Hypertensive retinopathy
Acute hypertensive retinopathy should be distinguished from retinal arteriolosclerosis. The presence of micro-vascular abnormalities in the ocular fundus increases the risk of heart and/or brain attack. At the clinical level, the current classification of chronic hypertensive retinopathy is based on the long-term risk of stroke. In research, a great number of studies are focused on the predictive value of retinal vascular diameters related to the general micro- and macrovascular disease.
Chondrocalcinosis
Chondrocalcinosis refers to deposition of calcium pyrophosphate crystals within cartilage or fibrocartilage, asvisualised on plain radiograph. Clinical features of chondrocalcinosis are various. The two common presentations of chondrocalcinosis are acute synovitis(pseudogout) and chronic arthritis, which can lead to asevere disability. Sporadic form of the disease is by far themost frequent. Aging is the main risk factor for the occurrence of sporadic chondrocalcinosis.
Prevalence of chondrocalcinosis varies from 7 to 10% in people agedaround 60 years old. A primary metabolic disorder or familial predisposition should be considered if chondrocalcinosis occurs in patients younger than 60 years. There is good evidence that hereditary hemochromatosis, hyperparathyroidism and hypomagnesemia are metabolic disorders that predispose to secondary chondrocalcinosis.
Mitochondrial dysfunction and mitophagy activation in blood mononuclear cells of fibromyalgia patients: implication in the pathogenesis of the disease.
Fibromyalgia is a chronic pain syndrome with unknown etiology. Recentstudies have shown some evidence demonstrating that oxidative stress may have a rolein the pathophysiology of fibromyalgia. However, it is still not clear whether oxidativestress is the cause or the effect of the abnormalities documented in fibromyalgia.Furthermore, the role of mitochondria in the redox imbalance reported in fibromyalgiais also controversial. We undertook this study to investigate the role of mitochondrialdysfunction, oxidative stress and mitophagy in fibromyalgia.
the role of oxidative stress and mitophagy in the pathophysiology of fibromyalgia.
A peptidyl-glucosamine derivative affects IKKalpha kinase activity in human
chondrocytes
Dept. of Biochemical Sciences, Sapienza University of Roma, P.le Aldo Moro, Roma, Italy;
The human chondrosarcoma cell line HTB-94 and human primarychondrocytes were stimulated with tumor necrosis factor (TNF)α after pre-treatmentwith GlcN or NAPA. Gene mRNA expression level was evaluated by real time-PCR.Inhibitor κB protein (IκB)α phosphorylation and p65 nuclear re-localization wereanalyzed by Western blotting; IKKα nuclear re-localization was also investigated byimmunocytochemistry and Western blotting. IKK kinase activity was studied by invitro kinase assay.
Results demonstrate that glucosamine and its peptidyl-derivativecan interfere with NF-κB signaling pathway by inhibiting IKKα activity in humanchondrocytes. However, the mechanism of action of the two molecules is notcompletely overlapping. While NAPA can both specifically inhibit the IKKα kinaseactivity and IKKα nuclear re-localization, GlcN only acts on IKKα nuclear relocalization.
Effects of glucocorticoid treatment on bone strength.
Manolides AS, Cullen DM, Akhter MP.ORC, Creighton University, Suite 4820, 610N, 30th Street, Omaha, NE, 68131, USA.
Glucocorticoids (GCs) are prescribed for the treatment of several diseases, but their long-term use causes osteoporosis. Current research suggests that GCs suppress the canonical Wnt/beta pathway, resulting in decreased expression of critical bone proteins. This study examined how bone structure and strength of high bone mass (HBM) mice and low density lipoprotein receptor-related protein 5 (LRP5) knockout (KO+/-) mice are affected by GC treatment in comparison to wild-type (WT) mice, and if changes were specific to either trabecular or cortical bone. Mice were treated with either prednisone or placebo. The femurs and L4 vertebral bodies were analyzed by micro-CT for structure and mechanically tested to determine strength and apparent material strength properties. Differences in all measured variables corresponding to GC treatment and genotype were tested using two-way ANOVA. GC treatment caused decreased structural strength parameters, weakened apparent material strength properties, and disruption of bone structure in HBM, but not LRP5+/- or WT, mice. Despite treatment-related loss, trabecular bone structure and strength remained elevated as compared to LRP5+/- and WT mice. In HBM femurs, both cortical and trabecular structure, but not strength parameters, were negatively affected by treatment. In HBM vertebral bodies, both structural and strength parameters were negatively affected by treatment.
in an urgent email from Port-au-Prince, Louise Ivers, our clinical director in Haiti, appealed for assistance from her colleagues in the Central Plateau.
Partners In Health (PIH),
