Bindung und Beziehung – eine Analyse aktueller psychoanalytischer Forschungsansätze

The issue of attachment has become increasingly important in research on fields such as developmental psychology, psychoanalysis but also infant research. This paper aims at discussing concepts from attachment theory, established by Bowlby, as well as object relations theory, concentrating on Klein’s and Bion’s contributions. These two theoretical models for understanding the specific individual emotional bond between an individual and its loved objects are elaborated and compared. Subsequently, the protective aspects of secure attachment are discussed and the harmful and psychically endangering qualities of insecure attachment are illustrated, showing that insecure attachment can be connected to psychopathology. Finally, further possibilities for research are pointed out and the potential of merging research methods from objects relations theory with attachment theory are discussed.     

Autonomic Arousal During Actigraphically Estimated Waking and Sleep in Male Veterans With PTSD

Physiological hyperarousal is manifested acutely by increased heart rate, decreased respiratory sinus arrhythmia, and increased skin conductance level and variability. Yet it is uncertain to what extent such activation occurs with the symptomatic hyperarousal of posttraumatic stress disorder (PTSD). We compared 56 male veterans with current PTSD to 54 males who never had PTSD. Subjects wore ambulatory devices that recorded electrocardiograms, finger skin conductance, and wrist movement while in their normal environments. Wrist movement was monitored to estimate sleep and waking periods. Heart rate, but not the other variables, was elevated in subjects with PTSD equally during waking and during actigraphic sleep (effect sizes, Cohen's d, ranged from 0.63 to 0.89). The length of the sleep periods and estimated sleep fragmentation did not differ between groups. Group heart rate differences could not be explained by differences in body activity, PTSD hyperarousal symptom scores, depression, physical fitness, or antidepressant use.     

Three-Dimensional Reconstruction of the Genial Spinal Canal

The aim of this anatomical study was to investigate the genial spinal canal histologically and to reconstruct it three-dimensionally to improve understanding of its anatomy and to reveal any differences between dentate and edentulous specimens. Two tissue blocks from the mandible between the left and right second incisors, one dentate and one edentulous, were fixed in 4.5% formaldehyde, decalcified and embedded in paraffin. Serial histological sections were prepared, stained with Azan and examined microscopically. Additionally, three-dimensional models of the blocks were reconstructed using microphotographs of the sections. The genial spinal canal in the dentate specimen contained a neurovascular bundle, which branched into a nerve innervating the incisor and a neurovascular bundle, whereas that in the edentulous specimen contained some nerves for vestibular gingival innervation and a vascular bundle. The results suggest differences in the genial spinal canal between dentate and edentulous mandibles. Further research is needed to confirm this finding. Clin. Anat., 33:1102–1108, 2020. © 2019 Wiley Periodicals, Inc.     

Pattern of TGFbeta receptor 1 expression differs between kras-mutated keratoacanthomas and squamous cell carcinomas of the skin

Purpose

Increasing evidence indicates that TGFbeta- and EGFR-signaling is involved in the pathogenesis of keratoacanthoma (KA) and squamous cell carcinoma (SCC) of the skin. We analyzed the expression pattern of TGFbeta-signaling components and screened for mutations in tgfbetaR1, egfr, kras and braf in KAs and SCCs.

Methods

Immunohistochemical analysis of TGFbeta1, TGFbetaR1, TGFbetaR2 and phospho-SMAD2/3 was performed on skin tumors (29 KAs, 30 well and 31 moderately differentiated SCCs). Mutation screening in hotspot regions of tgfbetaR1, egfr, kras and braf was performed through pyrosequencing of tumor DNA.

Findings

Expression of TGFbeta1, TGFbetaR1 and p-SMAD2/3 was increased in tumors as compared to surrounding skin. In KAs characteristic strong discontinuous membranous TGFbetaR1 expression pattern frequently associated with kras mutation was noted. SCCs showed continuous TGFbetaR1 expression, stronger p-SMAD2/3 expression and less frequent kras mutations. In tumors at sun-exposed sites stronger TGFbetaR1 expression was noted. One SCC showed tgfbetaR1 mutation, but no other mutations were found.

Conclusion

Although tgfbetaR1 germline mutations cause inherited KAs and our finding of strong discontinuous membranous expression in KAs suggests accumulation of functionally altered protein, we found no tgfbetaR1 mutations or influence on TGFbeta-signaling, but frequent kras mutations in this subgroup of KAs. Characteristic TGFbetaR1 expression pattern in KA can facilitate histopathologic distinction from SCC.     

Outcome of the frozen elephant trunk procedure as a redo operation

 Open in a separate windowOBJECTIVESThe goal of this study was to determine the outcome of patients undergoing an elective frozen elephant trunk (FET) procedure as a redo operation following previous cardiac surgery.METHODSOne hundred and eighteen consecutive patients underwent FET procedures between October 2010 and October 2019 at our centre. Patients were registered in a dedicated database and analysed retrospectively. Clinical and follow-up characteristics were compared between patients undergoing a FET operation as a primary (primary group) or a redo procedure (redo group) using logistic regression and Cox regression analysis. Emergency procedures (n = 33) were excluded from the analysis.RESULTSA total of 36.5% (n = 31) of the FET procedures were redo operations (redo group) and 63.5% (n = 54) of the patients underwent primary surgery (primary group). There was no significant difference in the 30-day mortality [primary group: 7.4%; redo group: 3.2%; 95% confidence interval (CI) (0.19–35.29); P = 0.63] and the 3-year mortality [primary group: 22.2%; redo group: 16.7%; 95% CI (0.23–3.23); P = 0.72] between redo and primary cases. Furthermore, the adjusted statistical analysis did not reveal significant differences between the groups in the occurrence of transient or permanent neurological deficit, paraplegia, acute renal failure and resternotomy. The redo group showed a higher rate of recurrent nerve palsy, which did not reach statistical significance [primary group: 3.7% (n = 2); redo group: 19.4% (n = 6); P = 0.091].CONCLUSIONSElective FET procedures as redo operations performed by a dedicated aortic team following previous cardiac surgery demonstrate an adequate safety profile.     

GDF15 promotes simultaneous astrocyte remodeling and tight junction strengthening at the blood–brain barrier

Perivascular astrocyte processes (PAP) surround cerebral endothelial cells (ECs) and modulate the strengthening of tight junctions to influence blood–brain barrier (BBB) permeability. Morphologically altered astrocytes may affect barrier properties and trigger the onset of brain pathologies. However, astrocyte-dependent mediators of these events remain poorly studied. Here, we show a pharmacologically driven elevated expression and release of growth/differentiation factor 15 (GDF15) in rat primary astrocytes and cerebral PAP. GDF15 has been shown to possess trophic properties for motor neurons, prompting us to hypothesize similar effects on astrocytes. Indeed, its increased expression and release occurred simultaneously to morphological changes of astrocytes in vitro and PAP, suggesting modulatory effects of GDF15 on these cells, but also neighboring EC. Administration of recombinant GDF15 was sufficient to promote astrocyte remodeling and enhance barrier properties between ECs in vitro, whereas its pharmacogenetic abrogation prevented these effects. We validated our findings in male high anxiety-related behavior rats, an animal model of depressive-like behavior, with shrunk PAP associated with reduced expression of the junctional protein claudin-5, which were both restored by a pharmacologically induced increase in GDF15 expression. Thus, we identified GDF15 as an astrocyte-derived trigger of astrocyte process remodeling linked to enhanced tight junction strengthening at the BBB.