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Summary: Background: Our understanding of the pathogenesis underlying keloid scar formation is still very limited, and the morphological distinction between hypertrophic and keloid scars remains difficult. Objectives: To test whether hypertrophic and keloid scars may reflect an inability to progress from immaturity to the desired mature normotrophic scar phenotype. Methods: Using whole‐biopsy imaging and an objectively quantifiable way to analyse immunoreactivity, we have compared the immunohistopathological profiles of young immature scars with mature normotrophic scars, hypertrophic scars, and keloids with their surrounding‐normal‐skin. Results: Abnormal scars (hypertrophic scars and keloids) maintain the immature scar phenotype, characterized by a CD34− (tumour biomarker) and α‐smooth muscle actin (α‐SMA)+ (myofibroblast) dermal region. This is in contrast to normal skin, surrounding‐normal‐skin and mature normotrophic scars that were CD34+/ α‐SMA−. Immature, hypertrophic and keloid scars showed abnormal epidermal differentiation (involucrin), but only hypertrophic scars and keloids showed increased epidermal thickness. Immature scars did show increased epidermal and dermal proliferation (Ki67), which was absent from abnormal scars, where mesenchymal hypercellularity (vimentin) and senescence (p16) were predominant. Keloidal collagen and α‐SMA were previously considered to distinguish between hypertrophic scars and keloids. However, α‐SMA staining was present in both abnormal scar types, while keloidal collagen was present mostly in keloids. There were no obvious signs of heterogeneity within keloid scars, and the surrounding‐normal‐skin resembled normal skin. Conclusions: Both abnormal scar types showed a unique CD34−/α‐SMA+/p16+ scar phenotype, but the differences between hypertrophic scars and keloids observed in this study were of a gradient rather than absolute nature. This suggests that scar progression to the mature normal scar phenotype is, for as yet unknown reasons, hindered in hypertrophic and keloid scars. What's already known about this topic? Hypertrophic and keloid scars both have sustained epidermal barrier dysfunction, suggesting the persistence of an immature scar phenotype.Morphological distinction between hypertrophic and keloid scars remains a topic of debate, although α‐smooth muscle actin (α‐SMA) and keloidal collagen have been considered distinguishing features of hypertrophic and keloid scars, respectively.It has been suggested that keloids are not simply homogeneous growths, as heterogeneity within keloid scars and possible involvement of the surrounding‐normal‐skin have been reported. What does this study add? An extensive whole‐biopsy imaging and quantifiable immunohistochemical assessment of immature, mature normal, hypertrophic and keloid scars, including normal skin surrounding keloids.Hypertrophic and keloid scars maintain dermal characteristics of immature scars, rather than transitioning into the normal mature phenotype.Differences between hypertrophic and keloid scars were of a gradient rather than absolute nature, with keloids showing the more extreme phenotype.There was no obvious heterogeneity within keloids, and the normal skin surrounding keloids resembled normal skin. What is the translational message? Keloids remain primarily a clinical diagnosis.A raised scar with the CD34−/α‐SMA+/p16+ phenotype with strong immunoreactivity for p16 and significant amounts of keloidal collagen, together with a thickened and strongly abnormal involucrin‐stained epidermis, would sway the diagnosis towards keloid scars.A hypertrophic scar seems more likely when the CD34−/α‐SMA+/p16+ phenotype shows very strong presence of α‐SMA+ in large dermal nodules, with lesser p16 staining and absent or negligible keloidal collagen. Linked Comment:Tapking et al. Br J Dermatol 2020; 182:832–833. Plain language summary available online [ABSTRACT FROM AUTHOR]

Summary: Background: Bullous pemphigoid (BP) is a subepidermal blistering disease characterized by autoantibodies against the two hemidesmosomal proteins, BP180 (type XVII collagen) and BP230. The multicentre prospective BLISTER (Bullous Pemphigoid Steroids and Tetracyclines) trial randomized 253 patients with BP to compare the benefits and harms between initial treatment with doxycycline or prednisolone. Objectives: To analyse distinct autoantibody profiles for the prediction of the disease course in a well‐characterized cohort of BP sera. Methods: One hundred and forty‐three patients of the BLISTER trial consented to participate in this serological study. Sera taken at baseline were analysed by (i) indirect immunofluorescence, (ii) anti‐BP180 NC16A (16th noncollagenous domain) and anti‐BP230 enzyme‐linked immunosorbent assay and (iii) immunoblotting with various substrates. Results were then linked with clinical parameters including age, Karnofsky score, number of blisters, related adverse events and mortality. Results: Disease activity correlated with immunoglobulin (Ig)G anti‐BP180 levels but not with levels of anti‐BP230 IgG and anti‐BP180 IgE. High levels of both anti‐BP180 IgG and anti‐BP230 IgG were associated with a low Karnofsky score. The presence of anti‐BP230 IgG was more frequent in older patients. Those with higher total IgE serum levels suffered from fewer adverse events. Higher IgG anti‐BP180 levels were associated with an increased 1‐year mortality rate. Conclusions: Analysis of the autoantibody profile is not only of diagnostic relevance but may also be helpful in predicting the course of the disease. What's already known about this topic? Serum levels of immunoglobulin (Ig)G autoantibodies against BP180 correlate with disease activity in bullous pemphigoid (BP).Reports about the correlation of serum anti‐BP180 IgE with disease severity are inconclusive.Karnofsky score is a predictor of death in BP but to date has not been shown to be related to serum autoantibody levels. What does this study add? High serum anti‐BP180 IgG levels are associated with an increased mortality in BP.Patients with BP with a lower Karnofsky score show higher serum levels of anti‐BP180 and anti‐BP230 IgG.High levels of total serum IgE appear to be related to a lower number of treatment‐related adverse events.Patients with BP with high anti‐BP180 IgG may be at risk of fatal outcomes, while in those with high total IgE, fewer adverse events can be expected. Linked Comment: Hashimoto and Tsuruta. Br J Dermatol 2018; 179:820–821. Plain language summary available online Respond to this article [ABSTRACT FROM AUTHOR]

Background Recent studies have demonstrated allergen-specific differences in the gene expression of inflammatory mediators in patch tested skin. Objectives To determine levels of various inflammatory mediators in the stratum corneum ( SC) after patch testing with common contact allergens and the skin irritant sodium lauryl sulfate ( SLS). Methods In total, 27 individuals who had previously patch tested positive to nickel, chromium, methylchloroisothiazolinone/methylisothiazolinone ( MCI/ MI) or para-phenylenediamine were retested and then patch tested with SLS and petrolatum, with petrolatum serving as the patch test control. At 72 h, the test sites were clinically graded and the SC samples collected on adhesive tape. Results The levels of 18 of the 32 quantified mediators differed significantly from that of the control patches for at least one of the tested substances. SLS and MCI/ MI induced the largest number of immunomediators. Interleukin ( IL)-16 levels were significantly higher in patch test reactions in all allergens than they were in the controls, while no significant difference was detected for SLS. Furthermore, a strong negative correlation was found between strength of patch test reaction and IL-1α levels. Conclusions Cytokine profiles in the SC of patch tested skin did not show a distinct allergen-specific pattern. However, MCI/ MI induced a larger and wider immune response than the other allergens, perhaps due to its potency as an irritant. The levels of IL-16 were significantly increased in patch test reactions to allergens but not to SLS; thus, they may help clinicians to differentiate between allergic contact dermatitis and irritant contact dermatitis. [ABSTRACT FROM AUTHOR]

Background The pathogenesis underlying keloid formation is still poorly understood. Research has focused mostly on dermal abnormalities, while the epidermis has not yet been studied. Objectives To identify differences within the epidermis of mature keloid scars compared with normal skin and mature normotrophic and hypertrophic scars. Methods Rete ridge formation and epidermal thickness were evaluated in tissue sections. Epidermal proliferation was assessed using immunohistochemistry (Ki67, keratins 6, 16 and 17) and with an in vitro proliferation assay. Epidermal differentiation was evaluated using immunohistochemistry (keratin 10, involucrin, loricrin, filaggrin, SPRR2, SKALP), reverse-transcriptase polymerase chain reaction (involucrin) and transmission electron microscopy (stratum corneum). Results All scars showed flattening of the epidermis. A trend of increasing epidermal thickness correlating to increasing scar abnormality was observed when comparing normal skin, normotrophic scars, hypertrophic scars and keloids. No difference in epidermal proliferation was observed. Only the early differentiation marker involucrin showed abnormal expression in scars. Involucrin was restricted to the granular layer in healthy skin, but showed panepidermal expression in keloids. Normotrophic scars expressed involucrin in the granular and upper spinous layers, while hypertrophic scars resembled normotrophic scars or keloids. Abnormal differentiation was associated with ultrastructural disorganization of the stratum corneum in keloids compared with normal skin. Conclusions Keloids showed increased epidermal thickness compared with normal skin and normotrophic and hypertrophic scars. This was not due to hyperproliferation, but possibly caused by abnormal early terminal differentiation, which affects stratum corneum formation. Our findings indicate that the epidermis is associated with keloid pathogenesis and identify involucrin as a potential diagnostic marker for abnormal scarring. [ABSTRACT FROM AUTHOR]

The article presents information on the updated set of guidelines prepared for the British Association of Dermatologists (BAD) for 2014. It states that the guidelines offers an up-to-date information for the management of infectious cutaneous warts due to papillomavirus infection. It stresses the morphological varieties of warts that turn to lesions such as seborrhoeic keratoses or seborrhoeic warts.

The objective of this study was to investigate the relationship between nitrogen isotopic fractionation (δ15N) and nitrogen-use efficiency (milk nitrogen/nitrogen intake; NUE) in pasture-fed dairy cows supplemented with increasing levels of urea to mimic high rumen degradable protein pastures in spring. Fifteen cows were randomly assigned to freshly cut pasture and either supplemented with 0, 250, or 336 g urea/d. Feed, milk, and plasma were analyzed for δ15N, milk and plasma for urea nitrogen concentration, and plasma for ammonia concentration. Treatment effects were tested using ANOVA and relationships between variables were established by linear regression. Lower dry matter intake (P = 0.002) and milk yield (P = 0.002) occurred with the highest urea supplementation (336 g urea/d) compared with the other two treatments. There was a strong linear relationship between milk δ15N - feed δ15N and NUE: [NUE (%) = 58.9 - 10.17 × milk δ15N - feed δ15N (‹) (r(2) = 0.83, P < 0.001, SE = 1.67)] and between plasma δ15N - feed δ15N and NUE: [NUE (%) = 52.4 - 8.61 × plasma δ15N - feed δ15N (‹) (r² = 0.85, P < 0.001, SE = 1.56)] . This study confirmed the potential use of δ15N to predict NUE in cows consuming different levels of rumen degradable protein. [ABSTRACT FROM AUTHOR]

Summary [ABSTRACT FROM AUTHOR]

Aims: The study aim was to determine the presence of total and faecal coliforms on kitchen surfaces, in tap water and on the hands of caregivers in households on both sides of the US–Mexico border. Methods and Results: Samples were collected in 135 randomly selected households in Ciudad Juarez, Mexico, and El Paso, Texas. Different surfaces throughout the kitchen and head of households’ hands were sampled using sterile cotton swabs moistened in D/E neutralizing solution. Sponge/dishcloth and drinking water samples were also obtained. Total and faecal coliforms were enumerated on m-Endo LES and mFC respectively. Total coliforms and Escherichia coli in drinking water samples were enumerated in accordance with the Quanti-TrayTM method. Sponge/dishcloth samples were the most commonly contaminated kitchen sites, followed by countertops and cutting boards. We recovered faecal coliforms from 14% of the hands of child caregivers, and this indicator was moderately associated with self-reported failure to wash hands after using the toilet (OR = 3·2; 95% CI: 0·9, 11·1). Conclusions: Hand washing should continue to be emphasized, and additional interventions should be directed to specific kitchen areas, such as sponges/dishcloths, tables/countertops and cutting boards. Significance and Impact of the Study: There is a need for additional interventions regarding kitchen sanitation. [ABSTRACT FROM AUTHOR]

Background Various anti-inflammatory drugs are available for the treatment of skin disorders. In these diseases, untoward immune responses to endogenous and/or environmental antigens are initiated by maturation and polarization of dendritic cells (DC). Objective To explore the suppressive effects of anti-inflammatory drugs on DC maturation and, in particular, polarization. Methods Exposure of DC to nickel in vitro results in DC maturation and secretion of both type 1 and type 2 cytokines, thereby providing a model to study the effects of anti-inflammatory drugs on DC responses. The inhibitory effects of anti-inflammatory drugs (ciclosporin, dexamethasone, diclofenac, dimethylfumarate, hydrocortisone, lactoferrin, 1-α,25-dihydroxyvitamin D3) on DC maturation (CD83, CD86, HLA-DR, CXCL8) and polarization (type 1: IL-12p70, TNF-α; type 2: IL-10, CCL17) were studied. Results All anti-inflammatory drugs, except for lactoferrin, had inhibitory effects on DC maturation. Hydrocortisone and dexamethasone exclusively suppressed the release of type 1 cytokines. A less pronounced, but similar profile was observed for dimethylfumarate and 1-α,25-dihydroxyvitamin D3. Ciclosporin suppressed both type 1 and 2 cytokines. In contrast, diclofenac suppressed only type 2 DC cytokine secretion. Conclusion The present results give more insight into the pharmacological effects of immunosuppressive drugs on the immune system, and can thereby contribute to a more rational selection of anti-inflammatory drugs for the treatment of inflammatory skin disorders. [ABSTRACT FROM AUTHOR]

Background There is an increasing demand for the clinical application of human skin substitutes (HSSs) for treating ulcers, burns and surgical wounds. Due to this increasing demand and due to the simultaneous requirement for the administration of topical antiseptic medications, there is a need to determine potential cytotoxic effects of these medications on HSSs compared with autograft skin. Objectives To perform such an evaluation. Methods Two different HSSs were used (autologous reconstructed epidermis on fibroblast-populated human dermis and allogeneic reconstructed epidermis on a fibroblast-populated rat collagen gel) and were compared with conventional full-thickness autograft. Twelve different antiseptics were applied topically to the stratum corneum in vitro for 24 h. The degree of cytotoxicity was analysed as detrimental changes in histology, metabolic activity (MTT assay) and RNA staining of tissue sections. Results The antiseptic medications tested showed different degrees of cytotoxicity. Acticoat®, Aquacel Ag®, Dermacyn®, Fucidin®, 0·5% silver nitrate solution and chlorhexidine digluconate were not cytotoxic for either HSS or autograft, and can therefore be used as required. Flamazine® and zinc oxide cream resulted in moderate cytotoxicity. However, application of Betadine®, cerium-silver sulfadiazine cream, silver sulfadiazine cream with 1% acetic acid and Furacine® resulted in a substantial decrease in cell viability and a detrimental effect on tissue histology when applied to autograft and especially to HSS. Conclusions Due to the potential cytotoxic effect of some antiseptics on HSS, it is advised that clinicians balance the cytotoxicity of the medication, its antiseptic properties and the severity of colonization in choosing which one to apply. [ABSTRACT FROM AUTHOR]

Background Chronic wounds represent a major problem to our society. Therefore, advanced wound-healing strategies for the treatment of these wounds are expanding into the field of tissue engineering. Objectives To develop a novel tissue-engineered, autologous, full-thickness skin substitute of entirely human origin and to determine its ability to heal chronic wounds. Methods Skin substitutes (fully differentiated epidermis on fibroblast-populated human dermis) were constructed from 3-mm punch biopsies isolated from patients to be treated. Acellular allodermis was used as a dermal matrix. After a prior 5-day vacuum-assisted closure therapy to prepare the wound bed, skin substitutes were applied in a simple one-step surgical procedure to 19 long-standing recalcitrant leg ulcers (14 patients; ulcer duration 0·5–50 years). Results The success rate in culturing biopsies was 97%. The skin substitute visibly resembled an autograft. Eleven of the 19 ulcers (size 1–10 cm2) healed within 8 weeks after a single application of the skin substitute. The other eight larger (60–150 cm2) and/or complicated ulcers healed completely ( n = 5) or continued to decrease substantially in size ( n = 3) after the 8-week follow-up period. Wound healing occurred by direct take of the skin substitute ( n = 12) and/or stimulation of granulation tissue/epithelialization ( n = 7). Skin substitutes were very well tolerated and pain relief was immediate after application. Conclusions Application of this novel skin substitute provides a promising new therapy for healing chronic wounds resistant to conventional therapies. [ABSTRACT FROM AUTHOR]

Whereas T lymphocytes are widely accepted as effector cells determining the pathogenesis of allergic contact dermatitis, contradictory results have been found regarding the roles of different T-cell subsets. The use of various experimental models, involving long-term cultured T-cell lines or clones, may explain these contradictory results. To investigate the involvement of distinct T-cell subsets in patients with nickel contact allergy. Different T-cell subsets were directly isolated from peripheral blood mononuclear cells (PBMCs) of nickel-allergic patients, and their proliferative capacity, type-1 or type-2 cytokine secretion [measured by interferon (IFN)-γ or interleukin (IL)-5 release] and phenotypical marker expression were analysed after stimulation with nickel. Only CD4+ CLA+ CD45RO+ and not CD8+ T cells proliferate and produce both type-1 (IFN-γ) and type-2 (IL-5) cytokines in response to nickel. Moreover, cells expressing the marker CLA in combination with CD4, CD45RO or CD69 are increased after nickel-specific stimulation. Interestingly, in addition, CD45RA+ CLA+ cells showed an increased frequency after allergen-specific stimulation. Analysis of nickel-reactive T cells for expression of distinct chemokine receptors showed that both proliferative capacity and cytokine production are restricted to subsets expressing CXCR3, CCR4 but not CCR6. Fluorescence-activated cell sorting analysis of chemokine receptors expressed on nickel-stimulated T cells confirmed these results; a subset of T cells expressing CLA and CXCR3, CCR4 and, most importantly, CCR10 increased in response to allergen, while these CLA+ nickel-reactive T cells were all negative for CCR6. These findings demonstrate that freshly isolated nickel-reactive T cells can be characterized as CD4+ CLA+ memory T cells which express the chemokine receptors CXCR3, CCR4 and CCR10, but not CCR6. [ABSTRACT FROM AUTHOR]

Summary Background There is little information on specific interactions between dermal fibroblasts and epidermal keratinocytes. The use of engineered skin equivalents consisting of organotypic cocultures of keratinocytes and fibroblasts offers an attractive approach for such studies. Objectives To examine the role fibroblasts play in generation and maintenance of reconstructed epidermis. Methods Human keratinocytes were seeded on collagen matrices populated with increasing numbers of fibroblasts and cultured for 2 weeks at the air–liquid interface. Results In the absence of fibroblasts, stratified epidermis with only three or four viable cell layers was formed. In the presence of fibroblasts, keratinocyte proliferation was stimulated and epidermal morphology was improved. Epidermal morphogenesis was also markedly improved in epidermis generated in organotypic keratinocyte monocultures grown in medium derived from dermal equivalents or from organotypic keratinocyte–fibroblast cocultures. These observations clearly indicate the proliferation-stimulating activity of soluble factors released from fibroblasts. Under all experimental conditions, onset of keratinocyte differentiation was shown by the expression of keratin 10 in all suprabasal cell layers. With increasing numbers of fibroblasts incorporated into the collagen matrix, the expression of markers associated with keratinocyte activation, e.g. keratins 6, 16 and 17 and the cornified envelope precursor SKALP decreased, and involucrin localization shifted toward the granulosum layer. This fibroblast-mediated effect was even more pronounced when the fibroblasts were precultured in the collagen matrices for 1 week instead of overnight. The basement membrane proteins collagen VII and laminin 5 were present at the epithelial–matrix border. The expression of integrin α6β4 and of E-cadherin was comparable with that seen in native skin and was not significantly modulated by fibroblasts.... [ABSTRACT FROM AUTHOR]

Investigates the effectiveness of topical immunotherapy with contact sensitizers for viral warts. Treatments of cutaneous warts; Comparison of efficacy between placebo and dinitrochlorobenzene; Side effects of dinitrochlorobenzene.

Thirty-four patients with haematological malignancies were studied to investigate the effect of empirical broad-spectrum antibiotic therapy (ceftazidime and gentamicin) on the gastro-intestinal flora. Twenty-five patients with acute myeloid leukaemia or post-autologous bone-marrow transplantation were given framycetin, nystatin and colistin (Fracon), and two patients with non-Hodgkin's Lymphoma were on co-trimoxazole, as long-term gut prophylaxis. Semi-quantitative microbiology was carried out on oropharyngeal swabs and quantitative microbiology on faecal specimens. The oropharyngeal flora consisted mainly of streptococci, coagulase-negative staphylococci and coryneforms, and was little affected by ceftazidime/gentamicin. A strain of Enterobacter cloacae resistant to ceftazidime and gentamicin colonized one patient, who later developed septicaemia. The faecal flora of patients on Fracon was dominated by enterococci; the few enterobacteria present were eliminated by ceftazidime/gentamicin. The anaerobic flora was absent in 15% of patients; in the remainder, it consisted mainly of Bacteroides spp., and was little affected by ceftazidime/gentamicin. The faecal flora of patients not on Fracon always contained anaerobes, and some strains of enterobacteria persisted throughout antibiotic treatment. None of the patients was colonized by Clostridium difficile or Pseudomonas aeruginosa. Broad-spectrum therapy with ceftazidime and gentamicin appeared to have little effect on the gastro-intestinal flora, except to encourage the overgrowth of enterococci and reduce the numbers of enterobacteria. [ABSTRACT FROM AUTHOR]

Click here for the corresponding questions to this CME article. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article regarding primary care management for melanoma patients.

Summary: 增生性瘢痕和瘢痕疙瘩是隆起性、异常性瘢痕的两种类型。增生性瘢痕生长在原创面边界内,最终生长变小,但瘢痕疙瘩生长超出原创面边界,不自行变小,治疗困难。瘢痕疙瘩通常发生在肤色较深的人。有时仍难以确定隆起的瘢痕是增生性瘢痕还是瘢痕疙瘩。 这项荷兰研究旨在确定这两种异常瘢痕是否都形成,因为它们保留了幼稚化、不成熟瘢痕的特征,而不是以正常的方式成熟。 作者研究了存在于皮肤外层(表皮)和内层(真皮)的细胞类型,发现增生性和瘢痕疙瘩与未成熟瘢痕而不是正常健康瘢痕非常相似,存在两个重要的方面:外层细胞没有适当成熟(外皮蛋白表达增加);正常皮肤的内层细胞表达一种称为 CD34 的蛋白,不具有收缩组织的细胞 (α‐SMA),但在异常瘢痕中,这种情况发生逆转,CD34 缺失,存在收缩细胞 (α‐SMA)。 与异常瘢痕不同,未成熟瘢痕内外层细胞表现为细胞生长增加 (Ki67)。异常瘢痕的外层要厚得多,内层有许多细胞(波形蛋白),但这些细胞已经停止生长(称为 p16)。 根据内层的外观很难将增生性瘢痕与瘢痕疙瘩分开,但增生性瘢痕有更多的细胞收缩,瘢痕疙瘩内层有很厚的结缔组织带。 总之,本研究结果提示,增生性瘢痕和瘢痕疙瘩保持了未成熟瘢痕的特征,不像正常瘢痕那样成熟。 本摘要涉及研究:增生性瘢痕和瘢痕疙瘩未能从 CD34‐α‐平滑肌肌动蛋白 (SMA)+未成熟瘢痕表型进展,并且表现出 α‐SMA 和 p16 表达的梯度差异 [ABSTRACT FROM AUTHOR]

Summary: Hypertrophic and keloid scars are two types of raised, abnormal scars. Hypertrophic scars grow within the borders of the original wound and eventually grow smaller, but keloids grow beyond the original wound borders, do not grow smaller on their own, and are difficult to treat. Keloids usually occur in people with darker skin colour. Sometimes it is still difficult to determine if a raised scar is a hypertrophic scar or a keloid. This study from the Netherlands aimed to find out if both these abnormal scars form because they retain characteristics of the young, immature scars, rather than maturing in a normal way. The authors examined the types of cells present in the outer (epidermis) and the inner (dermis) layer of the skin and found that the hypertrophic and keloid scars closely resembled immature scars, rather than normal healthy scars in two important ways: the outer layer cells did not mature properly (increased involucrin expression); the inner layer cells of normal skin express a protein called CD34 and do not have cells that function to contract tissue (α‐SMA), but in the abnormal scars this is reversed ‐ CD34 is missing and the (α‐SMA) contracting cells are present. Unlike abnormal scars, the cells of the inner and outer layer of immature scars showed increased cell growth (Ki67). The outer layer of the abnormal scars was much thicker and the inner layer had many cells (vimentin), but these cells had stopped growing (known as p16). It was difficult to separate the hypertrophic scars from the keloids based on what the inner layer looks like, but hypertrophic scars have more cells that contract and keloids have very thick bands of connective tissue in their inner layer. In conclusion, the results of this study suggest that hypertrophic and keloid scars maintain characteristics of immature scars and do not mature like normal scars do. This is a summary of the study: Hypertrophic and keloid scars fail to progress from the CD34−α‐smooth muscle actin (SMA)+immature scar phenotype and show gradient differences in α‐SMA and p16 expression [ABSTRACT FROM AUTHOR]

Two unrelated adult patients are described who both developed an exanthem with the characteristic morphology and distribution of the Gianotti–Crosti syndrome. The literature of adult cases of Gianotti–Crosti syndrome is reviewed with the suggestion that the syndrome may not be as uncommon as previously supposed. [ABSTRACT FROM AUTHOR]

The article provides an answer to a question concerning the warts that occur as a result of the human papilloma virus.

Develops a numerical approximation method for valuing multivariate contingent claims. Use of an n-dimensional extension of the lattice binomial method as basis for the approach; Closed-form solutions for the jump probabilities and amplitudes; Lattice valuation model for several assets; Application of the method in the case of European options.

A response by S. Gibbs, C. S. Kwok, and R. Holland to a letter to the editor on their article regarding the effectiveness of clear duct tape in eradicating common wart in the 2011 issue is presented.

Presents a letter to the editor about chronic urticaria responding to subcutaneous heparin sodium.

Comments on a study by Al-Gurairi et. al. on the treatment of viral warts using zinc sulphate published in the 2002 issue of the 'British Journal of Dermatology.' Method used for the collection of samples for clinical trials; Effectiveness of the treatment using zinc.

A normally fit European resident of East Africa developed a staphylococcal peri-nephric abscess following repeated episodes of furuncular myiasis caused by the tumbu fly, Cordylobia anthropophaga. A few lesions had required surgical intervention and one, presumably the source of sepsis, had become infected. There are very few descriptions in the literature of serious complications of myiasis and this is the first report of peri-nephric abscess from this source. This paper discuses the management of the myiasis and what factors determine the variation in host susceptibility and immune response to the infestation. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor about the clinical features of patient with pityriasis rotunda in Tanzania.

The article discusses the study which measures the usage of fluorouracil (FU) cream and the experience of patients who uses the cream as treatment. The study involves 112 patients with prescriptions of 5% FU cream to treat skin diseases such as Bowen disease (BD), solar keratosis, and superficial basal cell carcinoma (BCC) wherein the amount of the unused cream were measured. The study suggests that 97% of patients who uses the cream were very satisfied.

A letter to the editor is presented in response to the article about the diagnosis and treatment of tungiasis, published in the previous issue.