Excimer light effect on neurogenic inflammation in active versus stable psoriasis lesions.

Neurogenic inflammation, mediated by T helper 17 cell (Th17) and neurons that release neuropeptides such as substance P (SP), is thought to play a role in the pathogenesis of psoriasis. Excimer light is used in the treatment of psoriasis via induction of T cell apoptosis. The objective of this study is to study the effect of excimer light on active versus stable psoriasis and investigate the levels of substance P and its receptor in both groups. The study included 27 stable and 27 active psoriatic patients as well as 10 matched healthy controls. Clinical examination (in the form of local psoriasis severity index (PSI) and visual analogue scale (VAS)) was done to determine disease severity, level of itching, and quality of life. Tissue levels of SP and neurokinin-1 receptor (NK-1R) were measured by ELISA before and after 9 excimer light sessions in 43 patients. A statistically significant lower levels of PSI and VAS were reached after therapy with no significant difference between the stable and active groups. The mean tissue levels of SP before therapy were significantly higher than the control group. Lower levels of SP and NK-1 receptor were found after treatment overall and in each group. Excimer therapy can be effective for both stable and active plaque psoriasis and this effect could be partly through its role on ameliorating the neurogenic inflammation.

Possible role of rice bran extract in microglial modulation through PPAR-gamma receptors in alzheimer's disease mice model.

Alzheimer's Disease (AD), the most prevalent neurodegenerative disorder among elderly people, is ordinarily associated with progressive cognitive decline. Peroxisome proliferator-activated receptors-gamma (PPAR-γ) agonists can be targeted as a beneficial therapeutic strategy against AD. In the present study, we aimed to investigate the preventive and therapeutic effects of rice bran extract (RBE) as a possible PPAR-γ agonist on the microglial phenotype modulation in AD in mice compared to the effects of pioglitazone. This study included 64 adult male Swiss Albino mice divided into 8 groups, each group comprised 8 mice; control group, RBE group, lipopolysaccharide-induced neurodegeneration (a) (LPSa) group, (LPSb) group, RBE-preventive group (RBE + LPSa), pioglitazone-preventive group (PG + LPSa), RBE-treated group (RBE + LPSb), and pioglitazone-treated group (PG + LPSb). Cognitive functions were assessed by Y-maze and Morris water maze tests. The expression of PPAR-γ, CD45, arginase1, CD36, and CD163 genes was assessed by real time qPCR and the estimation of NF-kß protein level was done by Western blot technique. Moreover, the assessment of Aß42 and P-tau levels was performed by ELISA. Histopathological examination of brain tissues was performed for all the studied groups. Our results showed that RBE and pioglitazone could modulate microglial phenotype from M1 to M2 where they significantly decreased the expression of NF-κß and the pro-inflammatory microglial marker (CD45) in parallel with increasing the expression of the anti-inflammatory microglial and phagocytic markers (arginase1, CD163, and CD36). In addition, RBE and pioglitazone significantly increased PPAR-γ expression and reduced Aß42 deposition as well as p-tau protein levels. In conclusion, our study identified the possible role of PPAR-γ agonistic activity of RBE as a preventive and therapeutic agent in the treatment of the neuro-inflammation associated with AD.

Single-nucleotide polymorphisms of IL-10 and IL-28B as predictors of the response of IFN therapy in HCV genotype 4-infected children.

BACKGROUND AND AIMS: Single-nucleotide polymorphisms (SNPs) in the IL-10 gene (-1082 [rs1800896], -819 [rs3021097], and -592 [rs1800872]) and the IL-28B gene (rs12979860) in adults were shown to be associated with hepatitis C virus (HCV) clearance. The present study aimed to investigate the possible association of SNPs of IL-10 and IL-28B in predicting the treatment response of HCV genotype 4 in pediatric patients. PATIENTS AND METHODS: A restriction fragment length polymorphism-polymerase chain reaction and real-time polymerase chain reaction techniques were used to genotype 34 pediatric patients with HCV genotype 4 for IL-10 and IL-28B SNPs, respectively. Patients received pegylated interferon-α/ribavirin for 48 weeks subdivided according to their response to treatment into responders and nonresponders; also, 20 healthy individuals served as controls. RESULTS: A significant difference (P < 0.005) was observed in SNP of IL-28B rs12979860 frequencies between responders and nonresponders. In responders, CC genotype had greater frequency than CT and TT genotypes (60%, 30%, 10%), respectively, with C allele in its homozygous (CC) genotype more likely to respond to treatment than in its homozygous (TT) genotypes. SNPs of IL-10 at -819 (rs3021097) showed significant differences in their genotype frequencies between responders and nonresponders to therapy, and TT genotype had greater frequency in responders than CT and CC (55%, 20%, 25%), respectively. Genotypes with T allele (CT/TT) showed higher rates of response than those with no T allele (CC). CONCLUSIONS: SNPs of the IL-28B gene at (rs12979860) CC genotype as well as the IL-10 gene SNPs at -819 (rs3021097)TT genotype can be used for predicting response to treatment before patients are prescribed the expensive pegylated interferon-α/ribavirin therapy.

Assessment of tissue E-cadherin and its proteolytic serum fragment in pemphigus vulgaris before and after remission: A case-control study.

BACKGROUND: E-cadherin is a classic cadherin that mediates keratinocyte adhesion. AIMS: To assess the tissue expression of E-cadherin and its proteolytic serum fragment (soluble E-cadherin) in pemphigus vulgaris (PV) before and after clinical remission compared with controls. PATIENTS: Thirty-seven PV patients and thirty controls were enrolled. Pemphigus disease area index (PDAI) was calculated for patients at baseline and after remission. Punch biopsy specimens were taken from patients before, and after remission, and from controls for assessment of tissue E-cadherin by immunofluorescence. Similarly, serum samples were collected for assessment of serum soluble E-cadherin by ELISA. RESULTS: Presence, intensity, and mean intensity of tissue E-cadherin were significantly reduced in PV patients before treatment compared with controls (p < 0.001). Detected E-cadherin showed mainly a basal and suprabasal distribution with cell surface and a cytoplasmic expression. Serum E-cadherin was significantly higher in patients before treatment compared with controls (p = 0.006). With remission, tissue E-cadherin presence, intensity, mean intensity, and serum E-cadherin showed statistically significant improvement (p = 0.003, <0.001, <0.001, and 0.003 respectively). Tissue E-cadherin presence and serum E-cadherin level reached values equivalent to the controls (p = 0.49 and 0.44, respectively). CONCLUSIONS: Disruption of tissue E-cadherin and upregulation of serum soluble E-cadherin can contribute to the pathogenesis of PV. Clinical remission of PV is associated with normalization of tissue and serum E-cadherin.

Association of Vitamin D Deficiency with Chronic Stable Angina: A Case Control Study.

INTRODUCTION: Coronary heart disease is a major cause of death worldwide. Although the relationship between vitamin D status and cardiovascular diseases is not clearly understood, vitamin D deficiency could be a potentially modifiable and underestimated risk factor for ischemic heart diseases. This study aims to assess and compare vitamin D status between patient group with chronic stable angina and matched control group. METHODS: A case-control study was conducted on chronic stable angina patients and matched controls attending family medicine/internal medicine clinics at Cairo University Hospitals. Forty two adult patients with chronic stable angina and forty two matched controls were studied. Detailed medical history, examination, and laboratory tests (vitamin D, fasting lipid profile, and blood sugar) were collected from study participants of both groups. RESULTS: Severe vitamin D deficiency was found in 78.6% and 7.1% of cases and controls, respectively. Vitamin D level was found to be a significant predictor of chronic stable angina. Every unit (ng/ml) increase in vitamin D level decreases the chance of the subject to have chronic stable angina by 0.30 times. CONCLUSION: There is a significant association between vitamin D deficiency and the occurrence of chronic stable angina.

Vitamin D status in diabetic patients (type 2) and its relation to glycemic control & diabetic nephropathy.

BACKGROUND: Vitamin D deficiency appears to be lower in diabetic patients. Vitamin D may affect glycemic control & diabetic nephropathy. AIM: To assess vitamin D level in type 2 diabetic patients and its relation to their glycemic control and development of nephropathy compared to healthy controls. DESIGN: and Setting: Case control study including 82 participants (41 cases and 41 controls) from Family Medicine Clinic, Cairo University Hospitals. METHOD: Participants fulfilling the inclusion criteria were allocated into two groups, diabetes and control groups. History was taken, examination was done, and blood sample was withdrawn for analysis of Vitamin D levels and HBA1C. From the diabetic group only, serum creatinine was assessed and urine sample was collected for microalbuminuria. The results were analyzed using SPSS program version 21. RESULTS: Vitamin D level was lower in the diabetic group compared to control (65.5% and 56.1%). Vitamin D level was inversely proportionate to HbA1c levels in the diabetic patients (p value 0.000 & r -0.482), as well as to the A/C ratio (p value 0.01 & r -0.396). CONCLUSION: Vitamin D level appeared to be lower in diabetic patients and is associated with poor glycemic control & microalbuminuria.