Photoaging of the skin depends primarily on the degree of ultraviolet radiation (UVR) and on an amount of melanin in the skin (skin phototype). In addition to direct or indirect DNA damage, UVR activates cell surface receptors of keratinocytes and fibroblasts in the skin, which leads to a breakdown of collagen in the extracellular matrix and a shutdown of new collagen synthesis. It is hypothesized that dermal collagen breakdown is followed by imperfect repair that yields a deficit in the structural integrity of the skin, formation of a solar scar, and ultimately clinically visible skin atrophy and wrinkles. Many studies confirmed that acute exposure of human skin to UVR leads to oxidation of cellular biomolecules that could be prevented by prior antioxidant treatment and to depletion of endogenous antioxidants. Skin has a network of all major endogenous enzymatic and nonenzymatic protective antioxidants, but their role in protecting cells against oxidative damage generated by UV radiation has not been elucidated. It seems that skin's antioxidative defence is also influenced by vitamins and nutritive factors and that combination of different antioxidants simultaneously provides synergistic effect.

Human skin is constantly directly exposed to the air, solar radiation, environmental pollutants, or other mechanical and chemical insults, which are capable of inducing the generation of free radicals as well as reactive oxygen species (ROS) of our own metabolism. Extrinsic skin damage develops due to several factors: ionizing radiation, severe physical and psychological stress, alcohol intake, poor nutrition, overeating, environmental pollution, and exposure to UV radiation (UVR). It is estimated that among all these environmental factors, UVR contributes up to 80%. UV-induced generation of ROS in the skin develops oxidative stress, when their formation exceeds the antioxidant defence ability of the target cell. The primary mechanism by which UVR initiates molecular responses in human skin is via photochemical generation of ROS mainly formation of superoxide anion (O2 − ∙), hydrogen peroxide (H2O2), hydroxyl radical (OH∙), and singlet oxygen (1O2). The only protection of our skin is in its endogenous protection (melanin and enzymatic antioxidants) and antioxidants we consume from the food (vitamin A, C, E, etc.). The most important strategy to reduce the risk of sun UVR damage is to avoid the sun exposure and the use of sunscreens. The next step is the use of exogenous antioxidants orally or by topical application and interventions in preventing oxidative stress and in enhanced DNA repair.

Skin cells are constantly exposed to reactive oxygen species (ROS) and oxidative stress from exogenous and endogenous sources. UV radiation is the most important environmental factor in the development of skin cancer and skin aging. The primary products caused by UV exposure are generally direct DNA oxidation or generation of free radicals which form and decompose extremely quickly but can produce effects that can last for hours, days, or even years. UV-induced generation of ROS in the skin develops oxidative stress when their formation exceeds the antioxidant defense ability. The reduction of oxidative stress can be achieved on two levels: by lowering exposure to UVR and/or by increasing levels of antioxidant defense in order to scavenge ROS. The only endogenous protection of our skin is melanin and enzymatic antioxidants. Melanin, the pigment deposited by melanocytes, is the first line of defense against DNA damage at the surface of the skin, but it cannot totally prevent skin damage. A second category of defense is repair processes, which remove the damaged biomolecules before they can accumulate and before their presence results in altered cell metabolism. Additional UV protection includes avoidance of sun exposure, usage of sunscreens, protective clothes, and antioxidant supplements.

The histochemical and biomechanical relationships of limb muscles are examined in two groups of 15 men aged between 17 and 40 years. Seven muscles are chosen: biceps brachii, triceps brachii (TB), flexor digitorum superficialis, extensor digitorum, biceps femoris, tibialis anterior and gastrocnemius caput mediale (GCM). The aim of the preliminary study is to evaluate an alternative method based on a tensiomyographic (TMG) non-invasive measurement technique. The percentage of type I muscle fibres obtained with the histochemical method is 2.2 times higher for the slowest measured muscle (GCM) than for the fastest (TB). The contraction time of a muscle belly twitch response measured by TMG is 1.9 times higher for GCM than for TB. Statistical analysis of the data obtained by tensiomyographic and histochemical techniques shows a significant correlation between the contraction time of muscle response measured by TMG and the percentage of type I muscle fibres (correlation coefficient equals 0.93). Results of the study suggest using the TMG measuring technique as a basis for the estimation of the percentage of type I muscle fibres.

Dermatology and dermatologic surgery have rapidly evolved during the last two decades thanks to the numerous technological and scientific acquisitions focused on improved precision in the diagnosis and treatment of skin alterations. Given the proliferation of new devices for the treatment of vascular lesions, we have considerably changed our treatment approach. Lasers and non-coherent intense pulse light sources (IPLS) are based on the principle of selective photothermolysis and can be used for the treatment of many vascular skin lesions. A variety of lasers has recently been developed for the treatment of congenital and acquired vascular lesions which incorporate these concepts into their design. The list is a long one and includes pulsed dye (FPDL, APDL) lasers (577 nm, 585 nm and 595 nm), KTP lasers (532 nm), long pulsed alexandrite lasers (755 nm), pulsed diode lasers (in the range of 800 to 900 nm), long pulsed 1064 Nd:YAG lasers and intense pulsed light sources (IPLS, also called flash-lights or pulsed light sources). Several vascular lasers (such as argon, tunable dye, copper vapour, krypton lasers) which were used in the past are no longer useful as they pose a higher risk of complications such as dyschromia (hypopigmentation or hyperpigmentation) and scarring. By properly selecting the wavelength which is maximally absorbed by the target--also called the chromophore (haemoglobin in the red blood cells within the vessels)--and a corresponding pulse duration which is shorter than the thermal relaxation time of that target, the target can be preferentially injured without transferring significant amounts of energy to surrounding tissues (epidermis and surrounding dermal tissue). Larger structures require more time for sufficient heat absorption. Therefore, a longer laser-pulse duration has to be used. In addition, more deeply situated vessels require the use of longer laser wavelengths (in the infrared range) which can penetrate deeper into the skin. Although laser and light sources are very popular due to their non-invading nature, caution should be considered by practitioners and patients to avoid permanent side effects. These guidelines focus on patient selection and treatment protocol in order to provide safe and effective treatment. Physicians should always make the indication for the treatment and are responsible for setting the machine for each individual patient and each individual treatment. The type of laser or IPLS and their specific parameters must be adapted to the indication (such as the vessel's characteristics, e.g. diameter, colour and depth, the Fitzpatrick skin type). Treatments should start on a test patch and a treatment grid can improve accuracy. Cooling as well as a reduction of the fluence will prevent adverse effects such as pigment alteration and scar formation. A different number of repeated treatments should be done to achieve complete results of different vascular conditions. Sunscreen use before and after treatment will produce and maintain untanned skin. Individuals with dark ...