Emotion talk in the context of young people self-harming: facing the feelings in family therapy.

This article describes the use of emotion talk in the context of using a manualised approach to family therapy where the presenting problem is self-harm. Whilst we understand that there is an internal aspect to emotion, we also consider emotions to be socially purposeful, culturally constructed and interactional. We found that within the presenting families, negative emotions were often talked about as located within the young person. Through using 'emotion talk' (Fredman, 2004) in deconstructing and tracking emotions and exploring how emotions connected to family-of-origin and cultural contexts, we developed an interactional understanding of these emotions. This led to better emotional regulation within the family and offered alternative ways of relating. The article discusses the use of relational reflexivity, and using the therapist and team's emotions to enable the therapeutic process, encouraging reflexivity on the self of the therapist in relation to work with emotions. PRACTITIONER POINTS: Emotions can be seen as both a reflection of feelings experienced by the individual and as a communication.An interactional understanding of emotions can be used therapeutically.Therapists should explore emotional displays and track the interactional patterns within the therapeutic system.Therapists should self-reflexive about ways of doing emotions and use this awareness in practice.

Transcription factor Dlx2 protects from TGFß-induced cell-cycle arrest and apoptosis.

Acquiring resistance against transforming growth factor ß (TGFß)-induced growth inhibition at early stages of carcinogenesis and shifting to TGFß's tumour-promoting functions at later stages is a pre-requisite for malignant tumour progression and metastasis. We have identified the transcription factor distal-less homeobox 2 (Dlx2) to exert critical functions during this switch. Dlx2 counteracts TGFß-induced cell-cycle arrest and apoptosis in mammary epithelial cells by at least two molecular mechanisms: Dlx2 acts as a direct transcriptional repressor of TGFß receptor II (TGFßRII) gene expression and reduces canonical, Smad-dependent TGFß signalling and expression of the cell-cycle inhibitor p21(CIP1) and increases expression of the mitogenic transcription factor c-Myc. On the other hand, Dlx2 directly induces the expression of the epidermal growth factor (EGF) family member betacellulin, which promotes cell survival by stimulating EGF receptor signalling. Finally, Dlx2 expression supports experimental tumour growth and metastasis of B16 melanoma cells and correlates with tumour malignancy in a variety of human cancer types. These results establish Dlx2 as one critical player in shifting TGFß from its tumour suppressive to its tumour-promoting functions.

Effects of isoflurane on glutamate and taurine releases, brain swelling and injury during transient ischemia and reperfusion.

The volatile anesthetic agent isoflurane was thought to provide neuroprotection against ischemic damage; however, this effect remains controversial. Using the middle cerebral artery occlusion model and intracerebral microdialysis, the authors monitored the variations of glutamate and taurine concentrations in the extra-cellular space in male rats anesthetized with pentobarbital or isoflurane. Brain injury and edema were evaluated 24 h after ischemia. Isoflurane prevented the ischemia-induced efflux of glutamate and reduced the release of taurine. No difference in the size of the brain lesions was observed with both anesthetics, and isoflurane induced the formation of a bigger brain edema and reduced taurine release. These results suggest that inhibiting glutamate release during ischemia may not be sufficient to improve brain outcome after transient ischemia.

Acute effects of 17beta-estradiol on the extracellular concentration of excitatory amino acids and energy metabolites during transient cerebral ischemia in male rats.

Elevation of extracellular levels of amino acids has been implicated in the pathogenesis of stroke. The failure of brain energy metabolism due to the lack of oxygen and glucose contributes also to cell loss. Estrogen has been shown to protect brain cells against ischemia by a still unclear mechanism. We used intracerebral microdialysis to monitor the effects of acute 17beta-estradiol treatment on the release of glutamate and aspartate and on the levels of the energy metabolites glucose and lactate. In male rats subjected to 90 min of transient middle cerebral artery occlusion followed by 24-h reperfusion, acute treatment with 17beta-estradiol (0.8 mg/kg, i.v.) at the time of occlusion reduced the ischemic infarct by about 50%. In these treated rats, the ischemia-induced increases of extracellular levels of glutamate and aspartate were significantly and rapidly reduced. The reduction of glucose level during occlusion was not affected by 17beta-estradiol treatment; however, the increase of extracellular lactate was reduced during occlusion and reperfusion, probably due to the reduced glutamate-driven astrocytic glycolysis. These data suggest that acute treatment with 17beta-estradiol at the onset of occlusion significantly reduces the ischemia-induced excitotoxicity in the cortex, a mechanism that may participate in the neuroprotective effect on cellular survival.

17beta-estradiol effect on the extracellular concentration of amino acids in the glutamate excitotoxicity model in the rat.

Estrogen has demonstrated a neuroprotective role in a rat model of glutamate excitotoxicity and other neurodegenerative disorders. We studied the effect of 17beta-estradiol on glutamate-induced increases in amino acids levels (aspartate, histidine, taurine and GABA) in the rat cortex. Local perfusion of glutamate produced a transient increase of aspartate, histidine, taurine and GABA in the extracellular fluid. Pretreatment with 17beta-estradiol significantly reduced the increases of taurine and moderately attenuated that of histidine, whereas aspartate and GABA releases were not modified. The effect of 17beta-estradiol on histidine release was reversed by the antiestrogen tamoxifen, suggesting a receptor-dependent mechanism. Good correlations between the volumes of the glutamate-induced lesions and the extracellular concentrations of taurine and aspartate were observed. These findings suggest that the attenuation of the glutamate-induced release of taurine by 17beta-estradiol may participate in the neuroprotective effects of 17beta-estradiol and that increased levels of aspartate and taurine are markers for the severity of the glutamate-induced cortical lesions.