Motion of three-dimensional elastic films by anisotropic surface diffusion with curvature regularization

Short time existence for a surface diffusion evolution equation with curvature regularization is proved in the context of epitaxially strained three-dimensional films. This is achieved by implementing a minimizing movement scheme, which is hinged on the $H^{-1}$-gradient flow structure underpinning the evolution law. Long-time behavior and Liapunov stability in the case of initial data close to a flat configuration are also addressed.Comment: 44 page

New 675 nm Laser Device: The Innovative and Effective Non-Ablative Resurfacing Technique

Background and Objectives: Photo/chrono-aging is usually expressed as facial discolouration, wrinkles, redness, elastosis, laxity, and dehydration, thus representing major signs of ageing that often lead to a negative phycological impact on a patient's quality of life. Several types of treatment have been tested during the last decade, especially laser treatments. This article aims to share our experience in the treatment of photoaging with a new 675 nm laser source system on facial chrono-ageing. Materials and Methods: Thirty-five (35) patients were treated with the 675 nm laser device: 32 females (mean age 49 years) and 3 men (mean age 57 years), with Fitzpatrick skin types I-III (9% type I, 43% type II, 48% type III), facial wrinkles and hyperpigmented spots. The efficacy of this treatment was assessed using the Modified Fitzpatrick Wrinkles Scale (FWS), which was calculated before starting the treatment and after 6 months. The pain was evaluated using the VAS Pain Scale. Results: All 35 patients showed a significant improvement in facial wrinkles according to the FWS (from 1.96 to 1.73 at the 3-month follow-up, up to a value of 1.43 at 6 months). In a small group of patients, it was observed that 44% of them showed vascular moderate improvement and that 13% showed a vascular marked improvement after treatment. No side effects were detected except a mild erythematous rash in two patients, and the VAS Pain scale was assessed at 1.17. Conclusions: Red Touch allows a uniform and stable result to be achieved over time with minimum discomfort

Microwave technology for the treatment of abdomen localized adiposity 9 months follow-up

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Clinical evaluation on the performance and safety of a non-ablative fractional 1340 nm laser for the treatment of stretch marks in adolescents and young adults. a case series

A large part of the world's population suffers from Striae distensae (SD) or stretch marks, which create physical and psychological discomfort in people. We evaluate the SD clinical improvement by using a non-ablative fractional Nd:YAP 1340 nm laser. The research was performed on 25 patients of both sexes, with a mean age of 31 ± 13.09 years. Each patient underwent from a minimum of 3 to a maximum of 4 treatments, with an Nd:YAP (1340 nm) medical device, every four weeks, with 3- and 6-month follow-up, in these areas: back, abdomen, breast, flanks, lower limbs, buttocks, and thighs. Manchester Scar Scale assessed stretch marks improvement. Side effects, patient pain, and SD overall appearance improvement were also recorded for all patients. Digital photographs measured the aesthetic results. Treatment was well-tolerated (pain score 1.08 ± 0.76) by all patients. There were no long-term side effects, and 88% of patients revealed an SD excellent improvement showing good aesthetic results achieved by the treatment. The total mean pretreatment Manchester Scar Scale score decreased from 13.80 (±1.58) to 10.36 (±1.70) after 3 months (p < 0.01) and to 8.36 (±1.07) after 6 months (p < 0.01). An Nd:YAP (1340 nm) laser seems to be a safe and effective treatment, showing a higher security profile with no side effects

Albendazole negatively regulates keratinocyte proliferation

Abstract Background: Increased keratinocyte proliferation occurs in the skin of psoriatic patients and is supposed to play a role in the pathogenesis of this disorder. Compounds interfering with keratinocyte proliferation could be useful in the management of psoriatic patients. Aim: To investigate whether albendazole, an anti-helmintic drug that regulates epithelial cell function in various systems, inhibits keratinocyte proliferation in models of psoriasis. Methods: Aldara-treated mice received daily topical application of albendazole. Keratinocyte proliferation and keratin (K) 6 and K16 expression were evaluated by immunohistochemistry and Western blotting and inflammatory cells/mediators were analysed by immunohistochemistry and real-time PCR. In human keratinocytes (HEKa and HaCaT) treated with albendazole, cell cycle and proliferation, keratins and cell cycle-associated factors were evaluated by flow cytometry, colorimetric assay and Western blotting respectively. Results: Aldara-treated mice given albendazole exhibited reduced epidermal thickness, decreased number of proliferating keratinocytes and K6/K16 expression. Reduction of CD3- and Ly6G-positive cells in the skin of albendazole-treated mice associated with inhibition of IL-6, TNF-α, IL-1β, IL-17A, IL-36, CCL17, CXCL1, CXCL2 and CXCL5 expression. Treatment of keratinocytes with albendazole reduced K6/K16 expression and reversibly inhibited cell growth by promoting accumulation of cells in S-phase. This phenomenon was accompanied by down-regulation of CDC25A, a phosphatase regulating progression of cell cycle through S-phase, and PKR-dependent hyper-phosphorylation of eIF2α, an inhibitor of CDC25 translation. In Aldara-treated mice, albendazole activated PKR, enhanced eIF2α phosphorylation and reduced CDC25A expression. Conclusions: Data show that albendazole inhibits keratinocyte proliferation and exerts therapeutic effect in a murine model of psoriasis

Effective Intense Pulsed Light Protocol in the Treatment of Moderate to Severe Acne Vulgaris

no abstract availabl

Rat protein tyrosine phosphatase η physically interacts with the PDZ domains of syntenin

AbstractThe tyrosine phosphatase r-PTPη is able to suppress the malignant phenotype of rat thyroid tumorigenic cell lines. To identify r-PTPη interacting proteins, a yeast two-hybrid screening was performed and an insert corresponding to the full-length syntenin cDNA was isolated. It encodes a protein containing two PDZ domains that mediates the binding of syntenin to proteins such as syndecan, proTGF-α, β-ephrins and neurofascin. We show that r-PTPη is able to interact with syntenin also in mammalian cells, and although syntenin is a tyrosine-phosphorylated protein it is not a substrate of r-PTPη. The integrity of both PDZ domains of syntenin and the carboxy-terminal region of r-PTPη are required for the interaction between syntenin and r-PTPη

The selective antagonism of adenosine A2Breceptors reduces the synaptic failure and neuronal death induced by oxygen and glucose deprivation in rat CA1 hippocampus in vitro

Ischemia is a multifactorial pathology characterized by different events evolving in time. Immediately after the ischemic insult, primary brain damage is due to the massive increase of extracellular glutamate. Adenosine in the brain increases dramatically during ischemia in concentrations able to stimulate all its receptors, A1, A2A, A2B, and A3. Although adenosine exerts clear neuroprotective effects through A1 receptors during ischemia, the use of selective A1 receptor agonists is hampered by their undesirable peripheral side effects. So far, no evidence is available on the involvement of adenosine A2B receptors in cerebral ischemia. This study explored the role of adenosine A2B receptors on synaptic and cellular responses during oxygen and glucose deprivation (OGD) in the CA1 region of rat hippocampus in vitro. We conducted extracellular recordings of CA1 field excitatory post-synaptic potentials (fEPSPs); the extent of damage on neurons and glia was assessed by immunohistochemistry. Seven min OGD induced anoxic depolarization (AD) in all hippocampal slices tested and completely abolished fEPSPs that did not recover after return to normoxic condition. Seven minutes OGD was applied in the presence of the selective adenosine A2B receptor antagonists MRS1754 (500 nM) or PSB603 (50 nM), separately administered 15 min before, during and 5 min after OGD. Both antagonists were able to prevent or delay the appearance of AD and to modify synaptic responses after OGD, allowing significant recovery of neurotransmission. Adenosine A2B receptor antagonism also counteracted the reduction of neuronal density in CA1 stratum pyramidale, decreased apoptosis at least up to 3 h after the end of OGD, and maintained activated mTOR levels similar to those of controls, thus sparing neurons from the degenerative effects caused by the simil-ischemic conditions. Astrocytes significantly proliferated in CA1 stratum radiatum already 3 h after the end of OGD, possibly due to increased glutamate release. A2Breceptor antagonism significantly prevented astrocyte modifications. Both A2B receptor antagonists did not protect CA1 neurons from the neurodegeneration induced by glutamate application, indicating that the antagonistic effect is upstream of glutamate release. The selective antagonists of the adenosine A2B receptor subtype may thus represent a new class of neuroprotective drugs in ischemia

Antisense Oligonucleotide: Basic Concepts and Therapeutic Application in Inflammatory Bowel Disease

Several molecular technologies aimed at regulating gene expression that have been recently developed as a strategy to combat inflammatory and neoplastic diseases. Among these, antisense technology is a specific, rapid, and potentially high-throughput approach for inhibiting gene expression through recognition of cellular RNAs. Advances in the understanding of the molecular mechanisms that drive tissue damage in different inflammatory diseases, including Crohn’s disease (CD) and ulcerative colitis (UC), the two major inflammatory bowel diseases (IBDs) in humans, have facilitated the identification of novel druggable targets and offered interesting therapeutic perspectives for the treatment of patients. This short review provides a comprehensive understanding of the basic concepts underlying the mechanism of action of the oligonucleotide therapeutics, and summarizes the available pre-clinical and clinical data for oligonucleotide-based therapy in IBD