Is biological productivity enhanced at the New England shelfbreak front?

Author Posting. © American Geophysical Union, 2013. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research 118 (2013): 517–535, doi:10.1002/jgrc.20068.A two-dimensional (cross-shelf) numerical model of the mean seasonal circulation offshore of southern New England predicts upwelling at the shelfbreak front. Expected ramifications of this upwelling include enhancement of nutrient supply, phytoplankton biomass, and productivity. However, seasonal climatologies of chlorophyll based on both in situ data and satellite observations show no mean enhancement at the front. We investigate this apparent discrepancy with a four-component planktonic ecosystem model coupled to the two-dimensional physical model. Nutrient fields are restored to climatological values at depth, and upper ocean values evolve freely according to physical and biological forcing. Vertical diffusivity is based on seasonally averaged surface and bottom mixed layer depths compiled from in situ observations. The model reproduces the general pattern of the observed cross-shelf and seasonal variations of the chlorophyll distribution. It predicts a local enhancement of phytoplankton productivity at the shelfbreak in spring and summer as a result of the persistently upwelled nutrient-rich slope water. In the model, zooplankton grazing prevents accumulation of phytoplankton biomass at the site of the upwelling. The predicted enhancement of primary productivity (but not phytoplankton biomass) at the shelfbreak constitutes a hypothesis that could be tested in the future with suitable measurements from regional long-term observatories, such as the Ocean Observatories Initiative Pioneer Array.WGZ was supported by the Woods Hole Oceanographic Institution (WHOI) postdoctoral scholarship program, the WHOI Coastal Ocean Institute, and the National Science Foundation through grant OCE-1129125. DJM and GGG were supported by ONR grant N00014-06-1-0739. DJM gratefully acknowledges support of WHOI’s H. W. Jannasch Chair.2013-07-3

Properties of an equine herpesvirus 1 mutant devoid of the internal inverted repeat sequence of the genomic short region

AbstractThe 150kbp genome of equine herpesvirus-1 (EHV-1) is composed of a unique long (UL) region and a unique short (Us) segment, which is flanked by identical internal and terminal repeat (IR and TR) sequences of 12.7kbp. We constructed an EHV-1 lacking the entire IR (vL11ΔIR) and showed that the IR is dispensable for EHV-1 replication but that the vL11ΔIR exhibits a smaller plaque size and delayed growth kinetics. Western blot analyses of cells infected with vL11ΔIR showed that the synthesis of viral proteins encoded by the immediate-early, early, and late genes was reduced at immediate-early and early times, but by late stages of replication reached wild type levels. Intranasal infection of CBA mice revealed that the vL11ΔIR was significantly attenuated as mice infected with the vL11ΔIR showed a reduced lung viral titer and greater ability to survive infection compared to mice infected with parental or revertant virus

Inhibition of chemotherapy resistant breast cancer stem cells by a ROR1 specific antibody.

Breast cancers enduring treatment with chemotherapy may be enriched for cancer stem cells or tumor-initiating cells, which have an enhanced capacity for self-renewal, tumor initiation, and/or metastasis. Breast cancer cells that express the type I tyrosine kinaselike orphan receptor ROR1 also may have such features. Here we find that the expression of ROR1 increased in breast cancer cells following treatment with chemotherapy, which also enhanced expression of genes induced by the activation of Rho-GTPases, Hippo-YAP/TAZ, or B lymphoma Mo-MLV insertion region 1 homolog (BMI1). Expression of ROR1 also enhanced the capacity of breast cancer cells to invade Matrigel, form spheroids, engraft in Rag2-/-[Formula: see text] mice, or survive treatment with paclitaxel. Treatment of mice bearing breast cancer patient-derived xenografts (PDXs) with the humanized anti-ROR1 monoclonal antibody cirmtuzumab repressed expression of genes associated with breast cancer stemness, reduced activation of Rho-GTPases, Hippo-YAP/TAZ, or BMI1, and impaired the capacity of breast cancer PDXs to metastasize or reengraft Rag2-/-[Formula: see text] mice. Finally, treatment of PDX-bearing mice with cirmtuzumab and paclitaxel was more effective than treatment with either alone in eradicating breast cancer PDXs. These results indicate that targeting ROR1 may improve the response to chemotherapy of patients with breast cancer

The early UL3 gene of equine herpesvirus-1 encodes a tegument protein not essential for replication or virulence in the mouse

AbstractThe UL3 gene of equine herpesvirus-1 (EHV-1) is retained in the genome of defective interfering particles and encodes a ~33kDa myristylated protein. Further characterization showed that the UL3 gene is trans-activated only by the sole immediate early (IE) protein and encodes an early protein that is dispensable for EHV-1 replication and localizes in the tegument of purified virions. UL3-deleted EHV-1 (vL11ΔUL3) exhibits properties of host cell tropism, plaque size, and growth kinetics similar to those of the parental virus. Expression levels of EHV-1 proteins representative of all three gene classes in vL11ΔUL3-infected cells were identical to those in cells infected with parental virus. Mice intranasally infected with vL11ΔUL3 and parental virus showed no significant difference in mortality or virus lung titers. These findings suggest that the UL3 protein does not play a major role in the biology of EHV-1 in cell culture or virulence in the mouse

Need for and Access to Health Care and Medicines: Are There Gender Inequities?

Objective: Differences between women and men in political and economic empowerment, education, and health risks are well-documented. Similar gender inequities in access to care and medicines have been hypothesized but evidence is lacking. Methods: We analyzed 2002 World Health Survey data for 257,922 adult respondents and 80,932 children less than 5 years old from 53 mostly low and middle-income countries. We constructed indicators of need for, access to, and perceptions of care, and we described the number of countries with equal and statistically different proportions of women and men for each indicator. Using multivariate logistic regression models, we estimated effects of gender on our study outcomes, overall and by household poverty. Findings: Women reported significantly more need for care for three of six chronic conditions surveyed, and they were more likely to have at least one of the conditions (OR 1.41 [95% CI 1.38, 1.44]). Among those with reported need for care, there were no consistent differences in access to care between women and men overall (e.g., treatment for all reported chronic conditions, OR 1.00 [0.96, 1.04]) or by household poverty. Of concern, access to care for chronic conditions was distressingly low among both men and women in many countries, as was access to preventive services among boys and girls less than 5 years old. Conclusions: These cross-country results do not suggest a systematic disadvantage of women in access to curative care and medicines for treating selected chronic conditions or acute symptoms, or to preventive services among boys and girls

Increasing Throughput in Wireless Communications by Grouping Similar Bits

This letter proposes and studies a technique for grouping the bits transmitted through a wireless channel into codewords according to their quality (SNR). It proves that splitting the bits into multiple codewords of different rates provides a higher throughput than mixing heterogeneous quality bits into fixed-rate codewords. The letter first analyzes the pros and cons of different mappings of bits and codewords to the available time, frequency, and modulation resources. Then it describes the proposed scheme for a 16-QAM modulation and illustrates its benefits through simulations. Finally, it provides a mathematical proof of its superiority in a binary-input parallel AWGN channel with finite length error correcting codes. The proposed scheme can be applied to any communications channel using error correcting codes (ECC), but it is of particular interest for millimeter-wave (mmWave) wireless communications, where the channel quality is closely monitored and high order modulations are used over wide bandwidths. The simulations suggest that modest gains in throughput can be obtained with negligible additional complexity

Hospital Readmissions Reduction Program: An Economic and Operational Analysis

The Hospital Readmissions Reduction Program (HRRP), a part of the U.S. Patient Protection and Affordable Care Act, requires the Centers for Medicare and Medicaid Services to penalize hospitals with excess readmissions. We take an economic and operational (patient flow) perspective to analyze the effectiveness of this policy in encouraging hospitals to reduce readmissions. We develop a game-theoretic model that captures the competition among hospitals inherent in HRRP’s benchmarking mechanism. We show that this competition can be counterproductive: it increases the number of nonincentivized hospitals, which prefer paying penalties over reducing readmissions in any equilibrium. We calibrate our model with a data set of more than 3,000 hospitals in the United States and show that under the current policy, and for a large set of parameters, 4%–13% of the hospitals remain nonincentivized to reduce readmissions. We also validate our model against the actual performance of hospitals in the three years since the introduction of the policy. We draw several policy recommendations to improve this policy’s outcome. For example, localizing the benchmarking process—comparing hospitals against similar peers—improves the performance of the policy

Coronavirus disease 2019 among pregnant Chinese women : case series data on the safety of vaginal birth and breastfeeding

Funding Information: National Key Research and Development Program of China. Grant Numbers: 2016YFC1000203, 2018YFC1002804Peer reviewedPublisher PD