THE UNITY SPORTS BOOSTER CLUB MET ON WED. OCT 10 @UMS CAFETERIA. PRESIDENT JAMSEN CALLED MEETING TO ORDER WITH 9 MEMBERS PRESENT.
THE SECRETARY'S REPORT WAS GIVEN BY MISSY VOTH. APPROVED BY CRAIG BURWINKEL AND MARCIA CORNWELL.
THE TREASURER'S REPORT WAS GIVEN BY SOMMER STIEFEL. APPROVED BY ANDY OBERT AND MISSY VOTH.
FOOTBALL CONCESSIONS- LOOKING FOR HELP FROM 2-6PM ON SAT. OCT 13 FOR MIDDLE SCHOOL FOOTBALL JAMBOREE.
FOOTBALL SCOREBOARD- BEN MARTH SAID IT WOULD COST $38,000 FOR 18FT X 24FT SCOREBOARD. BILL DORETHY CHECKED WITH TIM SCHRAGE FROM PEPSI. WE ARE LOCKED IN WITH PEPSI UNTIL 2021.WE NEED MORE DETAILS FROM COACH MCLAUGHLIN ABOUT THE SCOREBOARD. WE WILL TABLE THIS MATTER UNTIL WE HAVE MORE INFO.
MVIT- IN REGARDS TO TROPHIES, STERLING AWARDS-$49 FOR THE BIG BASKETBALL FOR CHAMPIONSHIP TROPHY. PLAQUES ARE $14. MEDALS ARE $4. RESIN TROPHIES ARE $15 A PIECE. SPORTSMANSHIP TROPHY 9X12- $32 OR 8X10-$29.
MVIT- TICKET TAKERS...MARCIA CORNWELL WILL TAKE CARE OF GETTING. HOSPITALITY ROOM WILL BE OBERTS AND HOLLY KLUSMEYER IN CHARGE OF IT. ANNOUNCERS/SCORE KEEPERS WILL BE CASH IN CHARGE OF. SHERRI FULLER WILL TAKE CARE OF PIZZAS. MISSY VOTH WILL TAKE CARE OF ROPE HOLDERS. LOOKING INTO FINDING HONORARY COACHES.
NEW MEMBER DRAWING- WE HAVE A GIFT BASKET FOR MEMBERSHIP SIGNUP. SOMMER STIEFEL HAS PUT THIS TOGETHER FOR US.
PROJECT PRIORITIES-MOTION MADE TO PAY FOR UHS GOLF EXPENSES FROM SECTIONALS. THE AMOUNT WAS $412.90. MOTION TO APPROVE BY MISSY VOTH AND SECONDED BY ANDY OBERT.
MSBOYS BBALL- STARTED PRACTICE. SEASON STARTS ON MONDAY OCT. 29 WITH REX TRUEBE COLT CLASSIC.
MS XC- NOAH DENNINSON DID VERY WELL.
HS FOOTBALL- TWO MORE GAMES LEFT.
VOLLEYBALL - 18-5. WE WILL HOST REGIONALS.
HS GOLF- GRANT OHNEMUS AND GAGE MOELLER ARE GOING TO STATE FOR GOLF.
HS XC- REGIONALS ARE AT MACOMB.
THE NEXT MEETING WILL BE HELD NOVEMBER 14TH IN THE UMS CAFETERIA AT 7PM.
DONNA JANSEN MADE MOTION TO ADJOURN AND ANDY OBERT SECONDED IT.


If a student requires a helmet or adaptive device for physical activities, please bring it to each and every class.
Students are not required to purchase their own dance shoes at the beginning of the season—we have many pairs of tap shoes at the studio that have been graciously donated to us over the years. Students may borrow these shoes for tap classes and dance in their socks for ballet & jazz classes.


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Home Articles Personal Essay & Nostalgia Articles Nostalgia Behind the Cameras: A Tribute
Nostalgia Behind the Cameras: A Tribute
Written by John Howard Prin, LADC
Nostalgia Behind the Cameras: A Tribute (PDF) 1257 Kb
This article appeared in Mpls/St Paul Magazine
In the early days of television, broadcasters didn't have the high-tech gadgets of today. But they did have unique personalities, like that of WCCO-TV's Toby Prin.
Along with thousands of other midwestern viewers, I watched his round, jolly face smiling on the 19 inch black-and white screen. His bald head gleamed from the WCCO-TV studio's bright lights. His voice crooned the bubbly strains of "Doggie in the Window" over the speaker. As the camera tilted down to my father's stubby fingers stroking the keys of the Baldwin piano, I heard his familiar refrain—the words so many neighbors, friends and strangers across the miles of Minnesota and Wisconsin prairies and forests knew so well—"And now another Mailbox Melodies tune for you folks out there."
It was broadcast news of a folksier variety in 1954 when WCCO-TV personality Toby Prin entertained young viewers with songs on the live daily program "Mailbox Melodies."
Eight hours later, at 1:30 that morning, I was awakened by our creaky garage door opening. From my bed I heard the door bang shut and my dad's nonbroadcast voice in the kitchen. In his raspy, weary, cigar-chewing muttering, I detected him searching for my mom's rice pudding hidden somewhere in the refrigerator. This was his nightly ritual: Toby Prin's arrival home after another 18-hour day.
Later, as he did every so often, he came into my bedroom and whispered, "Good night, Johnny." Most times I was asleep, as were my brothers, Tommy and Dave, who were also on his appointed rounds. But sometimes I felt the touch of his pudgy hand on my cheek. I peeked from behind sleepy eyelids and saw the loving look on his face. What I didn't see were the wrinkles from heart spasms and intestinal aches that he hid so well.
The year was 1954. I was 10 years old. We lived in a tiny white colonial home in St. Louis Park.
In the mid-1950s, almost everybody who was anybody in the area had a TV set. The earliest models, 7-inch screens with flickering shadow images and scratchy-sounding speakers, were fast being replaced by fancier 17- or 19-inch models. As the new medium grew, so did Dad's public prominence.
In a restaurant or a store, fans young and old would shake Toby's hand, eagerly ask for his autograph and buzz excitedly about seeing their friends on last week's talent show. It never occurred to me that I had any choice other than to share Dad with everybody.
Dad was a pioneer. He was a celebrity in a boom industry. Although at home he was plain and unassuming and never dramatic, to the world he was robust, jolly and larger than life—by appearing regularly in others' living rooms, he became public property.
But he wasn't. Few fans were aware of Dad's collection of hats, both protection for his bald head as well as expressions of his character. Nor did they know of his pipe collection—dozens of finely carved dark woods displayed in racks in our den. People often assumed he was the life of the party at home. No; he avoided playing the piano or singing for guests, shrugging like the doctor who declines to venture a prognosis on his day off. Mostly, Toby Prin was known for his trademark, an ever-present cigar. Even when he went swimming, he'd puff away on a Dutch Master or White Owl, his face upturned comically to prevent it from going out.
In my college years, I heard about his early days as an entertainer on the Iron Range. When we'd visit our aunts and uncles, they would tell us how he'd played the parlor piano as a boy at his family home in Michigan, where he was the youngest of nine children born to an immigrant tin miner from England. Dad later moved to Minnesota and dated Mom, one of four daughters born to an immigrant laborer from Sweden. He got his start as a band leader on the Iron Range in the 1920s, when he used the stage name "Tiny Speck." It was Mom who persuaded him to seek the success he ultimately found in Twin Cities radio. His transition to television brought pride to everyone who was part of his history and "remembered him when."
My fondest memories center on my visits to WCCO's Ninth Street studio in downtown Minneapolis. I'd ride the bus to see him in the bustling chaos at Channel 4. He, along with the other "names," would be so busy that he couldn't take more than a second away from his basement cubicle to say hello before whisking me upstairs to the Client Room, a plush cavelike chamber reserved for bigwigs. There the privileged few could sit in oversized swivel chairs and observe the studio's goings-on through immense plate-glass windows. I loved my view of the enchanted kingdom beyond: the soundproofed realm of monitors, microphones, cameras, cables, boom arms, cardboard sets-crowned, of course, by the blinking red "On-TheAir" sign.
From this vantage point I spied Cedric Adams, monarch of WCCO's monochromatic empire and erstwhile columnist for the Minneapolis Star; Rollie Johnson, the freckled, bespectacled spokesman for sports; Bud Kraehling, the court jester of fair weather; John Gallos, the town crier; and Arlie Haberle, the first lady of fashion and society. I remember the day when a new face, a young announcer named Dave Moore, distinguished himself as a budding prince of broadcast news and commentary.
On the monitor screens flanking the technical director's domain, there also appeared competitors KSTP-TV and WTCN-TV, with their celebrities in clear view: Randy Merriman, champion of charm and game-show smiles; Mel Jass, all fast-moving hands and fast-talking sales pitches; and Casey Jones (Roger Awsumb), the kids'-show host in his too-clean overalls and cap.
All these celebrities and charmers graced the black-and-white world of live ballyhoo and bloopers where my father, the chubby minstrel of Channel 4, also made his living.
The good times didn't last long. Late in 1956, I sat stunned, along with Mom, Tommy and David in the Physicians and Surgeons Building across from the WCCO-TV studio. We tried to absorb the news that Dad was diabetic and had a serious heart ailment. At 51, his overweight and overwork were doing more than making him drowsy, cranky and forgetful —they were taxing his health to the danger point.
Our family had just finished the 18-month process of building a huge house in faraway Edina, then an untamed suburb of expansive lots with expensive country-style elegance.
From the day we moved in, Dad spent more and more time in doctors' offices, and the expenses of both new home and hospital visits became as burdensome as his efforts to fight fatigue, blackouts, high blood pressure, nerve blocks and, eventually, the amputation of his right leg.
Dad's working days at WCCO dwindled into unemployment. His best known show, Stillicious Talent Hunt, which he hosted as Uncle Toby for mobs of kids on Saturday mornings, went off the air because of his absences. When four months at the Mayo Clinic brought only a backlog of bills, my brothers and I secured jobs at local stores and restaurants. Mom, who had worked at Dayton's for three years, was promoted to full-time interior decorator at the Southdale store.
In 1960 we had to sell our Edina home and move to a smaller place like our earlier home. We all hoped Dad would get better, but the decline in his strength and weight and spirit were inexorable. The Dad we saw daily had the same smile and soft glow in his eyes, but his rosy cheeks were sagging and the torment in his soul had dimmed any sparkle in his temperament.
During my daily visits to Methodist Hospital (room 318), I gazed at his wasted-away torso (he was now 90 pounds, down from 355 pounds eight years before). I grimaced at the irony of his having become a real "Tiny Speck."
The whole family knew he would never leave that room again. I longed for the same loving, caring look in his eyes as when I was younger. But, on a dismal November day in 1965, at age 59, he died.
My main impression was of Dad working all day downtown at the station and his seldom being home, of his playing the piano or organ at nightclubs and bars from eight in the evening until one in the morning, and his entertaining at private parties or special affairs on his night off. The regret of our "missed" times together depressed me. He'd so seldom "been there," and he was from the generation of fathers, like his father before him, who just never told his kids that he loved them.
Yet one final memory surfaced. His faithful record of attendance at my high school hockey games was remarkable because I was the second-string varsity goalie for perennial power Edina. This meant I suited up for every game but sat on the sidelines. As the season reached an end, my chance finally came. Nervously, but competently, I stopped a flurry of enemy shots. The crowd jumped to its feet. The cheerleaders hollered my name. And Dad, standing on his artificial leg, whooped and hollered along with the rest of them. For that moment he had "been there," and the love in his eyes shined.
This article appeared in Mpls/St Paul Magazine-March 1988
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40+ Hot And Sexy Holland Roden Photos
Celebrity Ass, Celebrity Bikini, Celebrity Boobs, Hot Celebrities 138 Views
Holland Roden is famous for her role in the MTV teen series, Teen Wolf. But what Roden is more famous for is her sexy long red hair, which is natural by the way. The actress shows off her natural red hair in many of her movies and TV appearances, making her look hot. Whenever she poses in a bikini for photoshoots, her long red hair was always the stunner, along with her sexy bikini body. Check out our photo compilation of Holland Roden to see her beautiful red hair.
Born in Texas, Holland Roden's parents welcomed Holland Marie Roden on October 7, 1986. Before Holland became an actress, she spent her college years at UCLA studying molecular biology and women's studies. Right after her three years in pre-medical education, Holland started to do small roles for short films.
In 2004, Holland appeared in the short film, Consideration, where she played the character of Angela and in the short film, Back at the Ranch, as Dawn Leatherwood. After her brief film opportunity in 2004, it took two years for Holland to land into another acting opportunity. Then, she got a cast for an episode in CSI in 2007, as Kira Dellinger. The following year, Holland appeared in three more TV series, playing guest roles. She appeared in the canceled TV series, 12 Miles of Bad Road, Lost, and Cold Case.
Holland then turned to movies when she got a cast for the character, Sky, in the direct-to-DVD film, Bring It On: Fight to the Finish in 2009. In the same year, she got to guest star in the TV series, Weeds, for one episode. She also had a guest role on the comedy TV series, Community.
Roden's guest roles continued until 2011 when she appeared in Criminal Minds, The Event, and Memphis Beat. Her breakthrough TV role was when she starred in the MTV teen series, Teen Wolf. Roden portrayed the character, Lydia Martin and appeared in more than 100 episodes of the series.
The supernatural teen drama premiered in June 2011 with a total of six seasons until its final episode in September 2017.
Roden's character, Lydia Martin, is Allison's close friend and is also a popular girl at their high school. Although she did not reveal her boobs or ass, Roden still looked hot while portraying her role.
After the success of Teen Wolf, Holland continued to guest star in other TV series like Grey's Anatomy, Lore, and even MacGyver. While doing guest roles, she also had small appearances in short films like Morning Love and Fluffy. Her latest star role is in Escape Room 2, which will premiere in 2021.
When Roden was in Brazil in 2019, she got detained by the airport police because she allegedly had an invalid Brazilian passport. She got denied to enter the country for more than six hours and got treated aggressively by the police, according to her Instagram posts.
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Desperado Roller Coaster Lets it Ride
Editors' Choice Awards 2020
Weird & Amazing
The TripSavvy Team
United States Nevada Las Vegas
All Las Vegas
Ride Review of the Nevada Hypercoaster
Arthur Levine
Arthur is a travel writer with more than 25 years of experience. He has been covering theme parks, amusement parks, water parks, and attractions for TripSavvy since 2002.
Tripsavvy's Editorial Guidelines
Ken Lund/Flickr/CC BY-SA 2.0
As you drive south on I-15 from Las Vegas towards Los Angeles, the view is serene. Save for a few lonely cacti, the desert extends in all directions until it meets brick-red, scraggly hills. This picture-perfect scene goes on for miles until... what is that peculiar thing in the distance? Like a yellow phoenix rising from the sands, the incredibly tall, meandering track of the Desperado roller coaster punctures the blue sky. What is a roller coaster doing in the middle of nowhere? And why is it in the middle of a casino?
Coaster Stats
Thrill Scale (0=Wimpy!, 10=Yikes!): 8.5
Attraction type: Steel hypercoaster
Location: Buffalo Bill's, Primm, NV
Height: 209 feet
Drop: 225 feet
Speed: 90 mph
Manufacturer: Arrow Dynamics
Search for Buffalo Bill's Resort & Casino rates at TripAdvisor.
The Middle of Nowhere Is Now Somewhere
The Desperado is the centerpiece of the Primm Valley Casino Resorts in Primm, Nevada, about 45 minutes from Las Vegas. Gary Primm, the casino's founder, placed a Ferris wheel in front of his building in the early 80s to capture the attention of some of the millions of Vegas-bound travelers. With that modest move, he may have unknowingly sparked the trend to link theme park attractions with gambling.
Encouraged by the hordes of curious folks who stopped to ride his wheel and gamble in his casino, Primm expanded on his successful formula. Today, the resort includes three hotel/casinos and enough attractions and rides to rival a small amusement park. A sleek monorail shuttles passengers over the interstate between two of the casinos. There's a carousel, skyride, freefall tower, huge arcades, a log flume ride, carnival games, motion simulation theaters, and more. Primm turned the middle of nowhere into somewhere. And it's the roller coaster that really put the place on the map.
Through the Roof
The Desperado coaster is unique in many ways. For one, the loading station is inside Buffalo Bill's casino. The electric-yellow steel track winds around and into the bustling casino. As nearby slot machines beep and burp out winnings, nervous riders wait in line fretting over the train of cars about to whisk them through the roof for a hair-raising journey.
When it first opened, the Desperado had the official blessing of the Guiness Book of World Records as the world's tallest, fastest, and steepest roller coaster. It's since been eclipsed in all categories, but the heart-pounding, 225-foot first drop places it firmly in hypercoaster territory. With its steep decline, the Desperado clocks in at a top speed of 90 mph.
Like most hypercoasters, the Desperado does not loop, invert, or otherwise tip its riders upside down. The mission here is to terrorize with sheer height and speed. The initial drop, which enters a disorienting lights-out tunnel at ground level, is certainly panic inducing, but not necessarily the most terrifying feature of the ride.
As the coaster leaves the tunnel and climbs the second hill, it can provide a prolonged sense of negative-G weightlessness just before the cars are released for the second drop -- a dizzying 155-foot spiral fall. That strange feeling of weightlessness, repeated two more times before the third and fourth drops, can be especially powerful and disorienting. The weightless sensation, caused by negative Gs, is all the more frightening when contrasted with the intense positive G-forces imposed by the long and steep drops.
When the Desperado first opened, it really poured on the butterflies-in-your-stomach airtime. It has not aged gracefully however, and the negative-G moments have been less intense more recently. Keep in mind that many variables can affect a coaster ride: temperature, lubrication, wear and tear on the coaster train, and time of day, to name a few. Your results may vary.
There are more thrills to be had in and around the area. Check out other Las Vegas roller coasters.
A Loooong Ride: The 11 Biggest Roller Coasters.
Could You Handle the World's 10 Fastest Roller Coasters?
Las Vegas Takes You for a Ride—on Roller Coasters
You Have to Ride These 12 U.S. Roller Coasters At Least Once
Yikes! The World's 10 Tallest Roller Coasters will Freak You Out
The Coolest Launched Roller Coasters in the Country
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Patients with malignant diseases can be effectively treated with allogeneic hematopoietic stem cell transplantation (allo-SCT). Polymorphic peptides presented in HLA molecules, the so-called minor histocompatibility antigens (MiHA), play a crucial role in antitumor immunity as targets for alloreactive donor T cells. Identification of multiple MiHAs is essential to understand and manipulate the development of clinical responses after allo-SCT. In this study, CD8+ T-cell clones were isolated from leukemia patients who entered complete remission after allo-SCT, and MiHA-specific T-cell clones were efficiently selected for analysis of recognition of a panel of EBV-transformed B cells positive for the HLA restriction elements of the selected T-cell clones. One million single nucleotide polymorphisms (SNP) were determined in the panel cell lines and investigated for matching with the T-cell recognition data by whole genome association scanning (WGAs). Significant association with 12 genomic regions was found, and detailed analysis of genes located within these genomic regions revealed SNP disparities encoding polymorphic peptides in 10 cases. Differential recognition of patient-type, but not donor-type, peptides validated the identification of these MiHAs. Using tetramers, distinct populations of MiHA-specific CD8+ T cells were detected, demonstrating that our WGAs strategy allows high-throughput discovery of relevant targets in antitumor immunity after allo-SCT. Cancer Res; 70(22); 9073–83. ©2010 AACR.
Allogeneic hematopoietic stem cell transplantation (allo-SCT) is a curative treatment for malignant diseases (1). In case of relapse, persistent disease, or incomplete donor chimerism after transplantation, donor lymphocytes can be administered to initiate or enhance graft-versus-tumor (GVT) reactivity (2). Following HLA-matched allo-SCT, minor histocompatibility antigens (MiHA) are the target structures for donor-derived T cells. Presented in the context of HLA molecules, MiHAs are peptides derived from polymorphic proteins that differ between individuals due to genomic single nucleotide polymorphisms (SNP; refs. 3–6). T-cell responses directed against MiHAs have been monitored in detail in patients responding to donor lymphocyte infusion (DLI; refs. 7, 8). In these patients, detection of circulating MiHA-specific T cells coincided with rapid disappearance of malignant cells, indicating the in vivo efficacy of MiHA-specific T cells. Whether donor T cells mediate beneficial GVT effects or harmful graft-versus-host disease (GvHD) is likely to depend on the tissue distribution of the target antigen. Exclusive MiHA expression on malignant cells may result in a selective GVT effect, whereas T cells recognizing broadly expressed MiHAs may lead to detrimental GvHD (9).
Initially, biochemical identification of peptides eluted from HLA class I molecules recognized by MiHA-specific T cells was used for MiHA discovery (10–15). In addition, cDNA libraries were generated and screened for T-cell recognition to identify the MiHA-encoding gene transcript (8, 16–21). Finally, genetic linkage analysis has been applied to define the genomic region encoding the MiHA (22, 23). Irrespective of the MiHA identification method, ultimate validation of each MiHA was provided by the strict correlation between a specific SNP genotype and recognition by the T-cell clone.
SNPs between patient and donor may lead to MiHA expression by different mechanisms. The majority of MiHAs are encoded by "missense" SNPs that directly encode an amino acid polymorphism in the protein. In addition, SNPs "synonymous" in the normal open reading frame (ORF) have been shown to encode polymorphic amino acids in MiHA epitopes upon translation of alternative reading frames (ARF), as previously described for LB-ECGF-1H (8) and LB-ADIR-1F (15). MiHAs can also be generated by protein splicing, as illustrated for HwA-9, which is spliced together in a noncontiguous order by the proteasome (18). Furthermore, MiHAs can be encoded by gene transcripts that differ between patient and donor due to insertion or deletion of a single nucleotide, thereby inducing a shift in the translational reading frame, as shown by the LRH-1 MiHA (23). Finally, MiHAs may be encoded by gene transcripts that are homozygously deleted in the donor, as shown for MiHAs encoded by the UGT2B17 gene (17), or by intronic SNPs altering gene expression by RNA splicing, as shown for ACC-6 (19).
Although various MiHA identification approaches have led to the successful discovery of 20 HLA class I–restricted MiHAs, their laboriousness and low efficiency hampered identification of the majority of MiHAs recognized by T-cell clones. Development of advanced array-based SNP genotyping, and the fact that MiHAs are encoded by polymorphic genomic regions containing specific SNPs, enabled application of whole genome association scanning (WGAs) as an alternative approach for MiHA discovery (24). Association analysis may identify associating SNPs that directly encode the amino acid polymorphism or may serve as markers for MiHA-encoding SNPs that are not measured by the array. These markers are in linkage disequilibrium with MiHA-encoding SNPs and therefore associate with T-cell recognition. The feasibility of WGAs as an approach to identify new MiHAs has been shown by the discovery of individual MiHAs in BCL2A1 (24), CD19 (25), SLC1A5 (26), UGT2B17 (26), SLC19A1 (27), P2RX7 (28), and DPH1 (28).
To understand the development of GVT reactivity and GvHD, characterization of large numbers of MiHAs is essential. High-throughput identification and expression analysis of MiHAs in patients with various clinical responses after allo-SCT may provide insight into the fundamental difference and may allow manipulation of the balance between GVT reactivity and GvHD. Here, we report the successful application of WGAs for high-throughput characterization of MiHAs in GVT reactivity. T-cell clones were generated from two patients who received an HLA-matched allograft and responded to DLI for recurrence of the malignant disease. A panel of 80 EBV-transformed B-cell lines (EBV-LCL) was tested for recognition by each T-cell clone. More than 1 million SNPs were measured in the EBV-LCL and subsequently searched for association with the EBV-LCL recognition pattern of each T-cell clone. Strong association with a genomic region was found for 12 of the 17 T-cell clones evaluated. For 10 of these 12 T-cell clones, novel MiHAs with balanced population frequencies presented in the common HLA-A*0201 or B*0702 molecules could be identified, illustrating the value and efficiency of WGAs for MiHA discovery. Using tetramer analysis, the kinetics of MiHA-specific T-cell responses in the patients were shown to coincide with the clinical responses that were observed after DLI.
Patient H (HLA-A*0201, B*0702, B*4402, Cw*0501, Cw*0702, DRB1*04, DRB1*15, DRB4*01, DRB5*01, DQB1*03, DQB1*06, DPB1*04) had myelodysplastic syndrome refractory anemia with excess of blasts type 2. She was transplanted with a T-cell–depleted peripheral blood stem cell graft from a male HLA-matched unrelated donor. Chimerism analysis showed a decrease in the percentage of donor cells to 86% during the first 6 months after transplantation; therefore, the patient was treated with DLI. After DLI, the patient developed GvHD limited to skin and mouth, which coincided with a rapid and sustained conversion to 100% donor chimerism. Patient Z (HLA-A*0101, A*0201, B*0702, B*4402, Cw*0501, Cw*0702, DRB1*11, DRB1*15, DQB1*03, DQB1*06, DPB1*04, DPB1*14) is a patient with chronic myelogenous leukemia (CML) transplanted with a T-cell–depleted peripheral blood stem cell graft from his HLA identical sibling. More than 1 year after transplantation, the patient was successfully treated with DLI for cytogenetic relapse of CML. The patient did not develop GvHD.
Peripheral blood and bone marrow samples were collected from the patients, their donors, and third-party individuals after approval by the Leiden University Medical Center Institutional Review Board and informed consent according to the Declaration of Helsinki. Mononuclear cells were isolated by Ficoll gradient centrifugation and cryopreserved. Stable EBV-LCL were generated by in vitro transformation of thawed mononuclear cells of selected HLA-A*0201–positive and B*0702-positive individuals using EBV supernatant (29) followed by culture in Iscove's modified Dulbecco's medium (IMDM, Lonza) with 10% fetal bovine serum (FBS, Lonza).
Peripheral blood mononuclear cells (PBMC) obtained after DLI were thawed for isolation of T-cell clones. Monocytes were depleted using magnetic CD14 beads (Miltenyi Biotec) according to the manufacturer's instructions. CD14-negative cells were stained with allophycocyanin (APC)-conjugated anti-CD8 antibody (Invitrogen) and phycoerythrin (PE)-conjugated anti–HLA-DR antibody (Invitrogen). Propidium iodide (Sigma-Aldrich) was added to exclude dead cells, and viable HLA-DR+ CD8+ cells were single cell sorted by flow cytometry. Isolated T cells were collected in 96-well U-bottomed plates (Corning) in IMDM with 5% pooled human serum, 5% FBS, interleukin 2 (IL-2; 100 IU/mL), phytohemagglutinin (0.8 μg/mL, Murex Biotec Limited), and 5 × 104 irradiated allogeneic PBMC as feeder cells. Proliferating T-cell clones were restimulated every 10 to 14 days under identical stimulatory conditions at 2 × 105 T cells and 1 × 106 feeder cells per milliliter of culture medium. T-cell (5 × 103 per well) recognition of patient- and donor-derived EBV-LCL as well as third-party EBV-LCL (3 × 104 per well) were tested in 96-well U-bottomed plates in 100 to 150 μL IMDM with 5% pooled human serum, 5% FBS, and 20 IU/mL of IL-2. After overnight coincubation, release of IFN-γ was measured in culture supernatants by ELISA according to the manufacturer's instructions (Sanquin). For blocking studies, EBV-LCL were preincubated with saturating concentrations of antibodies against HLA-A*02 (BB7.2) and HLA-B*07 (VTM3A1) for 30 minutes at room temperature before addition of T cells.
T-cell receptor-β variable chain (TCRBV) usage was investigated by flow cytometry using specific monoclonal antibodies as included in the TCRBV repertoire kit (Beckman Coulter). T-cell clones with identical TCRBVs were analyzed by DNA sequencing of the CDR3 region of the TCRBV after amplification by PCR using specific forward and reverse primers. TCRBV products were purified with the Qiaquick PCR purification kit (Qiagen) and sequenced using the dye terminator cycle sequencing kit (ABI-PRISM, Perkin-Elmer), according to the manufacturer's instructions.
A panel of 80 HLA-A*0201– and B*0702-expressing EBV-LCL was selected for WGAs. To allow simultaneous analysis of all EBV-LCL for recognition by T-cell clones, triplicate samples of EBV-LCL were dispensed at 6 × 104 cells in 50 μL per well in 96-well polypropylene U-bottomed plates (Greiner Bio-One). After addition of 50 μL medium containing 20% DMSO, the panel plates were sealed, frozen, and stored at −140°C. To test the recognition of the EBV-LCL panel by each individual T-cell clone, plates were thawed, washed, and incubated for 2 days, and 5 × 103 MiHA-specific T cells were added to each well. After 24 hours, supernatants were used for IFN-γ ELISA. Of each EBV-LCL, genomic DNA from 5 × 106 cells was isolated using Gentra Puregene Cell Kit (Qiagen). According to the manufacturer's instructions, PCR-free whole genome amplification was performed. The DNA samples were subsequently fragmented, purified, and hybridized to Illumina Human1M-duo arrays containing probes for 1.1 million SNPs (Illumina). After hybridization, the bead arrays were stained and fluorescence intensities were quantified on an Illumina Bead Array 500GX Scanning Station. Raw data were analyzed using Illumina Genome Studio software, and SNP genotype reports were generated allowing WGAs analysis using the Plink software (http://pngu.mgh.harvard.edu/~purcell/plink, version 1.03; ref. 30). For WGAs, categorization of the test results in two separate groups is required. Therefore, EBV-LCL were divided into MiHApos and MiHAneg groups using five times the level of IFN-γ production in the absence of EBV-LCL as a threshold for recognition. WGAs was performed by combining T-cell recognition with SNP genotyping data. The level of matching between both patterns was calculated according to Fisher's exact test.
RNA from the patients and their donors was isolated from EBV-LCL using Trizol (Invitrogen) and transcribed into cDNA by reverse transcriptase (Invitrogen) using oligo-dT primers (Roche Diagnostics). Genes that were located in associating genomic regions were amplified by PCR using various forward and reverse primers that were selected to comprise entire gene transcript or specific SNP-containing regions (see Supplementary Table S1 online). PCR products were purified and analyzed by DNA sequencing, and the obtained patient and donor sequences were aligned to identify SNP disparities.
For each SNP that was identified by WGAs and gene sequencing, gene fragments comprising the polymorphic patient-type nucleotide flanked by 30 upstream and downstream nucleotides were translated into different reading frames. The online algorithm of NetMHC (31) was used to search for peptides with predicted binding to the appropriate HLA molecule. Peptide candidates were synthesized and dissolved in DMSO. Dilutions were prepared in IMDM and added to MiHAneg donor EBV-LCL (3 × 104 per well) in 96-well U-bottomed plates for 2 hours at 37°C. T cells (5 × 103 per well) were added, and after 24 hours, the culture supernatant was used for IFN-γ ELISA.
Tetramers were constructed by folding peptides in appropriate biotinylated MHC-monomers followed by multimerization using streptavidin conjugated to PE or APC as previously described with minor modifications (32). Patient samples were thawed and stained with FITC-conjugated CD4 and CD14 antibodies to exclude nonrelevant cells in flow cytometric analysis. MiHA-specific T cells were visualized using PE- or APC-conjugated tetramers and PE-Cy7–labeled anti-CD8. On average, 5 × 105 viable cells were analyzed per staining using a Becton Dickinson FACS CantoII and DIVA software.
CD8+ T cells were isolated from PBMCs obtained 5 or 6 weeks, and 8 weeks after DLI from patient H and patient Z, respectively. Single activated CD8+ T cells were isolated using flow cytometry based on expression of HLA-DR. Percentages of CD8+ T cells expressing HLA-DR were 11% (week 5) and 19% (week 6) for patient H and 3% (week 8) for patient Z (data not shown). Clonal expansion was observed for 195 T-cell clones from patient H and 37 T-cell clones from patient Z. All 232 clones were tested for recognition of patient- and donor-derived EBV-LCL by IFN-γ ELISA. The strategy followed for selection of MiHA-specific T-cell clones eligible for WGAs is depicted in Fig. 1A. In total, 62 T-cell clones from patient H and 16 T-cell clones from patient Z differentially recognized patient, but not donor, EBV-LCL, indicating recognition of MiHAs. All 78 patient-specific T-cell clones were investigated for HLA restriction using specific HLA class I, HLA-A*02, and B*07 blocking antibodies. Restriction to HLA-A*02 or B*07 was observed for 43 T-cell clones from patient H and 9 T-cell clones from patient Z. To identify whether T-cell clones recognized the same MiHA, we tested a panel of 30 HLA-A*02– and B*07-expressing EBV-LCL. In addition, TCRBV diversity was determined by flow cytometric analysis using specific TCRBV monoclonal antibodies and by DNA sequencing of the TCRBV CDR3 regions (33). This led to identification of 20 unique MiHA recognition patterns, including 13 MiHAs recognized by single T-cell clones and 7 MiHAs recognized by groups of T-cell clones (Table 1). TCRBV diversity was observed in five of the seven groups, indicating the presence of polyclonal T-cell responses targeting these MiHAs. Application of WGAs requires a balanced distribution between MiHApos and MiHAneg test samples. Recognition of 30 EBV-LCL was used to determine this parameter, resulting in exclusion of three clones recognizing rare (clones H11 and H15) or common (clone H9) MiHAs. Cross-reactivity to nonself HLA molecules was excluded by the lack of recognition of a panel of 25 HLA-A*02– and B*07-negative EBV-LCL.
T-cell clone selection and WGAs strategy for MiHA identification. Strategy outline for selection of CD8+ T-cell clones (A) and MiHA identification by WGAs (B). The digits in the arrows depict the number of clones that was selected at each step.
A panel of 80 HLA-A*0201– and B*0702-expressing EBV-LCL was generated to identify MiHA-encoding genes by WGAs. Genomic DNA was isolated from each individual EBV-LCL for SNP genotype analysis using Illumina Human 1M-duo bead chips. To estimate the quality of the array data, we extracted SNP genotypes for known MiHAs. For 16 of the 27 known MiHAs, probes were included on the Illumina Human 1M-duo bead array, and all SNP genotypes were accurately measured with call rates >95% and allele frequencies comparable with dbSNP data (see Supplementary Table S2 online). Next, recognition of all EBV-LCL by each WGAs-eligible T-cell clone was tested using IFN-γ ELISA. Figure 2 shows the recognition of all EBV-LCL for the selected T-cell clones. Clear clustering of MiHApos and MiHAneg EBV-LCL cells was observed for the majority of the T-cell clones. For clones H6 and H12, MiHApos EBV-LCL could not be clearly discriminated from MiHAneg EBV-LCL due to the large number of EBV-LCL that were intermediately recognized by the T cells. WGAs was performed by comparing each T-cell recognition pattern with all SNP genotypes. The level of matching between both patterns was calculated according to Fisher's exact test. By selecting SNP genotypes that significantly associated with a T-cell recognition pattern with P values <10−9, single genomic regions could be identified for 12 T-cell clones. The identified regions varied in length from 1 bp up to 100 kb, comprising a maximum number of three genes and containing 1 to 17 associating SNPs (see Supplementary Fig. S1 and Table S3 online). Lack of association with a genomic region was observed for five T-cell clones, including clones H6 and H12, which produced intermediate levels of IFN-γ upon coincubation with a number of EBV-LCL. Clones H13 and H14, which also failed to show association with a genomic region, recognized MiHAs with low population frequencies of 10% and 11%, respectively, suggesting that the power of WGAs was not sufficient to identify these MiHAs.
Recognition of a panel of 80 EBV-LCL by MiHA-specific T-cell clones. HLA-A*0201– and B*0702-restricted T-cell clones recognizing MiHAs with population frequencies between 10% and 90% were tested for recognition of a panel of 80 HLA-A*0201 and B*0702 EBV-LCL. Each dot represents the mean of triplicate IFN-γ production (ng/mL) as measured by ELISA after overnight coincubation of the T-cell clone (indicated on the X axis) with each EBV-LCL. Lines indicate the threshold of five times background IFN-γ production to segregate MiHApos from MiHAneg EBV-LCL.
The strongest associating SNPs within each region were further examined, and associating SNPs were found in coding and noncoding gene regions (Table 2). Associating missense SNPs, encoding amino acid polymorphisms in the normal ORF, were found in the genes WNK1, SSR1, PRCP, PDCD11, EBI3, and APOBEC3B. These SNPs may directly encode the MiHA. Clone H1 and its associating SNP rs12828016 located in exon 21 of the WNK1 gene is shown as a representative example in Fig. 3A. Associating synonymous SNPs were found in the genes ARHGDIB and GEMIN4, and associating SNPs in noncoding regions were found in the genes TTK, ERAP1, BCAT2, and ERGIC1. Associating synonymous SNPs and SNPs in noncoding regions may serve as marker SNPs for missense SNPs, which are not measured by the bead array. To search for these disparate missense SNPs, all genes comprising associating synonymous SNPs and SNPs in noncoding regions as identified by WGAs were investigated by analyzing cDNA derived from both patient and donor. Sequence analysis of gene transcripts revealed the presence of disparate missense SNPs in the genes ERAP1, BCAT2, and GEMIN4. Figure 3B shows clone H8 and its associating SNP rs26654 located in intron 1 of the ERAP1 gene as a representative example of a marker SNP, which is in linkage disequilibrium with SNP rs26654 located in exon 2 identified after gene sequencing. Sequence analysis revealed that ARHGDIB gene transcripts were completely identical between patient and donor, except for the single associating synonymous SNP rs4703 as identified by WGAs. These data suggest that this SNP directly encodes the MiHA in an ARF, as previously reported for other MiHAs (8, 15). The TTK and ERGIC1 genes, identified by strong association of SNPs in noncoding regions, did not show any SNP disparity between patient and donor in coding regions. In conclusion, WGAs in combination with gene sequencing led to identification of disparate missense SNPs for 10 of the 12 genes (Table 2).
Identification of candidate genes and MiHA-encoding SNPs by WGAs. Association results and selection of candidate MiHA-encoding SNPs are shown for WNK1 (A) and ERAP1 (B) genes as representative examples. Significance of association for each individual array SNP as expressed by P value is depicted. Each dot represents the array SNP relative to its physical position on the genome. The image below each plot shows the gene aligned to the chromosomal position as indicated on the X axis of the plot. Exons and introns are represented by dark and light boxes, respectively. A, for clone H1, the strongest associating SNP is located in exon 21 of the WNK1 gene and encodes an amino acid polymorphism. B, the strongest associating SNP for clone H8 is located in intron 1 of the ERAP1 gene. Sequence analysis revealed a disparate missense SNP in exon 2 of the ERAP1 gene.
Gene sequences containing missense and synonymous SNPs identified by WGAs and DNA sequencing were translated in the normal ORF and in all ARFs, respectively, and searched for peptides with predicted binding to HLA-A*0201 and B*0702 using the online algorithm of NetMHC (31). All peptide variants with predicted binding to HLA-A*0201 and B*0702 are shown in Table 3. Peptides of 9 to 11 amino acids with predicted binding to HLA-A*0201 or B*0702 were synthesized, exogenously pulsed on MiHAneg donor EBV-LCL, and tested for T-cell recognition. For nine polymorphic peptides, strong recognition of a single predicted candidate peptide or variable levels of recognition for candidate peptides of various lengths was observed (Table 3). The SSR1-derived HLA-A*0201 binding candidate peptide, however, was not recognized. Longer 14-mer and 21-mer SSR1-derived peptides spanning the identified patient-type amino acid polymorphism were clearly recognized, albeit at high peptide concentrations of 50 μmol/L (data not shown), thereby confirming that the missense SNP encodes the MiHA epitope, but leaving the precise composition of the epitope unknown. For all identified MiHA epitopes as shown in Table 3, as well as for the longer SSR1 peptides, no recognition of donor-type peptides was observed. This validated the identification of 10 novel MiHAs encoded by SNPs as identified by our approach of WGAs (Fig. 1B).
To analyze the kinetics of the T-cell responses specific for the novel MiHAs as identified by WGAs, donor samples as well as sequentially obtained peripheral blood samples from the patients were stained with tetramers and analyzed by flow cytometry. Except for LB-BCAT2-1R, we could construct stable tetramers that successfully stained the respective T-cell clones for all novel MiHAs. Tetramer analysis revealed the presence of T cells specific for the MiHAs in patient H, and for one MiHA in patient Z (Fig. 4). The frequencies of MiHA-specific T cells peaked at day 41 and 62 in patients H and Z, respectively, coinciding with conversion to full donor chimerism in patient H and disappearance of the BCR-ABL fusion product as a marker for disease in patient Z. No significant tetramer-positive events were detected using tetramers specific for LB-APOBEC3B-1K and for LB-EBI3-1I in patient Z.
MiHA-specific T-cell responses in patients H and Z. Tetramers were constructed to measure MiHA-specific CD8+ T cells in peripheral blood samples obtained at several time points, as indicated on the X axis. On the primary Y axis, the absolute number of tetramer-positive cells per milliliter of blood is depicted. The secondary Y axis depicts donor chimerism in patient H (A) and disease status in patient Z (B).
In this study, we developed an efficient strategy for T-cell selection and MiHA identification by WGAs. This WGAs-based strategy allowed detailed investigation of the specificity and diversity of antitumor T-cell responses in two patients successfully treated with HLA-matched allo-SCT and DLI. The strategy is based on efficient selection of MiHA-specific T-cell clones and a panel of 80 third-party EBV-LCL for simultaneous measurement of T-cell recognition and 1.1 million SNP genotypes. From the 17 selected T-cell specificities, 10 novel MiHAs were identified, illustrating the value of this WGAs-based strategy for broad characterization of MiHAs in clinical immune responses.
For 5 of the 17 selected T-cell specificities, we failed to show significant association with SNP genotypes by WGAs. Two T-cell clones recognized a limited number of EBV-LCL, suggesting that the power of the WGAs strategy may not be sufficient to identify MiHAs with low population frequencies. Two other T-cell clones for which we failed to show association with SNP genotypes by WGAs released intermediate levels of IFN-γ upon coincubation with a number of EBV-LCL, thereby hampering separation of EBV-LCL in MiHApos and MiHAneg groups. Finally, for one T-cell clone, a balanced segregation of MiHApos and MiHAneg EBV-LCL was observed; however, no significant association with any SNP genotype was detected. For this T-cell clone, association may be found by measuring more SNP genotypes, for example, by testing EBV-LCL from the International HapMap project, which have been genotyped for more than 4 million SNPs and recently shown to represent a valuable source for MiHA discovery (25–27).
Our WGAs-based strategy revealed a number of SNPs that associated with T-cell recognition with significant P values. We separated the missense SNPs from the synonymous SNPs and SNPs located in noncoding regions. Missense SNPs were directly analyzed for HLA binding prediction and identification of the MiHA peptide epitopes. All six missense SNPs were found to encode the MiHA epitope. Synonymous SNPs and SNPs in noncoding regions may serve as markers for MiHA-encoding SNPs that are not measured by the bead array. Therefore, genes comprising marker SNPs were first analyzed by gene sequencing to reveal all SNP disparities between patient and donor. For two T-cell clones, associating synonymous SNPs were found, of which one was shown to serve as a marker for a MiHA-encoding missense SNP and the other directly encoded the MiHA epitope translated in an ARF, as previously described for LB-ECGF-1H (8) and LB-ADIR-1F (15). Finally, for four T-cell clones, associating SNPs were located in noncoding regions. In two cases, intron SNPs were in linkage disequilibrium with MiHA-encoding missense SNPs, whereas no SNP disparities in coding gene regions were found for the other two T-cell clones.
For two T-cell clones showing strong association with intron SNPs, without SNP disparities in the coding regions of the associating genes of patient and donor, we explored the possibility that a monomorphic epitope is recognized, which may be under differential control of a SNP located in a regulatory region. The entire coding regions of the TTK and ERGIC1 genes were cloned into an expression vector and introduced into MiHA-negative cells, but no T-cell recognition of the transfected genes was observed (data not shown). Therefore, we consider it likely that these MiHAs are encoded by SNPs located outside known protein coding regions of the candidate genes, for example, by an intron SNP of an alternative mRNA splice variant, as previously described for ACC-6 (19), and we speculate that these MiHAs may be most difficult to identify by WGAs.
As a final step in the discovery of MiHA, specific recognition of patient-type peptide was established. All identified MiHA epitopes were accurately predicted using the binding algorithm of NetMHC (31), as shown by T-cell recognition of donor EBV-LCL pulsed with the predicted patient-type, but not donor-type, peptide variants. Weak, but patient-specific, recognition was observed for peptides derived from APOBEC3B and SSR1. The SSR1 epitope is a nonconventional peptide of 14 amino acids. Although recognition was weak, the T-cell clone differentially recognized patient-type, but not donor-type, 14-mer peptides demonstrating T-cell specificity for this polymorphism. Weak recognition of pulsed synthetic peptides may indicate posttranslational modification of endogenous epitopes, as previously described for the SMCY antigen (34). Another explanation may be that the T-cell clone expresses a T-cell receptor with a relatively low avidity, which is, however, sufficiently high to recognize MiHAs that are abundantly expressed at the cell surface of patient cells.
The MiHAs described in this study were identified as targets for T cells isolated from patients receiving DLI for incomplete donor chimerism or recurrent disease after allo-SCT. Specific tetramer staining of CD8+ T cells was shown for the majority of the novel MiHAs, and peak frequencies coincided with the development of clinical responses in the patients. Despite staining of the respective T-cell clones (data not shown), no tetramer-positive T cells were detected in the samples of patient Z using LB-APOBEC3B-1K and LB-EBI3-1I tetramers. Intermediate TCR avidity, as expressed by the intermediate EC50 value for recognition of APOBEC3B-derived peptides, may cause the lack of detection of the LB-APOBEC3B-1K–specific T cells. The absence of tetramer-positive T cells for LB-EBI3-1I may be explained by a low frequency of circulating T cells. Whereas the individual contribution of each MiHA-directed T-cell response cannot be determined, the induction of strong GVT reactivity and the absence of severe GvHD in both patients suggest involvement of one or more MiHAs with selective or predominant expression in malignant hematopoietic cells.
In conclusion, we present an efficient WGAs-based strategy for broad characterization of MiHAs. Our WGAs approach is valuable as a high-throughput method for detailed analysis of the specificity and diversity of T-cell responses in patients with different clinical responses as well as for selective identification of clinically relevant MiHAs with hematopoietic restricted expression.
We thank Lourdes Sampietro for help with the bead array analysis, Quinta Helmer for data file processing, Menno van der Hoorn and Guido de Roo for flow cytometric cell sorting, and Dirk van der Steen for tetramer production.
Grant Support: Dutch Cancer Society grant no. 05-3267 (C.E. Rutten) and European Union 6th Framework Programme, Allostem project no. 503319 (M. Griffioen).
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Guest Articles.
Emma Colenbrander
How Will Last-Mile Distributors Adapt to and Survive the COVID-19 Crisis?
Editor's note: This article is part of NextBillion's series "Enterprise in the Time of Coronavirus," which explores how the business and development sectors are responding to the pandemic. For news updates and analysis, virtual events, and links to useful resources related to the COVID-19 crisis, check out our coronavirus resource page.
COVID-19 is creating significant challenges for last-mile distributors (LMDs) around the world. At the Global Distributors Collective (GDC) we've spent the last few weeks consulting our members to understand the impact of COVID-19 on their businesses, how they are responding and what support they need.
In the face of unprecedented uncertainty, LMDs are proving to be both nimble and resilient. But – like many businesses – they urgently need financial and technical support to survive this crisis and to protect their ability to deliver impact as the crisis abates.
A Dramatic Slow-Down in Operations
Based on intel from our members, nearly all LMDs have scaled back or ceased operations completely because of government lockdowns, reduced access to communities, and/or precautions that members themselves are taking to protect their staff and customers. Many LMDs are also having trouble procuring stock because of affected supply chains – e.g., products getting stuck at port.
Some LMDs have been exempt from lockdowns and allowed to operate under the classification of essential service providers. In countries that have yet to implement lockdowns, some are continuing to trade while adhering to social distancing and taking other precautions. But many are planning for hibernation, and their immediate priority is conserving cash.
In general, LMDs report lower customer demand as a result of reduced incomes. Additionally, among the many LMDs that sell on credit, more customers are missing repayments, increasing default risks and exacerbating working capital constraints. But this isn't true across the board: Some of our members report that demand has remained stable or increased. This is primarily due to people spending more time at home (therefore seeking lighting and entertainment products), stockpiling essential goods (particularly cooking fuels), or being disconnected from services (increasing their need for products like water purifiers).
Supporting Staff, Agents and Customers
In situations where staff or agents are unable to work, LMDs are trying to keep them on payroll so they can continue to support their families – and so LMDs can retain their business capacity. It is particularly difficult to pay agents whose incomes are commission-based, and to keep staff engaged and motivated. But LMDs are finding creative ways to manage, for example by deploying field staff in other areas of the business and developing remote customer support capabilities.
Most LMDs are focusing on maintaining communication with customers and keeping them informed about the crisis, including sharing information about preventative measures – for instance, through SMS texts. Many LMDs are exploring how to re-organise payment terms, or delay payments, for customers experiencing hardship.
Helping LMDs to Adapt
Nearly all LMDs have cut non-essential costs and undertaken some form of scenario planning. Some have been able to negotiate extended or delayed payment terms on existing loans or stock purchases.
Where in-person sales are still possible, LMDs are focusing on areas where demand is highest (e.g.: in villages that are now growing, as the pandemic drives rural migrants out of cities back to their villages). Where in-person sales are no longer possible, LMDs are pivoting to online sales or sales via call centres, delivering products by post and providing customers with remote support.
LMDs are also positioning themselves to rebound as quickly as possible when the situation eases. As well as focusing on staff and agent retention, they are building up stock supplies, particularly in field locations close to customers. Many are continuing with their marketing activities, aware of the need to exercise sensitivity given the challenges that poor consumers are currently facing. LMDs that usually rely on in-person marketing are turning to radio, TV, printed and online press, and community/loudspeaker announcements. One LMD has set up a consumer referral program via SMS, to compensate for lost leads from word-of-mouth marketing.
This is new territory for many LMDs, and they have a growing need for technical assistance in digitising operations, providing remote support to customers, and testing new types of marketing so they can continue to operate. Support with crisis management – particularly scenario planning, financial management and risk mitigation – would also help, so they can identify areas for both cost-cutting and continued investment to protect their business capacity.
The GDC has a dedicated resource page, bringing together a curated set of resources specifically designed to support members. But additional focused, tailored support for LMDs is also needed, in the form of virtual trainings and simple downloadable tools, and through in-depth one-on-one mentoring.
A Role for LMDs to Distribute Essential Supplies
LMDs could also play a vital role in distributing critical supplies during the pandemic. However, country-level responses are being coordinated by governments and UN agencies that are often not aware of LMDs or their capabilities – such as the ability to communicate with customers at scale – which could be redeployed to support crisis response.
Nevertheless, these collaborations are happening. One GDC member is partnering with Unilever and DFID to distribute essential health/hygiene supplies and consumer goods, leveraging a network of 1,000 frontline health workers. Many other LMDs are eager to distribute products like face masks, sanitizers and soap, but there are challenges around sourcing quality products, and pricing or subsidising them appropriately.
We know of three LMDs who have raised funds to engage in free distribution of off-grid solar and water purification products, in response to the crisis. Several have partnered with INGOs to facilitate the delivery of food parcels. And other LMDs are exploring options to distribute solar systems and refrigerators to health centres.
The Urgent Need for Relief Funding
LMDs are looking at their cash runways, and understandably they are nervous. Most LMDs are small companies with little or no reserves. Relief funding, in the form of both grants and concessional debt, would prevent many LMDs from becoming insolvent, helping to protect their employees' jobs and their business capacity to deliver by covering fixed costs and ensuring stock availability.
Social impact investors are developing emergency loan facilities to support these enterprises, which could be tremendously beneficial. But taking on additional debt – even highly concessional debt – could make LMDs less attractive to future investors, reducing their chances of securing much-needed funding after the crisis. It could also force them to pivot to a model which prioritises profits over serving the poorest/most remote customer segments.
Emergency grant funding linked to ongoing salary payments or proof of other fixed costs would put LMDs in a stronger position to recover and attract investment after the pandemic has passed, ensuring they can continue to have an impact in last-mile communities. Funding could be made available on a strictly time-limited basis, linked to the imposition of lockdown conditions, and only offered to companies that were clearly viable prior to the crisis, in order to minimise the risk of market distortion.
Taking a Long-Term Perspective
The COVID19 crisis is fundamentally time-limited, but LMDs and their supporters need to take a longer-term view. Our members are asking us for support to manage this difficult period, but they are also asking us to continue with our "business as usual" activities, like providing training services, facilitating peer-to-peer learning, and generating marketing intelligence. One LMD told us that the huge volume of (well-intentioned) communications they were receiving about the crisis from the international development community was making their staff feel helpless and demotivated. Another LMD reported that an investor had pulled out of a transaction due to nervousness around COVID-19.
It is true that LMDs are at risk of becoming insolvent, and the longer the situation continues, the greater the risks become. But we won't be in crisis mode forever, and if LMDs get the right financial and technical support now, they will be in a strong position to bounce back.
What LMDs need more than ever is confidence in their resilience, their adaptability, and their capacity to serve last-mile communities. So please ask yourself what you can do to support the LMD sector through this crisis, and get in touch if you are interested in working with the GDC and our members – we'd love to chat.
Emma Colenbrander is Head of the Global Distributors Collective (GDC)
Photo courtesy of EU Civil Protection and Humanitarian Aid.
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Blog 2015 March Ukiah Valley Medical Center ...
Ukiah Valley Medical Center Appoints David R. Ploss, M.D., Cardiologist, as Chief Medical Officer
Mar 5, 2015 General
UKIAH, CA -- Local Cardiologist, David R. Ploss, M.D. has been appointed as Ukiah Valley Medical Center's (UVMC) new chief medical officer (CMO). As UVMC's senior physician leader, Dr. Ploss will help design, implement and ultimately oversee the organization's clinical quality, patient safety and performance improvement initiatives.
"It is exciting to have Dr. Ploss be part of our executive team during this crucial time at UVMC as we expand our ER/ICU and Trauma Center, form and build on relationships with community physicians, and pave the way for the future of health care in Mendocino county," said Gwen Matthews, president and chief executive officer of UVMC.
"Dr. Ploss' impressive credentials and experience, as well as his passion for excellence, will bring great value to our executive leadership team," shares Matthews. "I would like to thank Dr. Marvin Trotter for his service as CMO. We have made great strides in improving physician relations and patient care under his leadership. We are excited to see how Dr. Ploss can build on those successes."
Dr. Ploss is a cardiologist with twenty years of experience. He earned his medical degree in 1987 from Tufts University School of Medicine in Boston, Massachusetts. After completing a residency in internal medicine at University of California San Francisco he went on to complete a fellowship in cardiology at California Pacific Medical Center in San Francisco, CA. He then completed a second fellowship in cardiac electrophysiology at the West Los Angeles VA Medical Center in Los Angeles, CA.
Dr. Ploss left his vibrant practice of the Pacific Heart Group in Eureka to join the Adventist Heart Institute in Ukiah in 2014 and has since then grown the practice to include locations in Willits and Garberville. While a member of the medical community in Humboldt County, he served as Chief of Staff and Director of the Cardiac Catheterization Laboratory at St Joseph Hospital. Also, in tandem with the local Community Health Clinic System and the local hospitals, he helped to develop and direct a community Congestive Heart Failure Clinic. Prior to this, Dr. Ploss was in Dayton, Ohio where he developed the cardiac electrophysiology services at the Dayton Heart Center.
Dr. Ploss brings with him years of excellence and experience in medical practice as well as physician leadership. He is an active member of the Heart Rhythm Society, American College of Cardiology and the California Medical Association. He is interested in the arts and local politics and previously served as president of the Redwood Art Association.
Dr. Ploss believes that learning and leveraging his colleagues' knowledge and talents is the key to providing excellent patient care to the community. "I'm honored and excited to take on this new role. I look forward to working with my peers and the executive team to continue to improve our quality of care to make UVMC the best place to work and get care."
When not seeing patients, Dr. Ploss enjoys traveling, local politics, and the arts.
Adventist Heart Institute is an integrated heart center made up of a team of experienced cardiologists and cardiovascular surgeons who provide a coordinated continuum of care to patients in Lake, Mendocino and Napa counties. To learn more, visit www.AdventistHeart.org. To schedule an appointment, please call (707) 463-2400.
-- UVMC --
Ukiah Valley Medical Center is part of Adventist Health, a faith-based, not-for-profit integrated health care delivery system serving communities in California, Hawaii, Oregon and Washington. Our workforce of 28,900 includes more than 21,200 employees; 4,500 medical staff physicians; and 3,200 volunteers. Founded on Seventh-day Adventist health values, Adventist Health provides compassionate care in 19 hospitals, more than 170 clinics (hospital-based, rural health and physician clinics), 14 home care agencies, six hospice agencies and four joint-venture retirement centers. We invite you to visit www.uvmc.org for more information.
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Johnny Cecotto, de son vrai nom Alberto Cecotto Persello (né le 25 janvier 1956 à Caracas), est un coureur moto et pilote automobile vénézuélien d'origine italienne. Il s'est fait connaître en tant qu'adolescent prodige en 1975 lorsqu'il devient le plus jeune champion du monde de vitesse moto catégorie  à  et . Malgré un début de carrière prometteur, il subit de nombreuses blessures et problèmes mécaniques qui entravent son succès dans les courses de Grand Prix moto.

À , Cecotto se tourne vers la course automobile en tant que pilote de Formule 1. Il devient ensuite coureur de voitures de tourisme à succès. Il est le dernier d'un groupe restreint de pilotes qui ont concouru au plus haut niveau en moto et en course automobile, qui comprend entre autres John Surtees et Mike Hailwood.

Il est aussi le premier champion du monde originaire du continent américain.

À l'occasion du  anniversaire de la  en 1991, l'American Motorcyclist Association a convoqué un panel de journalistes de la presse motocycliste et d'anciens coureurs, qui ont qualifié la course de Johnny Cecotto en 1975 de « meilleure performance des 50 premières années de cette compétition ».

Carrière en moto
Cecotto naît à Caracas de parents immigrés italiens. Son père, propriétaire d'un magasin de motos, a remporté le championnat national vénézuélien sur une Norton . Il commence à courir à  en Amérique du Sud au guidon d'une Honda CB 750 Four et d'une Kawasaki 3 cylindres avant de gagner le soutien de l'importateur vénézuélien Yamaha.

Sur une Yamaha 350 TZ il remporte le championnat national vénézuélien de course sur route en 1973 à . Il défend avec succès son titre en récupérant le championnat national en 1974 et remporte également le championnat sud-américain de courses de motos sur route en 1974.

1975 - Déjà au sommet
Cecotto acquiert une notoriété internationale lors de l'épreuve des  de Daytona le 9 mars 1975, une des courses les plus inspirées de l'histoire de l'événement. À l'époque, la Daytona 200 est considérée comme l'une des courses de motos les plus prestigieuses au monde, attirant des champions du monde tels que Giacomo Agostini et Barry Sheene.

Cecotto arrive à Daytona en tant que recrue inconnue avec une  non modifiée sponsorisée par Venemotos, l'importateur vénézuélien de Yamaha. L'adolescent se qualifie en première ligne, à côté du poleman Kenny Roberts, de , Teuvo Länsivuori et Steve Baker.

Alors que Cecotto prend place sur la grille de départ, les officiels de la course remarquent qu'une flaque de liquide se forme sous sa moto et, à quelques instants du début de la course, prennent la décision de retirer Cecotto et sa moto de la grille pour des raisons de sécurité. Alors que la course commence, les officiels découvrent que le liquide n'est que de l'eau débordant du radiateur et qu'elle ne présente aucun danger pour la sécurité ; ils lui permettent de réintégrer la course depuis la dernière place. Cecotto,en seulement un tour, dépasse la moitié du peloton, deux tours plus tard, il est remonté à la  place. Au cinquième tour, il est  et, à la fin du dixième tour, . Au  tour, il dépasse Agostini pour la troisième place avant que sa moto ne commence à surchauffer, l'obligeant à réduire son rythme et à se contenter d'une troisième place derrière le vainqueur Gene Romero et Steve Baker .

Un mois après, Cecotto se rend en Europe où il poursuit son ascension avec la victoire lors de la prestigieuse course du championnat de formule 750 d'Imola 200, devant Patrick Pons et Steve Baker. Il a profité toutefois de la casse du moteur d'Agostini et du retrait du champion américain Kenny Roberts en raison d'une blessure au poignet.

Les GP de la saison 1975
Le 30 mars au GP de France,  course  de la saison, après que l'officiel Yamaha Ikujiro Takaī ait mené depuis le début sur le circuit du Castellet, le jeune Vénézuélien le passe dans le dernier tour au bout de la ligne droite du Mistral et remporte la victoire pour sa première participation à un grand prix, ainsi que le meilleur temps au tour. À  et , Cecotto devient le plus jeune vainqueur de toute l'histoire des Grands Prix, battant le record établi par Mike Hailwood en 1959. Cecotto ajoute à son exploit en signant également le doublé, car il mène le GP 350 de bout en bout, battant Agostini de . Il n'avait initialement prévu de participer qu'à deux ou trois épreuves européennes mais, après sa performance au Grand Prix de France, il a obtenu un parrainage complet pour le reste de la saison à bord d'un ex-Agostini TZ350

Après un abandon, chaîne cassée, au GP d'Espagne en , Cecotto s'incline en  derrière Agostini. Au GP d'Autriche, en , une chute collective l'élimine dès le premier tour et un nouveau départ est donné. Cecotto devait y débuter en  mais sa chute en  l'en a empêché. En mai au GP d'Allemagne, victimes d'ennuis de carburation, les deux Yamaha d'usine d'Agostini et de  abandonnent en , laissant la victoire à Johnny Cecotto. Le weekend suivant au GP des Nations à Imola, parti dernier, Agostini en  fait une remontée spectaculaire pour finir deuxième derrière Johnny Cecotto. À mi-saison en  (4 courses encore à disputer), Cecotto mène donc avec  devant Agostini (39) et Braun (26). En  (6 courses encore à disputer), Villa mène avec  devant les Français Rougerie (37) et Pons (32).

Au Dutch TT, les pilotes japonais Takaī et Kanaya sont repartis au Japon et c'est Cecotto qui récupère la  d'usine, mais il abandonne après un serrage. En  Agostini ne peut faire mieux que  à cause de problèmes de pneus et Cecotto, parti dernier n'a pu remonter qu'en  position. Le Vénézuélien disposait pour la première fois d'un cadre italien Bimota.

Au GP de Belgique le 6 juillet, la course des  voit une bataille entre les Harley et la Yamaha de Cecotto. Au dernier freinage à La Source, Rougerie arrive en tête mais est gêné par Villa, ce qui permet à Johnny Cecotto de passer et de gagner.

Au GP de Finlande, Cecotto tombe en panne d'allumage et Walter Villa remporte le GP , confortant son avance sur le Vénézuélien qui devient le seul à pouvoir lui contester le titre. Villa a  contre 42 à Cecotto. Johnny Cecotto bat Agostini en  et se rapproche du titre que désormais seul l'Italien peut lui ravir. C'est la première victoire d'une machine à cadre Bimota.

Au GP de Tchécoslovaquie en  Cecotto a cassé son moteur et Villa, parti avec deux minutes de retard, ne peut finir que , mais la victoire de Braun au GP suivant (Yougoslavie) donne le titre à l'italien. Compétitif en  avec deux victoires, c'est une chute au Grand Prix d'Allemagne puis des problèmes de moteur sur sa moto qui le laissent à la quatrième place du classement final. Agostini casse au cinquième tour et Cecotto, alors en tête est assuré d'être le champion du Monde des  cette année. Malheureusement, il abandonne à son tour, sélecteur cassé. Mais avec 4 victoires et  il est champion du monde dès sa première participation au championnat.

À l'âge de dix-neuf ans, il est alors le plus jeune champion du monde, jusqu'à ce que Loris Capirossi remporte le championnat du monde  en 1990 à l'âge de .

Les années 1976 à 80
En 1976, Cecotto revient courir la Daytona 200, désormais avec le soutien total de l'équipe de course d'usine Yamaha. La course se transforme rapidement en un duel entre Cecotto et son coéquipier, Kenny Roberts. Mais, leur rythme effréné s'avère vite trop élevé pour leurs pneus et au  des 52 tours, Roberts doit ralentir à cause de l'usure de son pneu arrière. À neuf tours de la fin, le pneu de Roberts explose, lui faisant presque perdre le contrôle de sa machine avant de retourner dans les stands. L'équipe de ravitaillement de Cecotto tente alors de le faire rentrer dans les stands pour vérifier son pneu, alors qu'il reste trois tours à parcourir, mais il ignore leur signal, continue et gagne la course devant  (Kawasaki) et  (Suzuki). Par la suite, ses pneus déchiquetés ont montré à quel point il était sur le point de subir le même sort que Roberts.

Pour les GP de 1976, Cecotto évolue désormais aussi en catégorie  au guidon d'une Yamaha YZR500 de l'année précédente sous les couleurs d'un équipe satellite soutenue par Yamaha, Venemotos. Barry Sheene (Suzuki) est favori et doit être son principal concurrent de la saison. Il commence la saison en remportant une deuxième place prometteuse derrière Sheene lors du Grand Prix de France d'ouverture de la saison, mais Cecotto a eu du mal à maîtriser la Yamaha, chutant 13 fois lors des courses suivantes. Il ne réussit pas à marquer d'autres points après cette manche française et peu de temps après le Grand Prix d'Italie, il abandonne complètement les  pour se concentrer sur la défense de son titre . Il termine la saison  à une décevante  place alors que Sheene remporte le championnat avec sa Suzuki RG 500 Gamma. Il perd également sa couronne en  dans une bataille serrée avec Walter Villa et sa Aermacchi-Harley-Davidson.

Alors que Cecotto possédait un don naturel pour le pilotage, certains observateurs ont émis l'hypothèse qu'il avait gagné trop tôt dans sa carrière sans comprendre pleinement comment il l'avait accompli. Le directeur de l'équipe Yamaha et ancien champion du monde, Rodney Gould, a déclaré : "Je pense que Cecotto allait vite et ne savait pas vraiment pourquoi. Maintenant, il ne sait pas pourquoi il va plus lentement et chute". Les résultats de Cecotto ont également été affectés par la désorganisation et le manque de préparation de l'équipe Venemotos. Selon son mécanicien d'usine Yamaha, Vince French, à plusieurs reprises, l'équipe n'a pas rempli les formulaires d'inscription officiels à la course ou n'a pas réussi à sécuriser l'espace de garage, retardant ainsi le temps d'entraînement vital. À d'autres occasions, l'équipe n'a pas fourni l'équipement requis par les organisateurs de la course, ce qui a entraîné des retards supplémentaires.

En 1977, le Continental Circus retourne en Amérique du Sud pour la première fois depuis 1963. Ce sont les succès de Cecotto qui ont suscité l'organisation de ce nouveau GP du Venezuela. C'est également la première fois depuis le GP du Japon 1967 que les championnats du Monde sortent d'Europe. Il est peut-être déjà un peu tard, mais la Formule 750 accède enfin au statut de championnat du Monde.

Devant son public au  Grand Prix moto du Venezuela de l'histoire du championnat, Johnny Ceccoto remporte aisément la catégorie . José Cecotto, frère aîné de Johnny a abandonné.

Au  GP de la saison au Grand Prix d'Autriche , Cecotto est grièvement blessé dans un accident impliquant quatre coureurs et qui coûte la vie au coureur suisse . La course des  est la première de la journée. A mi-course, Jon Ekerold mène devant Franco Uncini, Cecotto, Dieter Braun et Patrick Fernandez. Dans une grande courbe, Uncini part en travers entraînant Cecotto dans sa chute. La Harley tape les rails et rebondit sur la piste fauchant Braun et Fernandez. Les suivants, alertés par les drapeaux, ralentissent sauf le Suisse Stadelmann qui percute une des motos au milieu de la piste. Il s'ensuit une grande confusion et un retard dans les secours qui provoqueront la colère des pilotes. Hans Stadelmann est mort sur le coup. Fernandez et Cecotto seront immobilisés de longues semaines et Braun, touché à l'œil, mettra un terme à sa carrière.

Johnny Cecotto se remet de ses blessures à temps pour le Grand Prix de Suède qu'il termine à la deuxième place, à 2,9 secondes du vainqueur Barry Sheene. En  Cecotto remporte ensuite deux courses consécutives en Finlande et en Tchécoslovaquie où il remporte aussi le Grand Prix . Bien qu'il ait raté la majeure partie de la saison (6 courses) en raison de ses blessures, il est quand même quatrième au classement final du championnat en  et  en .

Cecotto débute la saison 1978 en remportant une deuxième fois l'Imola 200 en Formule 750, en étant second en première manche derrière Christian Sarron et vainqueur de la seconde. Toujours en avril, a lieu la  édition du "Moto-Journal 200", la manche française du Championnat du Monde 750 au Castellet. Johnny Cecotto remporte l'épreuve, disputée en une seule manche, devant Kenny Roberts et Steve Baker.En Grand Prix, seules les Yamaha 500 de Cecotto et  sont aux couleurs de la Yamaha Motor Company, les autres machines officielles courent sous des couleurs différentes. Cecotto ne participe plus qu'en  mais il affronte un nouveau rival pour le championnat du monde avec l'arrivée de Kenny Roberts. Au Venezuela, ils ne sont que douze au départ des 500 et ne seront que sept à l'arrivée, Barry Sheene l'emporte devant son coéquipier du team Herron-Texaco-Suzuki GB, l'américain . Cecotto, Katayama et Roberts ont cassé.

Bien qu'il marque quatre podiums (2 fois  en Espagne et en Allemagne et une fois  en Finlande) et une courte victoire par 1/10e de seconde sur Roberts au Dutch TT de 1978, il ne réussit pas à obtenir des résultats cohérents et il subit en outre quatre pannes mécaniques (Venezuela, France, Italie, Belgique). Roberts remporte le championnat du monde devant Sheene et Cecotto troisième.

Cecotto a plus de succès en Formule 750, où malgré quatre victoires de Roberts, il a remporté trois victoires et trois deuxièmes places et s'assure ainsi de son deuxième titre mondial.

Décidemment maudit sur ce circuit, Cecotto chute lors du Grand Prix d'Autriche 1979 au Salzburgring. Une rotule fracturée l'écarte des circuits jusqu'à l'été. Il a rejoint le championnat pour les dernières courses mais, ses blessures lui faisant toujours mal, il n'a pas réussi à obtenir des résultats cohérents, mais marque quelques points en Finlande et en France. C'est donc Roberts qui remporte son deuxième championnat du monde  consécutif.

En Formule 750, pour la dernière année de ce championnat, bien qu'il ait remporté 5 manches, les absences de Cecotto à la moitié des courses le relèguent à la troisième place du classement final, derrière Patrick Pons (qui devient le premier Français champion du monde dans un sport mécanique) et le Suisse Michel Frutschi vice-champion.

En 1980, en raison du succès de Roberts pour l'équipe Yamaha et des performances en baisse de Cecotto, Yamaha lui retire son soutien après la saison 1979. Il court donc en tant que pilote privé sur une  Yamaha à châssis Bimota et sur une Yamaha de production dans la catégorie . Il commence bien l'année avec une victoire en  au Grand Prix des Nations à Imola, puis une seconde place au Grand Prix de France . Cependant, après son succès initial, ses motos ont subi de nombreuses pannes mécaniques et il ne peut ajouter qu'une  place en fin de saison en RFA. Il ne peut donc pas mieux faire qu'une quatrième place au championnat .

C'est encore pire en  avec aucun podium, ce qui ne lui vaut qu'une septième place au championnat de la catégorie.

Après la saison 1980, il décide d'arrêter la course de motos à l'âge de  pour poursuivre une carrière en course automobile. Il prend sa retraite en ayant participé à 63 courses et glané en seulement 6 ans de compétitions au niveau mondial, 23 victoires et 46 podiums dans 4 catégories.

Résultats en Grand Prix moto
Source:

Résultats moto - Formule 750

(*) Deux manches par course.

Carrière en auto

Formule 1 et 2

Après quelques tentatives en 1980 et 1981 avec les écuries Onyx Racing - Mike Earle Racing, Minardi et Horag Hotz Racing sur des voitures à châssis March ou Minardi et des moteurs BMW, Cecotto fait ses vrais débuts sur quatre roues avec Minardi dans le Championnat d'Europe de Formule 2 de 1982. Lors de cette saison complète au volant de la voiture de l'équipe March-BMW, il remporte trois courses et termine la saison à égalité pour la première place avec son coéquipier Corrado Fabi, mais est relégué au deuxième rang par le système du nombre de victoires. Néanmoins, sa performance a attiré suffisamment d'attention pour qu'on lui offre une place en Formule 1.

En Formule 1, Cecotto participe à 23 courses, débutant le 13 mars 1983 avec l'équipe Theodore Racing. Il effectue des débuts prometteurs puisqu'il obtient une sixième place dès sa deuxième course. Cependant, l'équipe souffre d'un manque de financement et il est contraint de s'absenter les deux derniers manches. Pour la saison 1984, il rejoint l'équipe Toleman avec Ayrton Senna comme coéquipier. Lors des qualifications du Grand Prix de Grande-Bretagne, il se casse les deux jambes dans un accident, ce qui met effectivement fin à sa carrière en Formule 1. Sa sixième place à Long Beach était le meilleur résultat d'un pilote vénézuélien jusqu'à la victoire de Pastor Maldonado au Grand Prix d'Espagne, 29 ans plus tard.

Voitures de tourisme

Après s'être remis de ses blessures, Cecotto reprend la compétition dans la catégorie florissante des voitures de tourisme du groupe A pour la célèbre équipe Schnitzer Motorsport BMW, son meilleur résultat est une  place aux 24 Heures de Spa 1985 avec Dieter Quester et Markus Oestreich. Il se rend ensuite en Australie où il termine deuxième du James Hardie 1000 de 1985 sur le circuit Mount Panorama à Bathurst, au volant de la BMW 635 CSi qu'il conduisait à Spa, remportant conjointement le prix "Rookie of the Year" avec son copilote Roberto Ravaglia.

En 1986, il rejoint l'équipe RAS Sport Volvo basée en Belgique dans le cadre du championnat FIA Touring Car au volant d'une Volvo 240T turbocompressée. Cecotto termine  du championnat avec deux victoires (Hockenheim et Zolder), deux deuxièmes et deux troisièmes places. Il a également conduit une 240T à la victoire lors de la Guia Race de 1986 lors du Grand Prix de Macao, ainsi que l'InterTEC 500 de 1986 à Fuji au Japon aux côtés d'Anders Olofsson.
Après que Volvo se soit retirée à la fin de la saison 1986, Cecotto rejoint BMW et participe au championnat du monde des voitures de tourisme 1987 au volant d'une BMW M3 de l'équipe italienne CiBiEmme aux côtés du co-champion ETCC 1985 Gianfranco Brancatelli. Le duo remporte la troisième manche du championnat, les 500 km de Bourgogne à Dijon-Prenois, avant d'être la première voiture immatriculée en WTCC à terminer la première manche australienne, la James Hardie 1000 de 1987. Bien que Cecotto et Brancatelli n'aient terminé qu'à la  place à Bathurst, en tant que première voiture enregistrée à terminer, a obtenu des points pour la première place. Cecotto termine à la  place avec Brancatelli au Championnat du monde des voitures de tourisme 1987 avec 158 points.

De 1988 à 1992, Cecotto participe à la Deutsche Tourenwagen Meisterschaft (DTM, championnat allemand de voitures de tourisme). Au volant d'une BMW M3 Schnitzer Motorsport, il a terminé deuxième de la saison 1990. Il effectue également plusieurs courses d'endurance et s'adjuge les 24 Heures de Spa 1990 et les 24 Heures du Nürburgring 1992. En 1994 et 1998, il gagne le championnat allemand Super Tourenwagen Cup pour BMW. En 1995, il a participé au British Touring Car Championship (BTCC) pour BMW. En 2001 et 2002, il passe à l'Irmscher Opel Omega et remporte le championnat allemand V8Star Series deux années consécutives.

Résultats en courses auto

Résultats complets du Championnat d'Europe de Formule 2
Source:(Les courses en gras indiquent la pole position ; les courses en italique indiquent le tour le plus rapide)

Résultats complets du championnat du monde de Formule 1
Source:

Résultats complets du Championnat d'Europe des voitures de tourisme
Source:

(key) (Races in bold indicate pole position) (Races in italics indicate fastest lap)

Résultats complets du championnat du monde des voitures de tourisme
Source:

† Bien qu'il ait terminé  à Bathurst, la voiture enregistrée en WTCC la mieux classée, Cecotto, a obtenu la  place pour la manche.

Résultats complets de la Deutsche Tourenwagen Meisterschaft/Masters
Source:

Résultats complets de la Coupe d'Allemagne GT
Source:

Résultats complets de la Super Tourenwagen Cup
Source:

Résultats complets du championnat britannique des voitures de tourisme

Résultats des 24 Heures du Mans
Source:

Résultats complets de la Bathurst 1000

Activités ultérieures
Cecotto consacre actuellement la majeure partie de son temps à soutenir la carrière de coureur automobile professionnel de ses fils, Johnny Cecotto Jr. et Jonathan Cecotto.

Références

Annexes

Voir aussi
 Formule 750
 Johnny Cecotto Jr

Liens externes
 Johnny Cecotto official fan site
 Johnny Cecotto career statistics at MotoGP.com
 Johnny Cecotto sur WikiF1
 Johnny Cecotto sur DriverDB
 Johnny Cecotto sur RacingSportsCars
 Cecotto Home Page - Site officiel de Jonathan Cecotto

Pilote automobile vénézuélien
Pilote de moto vénézuélien
Pilote de DTM
Naissance en janvier 1956
Naissance à Caracas
Pilote de Formule 1
Pilote de Formule 2
Pilote Hart (moteur)
Pilote des 24 Heures du Mans
Pilote Championnat de Grande-Bretagne des voitures de tourisme
Champion du monde de vitesse moto
Vainqueur des 24 Heures de Spa
Vainqueur des 24 Heures du Nürburgring

redpajama_set_name: RedPajamaWikipedia


à à 쯳pan>Booker Foster was the last child of William è¥ Elder毳ter and Ann Booker.쯳pan>He was born ca 1764 in Amelia County, Virginia. He has been reported to have died in Maury County, Tennessee.쯳pan>He married Tabitha (has been reported as Susannah, are as Susannah (Foster?).꼯span>They (whoever she was) probably married ca 1775 as their first child was born ca 1777. Tabitha died after 1828.


text:
Pope Francis's Encyclical and an Urgent Response to Poverty
by Sister Simone Campbell
This post first appeared at the Talk Poverty blog.
Pope Francis waves as he is driven through the crowd ahead of his weekly general audience in St. Peter's Square, at the Vatican, Wednesday, Feb. 26, 2014. (AP Photo/Felipe Dana)
Pope Francis's historic, soaring encyclical on ecological and economic justice was made public just hours after the horrifying murders in the South Carolina church, where nine African-Americans were gunned down by a young white man. The juxtaposition makes me weep in the realization that such violence is yet more evidence of a brokenness in our world described so eloquently by the pope.
Pope Francis calls on all of us, especially those in power, to find bold, integrative solutions to all of these injustices.
In his encyclical, Pope Francis emphasized the importance of our interconnectedness. "Everything is connected. Concern for the environment thus needs to be joined to a sincere love for our fellow human beings and an unwavering commitment to resolving the problems of society." He also returned again and again to the injustice of inequality and "the intimate relationships between [people who are] poor and the fragility of the planet."
The encyclical strongly criticized consumerist, profit-seeking economies like ours as economies of exclusion, where short-term gains take precedence over long-term justice. Those who are left out – most often people who have been pushed into poverty – are denied just access to water, food, housing and other necessities of life, which are all basic human rights. Marketplace solutions favored by many will not address these needs, and the desire of some to privatize water and other resources will cause enormous harm to already struggling families.
Those who push technology as the answer to many of our problems are usually seeking short-term results, most often higher profits, at the expense of those at the economic margins. We see the results when low-income workers lose jobs to technology substitutes thought to improve efficiency and lower costs.
And, of course, it is most often poor communities that suffer the most from environmental degradation. People in poor communities are more often exposed to pollutants than those in wealthy areas, and they are less able to afford insurance and other protections during extreme weather events.
Pope Francis calls on all of us, especially those in power, to find bold, integrative solutions to all of these injustices. Those with the most wealth and power owe a "social debt" to people at the margins. They are therefore obligated to make sure they have all that is essential to their survival and wellbeing.
As the pope puts it, "Society as a whole, and the state in particular, are obliged to defend and promote the common good. In the present condition of global society, where injustices abound and growing numbers of people are deprived of basic human rights and considered expendable, the principle of the common good immediately becomes, logically and inevitably, a summons to solidarity and a preferential option for the poorest of our brothers and sisters."
In the end, the pope is calling for spiritual conversion and "an unwavering commitment to resolving the problems of society." Persistent poverty is one of our nation's most urgent problems, and it deserves an urgent response.
Sister Simone Campbell, SSS, is the executive director of NETWORK Lobby for Catholic Social Justice in Washington, DC, and the leader of Nuns on the Bus. As a lawyer and an advocate, she lobbies on issues of health care, economic policy and immigration reform. Follow her on Twitter: @sr_simone.
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TOPICS: Activism, Environment, Inequality
TAGS: catholic church, climate change, nuns on the bus, pope francis, sister simone campbell, widget