Seeds of the citrus fruits orange, mandarin, lime and grapefruit were analyzed. Petroleum ether‐extracted oils of such seeds amounted to more than 40% of each. Physical and chemical properties of the extracted oils are presented. Samples of the extracted oils were saponified and the unsaponifiables and fatty acid fractions isolated. The isolated unsaponifiables and fatty acids were analyzed by GLC. GLC analysis of the unsaponifiables revealed compositional patterns differ‐ent in number, type and relative concentration of fractions according to type of citrus seed oil, depending on the solvent system used for oil extraction and unsaponifiable matter isolation. The compositional patterns of the unsaponifiables were similar to that of cottonseed oil. Mandarin and grapefruit oils are free of cholesterol. The data demonstrate that the fatty acid compositional patterns of the oils differ; Mandarin seed oil contains the largest number of fatty acids, and grapefruit seed oil contains the lowest. The total amounts of volatile fatty acids in these oils are generally higher than those of other edible oils. Lime seed oil is similar, in the degree of unsaturation, to soybean oil. The orange oil pattern is similar to cottonseed oil. The amount of total essential fatty acids in lime seed oil is the highest of the oils studied.

Most superficial mycotic infections of human skin are due to dermatophytes. Children are frequently affected due to different predisposing factors, particularly overcrowding in classrooms. This study aimed to estimate the prevalence of dermatophytes infections and their related risk factors among school children in Menoufia Governorate, Egypt. Six public primary and preparatory schools were randomly selected and their pupils (n = 3464) were asked to complete a predesigned questionnaire covering both personal data and suspected risk factors for superficial dermatophyte infections. The children were also examined for dermatological diseases. Any suspected lesions were biopsied for mycological examination. The prevalence of clinically suspected dermatophytes infections was 1.41%, whereas the prevalence of culture confirmed cases was 0.98%. The most common clinical type was tinea capitis with a prevalence of 1.01%. Microsporum canis was the only isolated organism from the suspicious lesions with a 69.4% positivity rate. A higher prevalence was observed among boys, low socio-economic pupils and those with a family history of dermatophyte infections. Pet contact and sharing towels and caps among pupils were significant risk factors. Dermatophyte infection is still prevalent among basic school pupils. Fortunately, it is related to preventable risk factors. We recommend regular screening and use of educational health programmes for kids to control it.

BackgroundVitiligo is an autoimmune skin disorder in which the loss of melanocytes is mainly attributed to defective autoimmune mechanisms and, lately, there has been more emphasis on autoinflammatory mediators. Among these is the macrophage migration inhibitory factor, which is involved in many autoimmune skin diseases. However, little is known about the contribution of this factor to vitiligo vulgaris.ObjectiveTo determine the hypothesized role of migration inhibitory factor in vitiligo via estimation of serum migration inhibitory factor levels and migration inhibitory factor mRNA concentrations in patients with vitiligo compared with healthy controls. We also aimed to assess whether there is a relationship between the values of serum migration inhibitory factor and/or migration inhibitory factor mRNA with disease duration, clinical type and severity in vitiligo patients.MethodsEvaluation of migration inhibitory factor serum level and migration inhibitory factor mRNA expression by ELISA and real-time PCR, respectively, were performed for 50 patients with different degrees of vitiligo severity and compared to 15 age- and gender-matched healthy volunteers as controls.ResultsThere was a highly significant increase in serum migration inhibitory factor and migration inhibitory factor mRNA levels in vitiligo cases when compared to controls (p<0.001). There was a significant positive correlation between both serum migration inhibitory factor and migration inhibitory factor mRNA concentrations in vitiligo patients, and each of them with duration and severity of vitiligo. In addition, patients with generalized vitiligo have significantly elevated serum migration inhibitory factor and mRNA levels than control subjects.Study limitationsSmall number of investigated subjects.ConclusionsMigration inhibitory factor may have an active role in the development of vitiligo, and it may also be a useful index of disease severity. Consequently, migration inhibitory factor may be a new treatment target for vitiligo patients.

Background Psoriasis is an inflammatory disease that is mostly immune‐derived. It causes proliferation of skin cells, forming plaques. Psoriasis etiology is unknown. It might be multifactorial. Aims This work aimed to study Smad7 expression in psoriasis vulgaris patients in comparison with normal skin. Patients/Methods Thirty patients with psoriasis vulgaris in comparison with 20 age‐ and sex‐matched seemingly healthy individuals were selected. We used psoriasis area and severity index (PASI) to evaluate psoriasis severity. Skin biopsies were prepared from skin lesions (30), perilesions (30) and control (20) groups for histopathological and immunostaining evaluation of Smad7. Results Smad7 was progressively upregulated in proliferating keratinocytes from controls (58.18 ± 30.93) to perilesional (106 ± 38.93) and lesional (156.33 ± 62.01) skin (P < .001). Also, dermal inflammatory cells showed upregulation of Smad7 expression from control skin (40 ± 28.28) to skin lesions (137.33 ± 73.86) (P < .010). Smad7 expression showed a positive significant correlation with psoriasis severity (r = .452; P < .012). Conclusion Smad7 may be involved in increased keratinocyte proliferation as well as skin inflammation in psoriasis vulgaris patients.

Many of the histopathologic criteria used to diagnose melanoma overlap with atypical but otherwise benign naevi such as dysplastic or Spitz naevi. Galectin-3 is a member of the galectin gene family and is expressed at elevated levels in a variety of neoplastic cell types. The aim of the present study was to investigate the diagnostic value of galectin-3 expression compared with homatropine methyle bromide-45(HMB-45) (one of the established and widely used immunohistochemical melanocytic markers) together with assessment of its prognostic value in melanoma lesions. This study was carried out on 21 cases of melanoma and 20 benign pigmented naevi. Galectin-3 was expressed in all the examined benign and malignant melanocytic lesions. The nucleocytoplasmic pattern of galectin-3 appeared in malignant cases only with 42.86% sensitivity, 100% specificity, and 70.73% accuracy. This pattern tended to be associated with thick melanoma (P = 0.08) and reduced survival (P = 0.22). The intensity of galectin-3 assessed by H-score was significantly of higher values in malignant lesions compared with benign lesions (P < 0.0001). The best cut-off value for discrimination between benign and malignant melanocytic lesions was 295 with 95% sensitivity, 70% specificity, and 83% accuracy. The diagnostic power of galectin-3 in distinguishing between benign and malignant melanocytic lesions relies on the pattern and the intensity of its expression. The nucleocytoplasmic pattern of galectin-3 expression carries greater probability of a malignant phenotype and a poor prognostic impact on patients' outcome.

Background: Human JAKs are responsible for generating docking sites for human SSTAT phosphorylation. The role of JAKs in psoriasis pathogenesis has not been clearly explained. Aim: To investigate the role of JAK1 in psoriasis pathogenesis and to assess if this role is mediated through STAT3 or not, through evaluation of their immunohistochemical expression in the skin of psoriatic patients. Methods: This case–control study was carried out on 26 patients presenting with psoriasis vulgaris versus 26 age- and sex-matched apparently healthy volunteers. Psoriasis Area and Severity Index (PASI) scores were used to evaluate psoriasis severity. From all controls and cases (lesional and perilesional), skin biopsies were taken for histopathological and immunohistochemical JAK1 and STAT3 evaluation. Results: There was significant stepwise upregulation of JAK1 from controls to perilesional to lesional psoriatic skin of the patient group in both epidermis and dermis ( P ≤0.001 for both). Dermal JAK1 H-score was significantly associated with psoriasis severity ( P =0.01). STAT3 was significantly overexpressed in lesional psoriatic skin over nonlesional skin ( P <0.001). There were significant positive correlations between lesional H-scores for STAT3 and Psoriasis Area and Severity Index scores in epidermis ( r =0.63, P <0.001), and in dermis ( r =0.47, P =0.04). There was a significant positive correlation between JAK1 and STAT3 expression in epidermal lesional psoriatic skin ( r =0.44, P =0.03). Conclusion: JAK1 has a proinflammatory effect in psoriasis pathogenesis, which could be mediated through increasing STAT3 expression in psoriasis. JAK1 and STAT3 tissue expression could be markers of psoriasis severity. JAK1 may be used as a target for immunotherapy in psoriasis-management programs.

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Background: In-vitro studies showed that Leucine-rich glioma inactivated 3 (LGI3) is a keratinocyte-derived cytokine that stimulates melanin synthesis and is increased after ultra violet B (UVB) irradiation. So, we postulated that LGI3 may be involved in vitiligo aetiopathogenesis and may participate in narrow band ultra violet B (NB-UVB) induced pigmentation in vitiligo. oBjectives: To assess this hypothesis, lesional LGI3 immunohistochemical expression of vitiligo patients before and after NB-UVB phototherapy was studied, and its correlation with repigmentation was evaluated. Methods: Forty vitiligo patients and 20 age, sex, and skin phenotype-matched controls were enrolled. Patients were treated with NB-UVB thrice weekly for 12 weeks. VASI score was evaluated before and after NB-UVB sessions. For vitiligo patients, baseline LGI3 immunohistochemical staining was estimated, and compared to that of controls and to its post-treatment data in those patients. Results: Baseline LGI3 immunohistochemical studied parameters (expression, intensity, percentage and H score) were significantly lower in vitiligo cases than controls (p=0.003, 0.013, 0.001 and 0.001 respectively). After 12 weeks of NB-UVB phototherapy, these LGI3 immunohistochemical parameters were up-regulated and became comparable to that of controls (p >0.05 for all). There was a significant positive correlation between the improvement of both VASI score and LGI3 H score mean values (r=-0.349 , p=0.027). study liMitations: Small number of investigated subjects. conclusions: Decreased LGI3 protein may play an active role in vitiligo pathogenesis and its up-regulation after NB-UVB phototherapy, may actively participate in NB-UVB photo-induced melanogenesis.