5-hydroxymethylcytosine (5-hmC) is a modified form of cytosine recently found in mammalians and is believed, like 5-methylcytosine, to also play an important role in switching genes on and off. By utilizing a newly developed 5-hmC immunoassay, we determined the abundance of 5-hmC in human tissues and compared 5-hmC states in normal colorectal tissue and cancerous colorectal tissue. Significant differences of 5-hmC content in different tissues were observed. The percentage of 5-hmC measured is high in brain, liver, kidney and colorectal tissues (0.40–0.65%), while it is relatively low in lung (0.18%) and very low in heart, breast, and placenta (0.05-0.06%). Abundance of 5-hmC in the cancerous colorectal tissues was significantly reduced (0.02–0.06%) compared to that in normal colorectal tissues (0.46–0.57%). Our results showed for the first time that 5-hmC distribution is tissue dependent in human tissues and its abundance could be changed in the diseased states such as colorectal cancer.

her PhD at the University of Alberta studying white matter pathology in epilepsy. SUMMARYObjective: Brain imaging studies have shown widespread structural abnormalities in patients with temporal lobe epilepsy (TLE) within and beyond the affected temporal lobe, suggesting an altered network. Graph theoretical analysis based on white matter tractography has provided a new perspective to evaluate the connectivity of the brain. The alterations in the topologic properties of a whole brain white matter network in patients with TLE remain unknown. The purpose of this study was to examine the white matter network in a cohort of patients with left TLE and mesial temporal sclerosis (mTLE) compared to healthy controls. Methods: Anatomic brain networks of 16 patients with left mTLE were compared to those of 21 healthy controls. A white matter structural network was constructed from diffusion tensor tractography for each participant, and network parameters were compared between the patient and control groups. Results: Patients with left mTLE exhibited concurrent decreases of global and local efficiencies and widespread reduction of regional efficiency in ipsilateral temporal, bilateral frontal, and bilateral parietal areas. Communication hubs, such as the left precuneus, were also altered in patients with mTLE compared to controls. Significance: Our results demonstrate white matter network disruption in patients with left mTLE, supporting the notion that mTLE is a systemic brain disorder. KEY WORDS: Diffusion tensor imaging, Graph theory, Temporal lobe epilepsy, Network, Tractography, Diffusion tensor imaging.Temporal lobe epilepsy (TLE) is the most common focal epilepsy syndrome. Most TLE cases are associated with mesial temporal sclerosis (MTS), where hippocampal atrophy and/or T2 hyperintensity is observed on magnetic resonance imaging (MRI). Recently, quantitative MRI studies have provided new structural information in TLE by demonstrating extensive abnormalities within and beyond the temporal lobe, including reduced gray matter concentration/atrophy, 1 decreased cortical thickness, 2 and abnormal white matter in the temporal, frontal, and parietal lobes. The language and memory impairments seen in patients with TLE have also been related to altered blood oxygen level-dependent (BOLD) activation during memory and language tasks compared to healthy controls in functional MRI (fMRI) studies. 4 The growing knowledge of the brain structural and functional changes related to TLE has led to the notion that TLE is a network disorder that affects large neural networks involved in normal brain function.5 With the implementation of graph theoretical analysis on brain functional and structural measurements, features of the brain as an integrated system can be quantified to infer its capacity of information integration and segregation. 6 Graph theoretical analysis enables the abstraction and examination of the brain topologic architecture and properties at the network level, which provides a macroscopic perspective rather than the p...

This meta-analysis revealed that maternal vitamin D insufficiency is associated with increased risk of gestational diabetes.

Background Ischemic stroke is the second leading cause of death globally. The narrow time window for administering effective thrombolytic therapy motivates the search for alternative prevention strategies. Microglia and astrocyte activation-mediated inflammation play a pivotal role in ischemic stroke injury. Cottonseed oil (CSO) has been shown to exert anti-inflammatory effects against peripheral tissue injury, although CSO is mostly used as a solvent for lipid-soluble drugs. However, the role of CSO in neuroprotection against stroke has not been previously reported. Methods We treated adult male rats with CSO (1.3 ml/kg, subcutaneous injection, once every other day for 3 weeks) and then constructed a middle cerebral artery occlusion (MCAO) model followed by 24 h of reperfusion. Then, we measured the neurological scores, infarction volume, neuronal injury, and brain edema; we also measured the levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), degree of microglial and astrocytic activation, protein expression levels of Toll-like receptor 4 (TLR4), nuclear factor kappa B (NF-κB), C3d and S100A10, and the presence of A1 type astrocytes and A2 type astrocytes. Results We found that CSO treatment significantly improved the neurological deficit, reduced infarction volume, and alleviated neuronal injuries, blood–brain barrier (BBB) disruption, and brain edema. Additionally, CSO treatment significantly reduced microglial and astrocytic activation, inhibited TLR4 and NF-κB protein expression, and reduced the release of IL-1β, IL-6, and TNF-α. Finally, CSO treatment significantly decreased the number of C3d/glial fibrillary acidic protein (GFAP)-positive cells and C3d protein expression, and increased the number of S100A10/GFAP-positive cells and S100A10 protein expression. Conclusion Our results first found that CSO treatment alleviated ischemic stroke injury by reducing microglial and astrocytic activation and inflammation, which was related to the inhibition of TLR4/NF-κB pathway and the reduction of A1 phenotype neurotoxic astrocyte activation, suggesting that CSO could be a new strategy in the prevention of ischemic stroke.

Systemic administration of anti-sclerostin antibodies might be a useful strategy in total joint replacement when bone mass is deficient.