Doctors remove world’s largest kidney in Delhi hospital

Surgeons have removed the world’s largest kidney weighing 2.75 kg from a 45-year-old patient, authorities at Delhi’s Sir Ganga Ram Hospital said on Tuesday.

Subash Yadav (name changed) was diagnosed with chronic renal failure with severe pain in the abdomen, blood in urine and high fever. Little did he know that what was building inside his body was a kidney almost equivalent to the size of a baby. Normal kidneys weigh approximately 130 grams. The Guinness Book of World Records reports a kidney weighing 2.15 kg as the world’s largest, which was removed in Dhule, Maharashtra, in 2011.

Due to severe infection in the kidneys, Yadav’s condition was deteriorating with every passing day. Besides, it was leading to loss of blood. After consulting various doctors, Yadav landed at Sir Ganga Ram Hospital in the national Capital last month, and doctors decided to remove both the kidneys in a life-saving procedure.

“Due to excessive blood loss, I used to feel tired throughout the day,” said the 45-year-old man. “He was undergoing dialysis,” Dr Manu Gupta, consultant, urological surgeon, SGRH, told MAIL TODAY.

A nurse holds the world's largest kidney.

Last year, Yadav was diagnosed with autosomal dominant polycystic kidney disease (ADPKD) that is an inherited genetic systemic disease occurring in 1:700 to 1:1,000 individuals. It is a common inherited disorder with 12.5 million cases worldwide.

“It took us three hours of difficult dissection to remove the kidney that weighed 2.75 kg-20 times more than normal-and was stuck to the surrounding intestines. The second one, weighing 2.5 kg, was also removed a week later. Altogether, the patient’s body was bearing an extra weight of over 5 kg,” added Dr Gupta.

Dr Vinant Bhargav, consultant nephrologist at SGRH, said that pre-transplant nephrectomies (removal of kidneys) are occasionally necessary.

“The patient is recovering and awaiting kidney transplant,” Dr Bhargav told MAIL TODAY. The development of multiple kidney cysts results in slow enlargement of the kidney, leading to chronic kidney disease (CKD) in 50 per cent patients.

Doctors say children of such patients are screened young and followed up for life. “Patients may have symptoms of haematuria (blood in urine), abdominal pain, an abdominal mass, kidney failure and hypertension,” Dr Gupta told MAIL TODAY.

Chinese Scientists Genetically Modify Human Embryos .

In a world first, Chinese scientists have reported editing the genomes of human embryos. The results are published in the online journal Protein & Cell and confirm widespread rumours that such experiments had been conducted—rumours that  sparked a high-profile debate last month about the ethical implications of such work.

In the paper, researchers led by Junjiu Huang, a gene-function researcher at Sun Yat-sen University in Guangzhou, tried to head off such concerns by using ‘non-viable’ embryos, which cannot result in a live birth, that were obtained from local fertility clinics. The team attempted to modify the gene responsible for β-thalassaemia, a potentially fatal blood disorder, using a gene-editing technique known as CRISPR/Cas9. The researchers say that their results reveal serious obstacles to using the method in medical applications.

“I believe this is the first report of CRISPR/Cas9 applied to human pre-implantation embryos and as such the study is a landmark, as well as a cautionary tale,” says George Daley, a stem-cell biologist at Harvard Medical School in Boston. “Their study should be a stern warning to any practitioner who thinks the technology is ready for testing to eradicate disease genes.”

Some say that gene editing in embryos could have a bright future because it could eradicate devastating genetic diseases before a baby is born. Others say that such work crosses an ethical line: researchers warned in Nature in March that because the genetic changes to embryos, known as germline modification, are heritable, they could have an unpredictable effect on future generations. Researchers have also expressed concerns that any gene-editing research on human embryos could be a slippery slope towards unsafe or unethical uses of the technique.

The paper by Huang’s team looks set to reignite the debate on human-embryo editing—and there are reports that other groups in China are also experimenting on human embryos.

Problematic gene
The technique used by Huang’s team involves injecting embryos with the enzyme complex CRISPR/Cas9, which binds and splices DNA at specific locations. The complex can be programmed to target a problematic gene, which is then replaced or repaired by another molecule introduced at the same time. The system is well studied in human adult cell and in animal embryos. But there had been no published reports of its use in human embryos.

Huang and his colleagues set out to see if the procedure could replace a gene in a single-cell fertilized human embryo; in principle, all cells produced as the embryo developed would then have the repaired gene. The embryos they obtained from the fertility clinics had been created for use inin vitro fertilization but had an extra set of chromosomes, following fertilization by two sperm. This prevents the embryos from resulting in a live birth, though they do undergo the first stages of development.

Huang’s group studied the ability of the CRISPR/Cas9 system to edit the gene called HBB, which encodes the human β-globin protein. Mutations in the gene are responsible for β-thalassaemia.

Serious obstacles
The team injected 86 embryos and then waited 48 hours, enough time for the CRISPR/Cas9 system and the molecules that replace the missing DNA to act—and for the embryos to grow to about eight cells each. Of the 71 embryos that survived, 54 were genetically tested. This revealed that just 28 were successfully spliced, and that only a fraction of those contained the replacement genetic material. “If you want to do it in normal embryos, you need to be close to 100%,” Huang says. “That’s why we stopped. We still think it’s too immature.”

His team also found a surprising number of ‘off-target’ mutations assumed to be introduced by the CRISPR/Cas9 complex acting on other parts of the genome. This effect is one of the main safety concerns surrounding germline gene editing because these unintended mutations could be harmful. The rates of such mutations were much higher than those observed in gene-editing studies of mouse embryos or human adult cells. And Huang notes that his team likely only detected a subset of the unintended mutations because their study looked only at a portion of the genome, known as the exome. “If we did the whole genome sequence, we would get many more,” he says.

Ethical questions
Huang says that the paper was rejected by Nature and Science, in part because of ethical objections; both journals declined to comment on the claim (Nature’s news team is editorially independent of its research editorial team.)

He adds that critics of the paper have noted that the low efficiencies and high number of off-target mutations could be specific to the abnormal embryos used in the study. Huang acknowledges the critique, but because there are no examples of gene editing in normal embryos he says that there is no way to know if the technique operates differently in them.

Still, he maintains that the embryos allow for a more meaningful model—and one closer to a normal human embryo—than an animal model or one using adult human cells. “We wanted to show our data to the world so people know what really happened with this model, rather than just talking about what would happen without data,” he says.

But Edward Lanphier, one of the scientists who sounded the warning in Nature last month, says: “It underlines what we said before: we need to pause this research and make sure we have a broad based discussion about which direction we’re going here.” Lanphier is president of Sangamo Biosciences in Richmond, California, which applies gene-editing techniques to adult human cells.

Huang now plans to work out how to decrease the number of off-target mutations using adult human cells or animal models. He is considering different strategies—tweaking the enzymes to guide them more precisely to the desired spot, introducing the enzymes in a different format that could help to regulate their lifespans and thus allow them to be shut down before mutations accumulate, or varying the concentrations of the introduced enzymes and repair molecules. He says that using other gene-editing techniques might also help. CRISPR/Cas9 is relatively efficient and easy to use, but another system called TALEN is known to cause fewer unintended mutations.

The debate over human embryo editing is sure to continue for some time, however. CRISPR/Cas9 is known for its ease of use and Lanphier fears that more scientists will now start to work towards improving on Huang’s paper. “The ubiquitous access to and simplicity of creating CRISPRs,” he says, “creates opportunities for scientists in any part of the world to do any kind of experiments they want.”

A Chinese source familiar with developments in the field said that at least four groups in China are pursuing gene editing in human embryos.

World’s most powerful telescope set to launch in 2018 .

NASA is building the biggest telescope the world has ever seen, and it will give scientists the opportunity to ‘see’ cosmic events that occurred 13.5 billion years ago – just 220 million years following the Big Bang. Named the James Webb Space Telescope (JWST), it will be 100 times more powerful than the Hubble Space Telescope, and is tipped to be fully operational within the next three years.

“What the Webb will really be doing is looking at the first galaxies of the Universe,” project scientist Mark Clampin told the press at NASA’s Goddard Space Flight Centre in the US this week. “We will also be able, with these capabilities, to look in very dark parts of the universe where stars are being born.”

The JWST includes a mirror 6.5 metres in diameter, which is three times the size of Hubble’s mirror, and it will have 70 times its light-gathering capacity. It will include four cameras and spectrometers, the latter of which is designed to take in light, break it down into its spectral components, and digitise the signal as a function of a wavelength for scientists to interpret.

“We have sensors on board, equipment on board that will enable us to study the atmosphere of exoplanets spectroscopically, so we will be able to understand the composition of those atmospheres,” Matt Greenhouse, a JWST project scientist, told the press. “We can make big progress in the search for life.”

Unlike Hubble, which has spent the last 25 years orbiting Earth, the James Webb Space Telescope will go all the way out to one of the Lagrangian points – a set of five equilibrium points in every Earth-Moon System – 1.5 million kilometres (930,000 miles) away. This will keep it far enough away from the Sun so it’s not too hot, and will shelter it from radiation and “prevent it from being blinded by its own infra-red light,” Jean-Louis Santini reports for the AFP.

“It will follow Earth around the Sun over the course of the year. So it’s in a Sun centre orbit instead of an Earth centre orbit,” said Greenhouse. “Just as Hubble rewrote all the textbooks, Webb will rewrite [them] again.”

The telescope is expected to launch in October 2018.

Watch the video. URL:


Radiation Therapy Can Make Cancers 30x More Malignant

Study: Radiation Therapy May Make Cancers 30x More Malignant

Following on the heels of recent revelations that x-ray mammography may be contributing to an epidemic of future radiation-induced breast cancers, in a new article titled, “Radiation Treatment Generates Therapy Resistant Cancer Stem Cells From Aggressive Breast Cancer Cells,” published in the journal Cancer July 1st, 2012, researchers from the Department of Radiation Oncology at the UCLA Jonsson Comprehensive Cancer Center report that radiation treatment actually drives breast cancer cells into greater malignancy.

The researchers found that even when radiation kills half of the tumor cells treated, the surviving cells which are resistant to treatment, known as induced breast cancer stem cells (iBCSCs), were up to 30 times more likely to form tumors than the nonirradiated breast cancer cells. In other words, the radiation treatment regresses the total population of cancer cells, generating the false appearance that the treatment is working, but actually increases the ratio of highly malignant to benign cells within that tumor, eventually leading to the iatrogenic (treatment-induced) death of the patient.

Last month, a related study published in the journal Stem Cells titled, “Radiation-induced reprogramming of breast cells,” found that ionizing radiation reprogrammed less malignant (more differentiated) breast cancer cells into iBCSCs, helping to explain why conventional treatment actually enriches the tumor population with higher levels of treatment-resistant cells. [i]

A growing body of research now indicts conventional cancer treatment with chemotherapy and radiation as a major contributing cause of cancer patient mortality.  The primary reason for this is the fact that cancer stem cells, which are almost exclusively resistant to conventional treatment, are not being targeted, but to the contrary, are encouraged to thrive when exposed to chemotherapy and radiotherapy.

In order to understand how conventional treatment drives the cancer into greater malignancy, we must first understand what cancer is….

cancer lymphocyte

What Are Cancer Stem Cells, And Why Are They Resistant To Treatment?

Tumors are actually highly organized assemblages of cells, which are surprisingly well-coordinated for cells that are supposed to be the result of strictly random mutation. They are capable of building their own blood supply (angiogenesis), are able to defend themselves by silencing cancer-suppression genes, secreting corrosive enzymes to move freely throughout the body, alter their metabolism to live in low oxygen and acidic environments, and know how to remove their own surface-receptor proteins to escape detection by white blood cells. In a previous article titled “Is Cancer An Ancient Survival Program Unmasked?” we delved deeper into this emerging view of cancer as an evolutionary throw-back and not a byproduct of strictly random mutation.

Because tumors are not simply the result of one or more mutated cells “going rogue” and producing exact clones of itself (multi-mutational and clonal hypotheses), but are a diverse group of cells having radically different phenotypal characteristics, chemotherapy and radiation will affect each cell type differently.

Tumors are composed of a wide range of cells, many of which are entirely benign.

The most deadly cell type within a tumor or blood cancer, known as cancer stem cells (CSCs),has the ability to give rise to all the cell types found within that cancer.

They are capable of dividing by mitosis to form either two stem cells (increasing the size of the stem population), or one daughter cell that goes on to differentiate into a variety of cell types, and one daughter cell that retains stem-cell properties.

This means CSCs are tumorigenic (tumor-forming) and should be the primary target of cancer treatment because they are capable of both initiating and sustaining cancer.  They are also increasingly recognized to be the cause of relapse and metastasis following conventional treatment.

CSCs are exceptionally resistant to conventional treatment for the following reasons

  1. CSCs account for less than 1 in 10,000 cells within a particular cancer, making them difficult to destroy without destroying the vast majority of other cells comprising the tumor.[ii]
    1. CSCs are slow to replicate, making them less likely to be destroyed by chemotherapy and radiation treatments that target cells which are more rapidly dividing.
    1. Conventional chemotherapies target differentiated and differentiating cells, which form the bulk of the tumor, but these are unable to generate new cells like the CSCs which are undifferentiated.

    The existence of CSCs explains why conventional cancer treatment has completely missed the boat when it comes to targeting the root cause of tumors. One reason for this is because existing cancer treatments have mostly been developed in animal models where the goal is to shrink a tumor. Because mice are most often used and their life spans do not exceed two years, tumor relapse is very difficult, if not impossible to study.

    The first round of chemotherapy never kills the entire tumor, but only a percentage. This phenomenon is called the fractional kill. The goal is to use repeated treatment cycles (usually six) to regress the tumor population down to zero, without killing the patient.

    What normally occurs is that the treatment selectively kills the less harmful populations of cells (daughter cells), increasing the ratio of CSCs to benign and/or less malignant cells.  This is not unlike what happens when antibiotics are used to treat certain infections. The drug may wipe out 99.9% of the target bacteria, but .1% have or develop resistance to the agent, enabling the .1% to come back even stronger with time.

    The antibiotic, also, kills the other beneficial bacteria that help the body fight infection naturally, in the same way that chemotherapy kills the patient’s immune system (white blood cells and bone marrow), ultimately supporting the underlying conditions making disease recurrence more likely.

    The reality is that the chemotherapy, even though it has reduced the tumor volume, by increasing the ratio of CSCs to benign daughter cells, has actually made the cancer more malignant.

    Radiotherapy has also been shown to increase cancer stem cells in the prostate, ultimately resulting in cancer recurrence and worsened prognosis.[iii] Cancer stem cells may also explain why castration therapy often fails in prostate cancer treatment.[iv]

    Non-Toxic Natural Substances Which Target and Kill CSCs

    Natural compounds have been shown to exhibit three properties which make them suitable alternatives to conventional chemotherapy and radiotherapy:

    1. High margin of safety: Relative to chemotherapy agents such as 5-fluorouracil natural compounds are two orders of magnitude safer
    2. Selective Cytotoxicity: The ability to target only those cells that are cancerous and not healthy cells
    3. CSCs Targeting: The ability to target the cancer stem cells within a tumor population.

    The primary reason why these substances are not used in conventional treatment is because they are not patentable, nor profitable. Sadly, the criteria for drug selection are not safety, effectiveness, accessibility and affordability. If this were so, natural compounds would form an integral part of the standard of care in modern cancer treatment.

    Research indicates that the following compounds (along with common dietary sources) have the ability to target CSCs:

    1. Curcumin (Turmeric)
    1. Resveratrol (Red Wine; Japanese Knotweed)
    1. Quercetin (Onion)
    1. Sulforaphane (Brocolli sprouts)
    1. Parthenolide (Butterbur)
    1. Andrographalide (Andrographis)
    1. Genistein (Cultured Soy; Coffee)
    1. Piperine (Black Pepper)

    Additional research found on the Multidrug Resistance page indicate over 50 compounds inhibit multidrug resistance cancers in experimental models.

    [i] Radiation-induced reprogramming of breast cancer cells. Stem Cells. 2012 May ;30(5):833-44. PMID: 22489015

    [ii] Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nat Med. 1997 Jul ;3(7):730-7. PMID: 9212098

    [iii] Long-term recovery of irradiated prostate cancer increases cancer stem cells. Prostate. 2012 Apr 18. Epub 2012 Apr 18. PMID: 22513891

    [iv] Stem-Like Cells with Luminal Progenitor Phenotype Survive Castration in Human Prostate Cancer. Stem Cells. 2012 Mar 21. Epub 2012 Mar 21. PMID: 22438320

Serious Diabetes Complications Among Young People Becoming More Frequent

Major complications related to diabetes are becoming more frequent among young people. 

One common misconception surrounding diabetes is that you don’t have to worry about complications until you get older. A recent study conducted at the University of Colorado School of Medicine in Aurora has revealed that currently more young people in America are developing diabetic ketoacidosis (DKA), a potentially life-threatening condition tied to diabetes, at the time of their type 1 diabetes diagnosis compared to 15 years ago.

“Some of the factors associated with DKA at diagnosis are potentially modifiable,” the authors said in a statement. “For example, the association with family history suggests the importance of awareness of diabetic symptoms. However, economic factors are more difficult to modify. Increasing incidence of DKA correlated temporally with an increase in Colorado child poverty prevalence from 10 percent in 2000 to 18 percent in 2012.”

Lead author of the study Dr. Arleta Rewers and her colleagues assessed factors linked to DKA and trends in DKA at type 1 diabetes diagnosis between 1998 and 2012 in Colorado. Data included the medical records of 3,439 young people from the Barbara Davis Center for Diabetes in Denver who had been diagnosed with type 1 diabetes. A total of 1,339 young people — average age of 9.4 years — had also developed DKA at the time of their type 1 diabetes diagnosis.

The total number of young people with DKA at the time of their type 1 diabetes diagnosis increased by 55 percent over the course of the 14-year study. While incidences of DKA only jumped from 30 percent in 1998 to 35 percent in 2007, these rates experienced a noticeable increase to 46 percent in 2012. The research team concluded that delayed access to health care, lower quality of care, and lower income could’ve led to this notable rise in incidences of DKA.

“The recent increase of DKA incidence among youth with private insurance may be related to proliferation of high-deductible health plans,” the authors added. “To our knowledge, this is the only report of increasing incidence of DKA in the developed world. Further research on the reasons for the increase and interventions to decrease the incidence are warranted.”

According to the American Diabetes Association, DKA is characterized by dangerously high blood sugar and the presence of ketones, chemicals produced by the body when it breaks down fat for energy. The body creates ketones when it doesn’t have enough insulin to use glucose. Unfortunately, as ketones begin to buildup they make blood more acidic and poison the body. Although DKA can occur with any type of diabetes, it is considered rare among patients with type 2 diabetes.

Source: Dong F, Slover R, Klingensmith G, Rewers M, Rewers A. Incidence of Diabetic Ketoacidosis at Diagnosis of Type 1 Diabetes in Colorado Youth, 1998-2012. JAMA. 2016

How Changing Food Habits Changes Your Life with Dr. Joan Borysenko .

Join Liz Dawn as she welcomes Dr. Joan Borysenko for a topic that affects everyone in the world: FOOD and How Changing Food Habits, Changes Your Life. When you’ve got the right information, you can make powerful choices to change your life with your food choices. Joan will cut through confusing information and share very specifically which foods your body needs to heal and thrive. listen-herePrepare yourself for a new way of looking and thinking about food!

Dr. Joan Borysenko is a world-renowned expert in the mind/body connection and earned her doctorate in Medical Sciences from the Harvard Medical School, where she completed post-doctoral training in cancer cell biology.  In later years, she returned to Harvard Medical School to complete a second postdoctoral fellowship, this time in the new field of behavioral medicine. She then completed her third post-doctoral fellowship in psychoneuroimmunology.


Dr. Joan is also the New York Times bestselling author of Minding the Body, Mending the Mind. She also just release her latest book:  The PlantPlus Diet Solution.

Liz Dawn is the co-founder/co-creator of Mishka Productions and Celebrate Your Life events that brings to the world powerful life changing events that inspire, heal and transform your life! Visit their site at:  www.CelebrateYourLife.Org

Google Launches U.S. Wireless Service

Google Inc on Wednesday launched a new U.S. wireless service that switches between Wi-Fi and cellular networks to curb data use and keep phone bills low.


The service, Google’s first entry into the wireless industry, will work only on the company’s Nexus 6 phones and be hosted through Sprint Corp and T-Mobile’s networks, Google said in a statement.

The service, called Project Fi, will automatically switch between the two networks and more than 1 million open, free Wi-Fi spots, depending on which signal is strongest.

The service will cost $20 a month plus $10 per gigabyte of data used. Customers will get money back for unused data.

Sundar Pichai, Google’s senior vice president of products, said at a Barcelona conference last month the company was preparing to experiment with a mobile network, but that it did not intend to disrupt the wireless industry.

The service will be available on only one device and has limited carrier coverage, so it will not make Google a major wireless industry player, said Brian Blau, research director at Gartner.

If successful, however, Google’s service could pressure wireless providers to further lower prices and better adapt to the rise of tablets and wearable devices, Blau added. Though some carriers, such as T-Mobile and AT&T Inc, allow unused data to roll over, most mobile plans require customers to pay for a set amount of data each month.

But Google first has to “test out features they think are going to differentiate themselves,” Blau said, such as being able to transition from network connectivity to Wi-Fi.

If Google is able to provide those features, “it’s very possible they could become a major wireless player in the future,” Blau said.

Phone numbers will live in the cloud so that consumers can talk and text on any connected tablet, Google said.

The company already has a strong presence in the mobile market through its Android operating system, which hosts some of the most popular apps, such as Gmail and Google Maps.

Google shares rose 1.27 percent to $549.81 at mid-afternoon.

This revolutionary discovery could help scientists see black holes for the first time .

supermassive black hole

Artist’s concept of the black hole.

Of all the bizarre quirks of nature, supermassive black holes are some of the most mysterious because they’re completely invisible.

But that could soon change.

Black holes are deep wells in the fabric of space-time that eternally trap anything that dares too close, and supermassive black holes have the deepest wells of all. These hollows are generated by extremely dense objects thousands to billions of times more massive than our sun.

Not even light can escape black holes, which means they’re invisible to any of the instruments astrophysicists currently use. Although they don’t emit light, black holes will, under the right conditions, emit large amounts of gravitational waves — ripples in spacetime that propagate through the universe like ripples across a pond’s surface.

And although no one has ever detected a gravitational wave, there are a handful of instruments around the world waiting to catch one.

Game-changing gravitational waves

black hole(NASA Marshall Spaceflight Center)This illustration shows two spiral galaxies – each with supermassive black holes at their center – as they are about to collide.Albert Einstein first predicted the existence of gravitational waves in 1916. According to his theory of general relativity, black holes will emit these waves when they accelerate to high speeds, which happens when two black holes encounter one another in the universe.

As two galaxies collide, for example, the supermassive black holes at their centers will also collide. But first, they enter into a deadly cosmic dance where the smaller black hole spirals into the larger black hole, moving increasingly faster as it inches toward it’s inevitable doom. As it accelerates, it emits gravitational waves.

Astrophysicists are out to observe these waves generated by two merging black holes with instruments like the Laser Interferometer Gravitational-Wave Observatory.

“The detection of gravitational waves would be a game changer for astronomers in the field,” Clifford Will, a distinguished profess of physics at the University of Florida who studied under famed astrophysicist Kip Thorne told Business Insider. “We would be able to test aspects of general relativity that have not been tested.”

Because these waves have never been detected, astrophysicists are still trying to figure out how to find them. To do this, they build computer simulations to predict what kinds of gravitational waves a black hole merger will produce.

Learn by listening

In the simulation below, made by Steve Drasco at California Polytechnic State University (also known as Cal Poly), a black hole gets consumed by a supermassive black hole about 30,000 times as heavy.

The black lines you’re seeing are the orbits of the tiny black hole traced out as it falls into the supermassive black hole. What you’re hearing are gravitational waves.

“The motion makes gravitational waves, and you are hearing the waves,” Drasco wrote in a blog post describing his work.

Of course, there is no real sound in space, so if you somehow managed to encounter this rare cataclysmic event, you would not likely hear anything. However, what Drasco has done will help astrophysicists track down these illusive waves.

Just a little fine tuning

Gravitational waves are similar to radio waves in that both have specific frequencies. On the radio, for example, the number corresponding to the station you’re listening to represents the frequency at which that station transmits.

gwaves(Henze, NASA)3D visualization of gravitational waves produced by 2 orbiting black holes. Right now, astrophysicists only have an idea of what frequencies two merging black holes transmit because they’re rare and hard to find. In fact, the first ever detection of an event of this kind was only announced this month.

Therefore, astrophysicists are basically toying with their instruments like you sometimes toy with your radio to find the right station, except they don’t know what station will give them the signal they’re looking for.

What Drasco has done in his simulation is estimate the frequency at which an event like this would produce and then see how that frequency changes, so astrophysicists have a better idea of how to fine tune their instruments to search for these waves.

Detecting gravitational waves would revolutionize the field of astronomy because it would give observers an entirely new way to see the universe. Armed with this new tool, they will be able to test general relativity in ways never before made possible.

Watch the video. URL:

After 20 grueling hours, Maickel Melamed finished the Boston Marathon

Maickel Melamed, a college professor from Venezuela, crossed the finish line for the Boston Marathon at 4:00 this morning, a grueling 20 hours after the starting gun went off yesterday morning.

The 39-year-old suffers from muscular dystrophy, which attacks his muscles and nervous system, yet he’s a seasoned marathon runner who has completed in races around the world. He’s traveled to New York, Berlin, Chicago, and Tokyo to compete in the 26.2-mile leg-taming event.

As he drew closer to the finish line, the crowd around him grew despite the late hour. They were eager to see him through to the end, which they did:

Speaking to ABC News after a similar finish in the Chicago Marathon in 2013, Melamed explained the motivation behind his participation: “If you know you can do it, you have to do it.” Melamed wants to “spread a message of human dignity” by competing in and finishing these unlikely events, though he expects this morning’s finish to be his last before hanging up the racing shoes.

The rhetoric of the Boston Marathon is forever altered after the 2013 bombings that claimed lives and limbs of some runners. This year, bombing victim Rebekah Gregory successfully finished the race after losing her leg in the attack two years ago.

Actor and director Sean Astin had a similarly emotional experience finishing his long-distance run through Beantown. He dedicated his marathon to the youngest victim of the 2013 bombing, 8-year-old Martin Richard.

An unexpected microbe is killing organ transplant patients .

A 44-year-old man appeared to be recovering nicely after a double lung transplant at Northwestern Memorial Hospital in Chicago, Illinois. A week after the surgery, however, the patient, whose own lungs had been ruined by the inflammatory disease pulmonary sarcoidosis, grew confused and then became delirious. Although a brain scan found nothing wrong, tests showed that the amount of ammonia in his blood had spiked—and continued to rise even after dialysis to remove the toxin. Forty days after his surgery, he died.

Now, a new study implicates bacteria that normally live in the urinary tract as the cause of the man’s fatal illness and the deaths of other lung transplant patients. The work suggests a way to treat a rare but deadly complication of organ transplantation and cancer treatment.

Although our bodies normally produce small amounts of ammonia when we break down proteins, liver enzymes transform it into a safer compound, urea, which is excreted in our urine. In some organ transplant recipients and cancer patients, however, the amount of ammonia in the blood explodes. Although this condition, known as hyperammonemia, is unusual, “when it has occurred, it’s been disastrous,” says pulmonologist Mark Wylam of the Mayo Clinic in Rochester, Minnesota. The brain swells, and patients fall into a coma. “The end of the ordeal is that they die,” he says.

Not only is hyperammonemia resistant to treatment and usually fatal, but the cause has also been elusive. In 2013, Wylam and colleagues discovered the likely culprit in one case, a 64-year-old woman who died from hyperammonemia after a double lung transplant. They found that her blood and tissues were positive for a type of bacterium, Mycoplasma hominis, that often causes mild genital infections in women.

But the man who died at Northwestern Memorial Hospital showed no signs of M. hominis, thoracic surgeon Ankit Bharat of the Northwestern University Feinberg School of Medicine in Chicago and colleagues found. Instead, they detected a different bacterium, Ureaplasma urealyticum, in the man’s blood and in samples from his bladder, spleen, liver, and lungs.The team then tested tissue from three other lung transplant patients who had died from hyperammonemia, including the patient studied by Wylam and colleagues. All three showed evidence of infection with U. urealyticum or a kindred microbe, U. parvum. In contrast, 20 lung transplant recipients who didn’t develop hyperammonemia were negative for all three microbes, the researchers report online today in Science Translational Medicine.

The researchers also checked for the bacteria in two lung transplant recipients who had hyperammonemia but were still alive. Both patients carried U. urealyticum or U. parvumbacteria, and both recovered after antibiotic treatment.

Wylam, who wasn’t connected to the new study, says the results are convincing. “They have shown that U. urealyticum can also cause these unexplained cases of hyperammonemia.” The authors of the paper recommend testing lung transplant recipients who have hyperammonemia for Ureaplasma infection. The study also provides guidance about treating the condition. Although the man Bharat and colleagues studied had received the antibiotic azithromycin, the bacteria may have become resistant to it. The microbes are vulnerable to three families of antibiotics, so a combination of drugs would be a better choice to avoid resistance, Bharat says.

About two-thirds of us have Ureaplasma bacteria living in our urinary tract, where they feast on urea, breaking it down to produce energy and releasing ammonia as a byproduct. Why the bacteria occasionally trigger widespread infections and death isn’t clear. Cancer patients and transplant recipients have suppressed immune systems, and the microbes might take advantage of their weakened defenses. However, another possibility emerged when Bharat and colleagues found that the lungs of one donor already contained the bacteria before the organs were transplanted into the recipient. So donor organs could deliver the microbes to patients who develop hyperammonemia.

Ureaplasma microbes are hard to diagnose because they don’t like to grow in the cultures that hospitals often use to identify the culprits in bacterial infections. Unrecognized infections could be responsible for additional cases of hyperammonemia and even other illnesses, Bharat says. For example, he notes, the microbes could be causing disease in malnourished patients. “These organisms could be a bigger problem,” he says.

%d bloggers like this: