No Rest for the Warming

Climate change denialists are apt to grasp at straws, which may explain their heralding of a global warming “hiatus” or “pause” that since 1998 has supposedly invalidated scientific consensus and its models of climate change. Clearer and more clever heads have renamed the hiatus a “faux pause,” playing off the French faux pas which means false step or blunder. For one thing, the data showed only a relative slowdown in warming, not a pause; temperatures were still increasing. As Greg Laden says, “a hiatus or a pause in global warming is at present physically impossible.” Now a new paper published in Science suggests that even the extent of the slowdown was overestimated. Furthermore, the slowdown jibes with ongoing natural variations in surface temperature, as modulated by, for example, El Niño and La Niña events, and does not contradict the long-term upward trend. Greg says that any scientist championing the “pause” is either ignorant or “willfully obfuscating the science, in an effort to distract from the reality of human caused climate change.” Meanwhile, on Stoat, William M. Connolley notes a pointed revision to the Wikipedia entry on the so-called hiatus.

Advertisements

Outmaneuvering Antibiotic Resistance

A groundbreaking study published in PLOS ONE offers hope that scientists can reverse the development of antibiotic resistance among bacteria with the help of “a mathematical model that pinpoints optimal antibiotic cycling patterns.” On The Pump Handle, Kim Krisberg writes, “the research comes at a time of widespread concern that without a coordinated, well-funded response to growing antibiotic resistance, medicine could lose some of its most effective, life-saving tools.” The collaboration between biologists and mathematicians yielded a piece of software dubbed “Time Machine” that “computes which antibiotic goes with which mutation at which point in time to best manage the evolution of resistance.”

The promise of this software comes as the problem of antibiotic resistance becomes ever more urgent. On The Pump Handle, Liz Borkowski details a WHO report that documents strains of resistant pneumonia, E. coli, staph, tuberculosis, malaria, and flu worldwide. Borkowski also covers the recent outbreak of a “nightmare bacteria” called CRE due to contaminated medical equipment at a Los Angeles hospital. Meanwhile, last year, the CDC issued a warning about the threat of drug-resistant gonorrhea.

On Aetiology, Tara C. Smith provides some historical perspective, noting that the discoverer of penicillin warned about evolving resistance in 1945. Smith considers the possibility of moving beyond traditional antibiotics entirely, instead using viruses to consume bacteria, or using antimicrobial peptides like those produced by our immune systems to mutilate bacterial cell walls. But as Smith writes, “the peptides of our innate immune system are one of our first lines of defense against an immense variety of pathogens, and we don’t know what the outcome may be if we compromise this essential level of protection.”

Outmaneuvering Antibiotic Resistance

A groundbreaking study published in PLOS ONE offers hope that scientists can reverse the development of antibiotic resistance among bacteria with the help of “a mathematical model that pinpoints optimal antibiotic cycling patterns.” On The Pump Handle, Kim Krisberg writes, “the research comes at a time of widespread concern that without a coordinated, well-funded response to growing antibiotic resistance, medicine could lose some of its most effective, life-saving tools.” The collaboration between biologists and mathematicians yielded a piece of software dubbed “Time Machine” that “computes which antibiotic goes with which mutation at which point in time to best manage the evolution of resistance.”

The promise of this software comes as the problem of antibiotic resistance becomes ever more urgent. On The Pump Handle, Liz Borkowski details a WHO report that documents strains of resistant pneumonia, E. coli, staph, tuberculosis, malaria, and flu worldwide. Borkowski also covers the recent outbreak of a “nightmare bacteria” called CRE due to contaminated medical equipment at a Los Angeles hospital. Meanwhile, last year, the CDC issued a warning about the threat of drug-resistant gonorrhea.

On Aetiology, Tara C. Smith provides some historical perpective, noting that the discoverer of penicillin warned about evolving resistance in 1945. Many other antibiotics have since been developed and utilized—but one by one, they have also been outflanked. Smith considers the possibility of moving beyond traditional antibiotics entirely, instead using viruses to consume bacteria, or using antimicrobial peptides like those produced by our immune systems to mutilate bacterial cell walls. But as Smith writes, “the peptides of our innate immune system are one of our first lines of defense against an immense variety of pathogens, and we don’t know what the outcome may be if we compromise this essential level of protection.”

Genetic Modification as Medicine

On ERV, Abbie Smith provides an update on a pioneering treatment for hemophilia that uses viruses to insert missing genes in a patient’s DNA. Hemophilia results from from the mutation or deletion of a gene that makes a blood clotting agent called Factor IX; without it, hemophiliacs are at risk for uncontrolled bleeding. While Factor IX can be delivered pharmaceutically, utilizing viruses to modify patients’ DNA yields long-term improvements in natural Factor IX production. Abbie writes, “the amount of therapeutic Factor IX these patients needed (on average) dropped from 2613 IU/kg to 206. The people who got the ‘high’ dose of virus dropped that down to 92 IU/kg. They went from 15-16 ‘bleeding episodes’ a year, to one.” They also saved $2.5 million.

Next, Abbie revisits research on treating HIV by removing CCR5 receptors that the virus uses to enter white blood cells. Much excitement was generated in 2008 when the “Berlin Patient” was declared to be functionally cured of HIV after receiving bone marrow from a donor with a mutation that preludes manufacture of the CCR5 protein. Now scientists are considering using gene therapy to disable CCR5 production in HIV patients, but there’s a catch: some HIV quasispecies utilize other receptor proteins, and even a small population of such viruses can take over when a patient is not producing CCR5. For this reason, Abbie writes that this therapy may hold more promise as a vaccine for HIV than as a cure.

Meanwhile, HIV itself has been genetically modified to help some sufferers of acute lymphoblastic leukemia by training cytotoxic T cells to target cancerous B cells. Abbie writes, “for all the time HIV has stolen from people, from families, its nice to see it giving some time back.”