Exploring the impact of diet and nutrition on vitiligo: A systematic review of dietary factors and nutritional interventions.

BACKGROUND: Vitiligo, an autoimmune skin disorder linked to hormonal and genetic factors, results in reduced pigmentation due to a gradual decline in melanocyte activity. This systematic review delves into the role of dietary intervention and nutrition in managing vitiligo. METHODS: A comprehensive search on PubMed, Google Scholar, and European PMC identified 214 studies, with 14 meeting inclusion criteria post-screening. The selected studies primarily explored the impact of dietary supplements on disease activity. RESULTS: Heavy metal exposure, specifically Cd, Pb, and Hg, indicated potential links to heightened reactive oxygen species and vitiligo development. Conflicting evidence emerged regarding the role of trace minerals (Zn and Cu), with some studies suggesting deficiencies and others proposing excesses in vitiligo patients. Vitamins with anti-inflammatory properties like vitamin C, D, and B12, along with antioxidants, were investigated for their potential in repigmentation strategies. Additionally, polyunsaturated fatty acids (PUFAs), especially in varying types of fat consumption, were implicated. Emphasizing the need to reduce reliance on pharmacological and phototherapy interventions, the review uncovers novel roles for dietary supplements as adjuncts or flare reducers. CONCLUSION: While dietary interventions cannot be thought of as a standalone therapy, they still make a case for being used as adjuncts. Large scale clinical trials are warranted to establish strong evidence and protocols, and might also help reduce the dependency on pharmacological methods, which come with their adverse effect profiles.

IFNγ insufficiency during mouse intra-vaginal Chlamydia trachomatis infection exacerbates alternative activation in macrophages with compromised CD40 functions.

Chlamydia trachomatis (C.tr), an obligate intracellular pathogen, causes asymptomatic genital infections in women and is a leading cause of preventable blindness. We have developed in vivo mouse models of acute and chronic C. trachomatis genital infection to explore the significance of macrophage-directed response in mediating immune activation/suppression. Our findings reveal that during chronic and repeated C. trachomatis infections, Th1 response is abated while Treg response is enhanced. Additionally, an increase in exhaustion (PD1, CTLA4) and anergic (Klrg3, Tim3) T cell markers is observed during chronic infection. We have also observed that M2 macrophages with low CD40 expression promote Th2 and Treg differentiation leading to sustained C. trachomatis genital infection. Macrophages infected with C. trachomatis or treated with supernatant of infected epithelial cells drive them to an M2 phenotype. C. trachomatis infection prevents the increase in CD40 expression as observed in western blots and flow cytometric analysis. Insufficient IFNγ, as observed during chronic infection, leads to incomplete clearance of bacteria and poor immune activation. C. trachomatis decapacitates IFNγ responsiveness in macrophages via hampering IFNγRI and IFNγRII expression which can be correlated with poor expression of MHC-II, CD40, iNOS and NO release even following IFNγ supplementation. M2 macrophages during C. trachomatis infection express low CD40 rendering immunosuppressive, Th2 and Treg differentiation which could not be reverted even by IFNγ supplementation. The alternative macrophages also harbour high bacterial load and are poor responders to IFNγ, thus promoting immunosuppression. In summary, C. trachomatis modulates the innate immune cells, attenuating the anti-chlamydial functions of T cells in a manner that involves decreased CD40 expression on macrophages.

The tale of antibiotics beyond antimicrobials: Expanding horizons.

Antibiotics had proved to be a godsend for mankind since their discovery. They were once the magical solution to the vexing problem of infection-related deaths. German scientist Paul Ehrlich had termed salvarsan as the silver bullet to treatsyphilis.As time passed, the magic of newly discovered silver bullets got tarnished with raging antibiotic resistance among bacteria and associated side-effects. Still, antibiotics remain the primary line of treatment for bacterial infections. Our understanding of their chemical and biological activities has increased immensely with advancement in the research field. Non-antibacterial effects of antibiotics are studied extensively to optimise their safer, broad-range use. These non-antibacterial effects could be both useful and harmful to us. Various researchers across the globe including our lab are studying the direct/indirect effects and molecular mechanisms behind these non-antibacterial effects of antibiotics. So, it is interesting for us to sum up the available literature. In this review, we have briefed the possible reason behind the non-antibacterial effects of antibiotics, owing to the endosymbiotic origin of host mitochondria. We further discuss the physiological and immunomodulatory effects of antibiotics. We then extend the review to discuss molecular mechanisms behind the plausible use of antibiotics as anticancer agents.

Primary Palliative Care Education for Graduate Medical Trainees: Impacts and Needs.

As demand for palliative care (PC) services rise, there are insufficient numbers of PC specialists to provide PC for the US population. "Primary palliative care" refers to PC services that are administered by non-specialist PC providers. Educating trainees in graduate medical education (GME) programs is 1 strategy for expanding primary palliative care, though questions remain regarding the impact of PC education for GME trainees and where additional education is needed. This study is a multicenter, cross-sectional, web-based survey study of GME trainees assessing the needs for and impacts of primary palliative care education. The survey assessed the implementation of and participants' confidence with fundamental PC skills. The survey also asked about prior exposure to PC education and for participants' beliefs regarding areas that would be particularly helpful for future education. 170 residents and fellows from diverse training backgrounds participated in the survey out of 851 potential participants (response rate 19.98%). Exposure to PC education was associated with higher confidence and increased frequency of implementation of fundamental PC skills. Of the forms of education that were assessed, clinical/experiential education was associated most often with higher confidence and higher frequency of use of PC skills. Discussing goals of care, pain management for seriously ill patients, and communicating difficult information were those skills most frequently identified as important for additional training. This study demonstrates that by improving existing PC education or increasing access to PC education for GME trainees, it may be possible to improve primary palliative care.

Effect of the COVID-19 Pandemic Lockdown on the Management of Diabetic Retinopathy: A Cross-Sectional Study.

Introduction Worldwide, diabetic retinopathy (DR) is one of the leading causes of vision loss. Early treatment and screening for DR have a major role in reducing the rate of the disease and the coronavirus disease 2019 (COVID-19) pandemic-related restrictions have altered real-world practice patterns in managing DR. Aims and objectives To evaluate the impact of the COVID-19 pandemic on the management of DR amongst patients presenting to a tertiary eye care center in Gujarat, India. Methods This is a cross-sectional study comparison of ophthalmic findings of 72 patients who presented to a tertiary care hospital with the manifestation of DR before and after the COVID-19 outbreak and subsequent lockdown. All the patients underwent detailed ophthalmic examinations, including optical coherence tomography (OCT) and fundus fluorescein angiography (FFA). Results The mean age of participants was 54.5 years, with the mean duration of diabetes being five years since first detected. Diabetes was present in 26 patients out of 72. The number of follow-up visits to an ophthalmologist before COVID-19 was at least every one to three months, which significantly decreased after the lockdown of COVID-19. We found a significant progression of DR and clinically significant macular edema (CSME) in patients with diabetes. Before COVID-19, there were two mild non-proliferative diabetic retinopathy (NPDR), seven moderate NPDR, 15 severe NPDR, and 15 very severe NPDR, which were increased post lockdown to three, nine, 27, and 21, respectively. The proliferative diabetic retinopathy (PDR) vitreous hemorrhage (VH) and tractional retinal detachment (TRD) were also increased to 12 after lockdown as compared to only six before the COVID-19 lockdown. The causes for progression are inability to attend regular check-ups, inability to take proper treatment of diabetes and DR, poor control of diabetes, episode of COVID-19, history of high dose of steroid use, poor kidney function, and not knowing that there is a progression of the disease. A common reason for not visiting an ophthalmologist was fear of the unknown due to COVID-19. Conclusions COVID-19 has severely impacted the routine follow-up of DR and, in the subsequent years, there might be an increased incidence of severe outcomes due to DR. The second wave of COVID-19 and its lockdown have had very significant effects on the visual outcome of untreated DR patients.

Saga of monokines in shaping tumour-immune microenvironment: Origin to execution.

Cellular communication mediated by cytokines is an important mechanism dictating immune responses, their cross talk and final immune output. Cytokines play a major role in dictating the immune outcome to cancer by regulating the events of development, differentiation and activation of innate immune cells. Cytokines are pleiotropic in nature, hence understanding their role individually or as member of network cytokines is critical to delineate their role in tumour immunity. Tumour systemically manipulates the immune system to evade and escape immune recognition for their uncontrollable growth and metastasis. The developing tumour comprise a large and diverse set of myeloid cells which are vulnerable to manipulation by the tumour-microenvironment. The innate immune cells of the monocytic lineage skew the fate of the adaptive immune cells and thus dictating cancer elimination or progression. Targeting cells at tumour cite is preposterous owing to their tight network, poor reach and abundance of immunosuppressive mechanisms. Monocytic lineage-derived cytokines (monokines) play crucial role in tumour regression or progression by either directly killing the tumour cells with TNFα or promoting its growth by TGFß. In addition, the monokines like IL-12, IL-1ß, IL-6, IL-10 and TGFß direct the adaptive immune cells to secrete anti-tumour cytokines, TNFα, IFNγ, perforin and granzyme or pro-tumour cytokines, IL-10 and TGFß. In this review, we elucidate the roles of monokines in dictating the fate of tumour by regulating responses at various stages of generation, differentiation and activation of immune cells along with the extensive cross talk. We have attempted to delineate the synergy and antagonism of major monokines among themselves or with tumour-derived or adaptive immune cytokines. The review provides an update on the possibilities of placing monokines to potential practical use as cytokine therapy against cancer.

Berberine mediates tumor cell death by skewing tumor-associated immunosuppressive macrophages to inflammatory macrophages.

BACKGROUND: Berberine is a plant-derived alkaloid with potent anti-cancer activities. Berberine may redirect the tumor-promoting immunosuppressive M2 macrophages, to tumoricidal activated M1 macrophages. But such an anti-tumor function remains to be demonstrated. HYPOTHESIS: Polarization of macrophages to an immunosuppressive phenotype within the tumor microenvironment promotes tumor growth and contributes to resistance to chemotherapy. We examined if berberine would target macrophage polarization to reinstate anti-tumor immune response. STUDY DESIGN: Using a B16F10 mouse melanoma model, we assessed berberine-induced re-polarization of immunosuppressive M2 macrophages to anti-tumor M1 macrophages and subsequent T-cell activation within the immunosuppressive tumor microenvironment. METHODS: The B16F10 culture supernatant along with tumor antigen was used as tumor mimicking conditioned medium (CM). The bone marrow-derived macrophages were cultured in CM for 5 days. The CM-induced skewing of macrophages to M2-like phenotype was confirmed by flow cytometry and ELISA. The T-cells were co-cultured with macrophages to decipher the effect of berberine on T-cell differentiation. In vivo efficacy of berberine was analyzed using melanoma model of solid tumor. RESULTS: Berberine inhibited rIL-6-induced STAT-3 phosphorylation and IL-10 release from B16F10 cells. It enhanced tumor antigen-induced IL-1ß, IL-12 and TNFα, but suppressed IL-6 and TGF-ß release. Berberine significantly prevented the tumor antigen-mediated IL-10-enhanced IL-6 and TGF-ß expression. The CM skewed the bone marrow-derived macrophages to CD206-high but MHC-II-low M2-like tumor-associated macrophages. Berberine partially prevented the generation of these macrophages and was associated with reduced C/EBPß and Egr2 mRNA expression and lowered IL-10 and TGF-ß production. Berberine significantly reduced Arginase-1 expression in CM-treated M1 and M2-like macrophages. Berberine increased MHC-II and CD40 expression on the macrophages augmenting the CTL activity and the number of IFNγ-producing CD4+ T-cells. Berberine significantly lowered tumor volume, weight and enhanced the frequency of M1-like macrophages in mice. CONCLUSION: These data indicate that berberine interferes with pro-tumor macrophage polarization and IL-10 and TGF-ß release but restores Tcell anti-tumor cytotoxicity in the tumor microenvironment.

Caspase-1 inhibition by YVAD generates tregs pivoting IL-17 to IL-22 response in ß-glucan induced airway inflammation.

BACKGROUND: During Aspergillus fumigatus mediated lung inflammation, NLRP3 inflammasome is rapidly activated that aggravates IL-1ß production contributing to lung inflammation. Previously, we have shown the protective role of SYK-1 inhibition in inhibiting inflammasome activation during lung inflammation. In the current manuscript, we explored the protective role of direct caspase-1 inhibition during ß-glucan-induced lung inflammation. METHODS: We have mimicked the lung inflammation by administering intranasal ß-glucan in mice model. YVAD was used for caspase-1 inhibition. RESULTS: We have shown that caspase-1 inhibition by YVAD did not alter inflammasome independent inflammatory cytokines, while it significantly reduced inflammasome activation and IL-1ß secretion. Caspase-1 inhibited bone marrow derived dendritic cells (BMDCs), co-cultured with T cells showed decreased T-cell proliferation and direct them to secrete high TGF-ß and IL-10 compared to the T cells co-cultured with ß-glucan primed dendritic cells. Caspase-1 inhibition in BMDCs also induced IL-22 secretion from CD4+T cells. Caspase-1 inhibition in intranasal ß-glucan administered mice showed decreased tissue damage, immune cell infiltration and IgA secretion compared to control mice. Further, splenocytes challenged with ß-glucan show high IL-10 secretion and increased FOXp3 and Ahr indicating an increase in regulatory T cells on caspase-1 inhibition. CONCLUSION: Caspase-1 inhibition can thus be an attractive target to prevent inflammation mediated tissue damage during Aspergillus fumigatus mouse model and can be explored as an attractive therapeutic strategy.HIGHLIGHTSCaspase-1 inhibition protects lung damage from inflammation during ß-glucan exposureCaspase-1 inhibition in dendritic cells decreases IL-1ß production resulting in decreased pathogenic Th17Caspase-1 inhibition promotes regulatory T cells thereby inhibiting lung inflammation.

Can diallyl trisulfide, a dietary garlic-derived compound, activate ferroptosis to overcome therapy resistance in prostate cancer?

BACKGROUND: Therapy resistance is the underlying reason for poor outcome in prostate cancer (PCa) patients. Diallyl trisulfide (DATS) is an organosulfur compound present in garlic. DATS has been shown to target PCa cells by induction of apoptosis, increase in the production of reactive oxygen species, degradation of ferritin protein and increase in the labile iron (Fe) pool. AIM: We hypothesize that DATS could induce ferroptosis, an Fe-dependent, unique non-apoptotic form of regulated cell death to eliminate therapy resistance encountered by PCa patients. METHODS: In vitro and in vivo studies should be performed to test the hypothesis. RESULTS: As per the hypothesis, DATS would eliminate apoptotic resistance via inducing ferroptosis. CONCLUSION: Since apoptosis resistance has been reported to be the underlying mechanism of therapy resistance in PCa, DATS could be used to effectively target PCa cells by overcoming apoptosis resistance and inducing ferroptosis-mediated cell death of PCa cells.

Amyloid-like Structures Formed by Single Amino Acid Self-Assemblies of Cysteine and Methionine.

We report for the very first time the discovery of amyloid-like self-assemblies formed by the nonaromatic single amino acids cysteine (Cys) and methionine (Met) under neutral aqueous conditions. The structure formation was assessed and characterized by various microscopic and spectroscopic techniques such as optical microscopy, phase contrast microscopy, scanning electron microscopy, and transmission electron microscopy. The mechanism of self-assembly and the role of hydrogen bonding and thiol interactions of Cys and Met were assessed by Fourier transform infrared spectroscopy, thermogravimetric analysis, X-ray diffraction, and solid state NMR along with various control experiments. In addition, molecular dynamics simulations were carried out to gain insight into assembly initiation. Further, Thioflavin T and Congo red binding assays with Cys and Met structures indicated that these single amino acid assemblies may have amyloid-like characteristics. To understand the biological significance of the Cys and Met structures, cytotoxicity assays of the assemblies were performed on human neuroblastoma IMR-32 cells and monkey kidney cells (COS-7). The results revealed that both Cys and Met fibers were cytotoxic. The cell viability assay further supported the hypothesis that aggregation of single amino acid may contribute to the etiology of metabolic disorders like cystinuria and hypermethioninemia. The results presented in this study are striking, and to the best of our knowledge this is the first report which demonstrates that nonaromatic amino acids like Cys and Met can undergo spontaneous self-assembly to form amyloidogenic aggregates. The results presented are also consistent with the established generic amyloid hypothesis and support a new paradigm for the study of the etiology of single amino acid initiated metabolic disorders in amyloid related diseases.

Impaired mitochondrial dynamics underlie axonal defects in hereditary spastic paraplegias.

Mechanisms by which long corticospinal axons degenerate in hereditary spastic paraplegia (HSP) are largely unknown. Here, we have generated induced pluripotent stem cells (iPSCs) from patients with two autosomal recessive forms of HSP, SPG15 and SPG48, which are caused by mutations in the ZFYVE26 and AP5Z1 genes encoding proteins in the same complex, the spastizin and AP5Z1 proteins, respectively. In patient iPSC-derived telencephalic glutamatergic and midbrain dopaminergic neurons, neurite number, length and branching are significantly reduced, recapitulating disease-specific phenotypes. We analyzed mitochondrial morphology and noted a significant reduction in both mitochondrial length and their densities within axons of these HSP neurons. Mitochondrial membrane potential was also decreased, confirming functional mitochondrial defects. Notably, mdivi-1, an inhibitor of the mitochondrial fission GTPase DRP1, rescues mitochondrial morphology defects and suppresses the impairment in neurite outgrowth and late-onset apoptosis in HSP neurons. Furthermore, knockdown of these HSP genes causes similar axonal defects, also mitigated by treatment with mdivi-1. Finally, neurite outgrowth defects in SPG15 and SPG48 cortical neurons can be rescued by knocking down DRP1 directly. Thus, abnormal mitochondrial morphology caused by an imbalance of mitochondrial fission and fusion underlies specific axonal defects and serves as a potential therapeutic target for SPG15 and SPG48.

The effect of viewing distance on responses to the pattern glare test.

BACKGROUND: We investigated whether symptoms of pattern glare were affected by viewing distance, as distinct from spatial frequency, because of an association between symptoms and anomalies of accommodation and vergence. METHODS: One hundred young adults viewed gratings with spatial frequencies of 0.3, 2.3 and 9.4 cycles per degree (cpd) at four test distances (0.4, 0.8, 1.6 and 3.2 metres). Participants were asked to grade the presence of 15 symptoms of visual perceptual distortions and discomfort, on a scale from zero (no symptoms) to 10 (maximum perceptual and somatic symptoms). RESULTS: The viewing distance did not affect the nature and strength of symptoms, when viewing gratings with similar spatial frequencies. The symptoms increased with spatial frequency (p < 0.008 for all comparisons). CONCLUSIONS: The symptoms from the Pattern Glare Test do not appear to be modulated by the changes in accommodation and vergence associated with viewing distance, at least in an unselected sample of students. The highest spatial frequency of the current Pattern Glare Test was 9.4 cpd at 0.4 metre and this is insufficiently high to measure the reduction in symptoms at high spatial frequencies. If assessing relative aversion to gratings of different spatial frequencies, it may be useful to increase the testing distance to 0.6 metre so as to increase the spatial frequency of the third grating to 14.2 cpd.

Mindfulness-based cognitive therapy for preventing relapse in recurrent depression: a randomized dismantling trial.

OBJECTIVE: We compared mindfulness-based cognitive therapy (MBCT) with both cognitive psychological education (CPE) and treatment as usual (TAU) in preventing relapse to major depressive disorder (MDD) in people currently in remission following at least 3 previous episodes. METHOD: A randomized controlled trial in which 274 participants were allocated in the ratio 2:2:1 to MBCT plus TAU, CPE plus TAU, and TAU alone, and data were analyzed for the 255 (93%; MBCT = 99, CPE = 103, TAU = 53) retained to follow-up. MBCT was delivered in accordance with its published manual, modified to address suicidal cognitions; CPE was modeled on MBCT, but without training in meditation. Both treatments were delivered through 8 weekly classes. RESULTS: Allocated treatment had no significant effect on risk of relapse to MDD over 12 months follow-up, hazard ratio for MBCT vs. CPE = 0.88, 95% CI [0.58, 1.35]; for MBCT vs. TAU = 0.69, 95% CI [0.42, 1.12]. However, severity of childhood trauma affected relapse, hazard ratio for increase of 1 standard deviation = 1.26 (95% CI [1.05, 1.50]), and significantly interacted with allocated treatment. Among participants above median severity, the hazard ratio was 0.61, 95% CI [0.34, 1.09], for MBCT vs. CPE, and 0.43, 95% CI [0.22, 0.87], for MBCT vs. TAU. For those below median severity, there were no such differences between treatment groups. CONCLUSION: MBCT provided significant protection against relapse for participants with increased vulnerability due to history of childhood trauma, but showed no significant advantage in comparison to an active control treatment and usual care over the whole group of patients with recurrent depression.

Comfort from suicidal cognition in recurrently depressed patients.

BACKGROUND: Previous research has suggested that some individuals may obtain comfort from their suicidal cognitions. METHOD: This study explored clinical variables associated with comfort from suicidal cognition using a newly developed 5 item measure in 217 patients with a history of recurrent depression and suicidality, of whom 98 were followed up to at least one relapse to depression and reported data on suicidal ideation during the follow-up phase. RESULTS: Results indicated that a minority of patients, around 15%, reported experiencing comfort from suicidal cognitions and that comfort was associated with several markers of a more severe clinical profile including both worst ever prior suicidal ideation and worst suicidal ideation over a 12 month follow-up period. LIMITATIONS: Few patients self-harmed during the follow-up period preventing an examination of associations between comfort and repetition of self-harm. CONCLUSIONS: These results, although preliminary, suggest that future theoretical and clinical research would benefit from further consideration of the concept of comfort from suicidal thinking.

Pre-adult onset and patterns of suicidality in patients with a history of recurrent depression.

BACKGROUND: This report assesses the association between age of onset of major depression and later suicidality in a sample of 276 recurrently depressed patients recruited for the Oxford/Bangor Staying Well after Depression (SWAD) Trial, and interviewed when in remission. METHODS: The study enrolled adult patients with a history of at least three episodes of non-psychotic major depressive disorder from primary care and psychiatric care practices and through community advertisements. At study entry, all participants estimated the age of their first onset of a major depressive episode and completed both self-report and interview-based assessments of past and current suicidal ideation and behavior. Participants were divided into pre-adult and adult onset groups using a cut-off age of 18. RESULTS: Forty-eight percent of the sample reported a pre-adult age of onset. Pre-adult age of onset was significantly associated with suicidality, both from self-report and from interviewer assessment even when adjusting for differences in age, gender, employment status, length of the disorder and early adversity. LIMITATIONS: Relevant variables were all assessed through retrospective reports. CONCLUSIONS: Pre-adult age of onset is closely associated with risk for and severity of later suicidality, replicating, in a sample of patients assessed when in remission, findings from studies that assessed patients when currently depressed. The association of pre-adult age of onset with suicidality is not due to differences in sociodemographic variables, length of the disorder and early adversity.

Suicidal imagery in a previously depressed community sample.

This study sought to replicate previous findings of vivid suicide-related imagery in previously suicidal patients in a community sample of adults with a history of depression. Twenty-seven participants were interviewed regarding suicidal imagery. Seventeen participants reported prior suicidal ideation or behaviour in the clinical assessment, and the vast majority of these also reported experiencing suicide-related imagery when at their most depressed and despairing, in many cases in the form of flash-forwards to imagined future suicidal acts. Interestingly, five of the 10 participants who did not report suicidal ideation or behaviour in the clinical interview also described prominent imagery related to themes of death and suicide, but in several cases, these images were associated with meanings that seemed to act to reduce the likelihood of subsequent suicidal acts. Severity of prior suicidality was associated with lower levels of imagery-related distress and higher levels of imagery-related comfort. These findings support the idea that suicide-related imagery is an important component in the phenomenology of depression and despair and hint at potentially important differences in the meaning associated with such imagery between those individuals who report experiencing suicidal ideation or behaviour when depressed and those who do not. The findings are consistent with Joiner's model of acquired capability for suicide through habituation to pain and fear of suicide and suggest that it may be useful to tackle such imagery directly in the treatment of suicidal patients.

Can we harness computerised cognitive bias modification to treat anxiety in schizophrenia? A first step highlighting the role of mental imagery.

A new wave of computerised therapy is under development which, rather than simulating talking therapies, uses bias modification techniques to target the core psychological process underlying anxiety. Such interventions are aimed at anxiety disorders, and are yet to be adapted for co-morbid anxiety in psychosis. The cognitive bias modification (CBM) paradigm delivers repeated exposure to stimuli in order to train individuals to resolve ambiguous information in a positive, rather than anxiety provoking, manner. The current study is the first to report data from a modified form of CBM which targets co-morbid anxiety within individuals diagnosed with schizophrenia. Our version of CBM involved exposure to one hundred vignettes presented over headphones. Participants were instructed to actively simulate the described scenarios via visual imagery. Twenty-one participants completed both a single session of CBM and a single control condition session in counter-balanced order. Within the whole sample, there was no significant improvement on interpretation bias of CBM or state anxiety, relative to the control condition. However, in line with previous research, those participants who engage in higher levels of visual imagery exhibited larger changes in interpretation bias. We discuss the implications for harnessing computerised CBM therapy developments for co-morbid anxiety in schizophrenia.

Developing interpretation bias modification as a "cognitive vaccine" for depressed mood: imagining positive events makes you feel better than thinking about them verbally.

Two interpretation bias modification experiments found that mental imagery vs. verbal processing of positive material have differential emotional effects. In Experiment 1, participants were instructed to imagine positively resolved auditory descriptions or to listen to the same events while thinking about their verbal meaning. Increases in positive mood and bias were greater in the imagery than in the verbal condition, replicating E. A. Holmes, A. Mathews, T. Dalgleish, and B. Mackintosh (2006). An emotional vulnerability test showed that imagery (relative to the verbal condition) protected against a later negative mood induction. Experiment 2 created 2 new verbal conditions aimed to increase or reduce verbal comparisons. Results suggest making unfavorable comparisons with the highly positive material might be partially responsible for the inferiority of the verbal condition in Experiment 1. The findings demonstrate that imagery can play a key role in cognitive bias modification procedures and thus that task instructions are crucial. Imagining a positive event can make you feel better than thinking about the same event verbally. The authors propose that recruiting imagery will be useful in therapeutic innovations to develop a "cognitive vaccine" for depressed mood.