Can We Bridge the Gap? Mathematics and the Life Sciences, Part 1–Calculus-Based Modules, Programs, Curricula

This editorial serves as an introduction to Part 1 of the Special Issue Mathematics and the Life Sciences–a collection of articles showcasing ideas, examples, pedagogical frameworks, and curricular materials aiming to bridge the stubbornly persistent gap at the undergraduate level between the mathematical and the life sciences. The special issue features authors from public and private institutions of diverse types, sizes, and geographic locations: community colleges, liberal arts colleges, and research-oriented universities. We hope this special issue will serve as a resource to faculty who seek to make changes to their own course(s) or initiate curriculum reforms at their own schools. Part 1 focuses on educational initiatives that are appropriate for Calculus classes or require calculus as a prerequisite. Part 2 of the special issue features course materials and programs based on discrete mathematics, computational approaches, and statistics. Part 2 also includes articles on internship programs and co-curricular opportunities

Can We Bridge the Gap? Mathematics and the Life Sciences: Part 2–Discrete Models, Statistics, Co-Curricular Opportunities

This editorial serves as an introduction to Part 2 of the Special Issue Mathematics and the Life Sciences–a collection of articles showcasing ideas, examples, pedagogical frameworks, and curricular materials aiming to bridge the stubbornly persistent gap at the undergraduate level between the mathematical and the life sciences. The special issue features authors from public and private institutions of diverse types, sizes, and geographic locations: community colleges, liberal arts colleges, and research-oriented universities. We hope this special issue will serve as a resource to faculty who seek to make changes to their own course(s) or initiate curriculum reforms at their own schools. This Part 2 special issue features course materials and programs based on discrete mathematics, computational approaches, and statistics. It also includes articles on internship programs and co-curricular opportunities. Part 1 focuses on educational initiatives that are appropriate for calculus classes or require calculus as a prerequisite

Age-Structured and Vaccination Models of Devil Facial Tumor Disease

Tasmanian devil populations have been devastated by devil facial tumor disease (DFTD) since its first appearance in 1996. The average lifespan of a devil has decreased from six years to three years. We present an age-structured model to represent how the disease has affected the age and breeding structures of the population. We show that with the recent increase in the breeding of juvenile devils, the overall devil population will increase but not nearly to pre-DFTD levels. The basic reproductive number may be increased with the influx of young breeding devils. In addition, our model shows that the release of nearly 100 captive-bred, vaccinated devils into infected, wild populations may help eliminate the disease and hence enable the population\u27s recovery. Specifically, we demonstrate that with this release of captive-bred, vaccinated devils the basic reproductive number is decreased to below one

Paying Our Dues: The Role of Professional Societies in the Evolution of Mathematical Biology Education.

Mathematical biology education provides key foundational underpinnings for the scholarly work of mathematical biology. Professional societies support such education efforts via funding, public speaking opportunities, Web presence, publishing, workshops, prizes, opportunities to discuss curriculum design, and support of mentorship and other means of sustained communication among communities of scholars. Such programs have been critical to the broad expansion of the range and visibility of research and educational activities in mathematical biology. We review these efforts, past and present, across multiple societies-the Society for Mathematical Biology (SMB), the Symposium on Biomathematics and Ecology Education and Research (BEER), the Mathematical Association of America (MAA), and the Society for Industrial and Applied Mathematics (SIAM). We then proceed to suggest ways that professional societies can serve as advocates and community builders for mathematical biologists at all levels, noting that education continues throughout a career and also emphasizing the value of educating new generations of students. Our suggestions include collecting and disseminating data related to biomath education; developing and maintaining mentoring systems and research communities; and providing incentives and visibility for educational efforts within mathematical biology

Epidemiological and molecular assessment of a measles outbreak in a highly vaccinated population of northeast Italy.

SUMMARYTwo distinct measles outbreaks, unrelated from the epidemiological point of view but caused by genetically related strains, occurred in the Friuli Venezia Giulia region of northeastern Italy. Forty-two cases were reported during the period April–May 2008. In the first outbreak the index case was a teacher who introduced the virus into the Pordenone area, involving eight adolescents and young adults. The other concomitant outbreak occurred in the city of Trieste with 33 cases. The containment of the epidemics can be explained by the high MMR vaccine coverage in an area where the first dose was delivered to 93·4% and the second dose to 88·3% of the target children. Phylogenetic analysis of 14 measles virus strains showed that they belonged to a unique D4 genotype indistinguishable from the MVs/Enfield.GBR/14.07 strain, probably introduced from areas (i.e. Piedmont and Germany) where this genotype was present or had recently caused a large epidemic

Measles: An overview of a re-emerging disease in children and immunocompromised patients

Despite the availability of a safe and effective vaccine, in 2018, around 350,000 measles cases were reported worldwide, which resulted in an estimate of 142,300 deaths from measles. Additionally, in 2017, global measles cases spiked, causing the death of 110,000 people, mostly children under the age of 5 years and immunocompromised adults. The increase in measles incidence is caused by the ongoing reduction of vaccination coverage. This event has triggered public and scientific interest. For this reason, we reviewed the pathophysiology of measles infection, focusing on mechanisms by which the virus spreads systemically through the host organism. By reaching the lymphocytes from the airways through a \u201ctrojan horse\u201d strategy, measles induces an immunosuppression status. H and F glycoproteins, both expressed in the envelope, ensure attachment of the virus to host cells and spreading from one cell to another by binding to several receptors, as described in detail. The severity of the disease depends both on the age and underlying conditions of patients as well as the social and health context in which epidemics spread, and is often burdened by sequelae and complications that may occur several years after infection. Particular attention was paid to special groups that are more susceptible to severe or atypical measles. An overview of microbiology, symptoms, diagnosis, prevention, and treatment completes and enriches the review

Human Polyomaviruses in the Cerebrospinal Fluid of Neurological Patients.

BACKGROUND: Central nervous system (CNS) infections by human polyomaviruses (HPyVs), with the exception of JC (JCPyV), have been poorly studied. METHODS: In total, 234 cerebrospinal fluid (CSF) samples were collected from patients affected with neurological disorders. DNA was isolated and subjected to quantitative real-time PCR (Q-PCR) for the detection of six HPyVs: JCPyV, BKPyV, Merkel cell PyV (MCPyV), HPyV6, HPyV7, and HPyV9. Where possible, the molecular characterization of the viral strains was carried out by nested PCR and automated sequencing. RESULTS: JCPyV was detected in 3/234 (1.3%), BKPyV in 15/234 (6.4%), MCPyV in 22/234 (9.4%), and HPyV6 in 1/234 (0.4%) CSF samples. JCPyV was detected at the highest (p < 0.05) mean load (3.7 7 107 copies/mL), followed by BKPyV (1.9 7 106 copies/mL), MCPyV (1.9 7 105 copies/mL), and HPyV6 (3.3 7 104 copies/mL). The noncoding control regions (NCCRs) of the sequenced viral strains were rearranged. CONCLUSIONS: HPyVs other than JCPyV were found in the CSF of patients affected with different neurological diseases, probably as bystanders, rather than etiological agents of the disease. However, the fact that they can be latent in the CNS should be considered, especially in immunosuppressed patients

Zinc prevents vaginal candidiasis by inhibiting expression of an inflammatory fungal protein

This is the author accepted manuscript. The final version is available from the American Association for the Advancement of Science via the DOI in this recordData and materials availability: All data associated with this study are present in the paper or the Supplementary Materials. Raw data from the figures are given in data file S1.Candida causes an estimated half-billion cases of vulvovaginal candidiasis (VVC) every year. VVC is most commonly caused by Candida albicans, which, in this setting, triggers nonprotective neutrophil infiltration, aggressive local inflammation, and symptomatic disease. Despite its prevalence, little is known about the molecular mechanisms underpinning the immunopathology of this fungal infection. In this study, we describe the molecular determinant of VVC immunopathology and a potentially straightforward way to prevent disease. In response to zinc limitation, C. albicans releases a trace mineral binding molecule called Pra1 (pH-regulated antigen). Here, we show that the PRA1 gene is strongly up-regulated during vaginal infections and that its expression positively correlated with proinflammatory cytokine concentrations in women. Genetic deletion of PRA1 prevented vaginal inflammation in mice, and application of a zinc solution down-regulated expression of the gene and also blocked immunopathology. We also show that treatment of women suffering from recurrent VVC with a zinc gel prevented reinfections. We have therefore identified a key mediator of symptomatic VVC, giving us an opportunity to develop a range of preventative measures for combatting this disease.Wellcome TrustMedical Research Council (MRC)National Institute for Health and Care Research (NIHR)Biotechnology and Biological Sciences Research Council (BBSRC

A Yersinia Effector with Enhanced Inhibitory Activity on the NF-κB Pathway Activates the NLRP3/ASC/Caspase-1 Inflammasome in Macrophages

A type III secretion system (T3SS) in pathogenic Yersinia species functions to translocate Yop effectors, which modulate cytokine production and regulate cell death in macrophages. Distinct pathways of T3SS-dependent cell death and caspase-1 activation occur in Yersinia-infected macrophages. One pathway of cell death and caspase-1 activation in macrophages requires the effector YopJ. YopJ is an acetyltransferase that inactivates MAPK kinases and IKKβ to cause TLR4-dependent apoptosis in naïve macrophages. A YopJ isoform in Y. pestis KIM (YopJKIM) has two amino acid substitutions, F177L and K206E, not present in YopJ proteins of Y. pseudotuberculosis and Y. pestis CO92. As compared to other YopJ isoforms, YopJKIM causes increased apoptosis, caspase-1 activation, and secretion of IL-1β in Yersinia-infected macrophages. The molecular basis for increased apoptosis and activation of caspase-1 by YopJKIM in Yersinia-infected macrophages was studied. Site directed mutagenesis showed that the F177L and K206E substitutions in YopJKIM were important for enhanced apoptosis, caspase-1 activation, and IL-1β secretion. As compared to YopJCO92, YopJKIM displayed an enhanced capacity to inhibit phosphorylation of IκB-α in macrophages and to bind IKKβ in vitro. YopJKIM also showed a moderately increased ability to inhibit phosphorylation of MAPKs. Increased caspase-1 cleavage and IL-1β secretion occurred in IKKβ-deficient macrophages infected with Y. pestis expressing YopJCO92, confirming that the NF-κB pathway can negatively regulate inflammasome activation. K+ efflux, NLRP3 and ASC were important for secretion of IL-1β in response to Y. pestis KIM infection as shown using macrophages lacking inflammasome components or by the addition of exogenous KCl. These data show that caspase-1 is activated in naïve macrophages in response to infection with a pathogen that inhibits IKKβ and MAPK kinases and induces TLR4-dependent apoptosis. This pro-inflammatory form of apoptosis may represent an early innate immune response to highly virulent pathogens such as Y. pestis KIM that have evolved an enhanced ability to inhibit host signaling pathways