Pilot study of intense pulsed light for the treatment of systemic sclerosis-related telangiectases.

BACKGROUND: Telangiectases represent microvascular changes inherent in the systemic sclerosis (SSc) disease process. Intense pulsed light (IPL) is an effective treatment for non-SSc-related cutaneous telangiectases. OBJECTIVES: This pilot study aimed to examine the efficacy, safety and tolerability of IPL treatment in an open study of patients with SSc. METHODS: Patients underwent three treatments of IPL at monthly intervals and attended follow-up examinations at 1, 6 and 12 months after final treatment. Photographs, laser Doppler imaging (LDI) and thermography were used to measure changes at each visit. RESULTS: Seventeen patients completed the study. Photographs were graded (compared with baseline) as: at 1-month follow-up, four 'no change', four 'improved' and eight 'much improved'; at 6-month follow-up, four 'no change', eight 'improved'; and four 'much improved'; and at 12-month follow-up (eight images were available), three 'no change', two 'improved' and three 'much improved'. Perfusion as measured by LDI (perfusion units) was significantly reduced, compared with baseline [median 2·66, interquartile range (1·78-3·93)], at 1 month [1·70 (1·07-2·55), P = 0·006] and 6 months [2·05 (1·42-2·36), P = 0·008] post-treatment, but not at 12 months [1·61 (1·14-3·22), P =0·088]. No differences were found in skin temperature between baseline and follow-up visits. CONCLUSIONS: In this pilot study (the first of IPL treatment for SSc-related telangiectases) most patients improved after IPL treatment. However, the degree of improvement was not maintained in all patients at 6-12 months, suggesting that further treatments may be necessary. Longer term studies of this novel treatment approach are now required.

Polarisation-sensitive optical coherence tomography measurement of retardance in fibrosis, a non-invasive biomarker in patients with systemic sclerosis.

Polarisation-sensitive optical coherence tomography (PS-OCT) offers a novel, non-invasive method of assessing skin fibrosis in the multisystem disease systemic sclerosis (SSc) by measuring collagen retardance. This study aimed to assess retardance as a biomarker in SSc. Thirty-one patients with SSc and 27 healthy controls (HC) underwent PS-OCT imaging. 'Skin score' was assessed by clinical palpation (0-3 scale). A subset of ten patients and ten age/sex-matched HC had a biopsy and longitudinal imaging. Histological assessment included quantification of epidermal thickness, collagen content (to assess fibrosis) and matrix metalloproteinase (MMP) activity (in situ zymography). PS-OCT images were assessed for epidermal thickness (structure) and fibrosis (retardance). Positive correlation was observed between epidermal thickness as measured by histology and structural PS-OCT (r = 0.79; p < 0.001). Retardance was: HC mean 0.21 (SD 0.21) radian/pixel; SSc skin score 0, 0.30 (0.19); skin score 1, 0.11 (0.16); skin score 2, 0.06 (0.12); skin score 3, 0.36 (0.35). Longitudinal retardance decreased at one-week across groups, increasing at one-month for HC/skin score 0-1; HC biopsy site retardance suggests scarring is akin to fibrosis. Relationships identified between retardance with both biopsy and skin score data indicate that retardance warrants further investigation as a suitable biomarker for SSc-related fibrosis.

Pilot study of dual-wavelength (532 and 633 nm) laser Doppler imaging and infrared thermography of morphoea.

BACKGROUND: Little is known about the pathophysiology of localized scleroderma (skin fibrosis, also termed 'morphoea'), although it is likely that microvascular dysfunction is a contributing factor. OBJECTIVES: Our aim was to investigate different components of blood flow in morphoea using infrared thermography and dual-wavelength laser Doppler imaging (LDI). METHODS: Eight plaques of morphoea (in eight patients) were studied. Skin temperature and blood flow were assessed in both affected (within plaque) and adjacent unaffected (perilesional) skin. RESULTS: Skin temperature (representing blood flow) was higher in all areas of morphoea when compared with uninvolved skin. Perfusion within the plaques was found to be increased, when compared with uninvolved skin; in all cases as imaged by red wavelength (633 nm) LDI (representing blood flow through large, thermoregulatory vessels) and in six of eight cases by green wavelength (532 nm) LDI (representing nutritive capillary blood flow). The median (range) skin temperature difference between plaque and perilesional skin was 1.1 (0.7-2.2) degrees C and the median (range) ratios of plaque/perilesional perfusion as measured by red and green wavelength LDI were 1.3 (1.1-1.9) and 1.1 (0.8-1.5) arbitrary perfusion units, respectively. CONCLUSIONS: Microvascular perfusion is increased within morphoea plaques and the increased response detected by both thermography and red wavelength LDI, as compared with green wavelength LDI, suggests that the increase in perfusion is more marked in deeper, larger, rather than in superficial, smaller vessels.

An investigation into the blood-flow characteristics of telangiectatic skin lesions in systemic sclerosis using dual-wavelength laser Doppler imaging.

Superficial telangiectases associated with systemic sclerosis may be more responsive to treatment than those deeper in the dermis. We investigated whether dual-wavelength laser Doppler imaging (LDI) is sufficiently sensitive to ascertain the distribution of blood flow within telangiectases and whether blood flow relates to telangiectatic diameter. The perfusion and diameter of 20 telangiectases were measured in superficial and deeper layers of the skin using dual-wavelength LDI. Of 20 telangiectases, 18 had higher blood flow in the red (representing deeper blood flow), rather than the green (representing superficial blood flow) wavelength images. Clinically apparent diameters correlated with those of the superficial (r = 0.61, P = 0.01), but not with the deeper blood flow images. Hence, the apparent size of telangiectases at the skin surface does not predict blood flow through the microvessel(s) at deeper levels, and thus clinically apparent size is unlikely to predict treatment response. Dual-wavelength LDI may help predict treatment response.

Novel clinically relevant antibiotic resistance genes associated with sewage sludge and industrial waste streams revealed by functional metagenomic screening.

A growing body of evidence indicates that anthropogenic activities can result in increased prevalence of antimicrobial resistance genes (ARGs) in bacteria in natural environments. Many environmental studies have used next-generation sequencing methods to sequence the metagenome. However, this approach is limited as it does not identify divergent uncharacterized genes or demonstrate activity. Characterization of ARGs in environmental metagenomes is important for understanding the evolution and dissemination of resistance, as there are several examples of clinically important resistance genes originating in environmental species. The current study employed a functional metagenomic approach to detect genes encoding resistance to extended spectrum ß-lactams (ESBLs) and carbapenems in sewage sludge, sludge amended soil, quaternary ammonium compound (QAC) impacted reed bed sediment and less impacted long term curated grassland soil. ESBL and carbapenemase genes were detected in sewage sludge, sludge amended soils and QAC impacted soil with varying degrees of homology to clinically important ß-lactamase genes. The flanking regions were sequenced to identify potential host background and genetic context. Novel ß-lactamase genes were found in Gram negative bacteria, with one gene adjacent to an insertion sequence ISPme1, suggesting a recent mobilization event and/ the potential for future transfer. Sewage sludge and quaternary ammonium compound (QAC) rich industrial effluent appear to disseminate and/or select for ESBL genes which were not detected in long term curated grassland soils. This work confirms the natural environment as a reservoir of novel and mobilizable resistance genes, which may pose a threat to human and animal health.

Vasodilator iontophoresis a possible new therapy for digital ischaemia in systemic sclerosis?

OBJECTIVE: This study investigated whether whole finger vasodilator iontophoresis increases digital blood flow in patients with systemic sclerosis (SSc): If so, this might indicate a novel approach to therapy. METHODS: Eight patients and 8 healthy controls underwent whole finger iontophoresis using a specially designed chamber. Treatment was with 0.5% sodium nitroprusside (NaNP) or 1% acetylcholine chloride (ACh), and the procedure then repeated with the other vasodilator (randomly assigned order). Three treatments were carried out for each chemical; 2 min treatments were carried out bilaterally at 200 microA, a third was then carried out for 5 min on one digit only (randomly assigned to left or right). Blood flow increases were monitored with laser Doppler imaging (LDI). Maximum perfusion increase from baseline (MAX) and the area under the time perfusion curve (AUC), normalized for baseline, were calculated. Data were compared with a three-way analysis of variance test. RESULTS: Perfusion increased in both patients and controls, but significantly more so in controls (P(MAX) = 0.001, P(AUC) = 0.005, respectively). Values were significantly higher for the 5 min treatment compared with the 2 min treatment (P(MAX) = 0.011 and P(AUC) = 0.008 for both groups). No significant differences were found between the use of NaNP and ACh. CONCLUSIONS: The increased perfusion with both ACh and NaNP in the patient group (albeit to a lesser degree than in the control group) indicates that this local approach to vasodilation is effective. Increasing iontophoresis time causes more sustained vasodilation. Further studies are indicated to investigate a possible therapeutic effect in patients with severe digital ischaemia.

Gene therapy with autologous, interleukin 2-secreting tumor cells in patients with malignant melanoma.

We vaccinated metastatic melanoma patients with irradiated, autologous melanoma cells genetically engineered to secrete interleukin 2 (IL-2) to investigate whether an anti-tumor immune response would be induced. Melanoma cell cultures were established from surgical specimens and were engineered to secrete IL-2 by infection with recombinant retrovirus. Twelve patients were vaccinated subcutaneously one, two, or three times with approximately 10(7) irradiated, autologous, IL-2-secreting tumor cells. Treatment was well tolerated, with local reactions at 11 of 24 injection sites and minor systemic symptoms of fever and headache after 6 injections. One patient developed anti-tumor DTH after the first vaccination and showed an increased response after the second vaccination. Anti-autologous tumor CTLs could be detected prevaccination in the peripheral blood of seven patients and their activity increased after vaccination in four patients. No UICC-defined clinical responses were seen, but three patients had stable disease for 7-15 months, one of whom has not yet progressed (15+ months). Thus, patient vaccination with autologous, genetically engineered tumor cells is feasible and safe. Anti-tumor DTH and CTLs can be induced in some patients with such a vaccine.

Clinical and histological features of a group of patients with sporadic non-A, non-B hepatitis.

Twelve serologically proven cases of non-A, non-B (NANB) hepatitis have been described. The clinical course was mild in 11 patients. One patient, however, presented in portal systemic encephalopathy and required steroid treatment. Nine of the 12 patients continued to exhibit raised transaminase (AST) activities six or more months after the onset of the acute hepatitis. In these immunoglobulin concentrations were normal and autoantibodies were not present in significant titre. Four patients had evidence of previous hepatitis B infection, suggesting that the route of transmission of NANB might be similar to that of hepatitis B virus. A further four patients gave a history which suggests a possible parenteral mode of transmission. Liver biopsies were carried out both in the acute (8 cases) and chronic (6 cases) phases of the disease. Histological findings in liver biopsies covered the whole spectrum of acute and chronic hepatitis and 1 patient had cirrhosis. One notable feature in these biopsies was the presence of fatty changes.

Cell wall biosynthesis: glycan containing oligomers in developing cotton fibers, cotton fabric, wood and paper.

A series of oligomeric glycans can be extracted from the cell walls of developing cotton fibers with weak acid. Glycans that produce similar profiles on high pH anion chromatography with pulsed amperometric detection (HPAEC-PAD) are also found in a protein complex extracted from developing fibers and in amorphous aggregates found in association with immature fibers in developing, but not in mature cotton bolls. The quantity and composition of the glycans recovered from the carbohydrate-protein complex varies significantly with the time of day when the bolls are harvested. This diurnal variation is consistent with the hypothesis that secondary cell walls are deposited primarily at night. Incubation of re-hydrated cotton fibers in the presence of exogenous oligosaccharides, myo-inositol and glycerol substantially alters the apparent quantity of the oligomers extracted from the fibers. The same and similar glycans have also been extracted from cotton fabric, marine algae, various paper products and wood. While many of the oligomers isolated from the various cellulose sources display the same peaks by HPAEC-PAD, the specific number of oligomers and their relative quantities appear unique for each source of cellulosic material. Oligomeric glycans, as described in the preceding, are present in all cellulose sources that have been investigated. Their relative abundance changes in response to source, stage of development and other physiological variables. We hypothesize that the glycans are intermediates in the biological assembly of cellulose, and that their incorporation in cellulose is mediated by physicochemical and enzymatic mechanisms.

A comparison of ocular melanocyte and uveal melanoma cell invasion and the implication of alpha1beta1, alpha4beta1 and alpha6beta1 integrins.

BACKGROUND/AIMS: Posterior uveal melanoma is the most common intraocular tumour in adults, responsible for the death of approximately 35% of patients. Hepatic metastases are most frequent, and once diagnosed survival is usually less than 1 year. The beta1 family of integrins, alphavbeta3 and MMP-2 and MMP-9 have been implicated in the metastasis of several types of tumour. To study their involvement in uveal melanoma we analysed the expression of the beta1 integrins, alphavbeta3, MMP-2, and MMP-9 in 10 primary posterior uveal melanomas, and correlated expression with invasive potential in vitro. Comparable studies were undertaken on cultures of melanocytes. METHODS: Expression of integrins was studied by immunohistochemistry, secretion of MMP-2 and MMP-9 by zymography, and the invasive potential was assessed using a transwell model. RESULTS: MMP-2 was secreted by all uveal melanomas and seven of 10 secreted MMP-9. Among uveal melanoma, invasion levels of 4-25% were observed and the major integrins expressed were alpha1beta1, alpha2beta1, alpha3beta1, alpha5beta1, and avbeta3. Melanocytes did not express alpha1beta1, alpha4beta1, and alpha6beta1. CONCLUSION: The laminin binding alpha6beta1 integrin was not expressed by either melanocytes or tumours with spindle morphology, which are considered to have a better prognosis. It is possible that expression of the alpha6beta1 integrin may prove useful as a prognostic indicator.

Reduced expression of TAP-1 and TAP-2 in posterior uveal melanoma is associated with progression to metastatic disease.

In order to determine the effects of the loss or reduced expression of molecules associated with antigen presentation (transporter associated with antigen presentation [TAP]-1, TAP-2, low molecular weight protein [LMP]-2 and LMP-7), we examined the expression of these molecules in primary uveal melanoma lesions. Paraffin-embedded sections from 29 primary uveal melanoma lesions were analysed for expression of TAP-1, TAP-2, LMP-2 and LMP-7 using specific primary antibodies followed by a three-stage immunoperoxidase technique. Microscopic examination was undertaken to determine differences in expression of these molecules on the tumour and the surrounding stroma. Overall, 72% (21 out of 29) of the tumours showed some loss or reduced expression of TAP-1, TAP-2, LMP-2 and/or LMP-7. Statistical analysis of these results showed that progression to metastatic disease was strongly associated with reduced expression of TAP-1 (P < 0.05) and TAP-2 (P < 0.01), taking patient age, tumour site and histology into account. We conclude that the reduced expression of molecules important in eliciting an immune response, such as TAP-1 and TAP-2, may facilitate the metastatic spread of uveal melanoma lesions and may have important implications for prospective immunotherapy.

Cytokine modulation of antigen expression in human melanoma cell lines derived from primary and metastatic tumour tissues.

The constitutive and cytokine-mediated expression of MHC class I and II antigens and intercellular adhesion molecule-1 (ICAM-1) was evaluated on eight human melanoma cell lines derived from primary and metastatic malignancies from patients (WM human melanoma series) including three pairs of related cell lines derived from the same individual. The cytokines IL-1 beta, IL-4, IL-6, TNF alpha, TGF beta 2, IFN gamma and IFN alpha were assessed for their ability to modulate the expression of cell surface antigens. MHC class I and class II antigen expression was unregulated by IFN gamma, IFN alpha and/or TNF alpha in cell lines established from primary melanoma. In contrast the cell lines derived from metastatic deposits did not show an increase in expression of MHC antigens in response to these cytokines. Both primary and metastatic WM cell lines were shown to be resistant to spontaneous natural killer cell (NK) activity, but susceptible to effector lymphocytes mediating lymphotine activated killer (LAK) cytotoxicity as a result of activation by IL-2. Although the constitutive and cytokine-induced level of expression of ICAM-1 and MHC antigens varied between paired primary and metastatic cell lines, this did not correlate with susceptibility of the cell line target to NK or LAK cytotoxicity. Whereas the IFNs, TNF alpha, TGF beta 2 and IL-1 beta differentially modulated the expression of ICAM-1 and MHC class I, treatment with IFNs (but not IL-1 beta, TNF alpha or TGF beta 2) resulted in a significant reduction in the sensitivity of the melanoma cells to NK and LAK cytotoxicity. Constitutive ICAM-1 expression was positively correlated with the ability of WM cell lines to colonise the lungs of SCID mice upon i.v. injection. The acquisition of cytokine resistance and inability to demonstrate enhanced cell surface expression may represent an important feature associated with the development of the metastatic phenotype.

CD80-mediated induction of immunostimulation in two ocular melanoma cell lines is augmented by interferon-gamma.

Although the transfection of the T-cell costimulatory molecule CD80 cDNA into human tumours can augment their immunogenicity in vitro, its expression alone is ineffective in many tumour systems. We evaluated the influence of CD80 expression on the immunostimulatory activity of ocular melanoma cell lines and determined whether IFN-gamma could enhance the effect. Two ocular melanoma cell lines were transfected with CD80 cDNA. The immunostimulatory capacity of the CD80+ transfectants was determined by their ability to stimulate the proliferation of allogeneic peripheral blood mononuclear cells (PBMC). The influence of additional accessory molecules on PBMC proliferation was assessed by pre-treating the CD80 transfectants with IFN-gamma. The CD80+ transfectants induced proliferation of allogeneic PBMC. IFN-gamma treatment of the tumour cells induced upregulated expression of MHC class I, de novo expression of MHC class II and CD54, and enhanced the ability of the CD80+ transfectants to stimulate PBMC proliferation. CD4+ T cells were not required for the proliferative response against untreated CD80+ tumour cells but were necessary for the augmentation of proliferation observed following IFN-gamma treatment. CD80+ ocular melanoma cells possess immunostimulatory potential which is augmented by IFN-gamma induced upregulation of cell surface molecules. Further studies on the role of costimulatory molecules in inducing anti-tumour immunity in ocular melanoma may help to define new strategies for application of immunotherapeutic approaches to treat this aggressive disease.

Expression of integrins, degradative enzymes and their inhibitors in uveal melanoma: differences between in vitro and in vivo expression.

Posterior uveal melanoma is the most common intraocular malignancy in adults. Metastasis occurs in approximately 40% of all cases and spread is primarily to the liver. Once secondary hepatic disease has developed the prognosis is poor. Metastasis involves a series of adhesion and de-adhesion events, coupled with regulated tissue degradation to facilitate tumour cell invasion and spread to both local and distant sites. These processes are assisted by the expression of integrins and degradative enzymes by both tumour and host cells. Using a series of 10 uveal melanomas, we investigated the expression of a panel of integrins, degradative enzymes and their inhibitors that have been shown to be associated with metastasis. In addition, we undertook to establish if there might be differential expression in response to growth under artificial conditions. All the tumours expressed matrix metalloproteinases (MMP)-2 and-9, tissue inhibitor of metalloproteases (TIMP)-2, urokinase plasminogen activator (u-PA), plasminogen activator inhibitor (PAI)-1 and PAI-2. Differences in the expression of the integrins alpha1beta1, alpha2beta1 and alpha6beta1 were observed; in particular, these differences appeared to relate to expression as a consequence of growth in culture. In summary, uveal melanoma cells express both degradative enzymes and their respective inhibitors, which are important in metastasis. It would appear that differential expression of integrins is present, probably as a response to in vitro stimulation.

No alcohol, but wine is permitted: a survey of obstetric units in Scotland.

Many health-care professionals have expressed increasing concern over the growing use of licit and illicit substances. Considerable interest has also been shown in the effects of substance use on the developing fetus. In view of both the media and academic coverage of this subject, the possible dangers to health of both mother and child should (presumably) be common knowledge. It would seem reasonable, therefore, to assume that screening women in the early ante-natal period for their use of tobacco, alcohol and other drugs would be routine practice. This survey attempted to obtain an overview of the approach of ante-natal clinics to substance use and, if possible, identify any areas of need which might exist. The responses obtained indicate that the approach taken by midwives and obstetricians was not uniform. A number of factors were identified as influencing service provision.

Simulating nailfold capillaroscopy sequences to evaluate algorithms for blood flow estimation.

The effects of systemic sclerosis (SSc)--a disease of the connective tissue causing blood flow problems that can require amputation of the fingers--can be observed indirectly by imaging the capillaries at the nailfold, though taking quantitative measures such as blood flow to diagnose the disease and monitor its progression is not easy. Optical flow algorithms may be applied, though without ground truth (i.e. known blood flow) it is hard to evaluate their accuracy. We propose an image model that generates realistic capillaroscopy videos with known flow, and use this model to quantify the effect of flow rate, cell density and contrast (among others) on estimated flow. This resource will help researchers to design systems that are robust under real-world conditions.

Abnormal microvascular response is localized to the digits in patients with systemic sclerosis.

OBJECTIVE: To investigate the hypothesis that cutaneous microvascular perfusion of the dorsum of the hand (in response to local heating) and distal phalanx (in response to occlusion) is impaired in patients with systemic sclerosis (SSc) compared with healthy controls. METHODS: Twenty-nine patients with SSc and 29 control subjects were recruited. Perfusion was monitored using novel dual-wavelength laser Doppler imaging, allowing measurement of both smaller (capillaries) and larger (thermoregulatory) vessels. Postacclimatization, a baseline dorsum scan (red or green wavelength) was performed. A heating pad was placed on the dorsum (total stimulus time 6 minutes at 34-40 degrees C), and following removal of the pad, baseline wavelength scans were performed until perfusion returned to baseline values. This was then repeated for the second wavelength. The maximum perfusion increase due to heating (PEAK1) and area under the perfusion-time curve (AUC) were determined. In addition, scans (both wavelengths) of the index finger were performed prior to and during 2 minutes of suprasystolic occlusion, and the response upon occlusion release was monitored with single-point laser Doppler. The decrease in perfusion due to occlusion (from preocclusion baseline values) (%DECREASE) and the maximum increase (from baseline perfusion values under occlusion) in hyperemic perfusion upon removal of occlusion (PEAK/OCC) were calculated. RESULTS: PEAK1 and AUC values were not significantly different between patients and controls, as assessed with either wavelength. A significant difference between groups was found in the %DECREASE values with the green, but not the red, wavelength. A significant between-group difference was also found in PEAK/OCC values, using both wavelengths. CONCLUSION: This study suggests that SSc has no effect on microvascular perfusion in the dorsum of the hand, and that the abnormal microvascular response is localized to the digits, affecting both smaller and larger vessels.

Multiple locations on chromosome 3 are the targets of specific deletions in uveal melanoma.

PURPOSE: Loss of chromosome 3 is a frequent event in uveal melanomas, which is associated with hepatic metastases and a poor prognosis. The entire copy of chromosome 3 is usually lost (monosomy 3); however, a small subset of tumours demonstrate partial deletions of chromosome 3. Analysis of these tumours may allow the identification of tumour suppressor genes (TSGs) that are the molecular target of monosomy 3. Therefore, the purpose of this investigation was to determine the location of these partial deletions of chromosome 3 in uveal melanomas. METHODS: Microsatellite analysis and restriction fragment-length polymorphism analysis were performed on 52 primary uveal melanomas using 19 markers located on both arms of chromosome 3. Cytogenetic analysis and fluorescence in situ hybridisation were performed, where possible, to confirm molecular findings. RESULTS: Of 52 tumours studied, five tumours (10%) demonstrated LOH at one or more informative markers, but retention of heterozygosity was observed at other loci on chromosome 3, consistent with the presence of structural abnormalities to chromosome 3. Consistent with previous findings, the pattern of LOH in these tumours indicates the presence of deletions around 3p25-26 and on 3q, and that a new target region at 3p11-14 is preferentially deleted. CONCLUSIONS: These results indicate the presence of several tumour suppressor loci on chromosome 3 and support the notion that the high rate of monosomy 3 in uveal melanoma is driven by disruption of several TSGs located on both arms of chromosome 3.

Dual wavelength (532 and 633 nm) laser Doppler imaging of plaque psoriasis.

BACKGROUND: Increased blood flow occurs in plaques of psoriasis, and an increase in blood flow has been shown to occur in uninvolved skin adjacent to the active edge. OBJECTIVES: In order to gain more insight into the pathophysiology of the active edges of plaques of psoriasis, we investigated different components of the microcirculation in the lesional and nonlesional skin of patients with psoriasis, using dual wavelength laser Doppler imaging (LDI). METHODS: The cutaneous blood flow in 23 plaques on the forearms of 20 patients with chronic plaque psoriasis was recorded using dual wavelength LDI. Perfusion was determined within the plaque (P), in uninvolved skin adjacent to the plaque (A) and in nonadjacent skin (U). RESULTS: Perfusion in plaques was increased as imaged by either 633 nm (red wavelength) or 532 nm (green wavelength) compared with both adjacent and nonadjacent uninvolved skin: median (interquartile range) P/A(RED) = 3.7 (2.5-4.9), P/A(GREEN) = 1.3 (1.2-1.6), P/U(RED) = 4.2 (2.7-6.1), P/U(GREEN) = 1.5 (1.3-1.9). CONCLUSIONS: Vascular perfusion is increased within plaques of psoriasis compared with adjacent and nonadjacent uninvolved skin. The results suggest an area of increased perfusion in skin adjacent to plaques, when compared with nonadjacent skin, for both deeper (large) and superficial (small) vessels (imaged by 633 and 532 nm, respectively). We believe that this dual wavelength tool may be a suitable and useful way of assessing pathophysiology and treatment response in psoriasis.