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Amazon Best Sellers: Best Anatomy

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Amazon Best Sellers: Best Anatomy

New hybrid whale-dolphin discovered in Hawaii

Last year, a team of scientists spotted what they believed was a hybrid animal off the coast of Kauai, Hawaii.A new report from Cascadia Research Collectiveconfirms they did and the new sea creature is the result of a whale and a dolphin mating, the teams head researcher told CBS News.

What the researchers discovered was a hybrid of a melon-headed whale and a rough-toothed dolphin. In an interview with local newspaperThe Garden Island,the head of the project said the discovery is their most unusual finding. We had the photos and suspected it was a hybrid from morphological characteristics intermediate between species, Robin Baird said.

During their two-week project, scientists were able to get a biopsy sample from the creature and study its genetics. They were able to confirm that the animal was a hybrid. Based on the genetics, the father was a rough-toothed dolphin and the mother a melon-headed whale, Baird told CBS News via email.

One of the species that makes up this hybrid is very rare in Hawaii. Melon-headed whales usually dont swim in these waters, so when scientists spotted the whale, they put satellite tags on the animal. During this two-week study, scientists also spotted another rare species in the water, pantropical spotted dolphins, which they also tagged.

Bairds research team is going to be back in Kauais waters next month, when they hope to get more photos of the new hybrid whale-dolphin and water samples. They also hope to do testing on other species in the area.

Were hoping that just by talking to some tour operators and fishermen we might get tips and encounter something like pilot whales, Baird said.

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New hybrid whale-dolphin discovered in Hawaii

Hundreds of Thousands of Species in a Few Thousand Years?

A recent1 review paper proposed a controversial claimthat the vast majority of animal species arose contemporary with modern humans. Not surprisingly, this claim was met with backlash from the evolutionary community. On what basis did the authors make this wide-reaching claim? Is their assertion true? Furthermore, what ramifications do their data have for the creationist explanation of the origin of species from the originally created min or kinds?

The main focus of Stoeckle and Thalers paper is genetics. Specifically, they focus on a subset of DNA in human and animal cells, termed mitochondrial DNA (mtDNA). Their analysis of mtDNA is clear, straightforward, and carefully justifiedso much so that I will summarize their arguments by liberally quoting from their paper.

About 15 years ago, DNA barcoding was first proposed as a tool for practical taxonomy.2 Taxonomy is the field of science concerned with the classification of life, and scientists thought that taking small subsets of DNA would aid in identifying and classifying species. The particular mitochondrial sequence that has become the most widely used is the 648 base pair (bp) [think of base pairs as DNA letters] segment of the gene [a subsection of DNA sequence] encoding mitochondrial cytochrome c oxidase subunit I (COI).3

With a subset of a subset of DNA, Skeptics of COI barcoding raised a number of objections about its power and/or generality as a single simple metric applicable to the entire animal kingdom, including: the small fraction of the genome (about 5% of the mitochondrial genome and less than one millionth of the total organisms genome [total DNA in an organism]) might not be sensitive or representative.4

A simple example from humans illustrates this concern. For instance, on average any two humans differ at 0.2%0.5% of their mtDNA base pairs. Theoretically, if all mtDNA differences are evenly distributed around the human mtDNA genome, you would expect 12 mtDNA differences in each individuals 648 bp COI barcode. With numbers this low, one generation of an extra mutation or two in the COI barcode sequence might throw a real classification pattern (i.e., one based on comparisons of hundreds of anatomical and physiological features) into confusion.

However, since the early days of DNA barcoding, such objections have been mostly mollified. I can attest to this from my own experience in handling thousands of mtDNA sequences. As a representative of the mtDNA diversity among species and individuals, a subset of mtDNA sequence is a good first approximation. Though subsets arent always perfect representations of the whole sequence, they are good initial data points.

Furthermore, over several decades of mtDNA barcoding, scientists have discovered a specific clustering pattern among mtDNA barcodes from individuals across diverse species: a general observation is that barcode clusters correspond best to species in well-studied animal groups, where taxonomists have mostly decided and agreed upon what species are. Thus there is good support in several major phyla, including Chordata [e.g., vertebrates and a handful of other species], Arthropoda [e.g., insects, arachnids, and crustaceans], Mollusca [e.g., shellfish, octopi], Echinodermata [e.g., starfish]. We note that these phyla are estimated to contain about 34 of named animal species.5

This fact has two major ramifications: First, the cluster structure of the animal world found in COI barcode analysis is independent of any definition(s) of species. Second, domain experts judgments of species tend to agree with barcode clusters and many apparent deviations turn out to be exceptions that prove the rule.6 In other words, the initial fears of those skeptical of DNA barcoding have not been met. Instead, barcoding has been very successful.

In light of these successes, the authors acknowledge the unexpected implications for explanations for the origin of species: At its origin DNA barcoding made no claim of contributing to evolutionary theory,7 yet the pattern of DNA barcode variance is the central fact of animal life that needs to be explained by evolutionary theory.8

Expanding our scope beyond the narrow evolutionary focus of the authors, we can generalize their statement: These mtDNA barcode patterns need to be explained by any model purporting to account for the origin of species.

The barcode patterns take a very specific form: the clustering structure of COI barcodessmall variance within species and often but not always sequence gaps among nearest neighbor species is the primary fact that a model of evolution and speciation must explain. Furthermore, the average pairwise difference among individuals (APD; equivalent to population genetics parameter ) within animal species is between 0.0% and 0.5%. The most data are available for modern humans, who have an APD of 0.1% calculated in the same way as for other animals.9

Stoeckle and Thaler recognize the sweeping potential in these patterns: The agreement of barcodes and domain experts implies that explaining the origin of the pattern of DNA barcodes would be in large part explaining the origin of species. Understanding the mechanism by which the near-universal pattern of DNA barcodes comes about would be tantamount to understanding the mechanism of speciation.10

In their evolutionary model, Stoeckle and Thaler invoke two hypotheses account for the barcode cluster patterns: Either 1) COI barcode clusters represent species-specific adaptations, OR 2) extant populations have recently passed through diversity-reducing regimes whose consequences for sequence diversity are indistinguishable from clonal bottlenecks.11

Their conclusion? Modern human mitochondria and Y chromosome [another subset of DNA, but inherited paternally] originated from conditions that imposed a single sequence on these genetic elements between 100,000 and 200,000 years ago.12 In other words, to account for human CO barcode patterns, they favor the second hypothesissome sort of population dynamic (contraction) that reduced the genetic diversity of the population.

Stoeckle and Thaler then extrapolate their conclusions to controversial heights. To justify their extrapolation, they caution that one should not as a first impulse seek a complex and multifaceted explanation for one of the clearest, most data rich and general facts in all of evolution. Then they draw a parallel: The simple hypothesis is that the same explanation offered for the sequence variation found among modern humans applies equally to the modern populations of essentially all other animal species. Namely that the extant population, no matter what its current size or similarity to fossils of any age, has expanded from mitochondrial uniformity within the past 200,000 years.13 In other words, based on mtDNA barcodes, Stoeckle and Thaler claim that the vast majority of species have originated contemporary with modern humans.

Though Stoeckle and Thaler dont perform this step, lets revisit their data and take their results to the next logical conclusion. We can do this because creationists have no problems with the observations that Stoeckle and Thaler describe. Ive already mentioned that my own experience with mtDNA matches theirsbarcodes are a useful first approximation and should be treated as such. Yet this first approximation has revealed a consistent patternlow numbers of mtDNA differences within species and higher numbers of mtDNA differences between species.

Furthermore, since Stoeckle and Thaler explore the origin of individual speciesrather than the origin of whole classification groups, like mammalstheir reasoning applies almost seamlessly to the creationist explanation for the origin of species. Their claim that species arose recently is one that focuses on species within kindsnot one that explores changes from one kind into another. In other words, for Stoeckle and Thalers particular question, evolutionists and creationists agree on the question of common ancestry.

Nevertheless, they differ sharply on the question of timewhen these individual species arose. Unlike Stoeckle and Thaler, creationists invoke not two, but three potential explanations for low numbers of mtDNA sequence differences within species: (1) species-specific adaptations; (2) changing population sizes or past bottlenecks (see especially the discussion of American bison (Bison bison) mtDNA and African buffalo (Syncerus caffer) mtDNA in this paper; (3) time recent origin (e.g., within the last 4,5006,000 years).

We now have two decades worth of direct measurements of the rate at which human mtDNA mutates, and it matches exactly the 6,000-year timescale and rejects the evolutionary timescale (see Genetics Confirms the Recent, Supernatural Creation of Adam and Eve and references therein). Thus, taking Stoeckle and Thalers results to their logical conclusion, we can revise their statement to Modern human [mitochondrial DNA] originated from conditions that imposed a single sequence on these genetic elements14 about 6,000 years ago.

Lets now re-extrapolate these results to other species. The simple hypothesis is that the same explanation offered for the sequence variation found among modern humans applies equally to the modern populations of essentially all other animal species. Namely that the extant population, no matter what its current size or similarity to fossils of any age, has expanded from mitochondrial uniformity within the past 6,000 years.

We can refine this conclusion even more, with more spectacular implications for the creationist model: In the last two decades, the mtDNA mutation rate in a handful of invertebrate species has also been directly measured, and these rates14 are around 10 times higher (or more!) than the human mtDNA mutation rate (again, see this article and references therein). This would imply that multiple species within a genus (or perhaps even a family) have originated within the last 6,000 years.

In other words, these broad mtDNA barcode results suggest that, in general, the predictions15 I made for mtDNA mutation rates in diverse species are likely to be fulfilled. This is good evidence that Darwins ideas are well on their way to being replaced.

As this article was going to press, the theistic evolutionary organization BioLogos posted a critique of Stoeckle and Thalers paper. More specifically, BioLogos posted a critique of creationist responses to Stoeckle and Thaler. BioLogos took strong exception to the type of thesis that I advanced above. For example, consider the following quote from BioLogos: "Did Stoeckel [sic] and Thaler conclude that 90% of animal species appeared at same time as humans? The answer is No [emphasis theirs].

Did I miss a key element of the Stoeckle and Thaler paper?

Lets take a look at the BioLogos article, which was written by PhD biologist and professor Joel Duff. Duff clearly desired to minimize the implications of Stoeckle and Thalers paper. For example, Duff characterized the journal in which it was published as a low-profile Italian journal. He also downplayed the impact, saying that the extended press release didnt generate much reaction inside or outside of the scientific community. More strongly, Duff denounced claims like the one I made above as mischaracterization of the original research. He said it was an incorrect claim that most species originated about the same time.

Why?

To support his assertion, Duff proposed an examination of the original intent of the authors of this paper. Since an authors intent is invisible unless the author clearly states it, Duffs suggested methodology to justify his strong critique is a creative way to tackle a scientific controversy.

After examining Stoeckle and Thalers intent to Duffs satisfaction, Duffs journalism gets more questionable. Weve already examined his emphatic assertion: Did Stoeckel [sic] and Thaler conclude that 90% of animal species appeared at same time as humans? The answer is No. Duff justifies his forceful condemnation with a quote from Stoeckle and Thalers paper: the extant population, no matter what its current size or similarity to fossils of any age, has expanded from mitochondrial uniformity within the past 200,000 years.16 In light of this quote, Duff concludes, In other words, the genetic diversity observed in mitochondrial genomes of most species alive today can be attributed to the accumulation of mutations from an ancestral genome within the past 200,000 years, and Duff asserts that the authors never claim that most species came into existence within the past 200,000 years.

For a critique that began with a proposal to examine intent, Duff seems to have missed the actual intent of the authors. The title of their paper is, Why should mitochondria define species? After discussing and justifying at length the observation that mtDNA differences do, in fact, delineate species, the authors then make a startling statement: The pattern of DNA barcode variance is the central fact of animal life that needs to be explained by evolutionary theory17 [emphasis theirs]. In case the intent of their statement wasnt transparent, the authors make it explicit: The agreement of barcodes and domain experts implies that explaining the origin of the pattern of DNA barcodes would be in large part explaining the origin of species. Understanding the mechanism by which the near-universal pattern of DNA barcodes comes about would be tantamount to understanding the mechanism of speciation.18 They then spend the next chunk of their paper discussing what mtDNA barcodes imply about the mechanism of speciation. Clearly, Stoeckle and Thaler are concerned with much more than just the accumulation of mutations from an ancestral genome within the past 200,000 years. Instead, they have a strong focus on the origin of species.

But did the authors never claim that most species came into existence within the past 200,000 years? In one sense, if we split hairs, Duff is technically correct: In their paper, Stoeckle and Thaler never say so explicitly. Yet as weve just observed, the conclusion about the timing of the origin of species is implied. Furthermore, Thaler makes the conclusion explicit in the press releasethe very one that Duff cited:

Our paper strengthens the argument that the low variation in the mitochondrial DNA of modern humans also explains the similar low variation found in over 90% of living animal specieswe all likely originated by similar processes and most animal species are likely young19. [emphasis added]

How did Biologos miss this?

Duff advances a second argument in his critique of the implications of Stoeckle and Thalers paper. He says that the mtDNA results at best, [tell] us the minimum age of the species. It tells us little to nothing about the maximum age of a species [emphasis his]. For the maximum age, Duff thinks the fossil record is essential. Furthermore, he states that an examination of the mitochondrial genome of any species will only tell us when the common ancestor of all modern members of this species existed, which will almost invariably occur after the evolutionary origin of the species.

But how does Duff know that this is true? Ive already documented that fossils do not directly record genealogical relationships; only DNA does. Why would Duff defer the genealogical question of ancestry (a.k.a. the question of the origin of species) to an indirect field of science (paleontology) when a direct field (geneticsmtDNA) gives a clear answer?

Ive also documented that the process of speciation involves several stepsat a minimum, (1) the formation of one or more distinct individuals, (2) the multiplication of these distinct individuals into a population, and (3) the isolation of this distinct population from the parent species. How does Duff know that the supposed ancestors (recorded by fossils) of modern species were isolated enough from the other populations alive at the time to be called a new species? Duff is trying to win a scientific argument, not by data and by experimentation, but by assertion. This is not a scientific way to resolve the controversy.

BioLogos response is sad, if not ironic. Weve already documented the fact that our evolutionary opponents dont read our literature (Duff included , despite BioLogos professed commitment to dialogue with those who hold other views); yet they call us liars. Sometimes I wonder if they carefully read even the evolutionary literature. Either way, BioLogos main critique (of the implications of Stoeckle and Thalers paper) amounts to misrepresentation and speculation even approaching outright denial. If this is the best that the evolutionary community can do, then perhaps my scientific conclusions (above) are even stronger than they first appear.

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Hundreds of Thousands of Species in a Few Thousand Years?

TOday’s Movers: Seattle Genetics (NASDAQ:SGEN) Stock …

July 27, 2018 - By Vernon Prom

Investors sentiment increased to 1.61 in Q1 2018. Its up 0.38, from 1.23 in 2017Q4. It is positive, as 24 investors sold Seattle Genetics, Inc. shares while 53 reduced holdings. 31 funds opened positions while 93 raised stakes. 159.52 million shares or 12.47% more from 141.83 million shares in 2017Q4 were reported.

California State Teachers Retirement System reported 165,312 shares. 13,084 are held by Bluecrest Cap Ltd. Pictet Asset invested in 0.1% or 786,323 shares. Swiss Bankshares owns 0.02% invested in Seattle Genetics, Inc. (NASDAQ:SGEN) for 349,100 shares. Keybank National Association Oh invested in 0% or 8,414 shares. 4,998 were accumulated by Shell Asset Mngmt Company. Pnc Financial holds 6,727 shares. Utah Retirement Sys holds 0.02% of its portfolio in Seattle Genetics, Inc. (NASDAQ:SGEN) for 19,600 shares. Wells Fargo And Co Mn, a California-based fund reported 306,681 shares. The Connecticut-based Bridgewater Associate L P has invested 0.01% in Seattle Genetics, Inc. (NASDAQ:SGEN). Amundi Pioneer Asset Management has 21,523 shares. National Bank Of America Corp De accumulated 496,573 shares. Daiwa Securities accumulated 4,395 shares. Zurcher Kantonalbank (Zurich Cantonalbank), Switzerland-based fund reported 23,953 shares. Pub Employees Retirement Association Of Colorado invested in 20,183 shares or 0.01% of the stock.

Since February 1, 2018, it had 3 buys, and 12 sales for $266.62 million activity. Cline Darren S also sold $497,983 worth of Seattle Genetics, Inc. (NASDAQ:SGEN) shares. The insider SIEGALL CLAY B sold 18,832 shares worth $951,393. The insider HIMES VAUGHN B sold 5,000 shares worth $290,604. 10,457 shares were sold by DRACHMAN JONATHAN G, worth $552,452.

JP Morgan now has a $77 target on the $11.55 billion market cap company or 5.51 % upside potential. In analysts note issued to clients on Friday, 27 July, Seattle Genetics (NASDAQ:SGEN) shares have had their Overweight Rating kept by professional analysts at JP Morgan.

Among 8 analysts covering Seattle Genetics (NASDAQ:SGEN), 7 have Buy rating, 0 Sell and 1 Hold. Therefore 88% are positive. Seattle Genetics has $77.0 highest and $60.0 lowest target. $68.13s average target is -6.65% below currents $72.98 stock price. Seattle Genetics had 12 analyst reports since January 31, 2018 according to SRatingsIntel. SunTrust maintained it with Hold rating and $60.0 target in Wednesday, February 7 report. The stock of Seattle Genetics, Inc. (NASDAQ:SGEN) earned Buy rating by Needham on Wednesday, February 7. J.P. Morgan upgraded the shares of SGEN in report on Wednesday, February 14 to Buy rating. The rating was maintained by Morgan Stanley on Wednesday, March 21 with Overweight. The firm has Buy rating by RBC Capital Markets given on Tuesday, March 20. The firm has Buy rating given on Monday, June 11 by SunTrust. The company was maintained on Wednesday, February 7 by H.C. Wainwright. On Thursday, February 1 the stock rating was maintained by H.C. Wainwright with Buy. The stock of Seattle Genetics, Inc. (NASDAQ:SGEN) has Neutral rating given on Wednesday, February 7 by Bank of America. The firm has Overweight rating by JP Morgan given on Wednesday, February 14.

The stock increased 2.43% or $1.73 during the last trading session, reaching $72.98. About 1.60M shares traded or 72.55% up from the average. Seattle Genetics, Inc. (NASDAQ:SGEN) has declined 15.50% since July 28, 2017 and is downtrending. It has underperformed by 28.07% the S&P500.

Seattle Genetics, Inc., a biotechnology company, develops and commercializes targeted therapies to treat cancer worldwide. The company has market cap of $11.55 billion. It markets ADCETRIS, an antibody-drug conjugate for relapsed Hodgkin lymphoma and relapsed systemic anaplastic large cell lymphoma. It currently has negative earnings. The firm also develops SGN-CD33A that is in Phase III clinical trial to evaluate SGN-CD33A in combination with hypomethylating agents in previously untreated older patients, as well as in Phase 1/2 clinical trial for patients with relapsed or refractory acute myeloid leukemia ; ASG-22ME, which is in Phase I clinical trial for Nectin-4-positive solid tumors, including bladder cancer; SGN-LIV1A that is in Phase 1 clinical trial for patients with LIV-1-positive metastatic breast cancer; and SGN-CD19A, which is in Phase II clinical trial for patients with relapsed DLBCL, as well as in Phase II trial for patients with newly diagnosed DLBCL.

More notable recent Seattle Genetics, Inc. (NASDAQ:SGEN) news were published by: Streetinsider.com which released: Seattle Genetics (SGEN) Adcetris On-going Launch in 1L cHL is Positive Says SunTrust. on July 02, 2018, also Benzinga.com with their article: Benzingas Daily Biotech Pulse: Biogen, AC Immune Slip Despite Positive Trials, Sarepta Slapped With Clinical Hold published on July 26, 2018, Seekingalpha.com published: Mid-stage study underway for Seattle Genetics tisotumab vedotin in solid tumors; shares up 1% premarket on July 12, 2018. More interesting news about Seattle Genetics, Inc. (NASDAQ:SGEN) were released by: Seekingalpha.com and their article: Dont Sell Axon Enterprise Cramers Lightning Round (7/11/18) published on July 12, 2018 as well as Benzinga.coms news article titled: Benzingas Daily Biotech Pulse: Achaogen To Trim Workforce By 28%, Amgens Beat-And-Raise Quarter with publication date: July 27, 2018.

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TOday's Movers: Seattle Genetics (NASDAQ:SGEN) Stock ...

LR hospital hires cancer institute chief – arkansasonline.com

The outgoing director of the Winthrop P. Rockefeller Cancer Institute at the University of Arkansas for Medical Sciences has accepted a job at CHI St. Vincent.

Dr. Peter Emanuel turned in his resignation letter on May 4. His last day at UAMS is Tuesday.

Emanuel, 59, will join CHI St. Vincent on Sept. 1, according to a statement from the hospital. His position was not specified.

At the time of his resignation, he declined to give the reason for his departure, only citing unspecified challenges. He could not be reached for comment Friday afternoon.

UAMS is conducting a national search for a new cancer institute director, said Leslie Taylor, vice chancellor of communications and marketing. Dr. Laura Hutchins was appointed interim director in June. Hutchins is a professor in the College of Medicine Division of Hematology/Oncology, where she was division director from 1998 until September 2013.

Emanuel is a widely recognized expert in leukemia and lymphoma, a UAMS website states. He joined UAMS in 2007 after leaving the University of Alabama at Birmingham, where he was a professor of medicine, genetics and biochemistry.

From 2004 to 2006 he was the acting director of the National Cancer Institute-designated Comprehensive Cancer Center at the Alabama university.

During his time at UAMS, he oversaw the addition of the cancer institute's 12-story research and treatment tower, which opened in 2010. His annual salary was $500,000.

His resignation in May followed UAMS' decision to temporarily suspend its cardiac surgery program due to lead surgeon Dr. Gareth Tobler's retirement. That program restarted at the beginning of July, with the hospital contracting with four new physicians.

UAMS also laid off almost 260 employees in January to curb an anticipated $72.3 million deficit. Those layoffs included one full-time physician -- a general ear, nose and throat doctor who did not work at the cancer institute.

News of Emanuel's new role comes one day after an invoice that his wife, Carla Emanuel, sent seeking reimbursement from the Winthrop P. Rockefeller Cancer Institute became public.

The $4,000 bill lists events that she attended, phone calls she made and work she did to resolve problems with donors. Taylor said UAMS was not going to pay the bill because state procedures regarding vendors and invoices were not followed.

Taylor added that the invoice was the first one she was aware of from a spouse, and the institution does not normally reimburse people for attending fundraising events.

The Arkansas Times first reported on the invoice on Thursday.

Metro on 07/28/2018

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LR hospital hires cancer institute chief - arkansasonline.com

Journal of Investigational Allergology and Clinical Immunology

The Journal of Investigational Allergology and Clinical Immunology (J Investig Allergol Clin Immunol) provides an attractive and very active forum for basic and clinical research in allergology and clinical immunology. The journal publishes original works, reviews, short communications and opinions. It is the Official Journal ofthe Spanish Society of Allergology and Clinical Immunology (SEAIC). The journal will appear bimonthly (6 issues each year). The peer-review system, based on a team of internationally renowned and committed editors, guarantees the scientific quality of the papers.

2018; volume 28, Issue 3more issues

Dupilumab: A New Paradigm for the Treatment of Allergic DiseasesSastre J, Dvila I[summary] [PDF full-Text] Continual Medical Education (1.3 credits)

Alerglogica 2015: A National Survey on Allergic Diseases in the Adult Spanish PopulationOjeda P, Sastre J, Olaguibel JM, Chivato T, On behalf of the investigators participating in the National Survey of the Spanish Society of Allergology and Clinical Immunology Alergolgica 2015[summary] [PDF full-Text]

GLCCI1 Polymorphism rs37973 and Response to Treatment of Asthma With Inhaled CorticosteroidsRijavec M, avbi M, Lopert A, Flear M, Koroec P[summary] [PDF full-Text]

Circulating Helper T-Cell Subsets and Regulatory T Cells in Patients With Common Variable Immunodeficiency Without Known Monogenic DiseaseAzizi G, Mirshafiey A, Abolhassani H, Yazdani R, Jafarnezhad-Ansariha F, Shaghaghi M, Mortazavi-Jahromi SS, Noorbakhsh F, Rezaei N, Aghamohammadi A[summary] [PDF full-Text] [Supplemental Materials]

Common Proteins Located in Pigeon, Budgerigar, and Hen Droppings Related to Bird Fanciers LungRouzet A, Valot B, Reboux G, Millon L, Roussel S[summary] [PDF full-Text]

Fixed Drug Eruption Due to LorazepamAgull-Garca A, Garcs Sotillos M, Cols Sanz C[summary] [PDF full-Text]

Effects of Ole e 1 on Human Bronchial Epithelial Cells Cultured at the Air-Liquid InterfaceLpez-Rodrguez JC, Sols-Fernndez G, Barderas R, Villalba M, Batanero E[summary] [PDF full-Text] [Supplemental Materials]

Resolution of Type IV Hypersensitivity After Bone Marrow TransplantationLzaro M, Vzquez L, Laffond E, Moreno E, Macias EM, Dvila I[summary] [PDF full-Text]

Eosinophilic Esophagitis: Treatment With Different Doses of Omeprazole in Children Under 16 YearsGmez Torrijos E, Donado Palencia P, Sanchez Miranda MP, Moreno Lozano L, Extremera Ortega AM, Borja Segade JM, Galindo Bonilla PA, Garca Rodrguez R[summary] [PDF full-Text]

Prevalence of Clonal Mast Cell Disorders in Patients Presenting With Hymenoptera Venom Anaphylaxis Might Be Higher Than ExpectedVzquez-Revuelta P, Gonzlez-de-Olano D[summary] [PDF full-Text]

Prevalence of Severe Atopic Dermatitis in Adults in 3 Areas of SpainSicras-Mainar A, Navarro-Artieda R, Snchez L, Sastre J[summary] [PDF full-Text]

A Case of Work-Related Donkey Milk AllergyGiorgis V, Rolla G, Raie A, Geuna M, Boita M, Lamberti C, Nebbia S, Giribaldi M, Giuffrida MG, Brussino L, Corradi F, Bacco B, Gallo Cassarino S, Nicola S, Cavallarin L[summary] [PDF full-Text] [Supplemental Materials]

Cutaneous Pseudolymphoma Secondary to Exogenous Pigment in a Polychrome TattooMendez Diaz Y, Garca-Arpa M, Parra Cubillos A, De Lara Simn IM, Garca Rodriguez R, Gmez Torrijos E[summary] [PDF full-Text]

Delayed Hypersensitivity Reaction to Oral Dimethyl FumarateAntolin-Amerigo D, Snchez-Gonzlez MJ, Barbarroja- Escudero J, Ayuso-Peralta L, Belln-Heredia T, Ortega- Berruezo MA, Alvarez-Mon M, Rodrguez-Rodrguez M[summary] [PDF full-Text]

Late Diagnosis of Anaphylactic Reaction to Gadolinium-Based Contrast Media by Skin Tests 10 Years After OnsetHarr T, Jandus P[summary] [PDF full-Text]

Hymenoptera Venom Immunotherapy: How to Safely Switch to the Same Venom From a Different ManufacturerBil MB, Martini M, Berra D, Scarpa A, Losappio L, Quercia O, Lodi Rizzini F, Bignardi D, Cortellini G, Zisa G, Del Giudice A, Manzotti G, Marcotulli C, Murzilli F, Cilia M, Pravettoni V, Borrelli P, Pastorello EA[summary] [PDF full-Text]

Urticaria Induced by Ingestion of Anemonia sulcataDe Aramburu Mera T, Labella lvarez M, Baynova K, Bartolom Zavala B, Prados Castao M[summary] [PDF full-Text]

Blood Eosinophils, Fraction of Exhaled Nitric Oxide, and Serum Eosinophil Cationic Protein as Surrogate Markers for Sputum Eosinophils in Asthma: Influence of Treatment With Inhaled CorticosteroidsAlvarez Puebla MJ, Aroabarren Aleman E, Corcuera Garcia A, Ibaez Bereiz B, Iraola Iribar A, Olaguibel Rivera JM[summary] [PDF full-Text]

Epidemiological Study of the Allergic Population in the North of Gran CanariaSurez-Lorenzo I, Cruz-Niesvaara D, Rodrguez-Gallego C, Rodrguez de Castro F, Carrillo-Diaz T[summary] [PDF full-Text]

New Books

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Journal of Investigational Allergology and Clinical Immunology

Neuroscience | Drew University

The neuroscience major at Drew is a multidisciplinary program of study that allows students to explore the brain from the perspectives of many different disciplines, including anthropology, biology, chemistry, computer science, mathematics, physics, philosophy and psychology. After building a firm background in biology, psychology and chemistry, majors study neuroscience topics at more advanced levels. In biology, students tease apart the function of genes and molecules in the brain, investigate how neurons connect with each other in physiological systems and networks that provide the physical substrate for both our conscious and subconscious experiences, and explore animal behavior from an evolutionary viewpoint. In psychology, students look at the anatomical basis of behavior, and examine the data and theory of learning, memory, sensation, perception, language, motivation, reasoning, and creativity.

Explore the pharmacology of drugs designed to treat mental illnesses. Examine how a machine can be programmed to be able to process language and engage in visual perception in a computer science course.

One area of strength in Drews neuroscience program is its employment of laboratory and research experiences. Drews technologically sophisticated neuroscience laboratories are designed to give students broad access to applied experiences in studying the brain. All majors take laboratory courses in which they image live neurons with fluorescent microscopy, measure brain chemicals in animals, and examine changes in brain morphology due to drug exposure, and use computers to study neuroanatomy and neurophysiology and for data collection, statistical analysis and graphic presentations.

All members of the Neuroscience Program have active research programs and work with students on research projects throughout the year.

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Neuroscience | Drew University

Physiology – Oklahoma State UniversityStillwater

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Physiology is a specialized life science degree that introduces you to intensive, hands-on laboratory experiences. A Physiology major teaches you about animal physiology and anatomy. Youalso select among specialized upper-division courses, such as Embryology, Pharmacology, Environmental Physiology, Endocrinology, or Behavioral Neuroendocrinology.The physiology degree primarily serves to prepare you for graduate school or a medically-related professional school.

Courses to expect for this major include Physiology, Mammalian Physiology, Mammalian Physiology Lab, Vertebrate Morphology, Cell and Molecular Biology, Survey of Biochemistry, and Organic Chemistry.

Physiology graduates are prepared to enter a variety of career fields, including the public and private sector, graduate school, or professional programs, such as medical school or veterinary school. Our graduates enjoy successful careers in a variety of fields: Biotechnology Education Health Care Industry Medicine Pharmacology Physical Therapy Politics and Policy Research

Scholarships are available for prospective freshmen, transfer students, current students and continuing students through the University, College of Arts & Sciences, and respective Departments.

When students complete the OSU admission application, they are automatically considered for the University Level scholarships.

Students are eligible forCollege Levelscholarships within the College of Arts and Sciences after completing 12 hours at OSU. Some exceptions may apply. See specific scholarships for criteria.

The Department of Integrative Biology offersDepartmental Levelscholarships for eligible students.

Become an OK-LSAMP Scholar!OK-LSAMP is a consortium of Oklahoma colleges and universities working together to develop programs aimed at increasing the number of students from under-represented populations who receive degrees in Science, Technology, Engineering, and Mathematics (STEM) disciplines. The OK-LSAMP scholarship program provides scholars with increased opportunities and connections, including undergraduate research experiences, graduate school preparation, international experiences, and internships/externships with companies in the STEM fields.

Integrative Biology501 Life Sciences WestOklahoma State UniversityStillwater, Oklahoma 74078

405-744-5555

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Physiology - Oklahoma State UniversityStillwater

Immunology – shire.com

At Shire, our mission is to be champions for people around the world who are struggling with rare diseases. When it comes to rare and immune-mediated conditions, we serve individuals with these diseases and the physicians who treat them by providing therapies and services that can be tailored to each persons unique needseven as these needs change across the patient journey.

While each disease is different, the expectations of the individuals who live with them are similar. Shires strength in immunology is built on deep expertise in delivering complex therapies for a variety of conditions. To deliver on our promise as a rare champion, Shires goal is to provide:

Intelligent, adaptable treatments that help manage, and prevent serious conditions, supported by services that support these individuals in using the best therapy for them, and adjusting their approach as needs change. In hereditary angioedema (HAE), we help give patients the freedom to live their lives, aided by patient services and next-generation therapies that improve their treatment experience.

Ongoing progress that delivers new treatments and explores new ways of receiving them to continually advance the standard of care from symptom management to preventative therapies, as we work toward the ultimate goal of a cure. We offer the broadest immunoglobulin (IG) portfolio, and aspire to provide an intelligent set of flexible options to meet each patients need for effective care that fits their lives and improves the overall patient treatment experience. We also offer a broad biotherapeutic portfolio of products including Alpha-1, Albumin, Protein C, and pdFVIII designed to meet the needs of patients in both the hospital and at-home setting.

Manufacturing expertise to confidently manage the end-to-end challenges of developing complex therapies, including those created from human plasma, from securing donations through to delivering treatment.

We support patients with immune-mediated conditions including:

Alpha-1 Antitrypsin Deficiency (AAT or Alpha-1 deficiency) is a hereditary condition that results in reduced levels of alpha-1 antitrypsin (AAT) protein in the blood and lungs. This protein, which is made mostly in the liver, helps protect lung tissue from chemicals released by white blood cells.1People with low levels of AAT protein are at higher risk for developing lung diseases such as emphysema.

Hereditary Angioedema (HAE) is a rare disease that causes unexpected edema (swelling) in various parts of the body including extremities, the gastrointestinal tract, and upper airways. Depending on the severity of the disease, some people may have many attacks each month, while others will go months without an attack.

Primary immunodeficiency (PI) is a group of nearly 300 rare diseases wherein part of the immune system is missing or not functioning properly2,3. People with PI may be more susceptible to illness, take longer to recover and have recurring infections4, such as sinusitis, bronchitis, pneumonia, or gastrointestinal infections5. Physicians sometimes treat the infections while missing the underlying cause, leaving patients vulnerable to vital organ damage, physical disability, or even increased mortality risk6,7.

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Immunology - shire.com