Publications by authors named "Yilang Tang"

39 Publications

Shorter recovery times and better cognitive function-A comparative pilot study of magnetic seizure therapy and electroconvulsive therapy in patients with depressive episodes.

Brain Behav 2020 Dec 17;10(12):e01900. Epub 2020 Oct 17.

The National Clinical Research Center for Mental Disorders & Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Capital Medical University, Beijing, China.

Introduction: Magnetic seizure therapy (MST) is a new convulsive therapy that is as effective as traditional electroconvulsive therapy (ECT) in treating depression but with fewer cognitive side effects. The aim of this study was to compare the efficacy and cognitive effects between MST (100 Hz applied over the vertex) and bifrontal ECT for treating patients with depressive episodes.

Methods: Forty-five patients with depressive episodes were enrolled, with 18 receiving MST and 27 receiving ECT. MST was administered over the vertex with 100 Hz frequency. Treatment consisted of six sessions. The 17-item Hamilton Rating Scale for Depression (HAMD-17) was used to assess the severity of depression. The Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) was used to assess cognition. Assessments were performed at baseline and after the third and sixth treatment sessions.

Results: Both MST and ECT improved the patients' depressive symptoms significantly, yet no significant difference was found between the two groups (p > .05). The response rates and remission rates of MST and ECT were 72.2% versus 81.5% and 61.1% versus 63.0%, respectively. The MST group showed significant improvements in immediate memory (p < .001), delayed memory (p = .002), and attention (p < .001) than ECT. The recovery times for consciousness (p < .001), spontaneous breathing (p < .001), and orientation (p < .001) were shorter in MST group than ECT group. RBANS improvements were negatively correlated with the recovery time for orientation (r = .561, p < .001).

Conclusion: Magnetic seizure therapy showed similar efficacy to bifrontal ECT for treating depressive episodes. While MST may be an effective alternative to ECT, larger randomized trials are needed.
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http://dx.doi.org/10.1002/brb3.1900DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7749607PMC
December 2020

Factors associated with 30-day and 1-year readmission among psychiatric inpatients in Beijing China: a retrospective, medical record-based analysis.

BMC Psychiatry 2020 03 11;20(1):113. Epub 2020 Mar 11.

School of public health, Chinese Academy of Medical Sciences and Peking Union Medical College, No.3 Dong Dan San Tiao, Dongcheng District, Beijing, China.

Background: Psychiatric readmissions negatively impact patients and their families while increasing healthcare costs. This study aimed at investigating factors associated with psychiatric readmissions within 30 days and 1 year of the index admissions and exploring the possibilities of monitoring and improving psychiatric care quality in China.

Methods: Data on index admission, subsequent admission(s), clinical and hospital-related factors were extracted in the inpatient medical record database covering 10 secondary and tertiary psychiatric hospitals in Beijing, China. Logistic regressions were used to examine the associations between 30-day and 1-year readmissions plus frequent readmissions (≥3 times/year), and clinical variables as well as hospital characteristics.

Results: The 30-day and 1-year psychiatric readmission rates were 16.69% (1289/7724) and 33.79% (2492/7374) respectively. 746/2492 patients (29.34%) were readmitted 3 times or more within a year (frequent readmissions). Factors significantly associated with the risk of both 30-day and 1-year readmission were residing in an urban area, having medical comorbidities, previous psychiatric admission(s), length of stay > 60 days in the index admission and being treated in tertiary hospitals (p < 0.001). Male patients were more likely to have frequent readmissions (OR 1.30, 95%CI 1.04-1.64). Receiving electroconvulsive therapy (ECT) was significantly associated with a lower risk of 30-day readmission (OR 0.72, 95%CI 0.56-0.91) and frequent readmissions (OR 0.60, 95%CI 0.40-0.91).

Conclusion: More than 30% of the psychiatric inpatients were readmitted within 1 year. Urban residents, those with medical comorbidities and previous psychiatric admission(s) or a longer length of stay were more likely to be readmitted, and men are more likely to be frequently readmitted. ECT treatment may reduce the likelihood of 30-day readmission and frequent admissions. Targeted interventions should be designed and piloted to effectively monitor and reduce psychiatric readmissions.
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http://dx.doi.org/10.1186/s12888-020-02515-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7065326PMC
March 2020

Cutting Edge: IL-6-Driven Immune Dysregulation Is Strictly Dependent on IL-6R α-Chain Expression.

J Immunol 2020 02 10;204(4):747-751. Epub 2020 Jan 10.

Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, 55131 Mainz, Germany.

IL-6 binds to the IL-6R α-chain (IL-6Rα) and signals via the signal transducer gp130. Recently, IL-6 was found to also bind to the cell surface glycoprotein CD5, which would then engage gp130 in the absence of IL-6Rα. However, the biological relevance of this alternative pathway is under debate. In this study, we developed a mouse model, in which murine IL-6 is overexpressed in a CD11c-Cre-dependent manner. Transgenic mice developed a lethal immune dysregulation syndrome with increased numbers of Ly-6G neutrophils and Ly-6C monocytes/macrophages. IL-6 overexpression promoted activation of CD4 T cells while suppressing CD5 B-1a cell development. However, additional ablation of IL-6Rα protected IL-6-overexpressing mice from IL-6-triggered inflammation and fully phenocopied IL-6Rα-deficient mice without IL-6 overexpression. Mechanistically, IL-6Rα deficiency completely prevented downstream activation of STAT3 in response to IL-6. Altogether, our data clarify that IL-6Rα is the only biologically relevant receptor for IL-6 in mice.
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http://dx.doi.org/10.4049/jimmunol.1900876DOI Listing
February 2020

Hospitalization Pattern, Inpatient Service Utilization and Quality of Care in Patients With Alcohol Use Disorder: A Sequence Analysis of Discharge Medical Records.

Alcohol Alcohol 2020 Mar;55(2):179-186

Department of Psychiatry and Behavioral Sciences, Emory University, 12 Executive Park Drive NE, Suite 300, Atlanta, GA 30329, USA.

Aims: To identify and group hospitalization trajectory of alcohol use disorder (AUD) patients and its associations with service utilization, healthcare quality and hospital-level variations.

Methods: Inpatients with AUD as the primary diagnosis from 2012 to 2014 in Beijing, China, were identified. Their discharge medical records were extracted and analyzed using the sequence analysis and the cluster analysis.

Results: Eight-hundred thirty-one patients were included, and their hospitalization patterns were grouped into four clusters: short stay (n = 565 (67.99%)), mean psychiatric length of stay in 3 years: (32.25 ± 18.69), repeated short stay (n = 211 (25.39%), 137.76 ± 88.8 days), repeated long stay (n = 41 (4.93%), 405.44 ± 146.54 days), permanent stay (n = 14 (1.68%), 818.14 ± 225.22 days). The latter two clusters (6.61% patients) used 37.26% of the total psychiatric hospital days and 33.65% of the total psychiatric hospitalization expenses. All the patients in the permanent stay cluster and 41.77% of the patients in the short stay cluster were readmitted at least once within 3 years. Two-hundred thirty-four patients (28.16%) were admitted at least once for non-psychiatric reasons, primarily for diseases of circulatory and digestive systems. Cluster composition varied significantly among different hospitals.

Conclusion: Hospitalization pattern of patients with AUD varies greatly, and while most (>2/3) hospitalizations were short stay, those with repeated long stay and permanent stay used more than one third of the hospital days and expenses. Our findings suggest interventions targeting at certain patients may be more effective in reducing resource utilization.
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http://dx.doi.org/10.1093/alcalc/agz081DOI Listing
March 2020

Dietary tryptophan links encephalogenicity of autoreactive T cells with gut microbial ecology.

Nat Commun 2019 10 25;10(1):4877. Epub 2019 Oct 25.

DKTK Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany.

The interaction between the mammalian host and its resident gut microbiota is known to license adaptive immune responses. Nutritional constituents strongly influence composition and functional properties of the intestinal microbial communities. Here, we report that omission of a single essential amino acid - tryptophan - from the diet abrogates CNS autoimmunity in a mouse model of multiple sclerosis. Dietary tryptophan restriction results in impaired encephalitogenic T cell responses and is accompanied by a mild intestinal inflammatory response and a profound phenotypic shift of gut microbiota. Protective effects of dietary tryptophan restriction are abrogated in germ-free mice, but are independent of canonical host sensors of intracellular tryptophan metabolites. We conclude that dietary tryptophan restriction alters metabolic properties of gut microbiota, which in turn have an impact on encephalitogenic T cell responses. This link between gut microbiota, dietary tryptophan and adaptive immunity may help to develop therapeutic strategies for protection from autoimmune neuroinflammation.
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http://dx.doi.org/10.1038/s41467-019-12776-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6814758PMC
October 2019

Intention to leave and associated factors among psychiatric nurses in China: A nationwide cross-sectional study.

Int J Nurs Stud 2019 Jun 23;94:159-165. Epub 2019 Mar 23.

Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 12 Executive Park Drive NE, Suite 300, Atlanta, GA, 30329, USA; Mental Health Service Line, Atlanta VA Medical Center, Decatur, GA, 30033, USA. Electronic address:

Background: The retention of psychiatric nurses is an important concern for healthcare administrators in China. However, Chinese psychiatric nurses' intention to leave their jobs and the factors associated with it have been scarcely studied.

Objective: To investigate Chinese psychiatric nurses' intention to leave their jobs, and to explore the associations between the intention to leave and individual characteristics, job-related factors and job satisfaction.

Design: A cross-sectional, anonymous survey of a nationwide sample was conducted.

Settings: Thirty-two tertiary psychiatric hospitals in 29 provincial capital cities in China.

Participants: All 9907 nurses in 32 hospitals were targeted for this survey conducted in December 2017; 8493 responded (response rate = 85.7%), and 7933 (without logic errors in the data) were included in the analysis.

Methods: A questionnaire was used to investigate the respondent's intention to leave their job and to collect data on related factors, including individual characteristics (gender, age, marital status, educational background and self-rated health), job-related factors (professional title, working years, income, work hours, history of patient-initiated violence, perceived respect from patients, social recognition as well as physician-nurse coordination and trust) and job satisfaction. The short version of the Minnesota Satisfaction Questionnaire was used to assess job satisfaction. Chi-square tests and multilevel logistic regression analysis were used to examine associations between an intention to leave and other factors.

Results: Among 7933 respondents, 20.2% reported an intention to leave their current jobs. The multiple regression analysis showed that better self-rated health (i.e. OR = 0.373, 95%CI = 0.308-0.452 for good health, reference: poor health), working more than 20 years (OR = 0.479, 95%CI = 0.389-0.590, reference: 20 years or less), higher monthly income (i.e. OR = 0.521, 95%CI = 0.399-0.680 for 6001-8000 RMBs, reference: 4500 RMB or less), perceived patient respect (OR = 0.727, 95%CI = 0.623-0.849), physician-nurse coordination (OR = 0.549, 95%CI = 0.480-0.629) and being satisfied with one's job (OR = 0.373, 95%CI = 0.308-0.452) were negatively associated with an intention to leave; while those who were male (OR = 1.879, 95%CI = 1.605-2.199), working more than 40 hours per week (OR = 1.584, 95%CI = 1.374-1.825) and experienced patient-initiated violence in the past 12 months (OR = 1.566, 95%CI = 1.376-1.781) had a higher odds of reporting an intention to leave.

Conclusions: Self-rated health, monthly income, work hours, patient-initiated violence, perceived patient respect, physician-nurse coordination and job satisfaction are significant factors associated with a nurse's intention to quit their job. In order to retain nurses in Chinese tertiary psychiatric hospitals, the government and hospital administrators should consider ways to address these factors.
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http://dx.doi.org/10.1016/j.ijnurstu.2019.03.013DOI Listing
June 2019

Alternative Splice Forms of CYLD Mediate Ubiquitination of SMAD7 to Prevent TGFB Signaling and Promote Colitis.

Gastroenterology 2019 02 10;156(3):692-707.e7. Epub 2018 Oct 10.

Institute for Molecular Medicine, University Medical Centre, Johannes Gutenberg University of Mainz, Mainz, Germany. Electronic address:

Background & Aims: The CYLD lysine 63 deubiquitinase gene (CYLD) encodes tumor suppressor protein that is mutated in familial cylindromatosus, and variants have been associated with Crohn disease (CD). Splice forms of CYLD that lack exons 7 and 8 regulate transcription factors and functions of immune cells. We examined the expression of splice forms of CYLD in colon tissues from patients with CD and their effects in mice.

Methods: We performed immunohistochemical analyses of colon tissues from patients with untreated CD and patients without inflammatory bowel diseases (controls). We obtained mice that expressed splice forms of CYLD (sCYLD mice) without or with SMAD7 (sCYLD/SMAD7 mice) from transgenes and CYLD-knockout mice (with or without transgenic expression of SMAD7) and performed endoscopic analyses. Colitis was induced in Rag1 mice by transfer of CD4 CD62L T cells from C57/Bl6 or transgenic mice. T cells were isolated from mice and analyzed by flow cytometry and quantitative real-time polymerase chain reaction and intestinal tissues were analyzed by histology and immunohistochemistry. CYLD forms were expressed in mouse embryonic fibroblasts, primary T cells, and HEK293T cells, which were analyzed by immunoblot, mobility shift, and immunoprecipitation assays.

Results: The colonic lamina propria from patients with CD was infiltrated by T cells and had higher levels of sCYLD (but not full-length CYLD) and SMAD7 than tissues from controls. Incubation of mouse embryonic fibroblasts and T cells with transforming growth factor β increased their production of sCYLD and decreased full-length CYLD. Transgenic expression of sCYLD and SMAD7 in T cells prevented the differentiation of regulatory T cells and T-helper type 17 cells and increased the differentiation of T-helper type 1 cells. The same effects were observed in colon tissues from sCYLD/SMAD7 mice but not in those from CYLD-knockout SMAD7 mice. The sCYLD mice had significant increases in the numbers of T-helper type 1 cells and CD44 CD62L memory-effector CD4 T cells in the spleen and mesenteric lymph nodes compared with wild-type mice; sCYLD/SMAD7 mice had even larger increases. The sCYLD/SMAD7 mice spontaneously developed severe colitis, with infiltration of the colon by dendritic cells, neutrophils, macrophages, and CD4 T cells and increased levels of Ifng, Il6, Il12a, Il23a, and Tnf mRNAs. Co-transfer of regulatory T cells from wild-type, but not from sCYLD/SMAD7, mice prevented the induction of colitis in Rag1 mice by CD4 T cells. We found increased levels of poly-ubiquitinated SMAD7 in sCYLD CD4 T cells. CYLD formed a nuclear complex with SMAD3, whereas sCYLD recruited SMAD7 to the nucleus, which inhibited the expression of genes regulated by SMAD3 and SMAD4. We found that sCYLD mediated lysine 63-linked ubiquitination of SMAD7. The sCYLD-SMAD7 complex inhibited transforming growth factor β signaling in CD4 T cells.

Conclusions: Levels of the spliced form of CYLD are increased in colon tissues from patients with CD. sCYLD mediates ubiquitination and nuclear translocation of SMAD7 and thereby decreases transforming growth factor β signaling in T cells. This prevents immune regulatory mechanisms and leads to colitis in mice.
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http://dx.doi.org/10.1053/j.gastro.2018.10.023DOI Listing
February 2019

NF-κB inducing kinase (NIK) is an essential post-transcriptional regulator of T-cell activation affecting F-actin dynamics and TCR signaling.

J Autoimmun 2018 11 29;94:110-121. Epub 2018 Jul 29.

Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany. Electronic address:

NF-κB inducing kinase (NIK) is the key protein of the non-canonical NF-κB pathway and is important for the development of lymph nodes and other secondary immune organs. We elucidated the specific role of NIK in T cells using T-cell specific NIK-deficient (NIK) mice. Despite showing normal development of lymphoid organs, NIK mice were resistant to induction of CNS autoimmunity. T cells from NIK mice were deficient in late priming, failed to up-regulate T-bet and to transmigrate into the CNS. Proteomic analysis of activated NIK T cells showed de-regulated expression of proteins involved in the formation of the immunological synapse: in particular, proteins involved in cytoskeleton dynamics. In line with this we found that NIK-deficient T cells were hampered in phosphorylation of Zap70, LAT, AKT, ERK1/2 and PLCγ upon TCR engagement. Hence, our data disclose a hitherto unknown function of NIK in T-cell priming and differentiation.
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http://dx.doi.org/10.1016/j.jaut.2018.07.017DOI Listing
November 2018

Expression of IL-17F is associated with non-pathogenic Th17 cells.

J Mol Med (Berl) 2018 08 29;96(8):819-829. Epub 2018 Jun 29.

University Medical Center of the Johannes Gutenberg University Mainz, Institute for Molecular Medicine, 55131, Mainz, Germany.

IL-17A and IL-17F share the highest sequence homology of the IL-17 family and signal via the same IL-17RA/RC receptor heterodimer. To better explore the expression of these two cytokines, we used a double reporter mouse strain (IL-17 mice), where IL-17A expressing cells are marked by enhanced green fluorescent protein (eGFP) while red fluorescence protein (RFP) reports the expression of IL-17F. In steady state, we found that Th17 and γδ T cells only expressed IL-17A, while IL-17F expression was restricted to CD8 T cells (Tc17) and innate lymphoid cells (ILC type 3) of the gut. In experimental autoimmune encephalomyelitis, the vast majority of CNS-infiltrating Th17 cells expressed IL-17A but not IL-17F. In contrast, anti-CD3-induced, TGF-β-driven Th17 cells in the gut expressed both of these IL-17 cytokines. In line with this, in vitro differentiation of Th17 cells in the presence of IL-1β led primarily to IL-17A expressing T cells, while TGF-β induced IL-17F co-expressing Th17 cells. Our results suggest that expression of IL-17F is associated with non-pathogenic T cells, pointing to a differential function of IL-17A versus IL-17F.

Key Messages: Naïve mice: CD4 T cells and γδ T cells express IL-17A, and Tc17 cells express IL-17F. Gut ILC3 show differential expression of IL17A and F. Th17 differentiation with TGF-β1 induces IL-17A and F, whereas IL-1β induced cells expressing IL-17A. Th17 cells in EAE in CNS express IL-17A only. Gut Th17 cells induced by anti-CD3 express IL-17A and F together as skin γδ T cells of IMQ-treated mice.
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http://dx.doi.org/10.1007/s00109-018-1662-5DOI Listing
August 2018

Association between COMT gene polymorphisms, clinical symptoms, and cognitive functions in Han Chinese patients with schizophrenia.

Psychiatr Genet 2018 06;28(3):47-54

Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta.

Aim: Catechol-O-methyltransferase (COMT) gene variants may be involved in the pathogenesis of psychotic symptoms, and associated especially with negative symptom in schizophrenia, but their roles in cognitive function and treatment response remain unclear. The aim of this study was to explore the association between COMT gene polymorphisms, clinical symptoms (including cognitive function), and treatment response to antipsychotic medications in patients with schizophrenia.

Patients And Methods: A total of 200 Han Chinese inpatients with schizophrenia were recruited in accordance with Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (DSM-IV). In total, 96 of them completed assessments at baseline and after 8 weeks of antipsychotic treatment. Clinical symptoms were assessed using the Positive And Negative Syndrome Scale (PANSS), and cognitive function was evaluated using the Verbal Fluency Test, Trail Making Test A-B, Stroop Color-Word Test, and Wisconsin Card Sorting Test. Two single nucleotide polymorphisms, rs4680 and rs165599, on the COMT gene were genotyped.

Results: At baseline, we found no significant genotypic association between rs4680 and clinical symptoms or cognitive function. After 8 weeks of antipsychotic treatment, compared with patients with GG genotype, patients with AA/AG genotypes at rs4680 showed significantly higher scores on PANSS total, both at baseline and at the end of 8 weeks, especially in negative and general psychopathology symptoms. Patients with GG at rs165599 scored significantly higher on the Stroop test, suggesting better cognitive performance after 8 weeks of treatment. No significant association was found between rs165599 genotype and psychiatric symptoms as assessed by the PANSS and cognitive function tests at baseline.

Conclusion: Our findings suggest that the COMT gene polymorphisms may influence the response to antipsychotic treatment in Han Chinese patients with schizophrenia.
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http://dx.doi.org/10.1097/YPG.0000000000000194DOI Listing
June 2018

Impact of childhood trauma on sensorimotor gating in Chinese patients with chronic schizophrenia.

Psychiatry Res 2018 05 31;263:69-73. Epub 2018 Jan 31.

The National Clinical Research Center for Mental Disorders & Beijing Key Laboratory of Mental Disorders & Beijing Institute for Brain Disorders Center of Schizophrenia, Beijing Anding Hospital, Capital Medical University, No. 5 Ankang Lane, Dewai Avenue, Xicheng District, Beijing 100088, China. Electronic address:

We investigated the relationship between childhood trauma (CT) and sensorimotor gating in Chinese patients diagnosed with chronic schizophrenia. Seventy-five patients were assessed with the Childhood Trauma Questionnaire-Short Form (CTQ-SF), and then the modified paradigm, perceived spatial separation-induced prepulse inhibition (PSS PPI) and the perceived spatial co-location PPI (PSC PPI or classical PPI) were applied to test sensorimotor gating. Startling stimuli (90 dB) were presented either alone or preceded by discrete prepulse stimuli of 4 dB in a background 60-dB noise level. Associations between CT and various PPI paradigms were statistically analyzed. Univariate analysis revealed the absence of a significant correlation between CT and PPI paradigms (p > 0.05). However, multiple linear regression analyses revealed that sexual abuse and the positive and negative syndrome scale (PANSS) score were negatively correlated with PSS PPI (p = 0.029 and 0.008, respectively). On the other hand, female sex and history of smoking were positively correlated with PSS PPI (p = 0.044 and 0.043, respectively). In conclusion, the results of this study suggest that CT can be a predisposing factor that affects sensorimotor gating in schizophrenia patients.
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http://dx.doi.org/10.1016/j.psychres.2018.01.037DOI Listing
May 2018

IL-4 Receptor Alpha Signaling through Macrophages Differentially Regulates Liver Fibrosis Progression and Reversal.

EBioMedicine 2018 Mar 17;29:92-103. Epub 2018 Feb 17.

Institute of Translational Immunology, University Medical Center, Johannes Gutenberg University, Mainz, Germany; Research Center for Immunotherapy (FZI), University Medical Center, Johannes Gutenberg University, Mainz, Germany; Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Electronic address:

Chronic hepatitis leads to liver fibrosis and cirrhosis. Cirrhosis is a major cause of worldwide morbidity and mortality. Macrophages play a key role in fibrosis progression and reversal. However, the signals that determine fibrogenic vs fibrolytic macrophage function remain ill defined. We studied the role of interleukin-4 receptor α (IL-4Rα), a potential central switch of macrophage polarization, in liver fibrosis progression and reversal. We demonstrate that inflammatory monocyte infiltration and liver fibrogenesis were suppressed in general IL-4Rα as well as in macrophage-specific IL-4Rα (IL-4Rα) mice. However, with deletion of IL-4Rα spontaneous fibrosis reversal was retarded. Results were replicated by pharmacological intervention using IL-4Rα-specific antisense oligonucleotides. Retarded resolution was linked to the loss of M2-type resident macrophages, which secreted MMP-12 through IL-4 and IL-13-mediated phospho-STAT6 activation. We conclude that IL-4Rα signaling regulates macrophage functional polarization in a context-dependent manner. Pharmacological targeting of macrophage polarization therefore requires disease stage-specific treatment strategies.

Research In Context: Alternative (M2-type) macrophage activation through IL-4Rα promotes liver inflammation and fibrosis progression but speeds up fibrosis reversal. This demonstrates context dependent, opposing roles of M2-type macrophages. During reversal IL-4Rα induces fibrolytic MMPs, especially MMP-12, through STAT6. Liver-specific antisense oligonucleotides efficiently block IL-4Rα expression and attenuate fibrosis progression.
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http://dx.doi.org/10.1016/j.ebiom.2018.01.028DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5925448PMC
March 2018

Low post-traumatic stress disorder rate in Chinese in Beijing, China.

Asian J Psychiatr 2017 Dec 4;30:79-83. Epub 2017 Jul 4.

Department of Psychiatry, University of Oxford, UK.

Object: There have been significantly fewer community-based, epidemiological studies focusing on PTSD and its socio-demographic correlates among the Chinese than Western populations.

Method: The multistage household cluster random sampling method was used to select participants from18 districts and counties in Beijing; a total of 16,032 participants were assessed; face-to-face interviews and data collection was conducted using the semi-structured clinical interview for DSM-IV-TR Axis I Disorders-Patient Edition (SCID-I/P).

Result: The lifetime PTSD prevalence was 0.3%. Older age, low educational level, low personal monthly income, urban living, unemployment and being a farmer were all significantly associated with an increased risk of PTSD. Multivariate analysis showed that farmers and the unemployed were significantly associated with a higher risk for PTSD.

Conclusions: The prevalence rates of PTSD in Beijing were low compared with that of Western countries. Farming occupation and unemployment were independent risk factors for PTSD.
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http://dx.doi.org/10.1016/j.ajp.2017.07.003DOI Listing
December 2017

Reported maladaptive decision-making in unipolar and bipolar depression and its change with treatment.

Psychiatry Res 2017 11 9;257:386-392. Epub 2017 Aug 9.

Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, Georgia, United States. Electronic address:

Mood disorder patients frequently experience difficulty making decisions and may make sub-optimal decisions with adverse life consequences. However, patients' styles for decision-making when ill and after treatment have received little study to date. We assessed healthy controls (HC, n = 69) and patients with major depressive disorder (MDD, n = 61) or bipolar disorder (BP, n = 26) in a current major depressive episode using the Melbourne Decision-making Questionnaire. A subset of participants was re-evaluated after completing six weeks of pharmacotherapy. HC demonstrated significantly greater use of the healthy vigilance style, and significantly lower use of maladaptive decision-making styles, than the MDD and depressed BP patients. After six weeks of treatment, neither the MDD nor BP patients reported meaningful improvements in the vigilance style of decision-making, but scores on most maladaptive decision-making styles declined. BP patients who remitted reported significantly lower buckpassing and procrastination scores than healthy controls. Among MDD patients, however, the maladaptive passive buckpassing style of decision-making did not significantly diminish. For MDD patients, reported decision-making styles may remain impaired even after achieving remission. Among BP patients, low levels of adaptive vigilance decision-making may be a trait component of the illness, whereas for MDD patients, reported maladaptive passive decision-making styles are persistent.
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http://dx.doi.org/10.1016/j.psychres.2017.08.004DOI Listing
November 2017

NG2 plays a role in neuroinflammation but is not expressed by immune cells.

Acta Neuropathol 2017 08 31;134(2):325-327. Epub 2017 May 31.

Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.

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http://dx.doi.org/10.1007/s00401-017-1735-5DOI Listing
August 2017

Elevated levels of Bcl-3 inhibits Treg development and function resulting in spontaneous colitis.

Nat Commun 2017 04 28;8:15069. Epub 2017 Apr 28.

Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg, University of Mainz, Obere Zahlbarer Str 67, 55131 Mainz, Germany.

Bcl-3 is an atypical NF-κB family member that regulates NF-κB-dependent gene expression in effector T cells, but a cell-intrinsic function in regulatory T (Treg) cells and colitis is not clear. Here we show that Bcl-3 expression levels in colonic T cells correlate with disease manifestation in patients with inflammatory bowel disease. Mice with T-cell-specific overexpression of Bcl-3 develop severe colitis that can be attributed to defective Treg cell development and function, leading to the infiltration of immune cells such as pro-inflammatory γδT cells, but not αβ T cells. In Treg cells, Bcl-3 associates directly with NF-κB p50 to inhibit DNA binding of p50/p50 and p50/p65 NF-κB dimers, thereby regulating NF-κB-mediated gene expression. This study thus reveals intrinsic functions of Bcl-3 in Treg cells, identifies Bcl-3 as a potential prognostic marker for colitis and illustrates the mechanism by which Bcl-3 regulates NF-κB activity in Tregs to prevent colitis.
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http://dx.doi.org/10.1038/ncomms15069DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5414353PMC
April 2017

TGF-β inhibitor Smad7 regulates dendritic cell-induced autoimmunity.

Proc Natl Acad Sci U S A 2017 02 6;114(8):E1480-E1489. Epub 2017 Feb 6.

Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg University Mainz, 55131 Mainz, Germany;

TGF-β is an anti-inflammatory cytokine whose signaling is negatively controlled by Smad7. Previously, we established a role for Smad7 in the generation of autoreactive T cells; however, the function of Smad7 in dendritic cells (DCs) remains elusive. Here, we demonstrate that DC-specific Smad7 deficiency resulted in elevated expression of the transcription factors Batf3 and IRF8, leading to increased frequencies of CD8CD103 DCs in the spleen. Furthermore, Smad7-deficient DCs expressed higher levels of indoleamine 2,3-dioxygenase (IDO), an enzyme associated with tolerance induction. Mice devoid of Smad7 specifically in DCs are resistant to the development of experimental autoimmune encephalomyelitis (EAE) as a result of an increase of protective regulatory T cells (Tregs) and reduction of encephalitogenic effector T cells in the central nervous system. In agreement, inhibition of IDO activity or depletion of Tregs restored disease susceptibility. Intriguingly, when Smad7-deficient DCs also lacked the IFN-γ receptor, the mice regained susceptibility to EAE, demonstrating that IFN-γ signaling in DCs mediates their tolerogenic function. Our data indicate that Smad7 expression governs splenic DC subset differentiation and is critical for the promotion of their efficient function in immunity.
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http://dx.doi.org/10.1073/pnas.1615065114DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5338403PMC
February 2017

EBI2 Is Highly Expressed in Multiple Sclerosis Lesions and Promotes Early CNS Migration of Encephalitogenic CD4 T Cells.

Cell Rep 2017 01;18(5):1270-1284

Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, 55131 Mainz, Germany. Electronic address:

Arrival of encephalitogenic T cells at inflammatory foci represents a critical step in development of experimental autoimmune encephalomyelitis (EAE), the animal model for multiple sclerosis. EBI2 and its ligand, 7α,25-OHC, direct immune cell localization in secondary lymphoid organs. CH25H and CYP7B1 hydroxylate cholesterol to 7α,25-OHC. During EAE, we found increased expression of CH25H by microglia and CYP7B1 by CNS-infiltrating immune cells elevating the ligand concentration in the CNS. Two critical pro-inflammatory cytokines, interleukin-23 (IL-23) and interleukin-1 beta (IL-1β), maintained expression of EBI2 in differentiating Th17 cells. In line with this, EBI2 enhanced early migration of encephalitogenic T cells into the CNS in a transfer EAE model. Nonetheless, EBI2 was dispensable in active EAE. Human Th17 cells do also express EBI2, and EBI2 expressing cells are abundant within multiple sclerosis (MS) white matter lesions. These findings implicate EBI2 as a mediator of CNS autoimmunity and describe mechanistically its contribution to the migration of autoreactive T cells into inflamed organs.
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http://dx.doi.org/10.1016/j.celrep.2017.01.020DOI Listing
January 2017

Use of Orally Disintegrating Olanzapine During Electroconvulsive Therapy for Prevention of Postictal Agitation.

J Psychiatr Pract 2016 11;22(6):459-462

HERMIDA, JANJUA, TANG, JOB, and McDONALD: Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA SYRE: Advantage Anesthesia LLC, Atlanta, GA.

A major medical problem for patients undergoing electroconvulsive therapy (ECT) is the occurrence of postictal agitation (PIA). This phenomenon is associated with confusion and disorientation that can have severe clinical implications for the safety of the patient and health care professionals. Many different pharmacological strategies have been used to prevent PIA. We present data on 40 patients who suffered from PIA after a course of ECT and evaluate the prophylactic use of orally disintegrating olanzapine in the prevention of PIA in subsequent ECT treatments.
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http://dx.doi.org/10.1097/PRA.0000000000000185DOI Listing
November 2016

Alcohol and Opioid Use Disorder in Older Adults: Neglected and Treatable Illnesses.

Curr Psychiatry Rep 2016 09;18(9):87

Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, GA, USA.

The purpose of this article is to provide an overview of alcohol use disorder (AUD) and opioid use disorder (OUD) in older adults for general psychiatrists. The rapid growth of the geriatric population in the USA has wide-ranging implications as the baby boomer generation ages. Various types of substance use disorders (SUDs) are common in older adults, and they often take a greater toll on affected older adults than on younger adults. Due to multiple reasons, SUDs in older adults are often under-reported, under-detected, and under-treated. Older adults often use substances, which leads to various clinical problems. Space limitations prevents a comprehensive review; therefore, we primarily focus on alcohol use disorder and the problem of opioid use disorder, with more emphasis given to the latter, because the opioid use epidemic in the USA has gained much attention. We reviewed the literature on the topics, integrated across geriatric psychiatry, addiction psychiatry, research, and national trends. We discuss unique vulnerabilities of older adults to SUDs with regard to management of SUDs in older adults, medication-assisted treatment (MAT), and psychosocial treatments. We encourage general psychiatrists to raise their awareness of SUDs in older adults and to provide brief intervention or referral for further assessment.
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http://dx.doi.org/10.1007/s11920-016-0718-xDOI Listing
September 2016

Depression Worsening Associated With Lorcaserin: A Case Report.

J Clin Psychopharmacol 2015 Dec;35(6):747-8

Mood and Anxiety Disorders Program, Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA Mood and Anxiety Disorders Program, Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA.

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http://dx.doi.org/10.1097/JCP.0000000000000398DOI Listing
December 2015

Hematopoietic stem cell quiescence and function are controlled by the CYLD-TRAF2-p38MAPK pathway.

J Exp Med 2015 Apr 30;212(4):525-38. Epub 2015 Mar 30.

Division of Stem Cells and Cancer, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH), 69120 Heidelberg, Germany The German Cancer Consortium (DKTK), 69120 Heidelberg, Germany

The status of long-term quiescence and dormancy guarantees the integrity of hematopoietic stem cells (HSCs) during adult homeostasis. However the molecular mechanisms regulating HSC dormancy remain poorly understood. Here we show that cylindromatosis (CYLD), a tumor suppressor gene and negative regulator of NF-κB signaling with deubiquitinase activity, is highly expressed in label-retaining dormant HSCs (dHSCs). Moreover, Cre-mediated conditional elimination of the catalytic domain of CYLD induced dHSCs to exit quiescence and abrogated their repopulation and self-renewal potential. This phenotype is dependent on the interactions between CYLD and its substrate TRAF2 (tumor necrosis factor-associated factor 2). HSCs expressing a mutant CYLD with an intact catalytic domain, but unable to bind TRAF2, showed the same HSC phenotype. Unexpectedly, the robust cycling of HSCs lacking functional CYLD-TRAF2 interactions was not elicited by increased NF-κB signaling, but instead by increased activation of the p38MAPK pathway. Pharmacological inhibition of p38MAPK rescued the phenotype of CYLD loss, identifying the CYLD-TRAF2-p38MAPK pathway as a novel important regulator of HSC function restricting HSC cycling and promoting dormancy.
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http://dx.doi.org/10.1084/jem.20141438DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4387289PMC
April 2015

The deubiquitinating enzyme CYLD regulates the differentiation and maturation of thymic medullary epithelial cells.

Immunol Cell Biol 2015 Jul 20;93(6):558-66. Epub 2015 Jan 20.

Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.

The cross talk between thymocytes and the thymic epithelium is critical for T-cell development and the establishment of central tolerance. Medullary thymic epithelial cells (mTECs) are located in the thymic medulla and mediate the elimination of self-reactive thymocytes, thereby preventing the onset of autoimmunity. Previous studies identified the deubiquitinating enzyme CYLD as a critical regulator of T-cell development by activating proximal T-cell receptor signaling during the transition of double-positive to single-positive thymocytes. Here we evaluated the impact of the naturally occurring short-splice variant of the cyld gene (sCYLD) on the development and maturation of mTECs. We found that thymi of CYLD(ex7/8) mice, solely expressing sCYLD, displayed a reduced number of mature mTECs caused by a developmental block during the transition of immature to mature mTECs. Further, we could demonstrate an impaired negative selection of thymocytes in these mice. Our data demonstrate that inefficient negative selection in the thymus of CYLD(ex7/8) mice result from a defect in mTEC maturation.
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http://dx.doi.org/10.1038/icb.2014.122DOI Listing
July 2015

Cocaine-induced psychotic disorders: presentation, mechanism, and management.

J Dual Diagn 2014 ;10(2):98-105

a Department of Psychiatry and Behavioral Sciences , Emory University School of Medicine , Atlanta , Georgia , USA.

Cocaine, the third mostly commonly used illicit drug in the United States, has a wide range of neuropsychiatric effects, including transient psychotic symptoms. When psychotic symptoms occur within a month of cocaine intoxication or withdrawal, the diagnosis is cocaine-induced psychotic disorder (CIPD). Current evidence suggests those with CIPD are likely to be male, have longer severity and duration of cocaine use, use intravenous cocaine, and have a lower body mass index. Differentiating CIPD from a primary psychotic disorder requires a detailed history of psychotic symptoms in relation to substance use and often a longitudinal assessment. Treatment includes providing a safe environment, managing agitation and psychosis, and addressing the underlying substance use disorder. This review begins with a clinical case and summarizes the literature on CIPD, including clinical presentation, differential diagnosis, mechanism and predictors of illness, and treatment.
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http://dx.doi.org/10.1080/15504263.2014.906133DOI Listing
July 2015

Electroconvulsive therapy in a geriatric patient with normal pressure hydrocephalus without a shunt.

J ECT 2014 Dec;30(4):e55-6

Department of Psychiatry and Behavioral Sciences Emory University School of Medicine Atlanta, GA

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http://dx.doi.org/10.1097/YCT.0000000000000188DOI Listing
December 2014

Sex-specific association of brain-derived neurotrophic factor (BDNF) Val66Met polymorphism and plasma BDNF with attention-deficit/hyperactivity disorder in a drug-naïve Han Chinese sample.

Psychiatry Res 2014 Jul 14;217(3):191-7. Epub 2014 Mar 14.

Peking University Sixth Hospital/Institute of Mental Health, Beijing 100191, China; Key Laboratory of Mental Health, Ministry of Health, Peking University, Beijing 100191, China. Electronic address:

A functional polymorphism of the brain derived neurotrophic factor gene (BDNF) (Val66Met) has been suggested to be involved in the pathogenesis of attention-deficit/hyperactivity disorder (ADHD). It also has an impact on peripheral BDNF levels in psychiatric disorders. This study examined the association of Val66Met with plasma BDNF level of ADHD in Han Chinese children (170 medication - naïve ADHD patients and 155 unaffected controls, aged 6-16 years). The Val allele was showed a higher frequency in females with ADHD (n=84) than controls (P=0.029) from the case-control association study. The analysis of covariance (ANCOVA) indicated that the mean plasma BDNF levels of ADHD patients were significantly higher than that of controls (P=0.001). We performed both total sample and sex stratified analyses to investigate the effect of Val66Met genotype on the plasma BDNF levels, but only a trend of association was found in females with ADHD (n=84), with a tendency of lower plasma BDNF level in Val allele carriers than Met/Met genotype carriers (P=0.071). Our results suggested a sex-specific association between BDNF and ADHD. Furthermore, there was a possible sex-specific relationship between the BDNF Val66Met genotype and plasma BDNF levels. However, further studies are required to elucidate the role of BDNF in ADHD.
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http://dx.doi.org/10.1016/j.psychres.2014.03.011DOI Listing
July 2014

Adjunctive aripiprazole versus placebo for antipsychotic-induced hyperprolactinemia: meta-analysis of randomized controlled trials.

PLoS One 2013 1;8(8):e70179. Epub 2013 Aug 1.

Beijing Key Lab of Mental Disorders, Beijing Anding Hospital, Capital Medical University, Beijing, China.

Objective: To compare the safety and efficacy of adjunctive aripiprazole versus placebo for antipsychotic-induced hyperprolactinemia.

Methods:

Population: adult patients presenting with antipsychotic-induced hyperprolactinemia diagnosed by prolactin level with or without prolactin-related symptoms.

Interventions: adjunctive aripiprazole vs. adjunctive placebo.

Outcome Measures: adverse events and efficacy of treatment.

Studies: randomized controlled trials.

Results: Five randomized controlled trials with a total of 639 patients (326 adjunctive aripiprazole, 313 adjunctive placebo) met the inclusion criteria. Adjunctive aripiprazole was associated with a 79.11% (125/158) prolactin level normalization rate. Meta-analysis of insomnia, headache, sedation, psychiatric disorder, extrapyramidal symptom, dry mouth, and fatigue showed no significant differences in the adjunctive aripiprazole treatment group compared with the placebo group (risk difference (Mantel-Haenszel, random or fixed) -0.05 to 0.04 (95% confidence interval -0.13 to 0.16); I(2) =0% to 68%, P=0.20 to 0.70). However, sedation, insomnia, and headache were more frequent when the adjunctive aripiprazole dose was higher than 15 mg/day. Meta-analysis of the prolactin level normalization indicated adjunctive aripiprazole was superior to placebo (risk difference (Mantel-Haenszel, random) 0.76 (95% confidence interval 0.67 to 0.85); I(2) =43%, P<0.00001). The subgroup analysis confirmed that the subjects who received adjunctive aripiprazole 5 mg/day showed a degree of prolactin normalization similar to that of all participants. No significant differences between groups in discontinuation and improvements of psychiatric symptoms.

Conclusion: Adjunctive aripiprazole is both safe and effective as a reasonable choice treatment for patients with antipsychotic-induced hyperprolactinemia. The appropriate dose of adjunctive aripiprazole may be 5 mg/day.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0070179PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3731351PMC
March 2014

Sex dependent influence of a functional polymorphism in steroid 5-α-reductase type 2 (SRD5A2) on post-traumatic stress symptoms.

Am J Med Genet B Neuropsychiatr Genet 2013 Apr 15;162B(3):283-292. Epub 2013 Mar 15.

Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia.

A non-synonymous, single nucleotide polymorphism (SNP) in the gene coding for steroid 5-α-reductase type 2 (SRD5A2) is associated with reduced conversion of testosterone to dihydrotestosterone (DHT). Because SRD5A2 participates in the regulation of testosterone and cortisol metabolism, hormones shown to be dysregulated in patients with PTSD, we examined whether the V89L variant (rs523349) influences risk for post-traumatic stress disorder (PTSD). Study participants (N = 1,443) were traumatized African-American patients of low socioeconomic status with high rates of lifetime trauma exposure recruited from the primary care clinics of a large, urban hospital. PTSD symptoms were measured with the post-traumatic stress symptom scale (PSS). Subjects were genotyped for the V89L variant (rs523349) of SRD5A2. We initially found a significant sex-dependent effect of genotype in male but not female subjects on symptoms. Associations with PTSD symptoms were confirmed using a separate internal replication sample with identical methods of data analysis, followed by pooled analysis of the combined samples (N = 1,443, sex × genotype interaction P < 0.002; males: n = 536, P < 0.001). These data support the hypothesis that functional variation within SRD5A2 influences, in a sex-specific way, the severity of post-traumatic stress symptoms and risk for diagnosis of PTSD.
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http://dx.doi.org/10.1002/ajmg.b.32147DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3770127PMC
April 2013

Differential immune system DNA methylation and cytokine regulation in post-traumatic stress disorder.

Am J Med Genet B Neuropsychiatr Genet 2011 Sep 28;156B(6):700-8. Epub 2011 Jun 28.

Department of Psychiatry & Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia, USA.

DNA methylation may mediate persistent changes in gene function following chronic stress. To examine this hypothesis, we evaluated African American subjects matched by age and sex, and stratified into four groups by post-traumatic stress disorder (PTSD) diagnosis and history of child abuse. Total Life Stress (TLS) was also assessed in all subjects. We evaluated DNA extracted from peripheral blood using the HumanMethylation27 BeadChip and analyzed both global and site-specific methylation. Methylation levels were examined for association with PTSD, child abuse history, and TLS using a linear mixed model adjusted for age, sex, and chip effects. Global methylation was increased in subjects with PTSD. CpG sites in five genes (TPR, CLEC9A, APC5, ANXA2, and TLR8) were differentially methylated in subjects with PTSD. Additionally, a CpG site in NPFFR2 was associated with TLS after adjustment for multiple testing. Notably, many of these genes have been previously associated with inflammation. Given these results and reports of immune dysregulation associated with trauma history, we compared plasma cytokine levels in these subjects and found IL4, IL2, and TNFα levels associated with PTSD, child abuse, and TLS. Together, these results suggest that psychosocial stress may alter global and gene-specific DNA methylation patterns potentially associated with peripheral immune dysregulation. Our results suggest the need for further research on the role of DNA methylation in stress-related illnesses.
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http://dx.doi.org/10.1002/ajmg.b.31212DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3292872PMC
September 2011

Validation of the Autism Spectrum Screening Questionnaire, Mandarin Chinese Version (CH-ASSQ) in Beijing, China.

Autism 2011 Nov 20;15(6):713-27. Epub 2011 Jun 20.

Peking University Health Sciences Center, Institute of Mental Health, Beijing, China.

Background: This study screened children in Beijing, China, in order to establish the validity of a Mandarin Chinese translation of the ASSQ.

Methods: We recruited children diagnosed with autism spectrum disorders (ASDs), attention deficit/hyperactivity disorder (ADHD), childhood-onset schizophrenia (COS) (DSM-IV diagnoses made independently by two senior psychiatrists) and unaffected children attending a public school in Beijing. Their parents were asked to complete the CH-ASSQ.

Results: Data from the parents of 94 children with ASD (mean age: 81 ± 47 months), 45 with ADHD (106 ± 27 months), 26 with COS (166 ± 36 months), and 120 unaffected control (72 ± 16 months) were collected. The total scores of ASSQ in children with ASD, ADHD, COS, and unaffected controls were 25.3 ± 9.2, 10.4 ± 7.1, 12.2 ± 10.6, and 5.2 ± 6.6 respectively. Total ASSQ scores of children with ASD were significantly higher than in any other group (all p < .0001). ROC analysis of ASD versus unaffected control subjects showed the area under curve was 0.957, with a cutoff of 12 having the maximum sensitivity (0.957) and specificity (0.825).

Conclusions: Our pilot data suggest that CH-ASSQ successfully differentiates clinically diagnosed ASD patients from unaffected controls, as well as from patients with ADHD and COS. The instrument might therefore be useful for screening for ASD in urban Mandarin Chinese-speaking populations.
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http://dx.doi.org/10.1177/1362361310396383DOI Listing
November 2011