Are Group Psychotherapeutic Treatments Effective for Patients with Schizophrenia? A Systematic Review and Meta-Analysis

&lt;b&gt;&lt;i&gt;Background:&lt;/i&gt;&lt;/b&gt; Different psychotherapeutic treatments for schizophrenia are delivered in groups. However, little is known about the effectiveness of these group therapies for people with schizophrenia across different treatments with varying therapeutic orientations. This review aimed to (1) estimate the effect of different group psychotherapeutic treatments for schizophrenia and (2) explore whether any overall ‘group effect' is moderated by treatment intensity, diagnostic homogeneity and therapeutic orientation. &lt;b&gt;&lt;i&gt;Methods:&lt;/i&gt;&lt;/b&gt; A systematic search of randomised controlled trials exploring the effectiveness of group psychotherapeutic treatments for people with schizophrenia was conducted. Random-effect meta-analyses on endpoint symptom scores compared group psychotherapeutic treatments with treatment as usual and active sham groups. Findings on social functioning were described narratively, and meta-regression analyses on group characteristics were carried out. &lt;b&gt;&lt;i&gt;Results:&lt;/i&gt;&lt;/b&gt; Thirty-four eligible trials were included. A weak-to-moderate significant between-group difference in favour of group psychotherapeutic treatments was found for negative symptom scores (standard mean difference = -0.37, 95% confidence interval -0.60, -0.14; p &lt; 0.01, I&lt;sup&gt;2&lt;/sup&gt; = 59.8%) only when compared to treatment as usual and not to active sham groups. Improved social functioning was reported as a treatment outcome in the majority of studies compared to treatment as usual. The ‘group effect' on negative symptoms was positively related to ‘treatment intensity' (β = 0.32, standard error = 0.121; p &lt; 0.05). &lt;b&gt;&lt;i&gt;Conclusion:&lt;/i&gt;&lt;/b&gt; Group psychotherapeutic treatments can improve negative symptoms and social functioning deficits in the treatment of schizophrenia. The effect occurs across different treatments and appears to be non-specific. Future research should identify the underlying mechanisms for the positive effect of participating in groups and explore how they can be maximised to increase the therapeutic benefit.</jats:p

Altered Proliferation, Synthetic Activity, and Differentiation of Cultured Human sebocytes in the Absence of Vitamin A and Their Modulation by Synthetic Retinoids

Human sebocytes maintained in medium containing delipidized serum were studied for ultrastructural characteristics, cell proliferation, lipid synthesis, immunophenotype, and keratin expression before and after the addition of the synthetic retinoids isotretinoin and acitretin (10-8 - 10-5 M).Compared to the properties of sebocytes cultured in normal sebocyte medium (1–2 × 10-7 M vitamin A), the use of delipidized serum (undetectable amounts of vitamin A) resulted in prominent decrease of i) proliferation; ii) number of intracellular lipid droplets and synthesis of total lipids, especially triglycerides, squalene, and wax esters; and iii) labeling with monoclonal antibodies identifying progressive and late-stage sebocyte differentiation. Intercellular spaces narrowed and cell-to-cell contacts were established by abundant desmosomes. Lanosterol was induced. Keratins 14, 16, 17, and 18 were upregulated and the keratin 16: keratin 4 ratio, negatively correlating with sebocyte differentiation, increased.Addition of isotretinoin and acitretin exerted a biphasic effect. At concentrations ≤ 10-7 M, both compounds enhanced sebocyte proliferation and synthesis of total lipids, especially triglycerides and cholesterol, and decreased Ianosterol, keratin 16, and the keratin 16: keratin 4 ratio. In contrast, retinoid concentrations > 10-7 M inhibited sebocyte proliferation in a dose-dependent manner.Our findings indicate that vitamin A is essential for proliferation, synthetic activity, and differentiation of human sebocytes in vitro. Synthetic retinoids partially reinstate the altered functions of sebocytes maintained in medium containing delipidized serum. In contrast to the previously shown isotretinoin-specific response of cultured sebocytes in the presence of vitamin A, similar effects of isotretinoin and acitretin were obtained in its absence. This suggests different interactions of synthetic retinoids with vitamin A, possibly influencing their efficacy on the sebacceous gland

Group experiences of cognitive stimulation therapy (CST) in Tanzania: a qualitative study

BACKGROUND: Tanzania is a low-income country in which medication for dementia is largely unavailable. Cognitive Stimulation Therapy (CST) is a group-based psychological treatment for people with dementia (PwD), shown to improve cognition and quality of life (QoL). It has previously been culturally adapted and piloted in Tanzania, shown to produce similar outcomes. UK research into CST suggests processes inherent to the group nature are key to its success. This study sought to identify group processes within CST in Tanzania and understand their impact on CST principles and outcomes. METHODS: Data collection took place in rural Hai District, through qualitative semi-structured interviews. Sixteen PwD and four facilitators were recruited through convenience sampling and interviewed about their experiences of CST. Interviews were audio-recorded, translated, transcribed and analysed by thematic analysis. RESULTS: Two main themes emerged: 'Positive group experiences' and 'Negative group experiences'. From this, a number of group processes were identified, such as helping behaviours and feeling understood by the group. Positive processes supported CST principles and participant improvement. Facilitators were influential over group dynamics. The group processes identified impacted CST principles and treatment outcomes. CONCLUSIONS: This is the first study on group mechanisms of CST in Tanzania. It provides deeper insight into participants' experiences of CST, thus identifying specific processes underlying the quantitatively measured positive outcomes of CST in Tanzania by previous studies. It also reveals further cultural barriers to implementation, enabling amendments for optimization of treatment efficacy

Natural history of a visceral leishmaniasis outbreak in highland Ethiopia

In May 2005, visceral leishmaniasis (VL) was recognized for the first time in Libo Kemken, Ethiopia, a highland region where only few cases had been reported before. We analyzed records of VL patients treated from May 25, 2005 to December 13, 2007 by the only VL treatment center in the area, maintained by Médecins Sans Frontières-Ethiopia, Operational Center Barcelona-Athens. The median age was 18 years; 77.6% were male. The overall case fatality rate was 4%, but adults 45 years or older were five times as likely to die as 5-29 year olds. Other factors associated with increased mortality included HIV infection, edema, severe malnutrition, pneumonia, tuberculosis, and vomiting. The VL epidemic expanded rapidly over a several-year period, culminating in an epidemic peak in the last third of 2005, spread over two districts, and transformed into a sustained endemic situation by 2007

Selective Induction of Apoptosis in Melanoma Cells by Tyrosinase Promoter-Controlled CD95 Ligand Overexpression

Induction of apoptosis has been demonstrated previously by overexpression of CD95 ligand (CD95L) in cultured human melanoma cells. For in vivo approaches based on CD95L, however, targeted expression is a prerequisite and tyrosinase promoters have been considered for selection. Luciferase reporter gene assays performed for a representative panel of melanoma cell lines characterized by strong (SK-Mel-19), moderate (SK-Mel-13, MeWo), weak (A-375), and missing expression (M-5) of endogenous tyrosinase revealed high tyrosinase promoter activities in SK-Mel-19, SK-Mel-13, and MeWo, but only weak activities in A-375 and M-5 as well as in non-melanoma cell lines. After transfection of a CMV promoter CD95L expression construct, melanoma cells were found highly sensitive, as compared with non-melanoma cells. By applying a tyrosinase promoter CD95L construct, apoptosis was selectively induced in SK-Mel-19, SK-Mel-13, MeWo as well as in A-375, which was characterized by high CD95 surface expression and high sensitivity to agonistic CD95 activation. M5 and non-melanoma cell lines remained uninfluenced. Also, resistance to agonistic CD95 activation seen in MeWo characterized by weak CD95 surface expression was overcome by overexpression of CD95L. Our investigations provide evidence that tyrosinase promoter CD95L constructs may be of value for selective induction of apoptosis in therapeutic strategies for melanoma

The Bax/Bcl-2 Ratio Determines the Susceptibility of Human Melanoma Cells to CD95/Fas-Mediated Apoptosis

Defective cytochrome c release and the resulting loss of caspase-3 activation was recently shown to be essential for the susceptibility of human melanoma cells to CD95/Fas-induced apoptosis. Cytochrome c release from mitochondria is regulated by the relative amounts of apoptosis-promoting and apoptosis-inhibiting Bcl-2 proteins in the outer membrane of these organelles. The assignment of Bax/Bcl-2 ratios by quantitative Western blotting in 11 melanoma cell populations revealed a relation to the susceptibility to CD95-mediated apoptosis. We could show that a low Bax/Bcl-2 ratio was characteristic for resistant cells and a high Bax/Bcl-2 ratio was characteristic for sensitive cells. Low Bax expression was not a consequence of mutations in the p53 coding sequence. The Bax/Bcl-2 ratio was also in clear correlation with sensitivity to another cell death inducer, N-acetylsphingosine. Furthermore, Bcl-2 overexpression abolished apoptosis triggered by both apoptotic stimuli, confirming the critical role of the Bax/Bcl-2 ratio as a rheostat that determines the susceptibility to apoptosis in melanoma cells by regulating mitochondrial function. Interestingly, some chemotherapeutics lead to the activation of death pathways by CD95L upregulation, ceramide generation, direct activation of upstream caspases, or upregulation of proapoptotic genes. Taken together, these signals enter the apoptotic pathway upstream of mitochondria, resulting in activation of this central checkpoint. We therefore assumed that apoptosis deficiency of malignant melanoma can be circumvented by drugs directly influencing mitochondrial functions. For this purpose we used betulinic acid, a cytotoxic agent selective for melanoma, straightly perturbing mitochondrial functions. In fact, betulinic acid induced mitochondrial cytochrome c release and DNA fragmentation in both CD95-resistant and CD95-sensitive melanoma cell populations, independent of the Bax/Bcl-2 ratio