Work continued Tuesday on the new Gale Force roller coaster. The structure rises 125 ft from the sidewalk.Tuesday’s cloudy skies, light rain and less than gale force winds didn’t stop construction of the new Gale Force roller coaster at Playland’s Castaway Cove.Pieces of the new rails were still on the ground while work continued on the structural steel frame of the new 125-ft. attraction.Sections of rail, imported from Italy, rest alongside the steel frame of the new Gale Force roller coaster.Clay LaRosa, his brother Frank and a crew from La Rosa Construction were working on the concrete foundation and footings of the coaster when an OCNJDaily reporter visited the site.“If you look at all of the curves and angles of the steel, you realize something like this could not be built before the advent of the computer,” Clay said. “This isn’t the kind of design you can do with a pencil.”Imagined and designed by Castaway Cove owner Scott Simpson, Sansei Technology of Utah is overseeing construction. They also handled construction of the Cove’s landmark Double Shot ride.“The structural steel came from China and the rails came from Italy,” LaRosa said of the ride. “It’s not easy to (construct) but when it’s done it will be an engineering marvel.”A second coaster will be build alongside and through the Gale Force, he said, providing an extra thrill for those enjoying each ride.The Gale Force will replace the Python, Castaway Cove’s old, much smaller roller coaster.Upon completion, the new ride will be tested using human weight dummies before it is licensed to carry actual patrons. Will LaRosa be among those?“No!” he said with a laugh. “I’m too old.”Thrill Seekers – Prepare for some fun.View from the boardwalk.
Source:https://labblog.uofmhealth.org/lab-report/researchers-pinpoint-new-subtype-of-prostate-cancer Jun 14 2018Tumors with alterations in the CDK12 gene were more responsive to immunotherapy, suggesting precision medicine approachResearchers led by the University of Michigan Rogel Cancer Center have identified a new subtype of prostate cancer that occurs in about 7 percent of patients with advanced disease.The subtype is characterized by loss of the gene CDK12. It was found to be more common in metastatic prostate cancer compared to early stage tumors that had not spread.Tumors in which CDK12 was inactivated were responsive to immune checkpoint inhibitors, a type of immunotherapy treatment that has overall had limited success in prostate cancer.”Because prostate cancer is so common, 7 percent is a significant number. The fact that immune checkpoint inhibitors may be effective against this sub-type of prostate cancer makes it even more significant. This is an exciting prospect for patients who have CDK12 alterations and may benefit from immunotherapy,” says senior study author Arul Chinnaiyan, M.D., Ph.D., director of the Michigan Center for Translational Pathology.Researchers at the Rogel Cancer Center will lead a multisite clinical trial to assess checkpoint inhibitors as a treatment for metastatic prostate cancer with CDK12 loss.In this study, published in Cell, researchers looked at DNA and RNA sequencing data from 360 tumor samples from patients with metastatic castration-resistant prostate cancer. This is an aggressive, advanced form of the disease in which the cancer has spread throughout the body and no longer responds to traditional hormone-based treatments. Tumor samples were from U-M’s Mi-ONCOSEQ program and from samples collected through the Stand Up to Cancer-Prostate Cancer Foundation Dream Team.Researchers found loss of CDK12 in only about 1 percent of early prostate cancer samples. That jumped to 7 percent for metastatic cancer, which indicates a more-aggressive form of the disease.Related StoriesResearchers identify potential drug target for multiple cancer typesEmbrace your natural skin tone to prevent skin cancer, say expertsNew research links “broken heart syndrome” to cancer”It suggests that those early stage patients who have CDK12 loss are the ones who will develop metastatic disease. This could be a harbinger in early cancer,” Chinnaiyan says.By following the mechanism of how CDK12 loss impacts the cell, researchers found a process in which cells create neoantigens that are foreign to the immune system. This boosts immune-fighting T-cells, which may explain why these patients benefit from immune checkpoint blockade.This suggests that a precision medicine approach to prostate cancer could help better direct immunotherapy treatment. It could also explain why some prostate cancer patients have had exceptional responses to immunotherapy while the treatment has had lackluster results overall in prostate cancer.The team had first recognized a possible role for CDK12 in a 2015 paper that evaluated the genomic landscape of advanced prostate cancers. CDK12 has also been linked to ovarian cancer.Little is known about CDK12 on a molecular basis but scientists do know that CDK12 regulates several critical cellular processes and is essential for development. Eliminating it is likely lethal to most cell types. So why can tumors lose CDK12 and survive? Researchers suspect cancer must inherit something that allows it to grow in the face of CDK12 loss. More study is needed to understand this.”This very promising study suggests that CDK12 loss may be a biomarker for identifying prostate cancer patients who may respond to checkpoint immunotherapy,” says Howard Soule, Ph.D., executive vice president and chief science officer of the Prostate Cancer Foundation. “The Prostate Cancer Foundation is proud to have funded this team, which continues to make foundational strides in identifying actionable genomic mutations in prostate cancer and using this information to identify new classes of precision treatments that can be used to improve the lives of men with prostate cancer.”