Eating one's words: Part III. Mentalisation‐based psychotherapy for anorexia nervosa—an outline for a treatment and training manual

This paper presents a new outline for psychotherapy with personsn with anorexia nervosa. ‘Model on mentalisation’ is the intellectual and empirical framework for this contribution. Mentalisation is defined as the ability to understand feelings, cognitions, intentions and meaning in oneself and in others. The capacity to understand oneself and others is a key determinant of self‐organisation and affect regulation, and is acquired in early attachment relationships. Impaired mentalisation is documented and described as a central psychopathological feature in anorexia nervosa. Psychotherapeutic enterprise with individuals with compromised mentalising capacity should be an activity that is specifically focused on the rehabilitation of this function, with special emphasis on how the body is representing mental states. The paper describes psychotherapeutic goals, stances and techniques. It is intended that this outline will be further developed into manuals as a basis for therapy, training and research. Copyright © 2007 John Wiley & Sons, Ltd and Eating Disorders Association.     

Experiences of use of the cerebral palsy hemiplegic hand in young persons treated with upper extremity surgery.

The aim of this qualitative study was to explore the experiences of young persons using their hemiplegic hand in daily life activities following upper extremity surgery (UES). Ten persons, aged 12-24 years, were interviewed individually five to seven years after surgery. The analysis was guided by a comparative method. The findings show that the participants during this period had experienced changes which they related both to the treatment and to development. Data resolved into three main themes. Functional improvements are interwoven into daily life, the hand is easier to use and is used more, and changes in the appearance and in the internal feeling of the arm are of importance. This study reflects the patients' experiences of living with the outcome of UES and yields an important complement to objective, quantitative outcome studies.     

Evidence of secondary neuronal intestinal dysplasia in a rat model of chronic intestinal obstruction.

The etiology of neuronal intestinal dysplasia remains largely unknown. There is, however, supporting evidence of the existence of Hirschprung's disease or chronic intestinal obstruction associated with neuronal intestinal dysplasia. With the aim of investigating the possible development of neuronal intestinal dysplasia linked to chronic intestinal obstruction, we have examined the enteric nervous system response to long-term obstruction in a rat model. Three different surgical techniques were tested in Wistar male rats. In animals that survived longer than the cutoff chronic intestinal obstruction point (6 weeks), full-thickness biopsies and acetylcholinesterase (AChE), NADH, hematoxylin-eosin, and anti-S100 protein stainings were performed. The results of our model indicate that chronic intestinal obstruction induced different degrees of enteric nervous system dysplasia, including histological features of neuronal intestinal dysplasia. The relationship between chronic intestinal obstruction and anomalies of the enteric nervous system, including neuronal intestinal dysplasia, needs to be further studied.     

Red blood cells stimulate fibroblast-mediated contraction of three dimensional collagen gels in co-culture

OBJECTIVE AND DESIGN: Following injury, red blood cells (RBC) may interact with extracellular matrix (ECM). In the present study we hypothesised that RBC, and soluble factors from RBC, might mediate remodelling of ECM by affecting fibroblast-mediated contraction of three dimensional collagen gels. MATERIALS AND METHODS: Human lung fibroblasts (HFL-1), were cultured together with isolated RBC, conditioned medium from RBC (RBC-CM) and hemolysed RBC in type I collagen gels. Gel contraction was determined by an image analyser. RESULTS: Both RBC, RBC-CM and hemolysed RBC stimulated gel contraction by fibroblasts (P < 0.001), compared to fibroblasts alone. The RBC-CM stimulated (P < 0.01) gel contraction in a time and concentration dependent manner. A similar effect was observed when supernatant from hemolysed RBC was tested. The production of fibronectin was increased (P < 0.01) in the co-culture system, compared to fibroblasts cultured alone. CONCLUSIONS: The present study shows that RBC can interact with mesenchymal cells in vitro. The ability of RBC to modulate fibroblast-mediated contraction in vitro, might therefore be an important mechanism regulating repair processes after injury.     

Glucocorticoids modulate TGF-beta production

TGF- is thought to play a central role in pulmonary fibrosis inducing fibroblast differentiation and extracellular matrix synthesis. In human lung fibroblasts, it is still unclear how various TGB- isoforms affect TGF- production and whether glucocorticoids, commonly used agents to treat fibrotic lung disease, modulate these processes. To this end, human fetal lung fibroblasts (HFL-1) were cultured with various concentrations of glucocorticoids (budesonide, dexamethasone or hydrocortisone) with and without TFG-1, -2, and -3. TGF- mRNA was assessed by real time RT-PCR. Smad 2, 3, and 4 and AP-1 complex (c-fos and c-Jun) cellular localization were evaluated by immunostaining. TGF-2 and -3 stimulated TGF-1 production significantly (p < 0.01 relative to control). TGF-1 stimulated TGF-2 production (p < 0.01 relative to control). TGF-3 was undetectable. Glucocorticoids significantly inhibited TGF-1 and -2 production and reduced expression of the upregulated TGF-1 and -2 mRNA induced by exogenous TGF-1, -2 or -3 (p < 0.01 for each) but had no effect on Smads. Although c-jun-related nuclear staining was not intensified in TGF--stimulated cells, it was reduced by glucocorticoids. Thus, TGF- isoforms may stimulate production of various TGF- isoforms in the lung. Glucocorticoids then may block TGF- production by modulating mRNA levels and c-Jun.     

Wiedemann‐Rautenstrauch (neonatal progeroid) syndrome: New case with normal telomere length in skin fibroblasts

Wiedemann‐Rautenstrauch (neonatal progeroid) syndrome is an autosomal recessive condition with characteristic appearance of premature aging present at birth (aged face, natal teeth, and wrinkled skin). Other features of the syndrome are generalized lipoatrophy with specific fat accumulation in the lateral suprabuttock region, hypotrichosis, macrocephaly (pseudohydrocephalus), and mental retardation. We report on a new case that demonstrates all typical features of the syndrome. The girl is now 16 years and 10 months old and has had follow‐up from birth. We measured terminal restriction fragment (TRF) length to evaluate whether the patient's premature aging process is accompanied by shortening of telomere length in her cultured fibroblasts. Mean TRF of 13.5 kb found in our patient's fibroblasts is not shortened as compared to that of normal fibroblasts. Our results differ from those observed in Hutchinson‐Gilford progeria. © 2001 Wiley‐Liss, Inc.     

Micropapillary carcinoma of the parotid gland arising in mucinous cystadenoma

We describe a 45-year-old man who had a 2-year history of a slowly enlarging tumor in the left parotid gland. Histologically, the tumor was a mucinous cystadenoma with focal apocrine differentiation, which revealed a widespread invasive micropapillary adenocarcinoma component. A rim of lymphoid tissue surrounded the margins of the micropapillary carcinoma. The invasive micropapillary adenocarcinoma component was morphologically identical with the invasive micropapillary carcinoma of the mammary gland. The tumor is different from so-far recognized salivary gland tumor entities. Received: 25 October 1999 / Accepted: 13 June 2000     

Our experience with diagnostics of congenital disorders of glycosylation

The aim of this study is to report our 3years experience with the screening of congenital disorders of glycosylation. A common isoelectric focusing method with immunofixation was used for analysis of serum transferrin and alpha1-antitrypsin, apart from several other procedures. A group of about 1000 individuals, both healthy controls and patients, mostly with signs of a metabolic disease were examined. Here we present an overview of (1) hypoglycosylation findings, (2) distribution of protein variants, (3) misguiding rare Tf variants found in our set, and (4) association of some phenotypes with various diseases.     

Amplification and overexpression of HER-2/neu in parotid gland salivary duct carcinoma. Immunohistochemical study and fluorescence in situ hybridization

Salivary duct carcinoma (SDC) is highly malignant salivary gland tumour with aggressive clinical behaviour, characterised by its histological resemblance to invasive ductal carcinoma of the breast. Amplification of gene HER-2/neu and overexpression of its gene product have been shown to have both prognostic and treatment implications in breast cancer. The reports concerning the expression of c-erbB2/HER-2/neu in salivary gland tumours are few and controversial. Thus, eleven cases of SDC were evaluated for HER-2/neu status using immunohistochemistry (IHC) and fluorescent in situ hybridization (FISH). To the best of our knowledge, this is the first molecular genetic analysis of SDCs using FISH. HER-2/neu overexpression, identified as strong membrane staining, was observed in all but one case of SDC in majority of neoplastic cells while only four tumours, of nine cases analysed, revealed HER-2/neu gene amplification by means of FISH analysis. SDCs were associated with poor clinical outcome, 6 patients (55%) died of disseminated carcinoma within 4 to 44 months after therapy. There was no difference in outcome of patients with IHC positive-nonamplified and IHC positive-amplified tumours.