Challenging the Subcostal Incision Scar with the Two-staged Abdominoplasty: An Innovative Approach.

Abdominoplasty is a commonly sought-after procedure due to its life-transforming results, but is limited, as in any other operation, by a number of contraindications. One of these contraindications is a subcostal scar, which may jeopardize blood supply to the upper flap of the abdominoplasty, resulting in skin necrosis. Herein, we challenge this dogma by introducing the two-staged abdominoplasty with the utilization of a delayed flap in a 48-year-old multiparous woman presenting with a Kocher incision of open cholecystectomy, with good results and a complication-free course of 3 postoperative months. We recommend this approach in patients with subcostal scars. However, more research into the utilization of delayed flaps in abdominoplasty should be done to have a more well-founded conclusion.

Use of a Modified Nance Appliance for Esthetic Rehabilitation of a Child Patient with Rare Nonfamilial and Nonsyndromic Oligodontia.

Congenital absence of more than 6 teeth except the third molar is known as oligodontia. It can affect both primary and permanent dentitions. The affected individuals usually demonstrate esthetic, functional, and psychological concerns. The present case report is about a 4-year-old female patient with multiple missing (both primary and permanent) teeth with esthetic and social problems. On extraoral examination, the patient demonstrated upper lip relapse due to missing anterior teeth. On physical examination, no other abnormality was detected in relation to the hair, appendages, or presence of a cleft. On intraoral and radiographic examination, 21 teeth were missing, which included both the primary and the permanent tooth buds. To encourage a positive behavioral change, it was decided to carry out prosthetic intervention using a modified fixed Nance appliance and acrylic teeth. After the replacement of the missing teeth, a marked improvement in the profile and esthetics was seen.

Impact of gamma radiation on antioxidant activity in faba bean (Vicia faba L.) and the potential of meatballs formulation with inclusion of the powder of irradiated beans.

In the present study, the effect of gamma radiation on antioxidant activity in faba beans was investigated. Whole seeds were irradiated at doses of 0-10 kGy and the antioxidant activity in samples was assessed by measuring the DPPH radical scavenging activity and ferric reducing antioxidant power in the ethanolic extracts of seeds. Exposing of faba bean seeds to ascending doses of gamma irradiation induced significant gradual increases in the antioxidant activity in faba bean and the maximum increases were observed in samples irradiated at dose of 9 kGy. Therefore, the potential of meatballs formulation with inclusion of the powder of 9 kGy irradiated faba beans was investigated with evaluating the antioxidant capacity and oxidative stability in non-irradiated and 4.5 kGy irradiated meatballs. Meatballs formulated with 20% of faba bean powder were highly acceptable. Neither incorporation of irradiated faba bean in meatballs formulation nor irradiation treatments of the prepared meatballs could adversely affect the acceptability of samples. Incorporation of irradiated faba bean, especially at 9 kGy, in meatballs formulation improved the antioxidant activity and oxidative stability in non-irradiated and irradiated samples and increased their refrigerated shelf-life through delaying of the appearance of mold growth on samples. Therefore, healthier meat products with enhanced oxidative stability can be successfully formulated with inclusion of irradiated faba beans.

Suppression of hepatic apoptosis induced by acetaminophen using a combination of resveratrol and quercetin: an association of oxidative stress and interleukin-11 / Suspensión de la apoptosis hepática inducida por acetaminofén mediante una combinación de resveratrol y quercetina: una asociación de estrés oxidativo e interleucina-1

We sought to determine whether the combined polyphenolic compounds, resveratrol and quercetin can substantially protect against modulation of hepatic biomarkers of apoptosis and survival, p53-Bax axis and B-cell lymphoma 2 (Bcl-2) in an animal model of acetaminophen-induced acute liver injury via the association of oxidative stress and interleukin-11 (IL-11). The model group of rats received a single dose of acetaminophen (2 g/kg), whereas the protective group of rats was pre-treated for 7 days with combined doses of resveratrol (30 mg/kg) and quercetin (50 mg/kg) before being given a single dose of acetaminophen. All rats were then sacrificed 24 hours post acetaminophen ingestion. Acetaminophen overdose induced acute liver injury as demonstrated by profound liver parenchymal damage and increased levels of the liver injury enzymes, alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Acetaminophen significantly (p<0.05) modulated malondialdehyde (MDA), p53, apoptosis regulator Bax, Bcl-2, IL-11, interleukin-6 (IL-6), ALT, AST, superoxide dismutase (SOD), and glutathione peroxidase (GPx), which were significantly protected by resveratrol plus quercetin. We further demonstrated a significant (p<0.01) correlation between IL-11 scoring and the levels of p53, Bax, Bcl-2, and MDA. Thus, resveratrol plus quercetin effectively protect against acetaminophen-induced apoptosis, which is associated with the inhibition of oxidative stress and IL-11.

En el estudio se intentó determinar si los compuestos polifenólicos combinados, el resveratrol y la quercetina pueden proteger sustancialmente contra la modulación de los biomarcadores hepáticos de apoptosis y supervivencia, el eje p53-Bax y el linfoma de células B 2 (Bcl-2) en un modelo animal de lesión hepática aguda inducida por acetaminofén, a través de la asociación del estrés oxidativo y la interleucina-11 (IL-11). El grupo modelo de ratas recibió una dosis única de acetaminofén (2 g / kg), mientras que el grupo protector de ratas fue tratado durante 7 días con dosis combinadas de resveratrol (30 mg / kg) y quercetina (50 mg / kg) antes de recibir una dosis única de acetaminofén. Todas los animales fueron sacrificados 24 horas después de la ingestión de acetaminofén. La sobredosis de acetaminofén indujo una lesión hepática aguda, como se observó en el daño profundo del parénquima hepático y el aumento de los niveles de las enzimas en la lesión hepática, alanina aminotransferasa (ALT) y aspartato aminotransferasa (AST). Acetaminofén moduló significativamente (p <0.05) malondialdehído (MDA), p53, regulador de apoptosis Bax, Bcl2, IL-11, interleucina-6 (IL-6), ALT, AST, superóxido dismutasa (SOD) y glutatión peroxidasa ( GPx), los que se encontraron significativamente protegidos por el resveratrol y quercetina. Además se determinó una correlación significativa (p <0.01) entre la puntuación de IL-11 y los niveles de p53, Bax, Bcl-2 y MDA. En conclusión, el resveratrol más la quercetina protegen de manera efectiva contra la apoptosis inducida por acetaminofén, asociada con la inhibición del estrés oxidativo y la IL-11.

Resveratrol Pretreatment Ameliorates p53-Bax Axis and Augments the Survival Biomarker B-Cell Lymphoma 2 Modulated by Paracetamol Overdose in a Rat Model of Acute Liver Injury.

BACKGROUND: The potential protective effects of resveratrol (RES) on the modulation of hepatic biomarkers of apoptosis and survival, p53-Bax axis, and B-cell lymphoma 2 (Bcl-2) in an animal model of paracetamol-induced acute liver injury have not been investigated before. METHODS: The model group of rats received a single dose of paracetamol (2 g/kg, orally), whereas the protective group of rats were pretreated for 7 days with RES (30 mg/kg, i.p.) before they were given a single dose of paracetamol. All rats were then sacrificed 24-h post paracetamol ingestion. RESULTS: Histology images showed that paracetamol overdose induced acute liver injury, which was substantially protected by RES. Paracetamol significantly (p < 0.05) modulated p53, apoptosis regulator Bax, Bcl-2, tumor necrosis factor-alpha, interleukin-6, inducible nitric oxide synthase, malondialdehyde, superoxide dismutase, glutathione peroxidase, alanine aminotransferase, and aspartate aminotransferase, which were significantly protected by RES. We further demonstrated a significant (p< 0.01) correlation between either p53 or Bcl-2 scoring and the levels of inflammatory, nitrosative stress, and liver injury biomarkers. CONCLUSION: We demonstrate a substantial protection by RES pretreatment against paracetamol-induced modulation of p53-Bax axis, Bcl-2, and other acute liver injury biomarkers in rats.

Exercise augments the modulatory effects of vitamin E on pre-diabetes-induced aortopathy: a potential role of adiponectin.

Background: We tested the hypothesis that vitamin E may protect against pre-diabetes-induced aortic injury (aortopathy), and exercise can augment the action of vitamin E.Material and methods: Rats were either fed with a high fat and fructose diet (HFD) (model group) or a standard laboratory chow (control group) for 15 weeks before being sacrificed. The three protective groups were treated with vitamin E (HFD + Vit E), swimming exercises (HFD + Ex), and vitamin E plus swimming exercises (HFD + VitE + Ex), respectively.Results: Aortopathy was developed in the model group as demonstrated by substantial tissue ultrastructural alterations, which were partially protected by vitamin E and effectively protected with vitamin E plus swim exercise. Also, swimming exercises significantly (p < .05) increased the modulatory effects of vitamin E on dyslipidemia, insulin resistance, blood pressure, oxidative stress, inflammation, leptin, and adiponectin, except coagulation and thrombosis.Conclusions: Swim exercise augments the protective effects of vitamin E in a pre-diabetic animal model.

Inhibition of paracetamol-induced acute kidney damage in rats using a combination of resveratrol and quercetin / Inhibición de daño renal agudo inducido por paracetamol en ratas usando una combinación de resveratrol y quercetina

Paracetamol (also called acetaminophen, or APAP) overdose causes acute damage to the liver and kidneys in both humans and experimental animal models via the induction of the oxidative stress pathway. We sought to determine whether the combined antioxidants and anti-inflammatory compounds, resveratrol (RES) and quercetin (QUR) can protect against kidney injury induced by a toxic dose of APAP in a rat model of APAP-induced acute kidney injury. Rats were either received a single dose of APAP (2 g/kg) before being sacrificed after 24 hours or were pre-treated for 7 days with combined doses of RES (30 mg/kg) and QUR (50 mg/kg) before being given a single dose of APAP and then sacrificed 24 hours post APAP ingestion. Harvested kidney tissues were prepared for light microscopy staining, and tissue samples were assayed for (i) biomarkers of oxidative stress and antioxidant, malondialdehyde (MDA) and superoxide dismutase (SOD); and (ii) biomarkers of inflammation, tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Hematoxylin and eosin (H&E) stained images showed that APAP overdose induced acute kidney injury as demonstrated by widening of glomeruli space (Bowman space), tubular dilatation, numerous cellular debris in the renal tubules with tubular epithelial degeneration, and vacuolization, which were effectively protected by RES+QUR except a partial protection of the glomeruli space was observed. In addition, APAP significantly (p<0.05) modulated tissue levels of MDA, SOD, TNF-α, and IL-6, which were protected by RES+QUR. Furthermore, a significant (p<0.0001) positive correlation was observed between glomeruli space and TNF-α, (r=0.8899), IL-6 (r=0.8986), and MDA (r=0.8552), whereas glomeruli space scoring versus SOD showed negative correlation (r= - 0.7870). We conclude that resveratrol plus quercetin substantially protects against APAP-induced acute kidney injury in rats, possibly via the augmentation of antioxidants and inhibition of oxidative stress and inflammation.

La sobredosis de paracetamol (también llamado acetaminofen o APAP) causa un daño agudo en el hígado y los riñones, tanto en humanos como en modelos animales experimentales, a través de la inducción de la vía del estrés oxidativo. Intentamos determinar si los antioxidantes y los compuestos antiinflamatorios combinados, el resveratrol (RES) y la quercetina (QUR) pueden proteger contra la lesión renal inducida por una dosis tóxica de APAP en un modelo de rata de lesión renal aguda inducida por APAP. Las ratas recibieron una dosis única de APAP (2 g / kg) antes de ser sacrificadas después de 24 horas o se trataron previamente durante 7 días con dosis combinadas de RES (30 mg / kg) y QUR (50 mg / kg), antes de ser tratadas, se administró una dosis única de APAP y luego fueron sacrificadas 24 horas después de la ingestión. Los tejidos renales recolectados se tiñeron con H-E y fueron observados a través de microscopía óptica. Las muestras de tejido se analizaron para (i) biomarcadores de estrés oxidativo y antioxidante, malondialdehído (MDA) y superóxido dismutasa (SOD); y (ii) biomarcadores de inflamación, factor de necrosis tumoral alfa (TNF-α) e interleucina-6 (IL-6). Las imágenes teñidas con H & E mostraron que la sobredosis de APAP indujo daño renal agudo como lo demuestra la ampliación del espacio glomerular, la dilatación tubular, numerosos desechos celulares en los túbulos renales con degeneración epitelial tubular y la vacuolización, que se protegieron eficazmente con RES + QUR Se observó una protección parcial del espacio glomerular. Además, APAP modificó significativamente (p <0.05) los niveles tisulares de MDA, SOD, TNF-α e IL-6, que estaban protegidos por RES + QUR. Además, se observó una correlación positiva significativa (p <0,0001) entre el espacio glomerular y el TNF-α, (r = 0,8899), IL-6 (r = 0,8986) y MDA (r = 0,8552), mientras que la puntuación del espacio glomerular versus SOD mostró correlación negativa (r = - 0,7870). Concluimos que el resveratrol más quercetina protege sustancialmente contra la lesión renal aguda inducida por APAP en ratas, posiblemente a través del aumento de antioxidantes y la inhibición del estrés oxidativo y la inflamación.

Suppression of acetaminophen-induced hepatocyte ultrastructural alterations in rats using a combination of resveratrol and quercetin.

Ingestion of a toxic dose of the analgesic drug, acetaminophen (also called paracetamol or APAP), is among the most common causes of acute liver injury in humans. We tested the hypothesis that the combined polyphenolic compounds, resveratrol (RES) and quercetin (QUR), can substantially protect against hepatocyte ultrastructural damage induced by a toxic dose of APAP in a rat model of APAP-induced acute liver injury. The model group of rats received a single dose of APAP (2 g/kg), whereas the protective group of rats was pretreated for 7 days with combined doses of RES (30 mg/kg) and QUR (50 mg/kg) before being given a single dose of APAP. All rats were then sacrificed 24 hours post APAP ingestion. Harvested liver tissues were prepared for transmission electron microscopy (TEM) staining, and liver homogenates were assayed for biomarkers of inflammation, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), and oxidative stress, such as malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx). In addition, blood samples were assayed for the liver injury enzyme alanine aminotransferase (ALT) as an indicator of liver damage. TEM images showed that APAP overdose induced acute liver injury as demonstrated by profound hepatocyte ultrastructural alterations, which were substantially protected by RES+QUR. In addition, APAP significantly (p < 0.05) modulated TNF-α, IL-6, MDA, SOD, GPx, and ALT biomarkers, which were completely protected by RES+QUR. Thus, RES+QUR effectively protects against APAP-induced acute liver injury in rats, possibly via the inhibition of inflammation and oxidative stress.

Pre-diabetes induces ultrastructural alterations in the large blood vessel aorta in rats / La prediabetes induce alteraciones ultraestructurales en la aorta de los grandes vasos sanguíneos en ratas

Excessive consumption of carbohydrate and fat increases the risk of cardiovascular disease. We sought to determine the potential ultrastructural alterations in large blood vessels induced by a high fat and fructose diet (HFD) in a rat model of prediabetes. Rats were either fed with HFD (model group) or a standard laboratory chow (control group) for 15 weeks before being sacrificed. The harvested thoracic aorta tissues were examined using transmission electron microscopy (TEM), and blood samples were assayed for biomarkers of pre-diabetes.TEM images showed that HFD induced profound pathological changes to the aortic wall layers, tunica intima and tunica media ultrastructures in the pre-diabetic rats as shown by apoptotic endothelial cells with pyknotic nuclei, damaged basal lamina, deteriorated smooth muscle cells that have irregular plasma membranes, shrunken nucleus with clumped nuclear chromatin, damaged mitochondria and few cytoplasmic lipid droplets and vacuoles. In addition, HFD significantly (p<0.05) decreased adiponectin and increased biomarkers of lipidemia, glycaemia, inflammation, oxidative stress, vascular injury such as soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion protein 1 (sVCAM-1), endothelin-1 (ET-1), and coagulation and thrombosis such as Von Willebrand factor (vWF), and plasminogen activator inhibitor-1 (PAI-1), compared to normal levels of these parameters in the control group. Thus, we demonstrated that feeding rats with a HFDisable to develop a pre-diabetic animal model that is useful to study the aortic ultrastructural alterations.

El consumo excesivo de carbohidratos y grasas aumenta el riesgo de enfermedades cardiovasculares. Intentamos determinar las posibles alteraciones ultraestructurales en los grandes vasos sanguíneos, inducidas por una dieta alta en grasas y fructosa (HFD) en un modelo de rata de prediabetes. Las ratas se alimentaron con HFD (grupo modelo) o una comida de laboratorio estándar (grupo de control) durante 15 semanas antes de ser sacrificadas. Los tejidos de la aorta torácica recolectados se examinaron mediante microscopía electrónica de transmisión (TEM) y las muestras de sangre se analizaron para detectar biomarcadores de prediabetes. Las imágenes TEM mostraron que HFD indujo cambios patológicos profundos en las capas de la pared aórtica, túnica íntima y túnica media en la ratas pre-diabéticas como lo muestran las células endoteliales apoptóticas con núcleos picnóticos, lámina basal dañada, células musculares lisas deterioradas que tienen membranas plasmáticas irregulares, núcleo encogido con cromatina nuclear aglomerada, mitocondrias dañadas y pocas gotitas lipídicas citoplásmicas y vacuolas. Además, HFD presentó disminución significativa de adiponectina (p <0,05), y aumento de biomarcadores de lipidemia, glucemia, inflamación, estrés oxidativo, lesión vascular como la molécula de adhesión intercelular soluble 1 (sICAM-1), proteína de adhesión de células vasculares soluble 1 (sVCAM-1), endotelina 1 (ET-1), y la coagulación y la trombosis, como el factor de Von Willebrand (vWF), y el inhibidor del activador del plasminógeno-1 (PAI -1), en comparación con los niveles normales de estos parámetros en el grupo de control. Por tanto, la alimentación de ratas con HFD es capaz de desarrollar un modelo animal prediabético que es útil para estudiar las alteraciones ultraestructurales aórticas.

Insulin protects against hepatocyte ultrastructural damage induced by type 1 diabetes mellitus in rats.

Diabetic complications that affect vital organs such as the heart and liver represent a major public health concern. The potential protective effects of the hormone insulin against hepatocyte ultrastructural alterations induced secondary to type 1 diabetes mellitus (T1DM) in a rat model of the disease have not been investigated before. Therefore, rats were injected once with 65 mg/kg streptozotocin (T1DM group) and the protection group (T1DM+Ins) received a daily injection of insulin 48 h post diabetic induction by streptozotocin and continued until being sacrificed at week 8. The harvested liver tissues were examined using transmission electron microscopy (TEM) and blood samples were assayed for biomarkers of liver injury enzyme, glycemia, lipidemia, inflammation, and oxidative stress. TEM images showed that T1DM induced profound hepatocyte ultrastructural alterations as demonstrated by pyknotic nucleus, condensation of chromatin, irregular nuclear membrane, swollen mitochondria, dilated rough endoplasmic reticulum, damaged intercellular space, and accumulation of few lipid droplets inside the hepatocyte cytoplasm, which were substantially protected with insulin. In addition, the blood chemistry profile complements the TEM data as demonstrated by an increase in serum levels of alanine aminotransferase (ALT), dyslipidemia, C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and malondialdehyde (MDA) by T1DM that were significantly (p < 0.05) reduced with insulin injections. Thus, we conclude that insulin effectively protects against T1DM-induced liver injury in rats for a period of 8 weeks, possibly due to the inhibition of inflammation, oxidative stress, and dyslipidemia.

Vitamin E protects against hepatocyte ultrastructural damage induced by high fat diet in a rat model of pre-diabetes / La vitamina E protege contra el daño ultraestructural de los hepatocitos inducido por la dieta alta en grasas en un modelo de pre-diabetes en ratas

SUMMARY: We sought to investigate the potential protective effect of Vitamin E supplementation against hepatocyte ultrastructural alterations induced by high fat diet (HFD) in a rat model of pre-diabetes. Therefore, rats were either fed with HFD (model group) or a standard laboratory chow (control group) for 12 weeks before being sacrificed. The protective group fed on a HFD and started the treatment with vitamin E (100 mg/kg/day, i.p) from day 1 until being sacrificed at week 12. The harvested liver tissues were examined using transmission electron microscopy (TEM) and blood samples were assayed for biomarkers of liver injury and prediabetes. TEM images showed that HFD induced profound pathological changes to the hepatocyte ultrastructure as demonstrated by degenerated hepatocytes with damaged cytoplasm that have mitochondrial swelling, dilation of endoplasmic reticulum, blebbing of plasma membranes, and cytoplasmic accumulations of lipid droplets and vacuoles, which were substantially but not completely protected with vitamin E. In addition, HFD significantly (p<0.05) augmented biomarkers of liver injury and pre-diabetes such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-alpha (TNF-α), malondialdehyde (MDA), total cholesterol (TC), triglycerides (TG), and low density lipoprotein cholesterol (LDL-C), which were significantly (p<0.05) reduced with vitamin E except TNF-α and TC. Furthermore, none of these biomarkers were reduced to the control level by vitamin E. We conclude that vitamin E is a partial protective agent against HFD-induced liver injury and pre-diabetes.

RESUMEN: El objetivo de este estudio fue investigar el posible efecto protector de la administración de suplementos de vitamina E contra las alteraciones ultraestructurales de los hepatocitos inducidas por una dieta rica en grasas (DRG) en un modelo de prediabetes en ratas. Antes de ser sacrificadas las ratas fueron alimentadas con DRG (grupo modelo) o un alimento estándar de laboratorio (grupo control) durante 12 semanas. El grupo protector se alimentó con una DRG y comenzó el tratamiento con vitamina E (100 mg/kg/día, i.p) desde el día 1 hasta sacrificarlo en la semana 12. Los tejidos hepáticos recolectados se examinaron mediante microscopía electrónica de transmisión (MET) y se tomaron muestras de sangre y se analizaron los biomarcadores de daño hepático y prediabetes. Las imágenes de MET mostraron que el DRG indujo cambios patológicos profundos en la ultraestructura de los hepatocitos, como lo demuestran los hepatocitos degenerados con citoplasma dañado e hinchazón mitocondrial, dilatación del retículo endoplasmático, formación de ampollas en las membranas plasmáticas y acumulaciones citoplásmicas de gotas de lípidos y vacuolas, los que fueron sustancialmente protegidas con vitamina E. Además, DRG aumentó significativamente (p <0,05) los biomarcadores de daño hepático y prediabetes como alanina aminotransferasa (ALT), aspartato aminotransferasa (AST), factor de necrosis tumoral alfa (TNF-α), malondialdehído (MDA), colesterol total (CT), triglicéridos (TG) y lipoproteína de colesterol de baja densidad (LDL-C), la cual se redujo significativamente (p <0,05) con vitamina E, excepto TNF-α y CT. Ninguno de estos biomarcadores se redujo al nivel de control por la vitamina E. Concluimos que la vitamina E es un agente protector parcial contra la lesión hepática inducida por DRG y la prediabetes.

Swim exercise augments the protection of the knee joint against osteoarthritis development in diabetic rats treated with insulin / El ejercicio de natación aumenta la protección de la articulación de la rodilla contra el desarrollo de osteoartritis en ratas diabéticas tratadas con insulina

We recently reported that insulin can partially protect the knee joint against osteoarthritis (OA) development in a rat model of type 1 diabetes mellitus (T1DM). However, the combined protective effect of insulin and swim exercise against OA development secondary to diabetes has not been investigated before. Therefore, we hypothesized that swim exercise can augment the protection of the knee joint in diabetic rats treated with insulin. T1DM was induced in Sprague Dawley rats and treated with insulin and/ or swim exercise. Tissues harvested from the articular cartilage of the knee joint were examined by light microscopy, and blood samples were assayed for biomarkers of oxidative stress and inflammation. Treatment of diabetic rats with insulin and swim exercise substantially protected the articular cartilage and significantly (p<0.0001) inhibited the inflammatory biomarkers, tumor necrosis factor-alpha (TNFα) and interleukin-6 (IL-6), and the oxidative stress biomarker, malondialdehyde (MDA) measured as thiobarbituric acid reactive substances (TBARS) comparable to control. Whereas, a lesser effective protection was observed by insulin or swim exercise alone. Thus, we demonstrate a substantial protection against OA development in rats treated with combined insulin and swim exercise possibly due to a complete inhibition of biomarkers of inflammation and oxidative stress.

Recientemente informamos que la insulina puede proteger parcialmente la articulación de la rodilla contra el desarrollo de osteoartritis (OA) en un modelo de diabetes tipo 1 (DM1) en ratas. Sin embargo, el efecto protector combinado de la insulina y el ejercicio de natación contra el desarrollo de OA secundario a la diabetes no se ha investigado. Por lo tanto, planteamos la hipótesis de que el ejercicio de natación puede aumentar la protección de la articulación de la rodilla en ratas diabéticas tratadas con insulina. La DM1 se indujo en ratas Sprague Dawley y se trataron con insulina y/o ejercicio de natación. Los tejidos recogidos del cartílago articular de la articulación de la rodilla se examinaron mediante microscopía óptica, y las muestras de sangre se analizaron en busca de biomarcadores de estrés oxidativo e inflamación. El tratamiento de ratas diabéticas con insulina y ejercicio de natación protegió sustancialmente el cartílago articular y significativamente (p <0,0001) inhibió los biomarcadores inflamatorios, factor de necrosis tumoral alfa (TNF-α) e interleucina-6 (IL-6) y el biomarcador de estrés oxidativo, el malondialdehído (MDA) fue medido como sustancia reactivas al ácido tiobarbitúrico (TBARS), comparable al control. Se observó una menor protección efectiva mediante la insulina o el ejercicio de natación solo. Por lo tanto, demostramos una protección sustancial contra el desarrollo de OA en ratas tratadas con insulina combinada con el ejercicio de natación, posiblemente debido a una inhibición completa de biomarcadores de inflamación y estrés oxidativo.

Temperature dependent Raman and X-ray diffraction studies of anhydrous milk fat.

Raman spectroscopy was used to characterize the polymorphs and liquid state of anhydrous milk fat, with emphasis placed on the thermal evolution of the ester carbonyl stretching modes (1800-1700cm-1) and the comparative study of the Raman-active CC (1660cm-1) and CH (3000-2700cm-1) vibrational modes. Specific Raman signatures in the crystalline phase were found and attributed to the coexistence of two groups of triglycerides. This was confirmed using differential scanning calorimetry and X-ray diffraction methods. In the ester carbonyl band, the effect of changing temperature on both the number of modes and new defined intensity ratios was studied and enabled polymorph discrimination. CH stretching signals increased with polymorph stability, indicating the dominance of antisymmetric CH methylene vibrations as the anhydrous milk fats crystal lattice became more ordered. The change in intensity of the CH stretching bands as a function of temperature was used to probe the order-disorder transition.

Possible role of plasmacytoid dendritic cells in pityriasis lichenoides.

BACKGROUND: Plasmacytoid dendritic cells (pDCs) and their product, type I interferons (IFNs), have been implicated in the pathogenesis of several skin disorders characterized by an interface dermatitis (ID) pattern, such as lichen planus (LP). A type I IFN signature has previously been documented in pityriasis lichenoides (PL). Although pDCs are known to be the main source and most potent producers of local type I IFNs, their role in PL has not been investigated. AIM: To investigate the role of pDCs in PL. METHODS: In total, 20 cases of PL and 20 comparable cases of LP were immunohistochemically tested for pDC occurrence and type I IFN production using anti-blood-derived dendritic cell antigen-2 (BDCA2; a specific pDC marker) and anti-myxovirus protein A (anti-MxA) antibodies (indirect marker of pDC activity), respectively. MxA is a well-established surrogate marker for local type 1 IFN production. A semiquantitative scoring system was used. RESULTS: pDCs were present in all 40 cases with no statistically significant difference between the two groups. MxA expression was intense and diffuse in the majority of PL and LP cases. CONCLUSIONS: pDCs constitute a central component of the inflammatory infiltrate in PL, suggesting that PL shares with the other entities that exhibit an ID a common pDC-driven process through type I IFN production, which ultimately leads to the cytotoxic attack.

Plasmacytoid dendritic cells and type I interferon in the immunological response against warts.

BACKGROUND: Plasmacytoid dendritic cells (pDCs) are the most potent producers of type I interferons (IFNs), and are involved in the pathogenesis of several cutaneous infectious (especially viral), inflammatory/autoimmune and neoplastic entities. Their role in the pathogenesis and regression of human papilloma virus (HPV)-induced skin lesions has not been well studied. AIM: To investigate pDC occurrence and activity in HPV-induced skin lesions, including inflamed and uninflamed warts as well as epidermodysplasia verruciformis (EDV)-associated lesions. METHODS: In total 20 inflamed and 20 uninflamed HPV-induced skin lesions (including 7 EDV lesions) were retrieved from our database, and the tissue was immunohistochemically tested for pDC occurrence and activity using anti-BDCA-2 and anti-MxA antibodies, respectively. RESULTS: pDCs were present in all 20 inflamed warts and absent from all 20 uninflamed cases. MxA expression was also diffuse and strong in 75% (15/20) inflamed warts, but not in any of the uninflamed warts. CONCLUSIONS: pDCs constitute a central component of the inflammatory host response in inflamed warts, possibly contributing to their regression through production of type I interferons.