Transcranial direct current stimulation (tDCS) for working memory is an enticing treatment, but there is mixed evidence to date.

We tested the effects of electric field strength from uniform 2 mA dosing on working memory change from prestimulation to poststimulation. Second, we statistically evaluated a reverse-calculation method of individualizing tDCS dose and its effect on normalizing electric field at the cortex.

We performed electric field modeling on a dataset of 28 healthy older adults (15 women, mean age = 73.7, SD = 7.3) who received ten sessions of active 2 mA tDCS (N = 14) or sham tDCS (N = 14) applied over bilateral dorsolateral prefrontal cortices (DLPFC) in a triple-blind design. We evaluated the relationship between electric field strength and working memory change on an N-back task in conditions of above-median, high electric field from active 2 mA (N = 7), below-median, low electric field from active 2 mA (N = 7), and sham (N = 14) at regions of interest (ROI) at the left and right DLPF from uniform 2 mA doses appear to drive working memory improvements from tDCS. Individualized doses from reverse-calculation modeling significantly reduce electric field variance at the cortex. Taken together, using reverse-calculation modeling to produce the same, high electric fields at the cortex across participants may produce more effective future tDCS treatments for working memory.

In this study, we attempted to define the precise window of time for molar root elongation using a gain-of-function mutation of β-catenin model.

Both the control and constitutively activated β-catenin (CA-β-cat) mice received a one-time tamoxifen administration (for activation of β-catenin at newborn, postnatal day 3, or 5, or 7, or 9) and were harvested at the same stage of P21. Multiple approaches were used to define the window of time of postnatal tooth root formation.

In the early activation groups (tamoxifen induction at newborn, or P3 or P5), there was a lack of molar root elongation in the CA-β-cat mice. When induced at P7, the root length was slightly reduced at P21. However, the root length was essentially the same as that in the control when β-cat activated at P9. This study indicates that root elongation occurs in a narrow time of window, which is highly sensitive to a change of β-catenin levels. Molecular studies showed a drastic decrease in the levels of nuclear factor I-C (NFIC) and osterix (OSX), plus sharp reductions of odontoblast differentiation markers, including Nestin, dentin sialoprotein (DSP), and dentin matrix protein 1 (DMP1) at both mRNA and protein levels.

Murine molar root elongation is precisely regulated by the Wnt/β-catenin signaling within a narrow window of time (newborn to day 5).

Murine molar root elongation is precisely regulated by the Wnt/β-catenin signaling within a narrow window of time (newborn to day 5).In the past few years, the paramount role of cancer stem cells (CSCs), in terms of cancer initiation, proliferation, metastasis, invasion and chemoresistance, has been revealed by accumulating studies. However, this level of cellular plasticity cannot be entirely explained by genetic mutations. Research on epigenetic modifications as a complementary explanation for the properties of CSCs has been increasing over the past several years. Notably, therapeutic strategies are currently being developed in an effort to reverse aberrant epigenetic alterations using specific chemical inhibitors. In this review, we summarize the current understanding of CSCs and their role in cancer progression, and provide an overview of epigenetic alterations seen in CSCs. Importantly, we focus on primary cancer therapies that target the epigenetic modification of CSCs by the use of specific chemical inhibitors, such as histone deacetylase (HDAC) inhibitors, DNA methyltransferase (DNMT) inhibitors and microRNA-based (miRNA-based) therapeutics.

The possible contribution of head flexion posture while using a smartphone to the formation of “smartphone face,” is an increasing concern. Smartphone face describes the facial changes in a stooped posture receiving more gravitational pull on the jowl area.

In this study, we quantified facial sagging in different postural changes using a three-dimensional imaging technique.

Faces of 21 young (30.45±2.81yo, n=11) and old (59.50±3.37yo, n=10) Korean female subjects were scanned in different body postures including standing, supine, and head flexion (30°, 45°). The landmark displacements and volumetric changes in facial areas were assessed and correlated with skin elasticity. In addition, 22 Korean female subjects (45.45±3.81yo) were recruited to test the anti-gravity effect of facial cream A, which was formulated with Stem III complex™, for 8weeks.

The landmarks shifted inferior-laterally with the supine posture, while the upper face shifted more laterally and the lower face shifted more inferiorly. Ruboxistaurin in vivo With a head flexion posture, facial sagging occurred mainly toward the anterior direction with more prominent changes in the lower face. The changes were greater in the older group, and skin elasticity exhibited negative correlation with the shifting distances. A significant decrease in facial sagging was noted after an 8-week treatment of facial cream A.

The use of a three-dimensional imaging technique could accurately assess the gravity-induced facial changes in different postures. The head flexion posture particularly gives more gravitational pull to the lower face, which could contribute to the drooping jawline.

The use of a three-dimensional imaging technique could accurately assess the gravity-induced facial changes in different postures. The head flexion posture particularly gives more gravitational pull to the lower face, which could contribute to the drooping jawline.Maximal aerobic capacity (MAC) has been associated with preserved neural tissue or brain maintenance (BM) in healthy older adults, including the hippocampus. Amnestic mild cognitive impairment (aMCI) is considered a prodromal stage of Alzheimer’s disease. While aMCI is characterized by hippocampal deterioration, the MAC-hippocampal relationship in these patients is not well understood. In contrast to healthy individuals, neurocognitive protective effects in neurodegenerative populations have been associated with mechanisms of cognitive reserve (CR) altering the neuropathology-cognition relationship. We investigated the MAC-hippocampal relationship in aMCI (n = 29) from the perspectives of BM and CR mechanistic models with structural MRI and a memory fMRI paradigm using both group-level (higher-fit patients vs. lower-fit patients) and individual level (continuous correlation) approaches. While MAC was associated with smaller hippocampal volume, contradicting the BM model, higher-fit patients demonstrated statistically significant lower correlation between hippocampal volume and memory performance compared with the lower-fit patients, supporting the model of CR.