Predetermining glenoid dimensions using the scapular dimensions

European Journal of Orthopaedic Surgery & Traumatology - Variations of morphology of the glenoid cavity have been previously reported. These influence the surgical reconstruction or...     

Hesperidin Reduces Memory Impairment Associated with Adult Rat Hippocampal Neurogenesis Triggered by Valproic Acid

Treatment with valproic acid (VPA) deteriorates hippocampal neurogenesis, which leads to memory impairment. Hesperidin (Hsd) is a plant-based bioflavonoid that can augment learning and memory. This study aimed to understand the effect of Hsd on the impairment of hippocampal neurogenesis and memory caused by VPA. The VPA (300 mg/kg) was administered by intraperitoneal injection twice daily for 14 days, and Hsd (100 mg/kg/day) was administered by oral gavage once a day for 21 days. All rats underwent memory evaluation using the novel object location (NOL) and novel object recognition (NOR) tests. Immunofluorescent staining of Ki-67, BrdU/NeuN, and doublecortin (DCX) was applied to determine hippocampal neurogenesis in cell proliferation, neuronal survival, and population of the immature neurons, respectively. VPA-treated rats showed memory impairments in both memory tests. These impairments resulted from VPA-induced decreases in the number of Ki-67-, BrdU/NeuN-, and DCX-positive cells in the hippocampus, leading to memory loss. Nevertheless, the behavioral expression in the co-administration group was improved. After receiving co-administration with VPA and Hsd, the numbers of Ki-67-, BrdU/NeuN-, and DCX-positive cells were improved to the normal levels. These findings suggest that Hsd can reduce the VPA-induced hippocampal neurogenesis down-regulation that results in memory impairments.     

Origin of the dorsal scapular artery and its relation to the brachial plexus in Thais

We investigated the variations of the origin of the dorsal scapular artery (DSA) and its relation to the brachial plexus in 252 sides of the posterior cervical triangles of Thais. The origin of this artery on each part of the subclavian artery or other arterial branches was examined with special reference to their course in relation to the brachial plexus. The results show that the DSA originated from three sites; most commonly from the transverse cervical artery (69 %) followed by the direct branching from the second (2.8 %) or the third part (28.2 %) of the subclavian artery. When the DSA was branched from the transverse cervical artery, its course was always posterior or above the brachial plexus. When the DSA arose from the second or the third part of the subclavian artery, it always ran in the branches of the brachial plexus in various sites. The most frequent course was to pass between the upper and middle trunks of the brachial plexus (63.2 %). Other courses were far less frequent and found to pass between the anterior division of the upper trunk and the middle trunk of brachial plexus or between the roots of C₈ and T₁ with the frequency of 1.3 and 2.6 %, respectively.     

Caffeic Acid Alleviates Memory and Hippocampal Neurogenesis Deficits in Aging Rats Induced by D-Galactose

Hippocampal neurogenesis occurs throughout life, but it declines with age. D-galactose (D-gal) enhances cellular senescence through oxidative stress leading to neurodegeneration and memory impairment. Caffeic acid (CA) acts as an antioxidant via decreasing brain oxidative stress. This study aims to investigate the advantages of CA in alleviating the loss of memory and neurogenesis production in the hippocampus in aged rats activated by D-gal. Fifty-four male Sprague-Dawley rats were unpredictably arranged into six groups. In the D-gal group, rats were administered D-gal (50 mg/kg) by intraperitoneal (i.p.) injection. For the CA groups, rats received 20 or 40 mg/kg CA by oral gavage. In the co-treated groups, rats received D-gal (50 mg/kg) and CA (20 or 40 mg/kg) for eight weeks. The results of novel object location (NOL) and novel object recognition (NOR) tests showed memory deficits. Moreover, a decline of neurogenesis in the hippocampus was detected in rats that received D-gal by detecting rat endothelial cell antigen-1 (RECA-1)/Ki-67, 5-bromo-2′-deoxyuridine (BrdU)/neuronal nuclear protein (NeuN), doublecortin (DCX) by means of staining to evaluate blood vessel associated proliferating cells, neuronal cell survival and premature neurons, respectively. By contrast, CA attenuated these effects. Our results postulate that CA attenuated the impairment of memory in D-gal-stimulated aging by up-regulating levels of hippocampal neurogenesis.     

Effects of Asiatic Acid on Spatial Working Memory and Cell Proliferation in the Adult Rat Hippocampus

Asiatic acid is a pentacyclic triterpene from Centella asiatica. Previous studies have reported that asiatic acid exhibits antioxidant and neuroprotective activities in cell culture. It also prevents memory deficits in animal models. The objective of this study was to investigate the relationship between spatial working memory and changes in cell proliferation within the hippocampus after administration of asiatic acid to male Spraque-Dawley rats. Control rats received vehicle (propylene glycol) while treated rats received asiatic acid (30 mg/kg) orally for 14 or 28 days. Spatial memory was determined using the novel object location (NOL) test. In animals administered asiatic acid for both 14 and 28 days, the number of Ki-67 positive cells in the subgranular zone of the dentate gyrus was significantly higher than in control animals. This was associated with a significant increase in their ability to discriminate between novel and familiar object locations in a novel object discrimination task, a hippocampus-dependent spatial memory test. Administration of asiatic acid also significantly increased doublecortin (DCX) and Notch1 protein levels in the hippocampus. These findings demonstrate that asiatic acid treatment may be a potent cognitive enhancer which improves hippocampal-dependent spatial memory, likely by increasing hippocampal neurogenesis.     

Purple rice berry is neuroprotective and enhances cognition in a rat model of Alzheimer's disease

Alzheimer's disease, a neurodegenerative disease characterized by progressive memory loss and cognitive impairment, is the most common type of dementia in aging populations due to severe loss of cholinergic neurons in a specific area. Oxidative stress is known to be involved in the pathogenesis of this condition. Therefore, the cognition-enhancing and neuroprotective effects of rice berry (Oryza sativa), a purple-pigmented rice that is rich in antioxidant substances, was evaluated. Young adult male Wistar rats, weighing 180-220 g, were orally given rice berry once daily at doses of 180, 360, and 720 mg/kg of body weight for a period of 2 weeks before and 1 week after the induction of memory deficit and cholinergic lesions with AF64A, a specific cholinotoxin, via bilateral intracerebroventricular administration. One week following AF64A administration the rats were evaluated for spatial memory, neuron density, acetylcholinesterase activity, and hippocampal lipid peroxidation products. Our results showed that rice berry could significantly prevent memory impairment and hippocampal neurodegeneration in hippocampus. Moreover, it also decreased hippocampal acetylcholinesterase activity and lipid peroxidation product formation. These results suggest that rice berry has potential as an effective agent for neurodegeneration and memory impairment in Alzheimer's disease.