Ruptures and repairs of group therapy alliance. an untold story in psychotherapy research

Although previous studies investigated the characteristics of therapeutic alliance in group treatments, there is still a dearth of research on group alliance ruptures and repairs. The model by Safran and Muran was originally developed to address therapeutic alliance in individual therapies, and the usefulness of this approach to group intervention needs to be demonstrated. Alliance ruptures are possible at member to therapist, member to member, member to group levels. Moreover, repairs of ruptures in group are quite complex, i.e., because other group members have to process the rupture even if not directly involved. The aim of the current study is to review the empirical research on group alliance, and to examine whether the rupture repair model can be a suitable framework for clinical understanding and research of the complexity of therapeutic alliance in group treatments. We provide clinical vignettes and commentary to illustrate theoretical and research aspects of therapeutic alliance rupture and repair in groups. Our colleague Jeremy Safran made a substantial contribution to research on therapeutic alliance, and the current paper illustrates the enduring legacy of this work and its potential application to the group therapy context

Imatinib-mesylate for all patients with hypereosinophilic syndrome?

Some recent papers have focused on the activity of imatinib-mesylate, a selective inhibitor of tyrosine kinase, in idiopathic hypereosinophilic syndrome (HES) [1], [2], [3] and [4]. In this setting, a possible therapeutic target was identified by Cools et al. [2], who described the fusion tyrosine-kinase gene FIP1L1/PDGFRA as the result of an interstitial deletion within chromosome 4 in nine out of sixteen (56%) patients affected by HES. Of interest, although in this study the response to imatinib was strictly correlated with the presence of FIP1L1/PDGFRA rearrangement (all patients with such a molecular lesion treated with imatinib responded), only five out of nine responding patients evidenced the abnormal transcript [2]. Among the possible alternative mechanisms for the activation of the PDGFRA tyrosine-kinase domain, these authors suggested there may be a different fusion gene

Arsenic trioxide (ATO) and MEK1 inhibition synergize to induce apoptosis in acute promyelocytic leukemia cells

Recent studies suggest that components of the prosurvival signal transduction pathways involving the Ras-mitogen-activated protein kinase ( MAPK) can confer an aggressive, apoptosis-resistant phenotype to leukemia cells. In this study, we report that acute promyelocytic leukemia (APL) cells exploit the Ras-MAPK activation pathway to phosphorylate at Ser112 and to inactivate the proapoptotic protein Bad, delaying arsenic trioxide (ATO)-induced apoptosis. Both in APL cell line NB4 and in APL primary blasts, the inhibition of extracellular signal-regulated kinases 1/2 (ERK1/2) and Bad phosphorylation by MEK1 inhibitors enhanced apoptosis in ATO-treated cells. We isolated an arsenic-resistant NB4 subline (NB4-As-R), which showed stronger ERK1/2 activity (2.7-fold increase) and Bad phosphorylation (2.4-fold increase) compared to parental NB4 cells in response to ATO treatment. Upon ATO exposure, both NB4 and NB4-As-R cell lines doubled protein levels of the death antagonist Bcl-xL, but the amount of free Bcl-xL that did not heterodimerize with Bad was 1.8-fold greater in NB4-As-R than in the parental line. MEK1 inhibitors dephosphorylated Bad and inhibited the ATO-induced increase of Bcl-xL, overcoming ATO resistance in NB4-As-R. These results may provide a rationale to develop combined or sequential MEK1 inhibitors plus ATO therapy in this clinical setting

Vitamin C inhibits platelet expression of CD40 ligand

Upon stimulation with agonists, platelets express CD40 ligand (CD40L), a transmembrane protein implicated in the initiation and progression of atherosclerotic disease. We have recently discovered that oxidative stress plays a major role in platelet CD40L expression. In this study, we sought to determine whether vitamin C, a known antioxidant, is able to influence platelet CD40L expression. In vitro experiments were done by stimulating platelets with collagen in the presence or absence of vitamin C (50-100 mu M) or vehicle as control. An in vivo study was done in 10 healthy subjects who were randomized to intravenous infusion of placebo or 1 g vitamin C for 45 min in a crossover design. At the end of infusion platelet CD40L and O2- were measured. The in vitro study demonstrated that vitamin C dose dependently inhibited platelet CD40L expression without affecting agonist-induced platelet aggregation. In subjects treated with placebo no changes of platelet CD40L and O2- were observed; conversely, vitamin C infusion caused a significant and parallel decrease of platelet O2- (-70%, P < 0.001) and CD40L (-68%, P < 0.001). Platelet aggregation was not modified by either treatment. This study suggests that water-soluble antioxidants, which scavenge superoxide radicals, may reduce platelet CD40L expression. (c) 2005 Elsevier Inc. All rights reserved

Vitamin K deficiency bleeding leading to a diagnosis of Crohn’s Disease

We report the case of a 45 year old man who came to Emergency Room of Polyclinic for sudden onset of localized ecchymosis and widespread hematomas. He was subjected to blood count and first level investigations to assess coagulation. Based on the results, second level investigations were performed. Endoscopy of the gastrointestinal tract with histological examination revealed a diagnosis of Crohn's disease. Vitamin K deficiency causes the formation of vitamin K-dependent clotting factors that cannot perform their pro-coagulant action. Consequently, patients present with hemorrhagic manifestations. Clinical and laboratory features observed in this patient show that the deficiency of vitamin K-dependent coagulation factors may reveal a complex clinical condition such as an inflammatory bowel disease

Molecular signature of retinoic acid treatment in acute promyelocytic leukemia

Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia characterized by a block of differentiation at the promyelocytic stage. APL patients respond to pharmacological concentrations of all-trans retinoic acid ( RA) and disease remission correlates with terminal differentiation of leukemic blasts. The PML/RAR oncogenic transcription factor is responsible for both the pathogenesis of APL and for its sensitivity to RA. In order to identify physiological targets of RA therapy, we analysed gene expression profiles of RA-treated APL blasts and found 1056 common target genes. Comparing these results to those obtained in RA-treated U937 cell lines revealed that transcriptional response to RA is largely dependent on the expression of PML/RAR. Several genes involved in the control of differentiation and stem cell renewal are early targets of RA regulation, and may be important effectors of RA response. Modulation of chromatin modifying genes was also observed, suggesting that specific structural changes in local chromatin domains may be required to promote RA-mediated differentiation. Computational analysis of upstream genomic regions in RA target genes revealed nonrandom distribution of transcription factor binding sites, indicating that specific transcriptional regulatory complexes may be involved in determining RA response

Revision of the Student Adaptation to College Questionnaire (SACQ) for Use with Italian Students

Background: This multistudy report was aimed at examining the psychometric properties in the Italian context of the Student Adaptation College Questionnaire (SACQ) that represents the most important self-report measure for assessing how students adjust to university. Methods: Three studies were conducted in order to revise and improve the instrument for being more efficient in measuring adjustment to university. Results: The final result was the SACQ-SF consisting in 12 item assessing three dimensions: a) student’s perception of one’s study skills (Studying); b) student’s sense of satisfaction with courses and programs (Satisfaction with curriculum); c) student’s evaluation of the degree to which he has social skills and is making new friends (Social adjustment). Conclusions: Convergent and construct validity may be considered also adequate. In sum, the SACQSF can be considered a promising valuable and efficient instrument in measuring adjustment to university in the Italian context, and probably in the European one too. Further, as a brief instrument, it can be easily administered and used as a quick screening tool

Determination of cadmium (II) and zinc (II) in olive oils by derivative potentiometric stripping analysis

A method for the determination of cadmium (II) and zinc (II) in olive oils by derivative potentiometric stripping analysis after dry ashing of the sample is described. The metal ions were concentrated as their amalgams on a glassy carbon working electrode that was previously coated with a thin mercury film and then stripped by a suitable oxidant. Potential and time data were digitally converted into dt dE 121, and E was plotted vs. dt dE 121, thus increasing sensitivity of the method and improving resolution of the analysis. Quantitative analysis was carried out by the method of standard additions; a good linearity was obtained in the range of concentrations examined. Recoveries of 92\u2013102% for cadmium (II) and of 89\u201399% for zinc (II) were obtained from an olive oil spiked at different levels. The detection limits were 5.1 ng g 121 for cadmium (II) and 7.6 ng g 121 for zinc (II)

High performance liquid chromatographic determination of 2-furaldehyde and 5-hydroxymethyl-2-furaldehyde in honey

A method of determination of 2-furaldehyde (F) and 5-hydroxymethyl-2-furaldehyde (HMF) in honey by high-performance liquid chromatography (HPLC) is described. The method is based on the formation of the 2,4-dinitrophenylhydrazones of carbonyl compounds and subsequent reversed-phase separation of these derivatives. Derivatization is carried out by utilizing an acidic solution of 2,4-dinitrophenylhydrazine in acetonitrile. Precipitation of the derivatives of carbonyl compounds is thus avoided and direct injection of the sample into the HPLC system is allowed. The procedure offers a high specificity, since the derivatives of F and HMF are well separated from the other components of the mixture under examination. Recoveries of 95-99% were obtained from honey spiked at different levels with both analytes. The detection limit is of the order of 10 \u3bcg/kg of honey and reproducibility (mean of six determinations) is \ub13% for F and \ub12% for HMF

Molecular characterization of a t(1;3)(p36;q21) in a patient with MDS. MEL1 is widely expressed in normal tissues, including bone marrow, and it is not overexpressed in the t(1;3) cells

Patients with myeloid malignancies and either the 3q21q26 syndrome or t(1;3)(p36;q21) have been reported to share similar clinicopathological features and a common molecular mechanism for leukemogenesis. Overexpression of MDS1/EVI1 (3q26) or MEL1/PRDM16 (1p36), both members of the PR-domain family, has been directly implicated in the malignant transformation of this subset of neoplasias. The breakpoints in both entities are outside the genes, and the 3q21 region, where RPN1 is located, seems to act as an enhancer. MEL1 has been reported to be expressed in leukemia cells with t(1;3) and in the normal uterus and fetal kidney, but neither in bone marrow (BM) nor in other tissues, suggesting that this gene is specific to t(1;3)-positive MDS/AML. We report the molecular characterization of a t(1;3)(p36;q21) in a patient with MDS (RAEB-2). In contrast to previous studies, we demonstrate that MEL1, the PR-containing form, and MEL1S, the PR-lacking form, are widely expressed in normal tissues, including BM. The clinicopathological features and the breakpoint on 1p36 are different from cases previously described, and MEL1 is not overexpressed, suggesting a heterogeneity in myeloid neoplasias with t(1;3)