Category Archives: Cf

Calgarians are invited to enjoy a safe and fun-filled holiday mini-putt experience presented by Cadillac Fairview

CALGARY, AB, Nov. 4, 2021 /CNW/ - Cadillac Fairview (CF) is continuing with its traditions of spirited and engaging community experiences to deliver holiday cheer to Calgarians by transforming a portion of its parking lot into Frozen Fairways, an outdoor activity that merges two sports that are popular among Canadians: golf and hockey. From November 17 to 21, Calgarians are encouraged to safely take part in the five day holiday mini-putt experience that replaces a putter, greens and balls with a hockey stick and puck and artificial ice. Frozen Fairways features nine-holes, each with exciting Canadian twists including beloved activities like hockey and curling, and cultural staples like icing fishing and sugar shacks. Participants can reserve their time slot by pre-booking online. Tickets are $5 each and will go on sale starting on November 5. All proceeds from ticket sales will benefit local charities.

CF Chinook Centre logo (CNW Group/Cadillac Fairview Corporation Limited)

Additionally, Cadillac Fairview and RBC Loyalty & Rewards have come together to offer RBC credit cards exclusive perks, including advance to tickets, waived entry fees and more.

CF Chinook Centre continues to follow Alberta health guidelines with safety as a top priority for its community of guests and employees by integrating extensive health and safety measures in all of its holiday programming. As an outdoor event, the Frozen Fairways experience has enforced physical distancing measures, pre-screening (at home and onsite), regular and frequent sanitation procedures and minimized contact wherever possible. Additionally, to limit the number of guests visiting the activation and to minimize crowding, the experience is only accessible to guests via online registration. Each reservation includes one round of mini putt at the Frozen Fairways and groups will face off ten minutes apart. All guests are encouraged to wear masks and practice physical distancing on and off the course.

Story continues

Calgarians of all ages are welcome to participate in this shareworthy, festive and limited-time activity bringing family and friends together in a reimagined, safe and enjoyable way.

What:

CF Frozen Fairways

Where:

CF Chinook Centre Wednesday, November 17 to Sunday, November 21, 2021

Interview Opp:

Interview with Paige O'Neill, General Manager, CF Chinook Centre

Onsite Photo Opp:

Calgarians celebrate the holiday season at CF Chinook Centre's magical Frozen Fairways; imagery of Canadian-inspired Frozen Fairways mini-putt course.

For more information, event hours and to make reservations,visit https://shops.cadillacfairview.com/holiday.

About Cadillac FairviewCadillac Fairview (CF) is a globally focused owner, operator, investor, and developer of best-in-class real estate across retail, office, residential, industrial, and mixed-use asset classes. Wholly owned by the Ontario Teachers' Pension Plan, CF manages in excess of $35 billion of assets across the Americas and the United Kingdom, with further expansion planned into Europe and Asia.

Internationally, CF invests in communities with like-minded partners, including Stanhope in the UK, Lincoln Property Company in the U.S., and Multiplan in Brazil. The company's Canadian portfolio comprises 68 landmark properties, including the Toronto-Dominion Centre, CF Toronto Eaton Centre, Tour Deloitte, CF Carrefour Laval, CF Chinook Centre, and CF Pacific Centre.

Continually striving to make a positive impact in communities where it operates by promoting social connection, growth, and a sustainable future, CF's Purpose is Transforming Communities for a Vibrant Tomorrow. Learn more at cadillacfairview.com and follow CF on LinkedIn.

SOURCE Cadillac Fairview Corporation Limited

Cision

View original content to download multimedia: http://www.newswire.ca/en/releases/archive/November2021/04/c8531.html

See original here:

CF Chinook Centre Hosts Frozen Fairways Inviting Shoppers to take in New Outdoor Sports Experience from November 17 to 21 - Yahoo Finance

One of Canadas CF-18 Hornet fighter jets will fly over Beardys and Okemasis Cree Nation in honour of Indigenous veterans.

The community plans to hold their National Indigenous Veterans Day ceremony on Nov. 8, with the RCMP fighter jet scheduled to fly by at around 11 a.m.

Typically, RCAF fighters only fly past communities on request. RCAF public affairs officer David Lavallee said they carefully consider each application before committing to a fly over.

We support where we can and where appropriate, Lavallee explained during an interview on Friday. Certainly, a commemoration for National Indigenous Veterans Day is something that were more than happy to support.

Lavallee said Indigenous people have played significant roles in all aspects of the Canadian Forces, citing Sgt. Tommy Prince of the Canadian Army as just one example. The RCAF, he explained, is always happy to honour that legacy.

They played an important role and made important contributions, and its important that we acknowledge that, he said. This is a way where we can do that, and were certainly happy to (offer) support.

The CF-18 will fly over the event at no lower than 500 ft above the highest obstacle on its route. The events are carefully planned, coordinated and controlled for public safety reasons, and can be cancelled due to bad weather or poor flying conditions.

Beardys Chief and Council have officially declared Nov. 8-11 as Veterans Week in the community. Events include a wreath laying ceremony and veterans fundraising dinner on Nov. 8, a veterans virtual round table discussion on Nov. 9, a virtual Remembrance Day ceremony on Nov. 10, and a Pipe Ceremony and in-person Remembrance Day ceremony on Nov. 11.

Go here to read the rest:

CF-18 Hornet to fly over Beardy's and Okemasis in honour of Indigenous veterans - Prince Albert Daily Herald

INGELHEIM, Germany--(BUSINESS WIRE)--Boehringer Ingelheim, IP Group, the UK Cystic Fibrosis Gene Therapy Consortium (GTC, consisting of researchers from Imperial College London and the Universities of Oxford and Edinburgh) and Oxford Biomedica (OXB), announced today that Boehringer Ingelheim has exercised its options on intellectual property and know-how from the partners to progress and further accelerate the development of a potential, new treatment option for patients with CF. In the partnership, IP Group, acting on behalf of the three GTC host Universities, is granting exclusive global rights to develop, manufacture, register, and commercialize this lentiviral vector-based gene therapy for the treatment of cystic fibrosis. The GTC is additionally contributing its knowledge in pre-clinical research and clinical gene therapy development. OXB is adding its leading competence in manufacturing lentiviral vector-based therapies to Boehringer Ingelheims expertise in the development of novel breakthrough therapies for respiratory diseases.

CF is a rare, progressive, life-threatening disease that results in severe dysfunction and persistent infections of the lung affecting 70,000 people worldwide. It is caused by a defective or absent protein that results from mutations in the CFTR gene. This innovative development partnership among academia, life science investors, pharma, and biotech focusses on the advancement of BI 3720931, a novel, replication deficient lentiviral vector, in an inhaled formulation, which selectively introduces a healthy CFTR gene into the relevant target cells.

Professor Eric Alton, Coordinator of the GTC, said: The novel lung-targeting technology we have developed has demonstrated high gene transfer efficiency in pre-clinical models and offers the possibility of repeated administration to maintain a therapeutic effect, a benefit that other viral-based gene therapies may not be able to provide. Our novel therapy has the potential to improve CFTR function and modify disease in all CF patients, independent of the more than 2,000 different known gene mutations. The immediate target is those patients who are not eligible for CFTR modulators. The GTC is very excited to have reached this milestone after 21 years of focused effort. We are very grateful to our wonderful team and those with CF who have supported us in many ways including taking part in the multiple trials. We would like to thank our funders, both past and present, including the Health Innovation Challenge Fund (a partnership between Wellcome and the Department of Health and Social Care) and Just Gene Therapy, as well as the CF Trust, National Institute for Health Research and the Medical Research Council.

Since 2018, Boehringer Ingelheim has sponsored research and development activities with the GTC and OXB. The shared success achieved with our partners in this potentially revolutionary project makes us confident that we can now further accelerate this highly innovative therapeutic approach, said Clive R. Wood, Ph.D., Corporate Senior Vice President and Global Head of Discovery Research at Boehringer Ingelheim. With our leadership in the discovery and development of therapies in respiratory diseases combined with the gene therapy and manufacturing knowledge of our partners, we aim to bring the next breakthrough to patients suffering from CF, who are desperately waiting for better options.

John Dawson, Chief Executive Officer of Oxford Biomedica, said: We have enjoyed working with Boehringer Ingelheim, IP Group, and the GTC since 2018. Building on the great progress made to date, we are delighted that Boehringer Ingelheim, one of the worlds leading respiratory medicine organizations, has chosen to exercise the option to license OXB lentiviral vector manufacturing technology for this highly innovative inhaled cystic fibrosis gene therapy formulation developed by the GTC. This partnership is central to our companys mission of delivering life changing gene therapies to patients and has the potential to provide a new therapeutic option for many cystic fibrosis patients globally.

Under the terms of the option and license agreement with Boehringer Ingelheim, originally announced in August 2018, Boehringer Ingelheim will pay IP Group, on behalf of the GTC, an option exercise fee, near term, success based development, regulatory and sales milestone payments as well as royalties on net sales. OXB will receive an option exercise fee of 3.5 million and will be entitled to payments in an aggregate amount of up to 27.5 million upon achievement of various development, regulatory and sales milestones, in addition to a tiered low single digit royalty on net sales of a cystic fibrosis gene therapy product.

David Ramsden, Chief Executive of the Cystic Fibrosis Trust said: It is great news that Boehringer Ingelheim have committed to the next stage of the development of a gene therapy treatment for people with cystic fibrosis. This is an important step as it brings hope to the whole cystic fibrosis community and in particular to those who dont benefit from the currently available medicines. All of those who have helped us to invest long term in the work of the UK CF Gene Therapy Consortium should be proud of what they have made possible.

Please click on the following link for Notes to Editors:

http://www.boehringer-ingelheim.com/press-release/cystic-fibrosis-genetherapy-development-option-excercise

See the original post:

Boehringer Ingelheim and Partners to Accelerate Development of First-In-Class Gene Therapy for Patients with Cystic Fibrosis - Business Wire

LOS ANGELES -- When the Dodgers acquired Trea Turner at the Trade Deadline on July 30, Gavin Lux walked into manager Dave Roberts office and offered to play the outfield. Lux had no previous experience in the outfield, having played his whole baseball career as either a shortstop or a second baseman, a skill set that made him one of the top prospects in baseball.

But Lux understood what the roster looked like and he wanted to find a way to get in the lineup. When he was sent down to Triple-A Oklahoma City at the end of August, Lux was understandably upset. Once he got to the Minors, he borrowed Zach Reks outfield glove and got to work. After just three games in the outfield at Triple-A, the Dodgers called him back up.

I think its a credit to him [being] willing to do whatever it takes to help us win, Roberts said before Wednesday's Game 4 of the National League Championship Series against the Braves. And its not easy to be in a position that you havent played a whole lot of, certainly in this stage, and on the heels of what happened yesterday. I mean, it takes a tough ballplayer to withstand that stuff.

As expected, Luxs adjustment to the outfield has come with its fair share of ups and downs. Even after Luxs costly misplay in Game 3, the Dodgers started him back in center field in Wednesday's 9-2 Game 4 loss. Batting in the five-hole, he finished 0-for-2 before being taken out for defense in the sixth.

Gavin is extremely talented and has been put in a position thats extremely difficult in playing a position hes never played before September and now in the playoffs, Dodgers right-hander Walker Buehler said. And in talking to him after [Game 3], I think hes going to learn a lot just on how to make that specific play. Gavins confident enough and talented enough to handle that kind of stuff.

That specific play came in the fourth inning when a ball bounced off his glove near the wall in right-center. It set up the Braves four-run inning and was ruled an error after a scoring change. The Dodgers came back to win Game 3, 6-5, with an eighth-inning rally.

It came in Luxs 10th career start at the position and also after Lux helped get the Dodgers out of a potential big frame earlier in the game when he caught an Ozzie Albies fly ball and threw to second base to retire Eddie Rosario for a double play. During that sequence, Lux showed off the instincts and speed that make the Dodgers comfortable with using the former top prospect in center field.

On Wednesday, Lux was involved in another critical play when Joc Pederson shot a flare into center field. Lux played the ball conservatively, and Pederson tallied an RBI single. Back on the mound, starter Julio Uras raised his arms up in frustration. The ball had a 40 percent catch probability, according to Baseball Savant. It also gave the Braves a four-run lead.

Changing positions this late into the season is indeed extremely difficult, but Lux has responded by becoming an integral part of the Dodgers lineup this October, going 3-for-14 with four walks. He wrapped up the regular season by hitting .360 after getting recalled from the Minors.

The outfield isnt necessarily the position for Lux moving forward, but it gives him the best chance to play. And the Dodgers are going to stick with him. Even if it doesnt always look natural.

I think hes a heck of a ballplayer, Roberts said.

When asked how many times hes watched Cody Bellingers tying homer in Game 3, Roberts said hes gone through it about a dozen times. The way he has relived the moment will probably surprise you.

Now with this thing called TikTok, its around everywhere, so my kids show me this stuff, Roberts said.

Wait, so does Roberts have his own TikTok?

No. No, he said with a smile. I might have a burner Twitter account, but I dont have a TikTok account.

Maybe thatll change if the Dodgers win the World Series.

See the original post here:

'Tough ballplayer': Lux learning CF on the job - MLB.com

NEW YORK The shifting nature of adaptation for Pseudomonas aeruginosa microbes found in the upper respiratory tract of cystic fibrosis patients with chronic rhinosinusitis may provide treatment clues that are not obvious from lung-centered microbial sampling, new research suggests.

"Our findings underscore the importance of infection-site biogeography to pathogen evolution and the relevance of the sinuses to overall CF respiratory health," co-senior and co-corresponding author Jennifer Bomberger, a microbiology and molecular genetics researcher at the University of Pittsburgh School of Medicine, and her colleagues wrote.

As they reported in a paper published in Cell Reports on Tuesday, the researchers used whole-genome sequencing, targeted 16S ribosomal RNA gene sequencing, "microbial identification after passive clarity technique" hybridization chain reaction (MiPACT-HCR)-based imaging, phenotyping, and other approaches to assess samples collected over time from half a dozen adult CF patients. Rather than analyzing lung sputum samples, they focused on less characterized P. aeruginosa communities in the upper respiratory tract, where early colonization occurs.

"Much of what we know about P. aeruginosa communities in cystic fibrosis is from sputum samples from the lungs," Bomberger explained in an email, noting that "our study is different in that we are analyzing P. aeruginosa evolution in the upper respiratory tract (i.e. sinuses)."

The team's results revealed distinct genomic features and adaptation events in the upper respiratory tract during different stages of infection and in relation to the size of the P. aeruginosa community considered.

Whereas early-stage infections involving large P. aeruginosa populations showed signs of selection related to the host environment and related treatments, leading to a rise in aggregation-prone bugs, later-stage infections tended to involve smaller, host-restricted population fragments that were prone to genome degradation and "mutator"-driven genetic drift effects.

"We propose that following initial adaptive evolution in larger populations under strong selection for aggregation, P. aeruginosa persists in small, fragmented populations that experience stronger effects of genetic drift," the authors reported.

The results hinted that MiPACT-HCR imaging or genome degradation signatures such as pseudogenization may help in distinguishing between P. aeruginosa populations in the process of selection and the genetic drift-prone populations found at later stages of the infection process.

Such differences in population size, structure, and evolutionary patterns may help in guiding therapeutic approaches, Bomberger noted, since P. aeruginosa populations with alterations that have arisen randomly through genetic drift are less likely to respond to targeted treatments, whereas populations under selection may be more amenable to therapeutic approaches targeting key mutations.

"This information would allow researchers and clinicians to know if the community is undergoing selection or more genetic drift and how likely mutations are to suggest selective pressures that could be effectively targeted therapeutically," she said.

More:

Cystic Fibrosis Sinus Infections Involve Microbes With Shifting Evolution Patterns - GenomeWeb

A unique interaction between CFTR the protein defective in people with cystic fibrosis (CF) and two pro-inflammatory proteins may explain why some CF patients develop liver disease, researchers reported.

Their work suggests that the CFTR protein can act as an anchor, bringing certain proteins including the pro-inflammatory beta-catenin and the p65 subunit of NF kappa B together to prevent their activation.

When CFTR is missing or dysfunctional, these proteins are activated, which can lead to the overgrowth of cells lining the bile ducts called biliary epithelial cells or BECs and cause liver inflammation. (Bile ducts are thin tubes that go from the liver to the small intestine.)

This missing interaction is at the core of the pro-inflammatory environment in the fibrotic liver it adds insult to injury and makes the disease worse, Satdarshan (Paul) Monga, MD, a professor of pathology and medicine at the University of Pittsburgh and the studys senior author, said in a university press release.

Findings were reported in the study -Catenin-1 NFB-CFTR interactions in cholangiocytes regulate inflammation and fibrosis during ductular reaction published in the journal eLife.

Why liver disease affects some CF patients is not well understood. A team led by researchers at the University of Pittsburgh investigated this, looking at how the expansion of biliary epithelial cells, an important repair process following liver injury or disease, is associated with inflammation and fibrosis.

Researchers created two different mouse models using genetic tools. The KO1 model had beta-catenin loss in both hepatocytes (the main functional liver cells) and in BECs (also known as cholangiocytes). The KO2 model had loss of beta-catenin only in hepatocytes.

Beta-catenin is well known to play a key role in hepatocyte proliferation, allowing for liver repair with injury or disease.

Mice in both models were exposed for two weeks to a special diet (choline-deficient, ethionine-supplemented diet) that induces liver injury. They were then allowed to recover on a normal diet, and assessed two weeks, three months, and six months later.

In both models, researchers saw a greater degree of cell death, inflammation, and fibrosis than was evident in wild-type (normal) mice. However, the two models seemed to show different recovery profiles.

Two weeks after switching to normal diet, KO1 mice continued to show greater injury due to problems with hepatocyte proliferation. Even six months later, KO1 mice had evidence of progressive ductular reaction a proliferation of reactive bile ducts induced by liver injury which is associated with inflammation and fibrosis. This suggested a morphology close to that seen in CF patients.

Analysis of beta-catenin levels and the expression (activity) of Ctnnb1, the gene which encodes beta-catenin, showed an absence of beta-catenin at the six-month assessment in KO1 mice. In contrast, in wild-type mice also given the injury-inducing diet, beta-catenin was detected and fibrosis seemed to resolve after two weeks on a normal diet.

Better repair with time was also evident in KO2 mice after moving to a regular diet. By six months, fibrosis seemed to have resolved in this model and Ctnnb1expression was comparable to that of wild-type mice. Ductular reaction had also resolved in KO2 mice at six months, although not at three months.

We observed highly divergent injury-repair responses in the two models. KO2 mice showed progressive repair through expansion of BEC-derived beta-catenin-positive hepatocytes, and resolution of inflammation, [ductular reaction] and fibrosis, the researchers wrote.

Beta-catenins lack in the BECs of the KO1 model was thought to cause sustained activation of the NF kappa B protein a crucial regulator of immune and inflammatory responses upon injury, leading to greater inflammation. NF kappa B is activated through the interaction of the beta-catenin protein with p65 (a subunit of NF kappa B).

In contrast, in KO2 mice that lacked hepatocytes but not beta-catenin, thebeta-cateninp65 complex was able to be re-established, thus preventing chronic [NF kappa B] activation, the researchers wrote.

KO2 show gradual liver repopulation with BEC-derived b-catenin-positive hepatocytes, and resolution of injury, they noted, which mice in the KO1 model did not.

Researchers next worked with liver tissue samples from multiple sources, including CF patients, to determine if the interactions seen in mouse models and cell studies could be replicated. Specifically, they were looking for how p65 and beta-catenin may be interacting with the CFTR protein.

Turning off, or stopping, expression of the CFTR gene so that no CFTR protein is produced led to a pronounced activation of p65, the researchers found. Liver tissue from a CF patient was also seen to have lower-than-usual levels of total beta-catenin.

Doing an experiment and confirming for the first time that what we saw in mice was also what we see in patients with cystic fibrosis was very exciting and validating, said Shikai Hu, the studys first author.

Based on these results, the team suggested that the CFTR protein acts as a molecular anchor, interacting with beta-catenin-1 and p65 to prevent their activation. When CFTR is absent or defective, as in CF, these proteins become activated and ultimately induce progressive liver inflammation and fibrosis.

We report a novel beta-catenin-NF kappa B-CFTR interactome in BECs, and its disruption may contribute to hepatic pathology [liver disease] of CF, the researchers concluded.

More studies are need, they added, to further understand the molecular changes caused by CF in the liver.

Excerpt from:

Liver Disease in CF Appears Linked to Problems in CFTR Protein - Cystic Fibrosis News Today

A Michigan State University College of Human Medicine researcher has been awarded a federal grant to study a gene therapy treatment for cystic fibrosis, a potential cure for the rare, lethal disease that afflicts more than 30,000 people in the United States and 70,000 worldwide.

Dr. Xiaopeng Li

The grant from the National Institutes of Health will allow a team of researchers led by Xiaopeng Li, PhD, an associate professor in the Department of Pediatrics and Human Development, to study how CFTR gene (the causal gene for cystic fibrosis) mutations in the small airways in the lungs of cystic fibrosis patients lead to life-threatening infections.

The funding $2.1 million over four years is critical for this research, Li said. One reason we got the grant is we have a lot of data to show this is a feasible approach to treating the disease.

Li will lead a team that includes College of Human Medicine researchers Jeremy Prokop and Christopher Waters. The team also includes four pulmonologists Reda Girgis, Susan Millard and John Schuen from Spectrum Health and Helen DeVos Childrens Hospital Cystic Fibrosis Center, and Ryan Thomas from MSU's College of Human Medicine.

Marrying basic science and clinical medicine is a goal that is driving the collaboration between MSU and Helen DeVos Childrens Hospital/ Spectrum Health, said John Schuen, MD, chair, Cystic Fibrosis Translational Research Program. This relationship has already led to significant grant opportunities and published literature. Together, we will help uncover important discoveries at the cellular level that we hope will benefit our CF patients in the future.

The Cystic Fibrosis Translational Research Program is sponsored by the MSU-Spectrum Health Alliance and the Hunt for a Cure Foundation. The collaboration between MSU and Spectrum Health highlights the importance of our outstanding and expanding research partnership in the area of cystic fibrosis, said B. Keith English, MD, chair of the colleges Department of Pediatrics and Human Development.

The significance of the small airways in cystic fibrosis patients has not been well studied, Li said. Previous research, however, has shown that cells in the small airways of cystic fibrosis patients do not secrete bicarbonate, a substance necessary to maintain a proper pH balance on the cell surface. As a result, Li said, cystic fibrosis patients tend

to develop thick mucus obstruction in the small airways, making them susceptible to bacterial infections, which can lead to respiratory failure and death.

For years, patients have had to spend hours using drug therapies and airway clearance. More recently, CFTR modulators have been approved by the FDA but still do not provide a cure, with life expectancy in the mid-40s. It is a genetic disease with over 2,000 mutations in the CFTR gene. CF is usually diagnosed in infancy but even adults can discover that their chronic cough or recurrent pancreatitis is actually CF.

The study will look at why the cystic fibrosis small airways are so vulnerable to infection and the feasibility of replacing the defective gene with a normal gene, a procedure that would be tantamount to a cure Li said.

Its a particularly devastating disease, he said. Hopefully, one day we can apply this treatment to human patients.

Research reported in this publication was supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health under Award Number R01HL153165. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Read more:

MSU, Spectrum Health partner on over $2M NIH gene therapy study for cystic fibrosis - MSUToday

- 96-week interim results of TRIKAFTA (elexacaftor/tezacaftor/ivacaftor and ivacaftor) study show no loss of pulmonary function in people with at least one F508del allele, a first for any CFTR modulator

- Real-world data from people treated with KALYDECO (ivacaftor) over approximately 6 years show lower rates of mortality, lung transplant and pulmonary exacerbations than comparator cohort -

- Additional presentations highlight safety and efficacy profile of TRIKAFTA -

BOSTON, October 19, 2021--(BUSINESS WIRE)--Vertex Pharmaceuticals Incorporated (Nasdaq: VRTX) today announced that five scientific abstracts about the companys portfolio of cystic fibrosis (CF) medicines will be presented at the 2021 North American Cystic Fibrosis Conference (NACFC) taking place virtually November 2-5, 2021.

Key data being presented include 96-week interim results from an ongoing TRIKAFTA open-label extension study in people with CF ages 12 years and older with F508del/Minimal Function (F/MF) or F508del/F508del (F/F) genotypes, showing that the favorable safety profile and clinically meaningful improvements in lung function, respiratory symptoms and CFTR function as measured by sweat chloride observed in the Phase 3 pivotal studies were maintained through an additional 96 weeks of treatment (Poster #681). Additionally, a post hoc analysis of the annualized mean rate of change in percent predicted forced expiratory volume in 1 second (ppFEV1) showed there was no loss of pulmonary function over 96 weeks in this CF population, which is a first for any CFTR modulator to date.

Also presented at this years conference are data on results from a retrospective study of patients with gating mutations ages 6 years or older treated with KALYDECO showing that people treated with KALYDECO over approximately six years of follow up had significantly lower rates of mortality, lung transplant and pulmonary exacerbations (PEx) compared to a cohort of patients that were not eligible for and not receiving KALYDECO treatment (Poster #178).

Story continues

"The data were presenting this year clearly demonstrate that our portfolio of CFTR modulators has truly transformed the CF treatment landscape," said Carmen Bozic, M.D., Executive Vice President, Global Medicines Development and Medical Affairs, and Chief Medical Officer at Vertex. "The long-term follow up data from TRIKAFTA in particular demonstrates the unprecedented treatment effect of this medicine and reinforces the high bar it sets for safety and efficacy. Were committed to continuing to serially innovate in our CF program until we reach our goal of bringing transformative medicines to everyone with this disease."

Additional Presentations

In addition to the studies noted above, other presentations at NACFC include:

INTERIM RESULTS FROM THE HELIO STUDY: Interim analysis of a study of the real-world clinical effectiveness of TRIKAFTA in people with CF age 12 years and older with at least one F508del allele who were ineligible for another CFTR modulator, demonstrating clinically meaningful improvements in lung function and nutritional status at 6 months. In addition, the annualized PEx rate was lower with TRIKAFTA treatment. These results are consistent with findings from pivotal clinical trials (Poster #56).

QUALITATIVE STUDY OF PATIENTS TREATED WITH TRIKAFTA AND CAREGIVERS: Results from an ongoing qualitative study to evaluate (1) the real-world patient experience of TRIKAFTA treatment from the perspective of people with CF and caregivers and (2) the impact of TRIKAFTA on the caregiver experience. The impact of the SARS-CoV-2 pandemic was also included in the assessment of the patient and caregiver experience. Results from this study demonstrate that TRIKAFTA has a meaningful and substantial impact on the daily lives of people with CF and caregivers, including the ability to cope with living through the SARS-CoV-2 pandemic (Poster #285).

INTERIM RESULTS FROM A PHASE 3 OPEN-LABEL EXTENSION STUDY OF CHILDREN WITH CF AGES 6 YEARS AND OLDER: An interim analysis at week 24 of an ongoing, 96-week, Phase 3, open-label extension study designed to assess the long-term safety and efficacy of TRIKAFTA in children 6 years of age and older with at least one F508del allele. Results were consistent with the previously established safety profile of TRIKAFTA in this age group. Results also showed robust and clinically meaningful improvements in lung function, respiratory symptoms, and CFTR activity as measured by sweat chloride and indicate TRIKAFTA provides long-term benefit in this younger patient population (Poster #562).

About Cystic Fibrosis

Cystic fibrosis (CF) is a rare, life-shortening genetic disease affecting more than 83,000 people globally. CF is a progressive, multi-organ disease that affects the lungs, liver, pancreas, GI tract, sinuses, sweat glands and reproductive tract. CF is caused by a defective and/or missing CFTR protein resulting from certain mutations in the CFTR gene. Children must inherit two defective CFTR genes one from each parent to have CF, and these mutations can be identified by a genetic test. While there are many different types of CFTR mutations that can cause the disease, the vast majority of people with CF have at least one F508del mutation. CFTR mutations lead to CF by causing CFTR protein to be defective or by leading to a shortage or absence of CFTR protein at the cell surface. The defective function and/or absence of CFTR protein results in poor flow of salt and water into and out of the cells in a number of organs. In the lungs, this leads to the buildup of abnormally thick, sticky mucus, chronic lung infections and progressive lung damage that eventually leads to death for many patients. The median age of death is in the early 30s.

About KALYDECO (ivacaftor)

In people with certain types of mutations in the CFTR gene, the CFTR protein at the cell surface does not function properly. Known as a CFTR potentiator, ivacaftor is an oral medicine designed to facilitate the ability of CFTR proteins to transport salt and water across the cell membrane. KALYDECO (ivacaftor) was the first medicine to treat the underlying cause of CF in people with specific mutations in the CFTR gene.

INDICATION AND IMPORTANT SAFETY INFORMATION FOR KALYDECO (ivacaftor)

KALYDECO (ivacaftor) is a prescription medicine used for the treatment of cystic fibrosis (CF) in patients age 4 months and older who have at least one mutation in their CF gene that is responsive to KALYDECO. Patients should talk to their doctor to learn if they have an indicated CF gene mutation. It is not known if KALYDECO is safe and effective in children under 4 months of age.

Patients should not take KALYDECO if they take certain medicines or herbal supplements, such as: the antibiotics rifampin or rifabutin; seizure medications such as phenobarbital, carbamazepine, or phenytoin; or St. Johns wort.

Before taking KALYDECO, patients should tell their doctor if they: have liver or kidney problems; drink grapefruit juice or eat grapefruit; are pregnant or plan to become pregnant because it is not known if KALYDECO will harm an unborn baby; and are breastfeeding or planning to breastfeed because is not known if KALYDECO passes into breast milk.

KALYDECO may affect the way other medicines work, and other medicines may affect how KALYDECO works. Therefore the dose of KALYDECO may need to be adjusted when taken with certain medications. Patients should especially tell their doctor if they take antifungal medications such as ketoconazole, itraconazole, posaconazole, voriconazole, or fluconazole; or antibiotics such as telithromycin, clarithromycin, or erythromycin.

KALYDECO can cause dizziness in some people who take it. Patients should not drive a car, use machinery, or do anything that needs them to be alert until they know how KALYDECO affects them.

Patients should avoid food containing grapefruit while taking KALYDECO.

KALYDECO can cause serious side effects.

High liver enzymes in the blood have been reported in patients receiving KALYDECO. The patients doctor will do blood tests to check their liver before starting KALYDECO, every 3 months during the first year of taking KALYDECO, and every year while taking KALYDECO. For patients who have had high liver enzymes in the past, the doctor may do blood tests to check the liver more often. Patients should call their doctor right away if they have any of the following symptoms of liver problems: pain or discomfort in the upper right stomach (abdominal) area; yellowing of their skin or the white part of their eyes; loss of appetite; nausea or vomiting; or dark, amber-colored urine.

Abnormality of the eye lens (cataract) has been noted in some children and adolescents receiving KALYDECO. The patients doctor should perform eye examinations prior to and during treatment with KALYDECO to look for cataracts.

The most common side effects include headache; upper respiratory tract infection (common cold), which includes sore throat, nasal or sinus congestion, and runny nose; stomach (abdominal) pain; diarrhea; rash; nausea; and dizziness.

These are not all the possible side effects of KALYDECO. Please click here to see the full Prescribing Information for KALYDECO.

About TRIKAFTA (elexacaftor/tezacaftor/ivacaftor and ivacaftor)

In people with certain types of mutations in the CFTR gene, the CFTR protein is not processed or folded normally within the cell, and this can prevent the CFTR protein from reaching the cell surface and functioning properly. TRIKAFTA (elexacaftor/tezacaftor/ivacaftor and ivacaftor) is an oral medicine designed to increase the quantity and function of the CFTR protein at the cell surface. Elexacaftor and tezacaftor work together to increase the amount of mature protein at the cell surface by binding to different sites on the CFTR protein. Ivacaftor, which is known as a CFTR potentiator, is designed to facilitate the ability of CFTR proteins to transport salt and water across the cell membrane. The combined actions of elexacaftor, tezacaftor and ivacaftor help hydrate and clear mucus from the airways.

INDICATIONS AND IMPORTANT SAFETY INFORMATION FOR TRIKAFTA

TRIKAFTA is a prescription medicine used for the treatment of cystic fibrosis (CF) in patients ages 6 years and older who have at least one copy of the F508del mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene or another mutation that is responsive to treatment with TRIKAFTA. Patients should talk to their doctor to learn if they have an indicated CF gene mutation. It is not known if TRIKAFTA is safe and effective in children under 6 years of age.

Patients should not take TRIKAFTA if they take certain medicines or herbal supplements, such as: antibiotics such as rifampin or rifabutin; seizure medicines such as phenobarbital, carbamazepine, or phenytoin; St. Johns wort.

Before taking TRIKAFTA, patients should tell their doctor about all of their medical conditions, including if they: have kidney problems, have or have had liver problems, are pregnant or plan to become pregnant because it is not known if TRIKAFTA will harm an unborn baby, or are breastfeeding or planning to breastfeed because it is not known if TRIKAFTA passes into breast milk.

TRIKAFTA may affect the way other medicines work, and other medicines may affect how TRIKAFTA works. Therefore, the dose of TRIKAFTA may need to be adjusted when taken with certain medicines. Patients should especially tell their doctor if they take: antifungal medicines including ketoconazole, itraconazole, posaconazole, voriconazole, or fluconazole; antibiotics including telithromycin, clarithromycin, or erythromycin.

TRIKAFTA may cause dizziness in some people who take it. Patients should not drive a car, operate machinery, or do anything that requires alertness until they know how TRIKAFTA affects them.

Patients should avoid food or drink that contains grapefruit while they are taking TRIKAFTA.

TRIKAFTA can cause serious side effects, including:

Liver damage and worsening of liver function in people with severe liver disease that can be serious and may require transplantation. Liver damage has also happened in people without liver disease.

High liver enzymes in the blood, which is a common side effect in people treated with TRIKAFTA. These can be serious and may be a sign of liver injury. The patients doctor will do blood tests to check their liver before they start TRIKAFTA, every 3 months during the first year of taking TRIKAFTA, and every year while taking TRIKAFTA. Patients should call their doctor right away if they have any of the following symptoms of liver problems: pain or discomfort in the upper right stomach (abdominal) area; yellowing of the skin or the white part of the eyes; loss of appetite; nausea or vomiting; dark, amber-colored urine.

Abnormality of the eye lens (cataract) has happened in some children and adolescents treated with TRIKAFTA. If the patient is a child or adolescent, their doctor should perform eye examinations before and during treatment with TRIKAFTA to look for cataracts.

The most common side effects of TRIKAFTA include headache, upper respiratory tract infection (common cold) including stuffy and runny nose, stomach (abdominal) pain, diarrhea, rash, increase in liver enzymes, increase in a certain blood enzyme called creatine phosphokinase, flu (influenza), inflamed sinuses, and increase in blood bilirubin.

These are not all the possible side effects of TRIKAFTA. Please click here to see the full Prescribing Information for TRIKAFTA.

About Vertex

Vertex is a global biotechnology company that invests in scientific innovation to create transformative medicines for people with serious diseases. The company has multiple approved medicines that treat the underlying cause of cystic fibrosis (CF) a rare, life-threatening genetic disease and has several ongoing clinical and research programs in CF. Beyond CF, Vertex has a robust pipeline of investigational small molecule medicines in other serious diseases where it has deep insight into causal human biology, including pain, alpha-1 antitrypsin deficiency and APOL1-mediated kidney diseases. In addition, Vertex has a rapidly expanding pipeline of cell and genetic therapies for diseases such as sickle cell disease, beta thalassemia, Duchenne muscular dystrophy and type 1 diabetes mellitus.

Founded in 1989 in Cambridge, Mass., Vertex's global headquarters is now located in Boston's Innovation District and its international headquarters is in London. Additionally, the company has research and development sites and commercial offices in North America, Europe, Australia and Latin America. Vertex is consistently recognized as one of the industry's top places to work, including 11 consecutive years on Science magazine's Top Employers list and a best place to work for LGBTQ equality by the Human Rights Campaign. For company updates and to learn more about Vertex's history of innovation, visit http://www.vrtx.com or follow us on Facebook, Twitter, LinkedIn, YouTube and Instagram.

Special Note Regarding Forward-Looking Statements

This press release contains forward-looking statements as defined in the Private Securities Litigation Reform Act of 1995, including, without limitation, statements made by Dr. Carmen Bozic in this press release, statements regarding the potential benefits, safety and efficacy of TRIKAFTA and KALYDECO, and our plans to present data about our portfolio of CF medicines at the NACFC, including data from our TRIKAFA open-label extension study, a retrospective study of patients treated with KALYDECO, and additional scientific presentations regarding TRIKAFTA. While Vertex believes the forward-looking statements contained in this press release are accurate, these forward-looking statements represent the company's beliefs only as of the date of this press release and there are a number of risks and uncertainties that could cause actual events or results to differ materially from those expressed or implied by such forward-looking statements. Those risks and uncertainties include, among other things, that data from the company's development programs may not support registration, approval or further development of its compounds due to safety, efficacy or other reasons, risks related to approval and commercialization of our medicines, and other risks listed under the heading "Risk Factors" in Vertex's most recent annual report and subsequent quarterly reports filed with the Securities and Exchange Commission (SEC) and available through the company's website at http://www.vrtx.com and on the SECs website at http://www.sec.gov. You should not place undue reliance on these statements or the scientific data presented. Vertex disclaims any obligation to update the information contained in this press release as new information becomes available.

(VRTX-GEN)

View source version on businesswire.com: https://www.businesswire.com/news/home/20211019005260/en/

Contacts

Vertex Pharmaceuticals Incorporated Investors: Michael Partridge, +1 617-341-6108orBrenda Eustace, +1 617-341-6187orManisha Pai, +1 617-429-6891

Media: mediainfo@vrtx.com orU.S.: +1 617-341-6992orHeather Nichols: +1 617-839-3607orInternational: +44 20 3204 5275

The rest is here:

Vertex to Present Long-Term Data Demonstrating Significant Benefits of Treatment With CFTR Modulators at North American Cystic Fibrosis Conference...

CF President Jim Henningsen speaks to the Marion County Commission at a recent meeting. The county has committed $2 million as a local match for the new nursing education building. Image: Marion County via video

A study released by the Florida Hospital Association forecasts a statewide nursing shortage that could hit The Villages especially hard.

And in Ocala the College of Central Florida is racing to help meet the demand.

The study, by IHS Markit, projects a shortfall of 12% among RNs and 30% among licensed practical nurses by 2035.

Some areas will have extreme shortages. The Villages, for instance, could have only about 30% of the nurses it needs.

A few miles to the north, College of Central Florida President Jim Henningsen is answering the demand for health care education.

Weve already grown our nursing program by 50 percent in the last five years by making tough choices on older programs and closing them down to repurpose those resources, he said. But right now were full court in terms of trying to get funding done so that we can expand faster.

Hes lining up money from the Legislature, local sources and donors for a new $16 million nursing education building that could open in about two years. CFs two-year program would increase by 50 students to 325.

Read more:

CF seeks state and local funding for nursing education, as study projects dramatic shortfall - WMFE

Last Friday night was a special night for the Camden Fairview Cardinals, who are now 7-1 for the season. The Cardinals crushed the De Queen Leopards 62-3 in De Queen, and they are now one game away from clinching their first conference title since the 2013 season.

In the first half of last week's game, star quarterback Martavius Thomas broke the program's single-game passing record of 420 yards, by passing for 520 yards before the third quarter.

The defense for the Cardinals was equally dominant, bringing the team close to their third shutout of the season. Camden Fairview's defense accounted for 11 tackles for loss and four sacks against the Leopards. Cardinals defensive end Jacovey Barker had another monster performance by consistently making plays in the backfield and stalling De Queen's drives.

Martavius Thomas and Jacovey Barker are once again the Camden News Offensive and Defensive Players of the Week.

This is Thomas' fifth-time to be named the offensive player of the week, as he seems to perform better and better in every game he plays in. He was confident last week that he could beat the program's single game passing record of 420 yards, but he didn't expect to break it with 520 passing yards, but he has coaches behind him creating solid game plans and teammates to block and allow him to make open plays.

Thomas threw 23-for-29 for 520 yards, seven touchdowns, one interception and a quarterback rating of 144.3. He was highly efficient in his passing by spreading the ball throughout the field, consistently completing deep passes and exploiting coverage schemes. He had three receivers who accounted for at least 100 receiving yards and three receivers who caught two receiving touchdowns. Thomas has a great arsenal of weapons to dismantle opposing defenses, but his determination to get each of them the ball evenly is something that makes him dangerous as a passer. If an opposing defense locks down one key receiver, Thomas finds another one.

On the defensive side of the ball, the Cardinals once again had several dominant performances from their star players. Senior defensive end Jacovey Barker led the defense to another nearly shutout performance. Barker finished the game with seven solo tackles, three tackles for loss, three sacks and two quarterback hurries. Barker was constantly pressuring the backfield of the Leopards for the drives he was in. He made it difficult for the offense of De Queen to extend their drives.

Barker has accounted for 12 sacks in eight games this season, the most of any defender in the state of Arkansas. He is five sacks away to breaking the school record of most sacks in a season (16). He has a chance to break this record in the final two games of the season, as he is hungry and determined to not only break the record, but also dominate opposing offenses in the backfield. Barker has also accounted for 42 total tackles and 17 tackles for loss in the season.

Read more from the original source:

CF QB Martavius Thomas and DE Jacovey Barker named Camden News Players of the Week - Camden News