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In this work, the implementation of advanced functional coatings based on the combination of two compatible nanofabrication techniques such as electrospinning and dip-coating technology have been successfully obtained for the design of antifungal surfaces. In a first step, uniform and beadless electrospun nanofibers of both polyethylene oxide (PEO) and polyethylene (PEO)/chitosan (CS) blend samples have been obtained. In a second step, the dip-coating process has been gradually performed in order to ensure an adequate distribution of silver nanoparticles (AgNPs) within the electrospun polymeric matrix (PEO/CS/AgNPs) by using a chemical reduction synthetic process, denoted as in situ synthesis (ISS). Scanning electron microscopy (SEM) has been used to evaluate the surface morphology of the samples, showing an evolution in average fiber diameter from 157 ± 43 nm (PEO), 124 ± 36 nm (PEO/CS) and 330 ± 106 nm (PEO/CS/AgNPs). Atomic force microscopy (AFM) has been used to evaluate the roughness profile of the samples, indicating that the ISS process induced a smooth roughness surface because a change in the average roughness Ra from 84.5 nm (PEO/CS) up to 38.9 nm (PEO/CS/AgNPs) was observed. The presence of AgNPs within the electrospun fiber mat has been corroborated by UV-Vis spectroscopy thanks to their characteristic optical properties (orange film coloration) associated to the Localized Surface Plasmon Resonance (LSPR) phenomenon by showing an intense absorption band in the visible region at 436 nm. Energy dispersive X-ray (EDX) profile also indicates the existence of a peak located at 3 keV associated to silver. In addition, after doping the electrospun nanofibers with AgNPs, an important change in the wettability with an intrinsic hydrophobic behavior was observed by showing an evolution in the water contact angle value from 23.4° ± 1.3 (PEO/CS) up to 97.7° ± 5.3 (PEO/CS/AgNPs). The evaluation of the antifungal activity of the nanofibrous mats against Pleurotus ostreatus clearly indicates that the presence of AgNPs in the outer surface of the nanofibers produced an important enhancement in the inhibition zone during mycelium growth as well as a better antifungal efficacy after a longer exposure time. Finally, these fabricated electrospun nanofibrous membranes can offer a wide range of potential uses in fields as diverse as biomedicine (antimicrobial against human or plant pathogen fungi) or even in the design of innovative packaging materials for food preservation.

BackgroundUniversal newborn screening changed the way medical providers think about the presentation of cystic fibrosis (CF). Before implementation of universal screening, it was common for children with CF to present with failure to thrive, nutritional deficiencies, and recurrent infections. Now, nearly all cases of CF are diagnosed by newborn screening shortly after birth before significant symptoms develop. Therefore, providers often do not consider this illness in the setting of a normal newborn screen. Newborn screening significantly decreases the risk of complications in early childhood, yet definitive testing should be pursued if a patient with negative newborn screening presents with symptoms consistent with CF, including severe failure to thrive, metabolic alkalosis due to significant salt losses, or recurrent respiratory infections.Case presentationWe present a case of a 6-month-old infant male with kwashiorkor, severe edema, multiple vitamin deficiencies, hematemesis secondary to coagulopathy, and diffuse erythematous rash, all secondary to severe pancreatic insufficiency. His first newborn screen had an immunoreactive trypsinogen (IRT) value below the state cut-off value, so additional testing was not performed, and his growth trajectory appeared reassuring. He was ultimately diagnosed with CF by genetic testing and confirmatory sweat chloride testing, in the setting of his parents being known CF carriers and his severe presentation being clinically consistent with CF. Acutely, management with supplemental albumin, furosemide, potassium, and vitamin K was initiated to correct the presenting hypoalbuminemia, edema, and coagulopathy. Later, pancreatic enzyme supplementation and additional vitamins and minerals were added to manage ongoing deficiencies from pancreatic insufficiency. With appropriate treatment, his vitamin deficiencies and edema resolved, and his growth improved.ConclusionDue to universal newborn screening, symptomatic presentation of CF is rare and presentation with kwashiorkor is extremely rare in resource-rich communities. The diagnosis of CF was delayed in our patient because of a normal newborn screen and falsely reassuring growth, which after diagnosis was determined to be secondary to severe edematous malnutrition. This case highlights that newborn screening is a useful but imperfect tool. Clinicians should continue to have suspicion for CF in the right clinical context, even in the setting of normal newborn screen results.

Truffles are ascomycete hypogeous fungi belonging to the Tuberaceae family of the Pezizales order that grow in ectomycorrhizal symbiosis with tree roots, and they are known for their peculiar aromas and flavors. The axenic culture of truffle mycelium is problematic because it is not possible in many cases, and the growth rate is meager when it is possible. This limitation has prompted searching and characterizing new strains that can be handled in laboratory conditions for basic and applied studies. In this work, a new strain of Tuber borchii (strain SP1) was isolated and cultured, and its transcriptome was analyzed under different in vitro culture conditions. The results showed that the highest growth of T. borchii SP1 was obtained using maltose-enriched cultures made with soft-agar and in static submerged cultures made at 22 °C. We analyzed the transcriptome of this strain cultured in different media to establish a framework for future comparative studies, paying particular attention to the central metabolic pathways, principal secondary metabolite gene clusters, and the genes involved in producing volatile aromatic compounds (VOCs). The results showed a transcription signal for around 80% of the annotated genes. In contrast, most of the transcription effort was concentrated on a limited number of genes (20% of genes account for 80% of the transcription), and the transcription profile of the central metabolism genes was similar in the different conditions analyzed. The gene expression profile suggests that T. borchii uses fermentative rather than respiratory metabolism in these cultures, even in aerobic conditions. Finally, there was a reduced expression of genes belonging to secondary metabolite clusters, whereas there was a significative transcription of those involved in producing volatile aromatic compounds.

Allogeneic stem cell transplantation (Allo-SCT) implies that a donor and a recipient are not genetically identical. Allo-SCT is used to cure a variety of conditions, including hematologic malignancies using the graft versus tumor effect, nonmalignant hematologic, immune deficiencies, and, more recently, genetic disorders and inborn errors of metabolism. Given the immunosuppressive and myeloablative nature of some of the conditioning chemotherapy regimens used during the Allo-SCT, patients are often at high risk of infection, including viral infections affecting the gastrointestinal tract, following the transplant. Furthermore, other complications such as hepatic sinusoidal obstruction syndrome (SOS) or graft-versus-host disease may occur post-transplant and may require endoscopy to assist in the diagnosis. This review will provide newer insights into the importance of endoscopic techniques in the diagnosis of post-Allo-SCT complications with a focus on safety and timing. [ABSTRACT FROM AUTHOR]

Efficient lignin depolymerization is unique to the wood decay basidiomycetes, collectively referred to as white rot fungi. Phanerochaete chrysosporium simultaneously degrades lignin and cellulose, whereas the closely related species, Ceriporiopsis subvermispora, also depolymerizes lignin but may do so with relatively little cellulose degradation. To investigate the basis for selective ligninolysis, we conducted comparative genome analysis of C. subvermispora and P. chrysosporium. Genes encoding manganese peroxidase numbered 13 and five in C. subvermispora and P. chrysosporium, respectively. In addition, the C. subvermispora genome contains at least seven genes predicted to encode laccases, whereas the P. chrysosporium genome contains none. We also observed expansion of the number of C. subvermispora desaturase-encoding genes putatively involved in lipid metabolism. Microarray-based transcriptome analysis showed substantial up-regulation of several desaturase and MnP genes in wood-containing medium. MS identified MnP proteins in C. subvermispora culture filtrates, but none in P. chrysosporium cultures. These results support the importance of MnP and a lignin degradation mechanism whereby cleavage of the dominant nonphenolic structures is mediated by lipid peroxidation products. Two C. subvermispora genes were predicted to encode peroxidases structurally similar to P. chrysosporium lignin peroxidase and, following heterologous expression in Escherichia coli, the enzymes were shown to oxidize high redox potential substrates, but not Mn2. Apart from oxidative lignin degradation, we also examined cellulolytic and hemicellulolytic systems in both fungi. In summary, the C. subvermispora genetic inventory and expression patterns exhibit increased oxidoreductase potential and diminished cellulolytic capability relative to P. chrysosporium.

This research aimed to establish the relationship between carbon–nitrogen nutritional factors and copper sulfate on laccase activity (LA) by Pleurotus ostreatus. Culture media composition was tested to choose the nitrogen source. Yeast extract (YE) was selected as a better nitrogen source than ammonium sulfate. Then, the effect of glucose and YE concentrations on biomass production and LA as response variables was evaluated using central composite experimental designs with and without copper. The results showed that the best culture medium composition was glucose 45 gL−1 and YE 15 gL−1, simultaneously optimizing these two response variables. The fungal transcriptome was obtained in this medium with or without copper, and the differentially expressed genes were found. The main upregulated transcripts included three laccase genes (lacc2, lacc6, and lacc10) regulated by copper, whereas the principal downregulated transcripts included a copper transporter (ctr1) and a regulator of nitrogen metabolism (nmr1). These results suggest that Ctr1, which facilitates the entry of copper into the cell, is regulated by nutrient-sufficiency conditions. Once inside, copper induces transcription of laccase genes. This finding could explain why a 10–20-fold increase in LA occurs with copper compared to cultures without copper when using the optimal concentration of YE as nitrogen sources.

Strain degeneration has been defined as a decrease or loss in the yield of important commercial traits resulting from subsequent culture, which ultimately leads to Reactive Oxygen Species (ROS) production. Pleurotus ostreatus is a lignin-producing nematophagous edible mushroom. Mycelia for mushroom production are usually maintained in subsequent culture in solid media and frequently show symptoms of strain degeneration. The dikaryotic strain P. ostreatus (DkN001) has been used in our lab as a model organism for different purposes. Hence, different tools have been developed to uncover genetic and molecular aspects of this fungus. In this work, strain degeneration was studied in a full-sib monokaryotic progeny of the DkN001 strain with fast (F) and slow (S) growth rates by using different experimental approaches (light microscopy, malondialdehyde levels, whole-genome transcriptome analysis, and chitosan effect on monokaryotic mycelia). The results obtained showed that: (i) strain degeneration in P. ostreatus is linked to oxidative stress, (ii) the oxidative stress response in monokaryons is genotype dependent, (iii) stress and detoxifying genes are highly expressed in S monokaryons with symptoms of strain degeneration, (iv) chitosan addition to F and S monokaryons uncovered the constitutive expression of both oxidative stress and cellular detoxifying genes in S monokaryon strains which suggest their adaptation to oxidative stress, and (v) the overexpression of the cell wall genes, Uap1 and Cda1, in S monokaryons with strain degeneration phenotype indicates cell wall reshaping and the activation of High Osmolarity Glycerol (HOG) and Cell Wall Integrity (CWI) pathways. These results could constitute a hallmark for mushroom producers to distinguish strain degeneration in commercial mushrooms.

This past summer, humankind took one step towards a Gattaca-like future in which human beings may be genetically engineered before birth. As trumpeted by the headlines, researchers at the University of Oregon became the first American scientists to genetically alter human embryos using CRISPR-Cas9 (CRISPR) [1]. CRISPR is a naturally occurring bacterial immune response that can recognize and destroy the DNA of invading viruses [2]. In 2012, Berkeley scientist Jennifer Doudna and team demonstrated that CRISPR could be reprogrammed to target and alter ostensibly any gene of any organism on earth [3]. Although not the first gene-editing tool to be discovered, CRISPR is much more precise and cost-effective than its predecessors [4]. Consequently, Doudna’s discovery unlocked a plethora of unprecedented gene-editing applications including, but not limited to, the treatment of human disease, the study of human development, the more reliable creation of plants and animals with certain desirable characteristics, and the ability to alter the genomes of human embryos [5]. It is this last application of CRISPR that researchers at the University of Oregon explored when they reportedly eliminated the gene responsible for hypertrophic cardiomyopathy, a leading cause of death among young athletes, from viable human embryos last summer [6]. Although the researchers assert that these embryos were not intended for implantation—a move that would violate current law [7] — the experiment may be a harbinger of things to come. If made clinically available, this particular application of CRISPR may be used to alter human genomes in heritable ways, a practice known as germline modification. However, such alterations carry numerous, well-publicized risks [8]. For example, researchers have identified several technical issues associated with the technology such as off-target edits, mosaicism (i.e., the uneven uptake of edits in embryonic cells) [9], and, more recently, the possibility of causing cancer [10]. These risks, however, arguably constitute just the tip of the iceberg when it comes to the potential harms related to germline editing. Even if the technology can be made sufficiently effective from a technical standpoint, our relatively superficial understanding of the human genome renders attempts to modify the germline extremely risky. For instance, most diseases and disabilities are caused by a complex interplay of numerous genes [11]—an understanding of which still eludes us. Without complete comprehension of these interactions, we are unable to predict what effect changing just a few genes will have on the expression of others. We also lack a clear understanding of the multiple functions that individual genes play, such that the removal of a so-called “bad” gene could inadvertently impact beneficial pathways and processes [12]. Such outcomes are particularly problematic given the heritability of germline edits and their potential to affect countless unborn individuals. Germline editing also presents risks to society as a whole. For instance, the technology could be used to create children that conform to problematic societal ideals born from a history colored by discrimination and prejudice [13]. Germline editing also has the potential to exacerbate problematic wealth and power disparities given the likely expense of the procedure. Finally, the technology may detrimentally impact familial relations and the psyches of children designed to meet parental preferences [14]. While supporters of the technology claim that the medical benefits will likely outweigh these anticipated risks, surprisingly little has been done to parse out what these benefits may actually be. To address this lacuna, let’s take a closer look at some of the technology’s promised benefits against which its concomitant risks are to be weighed. First, despite frequent overblown claims about the revolutionary medical potential of germline editing, it must be emphasized that the technology likely cannot prevent the vast majority of health conditions, which emanate from a myriad of genetic and environmental factors not yet understood [15]. There is, however, a relatively small subset of diseases caused by single genes (e.g., Huntington’s and Tay Sachs), which are much better understood than polygenetic conditions and therefore constitute the best candidates for germline editing [16].* In the overwhelming majority of cases, however, an embryo screening technique called Preimplantation Genetic Diagnosis (PGD) can be used to prevent inheritance of these conditions [17]—an essential fact downplayed or even omitted in the discussions surrounding germline editing. PGD allows prospective parents who undergo in vitro fertilization—a procedure that would also accompany germline editing—to sequence the genomes of their embryos to identify the presence of any single-gene conditions (or other genetic risks, e.g., BRCA genes). Given the rarity of single-gene diseases, most couples affected by such conditions can create some portion of healthy embryos that may be implanted to produce offspring. Consequently, PGD can be used in most instances to prevent inheritance of single-gene conditions without the help of germline editing [18]. It is only in the exceedingly unlikely event that one reproductive partner carries two copies of a given disease gene while the other also possesses two copies—or one if the disease is dominant, i.e., only requires one copy of the gene to manifest—that the potential value of germline editing obtains is realized [19]. While such a couple could still raise healthy children by using third-party gametes (or, of course, via adoption), CRISPR could theoretically be used to edit the disease gene from the couple’s embryos to afford them an unaffected child, genetically related to both parents. While no doubt a desirable outcome, the number of individuals who may be uniquely helped by germline editing is limited. The question thus remains: does this benefit outweigh the technology’s many medical and social risks? To answer the question affirmatively places an enormous amount of importance on having a biological child that is almost tantamount to asserting a right to do so. While the concept of procreative liberty does indeed bestow certain rights on prospective parents, such as the negative right to enjoin the state from preventing a woman from conceiving or carrying a pregnancy to term, no American court has found an affirmative right to have a biological child [20]. It is also essential to note that enabling more people to have biological children for reasons unrelated to sterility is arguably a social, rather than a medical, benefit. Consequently, it must be asked whether this social benefit outweighs the related social risks discussed above. If the costs of germline modification may outweigh the benefits, then why do we continue to pursue the technology? Perhaps the answer is that we are pushing forward simply because we can. If that is indeed our approach to technological advancement, however, we may be headed for trouble. Given the rapidity with which technology is evolving, we will likely find ourselves in a future that poorly reflects our shared values as a society and species if we pursue every technological enhancement possible. To ensure that our powerful scientific capabilities help build a fair and inclusive world, we must instead engage in honest discussions regarding the true risks and benefits of a given technology before it is pursued. In the case of germline editing, that means proponents need to be more forthcoming about the technology’s limited medical benefits. Only then we will be able to responsibly decide whether and how to proceed with germline editing in a way that takes us closer to a future of our choosing. Photo by National Cancer Institute on Unsplash Endnote • The application of germline editing to monogenetic conditions is also likely less ethically controversial than targeting genes such as BRCA 1 and 2 that signal a risk rather than a certainty that a given condition will develop. Edits to such genes arguably constitute something beyond treatment—namely a genetic advantage conveyed by eliminating even the predisposition to disease—in a way that makes a slide toward pure enhancement uses of the technology more plausible. Works Cited [1] Heidi Ledford, “CRISPR Fixes Disease Gene in Viable Embryos,” Nature, August 2, 2017, https://www.nature.com/news/crispr-fixes-disease-gene-in-viable-human-embryos-1.22382. [2] Jennifer A. Doudna and Samuel H. Sternberg, A Crack in Creation, (Houghton Mifflin Harcourt, 2017), 34-59. [3] Ibid. [4] National Academies of Sciences, Engineering, and Medicine. 2017. Human Genome Editing: Science, Ethics and Governance. Washington, DC: The National Academies Press 1-8, accessed July 31, 2017 https://doi.org/10.17226/24623. [5] Ibid. [6] H. Ma et al., “Correction of a Pathogenic Gene Mutation in Human Embryos”, Nature (2017), accessed June 8, 2018, doi:10.1038/nature23305. [7] Consolidated Appropriations Act of 2016, Public Law 114-113 (adopted December 18, 2015). [8] Patrick Skerret, “Experts debate: Are we playing with fire when we edit human genes?”, STAT, November 15, 2017, https://www.statnews.com/2015/11/17/gene-editing-embryo-crispr/. [9] H. Ma et al., “Correction of a Pathogenic Gene Mutation in Human Embryos”, Nature (2017), accessed June 20, 2018, doi:10.1038/nature23305. [10] Haapaneimi et al., “CRISPR-Cas9 Gene Editing Induces p53-mediated DNA Damage”, Nature Medicine (2018), accessed June 20, 2018, https://doi.org/10.1028/s41591-018-0049-z; R. Ihry et al., “P53 Toxicity is a Hurdle to CRISPR/CAS9 Screening and Engineering in Human Pluripotent Stem Cells”, bioRxiv (2017), accessed June 20, 2018, https://doi.org/10.1101/168443. [11] “Frequently Asked Questions About Genetic Disorders”, National Human Genome Research Institute, accessed July 31, 2017, https://www.genome.gov/19016930/faq-about-genetic-disorders/. [12] See e.g., Moises Velasquez-Manoff, “The Upside of Bad Genes”, New York Times, June 17, 2017; “Protective Effect of Sickle Cell Trait Against Malaria-Associated Mortality and Morbidity”, CDC.gov, accessed June 20, 2018, https://www.cdc.gov/malaria/about/biology/sickle_cell.html; Sheri E. Gabriel et al., “Cystic Fibrosis Heterozygote Resistance to Cholera Toxin in the Cystic Fibrosis Mouse Model”, Science 266 (1994): 107-109; L. Kivela et al., “Presentation of Celiac Disease in Finnish Children Is No Longer Changing: A 50-Year Perspective,” J Ped 167 (2015): 1109-1115, accessed July 31, 2017, doi: http://dx.doi.org/10.1016/j.jpeds.2015.07.057. [13] See e.g., Jackie Scully, “Disability Bioethics: Moral Bodies, Moral Difference”, (Rowman & Littlefield, 2008), Chapter 2. [14] Michael Sandel, “The Case Against Human Perfection”, The Atlantic, April 2004. [15] “Frequently Asked Questions About Genetic Disorders”, National Human Genome Research Institute, accessed June 25, 2018, https://www.genome.gov/19016930/faq-about-genetic-disorders/. [16] Hank Greely, “Of Science, CRISPR-Cas9, and Asilomar”, Stanford Law and Science Blog, April 4, 2015, https://law.stanford.edu/2015/04/04/of-science-crispr-cas9-and-asilomar/. [17] Ibid; E. Lander, “Brave New Genome”, New England Journal of Medicine 2015, accessed June 8, 2018, DOI: 10.1056/NEJMp1506446. [18] Ibid. [19] Ibid. [20] Meyer v. Nebraska, 262 U.S. 390 (1923); Pierce v Society of Sisters, 268 U.S. 510 (1925); Farrington v. Tokushige, 273 U.S. 284 (1927); Prince v. Massachusetts, 321 U.S. 158 (1944); Wisconsin v. Yoder, 406 U.S. 205 (1972).

The Food and Drug Administration (FDA) made history this fall with its approval of Novartis’s Kymirah and Gilead’s Yescarta—the first gene therapies to ever be approved in the United States. [1,2] Both treatments belong to a new class of cancer therapeutics called CAR T-cell treatments, which use patients’ own immune cells to fight cancer.[1,2] These approvals may therefore mark the dawn of a new day for both gene therapy and the treatment of cancer. The manufacture of CAR T-cell treatments begins with the collection of T-cells, a type of white bloods cells, from a patient.[3] These cells are then genetically modified using a viral vector to express a protein known as chimeric antigen receptor (i.e., CAR). Once injected back into the patient, CAR causes the T-cells to seek and destroy cancer cells, combating the disease with seemingly unprecedented efficiency.[3] Kymirah, for example, caused 83% of 63 juvenile clinical trial subjects with a certain type of leukemia to go into remission within three months of receiving treatment.[1] Yescarta showed similar promise in clinical trials by sending 51% of the 100 adult subjects with B-cell lymphoma into complete remission.[2] Because these treatments must only be administered once, many see these drugs not as cancer treatments, but as cancer cures—a paradigmatic shift in the fight against cancer. Both drugs, however, are not without their serious side effects. For instance, both treatments can induce cytokine release syndrome (CRS), an immune system response to the presence of CAR T-cells that can cause high fever, flu-like symptoms, and potentially life-threatening neurological events.[1,2] Other serious side effects include: infection, hypotension, kidney damage, and hypoxia.[1.2] Given these significant risks, the FDA approved both Kymirah and Yescarta pursuant to a risk evaluation mitigation strategy (REMS), which, among other things, requires hospitals and clinics to obtain special certification in order to dispense these drugs.[1.2] To become certified, personnel must undergo training to recognize and treat CRS and hospitals and clinics must have the appropriate medications to treat CRS on hand.[1,2] Furthermore, due to their associated risks, both treatments are approved only as a drug of last resort (i.e., after all other treatments have failed).[1,2] By taking steps to reduce the risks associated with these uniquely effective treatments, the FDA seems to have appropriately accounted for the bioethical principles of nonmaleficence and beneficence. However, given their exorbitant costs, these drugs do pose some concerns for the bioethical principle of justice. Kymirah is currently sold by Novartis for $457,000, while Yescarta is available for the slightly less eye-popping price of $373,000.[4,5] Moreover, because these drugs will be available only at certified institutions, many will have to incur travel costs to gain access to these treatments. The hefty costs associated with these drugs have further stoked the uproar against rising drug prices.[4] Specifically, some to fear that, given the efficacy of these drugs, cancer will someday be a disease reserved only for the poor.[4] Such an outcome would for obvious reasons exacerbate the already problematic opportunity gaps that plague our country. Manufacturers of these drugs, however, attempt to justify high prices by pointing to the fact that these drugs effectively constitute cancer cures.[4,5] Consequently, patients must only pay once for these drugs instead multiple times over the course of several years as with traditional treatments. This justification, however, is made slightly less persuasive by the fact that these drugs are approved only as a last line of defense. As such, patients must endure costly treatment regimens before they’re asked to shell out almost half a million dollars for CAR T-cell therapies. Novartis, however, has said that it will only charge patients who respond to Kymirah within a month of receiving treatment; the company is currently working with the Centers for Medicare and Medicaid Services to design a payment plan to that effect.[6] Novartis has also stated that it “will offer an access program in the U.S. for eligible uninsured and underinsured patients” while “payers are developing their payment policies” for the drug.[6] Gilead has yet to make similar announcements regarding Yescarta. Debates regarding the costs of gene therapies are likely to heat up as more treatments of this kind are approved. Other drug companies also developing gene therapies have already indicated that their products, if approved, will carry similarly high price tags.[4] These companies, however, likewise justify the high costs. They claim that the prices are warranted given that these therapies: 1) can offer a cure for otherwise intractable conditions and 2) often target rare conditions and must therefore be priced highly in order to draw a profit.[4] It is possible, however, that, as with any technology, the price of these treatments will drop over time. That may be particularly true if CRISPR-Cas9, the most cost-effective gene-editing technique discovered to-date, eventually replaces viral vectors as the primary means for creating gene therapies. Also, insurers are discussing ways to devise alternative payment models for gene therapies such as paying for a treatment over time, the establishment of insurer risk pools, and the potential financing of one time payments.[6] How all this will play out remains to be seen, but pharmaceutical companies and policy-makers must take the appropriate steps to ensure that these promising new therapies don’t ultimately lead to the ghettoization of cancer and other genetic diseases. Works Cited 1. FDA News Release, FDA Approval Brings First Gene Therapy to the United States, (Aug. 30, 2017), https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm574058.htm. 2. FDA News Release, FDA Approves CAR-T Cell Therapy to Treat Adults with Certain Types of Large B-Cell Lymphoma, (Oct. 18, 2017), https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm581216.htm. 3. National Cancer Institute, CAR T Cells: Engineering Patient’s Immune Cells to Treat Their Cancers, (Aug. 31, 2017), https://www.cancer.gov/about-cancer/treatment/research/car-t-cells. 4. Gina Kolata, New Gene-Therapy Treatments Will Carry Whopping Price Tags, New York Times (Sept. 11, 2017), https://www.nytimes.com/2017/09/11/health/cost-gene-therapy-drugs.html. 5. Toni Clark and Bill Berkot, FDA Approves Gilead Cancer Gene Therapy; Price Set at $375,000, Reuters (Oct. 18, 2017), https://www.reuters.com/article/us-gilead-sciences-fda/fda-approves-gilead-cancer-gene-therapy-price-set-at-373000-idUSKBN1CN35H. 6. Arlene Weintrab, How to Cover Novartis’ $475K CAR-T Drug Kymirah? A’New Payment Model’ is the Only Way, Express Scripts Says, (Sept. 22, 2017), https://www.fiercepharma.com/financials/car-t-and-other-gene-therapies-need-new-payment-model-says-express-scripts.

This article describes some reasons that initiated protest movements in Russia and Egypt in 2011. The author thinks that the conflict in the political elite made was an important background that made thousands of people take to the streets of the cities. Russian and Egyptian political systems, that seem to be so different, had much in common in fact: hidden struggle between conservative «people of force» and liberals. The situation was aggravated by the coming elections and consequences of the international economic crisis. The research is based on Russian and Egyptian Media materials.