Therapeutic techniques and session impact: A practice-research network study in private practice.

Objective: This study investigated the relationship between therapeutic techniques and session impact, by examining the replicability of findings observed in a university-based training clinic (Boswell et al., 2010) in another practice-oriented setting: private practice.Method: N = 8 therapists completed session-level assessments of their technique use for N = 38 clients. The same client sample completed session-level assessments of session outcome. Technique-outcome associations were examined with multilevel models.Results: As in Boswell et al., common factors were associated with positive session impact. For clients who received higher average common factor techniques (relative to their own therapist's caseload), session impact was the poorest in sessions with higher behavioral change techniques use (relative to the client's own average). Moreover, clients with the lowest average common factor techniques (relative to their therapist's caseload) reported better session impact in sessions that involved a higher degree of session-level behavioral change techniques (relative to their own average).Conclusion: In line with Boswell et al., therapists should be mindful of the consistency of their routine technique use between- and within-clients, and this can be aided through collection of their own practice-oriented data.

Retinamide-induced apoptosis in glioblastomas is associated with down-regulation of Bcl-xL and Bcl-2 proteins.

Glioblastomas are among the most difficult neoplasms to treat with continued poor prognosis for long-term survival. Glioblastomas have developed effective mechanisms to resist chemotherapy including levels anti-apoptotic proteins, Bcl-xL and Bcl-2. Chemotherapy agents that promote down-regulation of Bcl-xL and Bcl-2 may enhance sensitivity to chemotherapy in glioblastomas. The ability of the synthetic retinoid N-(4-hydroxyphenyl) retinamide to modulate these anti-apoptotic proteins and to enhance apoptosis and chemotherapy was examined in glioblastoma cells. Expression of Bcl-2 family member proteins Bcl-xL and Bcl-2 were assessed in glioblastomas from three cell lines including U87, U251, and U138. Cells were treated with either retinamide alone or in combination with the chemotherapy agent, BCNU. The incidence of apoptosis was determined with flow cytometry analysis (FACS). Based on Western blots the levels of Bcl-2 and Bcl-xL were decreased in glioblastoma cells after treatment with retinamide. Retinamide treatment resulted in increased ratios of deamidated verses transamidated levels of Bcl-xL in U87 cells. BCNU chemotherapy combined with retinamide markedly down-regulated levels of both Bcl-xL and Bcl-2 proteins in glioblastoma and enhanced the incidence of apoptosis in U87 cells. These studies demonstrate that modulation of levels of the anti-apoptotic proteins, Bcl-xL and Bcl-2, may enhance the sensitivity of glioblastoma toward chemotherapy.

BCNU down-regulates anti-apoptotic proteins bcl-xL and Bcl-2 in association with cell death in oligodendroglioma-derived cells.

Oligodendroglial differentiation in gliomas is associated with enhanced sensitivity to chemotherapy. Antiapoptotic proteins, Bcl-xL and Bcl-2, are over-expressed in early passage cell lines derived from glioblastomas. Down-regulation of Bcl-xL and Bcl-2 with DNA antisense oligonucleotides promotes cell death in glioblastoma cells. Changes of expression of Bcl-xL and Bcl-2 after chemotherapy treatment have not been studied in glioma subtypes. The current experiments correlate decreased expression of both Bcl-xL and Bcl-2 after BCNU chemotherapy and cell death in two oligodendroglioma-derived cell lines. Expression of Bcl-2 family member proteins Bcl-xL, Bcl-2, and Bax were assessed in glioma cells both before and after chemotherapy treatment. Cell survival was assessed with a crystal violet bioassay. Levels of expression of Bcl-2 and Bcl-xL were elevated in two early passage oligodendroglioma-derived cell lines compared with a non-neoplastic glial cell line. BCNU chemotherapy markedly down-regulated expression of Bcl-xL and Bcl-2 proteins in both oligodendroglioma-derived cell lines. Changes in expression of Bcl-xL and Bcl-2 were associated with the increased sensitivity to chemotherapy. There were no changes noted in expression of Bax after BCNU treatment. Modulation of expression of the anti-apoptotic proteins, Bcl-xL and Bcl-2, in the two oligodendroglioma-derived cell lines was associated with increased sensitivity to BCNU chemotherapy. Down-regulation of Bcl-xL and Bcl-2 resulted in reversal of the ratio of Bax/Bcl-xL and Bax/Bcl-2 and enhanced cell death after treatment with BCNU. Mechanisms that control expression of the anti-apoptotic proteins Bcl-xL and/or Bcl-2 may be effective targets in treatment strategies in patients with malignant gliomas.

Lovastatin-induced up-regulation of the BH3-only protein, Bim, and cell death in glioblastoma cells.

The mechanism of lovastatin-induced cell death was examined in three established human glioblastoma cell lines; U87, U251, and U138. Changes in potential modifiers of apoptosis, including Bcl-2 family proteins and MAP kinase targets after such lovastatin treatment, were evaluated. Lovastatin (5 microm) treatment causes extensive cell death in two of the cell lines, U87 and U251; but only minimal in a third, U138. Lovastatin-induced death occurs in correlation with significantly increased levels of the BH3-only protein, Bim. The up-regulation of Bim levels was directly associated with an increased incidence of apoptosis. Lovastatin treatment in U87 cells results in activation of targets of three major mitogen-activating protein kinase cascades including Erk1/2, JNK and p38. Changes in levels of Bim, as well as increase phosphorylation of Erk1/2, c-jun, and p38 are all prevented by co-incubation of lovastatin and the isoprenylation metabolite, geranylgeranyl pyrophosphate. Inhibition of the MAP kinase pathways failed to block the increased expression of Bim expression or cell death. Further elucidation of the mechanisms of lovastatin-induced up-regulation of Bim and apoptosis in glioblastoma cells are important in determining a potential role for lovastatin as a chemotherapy agent.

Intrathecal baclofen withdrawal: a case report and review of the literature.

INTRODUCTION: Spasticity is an endpoint of a variety of neurologic disorders with upper motor neuron damage. There have been several studies demonstrating improvement in spasticity through administration of intrathecal baclofen. Withdrawal from oral baclofen has been well described. Intrathecal baclofen withdrawal has been less frequently reported. We present a case of withdrawal after intrathecal baclofen pump catheter failure. PATIENT: A 14-year-old boy presented with fevers, which were thought to be related to recent spine surgery and possible pneumonia. Eventual workup revealed evidence of intrathecal baclofen withdrawal owing to pump catheter failure. His fevers, with temperatures of up to 40 degrees C, and painful muscle spasms resolved and his clinical condition improved after pump exploration and resumption of intrathecal delivery. CONCLUSIONS: Intrathecal baclofen withdrawal can be life threatening. Prompt recognition and restoration of an adequate intrathecal baclofen dose is essential for recovery.

Efficacy of Eye Movement Desensitization in the treatment of cognitive intrusions related to a past stressful event.

Much of the Eye Movement Desensitization and Reprocessing (EMDR) efficacy research has been widely criticized, limiting scientific understanding of its therapeutic components. The present investigation of Eye Movement Desensitization (EMD) effectiveness included undergraduate students reporting current intrusive cognitions conceming a traumatic event. Forty-five participants received a single treatment session of either: (a) EMD, as described by Shapiro [J. Behav. Ther. Exp. Psychiatry 20 (1989b) 211], (b) an identical procedure which employed eye fixation on a stationary target, or (c) non-directive counseling. Standardized self-report, subjective rating, Daily Diary, and intrusive thought sampling measures were collected before and after treatment. Results indicated that participants in the eye fixation group reported marginally (p < .052) fewer cognitive intrusions than the non-directive group 1 week following treatment. No significant differences between the EMD and non-directive conditions or between the EMD and eye fixation conditions on this measure were found. During the treatment session, both desensitization groups were superior to the non-directive group in reducing reported vividness of the mental image of the original event. However, the non-directive group improved to the level of the two other groups by the following week. Rapid saccadic eye movements were therefore unrelated to immediate treatment effects for this sub-clinical sample, and non-directive treatment largely yielded eventual outcomes equivalent to the two desensitization conditions.