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"Campbell, Susan"
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Terrible typhoid Mary : a true story of the deadliest cook in America
\"What happens when a person's reputation has been forever damaged? With archival photographs and text among other primary sources, this riveting biography of Mary Mallon by the Sibert medalist and Newbery Honor winner Susan Bartoletti looks beyond the tabloid scandal of Mary's controversial life. How she was treated by medical and legal officials reveals a lesser-known story of human and constitutional rights, entangled with the science of pathology and enduring questions about who Mary Mallon really was. How did her name become synonymous with deadly disease? And who is really responsible for the lasting legacy of Typhoid Mary?\"--Amazon.com.
Book
Perineuronal nets decrease membrane capacitance of peritumoral fast spiking interneurons in a model of epilepsy
Brain tumor patients commonly present with epileptic seizures. We show that tumor-associated seizures are the consequence of impaired GABAergic inhibition due to an overall loss of peritumoral fast spiking interneurons (FSNs) concomitant with a significantly reduced firing rate of those that remain. The reduced firing is due to the degradation of perineuronal nets (PNNs) that surround FSNs. We show that PNNs decrease specific membrane capacitance of FSNs permitting them to fire action potentials at supra-physiological frequencies. Tumor-released proteolytic enzymes degrade PNNs, resulting in increased membrane capacitance, reduced firing, and hence decreased GABA release. These studies uncovered a hitherto unknown role of PNNs as an electrostatic insulator that reduces specific membrane capacitance, functionally akin to myelin sheaths around axons, thereby permitting FSNs to exceed physiological firing rates. Disruption of PNNs may similarly account for excitation-inhibition imbalances in other forms of epilepsy and PNN protection through proteolytic inhibition may provide therapeutic benefits.
Brain tumours are associated with epilepsy. Here the authors show, using a mouse model, that the degradation of perineuronal nets around fast spiking interneurons near the tumour contribute to seizures by increasing their membrane capacitance and firing.
Journal Article
Glutamate release by primary brain tumors induces epileptic activity
People with brain cancers called gliomas often have seizures due to secretion of the excitatory neurotransmitter glutamate from the tumor. Now, Harald Sontheimer and his colleagues report that blockade of a cystine-glutamate transporter in tumor cells by an FDA-approved drug can reduce glioma-induced epilepsy in mice.
Epileptic seizures are a common and poorly understood comorbidity for individuals with primary brain tumors. To investigate peritumoral seizure etiology, we implanted human-derived glioma cells into severe combined immunodeficient mice. Within 14–18 d, glioma-bearing mice developed spontaneous and recurring abnormal electroencephalogram events consistent with progressive epileptic activity. Acute brain slices from these mice showed marked glutamate release from the tumor mediated by the system x
c
−
cystine-glutamate transporter (encoded by
Slc7a11
). Biophysical and optical recordings showed glutamatergic epileptiform hyperexcitability that spread into adjacent brain tissue. We inhibited glutamate release from the tumor and the ensuing hyperexcitability by sulfasalazine (SAS), a US Food and Drug Administration–approved drug that blocks system x
c
−
. We found that acute administration of SAS at concentrations equivalent to those used to treat Crohn's disease in humans reduced epileptic event frequency in tumor-bearing mice compared with untreated controls. SAS should be considered as an adjuvant treatment to ameliorate peritumoral seizures associated with glioma in humans.
Journal Article
1968 : today's authors explore a year of rebellion, revolution, and change
\"Welcome to 1968--a revolution in a book. Essays, memoirs, and more by fourteen award-winning authors offer unique perspectives on one of the world's most tumultuous years\"--Provided by publisher.
Book
Mechanisms of Lung Cancer Development in Cystic Fibrosis Patients: The Role of Inflammation, Oxidative Stress, and Lung Microbiome Dysbiosis
Cystic fibrosis (CF) is a genetic disorder caused by mutations in the CFTR gene, leading to defective ion transport and impaired function of various organs. Chronic inflammation, oxidative stress, and microbial dysbiosis are key pathological features of CF patients, contributing to disease progression, lung damage, and an increased susceptibility to infections. Emerging evidence suggests that in CF patients these factors can promote cancer development, especially lung cancer. Chronic inflammation in CF, driven by immune cell dysfunction, results in the release of pro-inflammatory cytokines and reactive oxygen species (ROSs), fostering an environment conducive to cancer initiation. Oxidative stress can amplify cellular damage and hinder airway remodeling. ROSs not only damage cellular components such as lipids, proteins, and DNA but also disrupt lung homeostasis, creating a favorable environment for cancer development. Furthermore, the lung microbiome in CF patients is often dysbiotic, with a reduced diversity and the predominance of pathogenic bacteria such as Pseudomonas aeruginosa, which exacerbate inflammation and may contribute to carcinogenesis. This review explores the mechanisms linking CF to lung cancer, examining the potential clinical implications of these mechanisms for early detection, monitoring, and targeted therapies for lung cancer prevention in CF patients.
Journal Article
Dnmt1 and Dnmt3a maintain DNA methylation and regulate synaptic function in adult forebrain neurons
In dividing cells, the epigenetic mechanism of DNA methylation is catalyzed by enzymes that maintain DNA methylation or act as a
de novo
methyltransferase. In this study, the authors find that DNA methyltransferases Dnmt1 and 3a have an active role in the maintenance of DNA methylation in postmitotic excitatory neurons. Results indicate that there is a redundancy between the two enzymes in neurons and that DNA methylation is essential for normal synaptic plasticity and memory formation.
Dnmt1 and Dnmt3a are important DNA methyltransferases that are expressed in postmitotic neurons, but their function in the CNS is unclear. We generated conditional mutant mice that lack
Dnmt1
,
Dnmt3a
or both exclusively in forebrain excitatory neurons and found that only double knockout (DKO) mice showed abnormal long-term plasticity in the hippocampal CA1 region together with deficits in learning and memory. Although we found no neuronal loss, hippocampal neurons in DKO mice were smaller than in the wild type; furthermore, DKO neurons showed deregulated expression of genes, including the class I MHC genes and
Stat1
, that are known to contribute to synaptic plasticity. In addition, we observed a significant decrease in DNA methylation in DKO neurons. We conclude that Dnmt1 and Dnmt3a are required for synaptic plasticity, learning and memory through their overlapping roles in maintaining DNA methylation and modulating neuronal gene expression in adult CNS neurons.
Journal Article
The untold history of the United States : young readers edition. Volume 1, 1898-1945
A people's history of the American Empire, adapted for the next generation of young history buffs.
Book
There Are Some Questions Without Answers
The Spring 2025 Issue. Ploughshares is an award-winning journal of new writing. Since 1971, Ploughshares has discovered and cultivated the freshest voices in contemporary American literature, and now provides readers with thoughtful and entertaining literature in a variety of formats. Find out why the New York Times named Ploughshares \"the Triton among minnows.\" The Spring 2025 Issue, edited by Peggy Schumaker, features poetry and prose by Naomi Shihab Nye, Felicia Zamora, Tim Seibles, Lena Khalaf Tuffaha, Lia Purpura, Sonja Livingston, Marjorie Sandor, and more.
Journal Article