A retrospective, comparative, clinical study of occlusion rate of peripherally inserted central catheters fabricated of poly(vinyl alcohol)-based hydrogel composite.

Thrombotic accumulation is associated with surface interactions between blood proteins and vascular access devices. Catheter occlusion results from this process, and is a costly, common, occurrence with peripherally inserted central catheters (PICCs). Hydrophilic catheter materials exhibit antithrombotic properties.

Let's Match: Making Cannabis Policy Guided by Research.

Purpose: The growth and increasing sophistication of the legal cannabis industry necessitates further scientific inquiry to establish an evidence-based policy path forward. However, policymakers must balance public demand for cannabis reform with the lack of scientific consensus on key issues. This Commentary discusses Massachusetts' statutory provisions supporting cannabis research, advances in social equity driven by data, and critical policy issues, which invite questions without clear scientific answers.

Assessment of Fungicide Resistance via Molecular Assay in Populations of , Causal Agent of Apple Powdery Mildew, in New York.

, causal agent of apple powdery mildew, is a pathogen endemic worldwide where apples are produced. In the absence of durable host resistance, the disease is most effectively managed in conventional orchards with single-site fungicides. In New York State, increasingly erratic precipitation patterns and warmer temperatures due to climate change may create a regional environment more conducive to apple powdery mildew development and spread.

Trackability of a high-strength thromboresistant hydrogel catheter: An In vitro analysis comparing venous catheter forces in a simulated use pathway.

As the need for vascular access devices (VADs) continues to increase, so does the need for innovative designs and materials that can improve placement and optimize patient outcomes. Commercially available peripherally inserted central venous catheters (PICCs) are in high demand due to their ease of use and low cost. However, they are constructed of materials that can contribute to vascular injury and result in complications such as clotting, catheter failure, and infection.

Characterizations of an Emerging Disease: Apple Blotch Caused by (syn. ) in the Mid-Atlantic United States.

Apple orchards with minimal or reduced fungicide inputs in the Mid-Atlantic region of the United States have experienced outbreaks of severe premature defoliation with symptoms that matched those of apple blotch disease (ABD) caused by Fungal isolates obtained from symptomatic apple leaves and fruit produced uniform slow-growing, dark-gray colonies on peptone potato dextrose agar and had conidia. Internal transcribed spacer DNA sequences matched with and Koch's postulates were fulfilled when typical ABD symptoms occurred when reinoculated onto apple leaves and fruit. Spore dispersal in nonfungicide-treated orchards detected with quantitative PCR was low in early spring and dropped to undetectable levels in late May and early June before rising exponentially to highs in July and August, which coincided with symptom development.

Nuclear restriction of HIV-1 infection by SUN1.

Overexpression of the human Sad-1-Unc-84 homology protein 2 (SUN2) blocks HIV-1 infection in a capsid-dependent manner. In agreement, we showed that overexpression of SUN1 (Sad1 and UNC-84a) also blocks HIV-1 infection in a capsid-dependent manner. SUN2 and the related protein SUN1 are transmembrane proteins located in the inner membrane of the nuclear envelope.

'Honeycrisp' Bitter Pit Response to Rootstock and Region under Eastern New York Climatic Conditions.

There are still unknown factors at play in the causation of bitter pit in 'Honeycrisp' as well as in other apple varieties. To investigate some of these factors, we conducted a survey of 34 'Honeycrisp' orchard blocks distributed across two disparate production regions in eastern New York State, representing a variety of rootstocks, over three growing seasons. Weather, soil, horticultural traits, fruit quality traits, pick timing, leaf and peel minerals were evaluated for their impact on bitter pit (BP) incidence; factors were further evaluated for their interaction with region and rootstock.

Novel high-strength thromboresistant poly(vinyl alcohol)-based hydrogel for vascular access applications.

Adherence of proteins, cells, and microorganisms to the surface of biomaterials used for vascular access contribute to device failure by thrombosis, occlusions, and infections. Current technologies for inhibiting these complications are limited to coatings and additives that are limited in duration of efficacy and often induce adverse side effects. In this work, we developed a novel composite hydrogel structure comprising of a porous poly(vinyl alcohol) (PVA) that is impregnated with poly(acrylic acid) (PAA) and heat treated to create a physically cross-linked high-strength hydrogel material.

IFITM proteins inhibit placental syncytiotrophoblast formation and promote fetal demise.

Elevated levels of type I interferon (IFN) during pregnancy are associated with intrauterine growth retardation, preterm birth, and fetal demise through mechanisms that are not well understood. A critical step of placental development is the fusion of trophoblast cells into a multinucleated syncytiotrophoblast (ST) layer. Fusion is mediated by syncytins, proteins deriving from ancestral endogenous retroviral envelopes.

Xylosandrus germanus (Coleoptera: Curculionidae: Scolytinae) Occurrence, Fungal Associations, and Management Trials in New York Apple Orchards.

Xylosandrus germanus (Blandford) has caused increasing damage in high-density New York apple orchards since 2013, resulting in tree decline and death. We documented their occurrence and timing in > 50 orchards using ethanol-baited traps from 2014 to 2016. First captures ranged from 48 to 83 degree days (base 10 °C) from 1 January.

HIV Fusion in Dendritic Cells Occurs Mainly at the Surface and Is Limited by Low CD4 Levels.

HIV-1 poorly infects monocyte-derived dendritic cells (MDDCs). This is in large part due to SAMHD1, which restricts viral reverse transcription. Pseudotyping HIV-1 with vesicular stomatitis virus G protein (VSV-G) strongly enhances infection, suggesting that earlier steps of viral replication, including fusion, are also inefficient in MDDCs.

SUN2 Silencing Impairs CD4 T Cell Proliferation and Alters Sensitivity to HIV-1 Infection Independently of Cyclophilin A.

Linker of nucleoskeleton and cytoskeleton (LINC) complexes connect the nucleus to the cytoskeleton in eukaryotic cells. We previously reported that the overexpression of SUN2, an inner nuclear membrane protein and LINC complex component, inhibits HIV infection between the steps of reverse transcription and nuclear import in a capsid-specific manner. We also reported that SUN2 silencing does not modulate HIV infection in several cell lines.

Actin' on HIV: How Dendritic Cells Spread Infection.

Dendritic cells (DCs) capture HIV particles and transmit them to CD4 T cells. In a recent article published in Cell, Ménager and Littman (2016) perform an shRNA screen in DCs and find that actin nucleation and stabilization regulate HIV uptake and maintain the virus on membrane protrusions for efficient transfer.

Elimination of HIV-1-infected cells by broadly neutralizing antibodies.

The Fc region of HIV-1 Env-specific broadly neutralizing antibodies (bNAbs) is required for suppressing viraemia, through mechanisms which remain poorly understood. Here, we identify bNAbs that exert antibody-dependent cellular cytotoxicity (ADCC) in cell culture and kill HIV-1-infected lymphocytes through natural killer (NK) engagement. These antibodies target the CD4-binding site, the glycans/V3 and V1/V2 loops on gp120, or the gp41 moiety.

SUN2 Overexpression Deforms Nuclear Shape and Inhibits HIV.

Unlabelled: In a previous screen of putative interferon-stimulated genes, SUN2 was shown to inhibit HIV-1 infection in an uncharacterized manner. SUN2 is an inner nuclear membrane protein belonging to the linker of nucleoskeleton and cytoskeleton complex. We have analyzed here the role of SUN2 in HIV infection.

Fitness impaired drug resistant HIV-1 is not compromised in cell-to-cell transmission or establishment of and reactivation from latency.

Both the presence of latently infected cells and cell-to-cell viral transmission are means whereby HIV can partially evade the inhibitory activities of antiretroviral drugs. The clinical use of a novel integrase inhibitor, dolutegravir (DTG), has established hope that this compound may limit HIV persistence, since no treatment-naïve patient treated with DTG has yet developed resistance against this drug, even though a R263K substitution in integrase confers low-level resistance to this drug in tissue culture. Here, we have studied the impact of R263K on HIV replication capacity and the ability of HIV to establish or be reactivated from latency and/or spread through cell-to-cell transmission.

Latent HIV-1 can be reactivated by cellular superinfection in a Tat-dependent manner, which can lead to the emergence of multidrug-resistant recombinant viruses.

The HIV-1 latent reservoir represents an important source of genetic diversity that could contribute to viral evolution and multidrug resistance following latent virus reactivation. This could occur by superinfection of a latently infected cell. We asked whether latent viruses might be reactivated when their host cells are superinfected, and if so, whether they could contribute to the generation of recombinant viruses.

Productive entry of HIV-1 during cell-to-cell transmission via dynamin-dependent endocytosis.

HIV-1 can be transmitted as cell-free virus or via cell-to-cell contacts. Cell-to-cell transmission between CD4(+) T cells is the more efficient mode of transmission and is predominant in lymphoid tissue, where the majority of virus resides. Yet the cellular mechanisms underlying productive cell-to-cell transmission in uninfected target cells are unclear.

Cellular and molecular mechanisms involved in the establishment of HIV-1 latency.

Latently infected cells represent the major barrier to either a sterilizing or a functional HIV-1 cure. Multiple approaches to reactivation and depletion of the latent reservoir have been attempted clinically, but full depletion of this compartment remains a long-term goal. Compared to the mechanisms involved in the maintenance of HIV-1 latency and the pathways leading to viral reactivation, less is known about the establishment of latent infection.

Maraviroc and other HIV-1 entry inhibitors exhibit a class-specific redistribution effect that results in increased extracellular viral load.

HIV entry inhibitors, such as maraviroc (MVC), prevent cell-free viruses from entering the cells. In clinical trials, patients who were treated with MVC often displayed viral loads that were above the limit of conventional viral load detection compared to efavirenz-based regimens. We hypothesize that viruses blocked by entry inhibitors may be redistributed to plasma, where they artificially increase viral load measurements compared to those with the use of antiretroviral drugs (ARVs) that act intracellularly.

The viral protein Tat can inhibit the establishment of HIV-1 latency.

The establishment of HIV-1 latency can result from limiting levels of transcription initiation or elongation factors, restrictive chromatin modifications, transcriptional interference, and insufficient Tat activity. Since the viral protein Tat can counteract many of these factors, we hypothesized that the presence of exogenous Tat during infection might inhibit the establishment of latency. This was explored using a Jurkat model of latency establishment and reactivation.

The HIV-1 Vpu viroporin inhibitor BIT225 does not affect Vpu-mediated tetherin antagonism.

Among its many roles, the HIV-1 accessory protein Vpu performs a viroporin function and also antagonizes the host cell restriction factor tetherin through its transmembrane domain. BIT225 is a small molecule inhibitor that specifically targets the Vpu viroporin function, which, in macrophages, resulted in late stage inhibition of virus release and decreased infectivity of released virus, a phenotype similar to tetherin-mediated restriction. Here, we investigated whether BIT225 might mediate its antiviral function, at least in part, via inhibition of Vpu-mediated tetherin antagonism.

Vpu-mediated tetherin antagonism of ongoing HIV-1 infection in CD4(+) T-cells is not directly related to the extent of tetherin cell surface downmodulation.

Tetherin is a host cell restriction factor that acts against HIV-1 and other enveloped viruses. The antiviral activity of tetherin is antagonized by the HIV-1 protein Vpu, that downregulates tetherin from the cell surface. Here, we report the specific detection of cell surface tetherin levels in primary activated CD4(+) T-cells and in CD4(+) T-cell lines.

Transcription of preintegrated HIV-1 cDNA modulates cell surface expression of major histocompatibility complex class I via Nef.

Although transcription from unintegrated human immunodeficiency virus type 1 (HIV-1) DNA can occur inside infected cells, yielding all classes of viral mRNA transcripts, the translation of viral proteins is very limited. One of the proteins made is Nef, but it is unclear whether Nef produced in this way is able to play a role in immune evasion as occurs with integrated virus. We therefore asked whether transcription from preintegrated HIV-1 cDNAs could result in Nef-mediated modulation of cell surface major histocompatibility complex class I (MHC-I) expression.

Tetherin restricts direct cell-to-cell infection of HIV-1.

Background: Tetherin (BST-2/CD317/HM1.24) is an interferon (IFN)-inducible factor of the innate immune system, recently shown to exert antiviral activity against HIV-1 and other enveloped viruses by tethering nascent viral particles to the cell surface, thereby inhibiting viral release. In HIV-1 infection, the viral protein U (Vpu) counteracts this antiviral action by down-modulating tetherin from the cell surface.