Nate Henry (right), Nick’s identical twin, is healthy. Nick’s high levels of a molecule called suPAR may explain his illness. The data gets stronger and stronger that suPAR is the worst toxin you can have for the kidneys. Nick Henry first experienced the symptoms of kidney disease in 2004, shortly after the 19-year-old had a severe reaction to a spider bite. “I woke up one morning, and I was just swollen from head to toe,” he recalls. But doctors managed Henry’s disease, allowing him to return to his unusually active lifestyle—including baseball, softball, basketball, flag football, golf, and fishing—in his northeast Louisiana hometown of West Monroe. Shortly after he witnessed the death of his mother in a motor scooter accident in 2012, however, Henry’s renal health took a dramatic turn for the worse. “It’s almost as if my body went into shock,” he says. “Within a couple months, boom, I started swelling up again.”That swelling was a sign that his kidneys were no longer working normally. A biopsy confirmed that he had focal segmental glomerulosclerosis (FSGS), a severe form of kidney disease. In FSGS, the kidney’s glomeruli—the microscopic filtration units that sieve excess fluid and waste products from the blood—become overly leaky; essential proteins such as albumin seep out, disrupting blood chemistry and causing fluid to leak from the blood vessels into tissues throughout the body. Henry’s condition deteriorated so rapidly that by July 2014, his doctors in Shreveport, Louisiana, decided to remove both diseased kidneys. The next month, Henry received a transplanted kidney from his identical twin, Nate, who was healthy, even though FSGS can be genetic in origin.Within a day of the transplant, however, Henry felt like the swelling was coming back. At first, his doctors reassured him that he was doing fine. “Once they checked my urine, saw me spilling a bunch of protein again,” he says, “they realized [FSGS] was attacking the new kidney.” Three days after the surgery, Henry’s doctors conceded that the newly transplanted kidney had already become diseased. His transplant doctor, Neeraj Singh of Louisiana State University in Shreveport, says the recurrence was “one of the most dramatic cases I’ve seen.”Sign up for our daily newsletterGet more great content like this delivered right to you!Country *AfghanistanAland IslandsAlbaniaAlgeriaAndorraAngolaAnguillaAntarcticaAntigua and BarbudaArgentinaArmeniaArubaAustraliaAustriaAzerbaijanBahamasBahrainBangladeshBarbadosBelarusBelgiumBelizeBeninBermudaBhutanBolivia, Plurinational State ofBonaire, Sint Eustatius and SabaBosnia and HerzegovinaBotswanaBouvet IslandBrazilBritish Indian Ocean TerritoryBrunei DarussalamBulgariaBurkina FasoBurundiCambodiaCameroonCanadaCape VerdeCayman IslandsCentral African RepublicChadChileChinaChristmas IslandCocos (Keeling) IslandsColombiaComorosCongoCongo, The Democratic Republic of theCook IslandsCosta RicaCote D’IvoireCroatiaCubaCuraçaoCyprusCzech RepublicDenmarkDjiboutiDominicaDominican RepublicEcuadorEgyptEl SalvadorEquatorial GuineaEritreaEstoniaEthiopiaFalkland Islands (Malvinas)Faroe IslandsFijiFinlandFranceFrench GuianaFrench PolynesiaFrench Southern TerritoriesGabonGambiaGeorgiaGermanyGhanaGibraltarGreeceGreenlandGrenadaGuadeloupeGuatemalaGuernseyGuineaGuinea-BissauGuyanaHaitiHeard Island and Mcdonald IslandsHoly See (Vatican City State)HondurasHong KongHungaryIcelandIndiaIndonesiaIran, Islamic Republic ofIraqIrelandIsle of ManIsraelItalyJamaicaJapanJerseyJordanKazakhstanKenyaKiribatiKorea, Democratic People’s Republic ofKorea, Republic ofKuwaitKyrgyzstanLao People’s Democratic RepublicLatviaLebanonLesothoLiberiaLibyan Arab JamahiriyaLiechtensteinLithuaniaLuxembourgMacaoMacedonia, The Former Yugoslav Republic ofMadagascarMalawiMalaysiaMaldivesMaliMaltaMartiniqueMauritaniaMauritiusMayotteMexicoMoldova, Republic ofMonacoMongoliaMontenegroMontserratMoroccoMozambiqueMyanmarNamibiaNauruNepalNetherlandsNew CaledoniaNew ZealandNicaraguaNigerNigeriaNiueNorfolk IslandNorwayOmanPakistanPalestinianPanamaPapua New GuineaParaguayPeruPhilippinesPitcairnPolandPortugalQatarReunionRomaniaRussian FederationRWANDASaint Barthélemy Saint Helena, Ascension and Tristan da CunhaSaint Kitts and NevisSaint LuciaSaint Martin (French part)Saint Pierre and MiquelonSaint Vincent and the GrenadinesSamoaSan MarinoSao Tome and PrincipeSaudi ArabiaSenegalSerbiaSeychellesSierra LeoneSingaporeSint Maarten (Dutch part)SlovakiaSloveniaSolomon IslandsSomaliaSouth AfricaSouth Georgia and the South Sandwich IslandsSouth SudanSpainSri LankaSudanSurinameSvalbard and Jan MayenSwazilandSwedenSwitzerlandSyrian Arab RepublicTaiwanTajikistanTanzania, United Republic ofThailandTimor-LesteTogoTokelauTongaTrinidad and TobagoTunisiaTurkeyTurkmenistanTurks and Caicos IslandsTuvaluUgandaUkraineUnited Arab EmiratesUnited KingdomUnited StatesUruguayUzbekistanVanuatuVenezuela, Bolivarian Republic ofVietnamVirgin Islands, BritishWallis and FutunaWestern SaharaYemenZambiaZimbabweI also wish to receive emails from AAAS/Science and Science advertisers, including information on products, services and special offers which may include but are not limited to news, careers information & upcoming events.Required fields are included by an asterisk(*)The sudden failure of Henry’s new kidney is a recent chapter in a long-running medical mystery, dating to when kidney transplants became routine in the 1970s. Up to 30% of transplanted kidneys fail in FSGS patients—not because of immune rejection by the body, as doctors first suspected, but because the new organ immediately begins succumbing to the same disease process that ravaged the original ones. As he struggled to cope with that devastating turn of events (and relied on dialysis to stay alive), Henry traveled to Chicago, Illinois, to consult with Jochen Reiser, a kidney disease specialist who is chairperson of internal medicine at Rush University Medical Center there.Ever since he learned about such transplant failures 2 decades earlier, Reiser has been convinced that “there is something in the blood circulating that attacks the kidney. And we were out to catch that.” What he and colleagues claim to have “caught,” in an elegant but still unfolding story of molecular detective work over the past 10 years, is a protein known as soluble urokinase plasminogen activator receptor (suPAR). When Reiser analyzed blood samples from the Henry twins, the results aligned with the message he has been preaching with evangelical fervor for years. Nate, the healthy brother, had relatively low levels of suPAR; Nick’s were high—a driving force, Reiser believes, of his kidney failure. KidneyGlomerulusFunctional unit of kidneyPodocyteGlomerular basement membraneEndothelial cellsuPARsuPAR Slit diaphragmCapillary Chronic kidney disease affects 14% of the U.S. population, with estimates suggesting nearly 600 million people affected worldwide. The disease steadily erodes the kidneys’ ability to filter the blood, often leading to cardiovascular disease and premature death. Kidney disease—which can directly attack the filtration process, as in FSGS, or damage the kidney’s support structure—is particularly insidious because by the time the first diagnostic signs appear, patients have irreversibly “burned off” much of their kidney function. Historically, the leading risk factors have been high blood pressure, diabetes, and African-American ancestry. (Several mutations associated with increased risk are more common in African-Americans.)But research by Reiser and others has dramatically challenged that traditional picture of risk. If suPAR levels are low, people with the high-risk genes are no more likely to develop kidney disease than people without those gene variants, Reiser says. If suPAR levels are high, people are at greater risk of developing the disease regardless of whether they have the mutations.Molecular studies in animals as well as a growing number of analyses of large human populations associating suPAR with kidney disease have bolstered his confidence—and convinced him the disease could be treated by suppressing suPAR. Some other researchers aren’t convinced, noting that several clinical studies found no clear association between suPAR levels and FSGS. But on both sides of the debate there is widespread fascination with suPAR, a ubiquitous, Zelig-like bystander molecule that, at elevated levels in the blood, seems to presage many health calamities, such as heart attacks, diabetes, and premature death. Whatever suPAR’s precise role in kidney disease, the molecule appears to be a potent signal broadcast by an immune system under siege. It is exquisitely sensitive to inflammation, an accelerant for many diseases.”What is inflammation?” asks biochemist Jesper Eugen-Olsen of the University of Copenhagen, a pioneer in suPAR research. “It’s the language of cells. It’s how cells communicate with each other. When something is going wrong, the immune system is activated. It produces suPAR … and suPAR is a voice that just shouts, ‘Get on with it! Something is going on!’”A brash styleIn neither background nor appearance does Reiser conform with the public image of the director of a major metropolitan medical center. His 10th floor office at Rush sits just behind a corridor lined with photographs of hospital administrators going back to the 19th century—stern-faced, all-knowing medical patriarchs. Inside, Reiser, 46, sports a stylish striped blue suit, fashionably stubby beard, red socks, and slick dark hair. Known among colleagues as ambitious and scientifically gregarious, he has been eager to collaborate with anyone interested in exploring suPAR biology, and his brash, full-on style extends to the conspicuous display of large-format books celebrating the history of Aston Martins (he owns one) and Porsches on the coffee table in his office. Describing the speed of data collection for a paper that several years ago ended up in The New England Journal of Medicine (NEJM), he says, “It was like going from zero to 200 in no time,” adding sheepishly, “Car analogy.”Born and raised in the small German village of Remchingen, on the eastern edge of the Black Forest, Reiser got his medical degree and Ph.D. from Heidelberg University and did an overseas residency at Albert Einstein College of Medicine in New York City. Specializing in kidney disease, he went on to conduct research at Harvard Medical School in Boston and became chief of nephrology at the University of Miami Leonard M. Miller School of Medicine in Florida before being hired by Rush in 2012.Reiser’s arrival in the United States in 1999 coincided with renewed interest in solving the mystery of why up to 30% of FSGS patients who receive transplants see the disease recur in the new kidney. Just 3 years earlier, a group headed by Flavio Vincenti, a transplant specialist at the University of California, San Francisco (UCSF), and Virginia Savin, at the Medical College of Wisconsin in Milwaukee, announced a major clue. They reported in NEJM that they had amassed evidence for an FSGS-promoting factor in the blood of transplant recipients who’d experienced recurrences; they couldn’t isolate the exact protein, but when colleagues later injected an extract of such patients’ blood into rodents, the animals’ kidneys became permeable and spilled protein in the urine. That mysterious “permeability factor” became “the holy grail” of the field, according to Sanja Sever, a molecular biologist who studies kidney disease at Massachusetts General Hospital in Boston.While still in Germany, Reiser had trained his research efforts on a unique renal cell called the podocyte (so named because of its amoebic, faintly footlike extensions). That choice turned out to be fortunate. The kidney has about 1 million glomeruli, and in each one, hundreds of podocytes bridge the gap between the bloodstream and the urinary system. Their footlike extensions wrap around capillaries snaking through the kidneys and, along with two other layers of tissue, form a physical mesh of cells, like a three-ply screen door, that allows only small molecules—sodium ions, potassium ions, and metabolic wastes—to pass into the urinary tract. When the podocytes become damaged, however, they essentially lose their architectural integrity. The kidney filters then become leaky, allowing larger essential proteins such as albumin to escape from the blood and pass into the urine.It’s like a coffee filter, Sever says. “If there are holes in your filter, then you get some coffee grounds in your urine.” Podocyte damage can be reversed early in kidney disease. But, she says, “If you keep losing them, there’s a point of no return. … You are basically walking toward end-stage renal disease.” Kevin Beasley Albumin leakage A dangerous immune responseAnimal models suggest immature immune cells in the bone marrow release more suPAR when an organism is under attack. The molecule, an all-purpose marker of ill health, may be directly toxic to the kidney.A HEALTHY FILTERIn each glomerulus, the footlike extensions of cells called podocytes wrap around capillaries, fitting together tightly to create narrow “slit diaphragms.” The slits form a fine mesh that allows only small molecules to escape from the bloodstream into the urine.KIDNEY DISEASE What causes such damage? Reiser suspected that the mysterious blood-borne factor disrupts podocytes through receptor molecules on their cell surface. He focused on one: β3-integrin, a molecule whose activation perturbs the shape and motility of cells. When he looked for the molecular key that turned the lock of the integrin receptor, he discovered that oncologists had already been working on one such protein, urokinase PAR (uPAR), a cell surface receptor that plays a role in cancer metastasis. Reiser became even more intrigued when he learned that uPAR can be cleaved from cell surfaces and circulate in the blood—at which point it becomes a soluble cousin known as suPAR. Maybe suPAR was the mysterious kidney-destroying factor.In 2011, Reiser and colleagues reported in Nature Medicine that in cell culture, suPAR damaged human podocytes through the integrin pathway. The researchers supplemented that evidence with three mouse models showing that rodents with elevated levels of suPAR suffered kidney damage, although sometimes more slowly than in FSGS. With human clinical data suggesting that elevated suPAR levels correlated with the recurrence of FSGS in patients, a picture emerged in which the protein triggers a pathogenic process that ultimately produces holes in the coffee filter, leading to kidney disease.The findings both electrified and polarized the nephrology community. In a commentary for Nature Medicine, Martin Pollak of Harvard Medical School, who studies the genetics of kidney disease, and nephrologist Stuart Shankland of the University of Washington in Seattle described the findings as “paradigm shifting for our understanding of the pathogenesis of FSGS.”But some groups could not find the same clinical association between suPAR levels and recurrent disease in FSGS patients, and other groups questioned the protocol and interpretation of the animal models. And regardless of whether suPAR actually destroys the kidney, many nephrologists thought its levels were not very informative—by the time those specialists saw patients with kidney disease, suPAR levels were already high and offered no prognostic value. With Reiser claiming to have found the “holy grail” even as several groups were reporting discordant results, says one source, “People felt very emotional.”An omen of ill-healthBy that point, another key strand of the suPAR story had emerged in Europe. There, the focus was on the molecule as a potential biomarker for a range of diseases.The first clues came from AIDS patients. In Copenhagen, Eugen-Olsen and others examined blood collected from more than 300 HIV patients in the early 1990s, before life-saving antiretroviral therapies became available. All those patients had died, but a retrospective analysis showed their suPAR levels eerily correlated with disease progression: Higher levels were associated with an earlier death. Eugen-Olsen then spent several years collaborating with a hospital in the West African nation of Guinea-Bissau, testing suPAR levels in patients suspected of being HIV-infected. Again, higher suPAR levels predicted a quicker death among the infected. Surprisingly, however, suPAR also predicted mortality in patients who didn’t have AIDS; many turned out to have tuberculosis. That finding led him to hypothesize that suPAR might be a more general biomarker for chronic inflammation.In 2001, Eugen-Olsen founded the company ViroGates, which began to manufacture a relatively inexpensive test to measure suPAR levels in the blood. With the test in hand, he and colleagues in Copenhagen began to look at collections of blood samples banked in large-cohort prospective studies. In one called MONICA, which monitored healthy members of the Danish population for about 13 years, elevated levels of suPAR were associated with a higher risk of cardiovascular disease, type 2 diabetes, cancer, and premature death. Two other large European populations, enrolled in the Malmo Diet and Cancer Study and the Danish Inter99 Study, showed similar associations.The findings caught the attention of researchers at Emory University School of Medicine in Atlanta who had been looking for new and better biomarkers to predict risk of adverse cardiac events in people with heart disease. The researchers had built the Emory Cardiovascular Biobank with serum from several thousand patients. “We draw blood, and we follow them for years,” says Salim Hayek, a physician and research fellow at Emory. When two of Hayek’s colleagues, Danny Eapen and Arshed Quyyumi, delved into the biobank, they found that higher suPAR levels predicted heart attacks and death, as they reported in the Journal of the American Heart Association in 2014. (At the annual meeting of the American College of Cardiology last month, Hayek presented further evidence from the Emory group, suggesting that suPAR is a better predictor of cardiac events including heart attacks and death than any other biomarker in widespread clinical use.) Nick Henry had a kidney transplant, but his new organ quickly deteriorated, and he spends his nights on dialysis. An organ under attack In one scenario for a severe form of kidney disease, a blood-borne molecule called soluble urokinase plasminogen activator receptor (suPAR) disrupts the organ’s filtration units, or glomeruli, which remove waste and fluid from the bloodstream. Other molecules may intensify this attack. Jochen Reiser has spent years amassing evidence that suPAR mounts a powerful assault on the kidney. Kevin Beasley In addition to serving as an omen of ill health, suPAR seems to be a remarkably sensitive indicator of lifestyle insults. Studies have shown that the protein’s blood levels typically rise with obesity and with smoking. (Eugen-Olsen, an inveterate smoker, confesses that he quits when his suPAR levels rise and resumes when they subside again.) “Just looking at the data,” Hayek says, “clearly the environment is a much larger contributor to suPAR than genetics.”With its links to multiple diseases and environmental stresses, suPAR appears to sit at the nexus of immune signaling, chronic inflammation, and tissue damage. Among the protein’s normal sources are fat cells, immune cells, and endothelial cells, which produce low baseline levels. But a team led by Reiser and David Scadden of the Harvard Stem Cell Institute showed in 2017 that in mice, immature “stemlike” cells in the bone marrow can release a pulse of suPAR when the immune system detects an attack.Reiser believes suPAR is an ancient and unspecific way for the immune system to send urgent signals to the major organ systems when an organism faces a severe challenge from disease or the environment. Kidney damage, he says, is the long-term cost of that vital signaling mechanism. “As one example,” he says, “you get infected, you release more suPAR, you open your kidneys up, and you can dump the big molecules out into the urine. Almost like a primitive coupling of the immune system to vital organs.” In an acute infection, he says, the body urgently needs to flush out bacterial toxins, relatively big molecules. But if that inflammatory signaling becomes chronic, it takes its toll on kidney function—a trade-off that may have been acceptable earlier in human history, Reiser suggests, but is less so now. “If you live 40 years long, you can burn off the kidney this way, no problem,” he says. “If you live to be 80, 90, 100, you might burn off your kidneys too soon.”For Reiser, the Emory cardiac biobank offered a chance to put to rest the notion that high levels of suPAR are simply a nonspecific sign of failing kidneys, not a cause. When he saw the 2014 heart risk paper from the Emory group, he had the obvious question: Could the large databank show whether suPAR levels predicted the onset of kidney disease years later? He immediately fired off an email to Hayek.The Emory-based group quickly agreed to conduct follow-up renal examinations in more than 1300 patients who had no evidence of kidney dysfunction when they enrolled. The team found a strong link between high suPAR levels and the later development of kidney disease. For patients with the highest levels of suPAR, the risk was three times that of patients in the lowest group, and suPAR levels could predict kidney disease up to 5 years before the first symptoms appeared. “The effect was huge,” Hayek recalls.The association was so robust, he says, that when the group first submitted its findings for publication, “the first response we got from [NEJM] was: ‘How is that association so strong? Is that real? Something is wrong with your cohort.’” But after Hayek and Reiser found the same association in a second, unrelated cohort—the Women’s Interagency HIV Study—NEJM published their findings in 2015. “In that paper,” Reiser says, “we could show that suPAR is the strongest risk factor known in healthy people for new chronic kidney disease. Even stronger than hypertension, diabetes, black race—all of these risk factors that are known to be strong. When you adjust for those, suPAR had the strongest risk.”In the latest piece of evidence, published last summer in Nature Medicine, Reiser collaborated with researchers at the African American Study of Kidney Disease and Hypertension, based at Johns Hopkins University School of Medicine in Baltimore, Maryland, to compare the influence of suPAR and two gene mutations known to predispose African-Americans to kidney disease. A study of about 600 participants revealed that if suPAR levels remain low, “no notable differences” in kidney dysfunction were apparent between people who had the high-risk “disease genes” and people who did not. Conversely, high levels of suPAR strongly predicted kidney disease in African-Americans, regardless of whether the individual had the genetic variants.The proof is the cureYet nephrologists are still divided about whether suPAR actually attacks the kidneys—and if so, how aggressively. Doubters point to the conflicting clinical results and the slow progress of kidney damage in Reiser’s mice with elevated suPAR levels. The original 2011 animal and clinical data are “as complete as you can get,” Vincenti says. “But at some point, there has to be independent duplication of that data.”Several unresolved issues might explain the discrepancies. Different forms of suPAR can circulate in the blood, and some variants might be more pathogenic than whole suPAR. And a team led by Minnie Sarwal of UCSF, Dany Anglicheau of Necker Hospital in Paris, and Reiser has shown that in FSGS, a second blood-borne factor, an anti-CD40 autoantibody, works with suPAR to attack podocytes. “Everyone agrees it’s more complicated” than the initial findings in 2011 suggested, Reiser concedes. “But meanwhile, the data gets stronger and stronger that suPAR is the worst toxin you can have for the kidneys.” Bone marrow Jochen Reiser, Rush University Medical Center By Stephen S. HallApr. 19, 2018 , 12:15 PM Rush Production Group V. Altounian/Science What’s your risk of kidney disease, heart attack, or diabetes? A single molecule can tell MonocyteImmature myeloid cellNeutrophilPodocyte lost to urinary space The controversy may not be resolved to everyone’s satisfaction until a human trial indisputably shows that removing suPAR cures or slows the progression of kidney disease. Several groups are trying to develop a monoclonal antibody drug that would remove suPAR from the blood. One such group is Trisaq, a company Reiser and Sever founded in 2011. Vincenti said his group also has developed monoclonal antibodies to suPAR for clinical testing. “I was excited to try it in patients,” he says. “But we could not demonstrate, at least in our samples, that suPAR was a biomarker for either FSGS or recurrent FSGS. [That’s] held it back.”The first human proof may come not from a drug, but from a medical device. Miltenyi Biotec, a company in Bergisch Gladbach, Germany, makes apheresis devices, which remove substances from plasma, and it is developing a technology that would selectively scrub suPAR out of patients’ blood. “The key question,” notes CEO Stefan Miltenyi, “is if suPAR is the cause [of] renal diseases or just a bystander molecule.” Miltenyi hopes to launch a clinical trial in 2019.For FSGS patients such as Henry, who relies on 8-hour overnight sessions of dialysis to stay alive, a breakthrough therapy can’t come soon enough. But suPAR is already beginning to influence clinical decisions. Singh, Henry’s transplant physician, has used suPAR levels to manage the care of several kidney patients. And since 2013, every patient arriving at the emergency department at Copenhagen University Hospital Hvidovre has undergone suPAR testing to help physicians make triage and discharge decisions.Reiser often likens suPAR to cholesterol—a key marker and disease-associated molecule that can be monitored and, perhaps, ultimately controlled. But the main lesson of suPAR, he believes, is cautionary in an age of genomics and personalized medicine. Although a huge amount of attention (and government coin) has been devoted to identifying genes associated with disease, the environment can sometimes trump them. “I think that the gene adds to the risk profile—it’s part of the picture,” he concedes. “But the environment is a way-underestimated modifier that becomes way more important, quite frankly, than the underlying gene event. And this is … a beautiful illustration of exactly that principle.”
The No. 4-ranked Ohio State men’s tennis team opened up the spring schedule on a high note. OSU (2-0) defeated Butler and Xavier, 7-0 and 6-1, respectively, in matches in Columbus Wednesday night. The Buckeyes won all of their doubles matches and lost just one singles match against the Bulldogs and Musketeers. OSU redshirt junior Peter Kobelt, the No. 1-ranked singles player in the country, won both of his matches to improve to 16-3 on the season. The Buckeyes, which are coming off a 2012 campaign that saw them finish No. 4 in the final Intercollegiate Tennis Association top 25. OSU hopes to continue such success under coach Ty Tucker, who has guided the Buckeyes to seven consecutive Big Ten regular-season titles since 2006. This spring, under an experienced coaching staff and several key returners, the team is focusing on consistency and leadership. “The team goals are always the same, to overachieve and that seniors have their best years … we get a lot of mileage out of guys who have been three or four years into the program,” Tucker said. “If seniors are having their best years, it says a lot about the coaching staff because we were able to keep them motivated.” This spring, the Buckeyes face a daunting schedule that includes eight opponents currently ranked in the top 20 of the latest ITA poll (No. 6 Georgia, No. 24 LSU, No. 18 North Carolina, No. 7 Pepperdine, No. 22 Indiana, No. 9 Kentucky, No. 16 Illinois and No. 20 Michigan). Amid the challenges that loom ahead, some members of the team said they’re confident in their offseason preparation and high level of returning talent. “These guys play year-round, so the preparation is constant, and I think that’s unique to what we’re doing … that these guys are committed tennis players year-round,” said volunteer assistant coach David Schilling. “Because of that, when the season does come, these guys are really anxious to play, and it’s kind of like a reward for all their hard work.” Key returning contributors for the 2013 season are senior Connor Smith and redshirt freshman Chris Diaz, both of whom are ranked in the top 30 in singles nationally. Then there’s Kobelt, who is poised as the national favorite in the singles game. The redshirt junior has also quickly assumed a leadership role among his teammates. “(I want to) keep getting better every day. I’m not really worried about my results, I’ve had a pretty good season so far in the fall,” Kobelt said. “For me, it’s really about setting a good example for the guys and leading the best I can … that will give us the best opportunity to do well.” The Buckeyes also boast the longest active home win streak in Division I collegiate tennis, having won 148 consecutive matches played in Columbus, and rattling off a 19-0 home record in 2012. Being a constant threat at home is something Kobelt said he hopes continues. “It’s more mental for the teams that come and play us, because they all know the record, but it’s something that we try not to think about … but it’s a pretty cool record, and we’ll do everything we can to keep it intact,” he said. A home record such as the Buckeyes’ will contribute to the already promising stage set for the 2013 season. The balance of strong preparation, talent and leadership is causing coaches to deliver high praise to the 2013 squad. “This is probably the deepest team (Ty and I) have had. We’re 10, 11 guys deep on this team, and it’s a good blend of experience and some new, young talent,” Schilling said. “We’ve got a lot of guys who can play in some big matches for us.”
As Guyana joins the rest of the world in observing Child Protection Week under the theme “Children’s Safety and Security, Our Priority”, the haunting incidents of rape and sexual assault against women and girls continue to trouble this nation. The sad reality of this recently unfolded when a 21-year-old mother of one died following a sexual attack by a minibus driver. So severe were her injuries that a child is now left motherless. In 2015, there were over 230 reports of rape, but only 36 persons were charged. Compounding this actuality is also the fact that there is a stark court backlog on tackling cases of sexual violence.A recent United States Department report on human rights outlined that in Guyana, a high number of rape and sexual assaults are unreported to authorities, citing that this was most likely as a result of fear of stigma, a lack of confidence in authorities, retribution, or further violence.As with any form of violence, sexual violence tears at the fabric of a country’s well-being. However, when the agency responsible for helping victims of rape describes this horrendous crime as mere “deflowering”, the sad unravelled truth of our country’s approach to this crime is evident. “Deflowering” means to deprive (a woman) of her virginity, but is that what rape is? Mere deflowering? The Social Protection Ministry, in its statement on Guyana’s observances for Child Protection Week, stated that “incest and underage sexual activity in childhood (are) also of grave concern to the Childcare & Protection Agency (CPA), an arm of the Ministry. This deflowering of our children must stop.”It is frighteningly obvious that the Social Protection Ministry needs a trained psychologist to educate its staff about the true meaning of rape, particularly child rape, which is not simply “deflowering” even if the victim was virginal. Rape is more than “deflowering”; rape is sexual abuse, a lifelong scar. The Ministry needs to also be enlightened that rape and other forms of sexual assault have traumatic psychological, emotional, physical, social, interpersonal, and financial impact on victims. According to a study conducted by Rape Victims Advocates (RVA), each survivor reacts to sexual assault in their own unique way. Personal style, culture, and context of the survivor’s life may affect these reactions. Some victims may tell others right away what happened, others will wait weeks, months, or even years before discussing the assault, if they ever choose to do so.Earlier this year, Social Protection Minister Volda Lawrence came in for much criticism after she made some unfortunate remarks and had a casual approach in defence of a man, who was charged for sexual molestation. The Minister, in defence of the man, was quoted by another section of the media as saying, “This is a family issue that has been going on and on and on and on for whatever reason, I can’t tell you, because if I had a brother, even if there was an accusation, this is not how I would go about helping him.”What was rather disappointing is that the alleged molester’s sister further alleged that she told the Minister that her brother needed to be jailed for his involvement, but Lawrence asked her not to pursue such actions.Less than six months later, there is a statement issued by the Ministry the same Minister heads defining rape of children as simply “deflowering”.The Social Protection Ministry is where victims of such a dreadful crime seek refuge not only for their physical well-being but also for justice. As such, if rape/sexual assault victims’ tragedy is seen as mere “deflowering” by this ministry, then where can they truly seek help? This time around, President David Granger needs to do much more than modestly ask the Minister for an explanation.
Dear Editor,With each passing day, the inherent fault lines eroding the democratic purpose of the Guyana Elections Commission (GECOM) threaten to graduate into a devastating tsunami. In fact, the magnitude of evidence in the widely circulated public media from many disappointed stakeholders puts the rebranded image of the organisation as tantamount to that of an old-time cake shop being run with hundreds of millions of taxpayers’ money.It is clear that the undercurrents have further deepened, since the strongly-challengeable, unilateral appointment by President Granger of the Chairman, Justice (retired) James Patterson. Nothing significant has so far been done by the Chairman to remedy the problematic issues at GECOM. Rather, things seem to have gotten worse, rendering the decaying grey matter incapable of adjusting to, or overseeing, a meaningful input that would cleanse the infested cake shop operations.In essence, when appointed, Commissioners have to take to the public media to air the overwhelming internal inefficacies and dirty linen permeating GECOM. It is a clear sign that we are fast approaching breaking point!Numerous published evidence -based revelations provide a very dismal picture of the many distasteful happenings being conducted within the organisation. Under Chairman James Patterson’s watch, Chief Executive Officer Keith Lowenfield acts as a lord unto himself, and has become even more emboldened to unleash another imbued ‘Town Clerk-like’ display.It was recently reported that when asked about approaches to expending on public relations projects, Lowenfield informed GECOM’s statutory meeting that once the Finance Ministry gave the accounting officer the approval to expend funds for any purpose, the GECOM Secretariat was not required to bring the issue before the Sub-Committee or the Commission.The seriousness of this erroneous response cannot be understated. Lowenfield pretends to be not any wiser following highly prosecutable findings contained in the report of the 2017 Auditor General’s examination of GECOM’s financial activities. It is clear that the procurement mechanism is being continually abused under a created guise of so-called urgent requirements for the same activities year after year; election after election. In essence, the internally applied approaches are being deliberately manipulated to accommodate fraud and handpicked beneficiaries.In a public entity such as GECOM, properly accountable practices are enshrined in the approved procurement legislation to address procedures that must be followed in the pre-procurement cycle; the cycle, and the post- procurement cycle. Critically, procedures in the law are specific to how this firm procures in terms of mandatory compliance procedures that support accountability. Particularly, they address the tender process, including forms of tendering — whether selective, public, or special; and consider strongly the Terms of Reference for the critical activities.In the GECOM setting, these do not often change, and are repeatable, since they are often informed by the plan for the specific elections and the related budget. This column, on numerous occasions, called for release of the GECOM budget, which often seems absent, abstract or lacking, in the interest of transparency and accountability.It is therefore appalling that the Commission would entertain such responses from the CEO of the Secretariat when requests for clarification are made by Commissioners.Notably, the Chairman of the Commission and the CEO of the Secretariat had, months ago, indicated the readiness of the organisation to fulfill the rudiments of the November 12th Local Government Elections.One had expected that such confirmation would have been driven by structured planning and budgeting, approved by the Commission (including all commissioners). One had expected that the execution of the Secretariat’s plan would have been strongly monitored, supported by a structured schedule that is devoid of occurrences of fraudulent financial manipulation to benefit a few. One would have expected that the high-risk elements which undermine the required level of professionalism would have been identified, and approaches to mitigate them would have been employed.Sincerely,Neil Kumar