Background: Noise induces free radicals release and can damage the cochlear epithelium. The outer hair cell motor protein prestin is necessary for sharp frequency tuning and cochlear function. Otolin-1 is a glycoprotein; its mRNA expression is restricted to the inner ear. Genes involved in repairing the oxidative damage as human 8-oxoG DNA glycosylase 1 (hOGG1) can affect the cochlea susceptibility to noise. Prestin upregulation may represent a response to compensate for noise-induced hearing loss (NIHL). Objectives: We investigated the association between exposure to noise, the blood perstin and otolin-1level, hOGG1 polymorphisms, and oxidative DNA damage as indicated by serum 8-hydroxy-2'-deoxyguanosine (8-OHdG) concentrations. Materials and methods: In 300 patients with NIHL and 200 controls with normal hearing, blood prestin, otolin-1, and 8-OHdG levels were studied by ELISA; the hOGG1 polymorphism was genotyped by polymerase chain reaction amplification followed by digestion with restriction endonucleases. Results: The prestin, otolin-1, and 8-OHdG levels were significantly elevated in patients compared to controls (P < 0.05). Regression analysis showed that hOGG1 Cys/Cys genotype showed a significantly increased risk of hearing loss compared with the other genotypes exposed to the same environmental factors (95% confidence interval = 1.1–2.3, adjusted odds ratio = 1.5). This was associated with increased prestin, otolin-1, and 8-OHdG levels and the duration of noise exposure in months. Conclusion: These findings are consistent with the notion that prestin increases in an attempt to compensate for missing outer hair cells. Otolin-1 could be a circulatory biomarker for otoconia damage caused by noise, and the hOGG1 Cys/Cys genotype could be a susceptibility marker for NIHL. The hOGG1 Cys/Cys gene variant was more frequent in patients compared to controls exposed to the same environmental factors and more frequent in severe cases confirmed by elevated prestin, otolin-1, and 8-OHdG l levels.

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Introduction: Laryngeal carcinoma is the most common malignant head-and-neck tumor. Due to the low survival rate and the inadequate response to chemotherapy, effective therapy remains a challenge. Objectives: Therefore, the identification of new therapeutic options that preserve the larynx is needed. Hesperidin (Hsp) is a nontoxic plant flavanone that has proven effective against cancer. Materials and Methods: Hence, the current in vivo and in vitro study was conducted to determine whether Hsp might suppress metastasis of cancer larynx. Results: In an in vivo mouse metastasis model, Hsp suppressed metastasis of human Hep2 laryngeal cancer cells to the livers and lungs. In vitro assays, Hsp significantly inhibited angiopoietin 1 secretion (an angiogenic promotor) and increased annexin-V (an apoptotic indicator) in Hep2 cell culture at relatively low levels (10 µM). Conclusions: These studies suggest that Hsp deserves further investigation as a possible treatment option for laryngeal cancer.

Burns occur with high incidence worldwide causing high mortality and morbidity. [1] After skin injury, the skin depends on stem cells for its renewal involving inflammation, angiogenesis with cytokines, and growth factors production. [2] In pathological conditions as diabetes mellitus, healing is not completed or delayed. Chronic nonhealing burns have many precipitating factors as reduced angiogenesis and impairment in the cytokines production. [3] In diabetes, the adult stem cell cannot function properly resulting in impaired healing. [4] Adipose-derived stromal cells (ADSCs) treatments have been associated with promising outcomes in the wound healing. [5] Serpin B3, also known as "squamous cell carcinoma antigen-1", is a member of the serpin superfamily of serine protease inhibitors which are involved in the regulation of apoptosis, inflammation, and angiogenesis. [6] Keratinocyte growth factor-1 (KGF-1) is a member of the fibroblast growth factor family produced by fibroblasts, smooth muscle cells, and endothelial cells. [7] It is expressed in injured skin and extensively produced in the early healing process of the wound. [8] KGF-1 has been shown to induce migration and multiplication of keratinocytes that produce various growth factors and cytokines during the healing process. [9,10] Therefore, identification of the value and possible adverse effects of ADSCs for burn healing in normal and diabetic conditions using an animal model are needed before the human trials. The assessment of healing by Serpin B3 and KGF-1 as novel biomarkers and molecular targets of impaired diabetic wound healing. Objectives:The mechanisms underlying delayed healing in diabetes are not completely understood and biomarkers to identify and to treat such pathways are needed. The aim of the present study is to assess the clinical effect of adipose tissue-derived stem cells in accelerating third-degree burns healing in diabetic and normal mouse model and to restore skin integrity. Assessment of healing by Serpin B3 and keratinocyte growth factor-1 (KGF-1) as novel biomarkers and possible molecular targets of impaired diabetic wound healing. Materials and Methods: Forty male mice were set up as an experimental model for third-degree burn. They were randomly divided into four groups as follows: the control group, the diabetic (received high-fat diet) burnt group, the diabetic burnt group treated with adipose tissue-derived stem cells, and the nondiabetic burnt group treated with adipose tissue-derived stem cells. The rate of burn healing, the degree of angiogenesis, and collagen formation were evaluated by histological examination, Serpin B3 (enzyme-linked immunosorbent assay), and KGF-1 measured by real-time polymerase chain reaction. They were sacrificed after the 3 rd week for tissue sampling. Results: Adipose tissue-derived stem cells accelerate the healing of experimental burns. Serpin B3 was upregulated in adipose tissue-derived stem cells treated burns associated with denser collagen deposition, angiogenesis, and increased expressi...

Background: Angiogenesis is a key issue in the carcinogenesis progression. Gastrointestinal tract (GIT) cancer is a multi-stage disease, multifaceted, concerning convention of different signaling cascades. Abnormal angiogenesis have been related to pathogenesis of tumor. Objectives: We hypothesized inter-relationships between indices of angiogenesis biomarkers across the spectrum of GIT cancer and its relation to the pathogenesis and prognosis of the diseases. We also evaluated the consequence of estimating these indices in untimely tumor recognition. Methods: Forty patients were studied and divided into two groups: Group 1 (n=30) with GIT cancer and group 2 (n=10) with benign lesion. The cancer group subdivided into patients with gastric cancer (n= 12) and patients with colorectal cancer (n=18). 20 healthy controls (C) were involved in the study. Serum levels of all biochemical indices were estimated. Results: Significantly high serum levels of studied angiogenic biomarkers were detected in patients with GIT cancer compared to C and benign group (p<0.000l and p<0.001 for each respectively). Their levels being significantly higher in late stage of the disease versus early stage and in patients with high tumor burden versus patients with low tumor burden with the exception of Cathpsin-B and HA that showing no significant difference. Positive Significant correlations was present between all indices in cancer groups (p<0.001). Also, there was significant positive correlations between these biomarkers and stage of the tumor (p<0.01). Conclusions: There was a gradation in angiogenesis biomarkers in patients with GIT cancer which related to stage and size of the tumors. This may reflect the relative roles of these biomarkers in the biology of GIT cancer. Their estimation may have implications for our understanding of the pathphysiology of tumor, play a novel beneficial roles in early tumor detection and targeted tumor therapy by using antangiogenic therapy