SAN FRANCISCO — The Giants are in a rush.CEO Larry Baer and vice president of baseball operations Brian Sabean expect the club to contend every year, and in each of the past two seasons, the Giants failed to live up to expectations.Baer and Sabean are in a hurry to see the team return to the postseason and they’re eager to hasten the process.The duo wants to oversee a quick turnaround, but to ensure that happens, they know it’s imperative to slow down. After dismissing general manager Bobby …
SAN JOSE — With captain Joe Pavelski limp on the ice, the Sharks’ playoff outlook was bleak. They trailed the Vegas Golden Knights 3-0 with less than 10 minutes to play in Game 7.The Sharks responded to Pavelski’s apparent head injury with four goals on the ensuing five-minute power play to take a 4-3 lead and send the SAP Center into absolute chaos. They eventually won 5-4 in overtime.Logan Couture started the scoring just seven seconds into the power play, then turned and gestured to the …
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
8 November 2013Excavations will soon begin on a new site at the Cradle of Humankind in South Africa’s Gauteng province to investigate a find of “significant” fossils suspected to be those of our very early human ancestors.Professor Lee Berger, a research professor in Human Evolution from the Evolutionary Studies Institute at the University of the Witwatersrand and a National Geographic explorer-in-residence, will direct the expedition at the site, dubbed “Rising Star Cave”.Berger is best known for the discovery of Australopithecus sediba at the Malapa site at the Cradle – one of the most significant palaeoanthropological discoveries in recent times.The Cradle of Humankind is a World Heritage site situated about 40 kilometres north-west of Johannesburg.Berger said at the launch of the new expedition this week that “significant” fossils had been found in a chamber deep underground.“We do not know as yet what species of hominin we have found, and we will not speculate,” Berger said. “Our aim is to get the fossils out carefully, study them, compare them to other fossil material from around the world and then proceed to analyse and describe them.“This is part of the scientific process, and we are hoping to publish our findings – if all goes well – late in 2014.”The key challenge is the size and location of the cave: about 30 metres underground, it has a very small opening through which only slightly built people can fit.Berger used social media platforms to call for “tiny and small, specialised cavers and spelunkers with excellent archaeological, palaeontological and excavation skills”.From a list of 57 qualified applicants, Berger selected six scientists. “These are highly trained scientists with caving experience from the US, Canada and Australia who are currently in South Africa preparing for the excavation,” he said.The excavation and scientific analysis that follows will be featured in a National Geographic/NOVA television special.Members of the Speleological Exploration of South Africa will assist the expedition.Follow National Geographic’s Rising Star blog for updates on excavations.Wits University and SAinfo reporter
24 March 2015Nineteen black rhino were recently released at an undisclosed location in South Africa to create a new breeding population of the critically endangered animals.The animals form the 10th population to be facilitated through WWF South Africa’s Black Rhino Range Expansion Project and were made available through the Eastern Cape Parks and Tourism Agency. Growing rhino populations is part of WWF South Africa’s five-point rhino plan.Black rhino are more at risk of extinction than white rhino due to their low numbers. Since the start of the programme in 2003, around 160 black rhino have been relocated to form new breeding populations, and more than 50 calves have been born on project sites.Management plan“We are extremely proud of the agency’s contribution to the conservation of this species,” said Vuyani Dayimani, CEO of Eastern Cape Parks and Tourism Agency. “By doing this the agency is actively contributing to the achievement of the objectives of the national biodiversity management plan for black rhino in South Africa.”One of the key objectives of this plan is to grow the national population as rapidly as possible by harvesting animals from populations that are at or near ecological carrying capacity and using these animals to create new populations. This harvesting stimulates growth in the donor population and also makes animals available for the creation of new populations.“We are really grateful for Eastern Cape Parks and Tourism Agency’s progressive approach to the conservation of black rhino,” said Dr Jacques Flamand, head of the Black Rhino Range Expansion Project.Commitment“It requires a genuine commitment to conservation to entrust others with the care of such a large group of these precious animals; but this is for the greater good of the species. Establishing a new population is extremely exciting for us because this is essentially what the project works towards. To see our efforts come to fruition is very encouraging.”The Black Rhino Range Expansion Project aims to increase the numbers of black rhino by encouraging rapid population growth. It is a vital part of South Africa’s drive to reach a target of 3 000 black rhino. According to Dr Flamand: “South Africa now has significantly more black rhino than there would have been without the project’s intervention.“Founder populations released on to large areas of land have the potential to increase quickly in number. And moving rhinos from our major parks relieves pressure, allowing for more rapid growth both at source and in their new terrain.”SecurityThe Western Black rhino, a subspecies of the black rhino, was officially declared extinct in 2013 after last being seen in 2006.The recent translocation involved WWF and Eastern Cape Parks and Tourism Agency with help from SANParks and Ezemvelo KZN Wildlife. Six wildlife veterinarians participated in the project that saw darted animals being airlifted by helicopter to a central loading area where they were loaded into crates and prepared for a road trip to their new home.“The project was kept secret for security reasons and one of the highlights of the operation was the manner in which the different state agencies supported and assisted each other to ensure its success,” said Dayimani.As well as focusing on population growth, the Black Rhino Range Expansion Project supports security efforts on major rhino reserves. It is funded by WWF Netherlands and supported by the Ford Wildlife Fund. Founder populations for the project sites have come from game reserves managed by Ezemvelo KZN Wildlife and Eastern Cape Parks and Tourism Agency.Source: World Wildlife Fund South Africa
A Web Developer’s New Best Friend is the AI Wai… AT&T customers who have purchased or upgraded to the new iPhone 4 have started to receive SMS text messages pointing them to a newly published resource guide containing “important information about activating your device.” The link directs recipients to the page at www.att.com/iphone4upgradesupport which provides all the information needed regarding how to activate the new iPhone – yet another indication that iPhones may be shipping, as reported elsewhere, a day earlier than previously expected.According to the AT&T activation guide, there are just four “simple steps” to activating your new device. However, as previous iPhone owners know, AT&T’s and Apple’s activation systems tend to get bogged down as a large number of new iPhone owners attempt to activate their phones at the same time. Top Reasons to Go With Managed WordPress Hosting Last summer, with the launch of the iPhone 3GS, some users reported that it was taking up to 48 hours to complete the activation process. The issues caused by this overload of activation requests have gotten better over the years, at least – the 3GS delays were a vast improvement over the 3G problems that plagued the 3G launch.But when a company sells 600,000 phones on its launch day alone, as Apple has with the iPhone 4, activation issues are bound to happen.…or are they?According to numerous sources, Apple has begun sending out emails to some iPhone 4 customers informing them that their device will arrive on June 23rd – a day earlier than expected. The most obvious reasoning behind these missives is to spread out the activation process over the course of two days instead of one. Of course, new iPhone 4 users are just glad they’ll be getting the revamped device a day early, no matter the reason. And being the recipient of the text message doesn’t necessarily mean you’re among the chosen few to get your iPhone 4 early. Tags:#Apple#web sarah perez Related Posts 8 Best WordPress Hosting Solutions on the Market Why Tech Companies Need Simpler Terms of Servic…
Why IoT Apps are Eating Device Interfaces Role of Mobile App Analytics In-App Engagement audrey watters It makes sense that the Google suite of products would have a nicer version on Android than on iPhone, right? The newly released Google Docs app for Android is certainly a testament to that.Google added the ability to edit your Google Docs on your mobile devices last fall, a huge boon for those of us who tend to work on the go and who need to be able to access, edit, and share our work via our phones. But the mobile Web interface has still felt a little clunky, and a good reminder that really smartphones aren’t designed for word processing.The new Google Docs app, now available for Android, makes the process a lot less painful (well, minus the fact that you’re still working on with a small screen and keyboard, of course). While composition of new documents or spreadsheets may still be challenging, the app makes it very easy for you to share items with others and open files that you receive via Gmail. It’s also incredibly simple to upload documents to Google Docs via your phone. This isn’t simply a matter of uploading files (although that is an option). The new app is also integrated with the Android camera so if you snap a picture of a document, the app will translate it into text via OCR, using the new “Document from Photo” option. Of course, OCR isn’t always completely accurate, but it’s still a great way to easily input information into your Google Docs account. Tags:#Google#mobile#web Related Posts Note that there’s still no support for offline editing. And when you first load the app, it will take a while to sync your accounts. But once it does so, you’ll find you have access to all the files you store there. The app is available now via the Android Market. What it Takes to Build a Highly Secure FinTech … The Rise and Rise of Mobile Payment Technology
The Odisha government on Tuesday decided to celebrate the 150th birth anniversary of Mahatma Gandhi for two years from October 2 this year. The decision was taken at a meeting chaired by Chief Minister Naveen Patnaik at the Secretariat here. He said people belonging to all sections of society will be involved in the anniversary celebrations in the State.Observing that Mahatma Gandhi wanted to develop society on the principles of truth and non-violence, Mr. Patnaik said that he had proposed to include ‘Ahimsa’ in the preamble of the Constitution.Leader of the Opposition in the Assembly Narasingha Mishra, former Chief Minister Giridhar Gamang, Culture Minister Ashok Chandra Panda, Gandhian leader Bhabani Charan Patnaik and several MPs and legislators also attended the meeting.Mr. Panda informed that five sub-committees have been constituted for the celebration of the anniversary in a grand manner. Padayatras and memorial meetings will be held across the State during the two-year period, he added.The Minister said that Gandhiji’s birth anniversary would be celebrated in schools, colleges, urban local bodies, blocks and gram panchayats. A new website will be opened to propagate the messages of Gandhiji.In order to commemorating Mahatma Gandhi’s visit to Cuttack, a function will be organised in the city on March 23 next year, Mr. Panda said.Statues of Mahatma Gandhi will be erected at all district headquarters and one major road at the places Gandhiji visited will also be named after him. Gandhiji had visited Odisha eight times and toured different parts of the State.The Odisha government is also considering convening a special session of the Assembly in 2019.
Minnesota coach Jerry Kill has been released from the hospital after suffering a seizure late Saturday afternoon.The school confirmed Kill’s release Sunday. Gophers defensive coordinator Tracy Claeys told local reporters Sunday that Kill’s seizure was minor and that the coach could return to the team as early as Sunday afternoon.Kill was taken to the hospital Saturday as a precaution and was reported to be resting comfortably by Saturday night.Kill, 51, has had seizure disorder since being diagnosed with kidney cancer in 2005. He suffered a more severe seizure on the sideline during a game last September and had to be hospitalized for several days.That hasn’t stopped Kill in the past from getting right back out there.“What the hell am I supposed to do? Stop? I mean, sit in the chair and wait for the next dang seizure to come along?” Kill said last year.It’s the latest bit of adversity for the Gophers, who started the season 4-0 to generate optimism among the program’s long-suffering fans that a bowl game could be had.But they were thumped 31-13 at Iowa in the Big Ten opener, then delivered a sloppy and mistake-filled performance in the loss to the Wildcats on Saturday to fall to 0-2 in the conference.