Asthma and hay fever sufferers are being warned of a potentially deadly “pollen bomb” which could cause life-threatening attacks this weekend. Met Eireann’s pollen count forecast is showing high levels over the coming days as Ireland is set to scorch over the Easter holidays.The national forecaster warned: “With dry, settled and increasingly warm temperatures over the next few days the tree pollen risk will rise to high across all regions.” And the weekend will see spells of sunshine which will bring the mercury into the 20s.Sarah O’Connor, CEO of the Asthma Society of Ireland said: “Project pollen levels are high in coming days and, with pollen levels rising earlier than last year, people with hayfever really need to start managing the condition now, especially those with hayfever and asthma.“80 per cent of people with asthma also have hayfever. We have lots of information on asthma.ie on minimising hay fever symptoms for asthma patients, which for some people can cause a fatal asthma attack.“Hayfever is very misunderstood in Ireland and people often dismiss you as a hypochondriac or simply a complainer when you mention it. “As a hayfever sufferer, I can testify that it is a very debilitating condition that leaves you feeling really miserable and unwell.“The constant runny nose, itchy eyes and sneezing are extremely distracting, and the accompanying headache and fatigue have always really marked out the summer months for me. For me, it felt like a flu all summer long.”“Some tips to help prevent and/or reduce symptoms, include: keep windows closed in your bedroom at night, remaining indoors as much as possible, staying away from grassy areas, and putting Vaseline around your nostrils to trap pollen.“One person dies every five days here as a result of their asthma.”‘Pollen bomb’ to hit Donegal over Easter weekend was last modified: April 20th, 2019 by Staff WriterShare this:Click to share on Facebook (Opens in new window)Click to share on Twitter (Opens in new window)Click to share on LinkedIn (Opens in new window)Click to share on Reddit (Opens in new window)Click to share on Pocket (Opens in new window)Click to share on Telegram (Opens in new window)Click to share on WhatsApp (Opens in new window)Click to share on Skype (Opens in new window)Click to print (Opens in new window)
Are you sick? Should you rely on Darwinism or Science?by Jerry Bergman, PhDUnder the headline “Darwin can help your doctor,” a press release from the University of Groningen claimed that “Evolution and ecology inspire clinical research in infections and antimicrobial resistance”. The editors explain: “Taking an evolutionary view can inspire new ideas in clinical microbiology. For example, evolutionary studies can reveal why some antimicrobial dosing regimens are better than others in preventing the development of drug resistance.”As I read the review, it soon became apparent that the word evolution was tacked onto the report for no good reason except to give obeisance to Darwinism. The approach described in the report had nothing to do with Darwinism but was rather an example of the classic empirical experimental approach. This approach requires scientists to evaluate the proposed “antimicrobial dosing regimens” on patients and then study the outcome. For example, a sample of affected patients would be randomized into 5 treatment groups of 20 patients each, then the outcome of each group is compared. If statistical differences are found at the alpha 0.05 level or better (such as alpha 0.01) to insure the difference between the two is very unlikely due to chance, this lends evidence to the conclusion that the protocol found most effective is actually, as a whole, more effective. The report then added:Looking at microbial communities, rather than just the pathogenic micro-organisms, can also lead to new insights. That is why clinicians, bioinformaticians analysing pathogens and evolutionary biologists should all work together. These are the conclusions of a diverse group of scientists led by University of Groningen microbiologist Marjon de Vos, in a short review published by The Lancet Infectious Diseases on 30 April.Again, this is an example of an obvious truism. Of course, “clinicians, bioinformaticians analysing pathogens and evolutionary biologists should all work together.” I have to wonder what evolutionary biologists could possibly contribute. MicrobiologistDe Vos studies urinary tract infections. She realized that a lot could be gained by collaborating with different specialists … For example, … bacteria involved communicate with each other and can form a stable ecosystem, which affects their susceptibility to antibiotics.’ This realization led to an interdisciplinary workshop in 2017, which in turn resulted in the review paper now published in The Lancet Infectious Diseases.Still no answer as what this research has to do with evolution. So I read on.The consensus can be wrong, and has been wrong numerous times, when it comes to evoluition.The article then discussed cystic fibrosisThe review mentioned bioinformatics, which is an analysis of “the vast amount of genetic data collected on infectious diseases.” This also has nothing to do with evolution unless one is searching for long-term, millions of years, evolutionary trends. In this case, the bioinformatics technique is a fishing expedition looking for trends in gene expression patterns that may relate to the medical condition of concern. The doctors explain that cyclic antibiotic treatments in cystic fibrosis patients are used to treat chronic lung infections which are common in this condition. To minimize the development of drug resistance, treatment alternates with two different drugs. If the pathogens become resistant to one drug, ideally, the other will be effective. Obviously, this approach could result in multi-drug resistance.This is the claim I was expecting, which has nothing to do with evolution. I will cover the most common claim, that is antibiotic resistance due to mutations which create bacteria incorrectly termed “superbugs.”How do bacteria develop resistance to antibiotics?Although bacteria can become resistant due to mutations, all these mutations studied so far are either loss mutations, or damage-to-gene-expression mutations that damage the system that speeds up the removal of, or the inactivation of, antibiotics. None of these effects are the result of new cellular innovations, but are caused merely by damaging something in the bacteria.One type of mutation can alter the shape of the antibiotic binding site. The antibiotic works by fitting into the antibiotic binding site and, like a lock and key, if the keyhole is damaged, the key will no longer fit into the lock. Likewise, if the antibiotic binding site is distorted as a result of damage caused by mutations, the antibiotic will no longer fit into the antibiotic binding site, protecting the bacteria from the antibiotic.A side effect is the mutation can degrade or destroy the function for which the bacteria binding site was designed. For example, a neutral mutation in one amino acid that prevents the required antibody-enzyme interaction alters the binding site on the 4-quinolone antibiotic which disables the DNA gyrase enzyme in bacteria. The gyrase enzyme is an essential bacterial enzyme that catalyzes the ATP-dependent negative super-coiling of double-stranded closed-circular DNA. It reduces the twisting strain occurring while double-stranded DNA is being unwound by elongating RNA-polymerase.The classic example of mutations in the antibiotic mechanism which causes the bacteria to become immune to the antibiotic is ribosome point mutations that renders streptomycin and other mycin antibiotics ineffective. Mycin antibiotics function by attaching to specific receptor sites on the bacteria’s ribosomes which are required to produce protein to keep the bacteria alive. The result is this antibiotic action interferes with the bacteria protein-manufacturing process. The proteins the bacteria produce are, as a result of the mutation, either non-functional, or are not even produced. The result is the bacteria cannot grow and divide, or propagate.Bacterial mutations cause the bacteria to become streptomycin-resistant if the ribosome site, where the streptomycin attaches, is altered by mutations. As a result, the streptomycin no longer can bind on the host ribosome, and therefore it no longer can interfere with the ribosomal function of producing protein. Mutation-caused changes that enable the bacteria to become mycin-resistant can occur in several different locations on the ribosome.Mammalian ribosomes do not contain the specific site where myosin drugs attach, and for this reason the drug does not interfere with mammal ribosome function. Consequently, mycin drugs adversely affect bacterial growth without harming the host. Because fundamental differences exist between prokaryotic (bacterial) and eukaryotic ribosomes, these variations often are exploited in order to produce antibiotics to kill bacteria without harming the host. Actually, many antibiotics used are produced by fungi or other bacteria to protect them from enemy bacteria. Humans obtain them to protect them from the same pathogenic bacteria.Another example of a mutation-caused resistance is, in Mycobacterium tuberculosis bacteria, an enzyme in the bacteria that changes the antibiotic called isoniazid into its active form that kills the bacteria. If a mutation damages the enzyme that converts the antibiotic into its active form, the antibiotic remains in its inactive and harmless conformation. As a result, this mutation confers antibiotic resistance to the mutant bacteria. The mutation that damages the enzyme which prevents the antibiotic from killing the bacteria also cripples the bacteria, an effect called the fitness cost.When bacteria become resistant to antibiotics as a result of mutations, all the mutations studied so far are either loss mutations, or gene-expression mutations that result in speeding up the systems that removes or inactivates antibiotics. None are the result of new cellular innovations but are caused merely by altering the regulation control.all the mutations studied so far are either loss mutations, or gene-expression mutationsEvolution by retreatIn short, this brief discussion illustrates the fact that all known examples of antibiotic resistance are due to inbuilt systems designed to achieve symbiosis, or damage to some system in the host or pathogen that prevents it from properly defending itself. In short, so-called super bacteria are actually damaged bacteria that have an advantage in an environment loaded with antibiotics, such as in a hospital.Conversely, mutations that add new systems, such as a new regulatory system, energy-generating system, or transport system, have never been documented. Mutations increasing certain enzyme affinity may be beneficial, but often occur rapidly, indicating that design is involved. For example, mutations effecting hemoglobin-oxygen affinity help the host to acclimatize to a high altitude, but the same mutation can also cause polycythemia. This response is not evolution, but rather designed adaptation.Mutations that alter a protein which results in antibiotic resistance are also likely to weaken the organism. Mutations that both confer resistance, and allow the bacteria to survive, do not improve the bacteria fitness in its normal environment. The bacteria actually render them less able to survive in an antibiotic-free environment. Thus, when the bacteria becomes resistant to a drug, it is likely to become less fit in other ways. This is called the cost of resistance, or the fitness cost. Often the cost is very high and the mutation renders the resistant stain poorly able to survive in a non-antibiotic environment.The last claim covered in the The Lancet Infectious Diseases article was resistance plasmids. Resistance plasmids are small circular DNA that confers resistance to bacteria that can easily be exchanged between bacteria. The Lancet review admits “we still don’t know how changes in genes lead to the different characteristics of these pathogens. We need experiments by evolutionary biologists in order to understand the link between the genotype, the DNA sequence and the phenotype – for instance, the level of resistance.”Empty boastsThe 11-page Lancet article contained the word evolution 103 times and, after analyzing each example, the same problem was found as I have documented in this paper. Of interest is the article’s list of examples of the successes of microbial evolutionary medicine, including the exploitation of the alleged bacterial evolutionary molecular clock to trace transmission events over time in hospitals and continents in spite of the fact that the molecular clock has been a dismal failure, at least for long periods of time. “Darwin can help your doctor.” Science Daily. 30 April 2019. https://www.sciencedaily.com/releases/2019/04/190430103424.htm. “Darwin can help your doctor.” Science Daily. 30 April 2019. https://www.sciencedaily.com/releases/2019/04/190430103424.htm. Sandra B Andersen, et al. Microbial evolutionary medicine: from theory to clinical practice. The Lancet Infectious Diseases, 2019 DOI: 10.1016/S1473-3099(19)30045-3 Sandra B Andersen, et al. Microbial evolutionary medicine: from theory to clinical practice. The Lancet Infectious Diseases, 2019 DOI: 10.1016/S1473-3099(19)30045-3 Davies, A. P., et al., 2000. “Comparison of Fitness of Two Isolates of Mycobacterium tuberculosis, One of which had developed Multi-Drug Resistance during the Course of Treatment.” Journal of Infection, 41(2):184-187, Sept.; Davies, J. and M. Nomura, 1972. “The Genetics of Bacterial Ribosomes.” Annual Review of Genetics, 6:203-234. Didier, E. S., D. C. Bertucci, and L. Leblanc, 1999. “Inhibition of Microsporidia Growth in vitro.” Abstracts of the General Meeting American Society Microbiology, 99:11 Wieland, Carl, 1994. “Antibiotic Resistance in Bacteria.” Cen Tech J., 8(1):5-6, p. 5. Wieland, 1994, p. 6.Spetner, Lee, 1997. Not by Chance. Brooklyn, NY: The Judaica Press, p. 144.Lenski, Richard E., 2002. “Cost of Resistance” in Encyclopedia of Evolution. Volume 2, pp. 1008-1010. New York, NY: Oxford University Press. Mark Pagel (editor), p. 1009.Baquero, Fernando, 2002. “Antibiotic Resistance: Origins, Mechanisms, and Extent of Resistance” in Encyclopedia of Evolution. Volume 1, pp. 50-54. New York, NY: Oxford University Press. Mark Pagel (editor). p. 51. “Darwin can help your doctor.” Science Daily, 30 April 2019. https://www.sciencedaily.com/releases/2019/04/190430103424.htm. Andersen, Sandra B., 2019. Evolutionary medicine: from theory to clinical practice. The Lancet Infectious Diseases, online 30 April 2019. https://www.thelancet.com/action/showPdf?pii=S1473-3099%2819%2930045-3. Jeffrey Tomkins and Jerry Bergman, 2015. “Evolutionary Molecular Genetic Clocks–A Perpetual Exercise in Futility and Failure.” Journal of Creation, 29(2):26-35. Dr. Jerry Bergman has taught biology, genetics, chemistry, biochemistry, anthropology, geology, and microbiology at several colleges and universities including for over 40 years at Bowling Green State University, Medical College of Ohio where he was a research associate in experimental pathology, and The University of Toledo. He is a graduate of the Medical College of Ohio, Wayne State University in Detroit, the University of Toledo, and Bowling Green State University. He has over 1,300 publications in 12 languages and 40 books and monographs. His books and textbooks that include chapters that he authored, are in over 1,500 college libraries in 27 countries. So far over 80,000 copies of the 40 books and monographs that he has authored or co-authored are in print. For more articles by Dr Bergman, see his Author Profile.(Visited 301 times, 1 visits today)FacebookTwitterPinterestSave分享0
Rhodes University students are getting involved in weekly community service, which is the practical component of the Intetho ZoBomi philosophy course.Community service, part of the Intetho ZoBomi course, has a positive effect on primary school students. (Image: Rhodes University)Chili KierRhodes University has broken new ground by being one of the first tertiary institutions to introduce a weekly community service into one of its courses.The Intetho ZoBomi philosophy course gets students to mentor children from underprivileged schools.Intetho ZoBomi, which means existential conversations in isiXhosa, prompts students to question the society they live in and form opinions on issues such as racism or patriarchy so that they are equipped to dismantle it.The course encourages discussions on current issues too, such as service delivery or sexual violence. ZoBomi became a formally recognised subject at Rhodes in 2016, before which it was only available as a semester course.For the communityZoBomi is unusual because of the way in which it is structured. It includes the usual daily lectures and weekly tutorials, but it also offers community service hours at underprivileged schools in the surrounding area.Through getting involved in the local community, the course promotes unity and team building. (Image: Rhodes University)The community service component falls under the mandate of Service-Learning, which is focused on the mutual learning experience. The aim of Service-Learning is to combine meaningful service to the community with curriculum-based learning and critical reflection.Students take on two roles when doing community service. The first is mentorship, guiding children up to the age of 15 on academics, goals and ambitions in life and how it can be achieved.The second is to tutor children to improve their English skills. It aims to build a solid foundation on which the children can continue to hone their English writing and speaking abilities. The focus is on English because it is the language of instruction in most institutions and workplaces.Students praise the subjectA mentorship programme is facilitated by university students for matriculants as part of the Intetho ZoBomi course. (Image: Rhodes University)Annuschka Silence, a first year ZoBomi student is delighted with the subject. “ZoBomi created a space for me to relieve the stress from other subjects, because helping people helps me to feel at peace,” she said.Rhodes student and ZoBomi ZoBomi tutor, Phumelele Nkomozake encourages students to take the course as it not only helps underprivileged students to grasp tricky concepts, but it “provides an opportunity for introspection and self-discovery”.Through this course, university students are encouraged to take a second look at themselves and see how they can uplift others who may not have the same access to the basic facilities and resources.Sources: Rhodes UniversityWould you like to use this article in your publication or on your website? See Using Brand South Africa material.
Share Facebook Twitter Google + LinkedIn Pinterest By Jerry HagstromDTN Political CorrespondentORLANDO, Fla. (DTN) — Comparing President Donald Trump’s expected meeting with Chinese President Xi Jinping to conclude a new trade agreement to Trump’s recent meeting with North Korean leader Kim Jong Un, Agriculture Secretary Sonny Perdue said here Friday that a Trump-XI meeting could end “successfully or very detrimentally” for American agriculture.Trump walked away from his meeting with Kim in Vietnam because he decided the terms were not good enough, and the president “won’t sign an agreement that can’t be enforced,” Perdue told reporters after a speech at Commodity Classic, the gathering of more than 4,000 corn, soybean, wheat and sorghum growers and their families here.Perdue said he believes the agreement with China could double or triple exports for a wide range of U.S. products, including soybeans, rice, beef, ethanol and tree nuts. But he added that Trump wants China to agree to non-tariff items that will make big purchases possible.Perdue did not get into specifics Friday, but in the past, U.S. officials have said that improvements in China’s biotech approval process is a priority, but with agreements on intellectual property and technology transfer that affect all U.S. industry.A meeting between Trump and Xi has not yet been announced, although there are widespread rumors it will take place at Trump’s Mar-a-Lago Club resort in Florida in March.Perdue also said he hopes that an agreement with China is “imminent,” but he also told reporters that farmers may have to plant their crops while the negotiations continue.Farmers will have to make their decisions “based on market signals,” Perdue said, noting that they have always had to make decisions while dealing with uncertainty, and this year those uncertainties may include the relationship with China.Greeting a crowd that is beset with low commodity prices, incomes that have fallen and questions from bankers as spring planting approaches, Perdue opened his speech by acknowledging that “farming is tough” and that farmers are “burning through” capital they built up during the 2008-to-2013 period when commodity prices were high.Perdue also alluded to farmers’ reputation for complaining even when times are good, as he noted that when he was governor of Georgia, a farmer said he used to “whine,” but unfortunately the whine had come true.Perdue quickly added that he did not want to make light of the situation.Perdue acknowledged that some of those producers burning through capital are young farmers and said that his message to them is that their fathers and grandfathers had gone through tough times as well. He noted that USDA has direct and guaranteed loans that may be of help to them. The good years had attracted the children of farmers back to the farm, Perdue said, and if they can hang on, “I am bullish on agriculture.”Perdue also declared that the Environmental Protection Agency will issue a rule by June 1 for gas stations for year-round sale of E15, a type of gasoline that contains more ethanol than the E10 that is usually sold. Current rules do not allow its sale in the summer.Perdue acknowledged that he had misspoken when he said earlier in the week that the rule would not be ready by June 1. Andrew Wheeler, then the acting EPA administrator, told him after the shutdown the agency couldn’t get it done by the summer driving season, but with his confirmation pending, EPA found a way, Perdue said. Wheeler got confirmed this week.Jerry Hagstrom can be reached at firstname.lastname@example.orgFollow him on Twitter @hagstromreport(CC/AG)© Copyright 2019 DTN/The Progressive Farmer. All rights reserved.
Essential Reading! Get my 3rd book: Eat Their Lunch “The first ever playbook for B2B salespeople on how to win clients and customers who are already being serviced by your competition.” Buy Now There are a variety of ideas and beliefs available to you. Sadly, you are mostly infected with them, and less often do you intentionally select those ideas and beliefs that will best serve you. The ideas you picked up along the way on your journey to where you are now may or may not be serving you. If they are not serving you, that is reason enough to evaluate other ideas and beliefs.If you were to look at one part of your life where you are not generating the results you want—or need—you would invariably see a set of actions that are causing your poor results (even if the action that causes poor results is a lack of action). Behind those actions are beliefs that support the action, or lack thereof. For example, procrastination is an action that causes poor results, but the belief is that you can put off until tomorrow what you should do right now. The belief behind that belief is that you have plenty of time, even though all you have ever had or will ever have is the present moment in which to do anything.Say you want better results. The first thing you might do is to go to the marketplace and explore new ideas and beliefs that may interest you and which might suit you better. Once you are in the marketplace, you must decide where to start your search for something better. There are two places one should almost always look, where there is success, and where there is something with which you disagree.When Someone Has What You WantIf someone already has what you want, they have a set of beliefs and are taking a certain set of actions to produce the result you want. The fact that their ideas and beliefs and actions work for them doesn’t necessarily mean it is the one right answer, and it doesn’t mean that their way will necessarily be your way, but it’s worth exploring. There may also be people who have similar ideas and beliefs but have very different strategies and are taking different actions to produce the same result. Remember, this is a marketplace, and that means you are shopping.One of the ways you accelerate your growth and development is by discovering what already works. You don’t always have to learn everything yourself, especially if the beliefs and methods to produce that result have been reverse-engineered for you.If It Generates an Emotional ResponseThere is this spot at the very end of the marketplace where it is dimly lit and scary. From where you stand, it looks dangerous, and it may cause you to feel something like a cross between fear and revulsion. In this part of the marketplace, the ideas and beliefs and actions conflict with your beliefs, including some that are your most cherished and deeply-held beliefs. You don’t want to explore this part of the marketplace, because looking at any of these ideas might mean you have to give up what you already know and believe and prefer. And this is why you must venture into this part of the marketplace.There are ideas and beliefs you don’t like that underlie the very outcomes you want. There are actions you refuse to take that others are using to produce the very results you seek. What you see that conflicts with what you believe is an opportunity for growth and development.Seth Godin told me he doesn’t write as many books as he once did because his ALTmba produces better results faster. As a writer, I don’t like that, but I am sitting with it because there is a truth there worth considering.If you want to become the version of yourself that comes after this one, you must be willing to let go of the things that will keep you solidly locked in place.
Odisha’s sweetmeat traders’ association distributed 50,000 rasagolas free of cost to celebrate conferment of the geographical indication tag on the popular dessert here on Monday.“This is a matter of great pride for us that rasagola has been awarded the GI tag. The whole world has recognised that Odisha is the place of origin of the rasagola which is in circulation since the beginning of the famous Rath Yatra of Lord Jagannath,” said Pramod Prusty, vice-president of the Utkal Mistanna Byabasayee Samiti.As per the application submitted to the Registrar of Geographical Indication, the Odisha rasagolas are white in colour and round in shape but off-white rasagolas in various shades are also prepared. The UMBS, which was an applicant for the GI tag, demanded that the State government raise awareness about the tag’s benefits. “We want the government to start filing applications for GI tag for other famous sweets,” said Mr. Prusty.