Glacial Geology of Southeastern Massachusetts

Guidebook for field trips to the Boston area and vicinity : 68th annual meeting, New England Intercollegiate Geological Conference, October 8-10, 1976: Trip A-

The Late Quaternary geology of the Housatonic River basin in southwestern Massachusetts and adjacent Connecticut

Guidebook for field trips in western Massachusetts, northern Connecticut and adjacent areas of New York: 67th annual meeting October 10, 11, and 12, 1975: Trip B-7; C-

Sedimentation in a proglacial lake: Glacial Lake Hitchcock

Guidebook for field trips in Connecticut and south central Massachusetts: New England Intercollegiate Geological Conference 74th annual meeting, University of Connecticut, Storrs Connecticut , October 2 and 3, 1982: Trip Q-

Tetranectin Binds to the Kringle 1-4 Form of Angiostatin and Modifies Its Functional Activity

Tetranectin is a plasminogen kringle 4 domain-binding protein present in plasma and various tissue locations. Decreased plasma tetranectin or increased tetranectin in stroma of cancers correlates with cancer progression and adverse prognosis. A possible mechanism through which tetranectin could influence cancer progression is by altering activities of plasminogen or the plasminogen fragment, angiostatin. Tetranectin was found to bind to the kringle 1-4 form of angiostatin (AST(K1-4)). In addition, tetranectin inhibited binding of plasminogen or AST(K1-4) to extracellular matrix (ECM) deposited by endothelial cells. Finally, tetranectin partially counteracted the ability of AST(K1-4) to inhibit proliferation of endothelial cells. This latter effect of tetranectin was specific for AST(K1-4) since it did not counteract the antiproliferative activities of the kringle 1-3 form of angiostatin (AST(K1-3)) or endostatin. These findings suggest that tetranectin may modulate angiogenesis through interactions with AST

Gaps present a trade-off between dispersal and establishment that nourishes species diversity

We took advantage of two natural experiments to investigate processes that regulate tree recruitment in gaps. In the first, we examined the recruitment of small and large saplings and trees into 31 gaps resulting from treefalls occurring between 1984 and 2015 in the 2.25-ha core area of a 4-ha tree plot at Cocha Cashu in Peru. In the second, we identified the tallest saplings recruiting into 69 gaps created during a violent wind storm in February 2000. In the established tree plot, we were able to compare the composition of saplings in the disturbance zones of gaps prior to, during, and subsequent to the period of gap formation. Recruitment in gaps was compared with that in "nofall" zones, areas within the plot that had not experienced a treefall at least since the early 1980s. Our results confirmed earlier findings that a consistently high proportion (~60%) of established saplings survived gap formation. Light demanding species, as proxied by mortality rates, recruited under all conditions, but preferentially during periods of gap formation, a pattern that was especially strong among gap pioneers. Similar results were noted, separately, for small and large saplings and trees recruiting at >= 10 cm dbh. One hundred percent of previously untagged trees recruiting into gaps in the first post-disturbance census were gap pioneers, suggesting rapid development. This conclusion was strongly supported in a follow-up survey taken of 69 gaps 19 months after they had been synchronously created in a wind storm. Ten species of gap pioneers, eight of which are not normally present in the advance regeneration, had attained heights of 6-10 m in 19 months. The 10 gap pioneers were dispersed, variously, by primates, bats, birds, and wind and reached maximum frequency in different-sized gaps (range 1,000 m(2)). Both gap size and limited dispersal of zoochorous species into gaps serve as filters for establishment, creating a complex mosaic of conditions that enhances species diversity

Affine modifications and affine hypersurfaces with a very transitive automorphism group

We study a kind of modification of an affine domain which produces another affine domain. First appeared in passing in the basic paper of O. Zariski (1942), it was further considered by E.D. Davis (1967). The first named author applied its geometric counterpart to construct contractible smooth affine varieties non-isomorphic to Euclidean spaces. Here we provide certain conditions which guarantee preservation of the topology under a modification. As an application, we show that the group of biregular automorphisms of the affine hypersurface $X \subset C^{k+2}$ given by the equation $uv=p(x_1,...,x_k)$ where $p \in C[x_1,...,x_k],$ acts $m-$transitively on the smooth part reg$X$ of $X$ for any $m \in N.$ We present examples of such hypersurfaces diffeomorphic to Euclidean spaces.Comment: 39 Pages, LaTeX; a revised version with minor changes and correction

Surfactant protein D modulates HIV infection of both T-cells and dendritic cells

Surfactant Protein D (SP-D) is an oligomerized C-type lectin molecule with immunomodulatory properties and involvement in lung surfactant homeostasis in the respiratory tract. SP-D binds to the enveloped viruses, influenza A virus and respiratory syncytial virus and inhibits their replication in vitro and in vivo. SP-D has been shown to bind to HIV via the HIV envelope protein gp120 and inhibit infectivity in vitro. Here we show that SP-D binds to different strains of HIV (BaL and IIIB) and the binding occurs at both pH 7.4 and 5.0 resembling physiological relevant pH values found in the body and the female urogenital tract, respectively. The binding of SP-D to HIV particles and gp120 was inhibited by the presence of several hexoses with mannose found to be the strongest inhibitor. Competition studies showed that soluble CD4 and CVN did not interfere with the interaction between SP-D and gp120. However, soluble recombinant DC-SIGN was shown to inhibit the binding between SP-D and gp120. SP-D agglutinated HIV and gp120 in a calcium dependent manner. SP-D inhibited the infectivity of HIV strains at both pH values of 7.4 and 5.0 in a concentration dependent manner. The inhibition of the infectivity was abolished by the presence of mannose. SP-D enhanced the binding of HIV to immature monocyte derived dendritic cells (iMDDCs) and was also found to enhance HIV capture and transfer to the T-cell like line PM1. These results suggest that SP-D can bind to and inhibit direct infection of T-cells by HIV but also enhance the transfer of infectious HIV particles from DCs to T-cells in vivo

Human annexin A6 interacts with influenza a virus protein M2 and negatively modulates infection

Copyright © 2012, American Society for Microbiology. All Rights ReservedThe influenza A virus M2 ion channel protein has the longest cytoplasmic tail (CT) among the three viral envelope proteins and is well conserved between different viral strains. It is accessible to the host cellular machinery after fusion with the endosomal membrane and during the trafficking, assembly, and budding processes. We hypothesized that identification of host cellular interactants of M2 CT could help us to better understand the molecular mechanisms regulating the M2-dependent stages of the virus life cycle. Using yeast two-hybrid screening with M2 CT as bait, a novel interaction with the human annexin A6 (AnxA6) protein was identified, and their physical interaction was confirmed by coimmunoprecipitation assay and a colocalization study of virus-infected human cells. We found that small interfering RNA (siRNA)-mediated knockdown of AnxA6 expression significantly increased virus production, while its overexpression could reduce the titer of virus progeny, suggesting a negative regulatory role for AnxA6 during influenza A virus infection. Further characterization revealed that AnxA6 depletion or overexpression had no effect on the early stages of the virus life cycle or on viral RNA replication but impaired the release of progeny virus, as suggested by delayed or defective budding events observed at the plasma membrane of virus-infected cells by transmission electron microscopy. Collectively, this work identifies AnxA6 as a novel cellular regulator that targets and impairs the virus budding and release stages of the influenza A virus life cycle.This work was supported by the Research Fund for the Control of Infectious Disease (project 09080892) of the Hong Kong Government, the Area of Excellence Scheme of the University Grants Committee (grant AoE/M-12/-06 of the Hong Kong Special Administrative Region, China), the French Ministry of Health, the RESPARI Pasteur Network

Human surfactant protein D alters oxidative stress and HMGA1 expression to induce p53 apoptotic pathway in eosinophil leukemic cell line

This article is made available through the Brunel Open Access Publishing Fund. Copyright: © 2013 Mahajan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Surfactant protein D (SP-D), an innate immune molecule, has an indispensable role in host defense and regulation of inflammation. Immune related functions regulated by SP-D include agglutination of pathogens, phagocytosis, oxidative burst, antigen presentation, T lymphocyte proliferation, cytokine secretion, induction of apoptosis and clearance of apoptotic cells. The present study unravels a novel ability of SP-D to reduce the viability of leukemic cells (eosinophilic leukemic cell line, AML14.3D10; acute myeloid leukemia cell line, THP-1; acute lymphoid leukemia cell lines, Jurkat, Raji; and human breast epithelial cell line, MCF-7), and explains the underlying mechanisms. SP-D and a recombinant fragment of human SP-D (rhSP-D) induced G2/M phase cell cycle arrest, and dose and timedependent apoptosis in the AML14.3D10 eosinophilic leukemia cell line. Levels of various apoptotic markers viz. activated p53, cleaved caspase-9 and PARP, along with G2/M checkpoints (p21 and Tyr15 phosphorylation of cdc2) showed significant increase in these cells. We further attempted to elucidate the underlying mechanisms of rhSP-D induced apoptosis using proteomic analysis. This approach identified large scale molecular changes initiated by SPD in a human cell for the first time. Among others, the proteomics analysis highlighted a decreased expression of survival related proteins such as HMGA1, overexpression of proteins to protect the cells from oxidative burst, while a drastic decrease in mitochondrial antioxidant defense system. rhSP-D mediated enhanced oxidative burst in AML14.3D10 cells was confirmed, while antioxidant, N-acetyl-L-cysteine, abrogated the rhSP-D induced apoptosis. The rhSP-D mediated reduced viability was specific to the cancer cell lines and viability of human PBMCs from healthy controls was not affected. The study suggests involvement of SP-D in host’s immunosurveillance and therapeutic potential of rhSP-D in the eosinophilic leukemia and cancers of other origins.Department of Biotechnology, Indi