Nathan H. Lents

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Nathan H. Lents
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Nathan H. Lents in 2017
Born1978
OccupationAuthor
Professor
Nationality American
GenrePopular Science
Website
nathanlents.wordpress.com

Nathan H. Lents is an American scientist, author, and university professor. He has been on the faculty of John Jay College since 2006 [1] and is currently the director of the Cell and Molecular Biology program and the former head of the honors program and the campus Macaulay Honors College program. [2] Lents is noted for his work in cell biology, genetics, and forensic science, as well as his popular science writing and blogging on the evolution of human biology and behavior. Lents is also a visiting faculty member at the University of Lincoln in the UK and a fellow with the Committee for Skeptical Inquiry.

Contents

Early life and education

Lents was born and raised in Decatur, Illinois and graduated from St. Teresa High School. [3] He then attended Saint Louis University and graduated summa cum laude with a B.S degree in biology.[ citation needed ]

Lents moved to Saint Louis University School of Medicine for his doctoral work and graduated with a Ph.D. in Pharmacological and Physiological Sciences in 2004. [4] He completed postdoctoral training in cancer genomics at NYU Medical Center under the direction of Brian David Dynlacht. [5] He then joined the faculty of forensic science at John Jay College and the doctoral faculty of biochemistry at the CUNY Graduate Center.[ citation needed ]

Lents was promoted to Associate Professor with tenure in 2011 and attained the rank of full professor at John Jay College in 2016, his tenth year on the faculty. [6]

Research

While an undergraduate at Saint Louis University in the 1990s, Lents conducted research with Biology Department chair Robert I. Bolla on the biochemical interactions between soybean plants and the soybean cyst nematode, a key cause of soybean crop loss in the United States. Specifically, he discovered that the CF-9 gene cluster correlated with resistance to nematodes in soybean strains.[ citation needed ]

During this same time period, Lents also worked in the fermentation research division of agribusiness giant Archer Daniels Midland, conducting basic microbiology research on the soil bacteria Corynebacterium glutamicum , which is used in the production of amino acids for food additives. Specifically, he worked on the production of lysine, a product that was the subject of a global price-fixing conspiracy. ADM plead guilty to antitrust violations and was forced to pay $100 million, the largest antitrust fine in US history. Several top ADM executives served prison sentences, but none of the scientists in the lysine group were implicated in any wrongdoing.[ citation needed ]

Since 2000, Lents has published research reports in the area of cell and cancer biology, genetics, forensic science, as well as the teaching and learning of science, particularly evolution. [7] Lents has been funded by the National Institutes of Health, National Science Foundation, Susan G. Komen Breast Cancer Foundation, and the US Department of Education. [6] His early work focused on the cell cycle and cancer biology, particularly the G1 to S phase transition. Specifically, Lents and colleagues showed that activation of the MAP kinase cascade is necessary and sufficient for a key phosphorylation step in the activation of cyclin-dependent kinase 2, an important cell cycle enzyme. [8] In addition, as a PhD student, Lents developed an innovative "reverse mutational" approach to discovering key phosphorylation sites on the Retinoblastoma protein, one of the most important tumor suppressors. [9]

In 2008, Lents discovered a new splice variant for the Mdm2 oncogene that is induced upon treatment with DNA-damaging cancer chemotherapies. [10] His laboratory later discovered new genetic connections between Vitamin D, the transcription factor MZF1, and the CCN gene family, [11] work that has led him and others to call for exploration of the usefulness of vitamin D as a possible enhancement for cancer treatments. [12]

Lents has also published research in the area of forensic biology and toxicology. His laboratory was among the first to note that zinc supplements can be effective in masking the presence of certain drug metabolites during routine drug testing. [13] In 2016, he published work on the skin microbiome of decomposing human cadavers. [14] He also developed and patented a DNA-based forensic method of species identification of trace plant material. [15]

Most recently, Lents has turned his research focus to the evolutionary genetics of human uniqueness. His laboratory recently discovered a set of microRNA genes on human chromosome 21 that are not shared with other apes and that appear to have originated de novo through genomic rearrangements. [16]

Books

In 2016, Lents published his first book, Not So Different: Finding Human Nature in Animals with Columbia University Press. The book has received favorable reviews from Publishers Weekly , The Quarterly Review of Biology , Psychology Today , and several others.[ citation needed ] Lents says "…by exploring why animals behave as they do, we learn a lot about ourselves." He says the book is about us, it only pretends to be about animals. [17] Lents said his goal, when writing this book, was to: "dispel two big misconceptions: that evolution produces perfection or anything like it, and that humans are the pinnacle of evolution." [18]

In 2018, Houghton Mifflin Harcourt published his second book, Human Errors: A Panorama of Our Glitches, from Pointless Bones to Broken Genes, [19] which was listed by Publishers Weekly as a "Big Title" for spring 2018 in the Science category. [20] In this book, Lents explains that humans no longer need to rely on the body's physical ability because we learned to solve life's challenges by using our brains to invent tools and our social capabilities to allow for division of labor and cooperation. [17] Human Errors received many favorable reviews and was included on recommended summer reading lists in The Wall Street Journal , Discover Magazine, EndPoints, the Financial Times , and was "Book of the Month" for August 2018 in Geographical Magazine . [21]

Lents's next book will be published in early 2025 by HarperCollins and is tentatively titled Rewilding Sex: Modern Attitudes, Ancient Truths. Its subject will be the evolution of sex, gender, sexuality, and sexual relationships, and it will discuss how agriculture and civilization constrained and narrowed the diverse sexual expression of prehistoric humans. Lents will argue that human sexuality is "flexible", able to conform to the mandates of heteronormative power structures but not inherently monogamous. [22]

Intelligent Design criticism

Lents' book Human Errors elicited much criticism from supporters of Intelligent Design. Even though the book was intended for an audience that accepted the scientific consensus on evolution, it does argue that the quirks of evolution, not an intelligent designer, account for the flaws in the human body. [22] [23] Lents was thrust into the public eye as a defender of evolutionary science, especially in the context of education and politics in the United States. As part of this debate, Lents and a few colleagues deconstructed and rebutted a popular book on Intelligent Design, Darwin Devolves: The New Science About DNA That Challenges Evolution, written by creationist and biochemist Michael Behe. According to Lents, the exercise provided an opportunity both to clarify how evolution actually works and "how strongly bias can affect your interpretation of evidence". A version of this critique was published in the journal Science. [22] [24] Proponents of Intelligent Design reacted with a flurry of negative articles, but Lents responded to their arguments and personal attacks by keeping the discussion focused on the science. [18]

Science education

Lents has had articles published in journals and magazines, including Skeptic Magazine , The Wall Street Journal , The Observer , Psychology Today , [25] and The Chronicle of Higher Education .[ citation needed ] He regularly contributes modules for the Visionlearning science education project. He also maintains The Human Evolution Blog and authors most of its content. [26] He blogs for Psychology Today under the tagline "Beastly Behavior: How Evolution Shaped Our Minds and Bodies." [27]

Lents is the host and executive producer of the This World of Humans podcast, a collaboration with the Visionlearning project, focusing on new research in the area of biology and social science. [28]

In 2019, Lents was a featured presenter at CSICon, speaking about "Human Errors: What Our Quirks Tell Us about Our Past". [17]

As of 2022, Lents is a fellow with the Committee for Skeptical Inquiry. [29]

Media coverage

Lents has appeared on television, radio, and news articles commenting about forensic science, human evolution, and other science issues. His television appearances have included The Today Show , [30] 48 Hours , [31] The Whole Story with Anderson Cooper (CNN), [32] Access Hollywood , [33] The Brian Lehrer Show , [34] BBC World Service Television, [35] and Al Jazeera. [36]

Lents's work has been quoted by various publications, including the Associated Press, Vice, The New York Times , Scientific American and others. [37] His blog has been quoted by USA Today , the Daily Mirror , the Daily Mail , The Daily Telegraph , New York Magazine , the New York Post , IFL Science , People Magazine , and was mentioned on Live with Kelly and Ryan .[ citation needed ]

Personal life

Lents and his husband [38] Oscar live in Queens and have two children.[ citation needed ] In an April 2020 article for Psychology Today , Lents chronicled his personal battle with COVID-19. [39]

Related Research Articles

A microsatellite is a tract of repetitive DNA in which certain DNA motifs are repeated, typically 5–50 times. Microsatellites occur at thousands of locations within an organism's genome. They have a higher mutation rate than other areas of DNA leading to high genetic diversity. Microsatellites are often referred to as short tandem repeats (STRs) by forensic geneticists and in genetic genealogy, or as simple sequence repeats (SSRs) by plant geneticists.

<span class="mw-page-title-main">DNA repair</span> Cellular mechanism

DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encodes its genome. In human cells, both normal metabolic activities and environmental factors such as radiation can cause DNA damage, resulting in tens of thousands of individual molecular lesions per cell per day. Many of these lesions cause structural damage to the DNA molecule and can alter or eliminate the cell's ability to transcribe the gene that the affected DNA encodes. Other lesions induce potentially harmful mutations in the cell's genome, which affect the survival of its daughter cells after it undergoes mitosis. As a consequence, the DNA repair process is constantly active as it responds to damage in the DNA structure. When normal repair processes fail, and when cellular apoptosis does not occur, irreparable DNA damage may occur, including double-strand breaks and DNA crosslinkages. This can eventually lead to malignant tumors, or cancer as per the two hit hypothesis.

The argument from poor design, also known as the dysteleological argument, is an argument against the assumption of the existence of a creator God, based on the reasoning that any omnipotent and omnibenevolent deity or deities would not create organisms with the perceived suboptimal designs that occur in nature.

<span class="mw-page-title-main">ATM serine/threonine kinase</span>

ATM serine/threonine kinase or Ataxia-telangiectasia mutated, symbol ATM, is a serine/threonine protein kinase that is recruited and activated by DNA double-strand breaks, oxidative stress, topoisomerase cleavage complexes, splicing intermediates, R-loops and in some cases by single-strand DNA breaks. It phosphorylates several key proteins that initiate activation of the DNA damage checkpoint, leading to cell cycle arrest, DNA repair or apoptosis. Several of these targets, including p53, CHK2, BRCA1, NBS1 and H2AX are tumor suppressors.

Carcinogenesis, also called oncogenesis or tumorigenesis, is the formation of a cancer, whereby normal cells are transformed into cancer cells. The process is characterized by changes at the cellular, genetic, and epigenetic levels and abnormal cell division. Cell division is a physiological process that occurs in almost all tissues and under a variety of circumstances. Normally, the balance between proliferation and programmed cell death, in the form of apoptosis, is maintained to ensure the integrity of tissues and organs. According to the prevailing accepted theory of carcinogenesis, the somatic mutation theory, mutations in DNA and epimutations that lead to cancer disrupt these orderly processes by interfering with the programming regulating the processes, upsetting the normal balance between proliferation and cell death. This results in uncontrolled cell division and the evolution of those cells by natural selection in the body. Only certain mutations lead to cancer whereas the majority of mutations do not.

<span class="mw-page-title-main">Homeobox protein NANOG</span> Mammalian protein found in humans

Homeobox protein NANOG(hNanog) is a transcriptional factor that helps embryonic stem cells (ESCs) maintain pluripotency by suppressing cell determination factors. hNanog is encoded in humans by the NANOG gene. Several types of cancer are associated with NANOG.

<span class="mw-page-title-main">Cyclin E</span> Member of the cyclin family

Cyclin E is a member of the cyclin family.

Paul Montgomery Bingham is an American molecular biologist and evolutionary biologist, Associate Professor in the Department of Biochemistry and Cell Biology at Stony Brook University and Vice President for Research at Rafael Pharmaceuticals. He is known for his work in molecular biology, and has also published recent articles and a book on human evolution.

<span class="mw-page-title-main">Cyclin D</span> Member of the cyclin protein family

Cyclin D is a member of the cyclin protein family that is involved in regulating cell cycle progression. The synthesis of cyclin D is initiated during G1 and drives the G1/S phase transition. Cyclin D protein is anywhere from 155 to 477 amino acids in length.

<span class="mw-page-title-main">Cyclin-dependent kinase 6</span> Protein-coding gene in the species Homo sapiens

Cell division protein kinase 6 (CDK6) is an enzyme encoded by the CDK6 gene. It is regulated by cyclins, more specifically by Cyclin D proteins and Cyclin-dependent kinase inhibitor proteins. The protein encoded by this gene is a member of the cyclin-dependent kinase, (CDK) family, which includes CDK4. CDK family members are highly similar to the gene products of Saccharomyces cerevisiae cdc28, and Schizosaccharomyces pombe cdc2, and are known to be important regulators of cell cycle progression in the point of regulation named R or restriction point.

<span class="mw-page-title-main">Transcription factor Jun</span> Mammalian protein found in Homo sapiens

Transcription factor Jun is a protein that in humans is encoded by the JUN gene. c-Jun, in combination with protein c-Fos, forms the AP-1 early response transcription factor. It was first identified as the Fos-binding protein p39 and only later rediscovered as the product of the JUN gene. c-jun was the first oncogenic transcription factor discovered. The proto-oncogene c-Jun is the cellular homolog of the viral oncoprotein v-jun. The viral homolog v-jun was discovered in avian sarcoma virus 17 and was named for ju-nana, the Japanese word for 17. The human JUN encodes a protein that is highly similar to the viral protein, which interacts directly with specific target DNA sequences to regulate gene expression. This gene is intronless and is mapped to 1p32-p31, a chromosomal region involved in both translocations and deletions in human malignancies.

<span class="mw-page-title-main">Histone-modifying enzymes</span> Type of enzymes

Histone-modifying enzymes are enzymes involved in the modification of histone substrates after protein translation and affect cellular processes including gene expression. To safely store the eukaryotic genome, DNA is wrapped around four core histone proteins, which then join to form nucleosomes. These nucleosomes further fold together into highly condensed chromatin, which renders the organism's genetic material far less accessible to the factors required for gene transcription, DNA replication, recombination and repair. Subsequently, eukaryotic organisms have developed intricate mechanisms to overcome this repressive barrier imposed by the chromatin through histone modification, a type of post-translational modification which typically involves covalently attaching certain groups to histone residues. Once added to the histone, these groups elicit either a loose and open histone conformation, euchromatin, or a tight and closed histone conformation, heterochromatin. Euchromatin marks active transcription and gene expression, as the light packing of histones in this way allows entry for proteins involved in the transcription process. As such, the tightly packed heterochromatin marks the absence of current gene expression.

<span class="mw-page-title-main">Cyclin-dependent kinase 7</span> Protein-coding gene in the species Homo sapiens

Cyclin-dependent kinase 7, or cell division protein kinase 7, is an enzyme that in humans is encoded by the CDK7 gene.

<span class="mw-page-title-main">E2F3</span> Protein-coding gene in the species Homo sapiens

Transcription factor E2F3 is a protein that in humans is encoded by the E2F3 gene.

<span class="mw-page-title-main">CDH3 (gene)</span> Protein-coding gene in the species Homo sapiens

Cadherin-3, also known as P-Cadherin, is a protein that in humans is encoded by the CDH3 gene.

<span class="mw-page-title-main">HMGN1</span> Protein-coding gene in the species Homo sapiens

Non-histone chromosomal protein HMG-14 is a protein that in humans is encoded by the HMGN1 gene.

<span class="mw-page-title-main">40S ribosomal protein S27</span> Protein found in humans

40S ribosomal protein S27 also known as metallopan-stimulin 1 or MPS-1 is a protein that in humans is encoded by the RPS27 gene. Metallopanstimulin is a zinc finger protein proposed to be involved DNA repair as well as oncogenesis.

<span class="mw-page-title-main">Siddhartha Mukherjee</span> Indian-American physician, writer b. 1970

Siddhartha Mukherjee is an Indian-American physician, biologist, and author. He is best known for his 2010 book, The Emperor of All Maladies: A Biography of Cancer, that won notable literary prizes including the 2011 Pulitzer Prize for General Non-Fiction, and Guardian First Book Award, among others. The book was listed in the "All-Time 100 Nonfiction Books" by Time magazine in 2011. His 2016 book The Gene: An Intimate History made it to #1 on The New York Times Best Seller list, and was among The New York Times 100 best books of 2016, and a finalist for the Wellcome Trust Prize and the Royal Society Prize for Science Books.

<span class="mw-page-title-main">Retinoblastoma protein</span> Mammalian protein found in Homo sapiens

The retinoblastoma protein is a tumor suppressor protein that is dysfunctional in several major cancers. One function of pRb is to prevent excessive cell growth by inhibiting cell cycle progression until a cell is ready to divide. When the cell is ready to divide, pRb is phosphorylated, inactivating it, and the cell cycle is allowed to progress. It is also a recruiter of several chromatin remodeling enzymes such as methylases and acetylases.

Brian David Dynlacht, is an American biochemist and professor in the department of pathology of New York University Grossman School of Medicine at NYU Langone Health. Before moving his lab to New York University, he was an associate professor in the department of molecular and cellular biology at Harvard University. In 2002, while researching at the Harvard University, Dynlacht reported the discovery of CP110, which is now thought to be at the center of a molecular switch governing the centriole to ciliary transition in mammalian cells. His lab identified the first centriolar deubiquitinating enzyme, USP33, whose expression regulates centrosome biogenesis via deubiquitination of the centriolar protein CP110, and thus regulates the centrosome duplication.

References

  1. ↑ "Nathan H. Lents". John Jay College of Criminal Justice. 2014-03-23. Retrieved 2022-02-14.
  2. ↑ "Nathan H. Lents". John Jay College of Criminal Justice. 23 March 2014. Retrieved 9 May 2020.
  3. ↑ Lents, Nathan H (2004). CDK2, CAK, and pRB: interactions regulating G1 phase cell cycle progression (PhD Thesis). OCLC   123984250.[ page needed ]
  4. ↑ "Inaugural Distinguished Alumnus Award and Lecture". SLU Calendar.
  5. ↑ "Dynlacht Lab – NYU Cancer Institute – NYU School of Medicine". med.nyu.edu.
  6. 1 2 "NATHAN H. LENTS: Professor of Biology". jjay.cuny.edu. John Jay College of Criminal Justice. 23 March 2014. Archived from the original on 2 May 2020. Retrieved 2 May 2020.
  7. ↑ "Nathan H. Lents". scholar.google.com. Retrieved 2023-08-10.
  8. ↑ Lents, Nathan H; Keenan, Susan M; Bellone, Clifford; Baldassare, Joseph J (2002). "Stimulation of the Raf/MEK/ERK Cascade is Necessary and Sufficient for Activation and Thr-160 Phosphorylation of a Nuclear-targeted CDK2". Journal of Biological Chemistry. 277 (49): 47469–75. doi: 10.1074/jbc.M207425200 . PMID   12359725.
  9. ↑ Lents, Nathan H; Gorges, Laura L; Baldassare, Joseph J (2014). "Reverse Mutational Analysis Reveals Threonine-373 as a Potentially Sufficient Phosphorylation Site for Inactivation of the Retinoblastoma Tumor Suppressor Protein (pRB)". Cell Cycle. 5 (15): 1699–707. doi: 10.4161/cc.5.15.3126 . PMID   16880741.
  10. ↑ Lents, Nathan H; Wheeler, Leroy W; Baldassare, Joseph J; Dynlacht, Brian David (2008). "Identification and characterization of a novel Mdm2 splice variant acutely induced by the chemotherapeutic agents Adriamycin and Actinomycin D". Cell Cycle. 7 (11): 1580–6. doi:10.4161/cc.7.11.5985. PMC   3608406 . PMID   18469520.
  11. ↑ Piszczatowski, Richard T; Rafferty, Brian J; Rozado, Andre; Parziale, James V; Lents, Nathan H (2015). "Myeloid Zinc Finger 1 (MZF-1) Regulates Expression of the CCN2/CTGF and CCN3/NOV Genes in the Hematopoietic Compartment". Journal of Cellular Physiology. 230 (11): 2634–9. doi: 10.1002/jcp.25021 . PMID   25899830. S2CID   6888015.
  12. ↑ Piszczatowski, Richard T; Lents, Nathan H (2016). "Regulation of the CCN genes by vitamin D: A possible adjuvant therapy in the treatment of cancer and fibrosis". Cellular Signalling. 28 (10): 1604–13. doi:10.1016/j.cellsig.2016.07.009. PMID   27460560.
  13. ↑ Venkatratnam, Abhishek (1 July 2011). "Zinc Reduces the Detection of Cocaine, Methamphetamine, and THC by ELISA Urine Testing". Journal of Analytical Toxicology. 35 (6): 333–340. doi: 10.1093/anatox/35.6.333 . PMID   21740689.
  14. ↑ Johnson, Hunter R.; Trinidad, Donovan D.; Guzman, Stephania; Khan, Zenab; Parziale, James V.; DeBruyn, Jennifer M.; Lents, Nathan H. (22 December 2016). "A Machine Learning Approach for Using the Postmortem Skin Microbiome to Estimate the Postmortem Interval". PLOS ONE. 11 (12): e0167370. Bibcode:2016PLoSO..1167370J. doi: 10.1371/journal.pone.0167370 . PMC   5179130 . PMID   28005908.
  15. ↑ Srivastava, Tushar; Wu, Michael; Kakhnovich, Julia; Waithaka, Bridgit; Lents, Nathan H (2017). "A Three-Locus, PCR-based Method for Forensic Identification of Plant Material". Journal of Forensic Sciences. 63 (4): 1252–1260. doi:10.1111/1556-4029.13715. PMID   29194624. S2CID   206919448.
  16. ↑ Hunter R. Johnson; Jessica A. Blandino; Beatriz C. Mercado; José A. Galván; William J. Higgins; Nathan H. Lents (June 2022). "The evolution of de novo human-specific microRNA genes on chromosome 21". American Journal of Biological Anthropology. 178 (2): 223–243. doi:10.1002/ajpa.24504. S2CID   247240062.
  17. 1 2 3 Gerbic, Susan (7 August 2019). ""Human Errors: What Our Quirks Tell Us About Our Past." — An Interview With Nathan Lents". Skeptical Inquirer. Retrieved October 27, 2019.
  18. 1 2 Palmer, Rob (3 May 2021). "Nathan H. Lents on Our Not So Intelligent Design". Skeptical Inquirer. Archived from the original on 3 May 2021. Retrieved 3 May 2021.
  19. ↑ Lents, Nathan H. (2018). Human Errors: A Panorama of Our Glitches, from Pointless Bones to Broken Genes. Houghton Mifflin Harcourt. ISBN   978-1328974693.
  20. ↑ Segura, Jonathan. "Spring 2018 Adult Announcements". PublishersWeekly.com.
  21. ↑ "Book: Human Errors". 2017-10-16.
  22. 1 2 3 Palmer, Rob (7 September 2022). "Anticipating CSICon 2022: An Interview with Nathan H. Lents". Skeptical Inquirer. Archived from the original on 12 September 2022. Retrieved 24 September 2022.
  23. ↑ Hall, Harriet (May–June 2020). "Evolution's Flaws Are in Us". Skeptical Inquirer . Vol. 44, no. 3. Amherst, New York: Center for Inquiry. pp. 62–64. Archived from the original on 22 October 2020. Retrieved 1 January 2021.
  24. ↑ Lents, Nathan; Swamidass, S. Joshua; Lenski, Richard E. (8 February 2019). ""The end of evolution?"". Science. 363 (6427): 590. doi:10.1126/science.aaw4056. S2CID   59621727.
  25. ↑ "Nathan H. Lents, Ph.D. | Psychology Today". www.psychologytoday.com.
  26. ↑ Lents, Nathan. "The Human Evolution Blog". thehumanevolutionblog.com. Nathan Lents. Archived from the original on 2 May 2020. Retrieved 2 May 2020.
  27. ↑ "Beastly Behavior". Psychology Today.
  28. ↑ Website for This World of Humans podcast: www.visionlearning.com/en/twoh
  29. ↑ "Committee for Skeptical Inquiry Elects 14 New Fellows from Six Countries". Skeptical Inquirer. 1 February 2022. Archived from the original on 17 September 2022. Retrieved 19 September 2022.
  30. ↑ "Study: Handbags carry more bacteria than some toilets". TODAY.com.
  31. ↑ "Nathan Lents on 48 hours". CBS News .
  32. ↑ "The Whole Story with Anderson Cooper" . Retrieved 2023-08-10.
  33. ↑ "Exclusive: New Forensic Test Could Be Steven Avery's 'Secret Weapon' | Access Online". Access.
  34. ↑ "People – Nathan Lents". www.wnyc.org.
  35. ↑ "The Why Factor, The Family Tree". BBC World Service.
  36. ↑ "3 inventions that can catch you committing a crime". america.aljazeera.com.
  37. ↑ Rosenberg, Eli (2016-07-15). "K2's Sudden Surge Tests New York Authorities". The New York Times.
  38. ↑ Shostak, Stanley (17 February 2017). "Not So Different: Finding Human Nature in Animals". The European Legacy. 22 (4): 507–509. doi:10.1080/10848770.2017.1291895. S2CID   151502205.
  39. ↑ Lents, Nathan H. "I'm 41, Healthy, and Fit. And COVID-19 Still Got Me". psychologytoday.com/. Psychology Today. Retrieved 19 August 2020. My husband and I made the decision to keep my illness from all of our friends and family until I recovered. Our mothers are both worriers, and we saw no value in adding to their already excessive worry about us when there was absolutely nothing they (or anyone) could do to help us. My mom will be angry with me for some time, but I still think I made the right decision, especially since she's been checking on me constantly even though I'm now recovered.
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