511 research outputs found
Topological and magnetic phases of interacting electrons in the pyrochlore iridates
We construct a model for interacting electrons with strong spin orbit
coupling in the pyrochlore iridates. We establish the importance of the direct
hopping process between the Ir atoms and use the relative strength of the
direct and indirect hopping as a generic tuning parameter to study the
correlation effects across the iridates family. We predict novel quantum phase
transitions between conventional and/or topologically non-trivial phases. At
weak coupling, we find topological insulator and metallic phases. As one
increases the interaction strength, various magnetic orders emerge. The
topological Weyl semi-metal phase is found to be realized in these different
orders, one of them being the all-in/all-out pattern. Our findings establish
the possible magnetic ground states for the iridates and suggest the generic
presence of the Weyl semi-metal phase in correlated magnetic insulators on the
pyrochlore lattice. We discus the implications for existing and future
experiments.Comment: 6 pages, 5 figs. as published in PR
Insulin Resistance Does Not Impair Mechanical Overload-Stimulated Glucose Uptake, but Does Alter the Metabolic Fate of Glucose in Mouse Muscle
Skeletal muscle glucose uptake and glucose metabolism are impaired in insulin resistance. Mechanical overload stimulates glucose uptake into insulin-resistant muscle; yet the mechanisms underlying this beneficial effect remain poorly understood. This study examined whether a differential partitioning of glucose metabolism is part of the mechanosensitive mechanism underlying overload-stimulated glucose uptake in insulin-resistant muscle. Mice were fed a high-fat diet to induce insulin resistance. Plantaris muscle overload was induced by unilateral synergist ablation. After 5 days, muscles were excised for the following measurements: (1) [3H]-2-deoxyglucose uptake; (2) glycogen; 3) [5-3H]-glucose flux through glycolysis; (4) lactate secretion; (5) metabolites; and (6) immunoblots. Overload increased glucose uptake ~80% in both insulin-sensitive and insulin-resistant muscles. Overload increased glycogen content ~20% and this was enhanced to ~40% in the insulin-resistant muscle. Overload did not alter glycolytic flux, but did increase muscle lactate secretion 40–50%. In both insulin-sensitive and insulin-resistant muscles, overload increased 6-phosphogluconate levels ~150% and decreased NADP:NADPH ~60%, indicating pentose phosphate pathway activation. Overload increased protein O-GlcNAcylation ~45% and this was enhanced to ~55% in the insulin-resistant muscle, indicating hexosamine pathway activation. In conclusion, insulin resistance does not impair mechanical overload-stimulated glucose uptake but does alter the metabolic fate of glucose in muscle
VISEM-Tracking, a human spermatozoa tracking dataset
A manual assessment of sperm motility requires microscopy observation, which
is challenging due to the fast-moving spermatozoa in the field of view. To
obtain correct results, manual evaluation requires extensive training.
Therefore, computer-assisted sperm analysis (CASA) has become increasingly used
in clinics. Despite this, more data is needed to train supervised machine
learning approaches in order to improve accuracy and reliability in the
assessment of sperm motility and kinematics. In this regard, we provide a
dataset called VISEM-Tracking with 20 video recordings of 30 seconds
(comprising 29,196 frames) of wet sperm preparations with manually annotated
bounding-box coordinates and a set of sperm characteristics analyzed by experts
in the domain. In addition to the annotated data, we provide unlabeled video
clips for easy-to-use access and analysis of the data via methods such as self-
or unsupervised learning. As part of this paper, we present baseline sperm
detection performances using the YOLOv5 deep learning (DL) model trained on the
VISEM-Tracking dataset. As a result, we show that the dataset can be used to
train complex DL models to analyze spermatozoa
Impacts of Openness
This is the recording from the Impacts of Openness lightning talk session that was held on Friday, October 25, 2013, from 10:00 a.m. - noon in Watson Library, room 455 during the KU Libraries' celebration of Open Access Week.This event brings together several speakers from a variety of fields, each of whom will give a 10-minute presentation about the impact of openness in their work. More information about this event is available at http://openaccess.ku.edu/impacts-openness-lightning-talks-october-25
Short-term, high-fat diet accelerates disuse atrophy and protein degradation in a muscle-specific manner in mice
Background:
A short-term high-fat diet impairs mitochondrial function and the ability of skeletal muscle to respond to growth stimuli, but it is unknown whether such a diet alters the ability to respond to atrophy signals. The purpose of this study was to determine whether rapid weigh gain induced by a high-fat (HF) diet accelerates denervation-induced muscle atrophy.
Methods:
Adult, male mice (C57BL/6) were fed a control or HF (60Â % calories as fat) diet for 3Â weeks (3wHF). Sciatic nerve was sectioned unilaterally for the final 5 or 14Â days of the diet. Soleus and extensor digitorum longus (EDL) muscles were removed and incubated in vitro to determine rates of protein degradation and subsequently homogenized for determination of protein levels of LC3, ubiquitination, myosin heavy chain (MHC) distribution, and mitochondrial subunits.
Results:
When mice were fed the 3wHF diet, whole-body fat mass more than doubled, but basal (innervated) muscle weights, rates of protein degradation, LC3 content, mitochondrial protein content, and myosin isoform distribution were not significantly different than with the control diet in either soleus or EDL. However in the 14Â day denervated soleus, the 3wHF diet significantly augmented loss of mass, proteolysis rate, amount of the autophagosome marker LC3 II, and the amount of overall ubiquitination as compared to the control fed mice. On the contrary, the 3wHF diet had no significant effect in the EDL on amount of mass loss, proteolysis rate, LC3 levels, or ubiquitination. Fourteen days denervation also induced a loss of mitochondrial proteins in the soleus but not the EDL, regardless of the diet.
Conclusions:
Taken together, a short-term, high-fat diet augments denervation muscle atrophy by induction of protein degradation in the mitochondria-rich soleus but not in the glycolytic EDL. These findings suggest that the denervation-induced loss of mitochondria and HF diet-induced impairment of mitochondrial function may combine to promote skeletal muscle atrophy
Constitutively Active CaMKKα Stimulates Skeletal Muscle Glucose Uptake in Insulin-Resistant Mice In Vivo
In insulin-sensitive skeletal muscle, the expression of constitutively active Ca(2+)/calmodulin-dependent protein kinase kinase α (caCaMKKα) stimulates glucose uptake independent of insulin signaling (i.e., Akt and Akt-dependent TBC1D1/TBC1D4 phosphorylation). Our objectives were to determine whether caCaMKKα could stimulate glucose uptake additively with insulin in insulin-sensitive muscle, in the basal state in insulin-resistant muscle, and if so, to determine whether the effects were associated with altered TBC1D1/TBC1D4 phosphorylation. Mice were fed a control or high-fat diet (60% kcal) for 12 weeks to induce insulin resistance. Muscles were transfected with empty vector or caCaMKKα plasmids using in vivo electroporation. After 2 weeks, caCaMKKα protein was robustly expressed. In insulin-sensitive muscle, caCaMKKα increased basal in vivo [(3)H]-2-deoxyglucose uptake approximately twofold, insulin increased glucose uptake approximately twofold, and caCaMKKα plus insulin increased glucose uptake approximately fourfold. caCaMKKα did not increase basal TBC1D1 (Ser(237), Thr(590), Ser(660), pan-Thr/Ser) or TBC1D4 (Ser(588), Thr(642), pan-Thr/Ser) phosphorylation. In insulin-resistant muscle, caCaMKKα increased basal glucose uptake approximately twofold, and attenuated high-fat diet–induced basal TBC1D1 (Thr(590), pan-Thr/Ser) and TBC1D4 (Ser(588), Thr(642), pan-Thr/Ser) phosphorylation. In cell-free assays, CaMKKα increased TBC1D1 (Thr(590), pan-Thr/Ser) and TBC1D4 (Ser(588), pan-Thr/Ser) phosphorylation. Collectively, these results demonstrate that caCaMKKα stimulates glucose uptake additively with insulin, and in insulin-resistant muscle, and alters the phosphorylation of TBC1D1/TBC1D4
Regulation of Skeletal Muscle Glucose Transport and Glucose Metabolism by Exercise Training
Aerobic exercise training and resistance exercise training are both well-known for their ability to improve human health; especially in individuals with type 2 diabetes. However, there are critical differences between these two main forms of exercise training and the adaptations that they induce in the body that may account for their beneficial effects. This article reviews the literature and highlights key gaps in our current understanding of the effects of aerobic and resistance exercise training on the regulation of systemic glucose homeostasis, skeletal muscle glucose transport and skeletal muscle glucose metabolism
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