OBJECTIVEDepression is a common comorbidity of diabetes, undesirably affecting patients' physical and mental functioning. Psychological interventions are effective treatments for depression in the general population as well as in patients with a chronic disease. The aim of this study was to assess the efficacy of individual mindfulnessbased cognitive therapy (MBCT) and individual cognitive behavior therapy (CBT) in comparison with a waiting-list control condition for treating depressive symptoms in adults with type 1 or type 2 diabetes. RESEARCH DESIGN AND METHODSIn this randomized controlled trial, 94 outpatients with diabetes and comorbid depressive symptoms (i.e., Beck Depression Inventory-II [BDI-II] ‡14) were randomized to MBCT (n = 31), CBT (n = 32), or waiting list (n = 31). All participants completed written questionnaires and interviews at pre-and postmeasurement (3 months later). Primary outcome measure was severity of depressive symptoms (BDI-II and Toronto Hamilton Depression Rating Scale). Anxiety (Generalized Anxiety Disorder 7), well-being (Well-Being Index), diabetes-related distress (Problem Areas In Diabetes), and HbA 1c levels were assessed as secondary outcomes. RESULTSResults showed that participants receiving MBCT and CBT reported significantly greater reductions in depressive symptoms compared with patients in the waitinglist control condition (respectively, P = 0.004 and P < 0.001; d = 0.80 and 1.00; clinically relevant improvement 26% and 29% vs. 4%). Both interventions also had significant positive effects on anxiety, well-being, and diabetes-related distress. No significant effect was found on HbA 1c values. CONCLUSIONSBoth individual MBCT and CBT are effective in improving a range of psychological symptoms in individuals with type 1 and type 2 diabetes.

Patients with EH have an altered profile of pro-and anti-inflammatory cytokines, consistent with monocyte activation in the circulation. The importance of these changes for the pathogenesis of EH and/or its secondary complications remains to be elucidated.

SUMMARYThe balance between pro-and anti-inflammatory cytokines has been implicated in the pathogenesis of infectious and auto-immune diseases, and its modulation has been proposed as a potential therapeutic target. The results reported in the present study show that modulators of the reninangiotensin system, such as the angiotensin-converting enzyme (ACE )-inhibitor captopril and the angiotensin II receptor type I antagonist valsartan, have potent inhibitory effects on the lipopolysaccharide (LPS )-stimulated production of pro-inflammatory cytokines tumour necrosis factor (TNF ) and interleukin-1 (IL-1) in vitro. The anti-inflammatory cytokine IL-1Ra is increased by captopril, whereas IL-6 production is decreased by valsartan. These effects are exerted mainly at high concentrations of the drugs. Administration of one dose of captopril or valsartan in therapeutic dosages to patients with essential hypertension did not influence LPS-stimulated production of cytokines by whole blood. In conclusion, despite inhibitory effects on proinflammatory cytokine production in vitro, it is unlikely that captopril or valsartan could be used in anticytokine therapeutic strategies in vivo.

Tenascin-X (TNX) is an extracellular matrix glycoprotein whose absence in humans leads to a recessive form of Ehlers-Danlos Syndrome (EDS). TNX deficient patients have hypermobile joints and fragile skin, but unlike the classical type of EDS, no atrophic scars were observed. Anecdotal evidence suggested that wound healing in TNX deficient patients is abnormal, but no detailed study has been performed so far. To address the role of TNX in wound healing, we analyzed skin wound morphology and mechanical properties of scars in TNX knockout (KO) mice. Breaking strength of unwounded skin of KO mice is significantly lower (<50%) than that of wild-type (WT) mice. In the early stage of wound healing when TNX is hardly expressed in WT wounds (day 7), WT and KO skin are of similar strength. After 14 days, when TNX starts to be expressed at moderate levels in wounds of WT mice, the WT scars gain a further increase in breaking strength, whereas KO scars do not progress beyond the mechanical strength of uninjured KO skin. No obvious differences between KO and WT mice were noted in the rate of wound closure, or in expression of fibrillar collagens during wound healing. We conclude that TNX is unlikely to be involved in matrix deposition in the early phase of wound healing, but it is required in the later phase when remodeling and maturation of the matrix establishes and improves its biomechanical properties.

Vitamin B6, but not homocysteine, is an independent risk factor for AAA. The role of vitamin B6 in the pathogenesis of AAA needs to be further elucidated.