Aquatic food webs that incorporate multiple energy channels (e.g., nearshore benthic and pelagic) with varying productivity and turnover rates convey stability to biological communities by providing ...independent energy sources. Within the Lake Michigan food web, invasive dreissenid mussels have caused rapid changes to food web structure and potentially altered the channels through which consumers acquire energy. We used stable C and N isotopes to determine how Lake Michigan food web structure has changed in the past decade, coincident with the expansion of dreissenid mussels, decreased pelagic phytoplankton production, and increased nearshore benthic algal production. Fish and invertebrate samples collected from sites around Lake Michigan were analyzed to determine taxa-specific
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C:
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C (δ
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C) and
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N:
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N (δ
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N) ratios. Sampling took place during two distinct periods, 2002-2003 and 2010-2012, that spanned the period of dreissenid expansion, and included nearshore, pelagic and profundal fish and invertebrate taxa. The magnitude and direction of the δ
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C shift indicated significantly greater reliance upon nearshore benthic energy sources among nearly all fish taxa as well as profundal invertebrates following dreissenid expansion. Although the mechanisms underlying this δ
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C shift likely varied among species, possible causes include the transport of benthic algal production to offshore waters and increased feeding on nearshore prey items by pelagic and profundal species. δ
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N shifts were more variable and of smaller magnitude across taxa, although declines in δ
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N among some pelagic fishes suggest a shift to alternative prey resources. Lake Michigan fishes and invertebrates appear to have responded to dreissenid-induced changes in nutrient and energy pathways by switching from pelagic to alternative nearshore energy subsidies. Although large shifts in energy allocation (i.e., pelagic to nearshore benthic) resulting from invasive species appear to affect total production at upper trophic levels, changes in trophic structure and utilization of novel energy pathways may help to stabilize food webs following species invasions.
Obesity rates are climbing, representing a confounding and contributing factor to many disease states, including cancer. With respect to breast cancer, obesity plays a prominent role in the etiology ...of this disease, with certain subtypes such as triple-negative breast cancer having a strong correlation between obesity and poor outcomes. Therefore, it is critical to examine the obesity-related alterations to the normal stroma and the tumor microenvironment (TME). Adipocytes and adipose stem cells (ASCs) are major components of breast tissue stroma that have essential functions in both physiological and pathological states, including energy storage and metabolic homeostasis, physical support of breast epithelial cells, and directing inflammatory and wound healing responses through secreted factors. However, these processes can become dysregulated in both metabolic disorders, such as obesity and also in the context of breast cancer. Given the well-established obesity-neoplasia axis, it is critical to understand how interactions between different cell types in the tumor microenvironment, including adipocytes and ASCs, govern carcinogenesis, tumorigenesis, and ultimately metastasis. ASCs and adipocytes have multifactorial roles in cancer progression; however, due to the plastic nature of these cells, they also have a role in regenerative medicine, making them promising tools for tissue engineering. At the physiological level, the interactions between obesity and breast cancer have been examined; here, we will delineate the mechanisms that regulate ASCs and adipocytes in these different contexts through interactions between cancer cells, immune cells, and other cell types present in the tumor microenvironment. We will define the current state of understanding of how adipocytes and ASCs contribute to tumor progression through their role in the tumor microenvironment and how this is altered in the context of obesity. We will also introduce recent developments in utilizing adipocytes and ASCs in novel approaches to breast reconstruction and regenerative medicine.
Metaplastic breast carcinoma (MBC) is a rare breast cancer subtype with rapid growth, high rates of metastasis, recurrence and drug resistance, and diverse molecular and histological heterogeneity. ...Patient-derived xenografts (PDXs) provide a translational tool and physiologically relevant system to evaluate tumor biology of rare subtypes. Here, we provide an in-depth comprehensive characterization of a new PDX model for MBC, TU-BcX-4IC. TU-BcX-4IC is a clinically aggressive tumor exhibiting rapid growth in vivo, spontaneous metastases, and elevated levels of cell-free DNA and circulating tumor cell DNA. Relative chemosensitivity of primary cells derived from TU-BcX-4IC was performed using the National Cancer Institute (NCI) oncology drug set, crystal violet staining, and cytotoxic live/dead immunofluorescence stains in adherent and organoid culture conditions. We employed novel spheroid/organoid incubation methods (Pu·MA system) to demonstrate that TU-BcX-4IC is resistant to paclitaxel. An innovative physiologically relevant system using human adipose tissue was used to evaluate presence of cancer stem cell-like populations ex vivo
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Tissue decellularization, cryogenic-scanning electron microscopy imaging and rheometry revealed consistent matrix architecture and stiffness were consistent despite serial transplantation. Matrix-associated gene pathways were essentially unchanged with serial passages, as determined by qPCR and RNA sequencing, suggesting utility of decellularized PDXs for in vitro screens. We determined type V collagen to be present throughout all serial passage of TU-BcX-4IC tumor, suggesting it is required for tumor maintenance and is a potential viable target for MBC. In this study we introduce an innovative and translational model system to study cell–matrix interactions in rare cancer types using higher passage PDX tissue.
We examined the effects of chronic activity wheel running and imipramine administration on appetitive behavior after olfactory bulbectomy (OBX). Male Long–Evans rats were randomly assigned to the ...following conditions using a 2×2×2 design: (1) bilateral OBX or sham surgery, (2) voluntary activity wheel running or sedentary home cage, and (3) daily imipramine or saline injections. After 21 days of treatment, animals underwent behavioral testing for copulatory activity and sucrose preference. Bulbectomized animals exhibited decrements in copulatory performance and reductions in sucrose intake compared to sham animals. Within the bulbectomized groups, imipramine-treated rats either did not copulate or had reduced ejaculation frequencies. However, activity wheel running attenuated the copulatory deficits induced by OBX. The findings encourage studies of physical activity and male sexual dysfunction among depressed men being treated by pharmacotherapy.
The Mark III Collaboration has measured the {ital J}/{psi} leptonic branching fractions using the process {psi}(2{ital S}){r arrow}{pi}{sup +}{pi}{sup {minus}}{ital J}/{psi}, {ital J}/{psi}{r ...arrow}{ital l}{sup +}{ital l{minus}}. The results are {ital B}({ital J}/{psi}{r arrow}{ital e}{sup +}{ital e{minus}})=(5.92{plus minus}0.15{plus minus}0.20)% and {ital B}({ital J}/{psi}{r arrow}{mu}{sup +}{mu}{sup {minus}})=(5.90{plus minus}0.15{plus minus}0.19)%, where the first error is statistical and the second is systematic. Assuming lepton universality, the leptonic branching fraction of the {ital J}/{psi} is (5.91{plus minus}0.11{plus minus}0.20)%. This result is used to obtain the strong coupling constant {alpha}{sub {ital s}} and the QCD scale factor {Lambda}{sub MS} (M{bar S} denotes the modified minimal-subtraction scheme).
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