cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5121706.v1
title: Supplementary Material for: Therapieeffekte und Responder-Analysen bei Patientinnen mit Essstörungen: Eine naturalistische Studie

description: <i>Hintergrund:</i> Es gibt bisher einige kontrolliert randomisierte Studien (RCTs), die die Wirksamkeit der kognitiven Verhaltenstherapie (KVT) bei Essstörungen belegen, aber kaum Befunde über Effektstärken unter Praxisbedingungen. Da aber die überwiegende Anzahl ambulanter Psychotherapien bei Essstörungen in der Routineversorgung durchgeführt wird, erscheinen gerade hierfür Wirksamkeitsnachweise notwendig. <i>Patienten und Methode:</i> Die Stichprobe bestand aus 123 Frauen, die als Hauptdiagnose eine Essstörung gemä&zslig; dem Diagnostischen und Statistischen Manual Psychischer Störungen (DSM-IV) aufwiesen. Alle erhielten eine Manual-orientierte essstörungsspezifische KVT. Outcome-Maße bildeten Skalen des Eating Disorder Inventory-2 (EDI-2), des Brief Symptom Inventorys (BSI) und das Beck-Depressionsinventar (BDI). Es wurden Effektstärken berechnet und Responder- sowie Remissionsanalysen durchgeführt. Die Berechnungen wurden sowohl anhand der Intention-to-Treat (ITT)- als auch der Completer-Stichprobe (Completer) dargestellt. Ergebnisse: Auf den Essstörungsskalen zeigten sich Verbesserungen mit Effektstärken nach Cohen zwischen d = 0,50 bis d = 1,59 (ITT) und d = 0,34 bis d = 2,53 (Completer). Die störungsübergreifenden Outcome-Maße des BDI und BSI wiesen Werte von d = 0,89 bis d = 1,08 (BDI-ITT) sowie d = 0,65 bis d = 0,82 (Global Severity Index (GSI)-ITT) auf. Die Responder-Raten lagen für Patientinnen mit Anorexia nervosa bei 48,1%, mit Bulimia nervosa bei 50,8% und mit Essstörung nicht näher bezeichnet (NNB) bei 47,1%. <i>Schlussfolgerungen:</i> In der vorliegenden naturalistischen Studie ließen sich ähnliche, teilweise bessere Effektstärken als in RCTs hinsichtlich der Wirksamkeit der KVT bei Essstörungen finden. Es werden die Vergleichbarkeit der Ergebnisse mit RCTs sowie therapeutische Implikationen unter besonderer Beachtung von Unterschieden zwischen einzelnen Essstörungsformen diskutiert.
DOI: 10.6084/m9.figshare.5121718.v1
title: Supplementary Material for: Risk of Macrovascular Complications in Type 2 Diabetes Mellitus: Endothelial Microparticle Profiles

description: <i>Background:</i> While the adverse impact of diabetes on microvessels is well known, the risks of macroangiopathy are less well recognized. Here, we determine the differential risk and endothelial microparticle (EMP) profile of vascular complications in type 2 diabetes mellitus. <i>Methods:</i> Macroangiopathy was evaluated for cerebrovascular disease, coronary artery disease and peripheral artery disease; microangiopathy was evaluated for retinopathy, nephropathy and peripheral neuropathy. Clinical and laboratory factors were compared among 149 patients with no vascular complications or with microangiopathic and/or macroangiopathic complications. EMPs were also examined by flow cytometry using CD31, CD42b, annexin V (AV), and CD62E antibodies in the peripheral blood of patients. <i>Results:</i> Diabetes of long duration, an elevated hemoglobin A1c (HbA1c) and concomitant hypertension were significantly associated with the occurrence of vascular complications. Dyslipidemia and a high body mass index were significantly associated with macroangiopathy, while diabetes of long duration and a high concentration of HbA1c were associated with microangiopathy. The EMP (CD31+/CD42b–, CD31+/AV+) levels were higher in patients with macroangiopathy than in patients with microangiopathy and no complications. The EMP level was also independently associated with macroangiopathy in diabetic patients. <i>Conclusions:</i> Microangiopathy and macroangiopathy in diabetic patients appear to have a different pathophysiological basis. The measurement of EMP would be helpful to differentiate the risk of diabetic vascular complications.
DOI: 10.6084/m9.figshare.5121703
title: Supplementary Material for: Altered Expression of Myogenic Regulatory Factors in the Mouse Model of Amyotrophic Lateral Sclerosis

description: <i>Background:</i> In the superoxide dismutase 1 (SOD1)-G93A mouse model of amyotrophic lateral sclerosis (ALS), skeletal muscle is a key target of mutant SOD1 toxicity. However, the expression of factors that control the regenerative potential of the muscle is unknown in this model. <i>Objective:</i> To characterize the expression of satellite cell marker <i>Pax7</i> and myogenic regulatory factors (MRF) in skeletal muscle of SOD1-G93A mice at different stages of the disease. <i>Methods:</i> The expressions of <i>Pax7, Myod1, Myf5</i> and myogenin <i>(Myog)</i> were determined by quantitative real-time PCR and by Western blotting from the grouped gastrocnemius, quadriceps and soleus muscles of SOD1-G93A mice at presymptomatic, symptomatic and terminal stages of the disease, and from surgically denervated wild-type gastrocnemius muscles. <i>Results:</i><i>Pax7</i> mRNA and MYF5 protein were upregulated in presymptomatic mice, coinciding with increased muscle damage marker <i>Rrad</i> and chemokine <i>Ccl5.</i> All MRF transcripts and most proteins (excluding MYOG) were increased, starting from 3 months of age, simultaneously with increased expression of denervation marker Chrna1. However, in the terminal stage, no protein increase was evident for <i>Pax7</i> or any of the MRF despite the increased mRNA levels. The transcripts for chemokine <i>Ccl2</i> and chemokine receptor <i>Cxcr4 </i>were increased starting from the onset of symptoms. <i>Conclusions:</i> The characterization of <i>Pax7</i> and MRF in SOD1-G93A mice reveals a progressive induction of the myogenic program at the RNA level, but a blunted protein level response at late stages of the disease. Altered posttranscriptional and posttranslational mechanisms likely to operate, as well as the potential role of chemokine signaling in mutant SOD1 muscle, are discussed.
DOI: 10.6084/m9.figshare.5121712.v1
title: Supplementary Material for: Gamma-1-Syntrophin Mediates Trafficking of Gamma-Enolase towards the Plasma Membrane and Enhances Its Neurotrophic Activity

description: Syntrophins are scaffold proteins that can bind several signaling molecules and localize them to the plasma membrane. We demonstrate here that in neuroblastoma SH-SY5Y cells, brain-specific γ<sub>1</sub>-syntrophin binds the neurotrophic factor γ-enolase through its PDZ domain, and translocates it to the plasma membrane, as shown by immunoprecipitation, surface plasmon resonance, fluorescence colocalization and flow cytometry. Extensive colocalization of γ<sub>1</sub>-syntrophin and γ-enolase was observed in neurite growth cones in differentiated SH-SY5Y cells. Silencing of the γ<sub>1</sub>-syntrophin gene by RNA interference significantly reduced the re-distribution of γ-enolase to the plasma membrane and impaired its neurotrophic effects. We demonstrated that an intact C-terminal end of γ-enolase is essential for its γ<sub>1</sub>-syntrophin-assisted trafficking. The cleavage of two amino acids at the C-terminal end of γ-enolase by the carboxypeptidase cathepsin X prevents binding with the γ<sub>1</sub>-syntrophin PDZ domain. Collectively, these data demonstrate that γ<sub>1</sub>-syntrophin participates in γ-enolase translocation towards the plasma membrane, a pre-requisite for its neurotrophic activity. By disrupting this γ<sub>1</sub>-syntrophin-guided subcellular distribution, cathepsin X reduces γ-enolase-induced neurotrophic signaling.
DOI: 10.6084/m9.figshare.5121694
title: Supplementary Material for: Einfluss von Angststörungen und Depression auf den Therapieerfolg bei Patienten mit somatoformen Störungen

description: <i>Hintergrund:</i> Patienten mit somatoformen Stöungen leiden häufig komorbid unter Depressionen oder Angststörungen. Ziel der Studie ist es, deren Einfluss auf den Erfolg kognitiv-verhaltenstherapeutischer Therapie bei somatoformen Störungen zu klären. <i>Methode:</i> In einem längsschnittlichen Untersuchungsdesign wurde an 106 Patienten, die an einer ambulanten Gruppenintervention zur Bewältigung somatoformer Beschwerden teilgenommen haben, die Bedeutung komorbider Depression und Angststörungen für die Prädiktion des Therapieerfolgs untersucht. <i>Ergebnisse:</i> In bivariaten Analysen zeigten sich signifikante Zusammenhänge zwischen komorbider Angst, Intensität der somatoformen Störung und dem kurzfristigen und katamnestischen Therapieerfolg. Das Vorliegen einer Depression war nicht mit dem Therapieerfolg assoziiert. In multiplen Regressionsanalysen konnte jedoch nur eine hohe Intensität der somatoformen Störung als Prädiktor für den Therapieerfolg bestätigt werden. <i>Schlussfolgerung:</i> Auch schwerer beeinträchtigten Patienten mit somatoformen Störungen und Patienten mit komorbider Depression oder Angststörungen kann eine ambulante kognitiv-verhaltentherapeutische Therapie zur Symptombewältigung empfohlen werden.
DOI: 10.6084/m9.figshare.5121697
title: Supplementary Material for: Systematic Review of the Epidemiology of Complicated Peptic Ulcer Disease: Incidence, Recurrence, Risk Factors and Mortality

description: <i>Background/Aims:</i> The incidence of uncomplicated peptic ulcer has decreased in recent years. It is unclear what the impact of this has been on the epidemiology of peptic ulcer complications. This systematic review aimed to determine the incidence, recurrence and mortality of complicated peptic ulcer and the risk factors associated with these events. <i>Methods:</i> Systematic PubMed searches. <i>Results:</i> Overall, 93 studies were identified. Annual incidence estimates of peptic ulcer hemorrhage and perforation were 19.4–57.0 and 3.8–14 per 100,000 individuals, respectively. The average 7-day recurrence of hemorrhage was 13.9% (95% CI: 8.4–19.4), and the average long-term recurrence of perforation was 12.2% (95% CI: 2.5–21.9). Risk factors for peptic ulcer complications and their recurrence included nonsteroidal anti-inflammatory drug and/or acetylsalicylic acid use, <i>Helicobacter pylori</i> infection and ulcer size ≧1 cm. Proton pump inhibitor use reduced the risk of peptic ulcer hemorrhage. Average 30-day mortality was 8.6% (95% CI: 5.8–11.4) after hemorrhage and 23.5% (95% CI: 15.5–31.0) after perforation. Older age, comorbidity, shock and delayed treatment were associated with increased mortality. <i>Conclusions:</i> Complicated peptic ulcer remains a substantial healthcare problem which places patients at a high risk of recurrent complications and death.
DOI: 10.6084/m9.figshare.5121700
title: Supplementary Material for: Type 2 Diabetes and Late-Onset Alzheimer’s Disease

description: <i>Background/Aims:</i> To confirm in a cohort recruited in 1999–2001 our finding in a cohort recruited in 1992–1994 relating type 2 diabetes (T2D) to late-onset Alzheimer’s disease (LOAD). <i>Methods:</i> Participants were 1,488 persons aged 65 years and older without dementia at baseline from New York City. T2D was ascertained by self-report. Dementia and LOAD were ascertained by standard research procedures. Proportional hazard regression was used for analyses relating T2D and LOAD. <i>Results:</i> The prevalence of T2D was 17%. There were 161 cases of dementia and 149 cases of LOAD. T2D was related to dementia (hazard ratio = 1.7; 95% confidence interval = 1.4–2.9) and LOAD (1.6; 1.0–2.6) after adjustment for age, sex, education, ethnic group and apolipoprotein E Ε4. This association was weaker when only AD – excluding cases of mixed dementia – was considered (hazard ratio = 1.3; 95% confidence interval = 0.8–2.2). <i>Conclusion: </i>T2D is associated with LOAD. Cerebrovascular disease may be an important mediator.
DOI: 10.6084/m9.figshare.5121715.v1
title: Supplementary Material for: Chronic Obstructive Pulmonary Disease-Specific Gene Expression Signatures of Alveolar Macrophages as well as Peripheral Blood Monocytes Overlap and Correlate with Lung Function

description: <i>Background:</i> Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease characterized by progressive airflow limitation and significant extrapulmonary (systemic) effects that lead to co-morbid conditions, though the pathomechanism of COPD is largely undetermined. Alveolar macrophages (AM) derived from peripheral monocytes (MO) appear to play a key role in initiating and/or sustaining disease progression. <i>Objectives:</i> To identify disease- and cell type-specific gene expression profiles and potential overlaps in those in order to diagnose COPD, characterize its progression and determine the effect of drug treatment. <i>Method:</i> Global gene expression analysis was used for primary screening in order to obtain expression signatures of AMs and circulating MOs of COPD patients and healthy controls. The results of microarray analyses of AMs (20 controls and 26 COPD patients) and MOs (16 controls and 22 COPD patients) were confirmed and validated by real-time quantitative polymerase chain reaction. <i>Results:</i> We have identified gene sets specifically associated with COPD in AMs and MOs. There were overlapping genes between the two cell types. Our data also show that COPD-specific gene expression signatures in AMs and MOs correlate with percent of predicted FEV<sub>1</sub>. <i>Conclusion:</i> Disease-specific and overlapping gene expression signatures can be defined in lung-derived macrophages and also in circulating monocytes. Some of the validated expression changes in both cell types correlate with lung function and therefore could serve as biomarkers of disease progression.
DOI: 10.6084/m9.figshare.5121703.v1
title: Supplementary Material for: Altered Expression of Myogenic Regulatory Factors in the Mouse Model of Amyotrophic Lateral Sclerosis

description: <i>Background:</i> In the superoxide dismutase 1 (SOD1)-G93A mouse model of amyotrophic lateral sclerosis (ALS), skeletal muscle is a key target of mutant SOD1 toxicity. However, the expression of factors that control the regenerative potential of the muscle is unknown in this model. <i>Objective:</i> To characterize the expression of satellite cell marker <i>Pax7</i> and myogenic regulatory factors (MRF) in skeletal muscle of SOD1-G93A mice at different stages of the disease. <i>Methods:</i> The expressions of <i>Pax7, Myod1, Myf5</i> and myogenin <i>(Myog)</i> were determined by quantitative real-time PCR and by Western blotting from the grouped gastrocnemius, quadriceps and soleus muscles of SOD1-G93A mice at presymptomatic, symptomatic and terminal stages of the disease, and from surgically denervated wild-type gastrocnemius muscles. <i>Results:</i><i>Pax7</i> mRNA and MYF5 protein were upregulated in presymptomatic mice, coinciding with increased muscle damage marker <i>Rrad</i> and chemokine <i>Ccl5.</i> All MRF transcripts and most proteins (excluding MYOG) were increased, starting from 3 months of age, simultaneously with increased expression of denervation marker Chrna1. However, in the terminal stage, no protein increase was evident for <i>Pax7</i> or any of the MRF despite the increased mRNA levels. The transcripts for chemokine <i>Ccl2</i> and chemokine receptor <i>Cxcr4 </i>were increased starting from the onset of symptoms. <i>Conclusions:</i> The characterization of <i>Pax7</i> and MRF in SOD1-G93A mice reveals a progressive induction of the myogenic program at the RNA level, but a blunted protein level response at late stages of the disease. Altered posttranscriptional and posttranslational mechanisms likely to operate, as well as the potential role of chemokine signaling in mutant SOD1 muscle, are discussed.
DOI: 10.6084/m9.figshare.5121691
title: Supplementary Material for: Testicular Gene Expression in Cryptorchid Boys at Risk of Azoospermia

description: Despite timely and successful surgery, 32% of patients with bilateral and 10% with unilateral cryptorchidism will develop azoospermia. Cryptorchid boys at risk of azoospermia display a typical testicular histology of impaired mini-puberty at the time of the orchidopexy. During mini-puberty increased gonadotropin and testosterone secretion stimulate transformation of gonocytes into Ad spermatogonia. In the azoospermia risk group this transformation is to a great extent impaired. This study aimed to analyze data on whole genome expression signatures of undescended testes at risk of developing azoospermia. Twenty-three testicular biopsies from 22 boys were analyzed (19 testes from 18 boys with cryptorchidism and 4 contralateral descended testes from patients with testicular agenesis). Expression profiling identified 483 genes not or under-expressed in the azoospermia risk group compared with the control and low risk for azoospermia (LAZR) groups. Annotated loci were associated with spermatogenesis. Other significant genes were cellular defense response genes and hormone-controlled loci involved in spermatogenesis. Some genes transcribed in normal adult meiotic and post-meiotic germ cells are activated in healthy juvenile Ad spermatogonia. Thus, molecular events initiating the testicular expression program at the onset of puberty and maintaining it during adulthood occur very early in prepubertal testes. This molecular event is to a great extent impaired in the high risk for azoospermia (HAZR) group lacking Ad spermatogonia (stem cells for spermatozoa) indicating impaired mini-puberty.
DOI: 10.6084/m9.figshare.5121694.v1
title: Supplementary Material for: Einfluss von Angststörungen und Depression auf den Therapieerfolg bei Patienten mit somatoformen Störungen

description: <i>Hintergrund:</i> Patienten mit somatoformen Stöungen leiden häufig komorbid unter Depressionen oder Angststörungen. Ziel der Studie ist es, deren Einfluss auf den Erfolg kognitiv-verhaltenstherapeutischer Therapie bei somatoformen Störungen zu klären. <i>Methode:</i> In einem längsschnittlichen Untersuchungsdesign wurde an 106 Patienten, die an einer ambulanten Gruppenintervention zur Bewältigung somatoformer Beschwerden teilgenommen haben, die Bedeutung komorbider Depression und Angststörungen für die Prädiktion des Therapieerfolgs untersucht. <i>Ergebnisse:</i> In bivariaten Analysen zeigten sich signifikante Zusammenhänge zwischen komorbider Angst, Intensität der somatoformen Störung und dem kurzfristigen und katamnestischen Therapieerfolg. Das Vorliegen einer Depression war nicht mit dem Therapieerfolg assoziiert. In multiplen Regressionsanalysen konnte jedoch nur eine hohe Intensität der somatoformen Störung als Prädiktor für den Therapieerfolg bestätigt werden. <i>Schlussfolgerung:</i> Auch schwerer beeinträchtigten Patienten mit somatoformen Störungen und Patienten mit komorbider Depression oder Angststörungen kann eine ambulante kognitiv-verhaltentherapeutische Therapie zur Symptombewältigung empfohlen werden.
DOI: 10.6084/m9.figshare.5121685
title: Supplementary Material for: Androgen Receptor Mutations Are Associated with Altered Epigenomic Programming as Evidenced by <i>HOXA5</i> Methylation

description: Male external genital differentiation is accompanied by implementation of a long-term, male-specific gene expression pattern indicating androgen programming in cultured genital fibroblasts. We hypothesized the existence of an epigenetic background contributing to this phenomenon. DNA methylation levels in 2 normal scrotal fibroblast strains from 46,XY males compared to 2 labia majora fibroblast strains from 46,XY females with complete androgen insensitivity syndrome (AIS) due to androgen receptor (AR) mutations were analyzed by Illumina GoldenGate methylation arrays®. Results were validated with pyrosequencing in labia majora fibroblast strains from fifteen 46,XY patients and compared to nine normal male scrotal fibroblast strains. <i>HOXA5</i> showed a significantly higher methylation level in complete AIS. This finding was confirmed by bisulfite pyrosequencing of 14 CpG positions within the <i>HOXA5</i> promoter in the same strains. Extension of the 2 groups revealed a constant low <i>HOXA5</i> methylation pattern in the controls in contrast to a highly variable methylation pattern in the AIS patients. <i>HOXA5</i> represents a candidate gene of androgen-mediated promoter methylation. The constantly low <i>HOXA5</i> DNA methylation level of normal male scrotal fibroblast strains and the frequently high methylation levels in labia majora fibroblast strains in AIS indicate for the first time that androgen programming in sexual differentiation is not restricted to global gene transcription but also occurs at the epigenetic level.
DOI: 10.6084/m9.figshare.5121691.v1
title: Supplementary Material for: Testicular Gene Expression in Cryptorchid Boys at Risk of Azoospermia

description: Despite timely and successful surgery, 32% of patients with bilateral and 10% with unilateral cryptorchidism will develop azoospermia. Cryptorchid boys at risk of azoospermia display a typical testicular histology of impaired mini-puberty at the time of the orchidopexy. During mini-puberty increased gonadotropin and testosterone secretion stimulate transformation of gonocytes into Ad spermatogonia. In the azoospermia risk group this transformation is to a great extent impaired. This study aimed to analyze data on whole genome expression signatures of undescended testes at risk of developing azoospermia. Twenty-three testicular biopsies from 22 boys were analyzed (19 testes from 18 boys with cryptorchidism and 4 contralateral descended testes from patients with testicular agenesis). Expression profiling identified 483 genes not or under-expressed in the azoospermia risk group compared with the control and low risk for azoospermia (LAZR) groups. Annotated loci were associated with spermatogenesis. Other significant genes were cellular defense response genes and hormone-controlled loci involved in spermatogenesis. Some genes transcribed in normal adult meiotic and post-meiotic germ cells are activated in healthy juvenile Ad spermatogonia. Thus, molecular events initiating the testicular expression program at the onset of puberty and maintaining it during adulthood occur very early in prepubertal testes. This molecular event is to a great extent impaired in the high risk for azoospermia (HAZR) group lacking Ad spermatogonia (stem cells for spermatozoa) indicating impaired mini-puberty.
DOI: 10.6084/m9.figshare.5121679
title: Supplementary Material for: Brain Activity Supporting Working Memory Accuracy in Patients with Paranoid Schizophrenia: A Functional Magnetic Resonance Imaging Study

description: <i>Background:</i> Dysfunctional working memory (WM) has been recognized as one of the most consistent deficits in schizophrenia. Studies that investigated the neural correlates of WM-related pathology by comparing patients with schizophrenia and control participants have produced controversial results, reporting task-related hyper- or hypoactivity in frontoparietal networks. <i>Method:</i> We addressed this question by comparing BOLD signals for accurate responses during a WM task for emotional faces between a homogeneous group of high-performing patients and a control group. <i>Results:</i> Our results confirm previous findings of left prefrontal hyperactivity contrasted with hypoactivity in right prefrontal cortex to support WM performance. We also extend previous work by reporting enhanced activity in higher visual areas of patients during encoding and maintenance. <i>Conclusion:</i> Our findings and those of the literature can be integrated into a model, where preserved visual cognition in high-functioning patients with hypofrontality is explained by activation of contralateral homologue areas combined with enhanced recruitment of sensory areas.