Autoimmune bullous diseases are disorders in which the immune system mistakenly attacks certain molecules that act as \"glue\" in the various layers of the skin, leading to the formation of bullae or vesicles. A bulla is a liquid-containing lesion over five millimeters in size on the skin or mucous membranes. It forms due to a loss of cohesion between the epidermis and dermis, or between keratinocytes within the epidermis. Diagnosis is based on biopsies, which show the presence of autoantibodies and the depth of skin detachment. A blood test can be used to identify circulating autoantibodies.

Muscle satellite cell (SC) regulation is a complex process involving many key signalling molecules. Recently, the neurotrophin brain-derived neurotropic factor (BDNF) has implicated in SC regulation in animals. To date, little is known regarding the role of BDNF in human SC function in vivo. Twenty-nine males (age, 21 ± 0.5 years) participated in the study. Muscle biopsies from the thigh were obtained prior to a bout of 300 maximal eccentric contractions (Pre), and at 6 h, 24 h, 72 h, and 96 h postexercise. BDNF was not detected in any quiescent (Pax7+/MyoD-) SCs across the time-course. BDNF colocalized to 39% ± 5% of proliferating (Pax7+/MyoD+) cells at Pre, which increased to 84% ± 3% by 96 h (P < 0.05). BDNF was only detected in 13% ± 5% of differentiating (Pax7-/MyoD+) cells at Pre, which increased to 67% ± 4% by 96 h (P < 0.05). The number of myogenin+ cells increased 95% from Pre (1.6 ± 0.2 cells/100 myofibres (MF)) at 24 h (3.1 ± 0.3 cells/100 MF) and remained elevated until 96 h (cells/100 MF), P < 0.05. The proportion of BDNF+/myogenin+ cells was 26% ± 0.3% at Pre, peaking at 24 h (49% ± 3%, P < 0.05) and remained elevated at 96 h (P < 0.05). These data are the first to demonstrate an association between SC proliferation and differentiation and BDNF expression in humans in vivo, with BDNF colocalization to SCs increasing during the later stages of proliferation and early differentiation. Novelty BDNF is associated with SC response to muscle injury. BDNF was not detected in nonactivated (quiescent) SCs. BDNF is associated with late proliferation and early differentiation of SCs in vivo in humans.

The inner bark of cinnamon (Cinnamomum verum) is widely used as a spice. Cinnamon plants are also a valuable source of essential oil used for medicinal purposes. The present study aimed to investigate the composition and in vitro antioxidant activity of essential oil of C. verum bark (CvEO) and its protective effects in vivo on CCl4-induced hepatic and renal toxicity in rats. Groups of animals were pretreated for 7 days with CvEO (70 or 100 mg/kg body weight) or received no treatment and on day 7 a single dose of CCl4 was used to induce oxidative stress. Twenty-four hours after CCl4 administration, the animals were euthanized. In the untreated group, CCl4 induced an increase in serum biochemical parameters and triggered oxidative stress in both liver and kidneys. CvEO (100 mg/kg) caused significant reductions in CCl4-elevated levels of alanine transaminase, aspartate transaminase, alkaline phosphatase, γ-glutamyl transferase, lactate dehydrogenase, total cholesterol, triglycerides, low-density lipoprotein, urea, and creatinine and increased the level of high-density lipoprotein compared with the untreated group. Moreover, pretreatment with CvEO at doses of 70 and 100 mg/kg before administration of CCl4 produced significant reductions in thiobarbituric acid reactive substances and protein carbonyl levels in liver and kidney tissues compared with the untreated group. The formation of pathological hepatic and kidney lesions induced by the administration of CCl4 was strongly prevented by CvEO at a dose of 100 mg/kg. Overall, this study suggests that administration of CvEO has high potential to quench free radicals and alleviate CCl4-induced hepatorenal toxicity in rats.

Both the repeated-bout effect and increased flexibility have been linked to reduced muscle damage, fatigue, and strength loss after intense eccentric exercise. Our purpose was to compare the eccentric-training (ECC) response after first priming the muscles with either static flexibility training or a single intense bout of eccentric exercise. Twenty-five participants were randomly assigned to flexibility training (n = 8; 3×/week; 30 min/day), a single bout of intense eccentric exercise (n = 9), or no intervention (control; n = 8) during a 4-week priming phase, prior to completing a subsequent 4-week period of eccentric training of the knee flexors. Testing was completed prior to the priming phase, before ECC, during acute ECC (0 h, 24 h, and 48 h after bouts 1 and 4), and after ECC. Measures included muscle thickness (MT; via ultrasound); isometric, concentric, and eccentric strength; muscle power (dynamometer); electromyography; range of motion; optimal angle of peak torque; and soreness (visual analog scale). Flexibility training and single-bout groups had 47% less soreness at 48 h after the first bout of ECC compared with control (p < 0.05). The flexibility training group had 10% less soreness at 48 h after the fourth ECC bout compared with both the single-bout and control groups (p < 0.05). Isometric strength loss was attenuated for the flexibility training group (-9%) after the fourth ECC bout compared with control (-19%; p < 0.05). All groups had similar increases in strength, MT, and power after ECC (p < 0.05). Prior flexibility training may be more effective than a single session of eccentric exercise in reducing adverse symptoms during the acute stages of eccentric training; however, these benefits did not translate into greater performance after training.

Excess and incorrectly selected exercise can degrade athletic performance from an imbalance in redox homeostasis and oxidative stress, but well-planned training and nutrition can improve antioxidant capacity. The aim of the study was to investigate how nutrient intake could influence oxidative stress and cell lesion biomarkers after 5 days of training followed by a game. Blood was collected from 10 athletes at the start of training (basal), after training (pre-game), and postgame. Their acceleration capacity also was measured pre- and postgame. Blood analysis showed an increase in lactate concentration postgame (13%) and total antioxidant capacity increased both pre-game (13.1%) and postgame (12.7%), all in comparison with basal levels. An oxidative stress marker, protein carbonyl (PC), increased 3-fold over the course of the game, which correlated with a decreased acceleration (r = 0.749). For biomarkers of tissue damage, creatine kinase and aspartate transaminase (AST) increased postgame by 150% and 75%, respectively. The AST variation had a high negative correlation with energy and carbohydrate consumption and a moderate correlation with lipid and vitamin C intake. Protein intake had a positive but moderate correlation with reduced glutathione. The observed correlations suggest that nutritional monitoring can improve exercise physiological homeostasis and that PC serves as a good biomarker for oxidative stress and performance loss.

The TASER(®) is a self-defense weapon whose use has now become commonplace among law enforcement agencies. Electronic control weapons were first used in the USA in the 1990s and then adopted in Europe and France. We report a case of an 18-year-old male who presented a penetrating lesion of the middle phalanx of the left index finger. To the best of our knowledge, this is the first complex finger injury due to the TASER(®). It highlights the potential major risks to finger vitality and function with use of this electrical weapon.