Human psychopharmacology最新文献

{"title":"Effects of Caffeine and Stress on Persistence and Performance in an Unsolvable Visual Search Task in Humans.","authors":"Parssa Akbari, Sabrina R Comess, Olivia Henkoff, Phyllis Oduor, Sarah M Turgeon","doi":"10.1002/hup.70014","DOIUrl":"10.1002/hup.70014","url":null,"abstract":"<p><strong>Objective: </strong>To assess the effect of caffeine and stress on behavior during unsolvable tasks in humans.</p><p><strong>Methods: </strong>College students were given no gum, gum or gum containing 40 mg caffeine (Experiment 1); gum or 100 mg gum (Experiment 2); or the socially evaluated cold pressor test (SECPT) or warm water followed by gum or 100 mg caffeine gum (Experiment 3). Performance was considered to be the time to finish the solvable portion of a hidden picture task with a missing picture (HPT) or an anagram task with an unsolvable anagram (ANA; Experiment 1), the HPT or a word search task with a missing word (WST; Experiment 2), or a HPT (Experiment 3). Persistence was considered to be the amount of additional time participants spent trying to solve the unsolvable portion.</p><p><strong>Results: </strong>Experiment 1: 40 mg caffeine did not affect performance or persistence. Experiment 2: 100 mg caffeine increased the percent of total time participants persisted in the HPT from 38.0% to 51.7%. Experiment 3: stress improved performance in the HPT and caffeine and stress produced a significant interaction effect for persistence with trends toward increased persistence in stressed participants and decreased in unstressed.</p><p><strong>Conclusions: </strong>Caffeine increased time spent on an unsolvable task, particularly in stressed participants.</p>","PeriodicalId":520641,"journal":{"name":"Human psychopharmacology","volume":"40 5","pages":"e70014"},"PeriodicalIF":1.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144796632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal Use of Antidepressants in Pregnancy and the Risk of Postpartum Hemorrhage: An Electronic Health Record-Based Cohort Study.","authors":"William V Bobo, Launia White, David Hodge, Katherine Moore, Hannah Betcher, Alyssa M Larish, Cynthia Stoppel, Ardesheer Talati","doi":"10.1002/hup.70015","DOIUrl":"10.1002/hup.70015","url":null,"abstract":"<p><strong>Objectives: </strong>Prior studies have raised concerns about postpartum hemorrhage (PPH) risk associated with selective serotonin and serotonin-norepinephrine reuptake inhibitors (SSRIs and SNRIs), although limitations include possible confounding by maternal indications. The current study examined the risk of PPH associated with prenatal S/NRIs accounting for diagnosed maternal depression during pregnancy.</p><p><strong>Methods: </strong>The current study is a secondary analysis of data from a cohort of 2213 pregnancies (1997-2010) identified from a large electronic medical record-linkage system. Exposures were identified from electronic prescriptions records and resulted in three main groups: S/NRI-exposed pregnancies (S/NRI users), antidepressant-unexposed pregnancies (non-users), and S/NRI exposure in the year prior to (but not during) pregnancy (former users). Data used to identify PPH occurrences included obstetrician chart diagnoses, diagnosis codes, and recorded estimated blood loss (EBL). The risk of PPH by exposure group was estimated using unadjusted, minimally adjusted (maternal age at delivery, delivery year, parity, and maternal smoking), and depression-adjusted models (previous covariates and maternal depression). Supplemental analyses included an examination of PPH risk with prenatal bupropion monotherapy.</p><p><strong>Results: </strong>The study cohort consisted of 837 S/NRI users, 401 former users, and 786 non-users, as well as 114 bupropion users identified for additional analyses. The frequency of PPH was 11.6% in the overall cohort, and was 14.7% for S/NRI users, 10.2% for former users, and 8.7% for non-users. The risk of PPH was significantly higher for S/NRI users than non-users in unadjusted (OR 1.82 [95% CI 1.33, 2.49]), minimally adjusted (aOR 1.66 [1.19, 2.31]), and depression-adjusted models (aOR 1.46 [1.02, 2.10]). The risk of PPH was also higher for S/NRI former users than non-users in unadjusted models (OR 1.54 [1.05, 2.26]) but not minimally adjusted (aOR 1.42 [0.95, 2.11]) or depression-adjusted models (aOR 1.41 [0.95, 2.10]). No significant differences in PPH risk were observed between S/NRI users and former users, between bupropion users and non-users, or between S/NRI users and bupropion users.</p><p><strong>Conclusions: </strong>Prenatal S/NRI exposure was associated with an increased risk of PPH after adjusting for maternal depression, although residual confounding and confounding by other factors (including unmeasured factors) may be possible, as the risk of PPH appeared to be similar between S/NRI users and former users. Best-practice PPH risk management strategies should be adhered to for depressed patients, especially those who require treatment with antidepressants during pregnancy.</p>","PeriodicalId":520641,"journal":{"name":"Human psychopharmacology","volume":"40 5","pages":"e70015"},"PeriodicalIF":1.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144805574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasma levels of interleukin-8 and response to paroxetine in patients with major depressive disorder.","authors":"Xuan Guan,&nbsp;Zai-Quan Dong,&nbsp;Yan-Ni Hao,&nbsp;Xiao-Ling Shen,&nbsp;Qing-Lian Xie,&nbsp;Jian-Min Chen","doi":"10.1002/hup.2855","DOIUrl":"https://doi.org/10.1002/hup.2855","url":null,"abstract":"<p><strong>Objectives: </strong>Immune dysregulation plays a key role in major depressive disorder (MDD). However, little is known about the complicated involvement of various interleukins in MDD. This study was performed to investigate the correlation between plasma interleukin-8 (IL-8) levels and treatment outcome of paroxetine (a selective serotonin reuptake inhibitor) in patients with MDD.</p><p><strong>Methods: </strong>A total of 115 hospitalized patients (36 males and 79 females), aged from 18 to 72 years, were enrolled. Plasma levels of IL-8 were measured before treatment initiation (baseline) and at 8 weeks after oral paroxetine treatment. Efficacy of paroxetine was evaluated by use of the Hamilton Depression Rating Scale (HAMD-17). Baseline IL-8 levels were compared between responders and non-responders to paroxetine treatment.</p><p><strong>Results: </strong>Plasma IL-8 levels decreased significantly after an 8-week antidepressant treatment in responders, in association with a dramatic decrease in HAMD-17 scores. In non-responders, plasma IL-8 levels did not change significantly at 8 weeks after antidepressant treatment. Baseline plasma IL-8 levels were found to be significantly lower in responders than in non-responders, showing a correlation between IL-8 and antidepressant response to paroxetine.</p><p><strong>Conclusions: </strong>These results indicate that plasma IL-8 levels were related to treatment outcome of paroxetine, and therefore suggest that IL-8 could be a promising predicator of treatment response in individual patients with MDD.</p>","PeriodicalId":520641,"journal":{"name":"Human psychopharmacology","volume":" ","pages":"e2855"},"PeriodicalIF":1.7,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33487663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Facilitated extinction of conditioned fear responses by delta 9-tetrahyrdrocannabidol in humans: a pilot study.","authors":"Herman A Diggs,&nbsp;Norka E Rabinovich,&nbsp;David G Gilbert","doi":"10.1002/hup.2853","DOIUrl":"https://doi.org/10.1002/hup.2853","url":null,"abstract":"<p><strong>Objective: </strong>We sought to determine whether acute delta 9-tetrahyrdrocannabidol (THC) administration would facilitate fear extinction in young occasional cannabis users, given that animal models indicate THC facilitates extinction learning, and recent studies indicate THC administration may also enhance threat memory extinction in humans.</p><p><strong>Methods: </strong>On each of the 2 days, 24+ hour THC-deprived participants were conditioned to fear visual stimuli in a delay conditioning and extinction paradigm. Both CS+ and CS- were faces of negative emotional valence, with the CS+ paired with mild electric shock. Throughout both conditioning and extinction paradigms, EEG was measured to quantify event-related potentials for these learning processes. Following conditioning, individuals, in a randomized and counter-balanced order, smoked either an active THC cigarette (26.25 mg/2.7% THC) or a placebo marijuana cigarette (0.002% THC) on 1 day and the opposite cigarette on the second day. After smoking, CS+ and CS- were presented without shock, resulting in extinction of conditioned fear.</p><p><strong>Results: </strong>Relative to placebo, THC facilitated extinction of the conditioned response to the CS+, as reflected by reductions in late positive potential amplitude during extinction learning.</p><p><strong>Conclusions: </strong>The results indicate that acute THC administration may facilitate extinction of the conditioned fear response in humans.</p>","PeriodicalId":520641,"journal":{"name":"Human psychopharmacology","volume":" ","pages":"e2853"},"PeriodicalIF":1.7,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40624754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory markers at baseline correlate with subsequent clinical response to quetiapine in patients with bipolar disorder.","authors":"Marco Ferrari,&nbsp;Marco Godio,&nbsp;Stefano Martini,&nbsp;Camilla Callegari,&nbsp;Marco Cosentino,&nbsp;Franca Marino","doi":"10.1002/hup.2854","DOIUrl":"https://doi.org/10.1002/hup.2854","url":null,"abstract":"<p><strong>Objectives: </strong>Recent studies proposed the existence of a correlation between patients' inflammatory status and therapy response in bipolar disorder (BD). Here we investigated the correlation between levels of inflammatory markers and quetiapine (QUE) effects in BD patients.</p><p><strong>Methods: </strong>In 15 hospitalised BD patients, we investigated changes in inflammatory markers such as C-Reactive Protein (CRP), Erythrocyte Sedimentation Rate (ESR) and cytokines after a 6-week treatment with QUE monotherapy.</p><p><strong>Results: </strong>We found QUE treatment to significantly reduce CRP and IL-6 plasma levels. Moreover, we found higher CRP and IL-6 plasma levels at baseline correlated with better improvement of patients' clinical symptoms.</p><p><strong>Conclusion: </strong>The reported results, although preliminary, could be useful in clinical practice, providing not only markers for QUE response, but also allowing for identification of new targets and new therapies for the treatment of this condition.</p>","PeriodicalId":520641,"journal":{"name":"Human psychopharmacology","volume":" ","pages":"e2854"},"PeriodicalIF":1.7,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40353648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between the angiotensin-converting enzyme gene insertion/deletion polymorphism and first-episode patients with schizophrenia in a Chinese Han population.","authors":"Li Hui,&nbsp;Jing Qin Wu,&nbsp;Xuan Zhang,&nbsp;Jie Lv,&nbsp;Wei Li Du,&nbsp;Chang Gui Kou,&nbsp;Ya Qin Yu,&nbsp;Meng Han Lv,&nbsp;Da Chun Chen,&nbsp;Xiang Yang Zhang","doi":"10.1002/hup.2396","DOIUrl":"https://doi.org/10.1002/hup.2396","url":null,"abstract":"<p><strong>Background: </strong>Angiotensin-converting enzyme (ACE), a key enzyme of the renin-angiotensin system, can modulate dopamine turnover in the midbrain. Previous studies have revealed an association between ACE gene insertion/deletion (I/D) polymorphism and chronic schizophrenia, yet results are conflicting.</p><p><strong>Objective: </strong>The primary objective of this study was to examine whether the ACE gene I/D polymorphism is associated with first-episode patients with schizophrenia (FEP) in a Chinese Han population.</p><p><strong>Methods: </strong>The presence of the polymorphism was determined in 220 FEP and 538 healthy controls using a case-control design. We assessed the psychopathology in 212 FEP using the Positive and Negative Syndrome Scale (PANSS).</p><p><strong>Results: </strong>The allelic and genotypic frequencies of the ACE gene I/D polymorphism did not significantly differ between FEP and healthy controls (both p>0.05). However, the negative PANSS symptom was significantly higher in FEP with the D/D genotype than those with I/D and I/I genotypes (all p<0.05) even after Bonferroni corrections (all p<0.05). Furthermore, the D allele of the ACE gene was associated with higher negative PANSS symptom score in FEP.</p><p><strong>Conclusions: </strong>Our results indicated that even though the ACE gene I/D polymorphism did not associate with FEP, it may play a role in susceptibility to the negative PANSS symptom of FEP in a Chinese Han population.</p>","PeriodicalId":520641,"journal":{"name":"Human psychopharmacology","volume":" ","pages":"274-9"},"PeriodicalIF":1.7,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/hup.2396","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40299080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular pharmacodynamics of donepezil hydrochloride on the PR and QT intervals in patients with dementia.","authors":"Hirofumi Igeta,&nbsp;Yutaro Suzuki,&nbsp;Misuzu Tajiri,&nbsp;Toshiyuki Someya","doi":"10.1002/hup.2398","DOIUrl":"https://doi.org/10.1002/hup.2398","url":null,"abstract":"<p><strong>Objective: </strong>Although several case reports suggested that donepezil hydrochloride can induce bradycardia or atrioventricular block, the details remain unclear. We implemented a study of the impact of donepezil hydrochloride administration on PR, RR, and QT intervals.</p><p><strong>Methods: </strong>The subjects were 18 patients who were diagnosed with either dementia or cognitive disorder (DSM-IV-TR) and were hospitalized between January 2011 and December 2012. After hospitalization, they were treated with donepezil hydrochloride. Clinical parameters and electrocardiograms before and after the administration of donepezil hydrochloride were retrieved from the patients' medical records.</p><p><strong>Results: </strong>After the administration of donepezil hydrochloride, the mean PR interval significantly increased from 177.3 ± 30.9 to 186.8 ± 38.4 ms (p<0.001). And the mean RR interval also significantly increased from 850.3 ± 112.5 to 886.7 ± 136.4 ms (p=0.014). The mean difference in the PR interval before and after the administration of donepezil hydrochloride was 9.5 ± 17.1 (range=-21.0-44.0) ms. The QT intervals were unaffected by the administration of donepezil hydrochloride.</p><p><strong>Conclusions: </strong>Care should be taken when administering donepezil to patients with atrioventricular block, or patients taking other drugs that can prolong the PR interval. Copyright © 2014 John Wiley & Sons, Ltd.</p>","PeriodicalId":520641,"journal":{"name":"Human psychopharmacology","volume":" ","pages":"292-4"},"PeriodicalIF":1.7,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/hup.2398","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40299486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Positive perception of pharmacogenetic testing for psychotropic medications.","authors":"Matthew B Lanktree,&nbsp;Gwyneth Zai,&nbsp;Laura E Vanderbeek,&nbsp;Daniel E Giuffra,&nbsp;David S Smithson,&nbsp;Lucas B Kipp,&nbsp;Timothy R Dalseg,&nbsp;Mark Speechley,&nbsp;James L Kennedy","doi":"10.1002/hup.2383","DOIUrl":"https://doi.org/10.1002/hup.2383","url":null,"abstract":"<p><strong>Introduction: </strong>Pharmacogenetics attempts to identify inter-individual genetic differences that are predictive of variable drug response and propensity to side effects, with the prospect of assisting physicians to select the most appropriate drug and dosage for treatment. However, many concerns regarding genetic tests exist. We sought to test the opinions of undergraduate science and medical students in southern Ontario universities toward pharmacogenetic testing.</p><p><strong>Methods and results: </strong>Questionnaires were completed by 910 undergraduate medicine and science students from 2005 to 2007. Despite students' concerns that the results of genetic tests may be used for other purposes without consent (71%) or lead to discrimination (78%), an overwhelming number of students were in favor of pharmacogenetic testing (90%).</p><p><strong>Discussion: </strong>To our knowledge, this study is the first to survey a large sample for their attitude toward pharmacogenetic testing for psychotropic medications. Our results indicate that, although concerns remain and scientific advancements are required, respondents were in support of pharmacogenetic testing for medications used to treat schizophrenia. © 2014 The Authors. Human Psychopharmacology: Clinical and Experimental published by John Wiley & Sons, Ltd.</p>","PeriodicalId":520641,"journal":{"name":"Human psychopharmacology","volume":" ","pages":"287-91"},"PeriodicalIF":1.7,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/hup.2383","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40289737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of ADRA2A and MTHFR gene polymorphisms with weight loss following antipsychotic switching to aripiprazole or ziprasidone.","authors":"Siti Norsyuhada Roffeei,&nbsp;Gavin P Reynolds,&nbsp;Nor Zuraida Zainal,&nbsp;Mas Ayu Said,&nbsp;Ahmad Hatim,&nbsp;Syarinaz Ahmad Aida,&nbsp;Zahurin Mohamed","doi":"10.1002/hup.2366","DOIUrl":"https://doi.org/10.1002/hup.2366","url":null,"abstract":"<p><strong>Objectives: </strong>Various genetic polymorphisms have been reported to be associated with antipsychotic-induced weight gain. In this study, we aimed to determine whether risk polymorphisms in 12 candidate genes are associated with reduction in body mass index (BMI) of patients following switching of antipsychotics to aripiprazole or ziprasidone.</p><p><strong>Methods: </strong>We recruited 115 schizophrenia patients with metabolic abnormalities and who have been on at least 1 year treatment with other antipsychotics; they were then switched to either aripiprazole or ziprasidone. They were genotyped, and their BMI monitored for 6 months.</p><p><strong>Results: </strong>Significant associations with reduction in BMI at 6 months following switching were found in two of these genes: with rs1800544 of the ADRA2A gene (CC + CG [-0.32 ± 1.41 kg/m²] vs GG [-1.04 ± 1.63 kg/m²], p = 0.013) and with rs1801131 of the MTHFR gene (AA [-0.36 ± 1.53] vs AC + CC [-1.07 ± 1.53], p = 0.015).</p><p><strong>Conclusion: </strong>The study data indicated that carriage of the ADRA2A rs1800544 GG genotype and the MTHFR rs1801131 C allele are associated with BMI reduction in this population following switching of antipsychotics to aripiprazole and ziprasidone.</p>","PeriodicalId":520641,"journal":{"name":"Human psychopharmacology","volume":" ","pages":"38-45"},"PeriodicalIF":1.7,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/hup.2366","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32030845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Does omega-3 fatty acid supplementation enhance neural efficiency? A review of the literature.","authors":"Isabelle Bauer,&nbsp;Sheila Crewther,&nbsp;Andrew Pipingas,&nbsp;Laura Sellick,&nbsp;David Crewther","doi":"10.1002/hup.2370","DOIUrl":"https://doi.org/10.1002/hup.2370","url":null,"abstract":"<p><strong>Objective: </strong>While the cardiovascular, anti-inflammatory and mood benefits of omega-3 supplementation containing long chain fatty acids (LCPUFAs) such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are manifest, there is no scientific consensus regarding their effects on neurocognitive functioning. This review aimed to examine the current literature on LCPUFAs by assessing their effects on cognition, neural functioning and metabolic activity. In order to view these findings together, the principle of neural efficiency as established by Richard Haier (\"smart brains work less hard\") was extended to apply to the neurocognitive effects of omega-3 supplementation.</p><p><strong>Methods: </strong>We reviewed multiple databases from 2000 up till 2013 using a systematic approach and focused our search to papers employing both neurophysiological techniques and cognitive measures.</p><p><strong>Results: </strong>Eight studies satisfied the criteria for consideration. We established that studies using brain imaging techniques show consistent changes in neurochemical substances, brain electrical activity, cerebral metabolic activity and brain oxygenation following omega-3 supplementation.</p><p><strong>Conclusions: </strong>We conclude that, where comparison is available, an increase in EPA intake is more advantageous than DHA in reducing \"brain effort\" relative to cognitive performance.</p>","PeriodicalId":520641,"journal":{"name":"Human psychopharmacology","volume":" ","pages":"8-18"},"PeriodicalIF":1.7,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/hup.2370","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31909678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}