The difficulty of the follicular unit excision (FUE) hair transplantation procedure is currently attributed to hair curliness and subsurface angulation. Patients possessing the curliest hair shafts are considered the most challenging. Consequently, patients with these features are often denied FUE. However, this practice does not consider intrapatient variation in the graft attrition rate and the rates themselves, which are frequently low in very curly hair where the skin firmness/thickness is average. To better aid practitioners in predicting FUE performance, we have developed a new scoring system (the Sanusi FUE Score Scale [SFS Scale]) based on two major donor variables (hair and skin characteristics). Material and Method:The scale assigns scores to each of three hair subtypes (straight-wavy, curly, and coily-kinky) and each of three skin subtypes (thick/firm, soft/thin, and medium thickness/firmness). The scores were weighted based on the assessment of 13 experienced FUE practitioners from around the globe, who were asked to score each of the three skin and hair characteristics for their contribution to FUE difficulty. Results: On the contribution of skin characteristics to FUE difficulty, 12/13 (92%) practitioners assigned the highest (most difficult) score to thick/firm skin, with medium skin thickness/firmness being the least challenging. The same percentage of practitioners gave the highest difficulty score to coiled-kinky hair subtypes regarding the contribution of hair characteristics to FUE difficulty. All agreed that straight-wavy hair presents the least challenge to FUE performance. Tallying the scores of the skin and hair variables generates a final score range of 2-9, which is associated with five grades/classes of challenge in the FUE procedure, influencing the need for a specialized skill/nuanced approach or equipment. Conclusion:We developed a universal FUE donor scoring scale that accounts for the diversity of human hair and skin types. Further evaluation to determine the validity of this new classification system in predicting and grading FUE difficulty and patient outcomes is warranted.

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Type 2 diabetes is a chronic disease widespread throughout the world, with significant human, social, and economic costs. Its multifactorial etiology leads to persistent hyperglycemia, impaired carbohydrate and fat metabolism, chronic inflammation, and defects in insulin secretion or insulin action, or both. Emerging evidence reveals that oxidative stress has a critical role in the development of type 2 diabetes. Overproduction of reactive oxygen species can promote an imbalance between the production and neutralization of antioxidant defence systems, thus favoring lipid accumulation, cellular stress, and the activation of cytosolic signaling pathways, and inducing β-cell dysfunction, insulin resistance, and tissue inflammation. Over the last few years, microRNAs (miRNAs) have attracted growing attention as important mediators of diverse aspects of oxidative stress. These small endogenous non-coding RNAs of 19–24 nucleotides act as negative regulators of gene expression, including the modulation of redox signaling pathways. The present review aims to provide an overview of the current knowledge concerning the molecular crosstalk that takes place between oxidative stress and microRNAs in the physiopathology of type 2 diabetes, with a special emphasis on its potential as a therapeutic target.

1 The role of nitric oxide (NO) in the effects of low endotoxemia on gastric damage and blood flow has been evaluated in indomethacin-treated rats. 2 Pretreatment (À1 h) with endotoxin (40 mg kg À1 ) reduced gastric damage induced by indomethacin (20 mg kg À1 ) in conscious rats. 3 Endotoxin prevented the reduction in gastric blood flow (laser Doppler flowmetry) induced by indomethacin in pentobarbital-anaesthetised rats. 4 Pretreatment with an NO-synthase (NOS) inhibitor (L-NAME, 1 mg kg À1 ) reversed the protective effect of endotoxin on gastric blood perfusion. 5 Endotoxin did not modify the expression of mRNA for endothelial NOS or inducible NOS in the gastric corpus when evaluated 1 h postinjection. However, a 3.8-fold increase in inducible NOS mRNA and a 61% reduction in endothelial NOS mRNA were observed in the gastric corpus 4 h after endotoxin administration. 6 Evaluation of both total and Ca 2+ -dependent NOS activity by analysing the rate of conversion of L-arginine to L-citrulline in gastric corpus homogenates showed no differences between animals treated with endotoxin and those treated with saline 1 or 4 h beforehand. Ca 2+ -independent NOS activity was almost non-apparent in control as well as in endotoxin-treated rats at all the time points analysed. 7 Low endotoxemia preserves blood perfusion and protects the gastric mucosa against the deleterious effects of indomethacin through the endogenous NO release. NO synthesis in response to endotoxin does not involve the inducible NOS, but probably depends on the post-translational/ biochemical regulation in vivo of a Ca 2+ -dependent NOS, most probably endothelial NOS.

Gold-ceria nanoparticles (Au/CeO2) are known to have antioxidant properties. However, whether these nanoparticles can provide benefits in type 2 diabetes mellitus (T2D) remains unknown. This work aimed to study the effects of Au/CeO2 nanoparticles at different rates of gold purity (10, 4.4, 1.79 and 0.82) on leukocyte–endothelium interactions and inflammation in T2D patients. Anthropometric and metabolic parameters, leukocyte–endothelium interactions, ROS production and NF-κB expression were assessed in 57 T2D patients and 51 healthy subjects. T2D patients displayed higher Body Mass Index (BMI) and characteristic alterations in carbohydrate and lipid metabolism. ROS production was increased in leukocytes of T2D patients and decreased by Au/CeO2 at 0.82% gold. Interestingly, Au/CeO2 0.82% modulated leukocyte–endothelium interactions (the first step in the atherosclerotic process) by increasing leukocyte rolling velocity and decreasing rolling flux and adhesion in T2D. A static adhesion assay also revealed diminished leukocyte–endothelium interactions by Au/CeO2 0.82% treatment. NF-κB (p65) levels increased in T2D patients and were reduced by Au/CeO2 treatment. Cell proliferation, viability, and apoptosis assays demonstrated no toxicity produced by Au/CeO2 nanoparticles. These results demonstrate that Au/CeO2 nanoparticles at 0.82% exert antioxidant and anti-inflammatory actions in the leukocyte–endothelium interaction of T2D patients, suggesting a protective role against the appearance of atherosclerosis and cardiovascular diseases when this condition exists.