Ultrafast Charge Transfer at a Quantum Dot/2D Materials Interface Probed by Second Harmonic Generation

Hybrid quantum dot (QD) / transition metal dichalcogenide (TMD) heterostructures are attractive components of next generation optoelectronic devices, which take advantage of the spectral tunability of QDs and the charge and exciton transport properties of TMDs. Here, we demonstrate tunable electronic coupling between CdSe QDs and monolayer WS$_2$ using variable length alkanethiol ligands on the QD surface. Using femtosecond time-resolved second harmonic generation (SHG) microscopy, we show that electron transfer from photoexcited CdSe QDs to single-layer WS$_2$ occurs on ultrafast (50 fs - 1 ps) timescales. Moreover, in the samples exhibiting the fastest charge transfer rates ($\leq$ 50 fs) we observed oscillations in the time-domain signal corresponding to an acoustic phonon mode of the donor QD, which coherently modulates the SHG response of the underlying WS$_2$ layer. These results reveal surprisingly strong electronic coupling at the QD/TMD interface and demonstrate the usefulness of time-resolved SHG for exploring ultrafast electronic-vibrational dynamics in TMD heterostructures

A genetic basis for a postmeiotic X versus Y chromosome intragenomic conflict in the mouse.

Intragenomic conflicts arise when a genetic element favours its own transmission to the detriment of others. Conflicts over sex chromosome transmission are expected to have influenced genome structure, gene regulation, and speciation. In the mouse, the existence of an intragenomic conflict between X- and Y-linked multicopy genes has long been suggested but never demonstrated. The Y-encoded multicopy gene Sly has been shown to have a predominant role in the epigenetic repression of post meiotic sex chromatin (PMSC) and, as such, represses X and Y genes, among which are its X-linked homologs Slx and Slxl1. Here, we produced mice that are deficient for both Sly and Slx/Slxl1 and observed that Slx/Slxl1 has an opposite role to that of Sly, in that it stimulates XY gene expression in spermatids. Slx/Slxl1 deficiency rescues the sperm differentiation defects and near sterility caused by Sly deficiency and vice versa. Slx/Slxl1 deficiency also causes a sex ratio distortion towards the production of male offspring that is corrected by Sly deficiency. All in all, our data show that Slx/Slxl1 and Sly have antagonistic effects during sperm differentiation and are involved in a postmeiotic intragenomic conflict that causes segregation distortion and male sterility. This is undoubtedly what drove the massive gene amplification on the mouse X and Y chromosomes. It may also be at the basis of cases of F1 male hybrid sterility where the balance between Slx/Slxl1 and Sly copy number, and therefore expression, is disrupted. To the best of our knowledge, our work is the first demonstration of a competition occurring between X and Y related genes in mammals. It also provides a biological basis for the concept that intragenomic conflict is an important evolutionary force which impacts on gene expression, genome structure, and speciation

Recall errors in a weekly survey of diarrhoea in Guatemala: determining the optimal length of recall

We measured the recall error, optimal recall length and factors associated with diarrhoea in a weekly survey. Data was taken from a year-long randomized controlled trial in which characteristics of diarrhoeal episodes were recorded weekly. We labelled the recall period as days 1-6, day I being the day before the visit. Recall error was the percentage difference between the number of episodes reported to begin on a particular day and the mean for days I and 2. Generalized estimating equations were used to determine associations. Recall error was 37% on day 3 and 51% on day 5. The error was less in younger children (by 10%), severe episodes (by 29%) and when blood was present in the stool (by 18%). Diarrhoea was underreported when the recall period extended beyond 2 days. Surveys that use longer recall periods risk underestimating diarrhoea incidence and selectively capturing more severe episodes

The multicopy gene Sly represses the sex chromosomes in the male mouse germline after meiosis.

Studies of mice with Y chromosome long arm deficiencies suggest that the male-specific region (MSYq) encodes information required for sperm differentiation and postmeiotic sex chromatin repression (PSCR). Several genes have been identified on MSYq, but because they are present in more than 40 copies each, their functions cannot be investigated using traditional gene targeting. Here, we generate transgenic mice producing small interfering RNAs that specifically target the transcripts of the MSYq-encoded multicopy gene Sly (Sycp3-like Y-linked). Microarray analyses performed on these Sly-deficient males and on MSYq-deficient males show a remarkable up-regulation of sex chromosome genes in spermatids. SLY protein colocalizes with the X and Y chromatin in spermatids of normal males, and Sly deficiency leads to defective repressive marks on the sex chromatin, such as reduced levels of the heterochromatin protein CBX1 and of histone H3 methylated at lysine 9. Sly-deficient mice, just like MSYq-deficient mice, have severe impairment of sperm differentiation and are near sterile. We propose that their spermiogenesis phenotype is a consequence of the change in spermatid gene expression following Sly deficiency. To our knowledge, this is the first successful targeted disruption of the function of a multicopy gene (or of any Y gene). It shows that SLY has a predominant role in PSCR, either via direct interaction with the spermatid sex chromatin or via interaction with sex chromatin protein partners. Sly deficiency is the major underlying cause of the spectrum of anomalies identified 17 y ago in MSYq-deficient males. Our results also suggest that the expansion of sex-linked spermatid-expressed genes in mouse is a consequence of the enhancement of PSCR that accompanies Sly amplification

Higher Serum Vitamin D Concentration Is Associated with Better Balance in Older Adults with Supra-Optimal Vitamin D Status

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Transcriptional changes in response to X chromosome dosage in the mouse: implications for X inactivation and the molecular basis of Turner Syndrome.

BACKGROUND: X monosomic mice (39,XO) have a remarkably mild phenotype when compared to women with Turner syndrome (45,XO). The generally accepted hypothesis to explain this discrepancy is that the number of genes on the mouse X chromosome which escape X inactivation, and thus are expressed at higher levels in females, is very small. However this hypothesis has never been tested and only a small number of genes have been assayed for their X-inactivation status in the mouse. We performed a global expression analysis in four somatic tissues (brain, liver, kidney and muscle) of adult 40,XX and 39,XO mice using the Illumina Mouse WG-6 v1_1 Expression BeadChip and an extensive validation by quantitative real time PCR, in order to identify which genes are expressed from both X chromosomes. RESULTS: We identified several genes on the X chromosome which are overexpressed in XX females, including those previously reported as escaping X inactivation, as well as new candidates. However, the results obtained by microarray and qPCR were not fully concordant, illustrating the difficulty in ascertaining modest fold changes, such as those expected for genes escaping X inactivation. Remarkably, considerable variation was observed between tissues, suggesting that inactivation patterns may be tissue-dependent. Our analysis also exposed several autosomal genes involved in mitochondrial metabolism and in protein translation which are differentially expressed between XX and XO mice, revealing secondary transcriptional changes to the alteration in X chromosome dosage. CONCLUSIONS: Our results support the prediction that the mouse inactive X chromosome is largely silent, while providing a list of the genes potentially escaping X inactivation in rodents. Although the lower expression of X-linked genes in XO mice may not be relevant in the particular tissues/systems which are affected in human X chromosome monosomy, genes deregulated in XO mice are good candidates for further study in an involvement in Turner Syndrome phenotype.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

mTORC2 signaling drives the development and progression of pancreatic cancer

mTOR signaling controls several critical cellular functions and is deregulated in many cancers, including pancreatic cancer. To date, most efforts have focused on inhibiting the mTORC1 complex. However, clinical trials of mTORC1 inhibitors in pancreatic cancer have failed, raising questions about this therapeutic approach. We employed a genetic approach to delete the obligate mTORC2 subunit Rictor and identified the critical times during which tumorigenesis requires mTORC2 signaling. Rictor deletion resulted in profoundly delayed tumorigenesis. Whereas previous studies showed most pancreatic tumors were insensitive to rapamycin, treatment with a dual mTORC1/2 inhibitor strongly suppressed tumorigenesis. In late-stage tumor-bearing mice, combined mTORC1/2 and PI3K inhibition significantly increased survival. Thus, targeting mTOR may be a potential therapeutic strategy in pancreatic cancer

Thermal-Hydrodynamic Characteristics of Turbulent Flow in Corrugated Channels

The heat transfer-flow characteristics of turbulent flow inside corrugated channels heated by constant heat flux are numerically investigated. The rate of heat transfer, pressure drop, and performance evaluation criterion is determined for smooth channel and various designs of corrugated channels at the Reynolds number ranged from 5000 to 60,000. The effect of rib arrangement distributions of inward, outward, and inward-outward ribs are examined. The various rib configurations of corrugated channels are also tested. In addition, the influences of rib roughness parameters (height, pitch, and width) and rib shapes (semicircular, trapezoidal, and rectangular) are researched. The Reynolds-averaged Navier-Stokes equations (RANS) are used to model the governing flow equations. The computational model is validated through a reasonable agreement between the present numerical results and the outcomes of related works. For different geometrical and operating conditions, the results revealed that the rate of heat exchange in corrugated channels exceeds higher than that of smooth ones but with additional pressure loss. Moreover, the rib arrangements, rib configuration, and rib roughness parameters exhibit a relatively significant effect on the performance of the corrugated channels. On the other hand, the influence of the rib shapes seems to be small