ5/02634) and supported by the Poznan University of Medical Sciences in Poland (Statute sources: 502-20-22196440).
Disclosure of InterestNone Declared
Discovery, mode of action, resistance mechanisms, and plan of action for sustainable use of Group 14 herbicides
- Abigail L. Barker, John Pawlak, Stephen O. Duke, Roland Beffa, Patrick J. Tranel, Joe Wuerffel, Bryan Young, Aimone Porri, Rex Liebl, Raphael Aponte, Douglas Findley, Michael Betz, Jens Lerchl, Stanley Culpepper, Kevin Bradley, Franck E. Dayan
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- Journal:
- Weed Science / Volume 71 / Issue 3 / May 2023
- Published online by Cambridge University Press:
- 29 March 2023, pp. 173-188
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Protoporphyrinogen oxidase (PPO)-inhibiting herbicides remain an important and useful chemistry 60 yr after their first introduction. In this review, based on topics introduced at the Weed Science Society of America 2021 symposium titled “A History, Overview, and Plan of Action on PPO Inhibiting Herbicides,” we discuss the current state of PPO-inhibiting herbicides. Renewed interest in the PPO-inhibiting herbicides in recent years, due to increased use and increased cases of resistance, has led to refinements in knowledge regarding the mechanism of action of PPO inhibitors. Herein we discuss the importance of the two isoforms of PPO in plants, compile a current knowledge of target-site resistance mechanisms, examine non–target site resistance cases, and review crop selectivity mechanisms. Consistent and reproducible greenhouse screening and target-site mutation assays are necessary to effectively study and compare PPO-inhibitor resistance cases. To this end, we cover best practices in screening to accurately identify resistance ratios and properly interpret common screens for point mutations. The future of effective and sustainable PPO-inhibitor use relies on development of new chemistries that maintain activity on resistant biotypes and the promotion of responsible stewardship of PPO inhibitors both new and old. We present the biorational design of the new PPO inhibitor trifludimoxazin to highlight the future of PPO-inhibitor development and discuss the elements of sustainable weed control programs using PPO inhibitors, as well as how responsible stewardship can be incentivized. The sustained use of PPO inhibitors in future agriculture relies on the effective and timely communication from mode of action and resistance research to agronomists, Extension workers, and farmers.
Characterisation of age and polarity at onset in bipolar disorder
- Janos L. Kalman, Loes M. Olde Loohuis, Annabel Vreeker, Andrew McQuillin, Eli A. Stahl, Douglas Ruderfer, Maria Grigoroiu-Serbanescu, Georgia Panagiotaropoulou, Stephan Ripke, Tim B. Bigdeli, Frederike Stein, Tina Meller, Susanne Meinert, Helena Pelin, Fabian Streit, Sergi Papiol, Mark J. Adams, Rolf Adolfsson, Kristina Adorjan, Ingrid Agartz, Sofie R. Aminoff, Heike Anderson-Schmidt, Ole A. Andreassen, Raffaella Ardau, Jean-Michel Aubry, Ceylan Balaban, Nicholas Bass, Bernhard T. Baune, Frank Bellivier, Antoni Benabarre, Susanne Bengesser, Wade H Berrettini, Marco P. Boks, Evelyn J. Bromet, Katharina Brosch, Monika Budde, William Byerley, Pablo Cervantes, Catina Chillotti, Sven Cichon, Scott R. Clark, Ashley L. Comes, Aiden Corvin, William Coryell, Nick Craddock, David W. Craig, Paul E. Croarkin, Cristiana Cruceanu, Piotr M. Czerski, Nina Dalkner, Udo Dannlowski, Franziska Degenhardt, Maria Del Zompo, J. Raymond DePaulo, Srdjan Djurovic, Howard J. Edenberg, Mariam Al Eissa, Torbjørn Elvsåshagen, Bruno Etain, Ayman H. Fanous, Frederike Fellendorf, Alessia Fiorentino, Andreas J. Forstner, Mark A. Frye, Janice M. Fullerton, Katrin Gade, Julie Garnham, Elliot Gershon, Michael Gill, Fernando S. Goes, Katherine Gordon-Smith, Paul Grof, Jose Guzman-Parra, Tim Hahn, Roland Hasler, Maria Heilbronner, Urs Heilbronner, Stephane Jamain, Esther Jimenez, Ian Jones, Lisa Jones, Lina Jonsson, Rene S. Kahn, John R. Kelsoe, James L. Kennedy, Tilo Kircher, George Kirov, Sarah Kittel-Schneider, Farah Klöhn-Saghatolislam, James A. Knowles, Thorsten M. Kranz, Trine Vik Lagerberg, Mikael Landen, William B. Lawson, Marion Leboyer, Qingqin S. Li, Mario Maj, Dolores Malaspina, Mirko Manchia, Fermin Mayoral, Susan L. McElroy, Melvin G. McInnis, Andrew M. McIntosh, Helena Medeiros, Ingrid Melle, Vihra Milanova, Philip B. Mitchell, Palmiero Monteleone, Alessio Maria Monteleone, Markus M. Nöthen, Tomas Novak, John I. Nurnberger, Niamh O'Brien, Kevin S. O'Connell, Claire O'Donovan, Michael C. O'Donovan, Nils Opel, Abigail Ortiz, Michael J. Owen, Erik Pålsson, Carlos Pato, Michele T. Pato, Joanna Pawlak, Julia-Katharina Pfarr, Claudia Pisanu, James B. Potash, Mark H Rapaport, Daniela Reich-Erkelenz, Andreas Reif, Eva Reininghaus, Jonathan Repple, Hélène Richard-Lepouriel, Marcella Rietschel, Kai Ringwald, Gloria Roberts, Guy Rouleau, Sabrina Schaupp, William A Scheftner, Simon Schmitt, Peter R. Schofield, K. Oliver Schubert, Eva C. Schulte, Barbara Schweizer, Fanny Senner, Giovanni Severino, Sally Sharp, Claire Slaney, Olav B. Smeland, Janet L. Sobell, Alessio Squassina, Pavla Stopkova, John Strauss, Alfonso Tortorella, Gustavo Turecki, Joanna Twarowska-Hauser, Marin Veldic, Eduard Vieta, John B. Vincent, Wei Xu, Clement C. Zai, Peter P. Zandi, Psychiatric Genomics Consortium (PGC) Bipolar Disorder Working Group, International Consortium on Lithium Genetics (ConLiGen), Colombia-US Cross Disorder Collaboration in Psychiatric Genetics, Arianna Di Florio, Jordan W. Smoller, Joanna M. Biernacka, Francis J. McMahon, Martin Alda, Bertram Müller-Myhsok, Nikolaos Koutsouleris, Peter Falkai, Nelson B. Freimer, Till F.M. Andlauer, Thomas G. Schulze, Roel A. Ophoff
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- Journal:
- The British Journal of Psychiatry / Volume 219 / Issue 6 / December 2021
- Published online by Cambridge University Press:
- 25 August 2021, pp. 659-669
- Print publication:
- December 2021
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Background
Studying phenotypic and genetic characteristics of age at onset (AAO) and polarity at onset (PAO) in bipolar disorder can provide new insights into disease pathology and facilitate the development of screening tools.
AimsTo examine the genetic architecture of AAO and PAO and their association with bipolar disorder disease characteristics.
MethodGenome-wide association studies (GWASs) and polygenic score (PGS) analyses of AAO (n = 12 977) and PAO (n = 6773) were conducted in patients with bipolar disorder from 34 cohorts and a replication sample (n = 2237). The association of onset with disease characteristics was investigated in two of these cohorts.
ResultsEarlier AAO was associated with a higher probability of psychotic symptoms, suicidality, lower educational attainment, not living together and fewer episodes. Depressive onset correlated with suicidality and manic onset correlated with delusions and manic episodes. Systematic differences in AAO between cohorts and continents of origin were observed. This was also reflected in single-nucleotide variant-based heritability estimates, with higher heritabilities for stricter onset definitions. Increased PGS for autism spectrum disorder (β = −0.34 years, s.e. = 0.08), major depression (β = −0.34 years, s.e. = 0.08), schizophrenia (β = −0.39 years, s.e. = 0.08), and educational attainment (β = −0.31 years, s.e. = 0.08) were associated with an earlier AAO. The AAO GWAS identified one significant locus, but this finding did not replicate. Neither GWAS nor PGS analyses yielded significant associations with PAO.
ConclusionsAAO and PAO are associated with indicators of bipolar disorder severity. Individuals with an earlier onset show an increased polygenic liability for a broad spectrum of psychiatric traits. Systematic differences in AAO across cohorts, continents and phenotype definitions introduce significant heterogeneity, affecting analyses.
Antioxidant capacity as a novel biomarker of delirium after cardiac surgery
- J. Kaźmierski, A. Pawlak, P. Miler, H. Jerczyńska, J. Woźniak, E. Frankowska, K. Woźniak, A. Brzezińska, M. Wilczyński
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- Journal:
- European Psychiatry / Volume 64 / Issue S1 / April 2021
- Published online by Cambridge University Press:
- 13 August 2021, pp. S251-S252
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Introduction
Coronary-artery bypass graft (CABG) surgery is known to improve cardiac function and decrease mortality, albeit, this method of treatment is associated with a high risk of postoperative delirium. The pathophysiology of delirium after cardiac surgery is largely unknown.
ObjectivesTo investigate whether oxidative stress reflected by decreased preoperative and postoperative plasma antioxidant capacity (AC) is independently associated with delirium after cardiac surgery. Furthermore, to assess whether the association between AC and the level of soluble receptor for advanced glycation end-products (sRAGE) exists.
MethodsThe patients were examined 1 day preoperatively with the Mini International Neuropsychiatric Interview and MMSE test to screen for depression, anxiety disorders, and for cognitive impairment, respectively. Blood samples for AC and sRAGE levels were collected both preopertively and postoperatively. The CAM ICU and MDAS were used within the first 5 days postoperatively to screen for a diagnosis of delirium.
ResultsPostoperative delirium developed in 34% (61 of 177) of participants. Multivariate stepwise logistic regression analysis revealed that patients with low baseline AC are at significantly increased risk of developing delirium. Moreover, preoperative AC levels were inversly correlated with postoperative sRAGE concentrations (Spearman’s Rank Correlation -0.198; p<0.05). The most optimal cutoff values of the preoperative and postoperative AC that predict the development of delirium were 1.720 mM and 1.893 mM, respectively.
ConclusionsDecreased plasma AC levels are associated with delirium after cardiac surgery and inversly correlated with post-surgery sRAGE concentration. This may be an important pathophysiological consideration in the increased risk of postoperative delirium seen in cardiac surgery patients.
Raised preoperative monocyte chemoattractant protein-1 as the independent predictor of delirium after cardiac surgery. A prospective cohort study
- J. Kaźmierski, P. Miler, A. Pawlak, H. Jerczyńska, E. Frankowska, J. Woźniak, K. Woźniak, A. Brzezińska, M. Wilczyński
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- Journal:
- European Psychiatry / Volume 64 / Issue S1 / April 2021
- Published online by Cambridge University Press:
- 13 August 2021, p. S252
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Introduction
Delirium is a frequent and serious complication of cardiac surgery. However, the knowledge regarding pathogenesis of postoperative delirium is limited.
ObjectivesTo investigate whether increased levels of monocyte chemoattractant protein-1 (MCP-1) and hyper-sensitive C-Reactive Protein (hsCRP) are associated with postoperative delirium in cardiac surgery patients.
MethodsPatients were examined and screened for major depressive disorder (MDD) and cognitive impairment one day preoperatively, using the Mini International Neuropsychiatric Interview and The Mini-Mental State Examination Test. Blood samples were collected pre- and postoperatively for hsCRP and chemokine levels. Following surgical interventions, the Confusion Assessment Method for the Intensive Care Unit and the Memorial Delirium Assessment Scale with the cut-off score 10 were used to diagnose delirium.
ResultsPostoperative delirium screening was found positive in 34% (61 of 177) of patients. Both, pre- and postoperative hsCRP, and preoperative MCP-1 levels were associated with postoperative delirium in univariate comparisons; p=0.001; p=0.0004; p < 0.001, respectively. However, according to a multivariate stepwise logistic regression analysis only MCP-1 concentration raised before surgery was independently associated with postoperative delirium, and related to advancing age of participants (Spearman’s Rank Correlation 0.192; p=0.0103). According to ROC analysis, the most optimal cut-off for MCP-1 concentration in predicting the development of delirium was 371.81 ng/ml with sensitivity of 77.0% and specificity of 58.6%.
ConclusionsThe present study suggests that raised preoperative MCP-1 concentration is independently associated with delirium after cardiac surgery. Preoperative monitoring of pro-inflammatory markers combined with regular surveillance may be helpful in the prediction and early detection of postoperative delirium in this patient group.
YPSP01-14 - CD28 Gene Polymorphism With Respect To Affective Symptoms In Schizophrenia
- D. Frydecka, L. Karabon, J.A. Beszlej, E. Pawlak, E. Dobrzynska, M. Szewczuk-Boguslawska, A. Kiejna
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- Journal:
- European Psychiatry / Volume 25 / Issue S1 / 2010
- Published online by Cambridge University Press:
- 17 April 2020, 25-E1694
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Introduction
Schizophrenia is complex and clinically heterogeneous psychiatric disorder that has an evidenced genetic basis. Several reports indicate a possible role of the activation of the immune system in the pathogenesis of schizophrenia. CD28 is a molecule expressed on T-cells that provides the major co-stimulatory signal required for activation of immune response. For many years now, it has been strongly advocated that biological underpinnings of schizophrenia should be investigated with respect to subpopulations of subjects defined by homogenous symptomatology.
ObjectivesTo investigate the association of polymorphism of the CD28 gene (T17int3C) with respect to schizophrenia symptomatology.
Material and methods105 patients diagnosed with schizophrenia according to ICD-10 criteria and 380 controls were included in the study. The patients were diagnosed using the Operational Criteria for Psychotic Illness checklist (OPCRIT). Based on confirmatory factor analysis on OPCRIT items performed by Serretti et al. (2004), in our study we considered five factors of symptomatology (mania, positive symptoms, disorganization, depression and negative symptoms).
ResultsThere was significant difference in distribution of genotypes between patients with schizophrenia with co-occurring manic symptoms and without co-occurring manic symptoms (respectively CC and/or TC: 23% vs. 47%, TT: 77% vs. 53%, p=0,040). There was also difference in distribution of genotypes between patients with schizophrenia with co-occurring depressive symptoms and without cooccurring depressive symptoms (respectively CC and/or TC: 24% vs. 47%, TT: 76% vs. 53%, p=0,043).
ConclusionWe have shown that CD28 gene polymorphism might increase risk for affective (depressive and/or manic) symptom dimension in schizophrenic patients.
P-1233 - CTLA-4 and Cd28 Gene Polymorphism With Respect to Frontal Lobe Functions in Schizophrenia
- D. Frydecka, A. Beszlej, L. Karabon, E. Pawlak, A. Kiejna
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- Journal:
- European Psychiatry / Volume 27 / Issue S1 / 2012
- Published online by Cambridge University Press:
- 15 April 2020, p. 1
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Introduction
Genetic factors that modulate the immune response have been implicated as risk factors both for schizophrenia as well as for cognitive impairments (endophenotypes of schizophrenia). Regulation of immune response is mediated by two related receptors: CD28 is a major co-stimulator, whereas CTLA-4 performs negative regulatory functions. Balance of immune response depends on the expression of these regulatory molecules due to their genes polymorphisms.
AimThe study was carried out to investigate the association between polymorphisms of two genes: CTLA-4 (49A/G, −319C/T, CT60 A/G) and CD28 (+17C/T) and frontal lobe functions in patients with schizophrenia.
Methods118 patients diagnosed with schizophrenia (ICD-10) and 352 controls were included in the study. Frontal lobe functioning was assessed by Trail Making Test (TMT) and Stroop Test (SCWT).
ResultsThere was no significant difference in distribution of genotypes between patients and controls in the polymorphisms of CTLA-4 gene, but in polymorphism of CD28 gene (p = 0,0007). With respect to +17C/T CD28 gene polymorphism there was a trend level difference in performance on TMT: C allel carriers performed worse that T allel carriers (p = 0,054), suggesting weaker executive control function.
ConclusionsOur data support a role of CD28 +17 C/T gene polymorphisms for the predisposition to schizophrenia. Among patients the distribution of genotypes of CD28 gene polymorphism is similar to that found in patients with autoimmune disorders such as: early onset type 1 diabetes and Behçet's disease. Additionally, +17C/T CD28 gene polymorphism might be considered as a risk factor for cognitive impairment in schizophrenia.
1959 – Neuregulin-1 Gene Polymorphism With Respect To Cognitive Functioning In Schizophrenia
- D. Frydecka, A. Beszlej, P.M. Czerski, P. Kapelski, L. Karabon, A. Kiejna, B. Misiak, E. Pawlak-Adamska, M. Zagdanska, J. Hauser
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- Journal:
- European Psychiatry / Volume 28 / Issue S1 / 2013
- Published online by Cambridge University Press:
- 15 April 2020, 28-E1187
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Background
Neuregulin-1 (NRG1) may be an important factor in pathogenesis of schizophrenia due to its role in neurodevelopmental processes: myelination, neurotransmitter receptor expression and synaptic plasticity. NRG1 has been also implied to play role in cognitive impairments, which are considered to be endophenotypes of schizophrenia, i.e. subclinical, heritable and independent of clinical state traits associated with genetic susceptibility. Surprisingly, a recent meta-analysis (Dickinson, 2007) demonstrated that reliable and easy to administer Digit Symbol Coding Task (DSCT) discriminate people with schizophrenia from comparison individuals better than the more widely studied neuropsychological instruments.
PurposeThe study was carried out to investigate the association of a polymorphisms of the NRG1 gene (rs62510682) and schizophrenia with respect to performance on DSCT.
Material and methodsWe included 103 patients diagnosed with schizophrenia according to ICD-10 criteria and 578 controls in our study. The patients were evaluated for lifetime psychotic symptomatology using the Operational Criteria for Psychotic Illness (OPCRIT) checklist. DSCT was administered to 80 patients.
ResultsThe polymorphisms were in HWE both in the cases’ and controls’ groups. In single marker analysis, we did not find an association for the SNP tested. However; we have found that T allel carriers (TT and/or GT genotype) performed worse than G allel carriers (p=0.4) suggesting weaker cognitive processing efficiency.
ConclusionOur data do not support the role of the NRG1 gene polymorphism (rs62510682) in the predisposition to schizophrenia; however, the studied SNP might be considered to be a risk factor for cognitive impairment in schizophrenia.
EPA-0505 - NRG1 and DISC1 Gene Polymorphisms with Respect to Cognitive Endophenotype in Schizophrenia
- D. Frydecka, JA. Beszlej, A. Kiejna, E. Pawlak-Adamska, L. Karabon
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- Journal:
- European Psychiatry / Volume 29 / Issue S1 / 2014
- Published online by Cambridge University Press:
- 15 April 2020, p. 1
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Background:
Neuregulin-1 (NRG1) and DISC1 may be important factors in pathogenesis of schizophrenia due to their role in neurodevelopmental processes. NRG1 and DISC1 link directly into a common pathway mediated by Erb receptors and P13K/AKT1 signaling and have been implied to play role in cognitive impairments. Digit Symbol Coding Task (DSCT) from WAIS-R is a sensitive measure for cognitive decline in schizophrenia as well as it indexes poor prognosis and functional disability in schizophrenia.
Purpose:The study was carried out to investigate the association of a polymorphisms of the NRG1 gene (rs62510682) as well as of DISC1 gene (rs1538979) and schizophrenia with respect to performance on DSCT.
Material and methods:We included 103 patients diagnosed with schizophrenia according to ICD-10 criteria and 578 controls. In addition to unstructured interviews and review of medical records, the patients were evaluated for lifetime psychotic symptomatology using OPCRIT checklist. DCSTR was administered to 80 patients.
Results:The polymorphisms were in HWE for healthy controls and schizophrenia patients. In single marker analysis, we did not find an association for the SNPs tested. However; with respect to DCST we found that with respect to NRG1 gene T allel carriers performed worse than G allel carriers (p<0.5) and with respect to DISC1 gene patients with TC genotype performed worse than with CC genotype (p<0.05).
Conclusion:Our data do not support the role of NRG1 or DISC gene polymorphisms in the predisposition to schizophrenia; however, they might be considered as risk factors for the cognitive decline in schizophrenia.
2144 – IL-2, IL-6, IFN-gamma And Tgf-beta Genetic Polymorphism With Respect To Susceptibility To Schizophrenia
- D. Frydecka, A. Beszlej, L. Karabon, E. Pawlak-Adamska, A. Tomkiewicz, A. Partyka, B. Misiak, P. Piotrowski, M. Zagdanska, A. Kiejna
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- Journal:
- European Psychiatry / Volume 28 / Issue S1 / 2013
- Published online by Cambridge University Press:
- 15 April 2020, 28-E1316
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Background
Schizophrenia is a chronic severe psychiatric disorder with multiple environmental and genetic determinants. Several reports indicate the possible role of immune system dysregulation in the pathogenesis of schizophrenia. An accumulating body of evidence indicates an association of schizophrenia and its psychopathology with altered cytokine production. The variation of the level of cytokines might be partly due to their functional gene polymorphism.
PurposeThe study was carried out to investigate the association of schizophrenia with the following cytokine polymorphisms: IL-2 (-330T/G), IL-6 (-174G/C), IFN-gamma (+874 T/A), TGF-beta (+869 T/C and +915 G/C).
Material and methodsWe included 130 patients diagnosed with schizophrenia and 184 controls in our study. The patients were evaluated for lifetime psychotic symptomatology using the Operational Criteria for Psychotic Illness (OPCRIT) checklist. The patients having history of traumatic brain injury, neurologic disorders, substance abuse or immune related diseases were excluded from the study by detailed medical examination.
ResultsThe polymorphisms were in HWE both in the cases’ and controls’ groups. In single marker analysis, we did not find an association for the tested polymorphisms.
ConclusionOur data do not support the role of IL-2, IL-6, IFN-gamma and TGF-beta gene polymorphisms in the predisposition to schizophrenia in the Polish population.
Interleukin-receptor antagonist (IL1-RA) with respect to schizophrenia psychopathology
- D. Frydecka, B. Misiak, P. Sedlaczek, E. Pawlak-Adamska
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- Journal:
- European Psychiatry / Volume 33 / Issue S1 / March 2016
- Published online by Cambridge University Press:
- 23 March 2020, p. s220
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Introduction
The influence of the immune deregulation on the risk and psychopathology of schizophrenia is increasingly recognized in the literature.
AimTo assess the association between serum IL-1RA on schizophrenia psychopathology.
MethodsWe recruited 88 schizophrenia patients (38 males and 49 females, mean age 38.12 ± 12.67 years) and 88 healthy adult control subjects (68 males, 20 females, mean age 40.63 ± 7.99 years). Lifetime psychopathology was evaluated using Operational Criteria for Psychotic Illness (OPCRIT) checklist, while current psychopathology was assessed using Positive and Negative Syndrome Scale (PANSS). Serum samples were stored in aliquots at –80 °C. Serum levels of IL1-RA were measured using Immunoassay (ELISA).
ResultsThere were statistically significant differences between schizophrenia patients and healthy controls (median ± interquartile range: 350,81 ± 227.04 and 888.74 ± 762.63, respectively [pg/ml]) (U Mann–Whitney test, Z = –7.99, P < 0.0001). There were no differences in serum IL1-RA levels between male and female among patients with schizophrenia (U Mann–Whitney test, Z = –0.22, P = 0.82) nor among healthy control subjects (U Mann–Whitney test, Z = –0.17, P = 0.86). Among schizophrenia patients, there was a trend-level association between IL-1RA serum level with negative symptoms (Spearman correlation coefficient, r = –0.23, P = 0.056), positive symptoms (Spearman correlation coefficient r = –0.22, P = 0.066), and on a statistically significant level with general symptoms (Spearman correlation coefficient r = –0.28, P = 0.018).
ConclusionSerum IL1-RA level is higher in schizophrenia patients in comparison to healthy controls and it is associated with schizophrenia psychopathology.
Disclosure of interestThe authors have not supplied their declaration of competing interest.
On the bulk motion of the cerebrospinal fluid in the spinal canal
- A. L. Sánchez, C. Martínez-Bazán, C. Gutiérrez-Montes, E. Criado-Hidalgo, G. Pawlak, W. Bradley, V. Haughton, J. C. Lasheras
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- Journal:
- Journal of Fluid Mechanics / Volume 841 / 25 April 2018
- Published online by Cambridge University Press:
- 20 February 2018, pp. 203-227
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Radionuclide scanning images published in Nature by Di Chiro in 1964 showed a downward migration along the spinal canal of particle tracers injected in the brain ventricles while also showing an upward flow of tracers injected in the lumbar region of the canal. These observations, since then corroborated by many radiological measurements, have been the basis for the hypothesis that there must be an active circulation mechanism associated with the transport of cerebrospinal fluid (CSF) deep down into the spinal canal and subsequently returning a portion back to the cranial vault. However, to date, there has been no physical explanation for the mechanism responsible for the establishment of such a bulk recirculating motion. To investigate the origin and characteristics of this recirculating flow, we have analyzed the motion of the CSF in the subarachnoid space of the spinal canal. Our analysis accounts for the slender geometry of the spinal canal, the small compliance of the dura membrane enclosing the CSF in the canal, and the fact that the CSF is confined to a thin annular subarachnoid space surrounding the spinal cord. We apply this general formulation to study the characteristics of the flow generated in a simplified model of the spinal canal consisting of a slender compliant cylindrical pipe with a coaxial cylindrical inclusion, closed at its distal end, and subjected to small periodic pressure pulsations at its open entrance. We show that the balance between the local acceleration and viscous forces produces a leading-order flow consisting of pure oscillatory motion with axial velocities on the order of a few centimetres per second and amplitudes monotonically decreasing along the length of the canal. We then demonstrate that the nonlinear term associated with the convective acceleration contributes to a second-order correction consisting of a steady streaming that generates a bulk recirculating motion of the CSF along the length of the canal with characteristic velocities two orders of magnitude smaller than the leading-order oscillatory flow. The results of the analysis of this idealized geometry of the spinal canal are shown to be in good agreement not only with experimental measurements in an in-vitro model but also with radiological measurements conducted in human adults.
Current Understanding and Modeling of B Diffusion and Activation Anomalies in Preamorphized Ultra-Shallow Junctions
- B. Colombeau, A.J. Smith, N.E.B. Cowern, B.J. Pawlak, F. Cristiano, R. Duffy, A. Claverie, C.J. Ortiz, P. Pichler, E. Lampin, C. Zechner
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- Journal:
- MRS Online Proceedings Library Archive / Volume 810 / 2004
- Published online by Cambridge University Press:
- 17 March 2011, C3.6
- Print publication:
- 2004
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The formation of ultra-shallow junctions (USJs) for future integrated circuit technologies requires preamorphization and high dose boron doping to achieve high activation levels and abrupt profiles. To achieve the challenging targets set out in the semiconductor roadmap, it is crucial to reach a much better understanding of the basic physical processes taking place during USJ processing. In this paper we review current understanding of dopant-defect interactions during thermal processing of device structures – interactions which are at the heart of the dopant diffusion and activation anomalies seen in USJs. First, we recall the formation and thermal evolution of End of Range (EOR) defects upon annealing of preamorphized implants (PAI). It is shown that various types of extended defect can be formed: clusters, {113} defects and dislocation loops. During annealing, these defects exchange Si interstitial atoms and evolve following an Ostwald ripening mechanism. We review progress in developing models based on these concepts, which can accurately predict EOR defect evolution and interstitial transport between the defect layer and the surface. Based on this physically based defect modelling approach, combined with fully coupled multi-stream modelling of dopant diffusion, one can perform highly predictive simulations of boron diffusion and de/re-activation in Ge-PAI boron USJs. Agreement between simulations and experimental data is found over a wide range of experimental conditions, clearly indicating that the driving mechanism that degrades boron junction depth and activation is the dissolution of the interstitial defect band. Finally, we briefly outline some promising methods, such as co-implants and/or vacancy engineering, for further down-scaling of source-drain resistance and junction depth.
Does the Latent Track Occurrence in Amorphous Materials Result from a Transient Thermal Process?
- M. Toulemonde, Ch. Dufour, E. Paumier, F. Pawlak
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- Journal:
- MRS Online Proceedings Library Archive / Volume 504 / 1997
- Published online by Cambridge University Press:
- 10 February 2011, 99
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- 1997
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Heavy ion irradiations in the electronic stopping power (Se.) regime have been performed in amorphous materials. Latent tracks have been observed in amorphous semiconductors (a-Ge, a-Si) and their radii have been deduced from a phenomenological analysis in an amorphous metallic alloy, in vitreous silica and “polymer” like amorphous carbon. A transient thermal model is developed describing the energy diffusion by the electron gas, by the atomic lattice and the energy exchange between the two subsystems. According to Fick's law, the classical equations of heat flow in the two subsystems (electrons and atoms) are numerically solved in a cylindrical geometry taking into account the temperature dependence of all the parameters. A simulation of annealing of nuclear collisions induced defects in crystalline iron allows to determine a local temperature. Electronic defect creation occurs when Se. increases and becomes larger than a threshold which is correlated with the appearance of a molten phase. Using such a criterion, the radii of latent tracks are reproduced in both a - Ge and a - Si with the same value of the electron-phonon coupling despite large differences in their lattice thermodynamic parameters. Such a model is applied to amorphous metallic alloy Fe85B15, vitreous silica and amorphous carbon.