0Shares0000Allan Katerega celebrating the winner for AFC LeopardsNAIROBI, Kenya, Aug 11- The future of AFC Leopards’ Ugandan winger Allan Katterega maybe as well sealed with head coach Robert Matano making it clear that the players’ name ‘is no longer on his mind’ after a feud between the two last weekend in Nakuru.Katterega engaged the coach in an exchange of words after being substituted in Ingwe’s 1-0 loss against Bandari at the Afraha Stadium, lamenting of his withdrawal barely 40 minutes after being introduced. “I can’t work with that kind of a player because he lacks respect. Not only am I a coach to him but I am like his father as well. He has to respect me but creating a scene out of nothing in public, that’s embarrassing,” Matano told Capital Sport.The tough talking tactician, nicknamed ‘The Lion’ added; “He is not even on my mind. I already finished up that case in Nakuru and I don’t want even to talk about it. I have other players who are willing to work and it is those that I can talk about.”AFC Leopards head coach Robert Matano passes on instructions to his players at half time during their GOtv Shield match against Bidco United at the Thika Stadium on July 26, 2017.Photo/TIMOTHY OLOBULUThe coach has gone on to warn players who might follow in the Ugandan’s path that he will not be shy of getting rid of them, noting he will not condone any degree of indiscipline.“No player owns this team so no one is above anyone. It is a principle not only for my team but everywhere. If you cannot observe respect then you can’t work. It’s that simple,” the tactician insisted.AFC Leopards are battling to scale up the standings after quite a disappointing season and Matano’s arrival early June was meant to stabilize the team and take them back to the top.The club has lost three of its last five matches and are sitting13th in the Kenyan Premier League standings, worrying trends for a side that initially had a target of winning the Kenyan Premier League title, later downgraded to a top five aim.Matano though is confident his side will bounce back and will be among the top five teams at the end of the season.“We have to keep on working, because the journey is long. There are many matches left and we have to improve. It is mostly about the mentality because when you lose matches it tends to affect you. I am confident that we will be back on top,” the coach added.AFC Leopards defender Salim Abdallah attempts to cut away Western Stima’s Oromchan Villa during a Kenyan Premier League clash at Nyayo Stadium on July 29, 2017. PHOTO/Timothy OlobuluAFC Leopards’ next match will be away to Mathare United August 17 and Matano hopes his side will be able to bounce back. However, he is worried that they have not trained for a whole week due to the uncertainty of the elections.“If the game is confirmed we will have to play, we don’t have choice. That is the situation with almost all teams; they are not training. I am just hoping things can get back to normal then we start preparations. But for now, we just wait,” Matano offered.It is not only AFC whose training has been disrupted. Defending champions Tusker FC, Gor Mahia, Posta Rangers, Western Stima and Nakumatt are some of the teams whose training routines have been halted.“Well, we have been told to remain indoors and no training so there’s really nothing much we can do. It is the situation all over. I am hoping for peace though,” Gor Mahia head coach Dylan Kerr said.Thirsty for the title: Posta Rangers head coach Sammy Omollo has warned that his team is a strong title contender.His Posta Rangers counterpart Sammy Omollo said; “We really can’t put the players at risk by asking them to come for training and hence we decided to break. Hopefully by tomorrow (Saturday) we see how things are then we go back to normal.”Tusker’s George ‘Best’ Nsimbe said his team was back in training, but was hit hard with low numbers with most players yet to report back.Meanwhile, KPL Chief Executive Officer Jack Oguda says he will consult with the governing council on whether the midweek matches will go on as planned. Already, KPL postponed this weekend’s games due to the uncertainty.0Shares0000(Visited 1 times, 1 visits today)
Fairly regularly, papers appear in journals under the heading of Evolution. The ones dealing with genetics tend to be hard to follow. They are filled with jargon, correlation scores, charts and network diagrams. They employ algorithms and databases unfamiliar to the lay reader. Overall, though, they claim to find support for Darwin’s tree of life in the genes or metabolic networks of this or that group of organisms. Does Darwinism pop right out of the data, or does it take some massaging to make Darwin fit the observations? Let’s take one example that appeared in PNAS today for a look inside the engine room of how evidential support for evolution is manufactured.1 Kreimer et al set out to find the “evolution of modularity in bacterial metabolic networks.” What they were looking for, in other words, is whether the amount of modularity in the ways proteins interact follows their assumed evolutionary relationships. What is modularity? That had to be defined in the Materials & Methods section. First, they had to assign network scores to proteins based on what other proteins they interact with. In the process, they tossed out water, protons and electrons. Why? Because someone else in the references did so – who had also written a paper on “The effect of oxygen on biochemical networks and the evolution of complex life.” Already there seems to be some circularity in the reasoning. Next, they had to assign “modularity” values to the networks. (This refers roughly to the degree a network of interacting proteins could be isolated from other networks.) To do this, they used Newman’s algorithm, but they purposely avoided using an algorithm from another paper on the evolution of network modularity. The authors could probably justify these choices, but they were clearly making human judgment calls on what algorithms would produce meaningful results. Once they had modularity scores, they had to decide how to measure environmental influences on various bacteria species. They used the number of transporter genes found in databases as a proxy for environmental diversity; however, the paper admits that “the large scale KEGG data [Kyoto Encyclopedia of Genes and Genomes] used is not free from noise and missing information, and the representation used lacks reactions’ directionality, stoichiometry and more.” That word “more” sounds worrisome. How can they know they have meaningful data? Their reassurance was only general: “However, the large scope of the data used permits a very large-scale investigation across hundreds of networks and leads to the identification of general relations that run across the data.” OK, we’ll take their word for it. The worries do not stop there, though. Next they had to figure out the phylogenetic tree of their bacteria. Here they just borrowed one from another paper in the references. One might think this is odd, since the goal of the paper was to show evolution, not to assume it:The tree of life generated in ref. 21 was used to identify the phylogenetic relations between the species studied in our analysis and for inferring ancestral metabolic networks along the tree. This tree includes a relatively large number of species, covering most of the taxonomic groups for which metabolic data are available. Specifically, this tree was used to measure the distance of each extant and ancestral species to the last universal common ancestors of bacteria and to calculate the species pairwise phylogenetic distances (measured as the sum of distances from the two species to their last common ancestor).It appears they assumed a universal common ancestor from the start. And as shown by a paper reported here on 03/17/2006, scientific papers can perpetuate false “microparadigms” by referring to other papers uncritically. These worries notwithstanding, what remained was for the team to show a correlation between modularity and phylogeny. They generated a large circular diagram color-coded with modularity values for the assumed phylogenetic tree of bacteria. Unfortunately for their thesis, the color values appear random. To the rescue: the team had lots of explanations for why the anomalies were really not significant. There actually is a correlation if you look at it right, they said. Each exception had a ready explanation. Horizontal gene transfer, obligate parasitism, unusual environmental factors, a trend downward in modularity as one goes up the tree – there was no shortage of reasons why they found that modularity was only “moderately concordant with organismal phylogeny along the tree of life.” There is the tree-of-life assumption again. Let the disinterested reader evaluate the following claims and caveats in the paper. Are these valid explanations, or rescuing devices for a theory in crisis? Keep in mind that the goal of the paper was to establish the claim that all bacteria have evolved from a common ancestor, and the evolutionary tree should be visible in the modularity of their metabolic networks.Overall, our analysis is applied to a large set of 325 reconstructed bacterial metabolic networks (of which 138 appear on the phylogenetic tree), offering insights concerning the forces that have shaped the modularity of metabolic networks since the dawn of bacterial life.Given the moderate level of this overall correlation, it is instructive to examine a few specific cases, where different phylogenetic-modularity similarity patterns emerge.Obviously, habitat variability may also increase as larger classes are examined, so phylogenetic proximity probably involves both genetic and environmental similarities.Other cases, however, may involve substantial variation among strains of the same species…. Such divergence of modularity scores across closely related strains is likely to occur because of the loss of just very few central reactions, fragmenting the metabolic network and consequently altering modularity scores in a considerable manner…. Clearly, such loss of central reactions that affects major metabolic functions is probably detrimental and hence very rare….. Reassuringly, one may note that such variation in modularity among strains is probably not just a result of varying annotation practices that bias the Kyoto Encyclopedia of Genes and Genomes (KEGG) data….In summary, there is an overall rather marked correlation between network size and modularity, but it mainly arises because of the significantly lower modularity scores of small-sized networks. Interestingly, no significant correlation was observed between bacterial growth rate and modularity… despite the fact that network size is positively correlated with a faster growth rate….It is instructive to examine some of the outliers marked by an asterisk in Fig. 3a; specifically, a few species of Rickettsia and Borrelia have very small networks but high modularity scores. Although genetically very remote, these species have a shared lifestyle—they are obligate mammalian pathogens that are transmitted by parasitic insects such as fleas or ticks. This intricate life cycle requires a rapid and efficient shift between two very different environments, which probably dictated the emergence of niche-specific metabolic subsystems, increasing modularity. This may be an extreme example of the principle laid out by ref. 19, that environmental diversity promotes network modularity.Interestingly, among the host-associated organisms, endosymbionts have miniscule metabolic networks … but these networks are slightly more modular than those of commensals and pathogens … Furthermore, we find that thermophilic bacteria have significantly higher modularity scores than organisms in either mesophilic … or hyperthermophilic … environments, and facultative bacteria have lower modularity scores than aerobic bacteria … (after correcting for multiple hypotheses testing using the Bonferroni correction). However, the evolutionary forces that have shaped these differences remain unclear.Finally, we note that the genomic fraction of transporters and permeases, which may have been putatively thought to constitute a simple rough correlate of environmental diversity, does not manifest a significant correlation with network modularity.This overall trend, where ancestral modularity scores tend to be higher than those of the descendants, may be attributed to speciation and niche specialization of the organism and to the gradual addition of more peripheral metabolic pathways during evolution.An additional important force that has been assumed to effect the emergence of modularity in metabolic networks is HGT [horizontal gene transfer]. HGT refers to several biological mechanisms by which one organism may transfer genetic material to another organism that is not its descendant and is a major evolutionary force in prokaryotes.In summary, they concluded that the correlation of modularity to phylogeny is modest at best:This complex mixture of driving forces reinforces the notion that modularity can be thought of as a product of both the organism’s past evolutionary heritage and its present adaptation to a certain lifestyle and to available niches. The determination of whether modularity is a converging vs. a genetic trait remains an open challenge.After this, they unloaded a series of “methodological limitations” that might randomize the modest correlation even further. They left it to others to see if the correlation would hold up outside the limited scope of their study: “It remains to be seen whether the forces identified here in bacterial metabolic networks do play a similar or a different role in the evolution of modularity in other kinds of biological networks.” So what, exactly, was demonstrated?1. Kreimer, Borenstein, Gophna and Ruppin, “The evolution of modularity in bacterial metabolic networks,” Proceedings of the National Academy of Sciences USA, Published online on May 6, 2008, 10.1073/pnas.0712149105Every once in awhile we need to take our readers kicking and screaming into the stench of the baloney factory to show them how the Darwin sausage is made. We know you can only stand it for a few minutes at a time. This is the garbage that is force-fed to students. They have no choice; it’s the only thing on the menu. We bring you the very best smelly sausage. This was not cooked up in a corner; it was presented by the National Academy of Sciences, one of the most prestigious scientific societies in the world. It passed peer review. No one in the Academy criticized it. This can be considered representative of the very best the Darwinists have to offer in support of their world view that humans had bacteria ancestors by a chance process with no design. There were more rescuing devices in this paper than reasons to believe in evolution. Even when they assumed evolution and referred to other evolutionary papers, they could only find a modest correlation at best, with whopping outliers and anomalies that had to be explained away. Worse, they failed to even consider other explanations for the data. It was DIDO all the way – Darwin in, Darwin out, and DIGO, too: Darwin in, garbage out. The data were only incidental to the storytelling spree – mere props in the never-ending Darwin drama. Did you catch them conjuring up evolutionary “forces”? We think of forces in science like gravity and electromagnetism, but they redefined the word. To them, a force is any happenstance that steers the miracle-working potential of evolutionary tinkering. Did they ever explain how a new environment would generate the necessary random mutations that were supposed to create new, functional metabolic networks? Never; they merely assumed it would. Referring to horizontal gene transfer as a source of innovation only pushes the miracle onto another germ. Playing theoretical hot potato is not a scientific way to explain how complex interactions of highly-specific protein parts came about. Remember? They even admitted that tinkering with networks is probably detrimental and extremely rare – but in their view, tinkering is the only available source of innovation. At one point they said, “the evolutionary forces that have shaped these differences remain unclear,” but a few paragraphs later they were crowing about “the forces identified here”. Forces? What forces? Let’s see an equation. There were no forces; just obstacles. The telephone pole on the sidewalk does not force a bicycle rider to become an airplane pilot. More likely, it forces him into an opportunity for a concussion. Undoubtedly, the Darwin Party Propaganda Mill will add this paper to their mountain of evidence that supports Darwin. They will argue also that nothing in biology makes sense without evolution. They will use it to show how much useful science Darwinism is generating. In truth, the guys in the baloney factory spill their guts and sacrifice their brains into the mix to show their devotion to Charlie. Maybe that’s why the Good Book warned against eating meat offered to idols.(Visited 13 times, 1 visits today)FacebookTwitterPinterestSave分享0
Plants perform a wonder that has attracted the admiration of scholars from ancient Egypt, Greece and Rome to modern times: the ability to reproduce mathematically perfect patterns. This ability, called phyllotaxis, can be described mathematically with the Fibonacci Series and the Golden Angle. The beautiful spirals in sunflowers, artichokes, cacti, dandelion heads and other plants continue to fascinate children and adults today, but those are not the only examples. Leaves on a stem can emerge in phyllotactic patterns like a spiral staircase, and depending on the environment, plants can switch patterns at different stages in development. Scientists have learned a lot about the players in the phyllotaxis game, but still do not understand the script. The details of how genes and proteins produce the patterns remain elusive. In Current Biology,1 French biologists Jean-Christophe Palauqui and Patrick Laufs recounted some of the theories that have tried to explain phyllotaxis. Scientists know that the plant hormone auxin becomes concentrated in the shoot meristem where new organ primordia emerge, and that the PIN1 auxin transporter is able to polarize the localization of auxin. New work reported in the same issue of Current Biology implicates the PLETHORA (PLT) gene family, known to be active with root formation, with the processes going on in the meristem. Tinkering with the players can enhance or inhibit pattern formation. Just how these players interact, though, is not well understood. It’s not a simple case of gene turning on protein turning on hormone; each of the players signal each other back and forth in a complex choreography. In addition, the PLT genes seem able to stimulate mechanical forces in the primordia by the way they regulate PIN1 polarity and hence auxin distribution. There are also time delays between gene expression and downstream effects, such as 4 hours from the time PLT genes activate to the time PIN1 transcript levels are seen to increase. But then, auxin level can also feed back to regulate PIN1 expression. It appears, therefore, that the intra-player signaling is indirect and complex. The authors stated that the bewildering interactions of these players keeps biologists busy: “Elucidating the mechanism underlying PLT-mediated control of phyllotaxis will be challenging and likely depend on quantitative descriptions and modeling of PLT expression, PIN1 levels and polarization, auxin distribution, growth and mechanics,” they said. Even if these problems are solved with mechanistic theories some day, questions may still remain about how a seed with no phyllotaxis results in a mature plant with it. And beyond that, philosophers of aesthetics may continue to ponder how plants – and many other phenomena in nature unrelated to them, like spiral galaxies, hurricanes, conch shells, and the cochlea in the human ear – reproduce “divine proportions” that humans find beautiful (see article by Fred Willson at ICR and the 11/20/2003 entry). 1. Jean-Christophe Palauqui, Patrick Laufs, “Phyllotaxis: In Search of the Golden Angle,” Current Biology, Volume 21, Issue 13, R502-R504, 12 July 2011, DOI 10.1016/j.cub.2011.05.054. Explaining the mechanics of something does not explain its origin. You can understand how a robot on an assembly line works, and describe its structures and functions with flowcharts, equations and blueprints. That knowledge will not explain why it produces a Mercedes. Wikipedia trivializes the explanation as a consequence of natural selection, claiming that the solution was found within a decade of Darwin by Wilhelm Hofmeister. “Questions remain about the details,” the entry oversimplifies. If that were true, the scientists publishing in this week’s Current Biology would not remain baffled by it. The devil is often in the details. Hofmeister knew nothing of PIN1 and PLT, let alone the genetic code. His simplistic model of competing mechanical forces is so 1896; it cannot satisfy observers today, with our newer knowledge of genetic codes, proteins, and cell signals. If evolutionists do some day get all the mechanics worked out, the questions stated above will still remain. Considering that not all plants employ phyllotaxis, and that the patterns seem unnecessary for survival, unguided evolution reduces to an empty hand-waving story that “amazing stuff happens sometimes.” The same criticism can be leveled at any explanation employing impersonal, material causes. Take a deeper look at that sunflower. Here is a natural wonder that calls out for better science, deeper philosophy, and perhaps most of all, sound theology.(Visited 38 times, 1 visits today)FacebookTwitterPinterestSave分享0
Share Facebook Twitter Google + LinkedIn Pinterest The U.S. Department of Agriculture to temporarily stopped shipments to the United States of pork from Poland.The USDA has suspended entry of imports of fresh and frozen pork and pork products from Poland while it completes a review of that country’s export protocols. According to the USDA, “As part of a routine review of ongoing operations, it came to our attention that one Polish facility exporting pork to the U.S. has done so in contravention of the stringent requirements in place to prevent the spread of serious diseases of livestock, like ASF.”USDA’s action was taken out of an abundance of caution to ensure that the United States remains free of African Swine Fever (ASF), a highly contagious, trade-limiting pig disease with no cure. USDA has been closely monitoring ASF’s spread in Eastern Europe — parts of Poland have the disease — and in Asia. The disease underscores the need for the United States to be better prepared to address foreign animal diseases, including by establishing a more robust vaccine bank to deal with an outbreak of Foot-and-Mouth Disease (FMD), another trade-limiting disease endemic in many parts of the world. NPPC supports in the 2018 Farm Bill mandatory funding for an FMD vaccine bank and other disease-prevention programs.
Pagasa: Kammuri now a typhoon, may enter PAR by weekend LATEST STORIES LOOK: Vhong Navarro’s romantic posts spark speculations he’s marrying longtime GF Yoshihiro Kamegai of Japan v Jesus Soto-Karass of Mexico during the junior middleweights bout at The Forum on September 10, 2016 in Inglewood, California. Josh Lefkowitz/Getty Images/AFPJapanese boxer Yoshihiro Kamegai has the chance to grab the world junior middleweight title left behind by Saul “Canelo” Alvarez, but blocking his path is former world champion Miguel Cotto.Promoters announced Wednesday that Kamegai will face Cotto on August 26 at Los Angeles for the vacant World Boxing Organization junior middleweight crown.ADVERTISEMENT Lakers win 9th straight, hold off Pelicans More than 5,000 measles deaths in DR Congo this year — WHO Don’t miss out on the latest news and information. Panelo suggests discounted SEA Games tickets for students PLAY LIST 01:35Panelo suggests discounted SEA Games tickets for students02:49Robredo: True leaders perform well despite having ‘uninspiring’ boss02:42PH underwater hockey team aims to make waves in SEA Games01:44Philippines marks anniversary of massacre with calls for justice01:19Fire erupts in Barangay Tatalon in Quezon City01:07Trump talks impeachment while meeting NCAA athletes Sports Related Videospowered by AdSparcRead Next South Korea to suspend 25% of coal plants to fight pollution Mexican star Alvarez, who defeated Julio Cesar Chavez Jnr earlier this month, dropped the 154-pound title as he moves up to the middleweight ranks for a megafight on September 16 against unbeaten Gennady Golovkin for the Kazak star’s three world titles.Vying to replace Alvarez at 154 pounds are Kamegai, in his first world title bout at age 34, and 36-year-old Puerto Rican Cotto, whose first world championship bout was in 2004.FEATURED STORIESSPORTSSEA Games: Biñan football stadium stands out in preparedness, completionSPORTSMalditas save PH from shutoutSPORTSPrivate companies step in to help SEA Games hosting“I’m very excited to be back and showcase a high level fight for the fans,” Cotto said. “Kamegai is a great, tough fighter, but I will be ready for him and to capture the world title. I can’t wait to start training for this fight and get back in the ring.” MOST READ ‘Coming Home For Christmas’ is the holiday movie you’ve been waiting for, here’s why SEA Games: PH beats Indonesia, enters gold medal round in polo Tigresses lead BVR tournament Ilocos leg champs Cayetano dares Lacson, Drilon to take lie-detector test: Wala akong kinita sa SEA Games Cotto, 40-5 with 33 knockouts, has owned world titles at super lightweight, welterweight, super welterweight/junior middleweight and middleweight — the only Puerto Rican fighter to claim crowns in four different weight classes.“I fully understand who I’m going to be in the ring against, but Cotto’s record and history won’t matter once we are toe-to-toe,” Kamegai said. “I am looking forward to giving fans the kind of aggressive fight that they have seen from me before and having my arm raised in victory.”Kamegai, 27-3 with two drawn and 24 knockouts, is 3-2 with one drawn in his past six fights over the past three years, having stopped Mexico’s Jesus Soto Karass last September in his most recent bout.Cotto is 3-3 over the past five years, including a super welterweight title loss to Floyd Mayweather in 2012. His most recent bout was an unanimous decision loss to Alvarez in November 2015.ADVERTISEMENT View comments
CALGARY — Former NHL player and abuse survivor Sheldon Kennedy is removing his name from the Calgary child advocacy centre he founded.He says in a statement that the decision comes with some sadness, a great sense of relief and no regrets.Kennedy says having his name on the building means personal responsibility for its day-to-day operation and looking after front-line workers, donors, volunteers and victims.He says it has been rewarding work since he first pitched the centre in 2010, but it has taken a toll.Kennedy says he needs to take care of his mental health and find balance in his life.He says he’ll now focus on his family and on the Respect Group, a company he co-founded aimed at preventing bullying, abuse, harassment and discrimination.“Today, I am healthy and excited about my next chapter. I will continue the crusade, but with greater balance. I am also comforted to know that the Calgary Child Advocacy Centre and our community are ready to carry the torch,” Kennedy said in a statement Tuesday.“It has become clear that I will not be able to achieve the critical balance I need in my life without taking my name off the centre. Furthermore, our community will never fully own the issues with my name still on it. The time has come and the future is bright.”Kennedy declined to comment further.Kennedy was among the first to speak out about sexual abuse he suffered from coach Graham James. James was sentenced to 3 1/2 years in prison for abusing Kennedy and another young player.James later pleaded guilty to repeatedly abusing other players including retired NHL star Theo Fleury and Fleury’s cousin, Todd Holt, when they played for him in the Western Hockey League in the late 1980s and early ’90s.The Canadian Press