„Mild-behavioral-impairment“-Checkliste

Hintergrund: Das Syndrom einer leichten Verhaltensbeeinträchtigung („mild behavioral impairment syndrome“, MBI) ist definiert durch das Auftreten anhaltender neuropsychiatrischer Symptome im Alter. Die Mild-behavioral-impairment-Checkliste (MBI-C) dient der Erfassung von persistierenden neuropsychiatrischen Symptomen, welche die Präsenz des MBI definieren. Ziel: Erarbeitung einer deutschsprachigen Version der MBI-C und Beurteilung der klinischen Anwendbarkeit. Material undMethoden: ImAustausch mit dem federführenden Autor der englischen Originalversionwurde eine deutsche Version erstellt. Die Praktikabilität der Anwendung wurde im Rahmen einer Anwendbarkeitsstudie an einer Kohorte von 21 stationären alterspsychiatrischen Patienten überprüft. Dabei wurden die Compliance der Patienten, die Verständlichkeit, der Zeitaufwand, das Vorgehen bei der Auswertung und die Unterschiede zwischen den Angaben der Patienten und der Angehörigen beurteilt. Ergebnisse: Die erstellte Übersetzung der MBI-C gilt als offizielle deutsche Version und kann auf https://mbitest.org heruntergeladen werden. Alle Patienten beantworteten alle 34 Fragen vollständig, die Verständlichkeit zeigte sich als sehr gut, der durchschnittliche Zeitaufwand lag bei 16min. Es zeigten sich z. T. bedeutsame Unterschiede zwischen den Angaben der Patienten und der Angehörigen. Diskussion: Das MBI kann bei einem Teil der Personen mit neurodegenerativer demenzieller Erkrankung das ansonsten präsymptomatische Stadium markieren. Die MBI-C könnte somit bei der Früherkennung von neurodegenerativen Demenzen helfen. Diese Hypothese kann mithilfe der hier präsentierten sprachlich lokalisierten Version der MBI-C auch im deutschsprachigen Raumzukünftig überprüft werden

Adiponectin Fails in Improving Angiogenic Repair in Streptozocin-Treated or Leprdb/db Mice after Hind Limb Ischemia

Type 1 and 2 diabetes carry risk factors for the development of microvascular diseases with associated impairment of angiogenic repair. Here, we investigated whether adiponectin, an adipocyte-specific adipocytokine with antiatherosclerotic and antidiabetic properties, regulates angiogenic repair in response to tissue ischemia in Leprdb/db and streptozocin-treated diabetic mouse models. Methods. Adenoviral vectors containing the gene for β-galactosidase, full-length mouse adiponectin, and dominant-negative AMPKα2 were used in streptozocin-treated male Leprdb/db mice, after which hind limb blood flow was measured using a laser doppler blood flow analyzer. Results. The angiogenic repair of ischemic hind limbs was impaired in both streptozocin-treated and Leprdb/db mice compared to wild-type mice as evaluated by laser doppler flow and capillary density analyses. Adenovirus-mediated administration of adiponectin accelerated angiogenic repair after hind limb ischemia in WT mice, but not in Leprdb/db mice or mice treated with streptozocin. In vitro experiments using HUVECs highlighted the antiapoptotic and proangiogenic properties of adiponectin but could not demonstrate accelerated differentiation of endothelial cells into tube- like structures at elevated glucose levels. Conclusions. External administration of adiponectin at elevated glucose levels may not be useful in the treatment of diabetes mellitus-related vascular deficiency diseases

The effect of alexithymia and depressive feelings on pain perception in somatoform pain disorder

Objective: To investigate the relationship between alexithymia and depression and their influence on the subjective versus experimental pain perception in somatoform pain disorder. Methods: Three groups consisting of 40 patients with somatoform pain disorder, 40 patients with depression, and 40 healthy controls were matched. They completed questionnaires regarding alexithymia (TAS26) and depressive feelings (BDI-II). In addition, pain patients rated their subjective pain intensity (NRS). Quantitative sensory testings were conducted in all participants examining temperature (CPT, HPT) and mechanical (MPT, PPT) thresholds. Results: Analysis of variance showed that alexithymia was significantly increased in both patient groups compared to healthy controls, but with the highest amount in somatoform pain. Regression analyses confirmed that this finding was in part due to a high comorbidity of depressive feelings in both patient groups. We found a discrepancy between increased clinical pain ratings and elevated pressure pain thresholds, indicating a less intense mechanical pain perception in somatoform pain. Correlation analyses demonstrated a significant connection of subjective pain ratings and pressure pain thresholds with depressive feelings. Conclusion: Contrary to the results of other experimental pain studies on chronic muskuloskeletal pain syndromes, we could not confirm central sensitization in somatoform pain disorder. Our findings place the somatoform pain disorder more in the direction of affective disorder such as depression. These findings may improve a better understanding of the disease and also have direct therapeutic implications. The high occurrence of alexithymia and depressive feelings in somatoform pain should be considered in diagnostic and therapeutic regimens of these patients

Increased Alexithymia But No Profound Emotion Processing Disorder in Burnout Syndrome

Our objectives were to investigate alexithymia in burnout patients while controlling for depression and anxiety, as well as to evaluate whether alexithymia may be part of a profound emotional processing disorder or of a mentalization deficit. Alexithymia, depressive, and anxious feelings were compared in patients with burnout, depression, and healthy controls using an age-, sex-, and education-matched cross-sectional design (n= 60). A facial emotion recognition task and an emotional mentalizing performance test as well as physical and emotional violation experiences were conducted. Alexithymia was significantly increased in burnout patients, mediated by negative affect in this group. No impairment of facial emotion recognition or mental attribution could be shown. Burnout patients demonstrated slightly increased emotional abuse experiences in early childhood. The present results corroborate the supposition that alexithymia in burnout primarily depends on affect and may rise due to current strain and overload experience, rather than based on a profound developmental disorder in emotion processing

Impaired revascularization in a mouse model of type 2 diabetes is associated with dysregulation of a complex angiogenic-regulatory network

Objective - Diabetes is a risk factor for the development of cardiovascular diseases associated with impaired angiogenesis or increased endothelial cell apoptosis. Methods and Results - Here it is shown that angiogenic repair of ischemic hindlimbs was impaired in Lepr db/db mice, a leptin receptor-deficient model of diabetes, compared with wild-type (WT) C57BL/6 mice, as evaluated by laser Doppler flow and capillary density analyses. To identify molecular targets associated with this disease process, hindlimb cDNA expression profiles were created from adductor muscle of Lepr db/db and WT mice before and after hindlimb ischemia using Affymetrix GeneChip Mouse Expression Set microarrays. The expression patterns of numerous angiogenesis-related proteins were altered in Lepr db/db versus WT mice after ischemic injury. These transcripts included neuropilin-1, vascular endothelia growth factor-A, placental growth factor, elastin, and matrix metalloproteinases implicated in blood vessel growth and maintenance of vessel wall integrity. Conclusion - These data illustrate that impaired ischemia-induced neovascularization in type 2 diabetes is associated with the dysregulation of a complex angiogenesis-regulatory network. © 2005 American Heart Association, Inc

Microarray analysis of Akt1 activation in transgenic mouse hearts reveals transcript expression profiles associated with compensatory hypertrophy and failure

To investigate molecular mechanisms involved in the development of cardiac hypertrophy and heart failure, we developed a tetracycline-regulated transgenic system to conditionally switch a constitutively active form of the Akt1 protein kinase on or off in the adult heart. Short-term activation (2 wk) of Akt1 resulted in completely reversible hypertrophy with maintained contractility. In contrast, chronic Akt1 activation (6 wk) induced extensive cardiac hypertrophy, severe contractile dysfunction, and massive interstitial fibrosis. The focus of this study was to create a transcript expression profile of the heart as it undergoes reversible Akt1-mediated hypertrophy and during the transition from compensated hypertrophy to heart failure. Heart tissue was analyzed before transgene induction, 2 wk after transgene induction, 2 wk of transgene induction followed by 2 days of repression, 6 wk after transgene induction, and 6 wk of transgene induction followed by 2 wk of repression. Acute overexpression of Akt1 (2 wk) leads to changes in the expression of 826 transcripts relative to noninduced hearts, whereas chronic induction (6 wk) led to changes in the expression of 1,611, of which 65% represented transcripts that were regulated during the pathological phase of heart growth. Another set of genes identified was uniquely regulated during heart regression but not growth, indicating that nonoverlapping transcription programs participate in the processes of cardiac hypertrophy and atrophy. These data define the gene regulatory programs downstream of Akt that control heart size and contribute to the transition from compensatory hypertrophy to heart failure. Copyright © 2006 the American Physiological Society

The Proline 7 Substitution in the Preproneuropeptide Y Is Associated with Higher Hepatic Lipase Activity In Vivo

Hepatic lipase (HL) functions as a lipolytic enzyme that hydrolyzes triglycerides and phospholipids present in circulating plasma lipoproteins. Plasma HL activity is known to be regulated by hormonal and metabolic factors, but HL responsiveness to insulin as well as its role in modulating atherosclerotic risk is still controversial. We investigated on the influence of a known polymorphism in the neurotransmitter neuropeptide Y (NPY) on HL activity in two different cohorts consisting of diabetic and nondiabetic patients. HL activity was 24% and 34% higher on nondiabetic and diabetic subjects in the presence of the 7Pro allele in NPY, respectively. The presence of the 7Pro allele was an independent predictor of HL activity in multivariate analyses in both cohorts. These data suggest a regulatory effect of NPY on HL activity. Among carriers of the 7Pro allele, we also found a statistically significant lower absolute number of infarctions compared to noncarriers (p < 0 05) and a nonsignificant trend towards less myocardial infarction in the 7Pro allele diabetic carriers (p = 0 085). In conclusion, the common 7Pro allele in NPY was associated with higher HL activity in nondiabetic and diabetic subjects and its presence seems to coincide with a lower frequency of certain cardiovascular events