47 research outputs found
Effects of ultra-oxidized graphene oxide on the hydration of cement
While the use of concrete is widespread in the construction industry, cement’s poor flexural capacity and tendency to form cracks limit the potential strength development of concrete structures. Of late, concrete nanoreinforcement has gained attention, as it mitigates crack formation at the nanoscale, allowing for construction of more durable and stronger structures. Graphene oxide (GO) is a highly promising nanoreinforcement candidate due to its ease of dispersion in water, and subsequently the concrete mix. However, recent research has suggested that GO cement reinforcement is not only physical but chemical, as the hydrophilic GO provides water seeding points for cement hydration, leading to a denser microstructure which increases the flexural capacity of concrete. This research investigates the chemical interactions of GO and water, with the premise that if GO is synthesized with varying functional groups, its ability to seed water to cement will be altered. If the GO reinforcement to cement is chemical, then the physical properties of concrete with the different GO functional groups will be significantly altered. As such, four variants of GO were synthesized with varying chemical properties, but similar physical properties such as sheet sizes and thicknesses. The chemical difference between all GOs were confirmed via analytical characterization tests. Incorporation of these GOs in cement, mortar, and concrete confirmed significant impacts on strength, workability, and durability. Ultra-oxidized GOs, i.e. GOs with high presence of hydroxyl and epoxide groups showed >50% concrete mix workability, 30% increase in 28-day compressive strength, > 50% increase in 28-day flexural strength and a 42% reduction in 24 hour pore size development with respect to control concrete. Furthermore, different superplasticizer treatments to ultra-oxidized GO concretes showed consistently improved performance as well. Conversely, low hydroxyl GOs showed inconsistent results, with reduced workability and lower 28-day compressive strength of concrete with respect to control. The results confirm that GO nanoreinforcement is primarily a chemical interaction with concrete, incumbent on the presence of hydroxyl groups on the GO sheets. This research presents high potential for future implementation with physical reinforcement such as fibers or rebars. However, greater research must be undertaken to ensure GO nanoreinforcement does not impact or is not impacted by chemical admixtures in concrete
Efficiency of Estrogen Replacement Therapy in Osteoporosis
Estrogen therapy has been taken as a settled approach for both prevention and treatment of osteoporosis, especially in post-menopausal women as well as for the treatment of symptoms associated with menopause. Recent studies suggest that nuclear factor kappa-B ligand/receptor activator of nuclear factor kappa-B/osteoprotegerin system plays a signi cant role in osteoclastic activity regulation, with receptor activator of nuclear factor kappa-B ligand signaling in the presence of macrophage colony stimulating factor leading to increase in osteoclastic differentiation and functioning while osteoprotegerin neutralizing receptor activator of nuclear factor kappa-B ligand. Estrogen acts by increasing osteoprotegerin levels, and decreasing macrophage colony stimulating factor and receptor activator of nuclear factor kappa-B, thereby reducing bone resorption. Furthermore, estrogen is also known to be causing increased calcium absorption through gut and kidneys. The use of estrogen therapy in patients of osteoporosis is also considered to be highly cost effective. On the negative side, studies have shown that oral estrogen therapy can lead to complications like cholelithiasis, thrombophlebitis and pulmonary embolism, the most detrimental being endometrial cancer. But studies have shown that it can be virtually eliminated with the addition of progesterone in the cyclic combined regimen. Majority of bene cial effects occur with long term use of estrogen therapy, but the compliance by most of women appears to be poor and is usually due to lack of awareness, misconceptions, advice of physician and phobia of side effects. Additional studies should therefore be conducted to evaluate in detail the causes of non-compliance and strategies to improve compliance. The bene t of quality of life improvement with estrogen therapy should be taken into account and further evaluated via studies
IL-6 is increased in the cerebellum of autistic brain and alters neural cell adhesion, migration and synaptic formation
<p>Abstract</p> <p>Background</p> <p>Although the cellular mechanisms responsible for the pathogenesis of autism are not understood, a growing number of studies have suggested that localized inflammation of the central nervous system (CNS) may contribute to the development of autism. Recent evidence shows that IL-6 has a crucial role in the development and plasticity of CNS.</p> <p>Methods</p> <p>Immunohistochemistry studies were employed to detect the IL-6 expression in the cerebellum of study subjects. <it>In vitro </it>adenoviral gene delivery approach was used to over-express IL-6 in cultured cerebellar granule cells. Cell adhesion and migration assays, DiI labeling, TO-PRO-3 staining and immunofluorescence were used to examine cell adhesion and migration, dendritic spine morphology, cell apoptosis and synaptic protein expression respectively.</p> <p>Results</p> <p>In this study, we found that IL-6 was significantly increased in the cerebellum of autistic subjects. We investigated how IL-6 affects neural cell development and function by transfecting cultured mouse cerebellar granule cells with an IL-6 viral expression vector. We demonstrated that IL-6 over-expression in granule cells caused impairments in granule cell adhesion and migration but had little effect on the formation of dendritic spines or granule cell apoptosis. However, IL-6 over-expression stimulated the formation of granule cell excitatory synapses, without affecting inhibitory synapses.</p> <p>Conclusions</p> <p>Our results provide further evidence that aberrant IL-6 may be associated with autism. In addition, our results suggest that the elevated IL-6 in the autistic brain could alter neural cell adhesion, migration and also cause an imbalance of excitatory and inhibitory circuits. Thus, increased IL-6 expression may be partially responsible for the pathogenesis of autism.</p
NF-κB Signaling in the Brain of Autistic Subjects
Autism is a neurodevelopmental disorder characterized by problems in communication, social skills, and repetitive behavior. Recent studies suggest that apoptotic and inflammatory mechanisms may contribute to the pathogenesis of this disorder. Nuclear factor-κB (NF-κB) is an important gene transcriptional factor involved in the mediation of inflammation and apoptosis. This study examined the activities of the NF-κB signaling pathway in the brain of autistic subjects and their age-matched controls. The NF-κB activation is also determined in the brain of BTBR mice, which is a promising animal model for study of pathogenic mechanisms responsible for autism. Our results showed that the level of IKKα kinase, which phosphorylates the inhibitory subunit IκBα, is significantly increased in the cerebellum of autistic subjects. However, the expression and phosphorylation of IκBα are not altered. In addition, our results demonstrated that the expression of NF-κB (p65), and the phosphorylation/activation of NF-κB (p65) at Ser536 are not significantly changed in the cerebellum and cortex of both autistic subjects and BTBR mice. Our findings suggest that the NF-κB signaling pathway is not disregulated in the brain of autistic subjects and thus may not be significantly involved in the processes of abnormal inflammatory responses suggested in autistic brain
Goat Immunity to Helminthes
Goat hematology, especially, shares considerable attention since the last 1980s. Large number of discrepant normal hematologic values is reported. The discrepancies resulted came from the differences in age group, breed, and health standing of goats. This makes it further complex with variances in climate of the region, its environment, and size and methodology applied. With time, many inconsistencies, reasonably standardization in normal caprine kinetic hematologic values, are in place. Both goats and sheep are infested by the same key digestive tract helminthes (DTHs) diseases. Helminthes are exceedingly ubiquitous worm parasites that progressed to adopt with many erudite means to evade host immune system
Parasitism in Goats: Husbandry Management, Range Management, Gut Immunity and Therapeutics
Goats play a vital role in the economy of common man. It acts as pivotal point in the uplift of socio-economic status of females. The goats are such delicate and fragile animals that encounter a lot of infectious and non-infectious diseases including viruses, bacteria and gastrointestinal parasites (GIP). The goat being a range animal is selective feeder. It needs a lot of managemental practices which safeguards its health. This chapter focuses on management, impact of gastrointestinal parasites, role of intestinal immunity, various breeds reared in Pakistan, role of plant based phytochemicals to treat against GIT parasites and various models to predict the status of health in animals
The Therapeutic effect of Memantine through the Stimulation of Synapse Formation and Dendritic Spine Maturation in Autism and Fragile X Syndrome
Although the pathogenic mechanisms that underlie autism are not well understood, there is evidence showing that metabotropic and ionotropic glutamate receptors are hyper-stimulated and the GABAergic system is hypo-stimulated in autism. Memantine is an uncompetitive antagonist of NMDA receptors and is widely prescribed for treatment of Alzheimer's disease treatment. Recently, it has been shown to improve language function, social behavior, and self-stimulatory behaviors of some autistic subjects. However the mechanism by which memantine exerts its effect remains to be elucidated. In this study, we used cultured cerebellar granule cells (CGCs) from Fmr1 knockout (KO) mice, a mouse model for fragile X syndrome (FXS) and syndromic autism, to examine the effects of memantine on dendritic spine development and synapse formation. Our results show that the maturation of dendritic spines is delayed in Fmr1-KO CGCs. We also detected reduced excitatory synapse formation in Fmr1-KO CGCs. Memantine treatment of Fmr1-KO CGCs promoted cell adhesion properties. Memantine also stimulated the development of mushroom-shaped mature dendritic spines and restored dendritic spine to normal levels in Fmr1-KO CGCs. Furthermore, we demonstrated that memantine treatment promoted synapse formation and restored the excitatory synapses to a normal range in Fmr1-KO CGCs. These findings suggest that memantine may exert its therapeutic capacity through a stimulatory effect on dendritic spine maturation and excitatory synapse formation, as well as promoting adhesion of CGCs
Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-controlled trial
Background
Post-partum haemorrhage is the leading cause of maternal death worldwide. Early administration of tranexamic acid reduces deaths due to bleeding in trauma patients. We aimed to assess the effects of early administration of tranexamic acid on death, hysterectomy, and other relevant outcomes in women with post-partum haemorrhage.
Methods
In this randomised, double-blind, placebo-controlled trial, we recruited women aged 16 years and older with a clinical diagnosis of post-partum haemorrhage after a vaginal birth or caesarean section from 193 hospitals in 21 countries. We randomly assigned women to receive either 1 g intravenous tranexamic acid or matching placebo in addition to usual care. If bleeding continued after 30 min, or stopped and restarted within 24 h of the first dose, a second dose of 1 g of tranexamic acid or placebo could be given. Patients were assigned by selection of a numbered treatment pack from a box containing eight numbered packs that were identical apart from the pack number. Participants, care givers, and those assessing outcomes were masked to allocation. We originally planned to enrol 15 000 women with a composite primary endpoint of death from all-causes or hysterectomy within 42 days of giving birth. However, during the trial it became apparent that the decision to conduct a hysterectomy was often made at the same time as randomisation. Although tranexamic acid could influence the risk of death in these cases, it could not affect the risk of hysterectomy. We therefore increased the sample size from 15 000 to 20 000 women in order to estimate the effect of tranexamic acid on the risk of death from post-partum haemorrhage. All analyses were done on an intention-to-treat basis. This trial is registered with ISRCTN76912190 (Dec 8, 2008); ClinicalTrials.gov, number NCT00872469; and PACTR201007000192283.
Findings
Between March, 2010, and April, 2016, 20 060 women were enrolled and randomly assigned to receive tranexamic acid (n=10 051) or placebo (n=10 009), of whom 10 036 and 9985, respectively, were included in the analysis. Death due to bleeding was significantly reduced in women given tranexamic acid (155 [1·5%] of 10 036 patients vs 191 [1·9%] of 9985 in the placebo group, risk ratio [RR] 0·81, 95% CI 0·65–1·00; p=0·045), especially in women given treatment within 3 h of giving birth (89 [1·2%] in the tranexamic acid group vs 127 [1·7%] in the placebo group, RR 0·69, 95% CI 0·52–0·91; p=0·008). All other causes of death did not differ significantly by group. Hysterectomy was not reduced with tranexamic acid (358 [3·6%] patients in the tranexamic acid group vs 351 [3·5%] in the placebo group, RR 1·02, 95% CI 0·88–1·07; p=0·84). The composite primary endpoint of death from all causes or hysterectomy was not reduced with tranexamic acid (534 [5·3%] deaths or hysterectomies in the tranexamic acid group vs 546 [5·5%] in the placebo group, RR 0·97, 95% CI 0·87-1·09; p=0·65). Adverse events (including thromboembolic events) did not differ significantly in the tranexamic acid versus placebo group.
Interpretation
Tranexamic acid reduces death due to bleeding in women with post-partum haemorrhage with no adverse effects. When used as a treatment for postpartum haemorrhage, tranexamic acid should be given as soon as possible after bleeding onset.
Funding
London School of Hygiene & Tropical Medicine, Pfizer, UK Department of Health, Wellcome Trust, and Bill & Melinda Gates Foundation