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For a start, even the Australian bush fires were predicted by science:The scientist who predicted the bushfire emergency four decades agoDr Tom Beer’s pioneering 1980s research into bushfires and climate change has, to his dismay, proved all too accurate“I would blame most of that on the lobbying”,” says Pearman, now 78. “That lobbying has been extremely powerful in a country driven by the resource sector that includes uranium, coal and gas.”'What could I have done?' The scientist who predicted the bushfire emergency four decades agoHere are some actual predictions from Global Climate Models all of which have proven correct. Im even linking to the paper directly so you can go and read for yourself.- That the Earth would warm, and about how fast, and about how much(Arrhenius 1896, Callendar 1938, Plass 1956, Sawyer 1972, Broecker 1975; validated by Crowley 2000, Philipona et al 2004, Evans and Puckrin 2006, Lean and Rind 2008, Mann et al. 2008, etc)- That nighttime temperatures would increase more than daytime temperatures(Arrhenius 1896; validated by Dai et al. 1999, Sherwood et al. 2005, etc)- That winter temperatures would increase more than summer temperatures(Arrhenius 1896, Manabe and Stouffer 1980, Rind et al 1989; validated by Balling et al 1999, Volodin and Galin 1999, Crozier 2003, etc)- Polar amplification (that temperatures increase more as you move toward the poles)(Arrhenius 1896, Manabe and Stouffer 1980; validated by Polyakov et al 2001, Holland and Bitz 2003, etc)- That the Arctic would warm faster than the Antarctic(Arrhenius 1896, Manabe and Stouffer 1980; validated by Doran et al 2002, Comisa 2003, Turner et al 2007, etc)- That the Earth’s troposphere would warm and the stratosphere would cool(Manabe and Wetherald 1967, Manabe and Stouffer 1980; validated by Ramaswamy et al. 1996, 2006, De F. Forster et al 1999, Langematz et al 2003, Vinnikov and Grody 2003, Fu et al 2004, Thompson and Solomon 2005, etc)- The near constancy of relative humidity on global average(Manabe and Wetherall 1967; validated by Minschwaner and Dessler 2004, Soden et al 2005, Gettelman and Fu 2008, etc)- Scientists made a retrodiction (a model prediction based on established physics) for Last Glacial Maximum sea surface temperatures which was inconsistent with the paleo evidence for those times; better paleo evidence showed the models were right(Rind and Peteet 1985; validated by Farreral et al 1999, Melanda et al 2005, etc)- The clear sky super greenhouse effect from increased water vapor in the tropics(Vonder Haar 1986; validated by Lubin 1994, etc)- That coastal upwelling of ocean water would increase(Bakun 1990; validated by Goes et al 2005, McGregor et al 2007, etc)- The magnitude (0.3 C) and duration (two years) of the cooling from the Mt. Pinatubo eruption(Hansen et al 1992; validated by Hansen et al 1996, Soden et al 2002, etc)- The amount of water vapor feedback due to ENSO(Lau et al 1996; validated by Soden 2000, Dessler and Wong 2009, etc)- The rising of the tropopause and the effective radiating altitude(Thuburn and Craig 1997, Kushner et al 2001; validated by Santer et al 2003, Seidel and Randel 2006, etc)- The response of southern ocean winds to the ozone hole(Fyfe et al 1999, Kushner et al 2001, Sexton 2001; validated by Thompson and Solomon 2002, etc)- The expansion of the Hadley cells(Quan et al 2002; validated by Fu et al 2006, Hu and Fu 2007, etc)- They predicted a trend significantly different in amount and different in nature from UAH satellite temperatures, and then a bug was found in the satellite data which showed that surface temperatures were more accurate and reliable than UAH temperature data.(Christy et al 2003; validated by Santer et al 2003, Mears and Wentz 2005, Santer et al 2005, Sherwood et al 2005, etc)- The poleward movement of storm tracks(Trenberth and Stepaniak 2003; validated by Yin 2005, etc)Reality check december 2018:"Twenty years ago in Nature we concluded that recent warming was unprecedented in at least six centuries"https://www.nature.com/articles/33859This year in Nature, scientists concluded it's unprecedented in at least eleven millenniahttps://www.nature.com/articles/nature25464Even Exxon predicted in 1982 exactly how high global carbon emissions would be todayAccording to a graph displaying the “growth of atmospheric CO2 and average global temperature increase” over time, the company expected that, by 2020, carbon dioxide in the atmosphere would reach roughly 400 to 420 ppm. This month’s measurement of 415 ppm is right within the expected curve Exxon projected under its “21st Century Study-High Growth scenario.”IN 1982, EXXON SCIENTIST PROJECTED CARBON DIOXIDE CONCENTRATIONS IN THE ATMOSPHERE. (CREDIT: EXXON VIA INSIDE CLIMATE NEWS)Not only did Exxon predict the rise in emissions, it also understood how severe the consequences would be.“At the high end, some scientists suggest there could be considerable adverse impact including the flooding of some coastal land masses as a result of a rise in sea level due to melting of the Antarctic ice sheet,” it continued, stating this would only take place centuries after temperatures warmed by 3 degrees Celsius.”https://insideclimatenews.org/si...Watch to see Exxon scientist show how accurate their prediction was:SUMMARY:Global climate models aren’t given nearly enough credit for their accurate global temperature change projections. As the 2014 IPCC report showed, observed global surface temperature changes have been within the range of climate model simulations.Now a new study shows that the models were even more accurate than previously thought. In previous evaluations like the one done by the IPCC, climate model simulations of global surface air temperature were compared to global surface temperature observational records like HadCRUT4. However, over the oceans, HadCRUT4 uses sea surface temperatures rather than air temperatures.Climate models are even more accurate than you thought | Dana NuccitelliWere the predictions we made about climate change 20 years ago accurate? Here's a lookLiterature that suggests the models are on track after all. And while that may be worrisome for the planet, it’s good news for the scientists working to understand its future. Climate models are even more accurate than you thought The difference between modeled and observed global surface temperature changes is 38% smaller than previously thought. Global climate models aren’t given nearly enough credit for their accurate global temperature change projections.As the 2014 IPCC report showed, observed global surface temperature changes have been within the range of climate model simulations.Worrisome first quarter of 2017 climate trends » Yale Climate ConnectionsClimate Models - OSS FoundationSlow climate mode reconciles historical and model-based estimates of climate sensitivityRobust comparison of climate models with observations using blended land air and ocean sea surface temperatureshttps://www.researchgate.net/pub...Factcheck: Climate models have not 'exaggerated' global warmingBonus:CMIP6: the next generation of climate models explained | Carbon BriefFull answer:Roger Fjellstad Olsen's answer to How accurate have climate change predictions been in the past?

Brief Background on Anti-CD19 CAR-T ImmunotherapySo far, CAR-T immunotherapy has been most successful against CD19-positive tumors such as Acute lymphoblastic leukemia - Wikipedia (specifically B-ALL). CD19 is a cell surface molecule mainly expressed by mature B cells, meaning anti-CD19 CAR-T targets B cell tumors but also normal B cells. Despite considerable differences in CAR-T constructs used in different studies (1, 2, 3, 4), specificallydifferent short-chain variable fragments, scFv (the anti-CD19 antibody variable domain) that would be expressed on the CAR-T cell surface to bind to the CD19 expressed by the B cell tumor, anddifferent stimulating elements (CD28 or 4-1BB +/- CD3 ) that would get inserted into its cell membrane to signal within,so far anti-CD19 CAR-Ts have yielded impressive anti-tumor responses in relapsed or refractory populations. This is interpreted as a considerable advance since these were patients who'd failed standard therapies.Reversible Neurotoxicities as also Fatalities have occurred in various Anti-CD19 CAR-T Immunotherapy TrialsSince such studies began, different groups, including Juno, Novartis and Kite, testing CAR-T immunotherapy for B cell cancers have reported severe side effects including CRS or Cytokine release syndrome - Wikipedia and neurotoxicity as well as fatalities.CRS ranged from low-grade to high-grade fevers, muscle pain (myalgia) and severe hypotension (5).CNS (Central nervous system - Wikipedia) involvement is striking and unexpected since it occurred even in patients without disease in CNS. Neurotoxicity symptoms ranged from Ataxia - Wikipedia (lack of coordination), confusion and delirium to speech loss (aphasia), hallucinations, headaches, seizures (3, 4, 6, 7, 8, 9).While different studies reported anti-CD19 CAR-T associated-neurotoxicities in 13 to 53% of patients (10), they were reversible with speedy admission into critical care and aggressive management.Juno's ROCKET trial: Too Many Fatalities, All from Cerebral Edema. Why: Patient selection criteria and/or CAR-T construct and/or dose?Juno's ROCKET trial was different because it had far more fatalities and all from the same cause, cerebral edema, something previously unreported. Juno Therapeutics first reported 3 fatalities among enrolled patients with resistant/refractory B-ALL (11).Some additional background is necessary at this point. Early in tests of CAR-Ts, scientists observed that depleting patients of lymphocytes (aka lymphodepletion or conditioning) seemed to improve clinical response. Speculation is reducing patient's own circulating lymphocytes prior to infusing them with CAR-Ts reduces competition for cytokines such as IL-7 and IL-15 that CAR-Ts need to survive and expand. Accordingly, patients in Juno's ROCKET study also received conditioning consisting of Fludarabine - Wikipedia / Cyclophosphamide - Wikipedia, a nucleoside analog and an alkylating agent, respectively.FDA put this trial on hold after 3 patients died but then lifted the hold in a record short time, allowing it to resume after removing Fludarabine alone, implying it was the source of increased neurotoxicity. However, two more deaths occurred even after this modification in the conditioning regimen, which led to the FDA stopping this trial.It's difficult to decipher what led to these fatalities since all the relevant factors aren't (yet) in the public domain. However, comparing variables between different trials helps narrow down options (see below from 12) to patient selection and CAR-T construct and dose.Specifically, was there something different about their patient selection criteria and CAR-T construct, and did they use a different perhaps larger dose? This is becauseConditioning regimen of Fludarabine/Cyclophosphamide is commonly used in such trials with no reports of similar problems so that's out as a probable cause.Juno used autologous CAR-T cells (derived from patients themselves) as did Novartis and Kite.Juno used a similar CAR-T construct to the one currently being used by Kite in its anti-CD19 CAR-T trial (13). However, Juno tested it for ALL while Kite's ongoing trial is against non-Hodgkin's lymphoma (NHL). Safe in NHL (at least as of Aug 2017) but not in ALL patients would be an obvious speculation, and determining what the difference entails would be an obvious question to explore.Novartis (14) and Fred Hutchinson Cancer Research Center (15) are using a different CAR-T construct against ALL.Key difference is the signaling domain in their CAR-T is derived from 4-1BB while Juno and Novartis use one derived from CD28 (see below from 12).Studies suggest the CD28 signaling domain enhances anti-tumor activity (16) while the 4-1BB signaling domain confers longer persistence (16, 17).Though the Novartis (14) and FHCRC (15) trials are still ongoing, they already report high percentages of 82 (24 of 29) (18) and 93% (27 of 29) (19), respectively, complete response, which is disappearance of all clinical evidence of disease. No reports yet (as of Aug 2017) of fatalities due to cerebral edema.Unfortunately, patient selection criteria and CAR-T dose Juno used in their ROCKET trial aren't yet available in the public domain (as of Aug 2017) so conclusions about their role can only be speculative.Dose is an especially interesting consideration since one FHCRC study (19) done in collaboration with and funded by Juno showed a correlation between CAR-T cell dose and time of peak CAR-T expansion.What was additionally interesting about this study is that even though they infused CD4 and CD8 CAR-T cells at a 1:1 ratio, they found higher absolute numbers of CD8s at the peak of expansion.Since activated CD8 Cytotoxic T cell - Wikipedia are presumably the effector cells that actually kill the tumor cells, whether dose-dependent expansion of this type of 2nd generation CD8 CAR-Ts could contribute to cerebral edema in relapsing/refractory B-ALL at the dose Juno used in its ROCKET trial is a possibility to consider.Bibliography1. Grupp, Stephan A., et al. "Chimeric antigen receptor–modified T cells for acute lymphoid leukemia." New England Journal of Medicine 368.16 (2013): 1509-1518.; http://www.nejm.org/doi/pdf/10.1056/NEJMoa12151342. Kochenderfer, James N., et al. "Donor-derived CD19-targeted T cells cause regression of malignancy persisting after allogeneic hematopoietic stem cell transplantation." Blood 122.25 (2013): 4129-4139. https://pdfs.semanticscholar.org/cf2b/c433b1f370d1471e4df435a8e618594e0b67.pdf3. Davila, Marco L., et al. "Efficacy and toxicity management of 19-28z CAR T cell therapy in B cell acute lymphoblastic leukemia." Science translational medicine 6.224 (2014): 224ra25-224ra25. https://www.researchgate.net/profile/Marco_Davila2/publication/260271032_Efficacy_and_Toxicity_Management_of_19-28z_CAR_T_Cell_Therapy_in_B_Cell_Acute_Lymphoblastic_Leukemia/links/55518f8d08ae739bdb921e51.pdf4. Lee, Daniel W., et al. "T cells expressing CD19 chimeric antigen receptors for acute lymphoblastic leukaemia in children and young adults: a phase 1 dose-escalation trial." The Lancet 385.9967 (2015): 517-528. https://www.researchgate.net/profile/Rimas_Orentas/publication/266975072_T_cells_expressing_CD19_chimeric_antigen_receptors_for_acute_lymphoblastic_leukaemia_in_children_and_young_adults_a_phase_1_dose-escalation_trial/links/551ea0b30cf2a2d9e13c83d2/T-cells-expressing-CD19-chimeric-antigen-receptors-for-acute-lymphoblastic-leukaemia-in-children-and-young-adults-a-phase-1-dose-escalation-trial.pdf5. Lee, Daniel W., et al. "Current concepts in the diagnosis and management of cytokine release syndrome." Blood 124.2 (2014): 188-195. http://www.bloodjournal.org/content/bloodjournal/124/2/188.full.pdf?sso-checked=true6. Brentjens, Renier J., et al. "CD19-targeted T cells rapidly induce molecular remissions in adults with chemotherapy-refractory acute lymphoblastic leukemia." Science translational medicine 5.177 (2013): 177ra38-177ra38. https://www.researchgate.net/profile/Marco_Davila2/publication/236067161_CD19-Targeted_T_Cells_Rapidly_Induce_Molecular_Remissions_in_Adults_with_Chemotherapy-Refractory_Acute_Lymphoblastic_Leukemia/links/5551902808ae12808b392acd.pdf7. Maude, Shannon L., et al. "Chimeric antigen receptor T cells for sustained remissions in leukemia." New England Journal of Medicine 371.16 (2014): 1507-1517. http://www.nejm.org/doi/pdf/10.1056/NEJMoa14072228. Park, Jae H., et al. "Implications of minimal residual disease negative complete remission (MRD-CR) and allogeneic stem cell transplant on safety and clinical outcome of CD19-targeted 19-28z CAR modified T cells in adult patients with relapsed, refractory B-cell ALL." (2015): 682-682.9. Schuster, Stephen J., et al. "Sustained remissions following chimeric antigen receptor modified T cells directed against CD19 (CTL019) in patients with relapsed or refractory CD19+ lymphomas." (2015): 183-183.10. Wang, Zhenguang, Yelei Guo, and Weidong Han. "Current status and perspectives of chimeric antigen receptor modified T cells for cancer treatment." Protein & Cell (2017): 1-30. https://link.springer.com/content/pdf/10.1007%2Fs13238-017-0400-z.pdf11. DeFrancesco, Laura. "Juno's wild ride." (2016): 793-793. https://www.nature.com/nbt/journal/v34/n8/full/nbt0816-793.html12. Hartmann, Jessica, et al. "Clinical development of CAR T cells—challenges and opportunities in translating innovative treatment concepts." EMBO Molecular Medicine (2017): e201607485. http://embomolmed.embopress.org/content/embomm/early/2017/07/31/emmm.201607485.full.pdf13. A Phase 1-2 Multi-Center Study Evaluating KTE-C19 in Subjects With Refractory Aggressive Non-Hodgkin Lymphoma (ZUMA-1)14. Determine Efficacy and Safety of CTL019 in Pediatric Patients With Relapsed and Refractory B-cell ALL15. Laboratory Treated T Cells in Treating Patients With Relapsed or Refractory Chronic Lymphocytic Leukemia, Non-Hodgkin Lymphoma, or Acute Lymphoblastic Leukemia - Full Text View - ClinicalTrials.gov16. Zhao, Zeguo, et al. "Structural design of engineered costimulation determines tumor rejection kinetics and persistence of CAR T cells." Cancer cell 28.4 (2015): 415-428. https://www.researchgate.net/profile/Maud_Condomines/publication/283205585_Structural_Design_of_Engineered_Costimulation_Determines_Tumor_Rejection_Kinetics_and_Persistence_of_CAR_T_Cells/links/5633886508ae88cf81ba47ac.pdf17. Porter, David L., et al. "Chimeric antigen receptor T cells persist and induce sustained remissions in relapsed refractory chronic lymphocytic leukemia." Science translational medicine 7.303 (2015): 303ra139-303ra139. http://proaa9ff3.pic19.websiteonline.cn/upload/cart19+and+cll_dz87.pdf18. Grupp, Stephan A., et al. "Analysis of a global registration trial of the efficacy and safety of CTL019 in pediatric and young adults with relapsed/refractory acute lymphoblastic leukemia (ALL)." (2016): 221-221.19. Turtle, Cameron J., et al. "CD19 CAR–T cells of defined CD4+: CD8+ composition in adult B cell ALL patients." The Journal of clinical investigation 126.6 (2016): 2123. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4887159/pdf/JCI85309.pdfThanks for the R2A, Christopher VanLang.

Several types of nanoparticles, namely, liposomes, polymeric nanoparticles, solid lipid nanoparticles, dendrimers, appear to be taken up by bacteria. These structures have been explored mainly for their capacity to more efficiently deliver antibiotics. I highlight the few studies that directly compared bacterial uptake/activity of 'nanoparticled' cargo versus cargo alone. Key details that enhance bacterial nanoparticle uptake are italicized.From 1LiposomesLiposomes are small spherical vesicles with phospholipid bilayer walls, usually composed of an amphipathic lipid such as phosphatidylcholine. Incorporating cholesterol increases the membrane's rigidity. Liposomes encapsulate an aqueous space ranging from about 30 to 10000 nm in diameter.From 2Liposomes directly fuse with bacterial membranes, releasing their contents either within the bacterial cell membranes or into its interior. This can improve antibiotic delivery into the bacterial cells, side-stepping bacterial drug-resistance mechanisms such as bacterial membrane impermeability/low permeability or efflux systems (3).From 1Cationic liposome formulations bind more efficiently to skin-associated bacteria, Staphylococcus epidermidis and Proteus vulgaris (4).Liposome-encapsulated oleic acid was bactericidal against MRSA at a 12-fold lower concentration (5) compared to free oleic acid.Liposome-encapsulated Polymyxin B or vancomycin and teichoplanin had better antibacterial activity against drug-resistant Pseudomonas aeruginosa and MRSA, respectively (1). These liposomes also caused bacterial membrane lipid deformation suggesting they fused with it.Skin-associated Propionibacterium acnes (P. acnes). Lauric acid, a free fatty acid showed stronger anti-bacterial activity compared to palmitic and lauric acid. However, lauric acid is poorly water soluble, which limits its use in acne treatment. A study of lauric acid liposome formulation (LipoLA) showed it fused with P. acnes membranes, releasing lauric acid within and killing the bacteria (6).Metal liposomes: Metal matters. Platinum, zinc and titanium enter bacteria, gold doesn't.Wang et al made 16 nm gold nanospheres stabilized with citrate ions, which adhered well with the Salmonella typhimurium surface but were unable to get into the bacteria (7). A comparison of gold and platinum nanoparticles (8) showed the former interacted with Salmonella enteritidis but did not get inside, whereas platinum nanoparticles were observed inside the bacteria.Using flow cytometry (9), dynamic light scattering and transmission electron microscopy (10), Ashutosh et al found that Salmonella typhimurium directly uptake zinc and titanium nanoparticles.Key detail? A mammalian liver component called S9 enhances this metal nanoparticle uptake by bacteria. Experimental studies used either rat- or mouse-liver derived fraction S9. What is the role of this liver S9 fraction? It could supplement metabolic enzymes such as cytochrome P450 (10), enhance the formation of nanoparticle micelles facilitating uptake (11) or serve as a protein coating for the nanoparticles, again facilitating uptake (12).I won't cover silver nanoparticles since ionic silver is largely toxic to bacteria, and used as an antimicrobial agent itself.Polymeric nanoparticlesZhang, L., et al. (1) describe the advantages of polymeric nanoparticles for bacterial deliveryThey are structurally stable and can be synthesized with greater size precision.They have functional groups that can be chemically modified. Lectin, a protein that binds to bacterial cell wall carbohydrates, is frequently used for targeted antimicrobial delivery of polymeric nanoparticles. Lectin-conjugated polymeric nanoparticles containing gliadin specifically bound to Helicobacter pylori cell wall carbohydrate receptors and released the antimicrobial agent into the bacteria (13).Zhang et al describe two major types of polymeric nanoparticles for antimicrobial drug delivery. One is formed via spontaneous self-assembly of diblock copolymers consisting of hydrophilic and hydrophobic parts. The hydrophobic part forms the polymeric core holding the cargo while the hydrophilic part protects the core from degradation. The length of the hydrophobic chain controls the rate of cargo release. Biodegradable polymers such as poly(lactic acid) (PLA), poly(glycolic acid) (PGA), poly(lactide-co-glycolide) (PLGA), poly (?-carprolactone) (PCL), and poly(cyano- acrylate) (PCA) are used to form the hydrophobic polymeric core, while polyethylene glycol (PEG) is most commonly used as the hydrophilic part. The hydrophobic nature of the nanoparticle core allows polymeric nanoparticles to carry and deliver poorly water soluble cargo.In the other type of polymeric nanoparticle, linear polymers such as polyalkyl acrylates and polymethyl methacrylates form nanocapsules by emulsion polymerization. The cargo, antibiotics for example, are either absorbed or covalently conjugated to the nanoparticle surface.The caveat with covalent linkage is the need to empirically assess case-by-case whether the linkage inactivates cargo activity. For example, Abeylath et al found that covalent linkage inactivated penicillin but not beta-lactam or ciprofloxacin (14).Nanoparticles using poly (lactide-co-glycolide) [PLGA] loaded with antibiotics such as gentamicin (15), azithromicin and clarithromicin (16, 17) were more effective than corresponding intact antibiotic against Salmonella typhimurium. It's possible this is due to such nanoparticles adhering better to the bacteria. Dillen et al reported adhesion of PLGA containing cationic Eudragit nanoparticles to S. aureus (18). Bacterial cell walls tend to be negatively charged (19) so exploiting such electrostatic interactions helps bacterial nanoparticle uptake (20). PLGA has many other advantages including low toxicity, cargo flexibility, easy synthesis, precision engineering for surface properties (20).Solid lipid nanoparticlesLipid + surfactants for emulsification. Lipids can be free fatty acids such as palmitic, decanoic or behenic acids, or triglycerides such as trilaurin, trimyristin, or tripalmitin, or steroids such as cholesterol. Emulsifiers include soybean lecithin, phosphatidylcholine. Solid lipid nanoparticles have many advantages over other nanoparticles including greater cargo stability, bothhydrophilic and lipophilic cargo can be loaded, no need for organic solvents, greater precision in controlled cargo release and targeting, and improved bulk production.DendrimerA dendrimer is a polymer structure with enhanced surface area-to-volume ratio owing to extensive branching around a core unit. When a dendrimer has a high concentration of positively charged quaternary ammonium compounds on its surface, they bind more efficiently to negatively charged microbial cell walls. This increases bacterial membrane permeability, letting more dendrimers inside the bacteria (1, 21).I could not find a single study that directly compared cargo alone versus solid lipid nanoparticle- or dendrimer-encapsulated cargo uptake by bacteria.BibliographyZhang, L., et al. "Development of nanoparticles for antimicrobial drug delivery." Current medicinal chemistry 17.6 (2010): 585-594 Page on ucsd.eduNokhodchi, Ali, Ghobad Mohammadi, and Taravat Ghafourian. Nanotechnology tools for efficient antibacterial delivery to Salmonella. INTECH Open Access Publisher, 2012 Page on intechweb.orgMugabe, Clement, et al. "Mechanism of enhanced activity of liposome-entrapped aminoglycosides against resistant strains of Pseudomonas aeruginosa." Antimicrobial agents and chemotherapy 50.6 (2006): 2016-2022 Mechanism of Enhanced Activity of Liposome-Entrapped Aminoglycosides against Resistant Strains of Pseudomonas aeruginosaRobinson, Anne M., et al. "The interaction of phospholipid liposomes with mixed bacterial biofilms and their use in the delivery of bactericide." Colloids and Surfaces A: Physicochemical and Engineering Aspects 186.1 (2001): 43-53.Huang, Chun-Ming, et al. "Eradication of drug resistant Staphylococcus aureus by liposomal oleic acids." Biomaterials 32.1 (2011): 214-221 Page on nih.govYang, Darren, et al. "The antimicrobial activity of liposomal lauric acids against Propionibacterium acnes." Biomaterials 30.30 (2009): 6035-6040. Page on nih.govWang, Shuguang, et al. "Toxic effects of gold nanoparticles on Salmonella typhimurium bacteria." Toxicology and industrial health (2011): 0748233710393395 Page on nih.govSawosz, Ewa, et al. "Visualization of gold and platinum nanoparticles interacting with Salmonella enteritidis and Listeria monocytogenes." International journal of nanomedicine 5 (2010): 631 Page on nih.govKumar, Ashutosh, et al. "A flow cytometric method to assess nanoparticle uptake in bacteria." Cytometry Part A 79.9 (2011): 707-712 Page on wiley.comKumar, Ashutosh, et al. "Cellular uptake and mutagenic potential of metal oxide nanoparticles in bacterial cells." Chemosphere 83.8 (2011): 1124-1132 Page on researchgate.netSereemaspun, A., et al. "Inhibition of Human Cytochrome P450 Enzymes by Metallic Nanoparticles: A preliminary to Nanogenomics." International Journal of Pharmacology 4.6 (2008).Romberg, Birgit, Wim E. Hennink, and Gert Storm. "Sheddable coatings for long-circulating nanoparticles." Pharmaceutical research 25.1 (2008): 55-71 Sheddable Coatings for Long-Circulating NanoparticlesUmamaheshwari, R. B., and N. K. Jain. "Receptor mediated targeting of lectin conjugated gliadin nanoparticles in the treatment of Helicobacter pylori." Journal of drug targeting 11.7 (2003): 415-424.Abeylath, Thotaha Wijayahewage Sampath Chrysantha. "Glyconanobiotics: Novel carbohydrated nanoparticle polymers." (2007) http://scholarcommons.usf.edu/cgi/viewcontent.cgi?article=1586&context=etd&sei-redir=1&referer=http%3A%2F%2Fscholar.google.com%2Fscholar%3Fhl%3Den%26as_sdt%3D0%2C10%26q%3DGlyco%2BNanobiotics%253A%2BNovel%2Bcarbohydrate%2Bnanoparticle%2Bantibiotics%2Bfor%2BMRSA%2Band%2BBacillus%2Banthracis#search=%22Glyco%20Nanobiotics%3A%20Novel%20carbohydrate%20nanoparticle%20antibiotics%20MRSA%20Bacillus%20anthracis%22Ranjan, Ashish, et al. "Antibacterial efficacy of core-shell nanostructures encapsulating gentamicin against an in vivo intracellular Salmonella model." International journal of nanomedicine 4 (2009): 289 Page on nih.govMohammadi, Ghobad, et al. "Development of azithromycin–PLGA nanoparticles: Physicochemical characterization and antibacterial effect against Salmonella typhi." Colloids and Surfaces B: Biointerfaces 80.1 (2010): 34-39.Mohammadi, Ghobad, et al. "Physicochemical and anti-bacterial performance characterization of clarithromycin nanoparticles as colloidal drug delivery system." Colloids and Surfaces B: Biointerfaces 88.1 (2011: 39-44).Dillen, Kathleen, et al. "Adhesion of PLGA or Eudragit®/PLGA nanoparticles to Staphylococcus and Pseudomonas." International journal of pharmaceutics 349.1 (2008): 234-240.Al-Kobaisi, Muhannad F. "Jawetz, Melnick & Adelberg’s Medical Microbiology." Sultan Qaboos University Medical Journal 7.3 (2007): 273.Radovic-Moreno, Aleksandar F., et al. "Surface charge-switching polymeric nanoparticles for bacterial cell wall-targeted delivery of antibiotics." ACS nano 6.5 (2012): 4279-4287 Page on nih.govHuh, Ae Jung, and Young Jik Kwon. "“Nanoantibiotics”: a new paradigm for treating infectious diseases using nanomaterials in the antibiotics resistant era." Journal of Controlled Release 156.2 (2011): 128-145.Thanks for the A2A, Justin Dragna.