Early in vivo detection of denervation-induced atrophy by luminescence transient nanothermometry.

Denervation induces skeletal muscle atrophy due to the loss of control and feedback with the nervous system. Unfortunately, muscle atrophy only becomes evident days after the denervation event when it could be irreversible. Alternative diagnosis tools for early detection of denervation-induced muscle atrophy are, thus, required.

Time-Dependent Changes in Muscle IGF1-IGFBP5-PAPP System after Sciatic Denervation.

Denervation-induced muscle atrophy is a frequent cause of skeletal muscle diseases. However, the role of the most important muscle growth factor, insulin-like growth factor (IGF-1), in this process is poorly understood. IGF-1 activity is controlled by six IGF-1 binding proteins (IGFBPs).

Cardiovascular Responses of Women with Fibromyalgia to a Laboratory Stressor: Does Post-traumatic Stress Disorder Comorbidity Matter?

Objectives: This study compared cardiovascular responses to a laboratory trauma-unrelated stressor of two groups of women diagnosed with fibromyalgia (FM), one of them with comorbid post-traumatic stress disorder (PTSD), with a group of healthy controls in order to detect the possible existence of differences linked to comorbidity.

Design: Case-controls.

Methods: Eighteen women diagnosed with FM and comorbid PTSD, 18 women diagnosed with FM and no PTSD, and 38 healthy women were exposed to an arithmetic task with harassment while blood pressure and heart rate were measured during task exposure and recovery.

Melanocortin-4 receptor agonist (RO27-3225) ameliorates soleus but not gastrocnemius atrophy in arthritic rats.

Adjuvant-induced arthritis in rats decreases body weight and muscle mass. Melanocyte stimulating hormone administration to arthritic rats decreases inflammation and skeletal muscle wasting. In this study, we investigate whether activation of melanocortin-4 receptor by RO27-3225 administration is able to prevent the effect of arthritis on the expression of muscle-specific E3 ubiquitin ligases and MyoD in two different muscles, gastrocnemius (a mainly fast type muscle) and soleus (slow type).

Formoterol decreases muscle wasting as well as inflammation in the rat model of rheumatoid arthritis.

Adjuvant-induced arthritis is an experimental model of rheumatoid arthritis that is associated with body weight loss and muscle wasting. β2-adrenergic receptor agonists are powerful anabolic agents that trigger skeletal muscle hypertrophy and have been proposed as a promising treatment for muscle wasting in human patients. The aim of this work was to determine whether formoterol, a selective β2-adrenoreceptor agonist, is able to ameliorate muscle wasting in arthritic rats.

The melanocortin receptor type 3 agonist d-Trp(8)-γMSH decreases inflammation and muscle wasting in arthritic rats.

Background: Chronic inflammatory diseases induce cachexia that increases mortality and morbidity of the illness. Adjuvant-induced arthritis is an experimental model of rheumatoid arthritis that is associated with body weight loss and muscle wasting. Alpha-melanocyte stimulating hormone has an anti-inflammatory effect in arthritic rats and decreases muscle wasting.

Fenofibrate administration to arthritic rats increases adiponectin and leptin and prevents oxidative muscle wasting.

Chronic inflammation induces skeletal muscle wasting and cachexia. In arthritic rats, fenofibrate, a peroxisome proliferator-activated receptor α (PPARα (PPARA)) agonist, reduces wasting of gastrocnemius, a predominantly glycolytic muscle, by decreasing atrogenes and myostatin. Considering that fenofibrate increases fatty acid oxidation, the aim of this study was to elucidate whether fenofibrate is able to prevent the effect of arthritis on serum adipokines and on soleus, a type I muscle in which oxidative metabolism is the dominant source of energy.

Systemic α-melanocyte-stimulating hormone administration decreases arthritis-induced anorexia and muscle wasting.

Rheumatoid cachexia is associated with rheumatoid arthritis and it increases mortality and morbidity. Adjuvant-induced arthritis is an experimental model of rheumatoid arthritis that causes anorexia and muscle wasting. α-Melanocyte-stimulating hormone (α-MSH) has anti-inflammatory actions, and it is able to decrease inflammation in several inflammatory diseases including experimental arthritis.

Effect of cyclooxygenase-2 inhibition by meloxicam, on atrogin-1 and myogenic regulatory factors in skeletal muscle of rats injected with endotoxin.

Cyclooxygenase-2-induction by inflammatory stimuli has been proposed as a mediator of inflammatory cachexia. We analyse whether cyclooxygenase-2 inhibition by meloxicam administration is able to modify the response of skeletal muscle to inflammation induced by lipopolysaccharide endotoxin (LPS). Male rats were injected with 1 mg kg(-1) LPS at 17:00 h and at 10:00 h the following day, and euthanized 4, 24 or 72 hours later.

Long-term changes in corneal morphology induced by overnight orthokeratology.

Purpose: To assess long-term morphological and biometric corneal changes produced by overnight orthokeratology and to examine their recovery after cessation of contact lens wear.

Methods: Prospective, single-center, longitudinal trial. Fifteen right eyes with low to moderate myopia underwent overnight orthokeratology for 1 year.

Fenofibrate, a PPAR{alpha} agonist, decreases atrogenes and myostatin expression and improves arthritis-induced skeletal muscle atrophy.

Arthritis is a chronic inflammatory illness that induces cachexia, which has a direct impact on morbidity and mortality. Fenofibrate, a selective PPARα activator prescribed to treat human dyslipidemia, has been reported to decrease inflammation in rheumatoid arthritis patients. The aim of this study was to elucidate whether fenofibrate is able to ameliorate skeletal muscle wasting in adjuvant-induced arthritis, an experimental model of rheumatoid arthritis.

Short-term effects of overnight orthokeratology on corneal cell morphology and corneal thickness.

Purpose: To examine the morphological and biometric corneal changes produced over periods of 15 days and 1 month after overnight orthokeratology (OK).

Methods: Prospective, single-center, longitudinal trial. Twenty-seven right eyes of 27 subjects (group 1) with low to moderate myopia wore OK lenses for 1 month.

Genotype distribution of cervical human papillomavirus DNA in women with cervical lesions in Bioko, Equatorial Guinea.

Background: The HVP vaccine is a useful tool for preventing cervical cancer. The purpose of this study is to determine the most frequent HPV genotypes in Equatorial Guinea in order to develop future vaccination strategies to apply in this country.

Methods: A campaign against cervical cancer was carried out in the area on a total of 1,680 women.

Insulin-like growth factor-I modulation of cerebellar cell populations is developmentally stage-dependent and mediated by specific intracellular pathways.

Although development of transgenic animals overexpressing insulin-like growth factor-I has allowed the establishment of a role of this trophic factor in brain growth, detailed knowledge of the action of insulin-like growth factor-I on different brain areas is still lacking. We now provide evidence for a pleiotrophic role of this growth factor on cerebellar development. Insulin-like growth factor-I produced by cerebellar cultures is a survival factor for Purkinje cells and a mitogen/differentiation factor for cerebellar glioblasts.

Transynaptic modulation by insulin-like growth factor I of dendritic spines in Purkinje cells.

Purkinje cells synthesize insulin-like growth factor I and express insulin-like growth factor I receptors during their entire life. An additional source of insulin-like growth factor I for these cells is provided by climbing fiber afferents originating in the inferior olive nucleus. Recently we found that insulin-like growth factor I from the inferior olive is necessary for motor learning processes probably involving Purkinje cell synaptic plasticity.

Insulin-like growth factor I is an afferent trophic signal that modulates calbindin-28kD in adult Purkinje cells.

Recent evidence suggests that Purkinje cells are specific targets of insulin-like growth factor I (IGF-I) through their entire life span. During development, Purkinje cell numbers and their calbindin-28kD content increase after IGF-I treatment in culture. In the adult, part of the IGF-I present in the cerebellum is transported from the inferior olive, and modulates Purkinje cell function.

Orthograde transport and release of insulin-like growth factor I from the inferior olive to the cerebellum.

Insulin-like growth factor I (IGF-I) and its receptor are expressed in functionally related areas of the rat brain such as the inferior olive and the cerebellar cortex. A marked decrease of IGF-I levels in cerebellum is found when inferior olive neurons are lesioned. In addition, Purkinje cells in the cerebellar cortex depend on this growth factor to survive and differentiate in vitro.