Treatment of animals with Pyl A

alone increased NF-κB activity in the myometrium, which was enhanced with co-administration of LPS (Fig. 6a). The inability Alpelisib of Pyl A to inhibit NF-κB implies that CRTH2 is not involved in the mechanism of 15dPGJ2-mediated inhibition. In support of this, we demonstrated that CRTH2 is not required for 15dPGJ2-mediated inhibition of NF-κB in human amniocytes, myocytes and lymphocytes.[41] Surprisingly, myometrial COX-2 protein levels remained unchanged 4·5 hr post treatment in all groups. As preterm labour was typically induced following LPS/Pyl A treatment at 5·8 hr (SEM ± 0·7) it was expected that any COX-2 up-regulation in the myometrium should have already been apparent by 4·5 hr post treatment. It is possible that COX-2 was already up-regulated before intrauterine injection in preparation for term labour, which is one limitation of using a model at E16. Progesterone withdrawal in the mouse occurs late E16 and so downstream activation of pro-labour genes is not likely to have been initiated in our model.[44] Consistent

with this the majority of labour-associated find more proteins such as PGE2, PGF2α, the oxytocin receptor and Connexin-43 are not significantly up-regulated until E18.[45, 46] We have shown, however, that COX-2 is suppressed in pregnancy and is up-regulated from E16, which was not increased further in term labour.[47] We further explored the possibility that, despite seeing no change at the protein level, COX-2 was still activated by LPS and LPS plus Pyl A. Messenger RNA was indeed increased

in LPS-treated mice, and was further increased with co-injection of Pyl A (Fig. 6e). COX-2 requires peroxidases for activation and the endogenous peroxide tone of smooth muscle cells can be mimicked by nitration.[48] Previous studies have shown that peroxynitrite increases the activity of COX-2 with no alteration of COX-2 protein expression.[49, Protirelin 50] Consistent with our results, Aisemberg et al.[51] demonstrated an increase in LPS-induced mRNA COX-2 with no effect at the protein level. It is plausible that this is a result of LPS-induced NO leading to the formation of peroxynitrite, which in turn, activates COX-2 without alteration of protein expression. Alternatively, it is also plausible that the nitrated form of COX-2 is not recognized by the COX-2 antibody. Analysis of pup brain extracts collected from LPS-treated dams revealed a decrease in levels of phosphorylated p65 (ser 536). It is thought that this may reflect protein degradation induced by the pre-terminal state of the live pups (Fig. 6b). A significant increase in in utero fetal viability was achieved with Pyl A treatment (Fig. 5a) but this was not associated with altered NF-κB activity. This also highlights the contrasting effects of Pyl A compared with the 15dPGJ2 because we have previously shown that 15dPGJ2 inhibits NF-κB in the pup brain of dams treated with LPS.

Third, low transplantation rate and low mortality rate in dialysis

patients further retains the numbers Lumacaftor solubility dmso of the dialysis patient pool.29 Diabetes mellitus (DM) (43.2%), chronic glomerulonephritis (CGN) (25.1%), hypertension (8.3%) and chronic interstitial nephritis (2.8%) are four major underlying renal diseases of ESRD in 2007. DM has become the first leading cause of ESRD by outnumbering CGN since 2000.28 Unknown causes of ESRD are especially often reported as CGN. It implies that a significant portion of patients with hypertension and chronic interstitial nephritis might be underestimated as the underlying causes of ESRD. It needs more in-depth investigation to identify the exact pattern of primary diseases of ESRD. The study based on NHI dataset showed that old age, diabetes, hypertension, hyperlipidaemia and female sex were associated with a higher risk of developing CKD.12 A prospective cohort study by Wen et al.13 further demonstrated that older age, diabetes, hypertension, smoking, obesity and regular use of herbal medicine were more common in the CKD group, and CKD is prevalent in 37.2% of the population aged over 65 years. Furthermore, hypertension, diabetes, hyperlipidaemia, smoking, obesity, low socioeconomic state and regular user of Chinese herbal drugs were significant risk factors for CKD. The association of Chinese

herbal therapy with CKD and ESRD needs to be emphasized here. Herbal therapy is independently associated with risk of CKD in adults not using analgesics.30 Intake of Chinese herbs containing aristolochic HSP phosphorylation acid has Sorafenib price been reported as the cause

of advanced renal failure in Taiwan.31–33 Chinese herbal products containing aristolochic acid, Mu-ton and Fangi have been banned by the Department of Health (DOH) in Taiwan since 2003. The beneficial effect of this action still needs to be observed. Additionally, the second wave of the TW3H Survey (unpubl. data, 2009) stated that metabolic syndrome exerted a 34% higher risk for CKD stage 3–5, which is similar to reports from the USA, Japan and Korea.20,34,35 The above well-established risk factors of CKD may not explain why the high incidence and prevalence of ESRD has developed in Taiwan. Other potential risk factors needs to be further explored. First, chronic lead intoxication may play a key role in the pathogenesis of CKD in some victims of chronic exposure without obvious clinical presentations of intoxication.36 This nephrotoxic heavy metal may accumulate and contribute to CKD silently. Reducing lead overload by administration of i.v. ethylene diamine tetra acetate has been proved to slow down the deterioration of impaired renal function.37 Second, both hepatitis B and C are endemic diseases in Taiwan with seropositive rates of 12–15% for hepatitis B surface antigen and 3–5% for anti-hepatitis C virus in general populations.

The coronary arterioles dilated dose-dependently to the endothelium-dependent NO-mediated vasodilator serotonin. This vasodilation was inhibited in the same manner by NOS inhibitor NG-nitro-l-arginine methyl ester and by lumenal OxLDL (0.5 mg protein/mL). The inhibitory effect of OxLDL was reversed after treating the vessels with either l-arginine (3 mM) or arginase inhibitor LY2157299 datasheet difluoromethylornithine (DFMO; 0.4 mM). Consistent with vasomotor alterations, OxLDL inhibited serotonin-induced NO release from coronary arterioles and this inhibition

was reversed by DFMO. Vascular arginase activity was significantly elevated by OxLDL. Immunohistochemical analysis indicated that OxLDL increased arginase I expression in the vascular wall without altering

eNOS expression. Taken together, these results suggest that OxLDL up-regulates arginase I, which contributes to endothelial dysfunction by reducing l-arginine availability to eNOS for NO production and thus vasodilation. “
“Department of Cardiovascular Science, Faculty of Medicine, Dentistry & Health, University of Sheffield, Medical School, Sheffield, UK Atherosclerosis is a chronic inflammatory disease of the medium and large arteries driven in large part by the accumulation of oxidized low-density lipoproteins and other debris at sites rendered susceptible because of the geometry of the arterial tree. As lesions develop, they Trametinib ic50 acquire a pathologic microcirculation that perpetuates lesion progression, both by providing a means for further monocyte and T-lymphocyte recruitment into the arterial wall and by the physical and chemical stresses caused by micro-hemorrhage. This review summarizes work performed in our department investigating the roles

of signaling pathways, alone and in combination, that lead to specific programs of gene expression in the atherosclerotic environment. Focusing particularly on cytoprotective responses that might be enhanced therapeutically, the work has encompassed the anti-inflammatory effects of arterial laminar shear stress, mechanisms Tacrolimus (FK506) of induction of membrane inhibitors that prevent complement-mediated injury, homeostatic macrophage responses to hemorrhage, and the transcriptional mechanisms that control the stability, survival, and quiescence of endothelial monolayers. Lastly, while the field has been dominated by investigation into the mechanisms of DNA transcription, we consider the importance of parallel post-transcriptional regulatory mechanisms for fine-tuning functional gene expression repertoires. “
“Isolation of rodent endothelial cells from lymphatic capillaries with yields that allow extensive functional studies remains challenging due to low cell numbers, variable purity, and limited growth potential.

After 24 hr, the Th1 cells were pulsed www.selleckchem.com/products/LBH-589.html with [3H]thymidine for 12 hr to assess their proliferative capacity. In some experiments, Th1 cells were instead stimulated with streptavidin-coated magnetic beads (Dynal, Great Neck, NY) that had been previously incubated (1 hr at 4°) with biotinylated anti-CD3 and anti-CD28 antibody to asses the proliferative capacity of the Th1 cells. Th1 cells were harvested at different time-points either during the course of primary cultures

or in the secondary cultures. The cells were passed over Ficoll–Hypaque to remove the irradiated APCs, counted and disrupted with modified lysis buffer containing 10 mm KCl, 10 mm HEPES, 1% Nonidet P-40, 1 mm NaVO4, aprotinin (10 mg/ml), leupeptin (10 mg/ml), and 0·5 mm phenylmethylsulphonyl

fluoride. In some cases, the cells were lysed with hypotonic buffer (20 mm HEPES; pH 7·5, 5 mm NaF, 0·1 nm ethylenediaminetetraacetic acid, 10 μm Na2MoO4 and protease inhibitors) and the nuclei were pelleted with centrifugation at 14 000 g for 10 min. Following the removal of the cytoplasmic fraction, nuclear proteins were then extracted from the isolated nuclei in modified lysis buffer by sonification followed by agitation on a horizontal rotator on ice for 20 min. beta-catenin inhibitor Equivalent amounts of protein (50–100 μg) from Th1 cell lysates were separated on 12% sodium dodecyl sulphate–polyacrylamide gel electrophoresis (SDS–PAGE) Ready Gels (BioRad). The proteins were electrotransferred onto nitrocellulose (Amersham Life Sciences, Buckinghamshire, UK) and subsequently immunoblotted with different primary antibodies (1–3 μg/ml) and appropriate secondary antibodies: HRP-conjugated

goat anti-mouse IgG (1 : 1000), HRP-conjugated goat anti-rabbit IgG (1 : 1000) or HRP-conjugated goat anti-rat IgG (1 : 500). Immunodetection was performed by Super Signal West Pico Chemiluminescent Substrate (Pierce). To test for appropriate protein loading, some blots were stripped with the Western blot recycling kit (BioRad) and reprobed with the anti-actin antibody. To test for appropriate cytoplasmic/nuclear fractionation, some blots were stripped find more and reprobed with the anti-U1 SnRNP 70 antibody. Streptavidin-coated magnetic beads (Dynal) (30 μl) were incubated (30 min at 4°) with the appropriate biotinylated secondary antibody (either goat anti-rabbit IgG Fc Ab or rat anti-mouse IgG1 mAb) followed by incubation (30 min at 4°) with the appropriate primary antibody directed against the target protein. The Th1 cell lysates (100–200 μg/sample) were then incubated with the beads overnight at 4°. The magnetic beads with the immunoprecipitated protein were washed three times in lysis buffer, boiled with loading buffer for 5 min, resolved on 12% SDS–PAGE and immunoblotted with antibodies specific for p21Cip1 and the immunoprecipitated proteins.

The authors declare no conflicts of interest. “
“It has been proposed that mannose-binding Selleck Ibrutinib lectin (MBL) levels may impact

upon host susceptibility to tuberculosis (TB) infection; however, evidence to date has been conflicting. We performed a literature review and meta-analysis of 17 human trials considering the effect of MBL2 genotype and/or MBL levels and TB infection. No significant association was demonstrated between MBL2 genotype and pulmonary TB infection. However, the majority of studies did not report MBL2 haplotype inclusive of promoter polymorphisms. Serum MBL levels were shown to be consistently elevated in the setting of TB infection. While this may indicate that high MBL levels protect against infection with TB, the increase was also of a degree consistent with the acute-phase reaction. This analysis suggests that the relatively poorly characterized MBL2 genotypes reported are not associated significantly with susceptibility to pulmonary TB infection, but high MBL serum levels may be. Balanced polymorphisms

are the result of beneficial effects of resistance to prevalent infections due to physiological changes consequent on genetic variation. Well-characterized examples in human biology include haemoglobinopathies (sickle-cell and alpha-thalassaemia) and Plasmodium falciparum[1]. One of the most common polymorphisms on a global scale is that involving mannose-binding lectin (MBL), a pattern recognition receptor of the innate immune system. This liver-derived, acute-phase reactant recognizes pathogen-associated molecular patterns, R428 research buy Cell press killing microorganisms via activation of the lectin complement pathway and opsonophagocytosis [2,3]. MBL is also involved

in modulation of other inflammatory pathways contributing to autoimmune disease, apoptosis and vascular disease [4]. Despite its manifold effects in innate immune system pathways, there is a high frequency of MBL deficiency that arises due to polymorphisms of the MBL2 gene. The evolutionary advantage of MBL deficiency is unclear. MBL production is controlled by the MBL2 gene, and polymorphisms of the structural regions of the gene or its promoter are associated with relative or absolute serum MBL deficiencies [5]. The presence of key structural and promoter polymorphisms in a detailed MBL2 haplotype is reasonably well correlated with reduced serum MBL levels, and genotypic analyses are used frequently as surrogates for MBL serum levels. The MBL2 structural gene variants, B, C and D, are referred to collectively as O while A is the wild-type. Prior to recognition of the importance of MBL2 promoter polymorphism, MBL deficiency was defined on the basis of structural gene polymorphism alone and variably as the presence of any variant allele, [AO or OO] or compound heterozygosity for variant alleles [OO].

84 These reductions were independent of serum calcium and phosphate concentrations, and associated with attenuation of both renin mRNA expression in cardiac myocytes and renin, angiotensinogen and renin receptor mRNA

and protein expression in the kidneys.85 Renal fibrosis and inflammation is a process that is driven in part by over activity of the RAS, is ameliorated by standard RAS inhibition (ACE inhibitors (ACEi) or angiotensin receptor blockers), but which can be complicated by renin accumulation which in itself can have deleterious effects.86,87 This is a problem which Tan and colleagues examined with the addition of paricalcitol to a rat model of renal selleck chemical BGB324 manufacturer fibrosis treated with trandalopril.88 In this model, they demonstrated that paricalcitol in combination with an ACEi was effective at suppressing the excess renin production seen with the ACEi alone, and worked additively to reduce renal scar.88 In vivo, there is a paucity of data assessing vitamin D intervention in relation to the RAS system directly. In the controlled case-series by Park et al. they assessed the use of i.v. 1,25-OHD (2 µg twice weekly) for 15 weeks in a HD population, and found that both plasma renin activity and circulating angiotensin

II concentrations were significantly reduced; however, confounding factors such as drug use and the significant suppression of PTH was not controlled for.89 In an elegant translational study by Kong et al. after demonstrating that active vitamin D analogues could successfully MYO10 reduce renin expression both in the kidneys and

heart, with resultant improvements in cardiac mass and function equivalent and additive to the effects of an angiotensin receptor blocker (losartan) in rats, they observed that in as case-series of chronic HD patients the use of an active vitamin D analogue reduced plasma renin activity, which was independent of the reduction in PTH (P < 0.01).90 However, significance was reduced when the use of ARB/ACEI therapy was adjusted for (P = 0.064).90 However, this together with the experimental work of Tan mentioned above highlights the need for prospective trials to be conducted which focus on vitamin D supplements as a specific additive therapy in addition to standard RAS blockade strategies (further explored in Proteinuria section below). Vitamin D’s role in LVH and cardiac function in CKD has only been explored in a small number of studies, looking at predominantly 1,25-OHD administration in haemodialysis (HD) patients with conflicting results.77,89,91–95 Unfortunately, almost all studies have been of relatively short duration (∼3 months), making it difficult to draw firm conclusions about the effect of vitamin D on cardiac function.

Moreover, we compared the expression profiles of CD8+ TEM and TCM cells. We performed these assessment by direct ex vivo analyses of intrahepatic and blood CD8+ T cell subsets using 14 different X-396 concentration TCR Vβ-specific mAbs that cover

>90% of all T cells within these populations. Preferential usage of one or more TCR Vβ subset was observed in CD8+ TEM cells after immunization, and the skewed repertoire was maintained long-term following challenge. Female C57BL/6 and out-bred ICR mice (6–8 weeks old) were purchased from The Jackson Laboratory (Bar Harbor, ME, USA) and housed at The Walter Reed Army Institute of Medical Research (WRAIR) animal facility and handled according to institutional guidelines. All procedures were reviewed and approved by the WRAIR Animal Care and Use Committee and performed in facilities accredited by the Association for Assessment and Accreditation of Laboratory Animal Care International. Plasmodium berghei ANKA (uncloned) infections were periodically initiated in ICR mice by i.p. injection of reconstituted erythrocytes from cryopreserved stocks of mouse blood infected with parasites. The parasites were maintained in vivo by serial blood-stage passage to mice at 3- to 4-day intervals. Subsequent infections were initiated by allowing sporozoite-infected

mosquitoes to feed on uninfected mice, followed by a series of four blood-stage passages. For sporozoite selleck chemical production, Anopheles stephensi mosquitoes were allowed to feed to repletion of anesthetized, gametocyte-infected mice. Blood-engorged mosquitoes were housed at 22°C in 80% relative humidity and allowed free access to 10% sucrose in water. The presence

of oocysts was evaluated approximately 10 days after the PJ34 HCl blood meal and salivary gland sporozoites 7 days later. Sporozoites were dissected from the salivary glands of mosquitoes, as described previously (27), 16–21 days after an infective blood meal. The sporozoites were used either immediately or after attenuation with γ-radiation (15 000 rad) (Caesium-137 source Mark 1 series or Cobalt-60 Model 109; J.L. Shepard & Associates, San Fernando, CA, USA). Mice were primed i.v. with 75 K Pbγ-spz followed by two boost immunizations of 20 K Pbγ-spz 1 week apart. For challenges, mice received 10 K autologous infectious sporozoites 1 week after the last boost immunization. At various time points after immunization, mice were euthanized by CO2 inhalation. Livers were exposed and the inferior vena cava was cut for blood outflow. Livers were perfused with 10-mL phosphate buffered saline (PBS), removed and pressed through a 70 μm nylon cell strainer (BD Labware, Franklin Lakes, NJ, USA), and the liver cell suspension was processed as previously described (9). Briefly, the liver cells were resuspended in PBS and centrifuged at 300 g for 10 min. The pellet was resuspended in PBS containing 35% Percoll (Amersham Pharmacia Biotec, Uppsala, Sweden) and centrifuged at 800 g for 20 min.

Monocyte-derived DCs loaded with the B11-pmel17 fusion protein resulted in antigen-specific CD4+ and CD8+ T-cell proliferation in vitro. Furthermore, injection of the B11-pmel17 conjugate in huMR transgenic mice also resulted in induction of both humoral and cellular antigen-specific immunity 30. However, the use of MR-specific antibodies for antigen-targeting purposes in humans may induce adverse immune responses due to differences in glycosylation of the antibody with the endogenous MR in humans, which may arise from the cell line used for

MR-Ab production. These effects will not appear when using natural ligands of MR to target antigen. The use of natural ligands to target the MR has been successful. Injection https://www.selleckchem.com/products/Adrucil(Fluorouracil).html of DCs, ex vivo targeted with oxidized mannan-MUC1 conjugates, in mice resulted in the generation of high frequencies of MUC1-specific CTL and protection from tumor challenge 31, 32. These studies formed the basis of clinical trails using oxidized mannan–tumorantigen conjugates to target MR. In a phase I clinical trial, patients with advanced carcinoma of the breast, colon, stomach and rectum were treated with mannan conjugated to part of MUC1. Although

this resulted in antigen-specific humoral responses in half of the patients, and CTL responses in a minority of patients, no apparent clinical responses were detected 33. A pilot phase III clinical study on oxidized mannan conjugated to MUC1 in stage II breast cancer patients with early disease showed promising Selleck Opaganib results. Evaluation of patients 5 years after the last treatment revealed that all patients receiving immunotherapy were free of tumor recurrences. By contrast, the recurrence rate in patients receiving placebo was 27% 34. Since the MR shares its specificity for mannose residues with DC-SIGN, vaccination strategies using mannan to target MR are not specific and can involve other CLR, which can severely affect the desired response. Therefore, the urge to develop MR-specific vaccination strategies using other MR-restricted natural ligands is necessary. In this

study, we have shown that both 3-sulfo-LeA and tri-GlcNAc are potential glycans which can be used to develop MR-specific therapeutic strategies as these two ligands induce enhanced cross-presentation to CD8+ T cells as DCLK1 well as potent Th1 responses. Induction of antigen-specific CD4+ T cells is not only necessary for optimal generation of effector CD8+ T cells, but also play an important role in the maintenance of memory CD8+ T cells 22. Moreover, the presence of antigen-specific CD4 T cells has recently been shown to be pivotal for the mobilization of CTLs into the effector-site 23. Together, these findings provide new options for MR-targeting studies to use specific glycans that do not share glycan specificity with other CLRs, and besides showing strong capacity to induce cross-presentation also encompass a Th1 skewing potential.

Women with nocturia >1 had a mean BWT of 5.6 mm, with nocturia <1 a mean BWT of 4.9 mm. Women with daytime frequency selleckchem >7 had a mean BWT of 5.7 mm and those <7 had a mean BWT of 5.1 (P < 0.001). Women with a mean BWT of ≤ mm had a mean VAS score lower than women with

a BWT >5 mm (P < 0.001). They concluded that mean BWT implies the presence of OAB or urodynamic DO.91 Kuo HC et al. compared the differences of DWT and also urine nerve growth factor (NGF) levels between patients with OAB and controls to evaluate their suitability as potential biomarkers for OAB.92 Key results of this study documented that DWT decreased rapidly from empty bladder to a bladder volume of 250 mL and BAY 57-1293 ic50 slowly to the maximal bladder volume. DWT was not significantly different among subgroups at a 250 mL bladder volume. Although patients with OAB wet had a significantly greater DWT at the maximal bladder volume, this difference was not significant from controls

after correction of the volume factor. By contrast, urinary NGF levels were significantly increased in patients with OAB wet and those with urodynamic DO. A recent observational study by Lekskulchai and Dietz found a statistically significant correlation between DWT and DO, which indicated that patients with DO have a thicker DWT measured by translabial ultrasound.93 However, the low sensitivity based on ROC analysis concluded that DWT was not a useful diagnostic tool for DO, which contradicted to previously published study using a cut-off value of DWT.77,90 In published works regarding the measurements of DWT or BWT in men and women as a tool to confirm DO, as well as BOO, we found variable Fenbendazole findings. Most published data confirmed an increased DWT in men with

BOO compared with the controls.81,82,88 BWT tends to be greater in men than in women without LUTS; men with LUTS and benign prostatic enlargement show a moderate increase in BWT, and a small significant increase of BWT has been noted with age for both men and women.84 We postulate that the pathophysiology of OAB is complicated, especially in women. It is possible that some men with OAB or DO might have occult BOO, but most women with OAB or DO do not have BOO. This could explain why DWT of female OAB was not significantly increased compared with the controls. Although there were statistically significant differences in DWT at bladder capacity among OAB subgroups and controls, the differences of DWT or BWT between controls and OAB were small. We are not certain of the clinical significance of such a small difference in millimetersof thickness between the controls and patients with OAB or DO. Moreover, whether a small number of millimeters difference in thickness can be reproduced with repeated measurements by different investigators in different centers using different machines needs further investigation.

The individual

parameters were scored from 1 to 3, and a cumulative score between 0 and 19 was recorded for each biopsy. The observer was blinded (J.H.E). Values are expressed as the mean ± 2 SD. To compare the treatment group with controls, we used the Mann–Whitney U-test. To evaluate the differences between before treatment, during and after treatment, the normality of each type of measurement was evaluated using a KS test based on the residuals from a simple linear model using patient and time as factors. In no case was normality close to being rejected (P > 0.4 in all cases). Hence, one-way repeated-measures anova was used. However, to evaluate the differences between the two treatment groups, two-way repeated-measures anova was used. Three patients who received combined treatment were not evaluated at week 8 because they had started another psoriasis Caspase activation treatment due to exacerbations: two of those patients at week 4 (Fig. 1A; BL3 and BL6) and one patient at week 7 (Fig. 1A; BL1). For these patients, PASI www.selleckchem.com/products/chir-99021-ct99021-hcl.html evaluation was made at the time point their study participation was terminated, and they were not included

in the analysis at week 8. All measurements were taken using sigmastat 3.1 (Systat Software, San Jose, CA, USA). A P-value ≤ 0.05 was considered statistically significant. In order to evaluate whether clinical improvement of psoriasis following bathing in geothermal seawater combined with NB-UVB and NB-UVB alone is preceded by changes in systemic inflammatory markers, the clinical efficacy of each treatment regimen was evaluated first. As shown in Fig. 1C, both treatment regimens demonstrated significant clinical improvements. Furthermore, the data suggested that patients receiving combined treatment Thymidylate synthase demonstrated better clinical response, measured by the PASI score, than patients treated only with NB-UVB. This was seen both

after one week (% improvement: combined treatment 37.3 ± 10.3 versus NB-UVB treatment 18.3 ± 8.9, P < 0.05) and after three weeks (67.3 ± 11.9 versus 22.0 ± 12.0, P < 0.0001). However, this was not the main aim of the study, and larger cohort and another control group would be needed to fully address this interesting observation. Interestingly, bathing in the Blue Lagoon immediately following skin punch biopsy resulted in no infections and only minor skin irritation resolving in few days. In addition, the above clinical findings were confirmed by the histological Trozak’s score where patients in both treatment groups showed a significant histological improvement at week 3 (Trozak’s score: BL treatment = 10.3 ± 5.5 versus NB-UVB treatment = 8.0 ± 4.6; Fig. 2).