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Objectives: Poor sleep is a common side effect of cancer. Cannabis is increasingly used to manage cancer treatment-related symptoms, including sleep. This study investigated factors related to cannabis use for sleep among Canadian cancer survivors. Method: Adult Canadian cancer survivors (N = 940) were recruited via the Angus Reid Institute and completed an online, cross-sectional survey. Univariate and multiple binomial logistic regression models identified factors associated with cannabis use for sleep. Results: Of the participants (Mage = 64.5 yrs; Women = 51.1%; White = 92.9%), 25.1% (n = 236) currently use cannabis for sleep. Participants were at greater odds of using cannabis for sleep if they identified as a gender other than man or woman (AOR = 11.132), were diagnosed with multiple medical conditions (2:AOR = 1.988; 3+:AOR = 1.902), two psychological conditions (AOR = 2.171), multiple sleep disorders (AOR = 2.338), insomnia (AOR = 1.942), bone (AOR = 6.535), gastrointestinal (AOR = 4.307), genitourinary (AOR = 2.586), hematological (AOR = 4.739), or an unlisted cancer (AOR = 3.470), received hormone therapy only (AOR = 3.054), drink heavily (AOR = 2.748), or had mild insomnia (AOR = 1.828). Older participants (AOR=.972) and those with sleep apnea were less likely to use cannabis for sleep (AOR=.560). Conclusion: Given its prevalence, research is needed to understand how factors associated with cannabis use as a sleep aid among Canadian cancer survivors may influence its use and effectiveness and whether these factors are barriers to accessing evidence-based treatments. [ABSTRACT FROM AUTHOR]

Calanus finmarchicus is an abundant calanoid copepod in the New York Bight (NYB) that has energy-dense lipid stores. This study measured C. finmarchicus abundance, lipid storage and energy density and compared it to two other abundant calanoid species in the region. We compared the NYB C. finmarchicus preyfield characteristics with data from two other NW Atlantic coastal ecosystems, the Gulf of Maine (GoM) and Cape Cod Bay (CCB). Copepods from net tows were identified, enumerated, photographed and measured. These data were used to calculate animal biovolume and lipid content as well as the volumetric energy density of the copepod preyfield. C. finmarchicus were most abundant in spring and summer and the mean lipid storage of C. finmarchicus remained largely constant regardless of season and location within the NYB. Centropages typicus were abundant enough in the winter to be more energy-rich than C. finmarchicus. Temora longicornis, while also abundant, never surpassed the energy density of C. finmarchicus. C. finmarchicus in the NYB were comparably lipid-rich to those from the GoM and CCB. C. finmarchicus in the NYB can be a reliable energy source for local predators due to their high spring and summer abundances and year-round storage of high-energy wax esters. [ABSTRACT FROM AUTHOR]

The visual allure of microscopy makes it an intuitively powerful research tool. Intuition, however, can easily obscure or distort the reality of the information contained in an image. Common cognitive biases, combined with institutional pressures that reward positive research results, can quickly skew a microscopy project towards upholding, rather than rigorously challenging, a hypothesis. The impact of these biases on a variety of research topics is well known. What might be less appreciated are the many forms in which bias can permeate a microscopy experiment. Even well-intentioned researchers are susceptible to bias, which must therefore be actively recognized to be mitigated. Importantly, although image quantification has increasingly become an expectation, ostensibly to confront subtle biases, it is not a guarantee against bias and cannot alone shield an experiment from cognitive distortions. Here, we provide illustrative examples of the insidiously pervasive nature of bias in microscopy experiments - from initial experimental design to image acquisition, analysis and data interpretation. We then provide suggestions that can serve as guard rails against bias. [ABSTRACT FROM AUTHOR]

Simple Summary: Calcium is a versatile and ubiquitous signaling molecule that long-term dysregulation can increase the spread of cancer to various parts of the body but that short-term effects are understudied. Disseminated cancer cells in circulation have distinct extensions or protrusions, called microtentacles, that enhance their ability to attach to surfaces or other cells. In this study, we show rapidly increasing cellular calcium with the compounds of Ionomycin and Thapsigargin decreases the microtentacle frequency and clustering functions on cancer cells in a detached and suspended environment. Acute calcium-induced signaling events promoted changes to actin contraction and rearrangement responsible for suppressing microtentacles. The results from this study support clinical trial data from Thapsigargin derivatives, suggesting Ca2+ modulating therapies can potentially be used to promote cellular shape and structure changes in free-floating tumor cells to reduce metastasis. Cytoskeletal remodeling in circulating tumor cells (CTCs) facilitates metastatic spread. Previous oncology studies examine sustained aberrant calcium (Ca2+) signaling and cytoskeletal remodeling scrutinizing long-term phenotypes such as tumorigenesis and metastasis. The significance of acute Ca2+ signaling in tumor cells that occur within seconds to minutes is overlooked. This study investigates rapid cytoplasmic Ca2+ elevation in suspended cells on actin and tubulin cytoskeletal rearrangements and the metastatic microtentacle (McTN) phenotype. The compounds Ionomycin and Thapsigargin acutely increase cytoplasmic Ca2+, suppressing McTNs in the metastatic breast cancer cell lines MDA-MB-231 and MDA-MB-436. Functional decreases in McTN-mediated reattachment and cell clustering during the first 24 h of treatment are not attributed to cytotoxicity. Rapid cytoplasmic Ca2+ elevation was correlated to Ca2+-induced actin cortex contraction and rearrangement via myosin light chain 2 and cofilin activity, while the inhibition of actin polymerization with Latrunculin A reversed Ca2+-mediated McTN suppression. Preclinical and phase 1 and 2 clinical trial data have established Thapsigargin derivatives as cytotoxic anticancer agents. The results from this study suggest an alternative molecular mechanism by which these compounds act, and proof-of-principle Ca2+-modulating compounds can rapidly induce morphological changes in free-floating tumor cells to reduce metastatic phenotypes. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to enhance hepatocellular carcinoma (HCC) screening to achieve earlier diagnosis of patients with hepatitis C (HCV) cirrhosis in our Safety-Net population. Background: Adherence to HCC screening guidelines at Safety-Net hospitals is poor. Only 23% of patients with HCC at our health system had a screening exam within 1-year of diagnosis and 46% presented with stage IV disease. HCV-induced cirrhosis remains the most common etiology of HCC (75%) in our patients. Methods: In the setting of an established HCV treatment clinic, an HCC screening quality improvement initiative was initiated for patients with stage 3 fibrosis or cirrhosis by transient elastography. The program consisted of semiannual imaging. Navigators scheduled imaging appointments and tracked compliance. Results: From April 2018 to April 2021, 318 patients were enrolled (mean age 61 years, 81% Black race, 38% uninsured). Adherence to screening was higher than previously reported: 94%, 75%, and 74% of patients completed their first, second, and third imaging tests. Twenty-two patients (7%) were diagnosed with HCC; 55% stage I and 14% stage IV. All patients were referred and 13 (59%) received treatment. Median time to receipt of treatment was 77 days (range, 32–282). Median overall survival for treated patients was 32 months. Conclusions: Implementation of an HCC screening program at a safety-net hospital is feasible and facilitated earlier diagnosis in this study. Patient navigation and tracking completion of imaging tests were key components of the program's success. Next steps include expanding the program to additional at-risk populations. [ABSTRACT FROM AUTHOR]

Simple Summary: The recent discovery of the genetic identity of the tubulin carboxypeptidase (TCP) provides a unique opportunity to study the role of the detyrosination of α-tubulin (deTyr-Tub), as performed by the TCP, in breast epithelial cells and breast cancer cells. Previous research has shown that elevated deTyr-Tub conveys a poor prognosis in breast cancer and is upregulated in a coordinated manner at the invasive margin of patient tumor samples. Using TCP expression constructs, we have shown that increased deTyr-Tub promotes apoptosis in normal breast epithelial cells, that does not occur in the same cells with an oncogenic KRas mutation or Bcl-2/Bcl-xL overexpression. Furthermore, the addition of the TCP to the breast cancer cell lines MDA-MB-231 and Hs578t, also harboring Ras mutations, leads to increased focal gelatin degradation. Post-translational modifications (PTMs) of the microtubule network impart differential functions across normal cell types and their cancerous counterparts. The removal of the C-terminal tyrosine of α-tubulin (deTyr-Tub) as performed by the tubulin carboxypeptidase (TCP) is of particular interest in breast epithelial and breast cancer cells. The recent discovery of the genetic identity of the TCP to be a vasohibin (VASH1/2) coupled with a small vasohibin-binding protein (SVBP) allows for the functional effect of this tubulin PTM to be directly tested for the first time. Our studies revealed the immortalized breast epithelial cell line MCF10A undergoes apoptosis following transfection with TCP constructs, but the addition of oncogenic KRas or Bcl-2/Bcl-xL overexpression prevents subsequent apoptotic induction in the MCF10A background. Functionally, an increase in deTyr-Tub via TCP transfection in MDA-MB-231 and Hs578t breast cancer cells leads to enhanced focal gelatin degradation. Given the elevated deTyr-Tub at invasive tumor fronts and the correlation with poor breast cancer survival, these new discoveries help clarify how the TCP synergizes with oncogene activation, increases focal gelatin degradation, and may correspond to increased tumor cell invasion. These connections could inform more specific microtubule-directed therapies to target deTyr-tubulin. [ABSTRACT FROM AUTHOR]

Fluorescence microscopy images should not be treated as perfect representations of biology. Many factors within the biospecimen itself can drastically affect quantitative microscopy data. Whereas some sample-specific considerations, such as photobleaching and autofluorescence, are more commonly discussed, a holistic discussion of sample-related issues (which includes less-routine topics such as quenching, scattering and biological anisotropy) is required to appropriately guide life scientists through the subtleties inherent to bioimaging. Here, we consider how the interplay between light and a sample can cause common experimental pitfalls and unanticipated errors when drawing biological conclusions. Although some of these discrepancies can be minimized or controlled for, others require more pragmatic considerations when interpreting image data. Ultimately, the power lies in the hands of the experimenter. The goal of this Review is therefore to survey how biological samples can skew quantification and interpretation of microscopy data. Furthermore, we offer a perspective on how to manage many of these potential pitfalls. [ABSTRACT FROM AUTHOR]