Promoting contraceptive use among unmarried female migrants in one factory in Shanghai: a pilot workplace intervention

<p>Abstract</p> <p>Background</p> <p>In urban China, more single women are becoming pregnant and resorting to induced abortion, despite the wide availability of temporary methods of contraception. We developed and piloted a workplace-based intervention to promote contraceptive use in unmarried female migrants working in privately owned factories.</p> <p>Methods</p> <p>Quasi-experimental design. In consultation with clients, we developed a workplace based intervention to promote contraception use in unmarried female migrants in a privately owned factory. We then implemented this in one factory, using a controlled before-and-after design. The intervention included lectures, bespoke information leaflets, and support to the factory doctors in providing a contraceptive service.</p> <p>Results</p> <p>598 women participated: most were under 25, migrants to the city, with high school education. Twenty percent were lost when staff were made redundant, and implementation was logistically complicated. All women attended the initial lecture, and just over half the second lecture. Most reported reading the educational material provided (73%), but very few women reported using the free family planning services offered at the factory clinic (5%) or the Family Planning Institute (3%). At baseline, 90% (N = 539) stated that contraceptives were required if having sex before marriage; of those reporting sex in the last three months, the majority reporting using contraceptives (78%, 62/79) but condom use was low (44%, 35/79).</p> <p>Qualitative data showed that the reading material seemed to be popular and young women expressed a need for more specific reproductive health information, particularly on HIV/AIDS. Women wanted services with some privacy and anonymity, and views on the factory service were mixed.</p> <p>Conclusion</p> <p>Implementing a complex intervention with a hard to reach population through a factory in China, using a quasi-experimental design, is not easy. Further research should focus on the specific needs and service preferences of this population and these should be considered in any policy reform so that contraceptive use may be encouraged among young urban migrant workers.</p

Electronic Origin of High Temperature Superconductivity in Single-Layer FeSe Superconductor

The latest discovery of high temperature superconductivity signature in single-layer FeSe is significant because it is possible to break the superconducting critical temperature ceiling (maximum Tc~55 K) that has been stagnant since the discovery of Fe-based superconductivity in 2008. It also blows the superconductivity community by surprise because such a high Tc is unexpected in FeSe system with the bulk FeSe exhibiting a Tc at only 8 K at ambient pressure which can be enhanced to 38 K under high pressure. The Tc is still unusually high even considering the newly-discovered intercalated FeSe system A_xFe_{2-y}Se_2 (A=K, Cs, Rb and Tl) with a Tc at 32 K at ambient pressure and possible Tc near 48 K under high pressure. Particularly interesting is that such a high temperature superconductivity occurs in a single-layer FeSe system that is considered as a key building block of the Fe-based superconductors. Understanding the origin of high temperature superconductivity in such a strictly two-dimensional FeSe system is crucial to understanding the superconductivity mechanism in Fe-based superconductors in particular, and providing key insights on how to achieve high temperature superconductivity in general. Here we report distinct electronic structure associated with the single-layer FeSe superconductor. Its Fermi surface topology is different from other Fe-based superconductors; it consists only of electron pockets near the zone corner without indication of any Fermi surface around the zone center. Our observation of large and nearly isotropic superconducting gap in this strictly two-dimensional system rules out existence of node in the superconducting gap. These results have provided an unambiguous case that such a unique electronic structure is favorable for realizing high temperature superconductivity

Transgenic Expression of Entire Hepatitis B Virus in Mice Induces Hepatocarcinogenesis Independent of Chronic Liver Injury

Hepatocellular carcinoma (HCC), the third leading cause of cancer deaths worldwide, is most commonly caused by chronic hepatitis B virus (HBV) infection. However, whether HBV plays any direct role in carcinogenesis, other than indirectly causing chronic liver injury by inciting the host immune response, remains unclear. We have established two independent transgenic mouse lines expressing the complete genome of a mutant HBV (“preS2 mutant”) that is found at much higher frequencies in people with HCC than those without. The transgenic mice show evidence of stress in the endoplasmic reticulum (ER) and overexpression of cyclin D1 in hepatocytes. These mice do not show any evidence of chronic liver injury, but by 2 years of age a majority of the male mice develop hepatocellular neoplasms, including HCC. Unexpectedly, we also found a significant increase in hepatocarcinogenesis independent of necroinflammation in a transgenic line expressing the entire wildtype HBV. As in the mutant HBV mice, HCC was found only in aged—2-year-old—mice of the wildtype HBV line. The karyotype in all the three transgenic lines appears normal and none of the integration sites of the HBV transgene in the mice is near an oncogene or tumor suppressor gene. The significant increase of HCC incidence in all the three transgenic lines—expressing either mutant or wildtype HBV—therefore argues strongly that in absence of chronic necroinflammation, HBV can contribute directly to the development of HCC

Phase Diagram and High Temperature Superconductivity at 65 K in Tuning Carrier Concentration of Single-Layer FeSe Films

Superconductivity in the cuprate superconductors and the Fe-based superconductors is realized by doping the parent compound with charge carriers, or by application of high pressure, to suppress the antiferromagnetic state. Such a rich phase diagram is important in understanding superconductivity mechanism and other physics in the Cu- and Fe-based high temperature superconductors. In this paper, we report a phase diagram in the single-layer FeSe films grown on SrTiO3 substrate by an annealing procedure to tune the charge carrier concentration over a wide range. A dramatic change of the band structure and Fermi surface is observed, with two distinct phases identified that are competing during the annealing process. Superconductivity with a record high transition temperature (Tc) at ~65 K is realized by optimizing the annealing process. The wide tunability of the system across different phases, and its high-Tc, make the single-layer FeSe film ideal not only to investigate the superconductivity physics and mechanism, but also to study novel quantum phenomena and for potential applications.Comment: 15 pages, 4 figure

Angiotensin II Facilitates Breast Cancer Cell Migration and Metastasis

Breast cancer metastasis is a leading cause of death by malignancy in women worldwide. Efforts are being made to further characterize the rate-limiting steps of cancer metastasis, i.e. extravasation of circulating tumor cells and colonization of secondary organs. In this study, we investigated whether angiotensin II, a major vasoactive peptide both produced locally and released in the bloodstream, may trigger activating signals that contribute to cancer cell extravasation and metastasis. We used an experimental in vivo model of cancer metastasis in which bioluminescent breast tumor cells (D3H2LN) were injected intra-cardiacally into nude mice in order to recapitulate the late and essential steps of metastatic dissemination. Real-time intravital imaging studies revealed that angiotensin II accelerates the formation of metastatic foci at secondary sites. Pre-treatment of cancer cells with the peptide increases the number of mice with metastases, as well as the number and size of metastases per mouse. In vitro, angiotensin II contributes to each sequential step of cancer metastasis by promoting cancer cell adhesion to endothelial cells, trans-endothelial migration and tumor cell migration across extracellular matrix. At the molecular level, a total of 102 genes differentially expressed following angiotensin II pre-treatment were identified by comparative DNA microarray. Angiotensin II regulates two groups of connected genes related to its precursor angiotensinogen. Among those, up-regulated MMP2/MMP9 and ICAM1 stand at the crossroad of a network of genes involved in cell adhesion, migration and invasion. Our data suggest that targeting angiotensin II production or action may represent a valuable therapeutic option to prevent metastatic progression of invasive breast tumors

Expression of Transient Receptor Potential Ankyrin 1 (TRPA1) and Its Role in Insulin Release from Rat Pancreatic Beta Cells

<div><h3>Objective</h3><p>Several transient receptor potential (TRP) channels are expressed in pancreatic beta cells and have been proposed to be involved in insulin secretion. However, the endogenous ligands for these channels are far from clear. Here, we demonstrate the expression of the transient receptor potential ankyrin 1 (TRPA1) ion channel in the pancreatic beta cells and its role in insulin release. TRPA1 is an attractive candidate for inducing insulin release because it is calcium permeable and is activated by molecules that are produced during oxidative glycolysis.</p> <h3>Methods</h3><p>Immunohistochemistry, RT-PCR, and Western blot techniques were used to determine the expression of TRPA1 channel. Ca²⁺ fluorescence imaging and electrophysiology (voltage- and current-clamp) techniques were used to study the channel properties. TRPA1-mediated insulin release was determined using ELISA.</p> <h3>Results</h3><p>TRPA1 is abundantly expressed in a rat pancreatic beta cell line and freshly isolated rat pancreatic beta cells, but not in pancreatic alpha cells. Activation of TRPA1 by allyl isothiocyanate (AITC), hydrogen peroxide (H₂O₂), 4-hydroxynonenal (4-HNE), and cyclopentenone prostaglandins (PGJ₂) and a novel agonist methylglyoxal (MG) induces membrane current, depolarization, and Ca²⁺ influx leading to generation of action potentials in a pancreatic beta cell line and primary cultured pancreatic beta cells. Activation of TRPA1 by agonists stimulates insulin release in pancreatic beta cells that can be inhibited by TRPA1 antagonists such as HC030031 or AP-18 and by RNA interference. TRPA1-mediated insulin release is also observed in conditions of voltage-gated Na⁺ and Ca²⁺ channel blockade as well as ATP sensitive potassium (K_ATP) channel activation.</p> <h3>Conclusions</h3><p>We propose that endogenous and exogenous ligands of TRPA1 cause Ca²⁺ influx and induce basal insulin release and that TRPA1-mediated depolarization acts synergistically with K_ATP channel blockade to facilitate insulin release.</p> </div

A Distinct Macrophage Population Mediates Metastatic Breast Cancer Cell Extravasation, Establishment and Growth

Background: The stromal microenvironment and particularly the macrophage component of primary tumors influence their malignant potential. However, at the metastatic site the role of these cells and their mechanism of actions for establishment and growth of metastases remain largely unknown. Methodology/Principal Findings: Using animal models of breast cancer metastasis, we show that a population of host macrophages displaying a distinct phenotype is recruited to extravasating pulmonary metastatic cells regardless of species of origin. Ablation of this macrophage population through three independent means (genetic and chemical) showed that these macrophages are required for efficient metastatic seeding and growth. Importantly, even after metastatic growth is established, ablation of this macrophage population inhibited subsequent growth. Furthermore, imaging of intact lungs revealed that macrophages are required for efficient tumor cell extravasation. Conclusion/Significance: These data indicate a direct enhancement of metastatic growth by macrophages through their effects on tumor cell extravasation, survival and subsequent growth and identifies these cells as a new therapeutic target fo

Histone deacetylases in viral infections

Chromatin remodeling and gene expression are regulated by histone deacetylases (HDACs) that condense the chromatin structure by deacetylating histones. HDACs comprise a group of enzymes that are responsible for the regulation of both cellular and viral genes at the transcriptional level. In mammals, a total of 18 HDACs have been identified and grouped into four classes, i.e., class I (HDACs 1, 2, 3, 8), class II (HDACs 4, 5, 6, 7, 9, 10), class III (Sirt1–Sirt7), and class IV (HDAC11). We review here the role of HDACs on viral replication and how HDAC inhibitors could potentially be used as new therapeutic tools in several viral infections

Advances, challenges and future directions for stem cell therapy in amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative condition where loss of motor neurons within the brain and spinal cord leads to muscle atrophy, weakness, paralysis and ultimately death within 3–5 years from onset of symptoms. The specific molecular mechanisms underlying the disease pathology are not fully understood and neuroprotective treatment options are minimally effective. In recent years, stem cell transplantation as a new therapy for ALS patients has been extensively investigated, becoming an intense and debated field of study. In several preclinical studies using the SOD1G93A mouse model of ALS, stem cells were demonstrated to be neuroprotective, effectively delayed disease onset and extended survival. Despite substantial improvements in stem cell technology and promising results in preclinical studies, several questions still remain unanswered, such as the identification of the most suitable and beneficial cell source, cell dose, route of delivery and therapeutic mechanisms. This review will cover publications in this field and comprehensively discuss advances, challenges and future direction regarding the therapeutic potential of stem cells in ALS, with a focus on mesenchymal stem cells. In summary, given their high proliferation activity, immunomodulation, multi-differentiation potential, and the capacity to secrete neuroprotective factors, adult mesenchymal stem cells represent a promising candidate for clinical translation. However, technical hurdles such as optimal dose, differentiation state, route of administration, and the underlying potential therapeutic mechanisms still need to be assessed