Category: 7. Science

  • Most beautiful Galaxies ever captured by NASA telescopes: See pics

    Most beautiful Galaxies ever captured by NASA telescopes: See pics

    (Photograph: NASA, H. Ford (JHU), G. Illingworth (UCSC/LO), M.Clampin (STScI), G. Hartig (STScI), the ACS Science Team, and ESA)

    The Mice

    Otherwise known as NGC 4676, located 300 million light-years away in the constellation Coma Berenices, two galaxies are engaged in a celestial dance like the cat and mouse. For this case, mouse and mouse. They have been nicknamed “The Mice” because of the long tails of stars and gas emanating from each galaxy.

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  • Sessa B. Shaping the renaissance of psychedelic research. The Lancet. 2012;380:200–1.

    Google Scholar 

  • Nichols DE. Psychedelics. Pharmacol Rev. 2016;68:264–355.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Davis AK, Barrett FS, May DG, Cosimano MP, Sepeda ND, Johnson MW, et al. Effects of psilocybin-assisted therapy on major depressive disorder: a randomized clinical trial. JAMA Psychiatry. 2021;78:481–9.

    PubMed 

    Google Scholar 

  • Goodwin GM, Croal M, Feifel D, Kelly JR, Marwood L, Mistry S, et al. Psilocybin for treatment resistant depression in patients taking a concomitant SSRI medication. Neuropsychopharmacol Off Publ Am Coll Neuropsychopharmacol. 2023;48:1492–9.

    CAS 

    Google Scholar 

  • Results Posted | A Double-Blind Trial of Psilocybin-Assisted Treatment of Alcohol Dependence | ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT02061293. Accessed 15 July 2024.

  • Study Details | LSD Treatment for Persons With Alcohol Use Disorder | ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT05474989. Accessed 15 July 2024.

  • Study Details | Psilocybin-Assisted Psychotherapy in Adults With Alcohol Use Disorder (AUD) | ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT05646303. Accessed 15 July 2024.

  • Study Details | Psilocybin as a Treatment for Anorexia Nervosa: A Pilot Study | ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT04505189. Accessed 15 July 2024.

  • Study Details | Evaluation of Psilocybin in Anorexia Nervosa: Safety and Efficacy | ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT04661514. Accessed 15 July 2024.

  • Study Details | Psilocybin in Co-occuring Major Depressive Disorder and Borderline Personality Disorder | ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT05399498. Accessed 15 July 2024.

  • Study Details | The Safety and Tolerability of COMP360 in Participants With Post-traumatic Stress Disorder | ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT05312151. Accessed 15 July 2024.

  • Study Details | Phase 2 Clinical Trial of GH001 in Bipolar II Disorder | ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT05839509. Accessed 15 July 2024.

  • Study Details | Outpatient Buprenorphine Induction With Psilocybin for Opioid Use Disorder | ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT06067737. Accessed 15 July 2024.

  • Study Details | Psilocybin-facilitated Smoking Cessation Treatment: A Pilot Study | ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT01943994. Accessed 15 July 2024.

  • Study Details | A Phase 2, Randomized, Double-Blind, Placebo-Controlled Study to Evaluate the Efficacy and Safety of up to Two Doses of Psilocybin for the Treatment of Major Depressive Disorder in Adults With Cancer | ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT05947383. Accessed 15 July 2024.

  • Results Posted | Psychopharmacology of Psilocybin in Cancer Patients | ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT00465595. Accessed 15 July 2024.

  • Olson DE. Psychoplastogens: a promising class of plasticity-promoting neurotherapeutics. J Exp Neurosci. 2018;12:1179069518800508.

    PubMed 
    PubMed Central 

    Google Scholar 

  • Drevets WC, Ongür D, Price JL. Neuroimaging abnormalities in the subgenual prefrontal cortex: implications for the pathophysiology of familial mood disorders. Mol Psychiatry. 1998;3:220–6.

    CAS 
    PubMed 

    Google Scholar 

  • Drevets WC. Neuroimaging studies of mood disorders. Biol Psychiatry. 2000;48:813–29.

    CAS 
    PubMed 

    Google Scholar 

  • Cui L, Li S, Wang S, Wu X, Liu Y, Yu W, et al. Major depressive disorder: hypothesis, mechanism, prevention and treatment. Signal Transduct Target Ther. 2024;9:1–32.

    CAS 

    Google Scholar 

  • Molendijk ML, Bus BAA, Spinhoven P, Penninx BWJH, Kenis G, Prickaerts J, et al. Serum levels of brain-derived neurotrophic factor in major depressive disorder: state–trait issues, clinical features and pharmacological treatment. Mol Psychiatry. 2011;16:1088–95.

    CAS 
    PubMed 

    Google Scholar 

  • Malberg JE, Eisch AJ, Nestler EJ, Duman RS. Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus. J Neurosci. 2000;20:9104–10.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Olson DE. The Subjective effects of psychedelics may not be necessary for their enduring therapeutic effects. ACS Pharmacol Transl Sci. 2021;4:563–7.

    CAS 
    PubMed 

    Google Scholar 

  • Yaden DB, Griffiths RR. The subjective effects of psychedelics are necessary for their enduring therapeutic effects. ACS Pharmacol Transl Sci. 2021;4:568–72.

    CAS 
    PubMed 

    Google Scholar 

  • Lewis V, Bonniwell EM, Lanham JK, Ghaffari A, Sheshbaradaran H, Cao AB, et al. A non-hallucinogenic LSD analog with therapeutic potential for mood disorders. Cell Rep. 2023;42:112203.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Cameron LP, Tombari RJ, Lu J, Pell AJ, Hurley ZQ, Ehinger Y, et al. A non-hallucinogenic psychedelic analogue with therapeutic potential. Nature. 2021;589:474–9.

    CAS 
    PubMed 

    Google Scholar 

  • Cao D, Yu J, Wang H, Luo Z, Liu X, He L, et al. Structure-based discovery of nonhallucinogenic psychedelic analogs. Science. 2022;375:403–11.

    CAS 
    PubMed 

    Google Scholar 

  • Shahar O, Botvinnik A, Esh-Zuntz N, Brownstien M, Wolf R, Lotan A, et al. Role of 5-HT2A, 5-HT2C, 5-HT1A and TAAR1 Receptors in the Head Twitch Response Induced by 5-Hydroxytryptophan and Psilocybin: Translational Implications. Int J Mol Sci. 2022;23:14148.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Cameron LP, Patel SD, Vargas MV, Barragan EV, Saeger HN, Warren HT, et al. 5-HT2ARs mediate therapeutic behavioral effects of psychedelic tryptamines. ACS Chem Neurosci. 2023;14:351–8.

    CAS 
    PubMed 

    Google Scholar 

  • Desouza LA, Benekareddy M, Fanibunda SE, Mohammad F, Janakiraman B, Ghai U, et al. The hallucinogenic Serotonin2A receptor agonist, 2,5-Dimethoxy-4-Iodoamphetamine, promotes cAMP response element binding protein-dependent gene expression of specific plasticity-associated genes in the rodent neocortex. Front Mol Neurosci. 2021;14:790213.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Shao L-X, Liao C, Gregg I, Davoudian PA, Savalia NK, Delagarza K, et al. Psilocybin induces rapid and persistent growth of dendritic spines in frontal cortex in vivo. Neuron. 2021;109:2535–2544.e4.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Ly C, Greb AC, Cameron LP, Wong JM, Barragan EV, Wilson PC, et al. Psychedelics promote structural and functional neural plasticity. Cell Rep. 2018;23:3170–82.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Revenga M, de la F, Zhu B, Guevara CA, Naler LB, Saunders JM, Zhou Z, et al. Prolonged epigenomic and synaptic plasticity alterations following single exposure to a psychedelic in mice. Cell Rep. 2021;37:109836.

    PubMed Central 

    Google Scholar 

  • Vaidya VA, Marek GJ, Aghajanian GK, Duman RS. 5-HT2A receptor-mediated regulation of brain-derived neurotrophic factor mRNA in the hippocampus and the neocortex. J Neurosci. 1997;17:2785–95.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Vargas MV, Dunlap LE, Dong C, Carter SJ, Tombari RJ, Jami SA, et al. Psychedelics promote neuroplasticity through the activation of intracellular 5-HT2A receptors. Science. 2023. 17 February 2023. https://doi.org/10.1126/science.adf0435.

  • Hesselgrave N, Troppoli TA, Wulff AB, Cole AB, Thompson SM. Harnessing psilocybin: antidepressant-like behavioral and synaptic actions of psilocybin are independent of 5-HT2R activation in mice. Proc Natl Acad Sci. 2021;118:e2022489118.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Moliner R, Girych M, Brunello CA, Kovaleva V, Biojone C, Enkavi G, et al. Psychedelics promote plasticity by directly binding to BDNF receptor TrkB. Nat Neurosci. 2023;26:1032–41.

    PubMed 
    PubMed Central 

    Google Scholar 

  • Rush AJ, Trivedi MH, Wisniewski SR, Nierenberg AA, Stewart JW, Warden D, et al. Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: a STAR*D report. Am J Psychiatry. 2006;163:1905–17.

    PubMed 

    Google Scholar 

  • Stone MB, Yaseen ZS, Miller BJ, Richardville K, Kalaria SN, Kirsch I. Response to acute monotherapy for major depressive disorder in randomized, placebo controlled trials submitted to the US Food and Drug Administration: individual participant data analysis. BMJ. 2022;378:e067606.

    PubMed 
    PubMed Central 

    Google Scholar 

  • Fournier JC, DeRubeis RJ, Hollon SD, Dimidjian S, Amsterdam JD, Shelton RC, et al. Antidepressant drug effects and depression severity: a patient-level meta-analysis. JAMA. 2010;303:47–53.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Lukas RJ, Muresan AZ, Damaj MI, Blough BE, Huang X, Navarro HA, et al. Synthesis and characterization of in vitro and in vivo profiles of hydroxybupropion analogues: aids to smoking cessation. J Med Chem. 2010;53:4731–48.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Wang H-Q, Wang Z-Z, Chen N-H. The receptor hypothesis and the pathogenesis of depression: Genetic bases and biological correlates. Pharmacol Res. 2021;167:105542.

    CAS 
    PubMed 

    Google Scholar 

  • Stahl SM. Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications. 4th ed. New York, NY, US: Cambridge University Press; 2013.

    Google Scholar 

  • Undurraga J, Baldessarini RJ. Direct comparison of tricyclic and serotonin-reuptake inhibitor antidepressants in randomized head-to-head trials in acute major depression: Systematic review and meta-analysis. J Psychopharmacol (Oxf). 2017;31:1184–9.

    CAS 

    Google Scholar 

  • Haase J, Brown E. Integrating the monoamine, neurotrophin and cytokine hypotheses of depression — A central role for the serotonin transporter? Pharmacol Ther. 2015;147:1–11.

    CAS 
    PubMed 

    Google Scholar 

  • Oquendo MA, Placidi GPA, Malone KM, Campbell C, Keilp J, Brodsky B, et al. Positron emission tomography of regional brain metabolic responses to a serotonergic challenge and lethality of suicide attempts in major depression. Arch Gen Psychiatry. 2003;60:14–22.

    PubMed 

    Google Scholar 

  • Drevets WC, Videen TO, Price JL, Preskorn SH, Carmichael ST, Raichle ME. A functional anatomical study of unipolar depression. J Neurosci. 1992;12:3628–41.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Liu W, Ge T, Leng Y, Pan Z, Fan J, Yang W, et al. The role of neural plasticity in depression: from hippocampus to prefrontal cortex. Neural Plast. 2017;2017:6871089.

    PubMed 
    PubMed Central 

    Google Scholar 

  • Chan SWY, Harmer CJ, Norbury R, O’Sullivan U, Goodwin GM, Portella MJ. Hippocampal volume in vulnerability and resilience to depression. J Affect Disord. 2016;189:199–202.

    PubMed 

    Google Scholar 

  • Bartkowska K, Paquin A, Gauthier AS, Kaplan DR, Miller FD. Trk signaling regulates neural precursor cell proliferation and differentiation during cortical development. Development. 2007;134:4369–80.

    CAS 
    PubMed 

    Google Scholar 

  • Minichiello L. TrkB signalling pathways in LTP and learning. Nat Rev Neurosci. 2009;10:850–60.

    CAS 
    PubMed 

    Google Scholar 

  • Bus BaA, Molendijk ML, Tendolkar I, Penninx BWJH, Prickaerts J, Elzinga BM, et al. Chronic depression is associated with a pronounced decrease in serum brain-derived neurotrophic factor over time. Mol Psychiatry. 2015;20:602–8.

    CAS 
    PubMed 

    Google Scholar 

  • Talaee N, Azadvar S, Khodadadi S, Abbasi N, Asli-Pashaki ZN, Mirabzadeh Y, et al. Comparing the effect of fluoxetine, escitalopram, and sertraline, on the level of BDNF and depression in preclinical and clinical studies: a systematic review. Eur J Clin Pharmacol. 2024;80:983–1016.

    PubMed 

    Google Scholar 

  • Madsen CA, Navarro ML, Elfving B, Kessing LV, Castrén E, Mikkelsen JD, et al. The effect of antidepressant treatment on blood BDNF levels in depressed patients: a review and methodological recommendations for assessment of BDNF in blood. Eur Neuropsychopharmacol. 2024;87:35–55.

    CAS 
    PubMed 

    Google Scholar 

  • Ray MT, Shannon Weickert C, Webster MJ. Decreased BDNF and TrkB mRNA expression in multiple cortical areas of patients with schizophrenia and mood disorders. Transl Psychiatry. 2014;4:e389.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Rahmani F, Saghazadeh A, Rahmani M, Teixeira AL, Rezaei N, Aghamollaii V, et al. Plasma levels of brain-derived neurotrophic factor in patients with Parkinson disease: a systematic review and meta-analysis. Brain Res. 2019;1704:127–36.

    CAS 
    PubMed 

    Google Scholar 

  • Kim OY, Song J. The importance of BDNF and RAGE in diabetes-induced dementia. Pharmacol Res. 2020;160:105083.

    CAS 
    PubMed 

    Google Scholar 

  • Davarpanah M, Shokri-mashhadi N, Ziaei R, Saneei P. A systematic review and meta-analysis of association between brain-derived neurotrophic factor and type 2 diabetes and glycemic profile. Sci Rep. 2021;11:1–14.

    Google Scholar 

  • Nutt D, King LA, Saulsbury W, Blakemore C. Development of a rational scale to assess the harm of drugs of potential misuse. The Lancet. 2007;369:1047–53.

    Google Scholar 

  • Yanagita T. Intravenous self-administration of (−)-cathinone and 2-amino-1-(2,5-dimethoxy-4-methyl)phenylpropane in rhesus monkeys. Drug Alcohol Depend. 1986;17:135–41.

    CAS 
    PubMed 

    Google Scholar 

  • Deneau G, Yanagita T, Seevers MH. Self-administration of psychoactive substances by the monkey. Psychopharmacologia. 1969;16:30–48.

    CAS 
    PubMed 

    Google Scholar 

  • Becker AM, Klaiber A, Holze F, Istampoulouoglou I, Duthaler U, Varghese N, et al. Ketanserin reverses the acute response to LSD in a randomized, double-blind, placebo-controlled, crossover study in healthy participants. Int J Neuropsychopharmacol. 2023;26:97–106.

    CAS 
    PubMed 

    Google Scholar 

  • Kometer M, Schmidt A, Jäncke L, Vollenweider FX. Activation of serotonin 2A receptors underlies the psilocybin-induced effects on α oscillations, N170 visual-evoked potentials, and visual hallucinations. J Neurosci. 2013;33:10544–51.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Holze F, Vizeli P, Ley L, Müller F, Dolder P, Stocker M, et al. Acute dose-dependent effects of lysergic acid diethylamide in a double-blind placebo-controlled study in healthy subjects. Neuropsychopharmacology. 2021;46:537–44.

    CAS 
    PubMed 

    Google Scholar 

  • Valle M, Maqueda AE, Rabella M, Rodríguez-Pujadas A, Antonijoan RM, Romero S, et al. Inhibition of alpha oscillations through serotonin-2A receptor activation underlies the visual effects of ayahuasca in humans. Eur Neuropsychopharmacol. 2016;26:1161–75.

    CAS 
    PubMed 

    Google Scholar 

  • Kometer M, Schmidt A, Bachmann R, Studerus E, Seifritz E, Vollenweider FX. Psilocybin biases facial recognition, goal-directed behavior, and mood state toward positive relative to negative emotions through different serotonergic subreceptors. Biol Psychiatry. 2012;72:898–906.

    CAS 
    PubMed 

    Google Scholar 

  • Vollenweider FX, Vollenweider-Scherpenhuyzen MFI, Bäbler A, Vogel H, Hell D. Psilocybin induces schizophrenia-like psychosis in humans via a serotonin-2 agonist action. NeuroReport. 1998;9:3897.

    CAS 
    PubMed 

    Google Scholar 

  • Quednow BB, Kometer M, Geyer MA, Vollenweider FX. Psilocybin-Induced deficits in automatic and controlled inhibition are attenuated by ketanserin in healthy human volunteers. Neuropsychopharmacology. 2012;37:630–40.

    CAS 
    PubMed 

    Google Scholar 

  • Preller KH, Herdener M, Pokorny T, Planzer A, Kraehenmann R, Stämpfli P, et al. The fabric of meaning and subjective effects in LSD-Induced states depend on serotonin 2A receptor activation. Curr Biol. 2017;27:451–7.

    CAS 
    PubMed 

    Google Scholar 

  • Klaiber A, Schmid Y, Becker AM, Straumann I, Erne L, Jelusic A, et al. Acute dose-dependent effects of mescaline in a double-blind placebo-controlled study in healthy subjects. Transl Psychiatry. 2024;14:1–8.

    Google Scholar 

  • Holze F, Madsen MK, Svarer C, Gillings N, Stenbaek DS, Rudin D, et al. Ketanserin exhibits dose- and concentration-proportional serotonin 2A receptor occupancy in healthy individuals: relevance for psychedelic research. Eur Neuropsychopharmacol. 2024;88:43–48.

    CAS 
    PubMed 

    Google Scholar 

  • Casey AB, Cui M, Booth RG, Canal CE. “Selective” serotonin 5-HT2A receptor antagonists. Biochem Pharmacol. 2022;200:115028.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Madsen MK, Fisher PM, Burmester D, Dyssegaard A, Stenbæk DS, Kristiansen S, et al. Psychedelic effects of psilocybin correlate with serotonin 2A receptor occupancy and plasma psilocin levels. Neuropsychopharmacology. 2019;44:1328–34.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Corne SJ, Pickering RW. A possible correlation between drug-induced hallucinations in man and a behavioural response in mice. Psychopharmacologia. 1967;11:65–78.

    CAS 
    PubMed 

    Google Scholar 

  • Halberstadt AL, Chatha M, Klein AK, Wallach J, Brandt SD. Correlation between the potency of hallucinogens in the mouse head-twitch response assay and their behavioral and subjective effects in other species. Neuropharmacology. 2020;167:107933.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Fiorella D, Rabin RA, Winter JC. The role of the 5-HT2A and 5-HT2C receptors in the stimulus effects of hallucinogenic drugs I: Antagonist correlation analysis. Psychopharmacology (Berl). 1995;121:347–56.

    CAS 
    PubMed 

    Google Scholar 

  • Halberstadt AL, Koedood L, Powell SB, Geyer MA. Differential contributions of serotonin receptors to the behavioral effects of indoleamine hallucinogens in mice. J Psychopharmacol (Oxf). 2011;25:1548–61.

    CAS 

    Google Scholar 

  • Canal CE, Olaghere da Silva UB, Gresch PJ, Watt EE, Sanders-Bush E, Airey DC. The serotonin 2C receptor potently modulates the head-twitch response in mice induced by a phenethylamine hallucinogen. Psychopharmacology (Berl). 2010;209:163–74.

    CAS 
    PubMed 

    Google Scholar 

  • Hutten NRPW, Mason NL, Dolder PC, Theunissen EL, Holze F, Liechti ME, et al. Low Doses of LSD Acutely Increase BDNF Blood Plasma Levels in Healthy Volunteers. ACS Pharmacol Transl Sci. 2021;4:461–6.

    CAS 
    PubMed 

    Google Scholar 

  • de Almeida RN, de Galvão ACM, da Silva FS, Silva EADS, Palhano-Fontes F, Maia-de-Oliveira JP, et al. Modulation of serum brain-derived neurotrophic factor by a single dose of ayahuasca: observation from a randomized controlled trial. Front Psychol. 2019;10:1234.

    PubMed 
    PubMed Central 

    Google Scholar 

  • Becker AM, Holze F, Grandinetti T, Klaiber A, Toedtli VE, Kolaczynska KE, et al. Acute effects of psilocybin after escitalopram or placebo pretreatment in a randomized, double-blind, placebo-controlled, crossover study in healthy subjects. Clin Pharmacol Ther. 2022;111:886–95.

    CAS 
    PubMed 

    Google Scholar 

  • Holze F, Ley L, Müller F, Becker AM, Straumann I, Vizeli P, et al. Direct comparison of the acute effects of lysergic acid diethylamide and psilocybin in a double-blind placebo-controlled study in healthy subjects. Neuropsychopharmacology. 2022;47:1180–7.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Holze F, Vizeli P, Müller F, Ley L, Duerig R, Varghese N, et al. Distinct acute effects of LSD, MDMA, and D-amphetamine in healthy subjects. Neuropsychopharmacology. 2020;45:462–71.

    CAS 
    PubMed 

    Google Scholar 

  • Rocha JM, Rossi GN, de Lima Osório F, Bouso JC, de Oliveira Silveira G, Yonamine M, et al. Effects of ayahuasca on the recognition of facial expressions of emotions in naive healthy volunteers: a pilot, proof-of-concept, randomized controlled trial. J Clin Psychopharmacol. 2021;41:267.

    PubMed 

    Google Scholar 

  • Vogt SB, Ley L, Erne L, Straumann I, Becker AM, Klaiber A, et al. Acute effects of intravenous DMT in a randomized placebo-controlled study in healthy participants. Transl Psychiatry. 2023;13:172.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Shafiee A, Arabzadeh Bahri R, Rafiei MA, Esmaeilpur Abianeh F, Razmara P, Jafarabady K, et al. The effect of psychedelics on the level of brain-derived neurotrophic factor: a systematic review and meta-analysis. J Psychopharmacol (Oxf). 2024;38:425–31.

    Google Scholar 

  • Le Nedelec M, Glue P, Winter H, Goulton C, Broughton L, Medlicott N. Acute low-dose ketamine produces a rapid and robust increase in plasma BDNF without altering brain BDNF concentrations. Drug Deliv Transl Res. 2018;8:780–6.

    PubMed 

    Google Scholar 

  • Ly C, Greb AC, Vargas MV, Duim WC, Grodzki ACG, Lein PJ, et al. Transient stimulation with psychoplastogens is sufficient to initiate neuronal growth. ACS Pharmacol Transl Sci. 2021;4:452–60.

    CAS 
    PubMed 

    Google Scholar 

  • Raval NR, Johansen A, Donovan LL, Ros NF, Ozenne B, Hansen HD, et al. A Single dose of psilocybin increases synaptic density and decreases 5-HT2A receptor density in the pig brain. Int J Mol Sci. 2021;22:835.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Zhao X, Du Y, Yao Y, Dai W, Yin Y, Wang G, et al. Psilocybin promotes neuroplasticity and induces rapid and sustained antidepressant-like effects in mice. J Psychopharmacol (Oxf). 2024;38:489–99.

    CAS 

    Google Scholar 

  • Calder AE, Hasler G. Towards an understanding of psychedelic-induced neuroplasticity. Neuropsychopharmacology. 2023;48:104–12.

    PubMed 

    Google Scholar 

  • Benekareddy M, Nair AR, Dias BG, Suri D, Autry AE, Monteggia LM, et al. Induction of the plasticity-Associated immediate early gene Arc by stress and hallucinogens: role of brain-derived neurotrophic factor. Int J Neuropsychopharmacol. 2013;16:405–15.

    CAS 
    PubMed 

    Google Scholar 

  • Ito H, Nyberg S, Halldin C, Lundkvist C, Farde L. PET imaging of central 5-HT2A receptors with carbon-11-MDL 100,907. J Nucl Med. 1998;39:208–14.

    CAS 
    PubMed 

    Google Scholar 

  • Beliveau V, Ganz M, Feng L, Ozenne B, Højgaard L, Fisher PM, et al. A High-Resolution in vivo atlas of the human brain’s serotonin system. J Neurosci. 2017;37:120–8.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Pompeiano M, Palacios JM, Mengod G. Distribution of the serotonin 5-HT2 receptor family mRNAs: comparison between 5-HT2A and 5-HT2C receptors. Mol Brain Res. 1994;23:163–78.

    CAS 
    PubMed 

    Google Scholar 

  • Davoudian PA, Shao L-X, Kwan AC. Shared and distinct brain regions targeted for immediate early gene expression by ketamine and psilocybin. ACS Chem Neurosci. 2023;14:468–80.

    CAS 
    PubMed 

    Google Scholar 

  • Korpi ER, den Hollander B, Farooq U, Vashchinkina E, Rajkumar R, Nutt DJ, et al. Mechanisms of action and persistent neuroplasticity by drugs of abuse. Pharmacol Rev. 2015;67:872–1004.

    CAS 
    PubMed 

    Google Scholar 

  • Tuvikene J, Pruunsild P, Orav E, Esvald E-E, Timmusk T. AP-1 Transcription factors mediate BDNF-Positive feedback loop in cortical neurons. J Neurosci. 2016;36:1290–305.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • López-Giménez JF, González-Maeso J Hallucinogens and Serotonin 5-HT2A Receptor-Mediated Signaling Pathways. In: Halberstadt AL, Vollenweider FX, Nichols DE, editors. Behav. Neurobiol. Psychedelic Drugs, Berlin, Heidelberg: Springer; 2018. p. 45–73.

  • Rantamäki T. TrkB neurotrophin receptor at the core of antidepressant effects, but how? Cell Tissue Res. 2019;377:115–24.

    PubMed 

    Google Scholar 

  • Luttrell LM, Lefkowitz RJ. The role of β-arrestins in the termination and transduction of G-protein-coupled receptor signals. J Cell Sci. 2002;115:455–65.

    CAS 
    PubMed 

    Google Scholar 

  • Smith JS, Lefkowitz RJ, Rajagopal S. Biased signalling: from simple switches to allosteric microprocessors. Nat Rev Drug Discov. 2018;17:243–60.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Kim K, Che T, Panova O, DiBerto JF, Lyu J, Krumm BE, et al. Structure of a hallucinogen-activated Gq-Coupled 5-HT2A serotonin receptor. Cell. 2020;182:1574–1588.e19.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Wallach J, Cao AB, Calkins MM, Heim AJ, Lanham JK, Bonniwell EM, et al. Identification of 5-HT2A receptor signaling pathways associated with psychedelic potential. Nat Commun. 2023;14:8221.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Glatfelter GC, Pottie E, Partilla JS, Stove CP, Baumann MH. Comparative pharmacological effects of lisuride and lysergic acid diethylamide revisited. ACS Pharmacol Transl Sci. 2024;7:641–53.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Rodriguiz RM, Nadkarni V, Means CR, Pogorelov VM, Chiu Y-T, Roth BL, et al. LSD-stimulated behaviors in mice require β-arrestin 2 but not β-arrestin 1. Sci Rep. 2021;11:1–14.

    Google Scholar 

  • Schmid CL, Raehal KM, Bohn LM. Agonist-directed signaling of the serotonin 2A receptor depends on β-arrestin-2 interactions in vivo. Proc Natl Acad Sci. 2008;105:1079–84.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Schmid CL, Bohn LM. Serotonin, but not N-Methyltryptamines, activates the serotonin 2A receptor via a β-Arrestin2/Src/Akt signaling complex in vivo. J Neurosci. 2010;30:13513–24.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Smith RL, Barrett RJ, Sanders-Bush E. Neurochemical and behavioral evidence that quipazine-ketanserin discrimination is mediated by serotonin2A receptor. J Pharmacol Exp Ther. 1995;275:1050–7.

    CAS 
    PubMed 

    Google Scholar 

  • Kaplan AL, Confair DN, Kim K, Barros-Álvarez X, Rodriguiz RM, Yang Y, et al. Bespoke library docking for 5-HT2A receptor agonists with antidepressant activity. Nature. 2022;610:582–91.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Marek GJ, Martin-Ruiz R, Abo A, Artigas F. The selective 5-HT2A receptor antagonist M100907 enhances antidepressant-like behavioral effects of the SSRI fluoxetine. Neuropsychopharmacology. 2005;30:2205–15.

    CAS 
    PubMed 

    Google Scholar 

  • Liu J-L, Li M, Dang X-R, Wang Z-H, Rao Z-R, Wu S-X, et al. A NMDA receptor antagonist, MK-801 impairs consolidating extinction of auditory conditioned fear responses in a pavlovian model. PLOS ONE. 2009;4:e7548.

    PubMed 
    PubMed Central 

    Google Scholar 

  • Dalton GL, Wu DC, Wang YT, Floresco SB, Phillips AG. NMDA GluN2A and GluN2B receptors play separate roles in the induction of LTP and LTD in the amygdala and in the acquisition and extinction of conditioned fear. Post-Trauma Stress Disord. 2012;62:797–806.

    CAS 

    Google Scholar 

  • Planchez B, Surget A, Belzung C. Animal models of major depression: drawbacks and challenges. J Neural Transm. 2019;126:1383–408.

    CAS 
    PubMed 

    Google Scholar 

  • Belovicova K, Bogi E, Csatlosova K, Dubovicky M. Animal tests for anxiety-like and depression-like behavior in rats. Interdiscip Toxicol. 2017;10:40–43.

    PubMed 

    Google Scholar 

  • Hendrie C, Pickles A. The failure of the antidepressant drug discovery process is systemic. J Psychopharmacol (Oxf). 2013;27:407–16.

    Google Scholar 

  • Pehrson AL, Roberts D, Khawaja A, McNair R. The role of serotonin neurotransmission in rapid antidepressant actions. Psychopharmacology (Berl). 2022;239:1823–38.

    CAS 
    PubMed 

    Google Scholar 

  • Béïque J-C, Imad M, Mladenovic L, Gingrich JA, Andrade R. Mechanism of the 5-hydroxytryptamine 2A receptor-mediated facilitation of synaptic activity in prefrontal cortex. Proc Natl Acad Sci USA. 2007;104:9870–5.

    PubMed 
    PubMed Central 

    Google Scholar 

  • Andrade R. Serotonergic regulation of neuronal excitability in the prefrontal cortex. Neuropharmacology. 2011;61:382–6.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Muschamp JW, Regina MJ, Hull EM, Winter JC, Rabin RA. Lysergic acid diethylamide and [−]-2,5-dimethoxy-4-methylamphetamine increase extracellular glutamate in rat prefrontal cortex. Brain Res. 2004;1023:134–40.

    CAS 
    PubMed 

    Google Scholar 

  • Vollenweider FX, Preller KH. Psychedelic drugs: neurobiology and potential for treatment of psychiatric disorders. Nat Rev Neurosci. 2020;21:611–24.

    CAS 
    PubMed 

    Google Scholar 

  • Aghajanian GK, Marek GJ. Serotonin, via 5-HT2A receptors, increases EPSCs in layer V pyramidal cells of prefrontal cortex by an asynchronous mode of glutamate release. Brain Res. 1999;825:161–71.

    CAS 
    PubMed 

    Google Scholar 

  • Baki L, Fribourg M, Younkin J, Eltit JM, Moreno JL, Park G, et al. Cross-signaling in metabotropic glutamate 2 and serotonin 2A receptor heteromers in mammalian cells. Pflüg Arch – Eur J Physiol. 2016;468:775–93.

    CAS 

    Google Scholar 

  • Fribourg M, Moreno JL, Holloway T, Provasi D, Baki L, Mahajan R, et al. Decoding the Signaling of a GPCR Heteromeric Complex Reveals a Unifying Mechanism of Action of Antipsychotic Drugs. Cell. 2011;147:1011–23.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Moreno JL, Miranda-Azpiazu P, García-Bea A, Younkin J, Cui M, Kozlenkov A, et al. Allosteric signaling through an mGlu2 and 5-HT2A heteromeric receptor complex and its potential contribution to schizophrenia. Sci Signal. 2016;9:ra5–ra5.

    PubMed 
    PubMed Central 

    Google Scholar 

  • Olivero G, Grilli M, Vergassola M, Bonfiglio T, Padolecchia C, Garrone B, et al. 5-HT2A-mGlu2/3 receptor complex in rat spinal cord glutamatergic nerve endings: A 5-HT2A to mGlu2/3 signalling to amplify presynaptic mechanism of auto-control of glutamate exocytosis. Neuropharmacology. 2018;133:429–39.

    CAS 
    PubMed 

    Google Scholar 

  • Saha S, González-Maeso J. The crosstalk between 5-HT2AR and mGluR2 in schizophrenia. Neuropharmacology. 2023;230:109489.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Saha S, Gonzalez-Maeso J Translation-independent association of mRNAs encoding protomers of the 5-HT2A-mGlu2 receptor complex in living cells. 2024:2024.06.17.599432.

  • Taddeucci A, Olivero G, Roggeri A, Milanese C, Giorgio FPD, Grilli M, et al. Presynaptic 5-HT2A-mGlu2/3 receptor–receptor crosstalk in the prefrontal cortex: metamodulation of glutamate exocytosis. Cells. 2022;11:3035.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Jakab RL, Goldman-Rakic PS. 5-Hydroxytryptamine2A serotonin receptors in the primate cerebral cortex: Possible site of action of hallucinogenic and antipsychotic drugs in pyramidal cell apical dendrites. Proc Natl Acad Sci. 1998;95:735–40.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Miner LAH, Backstrom JR, Sanders-Bush E, Sesack SR. Ultrastructural localization of serotonin2A receptors in the middle layers of the rat prelimbic prefrontal cortex. Neuroscience. 2003;116:107–17.

    CAS 
    PubMed 

    Google Scholar 

  • Gewirtz JC, Chen AC, Terwilliger R, Duman RC, Marek GJ. Modulation of DOI-induced increases in cortical BDNF expression by group II mGlu receptors. Pharmacol Biochem Behav. 2002;73:317–26.

    CAS 
    PubMed 

    Google Scholar 

  • Gewirtz JC, Marek GJ. behavioral evidence for interactions between a hallucinogenic drug and group II metabotropic glutamate receptors. Neuropsychopharmacology. 2000;23:569–76.

    CAS 
    PubMed 

    Google Scholar 

  • Casarotto PC, Girych M, Fred SM, Kovaleva V, Moliner R, Enkavi G, et al. Antidepressant drugs act by directly binding to TRKB neurotrophin receptors. Cell. 2021;184:1299–1313.e19.

    CAS 
    PubMed 
    PubMed Central 

    Google Scholar 

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  • Fusion breakthrough uses inverted D plasma to solve key energy challenge

    Fusion breakthrough uses inverted D plasma to solve key energy challenge

    Scientists at the DIII-D National Fusion Facility are investigating a different approach to tokamak operation that has yielded promising results for the design of future fusion power plants. 

    Recent experiments have demonstrated that a plasma configuration known as “negative triangularity” can achieve the high-performance conditions necessary for sustained fusion energy, while also addressing a critical challenge related to heat management inside the reactor.

    In 2023, the DIII-D facility conducted a dedicated experimental campaign to assess this operational method. 

    The findings show that negative triangularity plasmas can produce stable conditions that meet and, in some cases, exceed the requirements for future fusion pilot plants. 

    These results are notable because the fusion community had previously projected that this plasma shape would be less stable than conventional approaches.

    Altering cross-sectional shape of plasma

    Tokamak devices are central to fusion energy research. They use powerful magnetic fields to contain and shape plasma—a state of matter where atoms are heated to extreme temperatures, causing them to separate into ions and electrons. 

    The goal is to harness the energy released when these atomic nuclei fuse together. To make a fusion power plant economically viable, a tokamak must simultaneously achieve high plasma pressure, current, and density, all while effectively confining the heat.

    The negative triangularity configuration alters the cross-sectional shape of the plasma from the conventional “D” shape to an inverted “D,” with the curved portion facing the tokamak’s inner wall. 

    In the DIII-D experiments, this shape demonstrated unexpectedly low levels of instability. Researchers were able to achieve high pressure, density, and current concurrently, and observed that the plasma’s heat confinement was very good under these conditions.

    Conjunction with ‘divertor detachment’

    A significant challenge in tokamak design is the core-edge integration issue. This refers to the difficulty of maintaining a sufficiently hot plasma core, where fusion reactions occur, while keeping the plasma edge cool enough to prevent heat from damaging the interior walls of the device. The negative triangularity experiments offered a potential solution to this problem.

    For the first time, researchers operating with a negative triangularity shape achieved high plasma confinement in conjunction with “divertor detachment.” 

    This condition creates a cooler boundary layer that reduces the amount of heat and the electron temperature at the material surfaces. This was accomplished while maintaining an instability-free plasma edge, suggesting an integrated solution for the core and the edge. 

    Scientists are now using advanced simulation tools to study these divertor conditions more closely, which will help them confidently extrapolate the findings to future fusion power plant designs.’

    Better suppression of plasma instabilities

    “These features collectively indicate the promising potential of negative triangularity and support further investigation of this regime for development as a fusion pilot plant design,” concluded the researchers in a press release. 

    The advantages of negative triangularity include better suppression of plasma instabilities, which cause the expulsion of particles and energy. This can also help reduce damage to the tokamak wall, which is a concern in fusion reactors.

    Earlier, in January this year, SMART (Small Aspect Ratio Tokamak), the world’s only fusion reactor with ‘negative triangularity’ constructed at the University of Sevilla in Spain, produced its first plasma.

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  • Living on Mars would suck

    Living on Mars would suck

    The billionaire owners of Space X and Blue Origin have competing visions of a space-based future. Elon Musk wants a self-sustaining settlement on Mars as a backup for humanity in case the Earth gets destroyed. Jeff Bezos wants us to move heavy industry and all polluting industries to space to save Earth’s climate, and envisions a trillion humans living in space.

    Meanwhile, the United States and China are locked in a race of their own for dominance of space, with Chinese advancements far outpacing America’s. The nuclear-wielding superpowers could wind up competing over territory on the moon and Mars.

    Mars, for all its flaws — and there are many, including radiation, dust storms, and unbreathable air — is the only planet in our solar system that’s a candidate for settlement. Its day and night cycle closely resembles Earth’s, its dramatic temperature swings are moderate compared to other planets, and it contains the basic building blocks of life.

    But the science journalist, author, and astrophysicist Adam Becker says it’s just not worth it.

    His recent book, More Everything Forever: AI Overlords, Space Empires, and Silicon Valley’s Crusade to Control the Fate of Humanity, challenges the fashionable ideologies guiding tech leaders today, including long-termism, effective altruism, transhumanism, and space colonization.

    As Becker puts it, it’s about “the horrible ideas that tech billionaires have about the future that they’re trying to shove down our throats, and why they don’t work.”

    Becker told Today, Explained co-host Sean Ramewaram why he thinks Mars is worth exploring for scientific inquiry, but not as a Plan B for Earth.

    Below is an excerpt of their conversation, edited for length and clarity. There’s much more in the full podcast, so listen to Today, Explained wherever you get podcasts, including Apple Podcasts, Pandora, and Spotify.

    So, you think Mars is a horrible idea?

    Mars is a horrible idea. Mars is a terrible place; it’s awful. There’s nothing to breathe. You’ll die of cancer if you hang out there for too long because it’s covered in radiation. The dirt is poisoned. The gravity’s too low. It gets hit with asteroids more often than Earth does. There’s no biosphere. There’s nothing to eat. There’s nothing to breathe. If you hung out on the surface of Mars without a spacesuit, you would asphyxiate while the saliva boils off your tongue.

    But you’re an astrophysicist, author, and journalist, which means at some point you were a young child who dreamt of space. And part of the dream of space is Mars, right?

    When I was a kid, I thought that the future was in space. I watched a lot of Star Trek because I’m a huge nerd, and a young growing nerd needs to consume healthy amounts of Star Trek in order to grow up to be a big, strong nerd. When I was a kid, I thought of Star Trek as a documentary about the future. Not literally a documentary, but I thought, “Yeah, this is what we’re shooting for; this is what we want. We want to be in space, that’s where the good future is.” And then I grew up.

    Notably, there weren’t a lot of billionaires on Star Trek, or they didn’t talk about it, at least.

    No. In fact, what they talked about was that there was no money.

    So, you grow up, and you see the intersection of space and money, and you change your mind about how you feel about space? Or at least Mars.

    I love space. I did a PhD in astrophysics for a reason. I think that space research and exploring space with robots and satellites is amazing. But seeing billionaires turning space into another status icon for the ultra wealthy? It’s gross.

    Musk talks about Mars as if it’s the inevitable future of humanity, that going to Mars is a project to save humanity like some giant philanthropic effort, and it’s just nonsense. He says we have to go to Mars in case there’s a disaster here on Earth, and we have to put a million people on Mars by 2050, and they have to be able to survive even if the rockets from Earth stop coming.

    I’m like, dude, that is not happening. Mars is awful, and there is nothing that could happen to Earth that would make it a worse place than Mars. You could have an asteroid hit as bad as the one that killed off the dinosaurs 66 million years ago. And the day that that happened, which is the worst day in the history of complex life on Earth, was a nicer day than any day on Mars in the last few billion years.

    What about the Bezos argument for space colonization?

    I will say one nice thing about one billionaire: Jeff Bezos at one point made fun of Musk for promoting Mars. He’s like, Mars sucks. I’m like, yeah, you know what? Jeff Bezos is right. Mars does suck. It’s everything he said after that that was a problem. Because Bezos also has a specific vision for space. He says we need to go out into space to live in hundreds of thousands or millions of enormous space stations so we can have a trillion humans living in space in a couple of centuries.

    And before you tell us what you think of that idea, we see a lot of this in the science fiction that we love to watch, from Star Trek to Interstellar to 2001: A Space Odyssey.

    Absolutely. But science fiction is fiction. It is a set of stories that we tell not to predict the future, but as a setting to explore some questions about being human. One of the great science fiction authors of all time, Ursula Le Guin, said that science fiction is not a guide to the future.

    Like any good millennial, there are tweets that live rent free in my head, and one of them is the Torment Nexus tweet, where it says: Science fiction author: “In my book I invented the Torment Nexus as a cautionary tale.” Tech company: “At long last, we have created the Torment Nexus from classic sci-fi novel Don’t Create the Torment Nexus.”

    “We should be focusing on actually making this world a better place. Mars is not hope. It’s not even a fantasy. It’s a delusion.”

    I agree that science fiction can give us something to aspire to, but it’s not the literal technology in the science fiction stories. Those things are narrative devices, like warp drive. We shouldn’t aspire to warp drive because — just going to throw this out there as a physicist — that ain’t happening.

    One of the things I love about Star Trek is it shows a future to aspire to in terms of how the people relate to each other and the kind of world that they’ve built, independent of the technology. Star Trek was groundbreaking, even in the original series, in showing a diverse group of people on an aspirational mission of exploration and self-actualization, and working together as friends to explore the world that we live in. That is a future to aspire to.

    That is not what Bezos has in mind. Bezos’s idea is to put a trillion people in space, and he says he wants this because if we stay here on Earth in a few centuries, we’re going to run out of resources and run out of energy. And he’s right about that. If you assume the current rate of constant growth in usage of energy, then a few centuries after that, you’re using all of the energy output of the sun.

    But what you’re saying is there’s an alternative, and that is to not use all of our resources.

    Yeah, or at least to safeguard them more wisely and use them in a more sustainable way. But Bezos wants perpetual growth in energy usage per capita. He’s used that specific phrase. He wants each individual person to use more and more energy forever. And then he talks about how if we had a trillion people, there’d be a thousand Mozarts and a thousand Einsteins. What about the Mozarts and Einsteins that are living and dying in poverty right now?

    It sounds like, for all you disagree with these tech billionaires when it comes to Mars or space colonization, we all have to agree that life on Earth is not infinite. Our sun, the source of life here on Earth, will eventually die. I know it’s very far away. But we made it to the moon, and making it to Mars feels like it could be a step in the right direction.

    When I sat on the steps of the Air and Space Museum here in Washington, DC, and asked people whether we should go to Mars, they didn’t talk about Elon Musk and Jeff Bezos. They talked about the idea that space is infinite, and as a human race, it’s something we should pursue. Do you really think that we should skip the stepping stone, just because these guys have some wrongheaded ideas about why we should be taking that step in the first place?

    I don’t think Mars sucks because the billionaires want to go there. I think Mars sucks and the billionaires want to go there. And why do they want to go there? Well, they’re not particularly original guys. Mars has been in our cultural psyche for a very long time, and so has the idea of sending the human race out into space.

    I think, instead, we should be focusing on actually making this world a better place. Mars is not hope. It’s not even a fantasy. It’s a delusion. It is not a place where we are going to find our fate, unless that fate is painful death.

    You don’t even see a reason to go there so that we can experiment with what it would be like to live on another planet long term? You don’t even see a use for that because it might teach us something about the actual moonshot that we discover in a hundred or a thousand years, which is there’s some planet in some distant galaxy that’s just like home.

    If we find a planet around another star, even in our own galaxy, forget distant galaxies, that’s just like home, we’re not going. It’s not happening. The speed-of-light limit is a hard stop. We are not going. And no one is coming to save us. I find that hopeful. We have to save ourselves.

    There’s a story that I think is apocryphal; toward the end of his life, somebody asked the great architect and visionary R. Buckminster Fuller if he was sad that he was going to die without ever having gone to space. And his answer was, “We’re in space.” We live in space! And we live in the most special and amazing place in space.

    This is a place that we evolved to live, and everything about it is so well suited for us, and it’s not just the distance of the planet from our sun. It’s not just the mix of gases in our atmosphere. It is everything about this biosphere.

    We can eat the fruit off the trees. We live in a place where food literally grows on trees. It’s awesome! This is an amazing place, and we should continue to learn about the universe that we are a part of as we build a better home for ourselves here where we belong.

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  • Why Saturday’s ‘Black Moon’ Sets Up A ‘Blood Moon’ And Three Solar Eclipses

    Why Saturday’s ‘Black Moon’ Sets Up A ‘Blood Moon’ And Three Solar Eclipses

    Topline

    The new moon on Saturday, Aug. 23, will pass unseen. Lost in the sun’s glare, it will get closest to our star — from Earth’s point of view — at precisely 2:06 a.m. EDT. Lost in the sun’s glare, its absence from the night sky signals the end of one orbit of the Earth by the moon, and the beginning of another, but this month it sets up not one, but three eclipses — one lunar and three solar — stretching through 2044.

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  • See Sunday’s Newborn Moon With Mars After Rare ‘Black Moon’ Weekend

    See Sunday’s Newborn Moon With Mars After Rare ‘Black Moon’ Weekend

    Moon gazers across the globe will get the chance to look for a newborn moon in the early evening sky just after sunset on Sunday, Aug. 24, 2025. Always a monthly highlight for skywatchers, the razor-thin crescent in the early evening sky will appear low in the west shortly after sunset, accompanied by the red planet Mars. It comes just a day after a rare seasonal “black moon.”

    Where And When To Look

    The waxing crescent moon will become visible in the western sky shortly after sunset where you are on Sunday evening. Because it’s yet to emerge far from the glare of the sun, it will set about 50 minutes after sunset — meaning observers have less than an hour to spot it.

    Look low toward the western horizon, ideally from a spot with an open, unobstructed view.

    What You’ll See

    The moon will appear as a delicate crescent in the constellation Virgo, with most of its surface impossible to see. Just above and to the left of the crescent moon, Mars will be visible.

    Mars reached opposition on Jan. 16, when it made its closest approach to Earth since 2022. It’s been prominent ever since, and will continue to be visible shortly after sunset for a few more months, though it’s now receding quickly from Earth. It will eventually become lost in the sun’s glare in late November. The red planet will next come to opposition on Feb. 19, 2027.

    Observing Tips

    Catching a crescent this slim requires good timing, a good location, some patience and possibly a pair of binoculars. Head outside about 20 to 30 minutes after sunset and begin scanning low in the west. A clear horizon free from buildings or trees is essential for success.

    A pair of binoculars may help you find the faint crescent close to the horizon, particularly if it’s hazy. Although you may need help finding it, as soon as you have it, you’ll likely be able to find it with the naked eye.

    Although the moon will only be visible this slim for one night, if it’s cloudy, it’s worth looking again the next night. On Sunday, Aug. 25, the waxing crescent moon, now 8% illuminated, will shine just below and to the right of Mars in the western sky after sunset.

    What’s Next In The Night Sky

    The moon’s slim crescent on Aug. 24 and Aug. 25 kicks off a few nights of beautiful moon views. On Tuesday, Aug. 26, a 14%-lit crescent moon slides between Mars and Spica, Virgo’s brightest star, while on Wednesday, Aug. 27, a 21%-lit crescent moon will sit beside Spica and Mars, with bright star Arcturus directly above. Stargazers can try the classic “Arc to Arcturus, spike to Spica” star-hop, beginning from the arc of stars in the Big Dipper’s handle.

    Wishing you clear skies and wide eyes.

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  • Scientists found the missing nutrients bees need — Colonies grew 15-fold

    Scientists found the missing nutrients bees need — Colonies grew 15-fold

    A new study led by the University of Oxford in collaboration with Royal Botanic Gardens Kew, University of Greenwich, and the Technical University of Denmark could provide a cost-effective and sustainable solution to help tackle the devastating decline in honeybees. An engineered food supplement, designed to provide essential compounds found in plant pollen, was found to significantly enhance colony reproduction. The results were published on August 20 in the journal Nature.

    The challenge: addressing a critical nutrient deficiency

    Climate change and agricultural intensification have increasingly deprived honeybees of the floral diversity they need to thrive. Pollen, the major component of their diet, contains specific lipids called sterols necessary for their development. Increasingly, beekeepers are feeding artificial pollen substitutes to their bees due to insufficient natural pollen. However, these commercial supplements — made of protein flour, sugars, and oils — lack the right sterol compounds, making them nutritionally incomplete.

    In the new study, the research team succeeded in engineering the yeast Yarrowia lipolytica to produce a precise mixture of six key sterols that bees need. This was then incorporated into diets fed to bee colonies during three-month feeding trials. These took place in enclosed glasshouses to ensure the bees only fed on the treatment diets.

    Key findings:

    • By the end of the study period, colonies fed with the sterol-enriched yeast had reared up to 15 times more larvae to the viable pupal stage, compared with colonies fed control diets.
    • Colonies fed with the enriched diet were more likely to continue rearing brood up to the end of the three-month period, whereas colonies on sterol-deficient diets ceased brood production after 90 days.
    • Notably, the sterol profile of larvae in colonies fed the engineered yeast matched that found in naturally foraged colonies, suggesting that bees selectively transfer only the most biologically important sterols to their young.

    Senior author Professor Geraldine Wright (Department of Biology, University of Oxford), said: “Our study demonstrates how we can harness synthetic biology to solve real-world ecological challenges. Most of the pollen sterols used by bees are not available naturally in quantities that could be harvested on a commercial scale, making it otherwise impossible to create a nutritionally complete feed that is a substitute for pollen.”

    Lead author Dr Elynor Moore (Department of Biology, University of Oxford at the time of the study, now Delft University of Technology) added: “For bees, the difference between the sterol-enriched diet and conventional bee feeds would be comparable to the difference for humans between eating balanced, nutritionally complete meals and eating meals missing essential nutrients like essential fatty acids. Using precision fermentation, we are now able to provide bees with a tailor-made feed that is nutritionally complete at the molecular level.”

    From pollen to precision nutrition: Identifying and producing key bee sterols

    Before this work, it was unclear which of the diverse sterols in pollen were critical for bee health. To answer this, the researchers chemically assessed the sterol composition of tissue samples harvested from pupae and adult bees. This required some extraordinarily delicate work; for instance, dissecting individual nurse bees to separate the guts. The analysis identified six sterol compounds that consistently made up the majority in bee tissues: 24-methylenecholesterol, campesterol, isofucosterol, β-sitosterol, cholesterol, and desmosterol.

    Using CRISPR-Cas9 gene editing, the researchers then engineered the yeast Yarrowia lipolytica to produce these sterols in a sustainable and affordable way. Y. lipolytica was selected since this yeast has a high lipid content, has been demonstrated as food-safe, and is already used to supplement aquaculture feeds. To produce the sterol-enriched supplement, engineered yeast biomass was cultured in bioreactors, harvested, then dried into a powder.

    Co-author Professor Irina Borodina (The NNF Center for Biosustainability, Technical University of Denmark) said: “We chose oleaginous yeast Yarrowia lipolytica as the cell factory because it is excellent at making compounds derived from acetyl-CoA, such as lipids and sterols, and because this yeast is safe and easy to scale up. It is used industrially to produce enzymes, omega-3 fatty acids, steviol glycosides as calorie-free sweeteners, pheromones for pest control, and other products.”

    Benefits for agriculture and biodiversity

    Pollinators like honeybees contribute to the production of over 70% of leading global crops. Severe declines — caused by a combination of nutrient deficiencies, climate change, mite infestations, viral diseases, and pesticide exposure — poses a significant threat to food security and biodiversity. For instance, over the past decade, annual commercial honey bee colony losses in the U.S have typically ranged between 40 and 50%, and could reach 60 to 70% in 2025. This new engineered supplement offers a practical means to enhance colony resilience without further depleting natural floral resources. Since the yeast biomass also contains beneficial proteins and lipids, it could potentially be expanded into a comprehensive bee feed.

    Co-author Professor Phil Stevenson (RBG Kew and Natural Resources Institute, University of Greenwich) added: “Honey bees are critically important pollinators for the production of crops such as almonds, apples, and cherries and so are present in some crop locations in very large numbers, which can put pressure on limited wildflowers. Our engineered supplement could therefore benefit wild bee species by reducing competition for limited pollen supplies.”

    Danielle Downey (Executive Director of honeybee research nonprofit Project Apis m., not affiliated with the study) said: “We rely on honey bees to pollinate one in three bites of our food, yet bees face many stressors. Good nutrition is one way to improve their resilience to these threats, and in landscapes with dwindling natural forage for bees, a more complete diet supplement could be a game changer. This breakthrough discovery of key phytonutrients that, when included in feed supplements, allow sustained honey bee brood rearing has immense potential to improve outcomes for colony survival, and in turn the beekeeping businesses we rely on for our food production.”

    Next steps and future applications

    Whilst these initial results are promising, further large-scale field trials are needed to assess long-term impacts on colony health and pollination efficacy. Potentially, the supplement could be available to farmers within two years.

    This new technology could also be used to develop dietary supplements for other pollinators or farmed insects, opening new avenues for sustainable agriculture.

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  • Impact of material properties for improved Pseudomonas aeruginosa biofilm inactivation with 280 nm UV LEDs

    Impact of material properties for improved Pseudomonas aeruginosa biofilm inactivation with 280 nm UV LEDs

    Inactivation rates on different materials

    Inactivation potential for 280 nm UV LEDs on pure culture P. aeruginosa biofilm was assessed across eight materials: extruded Polytetrafluoroethylene (PTFE), Acrylonitrile Butadiene Styrene (ABS), Viton®, Silicone, High Density Poly Ethylene (HDPE), Stainless Steel, Porex (expanded PTFE), and Polycarbonate. Biofilm growth was quantified using standard plate counts, and data were analyzed using a non-linear model to determine the dose–response curve for each material tested. The UV LED irradiation reduced cell viability across all tested materials. As illustrated in Fig. 2, the dose–response curves have two regions of interest: slope and tailing.

    Fig. 2

    Geeraerd’s model biodosimetry (dose–response) curves for pure culture P. aeruginosa biofilm grown in CDC biofilm reactor and inactivated with 280 nm UV LED irradiation for (a) ABS (n = 4), (b) HDPE (n = 4), (c) Polycarbonate (n = 3), (d) Porex (n = 3), (e) PTFE (n = 3), (f) Silicone (n = 5), (g) Stainless steel (n = 4), (h) Viton (n = 3).

    The sloped (log-linear) region represents the rate of inactivation, whereas the tailing region demonstrates that increasing fluence does not result in additional log reduction for that test condition. Tailing may occur in instances where there is a resistant subpopulation of a microbe or if there is shielding/shadowing of a subset of microbes, which would prevent them from being exposed to germicidal light. Geeraerd’s Model can quantify this effect in the Nres term, which can provide insights into the impact of material surface in addition to microbial effects. Silicone, polycarbonate, and ABS demonstrated rapid inactivation with steep initial increases in log reduction values at lower fluence levels, achieving over 1.5 LRV at ~ 10 mJ/cm2. PTFE and ABS required higher fluences, ~ 12 mJ/cm2 and ~ 35 mJ/cm2, respectively, to achieve 1.5 LRV. Conversely, stainless steel, HDPE and Viton® did not achieve 1.5 LRV before exhibiting tailing. These observations suggest that surface characteristics play a crucial role in the susceptibility of biofilms to UV LED inactivation. Material surface impacts biofilm attachment and accumulation, which can account for differences in inactivation potential.

    The fluence required to reach the tailing region of log reduction varied among the materials. Silicone and polycarbonate reached their maximum log reduction at around 10 mJ/cm2, while Porex, stainless steel and Viton® required 15 mJ/cm2, PTFE required approximately 25 mJ/cm2, and ABS and HDPE required upwards of 35 mJ/cm2. These results indicate that the effectiveness of 280 nm UV LED biofilm inactivation is highly dependent on the material’s properties and the applied fluence. The variability in LRV across tested materials demonstrates the importance of further surface characterization for results to be fully contextualized and analyzed.

    The calculated inactivation rate constants (k value), residual standard errors and the peak LRV achieved for each material are provided in Table 1. These values allow for a comparison of UV LED effectiveness across material types and further illustrate the impacts and variability that material surface can have on experimental results.

    Table 1 Inactivation rate constants (k) for coupons tested for biofilm formation and inactivation in the CDC biofilm reactor when exposed to 280 nm UV LEDs.

    Inactivation rate constants provide a clear picture of the inactivation effectiveness across the materials tested. A one-way analysis of variance  (ANOVA) revealed a statistically significant difference in k values among various material types (p = 3.92e−9). To further investigate these differences, a Tukey’s Honestly Significant Difference (HSD) test was run, which identified several significant comparisons. The most notable significant differences were observed between Porex and ABS, with a mean difference of 0.1527 (p = 0.000126), indicating that Porex is significantly more effective than ABS. Similarly, significant differences were found between Silicone and ABS (p = 0.00014), and PTFE and ABS (p = 0.0284), suggesting that both Silicone and PTFE also demonstrate higher effectiveness compared to ABS. In contrast, the comparisons between HDPE and ABS (p = 1.00), Polycarbonate and HDPE (p = 0.0821), as well as those between Silicone and PTFE (p = 0.535), showed no significant differences. These findings highlight the differences between materials and emphasize the importance of material choice when considering inactivation effects within a system.

    Potential role of surface properties for UV inactivation of biofilms

    With the limited number of published studies which employ UV LEDs for the inactivation of biofilm on material surfaces, the comparison of collected k values to published values is difficult. Pousty et al.2 employed 270 nm emitting LEDs to inactivate pure culture P. aeruginosa biofilm on three material types (PTFE, polycarbonate and PVC) and observed k-values of 0.133 ± 0.023, 0.416 ± 0.089 and 0.416 ± 0.089, respectively. The k values for PTFE and polycarbonate used in both studies fall within the confidence interval, indicating similar inactivation effectiveness between the experiments.

    Chemicals used for surface inactivation, such as chlorine (Cl2), are commonplace in many homes and industries alike; however, these chemicals may have limited use cases due to surface or human sensitivity and the inability for their inactivation to be augmented using additive effects. Surface reflectance has been shown to impact UV irradiation, and it is hypothesized that increased surface reflection may present an additive inactivation impact for surface inactivation50,51. The diffuse reflectance for each material, measured in triplicate in increments of 0.5 nm, from 200 to 400 nm, is illustrated in Fig. 3 provides the reflectance percentage at 280 nm for each material.

    Fig. 3
    figure 3

    Diffuse reflectance measurements of materials (ah) used for biofilm formation in CDC biofilm reactors for inactivation by 280 nm UV LED irradiation (n = 3). Shaded areas represent 95% confidence intervals around the mean.

    The diffuse reflectance at 280 nm demonstrated a broad range of values, reflecting their varying interactions with UV light. Viton®, a firm black rubber, exhibited the lowest reflectance at 5.2%, followed by Silicone, a soft, transparent rubber, with a reflectance of 6.83%. Polycarbonate, a frosted glass-like material, showed slightly higher reflectance at 7.4%, closely followed by ABS, a hard black plastic, at 8.4%. HDPE, an opaque white plastic, reflected 12.8% of UV light at 280 nm, while Stainless Steel (316L), known for its shiny silver surface, had a reflectance of 16.7%. The two most reflective materials were PTFE, a hard white plastic, and Porex, a flexible white plastic sheet, which demonstrated reflectance of 44.2% and 84.4% respectively, at 280 nm. This variation in reflectance at 280 nm highlights the importance of material properties in UV light interaction and their potential for effective biofilm inactivation.

    A one-way ANOVA was conducted on surface reflectance across the materials and revealed a significant effect of material type (p < 2e−16). Significant differences in reflectance between material pairs were also noted. HDPE demonstrated a substantially higher reflectance compared to ABS, with a difference of 16.54% (p < 0.0001), while the difference between Porex and ABS was even more pronounced at 75.71% (p < 0.0001). A two-way ANOVA examining the interaction between material and wavelength also yielded significant results for material type (p < 2e−16), wavelength (p < 2e−16), and the interaction of material with wavelength (p < 2e−16). This indicates that both the type of material and the wavelength significantly influence reflectance, and the interaction suggests the effect of material on reflectance varies with wavelength. These findings highlight the complex relationship and indicate that surface reflection can contribute to an increase in inactivation capacity. However, a greater dataset with increased material types would have to be tested to identify the extent of the impacts.

    Surfaces with increased roughness or variation can contribute to increased biofilm attachment52,53,54. The surface roughness values are shown in Table 2, where Ra represents the average roughness of the material above the mean line, Rz is the average maximum height of the profile, and Rsm is the mean width of the profile elements.

    Table 2 Surface roughness (Ra, Avg. roughness; Rz, Roughness depth; RSm, Peak spacing) of tested materials.

    A correlation analysis revealed a significant correlation between surface reflectance and surface roughness (p = 0.04). These findings indicate that higher surface roughness is associated with increased diffuse reflectance. To understand the impacts on inactivation due to surface roughness, a further correlation analysis was run between k value and surface roughness (p = 0.202) and surface roughness and Nres (p = 0.484), suggesting neither correlation is statistically significant for the materials tested in this study. This indicated that surface roughness alone does not govern the potential for a material to be inactivated.

    Additionally, a linear regression was run to understand the impacts of surface roughness versus k values (p = 0.202, R2 = 0.255) and Nres (p = 0.484, R2 = 0.0848). However, the regressions were not significant. While there appears to be a small relationship between roughness and k-values, in this study, the lack of statistical significance suggests that roughness does not provide predictive power for k values or Nres.

    The materials which measured with higher Ra and Rz values, such as silicone rubber (Ra = 13.7 µm, Rz = 108.7 µm) and Porex (Ra = 19.84 µm, Rz = 100.01 µm), provide more surface area and microenvironments for biofilm attachment and formation. In contrast, materials like ABS (Ra = 3.26 µm, Rz = 22.8 µm) and stainless steel (Ra = 3.45 µm, Rz = 33.3 µm) have smoother surfaces, which can inhibit biofilm attachment due to the minimal surface texture. This is represented in this study as materials with higher roughness also resulted in higher maximum LRVs. Silicone (Ra = 13.69 µm) and Porex (Ra = 19.86 µm) were measured as the two roughest materials, but also demonstrated the first and third largest LRVs, 2.05 and 1.75 CFU/cm2, respectively. Furthermore, the modelled Nres for both silicone and porex, 1.86 and 1.75, were amongst the largest of the tested materials. This demonstrates that these materials have the potential to provide favourable conditions for microbial shielding, allowing for a larger resistant sub-population than the other tested materials.

    However, this observation does not hold for all materials, for example, HDPE, which measured comparatively low on surface roughness (Ra = 4.63 µm, Rz = 45.89 µm) but exhibited a higher LRV (LRV max. = 1.17). This change could be attributed to additional surface characteristics of HDPE, such as zeta potential, less electrostatic repulsion or hydrophobicity55,56.

    Other approaches to enhance biofilm inactivation with UV LEDs

    Optimization of UV LED parameters, including wavelength, intensity, and exposure time, is crucial for maximizing biofilm inactivation across material types. Identifying surface characteristics such as roughness and reflectivity allows for the tailoring of UV LED inactivation processes to specific use cases. For instance, ABS required a fluence of 20 mJ/cm2 to achieve maximum inactivation, while PTFE and Viton® reached peak inactivation at 10 mJ/cm2. Understanding the differences between material types and their respective inactivation needs allows for only the required fluences to be applied.

    These findings have practical implications for the selection of materials in applications requiring biofilm inactivation using UV LEDs. Materials like ABS, PTFE, and Porex, which show higher and rapid inactivation, are recommended for applications where quick and effective biofilm control is essential. Conversely, materials like HDPE and Polycarbonate, which exhibit lower inactivation rates, may require higher fluence or prolonged exposure for effective biofilm control. Further research is recommended to optimize UV LED parameters for each material to enhance inactivation efficiency. Ultimately, future work should investigate additional material types and the potential synergistic effects with other variables (e.g., light wavelength) to advance the possibilities of UV LED biofilm inactivation.

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  • Most of Earth’s species came from explosive bursts of evolution

    Most of Earth’s species came from explosive bursts of evolution

    The British evolutionary biologist JBS Haldane is said to have quipped that any divine being evidently had ‘an ordinate fondness for beetles’. This bon mot conveyed an important truth: the ‘tree of life’ – the family tree of all species, living or extinct – is very uneven. In places, it resembles a dense thicket of short twigs; elsewhere it has only sparse but long branches. A few groups tend to predominate: as Haldane pointed out, more than 40% of extant insects are beetles, while 60% of birds are passerines, and more than 85% of plants are flowering plants.

    But is such a concentration of species within a few exceptionally large groups a universal phenomenon of life on Earth? This question, important for our understanding of evolution and ecology, has long been the subject of controversy among biologists. But until recently, it was difficult to answer due to our poor knowledge of the number of species in existence, their evolutionary relationships, and the age of each group. But now, scientists in the US finally have provided an answer, published in Frontiers in Ecology and Evolution.

    “Here we show for the first time that most living species do indeed belong to a limited number of rapid radiations: that is, they form groups with many species which evolved in a relatively short period of time,” said Dr John J. Wiens, a professor at the University of Arizona.

    “Specifically, if we look among the kingdoms of life, among animal phyla, and among plant phyla, we find in each case that more than 80% of known species belong to the minority of groups with exceptionally high rates of species diversification.”

    Wiens and his coauthor Dr Daniel Moen, an assistant professor at the University of California Riverside, here analyzed the distribution of species richness and diversification rates across ‘clades’ – groups of species that each evolved from a single ancestor, such as phyla, classes, or families.

    Out on a limb

    They did this for land plants, insects, vertebrates, for all animals, and for all species across life. They analyzed data on each clade’s species richness, age, and estimated diversification rate: that is, the accumulation of new species over time.

    They focused on 10 phyla, 140 orders, and 678 families of land plants, jointly spanning more than 300,000 species; 31 orders and 870 families of insects, encompassing more than one million known species; 12 classes of vertebrates, encompassing more than 66,000 species; and 28 phyla and 1,710 families of animals with more than 1.5 million species. Finally, they analyzed 17 kingdoms and 2,545 families across all of life, including more than 2 million species.

    The results were clear and consistent: irrespective of hierarchical level or group of organisms, the majority of extant species proved to be restricted to a few disproportionately large clades with higher-than-average diversification rates.

    ‘Rapid radiations’ of species are thought to occur when a new ecological niche opens up: for example, when a flock of grassquit birds dispersed from Central America to the virgin territory of the Galápagos Islands approximately 2.5 million years ago to diversify into the famous Darwin’s finches; or when an evolutionary innovation like powered flight prompted the radiation of bats 50 million years ago.

    Seeing the forest for the trees

    “Our results imply that most of life’s diversity is explained by such relatively rapid radiations. We also suggest key traits that might explain these rapid radiations, based on our results and results of earlier studies,” said Wiens.

    “These traits include multicellularity in plants, animals, and fungi across the kingdoms of life; the invasion of land and the adoption of a plant-based diet in arthropods among animal phyla; and the emergence of flowers and insect pollination in flowering plants among plant phyla,” said Wiens.

    However, one ‘known unknown’ remains: the distribution of species within the kingdom bacteria. Approximately 10,000 species of bacteria are known to science, but current estimates for the true number range from millions to trillions. However, the origin of bacteria dates back to 3.5 billion years ago, and so the overall diversification rate among them is actually quite low.

    “If actual bacterial richness really is much higher than described richness for other groups, then a clade with low diversification rates [namely bacteria] would contain the majority of species across life – this would be in stark contrast to our results. Therefore, we caution that our results apply primarily to known species diversity,” wrote the authors.

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  • Antarctica’s Biodiversity at Risk Amid Research Gaps

    Antarctica’s Biodiversity at Risk Amid Research Gaps

    Long-term studies help scientists understand how species and ecosystems change, adapt, or struggle. With today’s fast-paced global shifts and growing environmental threats, this kind of monitoring is more important than ever. Antarctica is changing fast, and that’s a big deal for the plants and animals specially built to survive its extreme conditions. Keeping a close eye on these changes helps researchers protect what’s most vulnerable.

    A new study from University of Wollongong researchers urges a significant boost in long-term monitoring to protect Antarctica’s fragile ecosystems. As climate change reshapes the continent, consistent research helps scientists and policymakers respond with innovative strategies and strong protections.

    From mosses to microbes, Antarctica’s lesser-known life forms play vital roles in its ecosystem. Their survival affects not just the icy south, but ecosystems around the world.

    The study warns that without large-scale monitoring, we risk losing biodiversity that’s deeply connected to life on other continents. Protecting Antarctica means protecting a piece of Earth’s ecological puzzle.

    Scientists reviewed nearly 140 long-term studies on Antarctic life. While over half lasted a decade or more, most focused on penguins and marine mammals. The tiny but mighty organisms, like mosses and lichens, got far less attention.

    Most studies have been conducted in the more accessible West Antarctic Peninsula. Remote East Antarctica? Barely explored.

    Study lead author Dr Melinda Waterman said, “Antarctica’s biodiversity is still largely a mystery. From emperor penguins to freeze-tolerant plants and tiny animals to microbes that live on air, how are they responding to growing threats?”

    “Many of the species thriving beneath the ice shelves and across the harsh tundra are so little studied that we’re only beginning to understand their roles. Long-term monitoring is our window into this hidden world, showing how subtle changes can ripple through entire ecosystems.”

    Distinguished Professor Sharon Robinson AM, who has spent more than 30 years studying Antarctic plants, said tiny organisms support the continent’s entire food web. “Every moss patch, microscopic worm, and deep-sea coral is part of a fragile balance. If we lose them, the consequences could be global. Sustained research gives policymakers the evidence needed to act on climate change and help Antarctica’s wildlife endure.”

    Journal Reference:

    1. Shae Jones, Diana King, Vonda Cummings, Sharon Robinson, and Melinda Waterman. Research bias in long-term monitoring of Antarctic nearshore marine and terrestrial biota. Global Change Biology: DOI: 10.1111/gcb.70392

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