Category Archives: Gene Medicine

DURHAM, N.C. (WTVD) Duke University School of Medicine researchers have helped discover a new coronavirus gene mutation that helps the virus spread faster.

Dr. David Montefiori is a professor of surgery who also serves as Director of the Laboratory for AIDS Vaccine Research and Development. He explained that the gene mutation causes a new strain of coronavirus.

Were looking at the genetic sequence of the virus. And in particular, were looking at the sequence of the spike protein. This is a protein thats on the surface of a virus, that the virus uses to attach to a cell and to get into a cell, Dr. Montefiori said.

Scientists around the world study sequences taken from people infected with viruses. They then deposit the sequences into a central database originally designed to help researchers study the flu.

Once those sequences are deposited into the database, scientists have access to those sequences to analyze them. And my colleague at Los Alamos National Laboratory Dr. Bette Korber, who is an expert at analyzing sequences, and we have been collaborating together for many years on HIV, she immediately started analyzing the spike sequences in that database that were coming in from around the world, Dr. Montefiori said. And we were both interested in whether or not mutations might arise that showed evidence of spreading in the human population that many people would show evidence of being infected with a virus that carries a mutation in it.

He explained how the mutation spread quickly.

(Dr. Korber) noticed this mutation that we call D614G in the spike protein that was found in about six people in very early March. So it became a mutation of interest because of showing some evidence of spreading, suggesting that it might have a fitness advantage. And within weeks, it was found in more and more people, Dr. Montefiori said. As more and more sequences came into the database, more and more of those sequences had this mutation. And it just kept spreading. By the end of April, it was now the dominant strain of the virus globally.

Researchers dont believe the strain is more deadly than the original coronavirus strain, they are still concerned.

It appears to spread faster. And thats probably why the virus liked the mutation, and why its so dominant because it provided an advantage to the virus to spread easier. And thats what a virus wants to do to survive. It wants to be able to transmit, Dr. Montefiori said.

Dr. Montefiori did not believe this mutation is the cause for the US having so many more cases, hospitalizations and deaths than any other country.

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Duke researchers help discover new strain of coronavirus that spreads faster because of gene mutation - WGHP FOX 8 Greensboro

Chong-Hou Lok, Dong Zhu, Jia Wang, Yu-Tang Ren, Xuan Jiang, Shu-Jun Li, Xiu-Ying Zhao

Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Beijing, Peoples Republic of China

Correspondence : Xiu-Ying ZhaoBeijing Tsinghua Changgung Hospital,School of Clinical Medicine, Tsinghua University, Beijing 10220, Peoples Republic of ChinaEmail zxya00340@btch.edu.cn

Introduction: Understanding drug resistance is important in drug selection for Helicobacter pylori (H. pylori) eradication, and drug resistance data are lacking in Beijing.Purpose: This cross-sectional study aimed to isolate H. pylori from patients with gastroduodenal diseases and to analyze drug resistance to clarithromycin (CLA) and levofloxacin (LEV), which are used frequently in China.Patients and Methods: One hundred and seventy-six patients with gastroduodenal diseases undergoing gastroduodenoscopy were selected by convenient sampling. Gastric mucosa samples were cultured and sub-cultured using a new medium broth. Active H. pylori strains were confirmed by microscopy observation as Gram-negative curved bacilli with positive test results for urease, oxidase, and catalase, and H. pylori 16S rRNA amplification by polymerase chain reaction (PCR). CLA and LEV resistance was identified by minimum inhibitory concentration (MIC) tests and sequencing of 23S rRNA, gyrA, and gyrB genes.Results: From the 176 clinical samples, 112 (112/176, 63.6%) were confirmed with H. pylori infection and 65 (65/176, 36.9%) active H. pylori strains were obtained and further confirmed by MIC assay. Overall, the rates of CLA-resistant and LEV-resistant mutations in the 112 samples were 50.9% and 33.0%, respectively. Mutation related to CLA resistance was A2143G in the 23S rRNA gene and mutations associated with LEV resistance were N87K, D91G, and D91Y in the gyrA gene. Of 112 samples, 22 (19.6%) presented dual resistance to CLA and LEV. Resistance of the H. pylori strains to CLA (r=0.846, P< 0.001) and LEV (r=0.936, P< 0.001) had a strong correlation in phenotypic and genotypic level.Conclusion: The results indicated that resistance of CLA and LEV is severe among patients with gastroduodenitis. A good consistency could be found as to drug resistance between genotypic or phenotypic assay, suggested extending the detection of H. pylori drug resistance from the MIC method to a genotypic assay.

Keywords: Helicobacter pylori, clarithromycin, levofloxacin, antibiotic resistance

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Phenotype and Molecular Detection of Clarithromycin and Levofloxacin R | IDR - Dove Medical Press

TOKYO & MUNICH--(BUSINESS WIRE)--Daiichi Sankyo Company, Limited (hereafter, Daiichi Sankyo) today announced that the European Medicines Agency (EMA) has validated the Marketing Authorization Application (MAA) for trastuzumab deruxtecan, a HER2 directed antibody drug conjugate (ADC), for the treatment of adults with unresectable or metastatic HER2 positive breast cancer who have received two or more prior anti-HER2 based regimens. Trastuzumab deruxtecan was granted accelerated assessment by the EMAs Committee for Medicinal Products for Human Use (CHMP).

Validation confirms that the application is complete and commences the scientific review process by the EMAs CHMP. Accelerated assessment is granted by the CHMP to products expected to be of major interest for public health and therapeutic innovation and can significantly reduce the review timelines.

The accelerated assessment highlights the significant unmet need for patients with HER2 positive metastatic breast cancer that trastuzumab deruxtecan aims at addressing, said Gilles Gallant, BPharm, PhD, FOPQ, Senior Vice President, Global Head, Oncology Development, Oncology R&D, Daiichi Sankyo. Trastuzumab deruxtecan is already available for patients in the U.S. and Japan, and we look forward to working with the EMA to bring this important new medicine to patients in the EU as quickly as possible.

The MAA is based on the positive results from the pivotal phase 2 DESTINY-Breast01 trial of trastuzumab deruxtecan monotherapy in patients with HER2 positive metastatic breast cancer who had received two or more prior anti-HER2 regimens. The results of the DESTINY-Breast01 trial are published in The New England Journal of Medicine.

About HER2

HER2 is a tyrosine kinase receptor growth-promoting protein expressed on the surface of many types of tumors including gastric, breast and lung cancers. HER2 overexpression is associated with a specific HER2 gene alteration known as HER2 amplification and is often associated with aggressive disease and poorer prognosis.1

About HER2 Positive Breast Cancer

Approximately one in five breast cancers are HER2 positive.2,3 Despite recent improvements and approvals of new medicines, there remain significant clinical needs for patients with HER2 positive metastatic breast cancer.4,5 This disease remains incurable with patients eventually progressing after available treatment.5

About Trastuzumab Deruxtecan

Trastuzumab deruxtecan (fam-trastuzumab deruxtecan-nxki in the U.S. only) is a HER2 directed ADC and is the lead ADC in the oncology portfolio of Daiichi Sankyo and the most advanced program in AstraZenecas ADC scientific platform.

ADCs are targeted cancer medicines that deliver cytotoxic chemotherapy (payload) to cancer cells via a linker attached to a monoclonal antibody that binds to a specific target expressed on cancer cells. Designed using Daiichi Sankyos proprietary DXd ADC technology, trastuzumab deruxtecan is comprised of a HER2 monoclonal antibody attached to a novel topoisomerase I inhibitor payload by a tetrapeptide-based linker.

Trastuzumab deruxtecan (5.4 mg/kg) is approved in the U.S. and Japan for the treatment of adult patients with unresectable or metastatic HER2 positive breast cancer who received two or more prior anti-HER2-based regimens based on the DESTINY-Breast01 trial.

Trastuzumab deruxtecan has not been approved in the EU, or countries outside of Japan and the U.S., for any indication. It is an investigational agent globally for various indications.

About the Trastuzumab Deruxtecan Clinical Development Program

A comprehensive development program for trastuzumab deruxtecan is underway globally with six pivotal trials evaluating the efficacy and safety of trastuzumab deruxtecan monotherapy across multiple HER2 cancers including breast, gastric, and lung cancers. Trials in combination with other anticancer treatments, such as immunotherapy, also are underway.

In May 2020, trastuzumab deruxtecan received Breakthrough Therapy Designation from the U.S. Food and Drug Administration (FDA) for the treatment of patients with HER2 positive unresectable or metastatic gastric or gastroesophageal junction adenocarcinoma who have received two or more prior regimens including trastuzumab, and Orphan Drug Designation for gastric cancer, including gastroesophageal junction cancer. In March 2018, trastuzumab deruxtecan received a SAKIGAKE designation for potential use in the same HER2positive patient population and a supplemental New Drug Application was submitted to the Japan Ministry of Health, Labour and Welfare (MHLW) for approval in April 2020.

In May 2020, trastuzumab deruxtecan also received Breakthrough Therapy Designation for the treatment of patients with metastatic non-small cell lung cancer (NSCLC) whose tumors have a HER2 mutation and with disease progression on or after platinum-based therapy.

About the Collaboration between Daiichi Sankyo and AstraZeneca

In March 2019, Daiichi Sankyo and AstraZeneca entered into a global collaboration to jointly develop and commercialize trastuzumab deruxtecan worldwide, except in Japan where Daiichi Sankyo maintains exclusive rights. Daiichi Sankyo is solely responsible for the manufacturing and supply.

About Daiichi Sankyo

Daiichi Sankyo Group is dedicated to the creation and supply of innovative pharmaceutical therapies to improve standards of care and address diversified, unmet medical needs of people globally by leveraging our world-class science and technology. With more than 100 years of scientific expertise and a presence in more than 20 countries, Daiichi Sankyo and its 15,000 employees around the world draw upon a rich legacy of innovation and a robust pipeline of promising new medicines to help people. In addition to a strong portfolio of medicines for cardiovascular diseases, under the Groups 2025 Vision to become a Global Pharma Innovator with Competitive Advantage in Oncology, Daiichi Sankyo is primarily focused on providing novel therapies in oncology, as well as other research areas centered around rare diseases and immune disorders. For more information, please visit: http://www.daiichisankyo.com

References :

1Iqbal N, et al. Mol Biol Int. 2014; 2014: 852748

2Tandon A, et al. J Clin Oncol. 1989;7(8):1120-8.

3Sledge G, et al. J Clin Oncol. 2014;32(19):1979-1986.

4de Melo Gagliato D, et al. Oncotarget. 2016;7(39):64431-46.

5National Comprehensive Cancer Network (NCCN). NCCN Guidelines. Breast Cancer. Accessed June 2020.

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EMA Validates and Grants Accelerated Assessment for Trastuzumab Deruxtecan for the Treatment of HER2 Positive Metastatic Breast Cancer - Business Wire

My husband, Matteo Adinolfi, who has died aged 91 from Covid-19, was an internationally esteemed immunologist focusing on prenatal diagnosis of gene disorders, and a talented amateur artist.

Matteo was born in Eritrea. His parents, Attilio Adinolfi and his wife, Maria (nee Sellitti) had moved there from Italy, to escape fascism. In 1943, on a visit back to Naples, the family was trapped by the advancing war and unable to return to Africa.

Attilio joined the navy; Matteo and his mother and two sisters survived the bombardments by fleeing from one hill to another, foraging for food and finding shelter where they could. At the end of the war, Matteo was emaciated and extremely ill with gastroenteritis.

After he recovered, his experience motivated him to study medicine in Naples in 1954. He then worked at the University of Naples until 1962. Once, while sharing a pizza with an American geneticist visiting Naples, he heard about a new electrophoretic starch gel the visitor had invented for identification of plasma proteins he wrote the formula on a paper napkin. Matteos curiosity led him to prepare the gel and test the blood of a lamprey eel from the laboratory aquarium. To his surprise, the lamprey haemoglobin closely resembled a single strand of four-chain human haemoglobin. The paper, published in Nature (1955), received international attention and got him known as the famous lamprey Adinolfi.

In 1962 he moved to London and joined the experimental haemotology research unit at the Wright Fleming Institute, at the same time practising at St Marys hospital. He was awarded his PhD in immunology at the University of London in 1966 and became a senior lecturer at the paediatric research unit at Guys hospital and medical school. Over the next 30 years, he worked as a consultant, teacher and researcher in London at Guys and at University College hospital and in Lambeth, Southwark and Lewisham Area Health Authority. He was appointed professor of developmental immunology at the University of London in 1983. In 1994 he was elected an honorary fellow of the Royal Society of Medicine. The same year he went to the Galton Institute; he retired in 2004, aged 76.

Besides the lamprey haemoglobin work in Naples, in recent years at Guys hospital, Matteo and international colleagues developed laser microscopy in prenatal diagnoses of chromosome disorders and single-cell gene defects.

Matteo published hundreds of scientific papers, contributed chapters to many books and organised courses in many countries.

AMaking art was another of his passions. A prolific artist, he was proficient with collage, sculpture, drawing and printmaking. He and others founded the popular 407 Art Club at Guys hospital. He and I met at an etching class at the City Literary Institute in 1978, lived together from then, and married in 1985.

Matteo is survived by me and by his children, Carlo, Nora and Marina, from his first marriage, to Annetta De Giorgio, which ended in divorce. His second wife, Camille (nee Guthrie), died in 1975.

Link:
Matteo Adinolfi obituary | From the Guardian - The Guardian

Daix (France), July 6, 2020 Inventiva (Euronext: IVA) ("Inventiva" or the "Company"), a clinical-stage biopharmaceutical company developing oral small molecule therapies for the treatment of non-alcoholic steatohepatitis (NASH), mucopolysaccharidoses (MPS) and other diseases with significant unmet medical need, today announced the decision by the investigator to reduce the number of patients to be enrolled in the investigator-initiated Phase II clinical trial of lanifibranor in patients with TD2M and NAFLD being conducted by Prof. Cusi at the University of Florida.

This trial aims to evaluate the metabolic effects of lanifibranor and its potential efficacy on liver triglycerides inT2DM patients with NAFLD and provide additional clinical data supporting lanifibranors potential for the treatment of NASH.

Originally, the trial was expected to enroll 64 patients to be treated with a single daily dose of lanifibranor (800 mg/day) or placebo for a 24-week period and 10 subjects in a healthy, non-obese control group. However, given the observed effects of lanifibranor in reducing steatosis during the Phase IIb NATIVE clinical trial evaluating lanifibranor for the treatment of NASH, the investigator Prof. Cusi has decided to reduce the number of patients to be evaluated to 34 patients from 64 originally, while maintaining the same statistical powering in the trial.

At present, this investigator-initiated trial has recruited 23 patients, 15 of which have completed the 24-week period of treatment. Results from this trial are currently expected in 2021. However, due to the COVID-19 pandemic, the recruitment and screening of new patients has been suspended at the University of Florida, where the trial is being conducted, and the results could therefore be delayed.

The table below sets forth data from the Phase IIb NATIVE clinical trial with respect to the pre-specified analysis of changes in CRN steatosis score in the subset of T2DM patients, as compared to the overall population of patients treated in the trial. These data contributed to the investigators decision to reduce target enrollment in the ongoing investigator-initiated NAFLD trial.

* Statistically significant in accordance to the statistical analysis plan (SAP)

Prof. Ken Cusi, M.D., F.A.C.P., F.A.C.E., Professor of Medicine, Chief, Division of Endocrinology, Diabetes and Metabolism, University of Florida, said: The results recently shown by lanifibranor in NASH patients with respect to its ability to reduce steatosis and significantly improve insulin sensitivity and glycemic control are higher than I expected and support lanifibranors potential for the treatment of patients with NASH. I now look forward to advancing this trial and developing data to support the hypothesis that lanifibranor can have a significant impact on hepatic triglycerides in patients with type 2 diabetes and NAFLD.

Pierre Broqua, CSO and cofounder of Inventiva, stated: We are very pleased with this decision following the positive results of lanifibranor during the Phase IIb clinical trial in NASH. Type 2 diabetes patients with NASH are generally exposed to an increased risk of poor clinical outcomes and are therefore in a critical need for an efficacious NASH treatment. We were thus particularly pleased to see significant improvements in CRN steatosis scores in patients with type 2 diabetes in the NATIVE trial and look forward to data from Prof. Cusis trial, which could further support lanifibranors potential in this population.

About lanifibranor

Lanifibranor, Inventivas lead product candidate, is an orally-available small molecule that acts to induce anti-fibrotic, anti-inflammatory and beneficial vascular and metabolic changes in the body by activating all three peroxisome proliferatoractivated receptor (PPAR) isoforms, which are wellcharacterized nuclear receptor proteins that regulate gene expression. Lanifibranor is a PPAR agonist that is designed to target all three PPAR isoforms in a moderately potent manner, with a wellbalanced activation of PPAR and PPAR, and a partial activation of PPAR. While there are other PPAR agonists that target only one or two PPAR isoforms for activation, lanifibranor is the only panPPAR agonist in clinical development. Inventiva believes that lanifibranors moderate and balanced panPPAR binding profile contributes to the favorable tolerability profile that has been observed in clinical trials and preclinical studies to date.

About the study of lanifibranor in type 2 diabetes (T2DM) patients with non-alcoholic fatty liver disease (NAFLD)

The trial being conducted by Prof. Kenneth Cusi, Chief of the Division of Endocrinology, Diabetes & Metabolism in the Department of Medicine at the University of Florida, Gainesville, is expected to enroll 34 patients treated for a 24-week period with a single daily dose of lanifibranor (800 mg/day) or placebo and 10 subjects in a healthy, non-obese control group. The studys overall objective is to measure the metabolic effects of lanifibranor and its potential efficacy on liver triglycerides in T2DM patients with NAFLD. The primary endpoint is the change in liver triglycerides as assessed by proton magnetic resonance spectroscopy. Secondary endpoints include changes in liver fibrosis, evidence of metabolic improvements in insulin resistance, de novo lipogenesis, free fatty acids and lipids, as well as safety. Results from this trial are currently expected in 2021. However, due to the COVID-19 pandemic, the recruitment and screening of new patients has been suspended at the University of Florida, where the trial is being conducted, and the results could therefore be delayed.

About Inventiva

Inventiva is a clinical-stage biopharmaceutical company focused on the development of oral small molecule therapies for the treatment of NASH, MPS and other diseases with significant unmet medical need.

Leveraging its expertise and experience in the domain of compounds targeting nuclear receptors, transcription factors and epigenetic modulation, Inventiva is currently advancing two clinical candidates, as well as a deep pipeline of earlier stage programs.

Lanifibranor, its lead product candidate, is being developed for the treatment of patients with NASH, a common and progressive chronic liver disease for which there are currently no approved therapies. Inventiva recently announced positive topline data from its Phase IIb clinical trial evaluating lanifibranor for the treatment of patients with NASH.

Inventiva is also developing odiparcil, a second clinical stage asset, for the treatment of patients with subtypes of MPS, a group of rare genetic disorders. A Phase I/II clinical trial in children with MPS VI is currently under preparation following the release of positive results of the Phase IIa clinical trial in adult MPS VI patients at the end of 2019.

In parallel, Inventiva is in the process of selecting an oncology development candidate for its Hippo signalling pathway program. Furthermore, the Company has established a strategic collaboration with AbbVie in the area of autoimmune diseases. AbbVie has started the clinical development of ABBV157, a drug candidate for the treatment of moderate to severe psoriasis resulting from its collaboration with Inventiva. This collaboration enables Inventiva to receive milestone payments upon the achievement of pre-clinical, clinical, regulatory and commercial milestones, in addition to royalties on any approved products resulting from the collaboration.

The Company has a scientific team of approximately 70 people with deep expertise in the fields of biology, medicinal and computational chemistry, pharmacokinetics and pharmacology, as well as in clinical development. It also owns an extensive library of approximately 240,000 pharmacologically relevant molecules, approximately 60% of which are proprietary, as well as a whollyowned research and development facility.

Inventiva is a public company listed on compartment C of the regulated market of Euronext Paris (Euronext: IVA ISIN: FR0013233012). http://www.inventivapharma.com

Contacts

InventivaFrdric CrenChairman & CEOinfo@inventivapharma.com+33 3 80 44 75 00

Brunswick GroupYannick Tetzlaff / Tristan Roquet Montegon /Aude LepreuxMedia relationsinventiva@brunswickgroup.com+33 1 53 96 83 83

Westwicke, an ICR CompanyPatricia L. BankInvestor relationspatti.bank@westwicke.com +1415513 1284

Important Notice

This press release contains forward-looking statements, forecasts and estimates with respect to Inventivas clinical trials, clinical trial data releases, clinical development plans and anticipated future activities of Inventiva. Certain of these statements, forecasts and estimates can be recognized by the use of words such as, without limitation, believes, anticipates, expects, intends, plans, seeks, estimates, may, will and continue and similar expressions. Such statements are not historical facts but rather are statements of future expectations and other forward-looking statements that are based on management's beliefs. These statements reflect such views and assumptions prevailing as of the date of the statements and involve known and unknown risks and uncertainties that could cause future results, performance or future events to differ materially from those expressed or implied in such statements. Actual events are difficult to predict and may depend upon factors that are beyond Inventiva's control. There can be no guarantees with respect to pipeline product candidates that the clinical trial results will be available on their anticipated timeline, that future clinical trials will be initiated as anticipated, or that candidates will receive the necessary regulatory approvals. Therefore, actual results may turn out to be materially different from the anticipated future results, performance or achievements expressed or implied by such statements, forecasts and estimates. Given these uncertainties, no representations are made as to the accuracy or fairness of such forward-looking statements, forecasts and estimates. Furthermore, forward-looking statements, forecasts and estimates only speak as of the date of this press release. Readers are cautioned not to place undue reliance on any of these forward-looking statements.

Please refer to the Universal Registration Document filed with the Autorit des Marchs Financiers on June 19, 2020 under n D.20-0551 for additional information in relation to such factors, risks and uncertainties.

Except as required by law, Inventiva has no intention and is under no obligation to update or review the forward-looking statements referred to above. Consequently, Inventiva accepts no liability for any consequences arising from the use of any of the above statements.

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Inventiva announces the decision by the investigator to reduce the number of patients in the ongoing Phase II trial evaluating lanifibranor in type 2...

CHAPTER TWELVE

GRAND CANYON SUITE

Kemo Sabe, how many outlaws are left? Tonto asked the Ranger during a lull in the melee.

The Masked man, standing high in Silvers stirrups surveyed the battleground quickly, his dark piercing eyes catching all the important details in their scan of the cacophony.

He turned and looked towards Tonto.

About twenty or twenty five Tonto, now we outnumber them! he said enthusiastically.

Just as quickly as the battle waned, it resumed as the remaining outlaws charged once more.

Bracing themselves for the brutal onslaught, the tired ranchers formed a defensive wall. The Lone Ranger, Tonto, Monte Hale, Rex Allen, Gabby Hayes, the Harts, Tex Ritter and crew, Tim McCoy and his outriders; all lined up, their pistols still hot and smoking as they stood tall and defiant to face the bloodthirsty outlaws final surge!

The outlaws, battered, bruised and wounded stared ahead at the growing line of vengeful determined ranchers.

Fear grew within their villainous breasts as man by man, they looked to the man beside them. Left, then right, each man assessed his sideman and finally, faced front again.

By now the moon was almost mid sky, and the shadows of the ranchers were eerie dancers on the uneven beat up ground. Slowly, gun barrel reflections of white light met each outlaws gaze as they surveyed the wide line of vengeance before them.

More men joined in the ever widening swath of ranchers . Bob Nolan, Pat Brady, Dusty Rogers, and Sunset Carson had galloped up and merged with the ranchers.

The masked outlaw leader, waiting in line with the outlaws, waved the desperate men forward. Over poorly lit ground, they walked slowly at first, guns raised in preparation for a final shoot out! The masked leader walked one step behind, examining all he could see.

The Lone Ranger yelled out.

Forward men!

Like two columns of marching Roman centurions, the desperate groups moved towards a certain collision with destiny. A charged silence filled the air between the two approaching masses of men. The ground, trampled and torn, bore signs of recent violence, and the anger in the air screamed the promise of more!

Fear showed in every outlaws numbers as the ranchers neared. The masked leader, still walking a step behind, sensing certain defeat, yelled

CHARGE!!!

The outlaws, waiting for the sign to attack, ran forward desperately. Guns held high, each outlaw fired his brace of ammunition. Reloading, they fired again, and again.

The ranchers led by the Ranger and Roy, met the villainous onslaught with courage born of confidence. The outlaw bullets did little harm to the revenge driven cattlemen. A few fell back with slight wounds, then recovering from the hot stings, rejoined their comrades.

GETEM BOYS! the Ranger shouted as he lifted his pistol, and fired, and fired.

Roy Rogers, beside the Ranger, charged into the mass of fighting men, pistols held high and blazing. All around him, rancher fought outlaw, and with one sure result; death or capture for the evil doer!

The masked leader, fighting for his life with a rancher spotted Roy out of the corner of his eye. he feigned left, then punched right felling the exhausted rancher. Roy, seeing the man fall, plunged towards the mysterious leader.

Rogers! Come get me he taunted.

Roy reached the hooded man, and leaping upon the outlaw leader, pulled him to the ground.

The leader, somewhat hampered by his disguise, rolled Roy off into the moist hardback.

Give yourself up! Roy shouted.

Roy stood up, and slipped.

The masked leader, sensing that defeat was close at hand, jumped up and mounted his horse in desperation. Taking a quick look around the melee, he reined his horse around, back again and then fled!

Come back, you coward! Roy shouted.

The masked leader kicked at the lunging cowboy. Missing Roy by a couple of inches, he spurred his horse onward.

Roy Rogers, ducking to avert the outlaw leaders silver tipped boot, fell onto the trampled ground again.

The masked leader galloped desperately away from the battle scene. One thought filled his mind-ESCAPE!! Pushing his mount mercilessly, he looked back and saw Roy rising from the ground dazed somewhat. Turning frontwards, he leaned down and fled for his life!

Roy Rogers, getting up from the ground looked up to see through blurry eyes. Shaking his head to clear the cobwebs, he called out.

Here Trigger and he whistled.

Trigger, not far away, galloped enthusiastically towards Roy. Roy, running alongside Trigger, mounted him mid gallop. He quickly reined Trigger around toward the fleeing outlaw leader.

Come on boy, hes got a big lead on us! Roy shouted to Trigger.

Trigger accelerated strongly, the cool night air rushing across his face and bruising his lungs. Dust flew as his hooves beat out a tune that could only be called JUSTICE!

Roy urged Trigger on, as the outlaw ahead pushed his mount brutally. the distance between them was steadily decreasing. One hundred, ninety, eight yards and closer.

A shot from the outlaw puffed back and went wide. A second came a little closer. Roy pulled his silver handled pistol out and took careful bead, then fired once.

By now, Roy and Trigger had closed the gap down to twenty yards.

Roy pushed Trigger onward, with the outlaw this close nothing could stop them. Triggers golden mane, waving in the rushing wind shimmered ghostly in the moonlight. Like a pair of rushing gladiators smelling victory, Roy and Trigger were transformed into avenging angels.

The outlaw leader, now scant yards away, looked back with fear in his eyes. His horse, stopped short as Trigger and Roy outran the pair briefly. Turning quickly, Roy and Trigger met the outlaw pairs attack head on.

Trigger reared up in response to the chestnuts menacing hooves. Roy, balancing on Triggers back, tensed in preparation for the final battle. Trigger struck out with his left hoof, the chestnut reeled back. Striking out in retaliation, the chestnut nicked Triggers shoulder drawing blood with a sharp shoe. Trigger, lashed out with both hooves, the other horse recoiled in fear and stepped back and down again. Trigger landed on his front hooves and attacked again and again.

Silhouetted in the moonlight, the mounted riders looked like ghosts dueling eternally over some long forgotten disagreement. Triggers mane, adopting the shimmery translucence of the silvery light, whirled as if tethered to an invisible line. Roys figure, against the moon, loomed mightily over the masked leaders as the horses, tired by their exertion, planted themselves firmly on the ground. The chestnut, beaten by Triggers pummeling hooves, succumbed to the golden stallion.

Roy, sensing victory for Trigger, urged him closer to the outlaw pair. Leaping from his saddle, Roy landed on the frantic outlaw leader and pulled him to the ground.

Roy, atop the masked leader, punched once, twice. The masked evildoer, arched his back and sent Roy flying through the air.

Blood dripping out of the leaders mask minimized his vision. His fear of dying drove him on! The leader ran and jumped on Roy dazing him temporarily.

Taking his pistol out of his holster he grabbed the barrel end and swung towards Roy.

Ducking to avoid the heavy pistol end, Roy swung out with his right fist. Connecting with the outlaws blood drenched chin solidly, Roy felt a snap.

The leaders head jerked back and his body followed. The masked outlaw rolled off Roy onto the ground, his pistol falling harmlessly to the side.

Roy sat up and knelt beside the stunned outlaw. He wiped his mouth with his gloved hand.

Finding his hat in the dirt, Roy picked it up and knocked the dust off. Placing it on his head, he turned and looked at the outlaw.

In the moonlight his menace was diminished, thickening blood shone black in the silvery glow. Roy stood up and rolled the masked leader over. He reached down and pulled the mask off.

The moonlight fell upon the face of Sheriff Bill Stockton!

Roy whistled.

So, our suspicions were right he said.

Roy walked over to Trigger, took his lasso off and tied Bill up. Wrapping the outlaw sheriff tightly, Roy threw him onto his tired chestnut. Whinnying in protest, the horse struggled with the dead weigh of the sheriff/outlaw leader.

Come on boy. Well go slow Roy said soothingly.

Breathing the cool prairie air, Roy whistled a nameless tune. Trigger, nodding in response, sauntered over beside where Roy was standing. Roy placed his left foot in the stirrup, grasped the horn, and back, then swung up into the well worn saddle.

Lets go Trigger, take it easy. Weve got ourselves a tag along Roy said as he rubbed the palominos neck.

Trigger whinnied and tossed his head from left to right.

Dont worry, well get your cut washed out too. If youre lucky, the vetll have a girl patient there too. Or well get Tonto to fix you up. Roy said to comfort Trigger.

Roy turned Trigger. The chestnut caboose followed and headed off towards Rexs place.

As the masked outlaw leader fled from Roy, the remaining villains were battling viciously. Like trapped wolves they used every weapon at their disposal; teeth, knives, boots, even mud. The sounds of hand to hand combat intermingled with the echoes of gunfire drifted over to the ranch where Mary Sterling waited for the battle to end and peace to begin once more.

Now and then, Gabbys voice could be heard over the lull.

Got ya varmint of Drop it polecat. Ive got you covered.

As the outlaw numbers diminished, strength and resolve of the ranchers increased.

Twisting his head quickly y from side to side and scanning as well as he could in the moonlight, Aces sharp vision caught the lunar sparkle from the masked leaders disguise. Much to his surprise, the leader glanced back, kicked out at a flying Roy Rogers, then turned and galloped off!

Above the din, he yelled to the surviving outlaws.

Men- Scatter!

Each man found his horse, then fled as well as he could. The ranchers, led by the Lone Ranger and Tonto, fell upon the fleeing outlaws.

Quick men! Theyre leaving! he shouted.

Silver responded to the masked mans gentle commands- left here to cut a retreat, right to block an outlaw. Tonto found the fleeing Ace Parker and gave chase. Within a few hundred yards, Tonto and Scout overtook the villainous gunman. The Indian flung Ace to the ground, Aces head ricocheting off a rock. With savage fury Tonto swung once, twice, three, and out Ace Parker went. Collapsing into a heap on the ground and bleeding from half a dozen wounds, he whispered.

You got me Indian. You got me.

All around the melee, whoops of victory filled the air. Triumphant ranchers pulled back fleeing outlaws. Some men gathered the fallen together in a line. The outlaws, some bound, some not, all bore signs of battle weariness. and failure. The grinning ranchers, their faces battered but jubilant, slapped got down to the business of securing the prisoners.

Rex Allen found Koko, and pursued Trig Larson. Trig Larson, too scared and confused to find a horse, bolted desperately. Rex, in a couple of Kokos strides caught up him. He lept upon the fleeing outlaw. They went down. Rex, landing squarely on Trigs back heard a crack. Trig Larson let out a yell of pain.

Ya broke my arm Allen! I give up he howled.

Rex Allen stepped off Larson, and lifted him up by his good arm. A surge of anger came over Rex. He wanted to beat Trig Larson within an inch of his life, but he couldnt. They had won.

Lets go Larson. You walk, I ride Rex said grimly.

Trig Larson, downcast, started back towards Rexs place. Rex, atop Koko, held back tears of gratitude.

Somehow tonight, the deaths of his friends and fellow ranchers had been avenged, and the dead now knew.

One by one, the escaping outlaws found their retreat blocked by the inspired ranchers. The Corrigans, Haydens, Ritters and Pierce Lyden all found their targets and bore down. Some fights were quick, some long, but the prospect of peace drove the ranchers to a feverish pace. In the end, not one outlaw was left standing. Some got killed in the battle, some just got shot escaping.

Rex the Lone Ranger said to the exhausted ranch owner as he sauntered into the corral area, Its all over now.

Rex , took his dirty hat off, and brushed his hand against the crest and sides. He put his hat back on and smiled a tired smile.

Lone Ranger, I hope youre right he said, his hand on the Rangers shoulder.

The Ranger stood atop Silver and yelled.

Men-bring the outlaws here. Well tie them to the fence,

The men grumbled. One man spoke up.

Lets lynchem!

They killed my pa!

They killed my uncle!

The Ranger and Tonto looked around. The men were poised to finish the night with more violence. Rex looked at the pair, concern showing on his face.

Men, we have to hold them for the law. If we dont, were not better than

Roy Rogers came around the corner. Reining Trigger back he dismounted and walked over to where the Ranger, Rex and Tonto stood. The flickering light evidenced Roys battle scars. His dungarees and shirt, were now stained brown and red.

What took so long Roy? Rex asked.

Roy pointed to the chestnut behind Trigger where the masked leader/Bill Stockton lay gagged and unmoving.

He did Roy said smiling. But we took care of the both of them, didnt we Trigger.

Trigger whinnied in response to Roys praise.

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Bing and Ol' Medicine Hat - Todayville.com

Hansa grants Sarepta exclusive license to develop and promote imlifidase as a potential pre-treatment prior to the administration of gene therapy in Duchenne muscular dystrophy and Limb-girdle muscular dystrophy, for patients with neutralizing antibodies (NAbs) to adeno-associated virus (AAV).

Under the terms of the license: Hansa will receive a USD 10 million upfront payment and is eligible for up to USD 397.5 million in development, regulatory and sales milestone payments. Hansa will book all sales of imlifidase and would be eligible for royalties in the high single-digits to mid-teens on any gene therapy sales enabled through pre-treatment with imlifidase in NAb-positive patients.

Lund, Sweden July 2, 2020. Hansa Biopharma (Hansa), the leader in immunomodulatory enzyme technology for rare IgG mediated diseases, announced today that it has entered into an agreement with Sarepta Therapeutics Inc. (Sarepta), the leader in precision genetic medicine for rare diseases, through which Sarepta is granted an exclusive, worldwide license to develop and promote imlifidase as a pre-treatment to enable Sarepta gene therapy treatment in Duchenne muscular dystrophy (DMD) and Limb-girdle muscular dystrophy (LGMD). The pre-treatment is intended for patients with pre-existing neutralizing antibodies (NAb-positive patients) to adeno-associated virus (AAV), the technology that is the basis for Sareptas gene therapy products.

Sarepta will be responsible for conducting pre-clinical and clinical studies with imlifidase and any subsequent regulatory approvals. Sarepta will also be responsible for the promotion of imlifidase as a pre-treatment to Sareptas gene therapies following potential approval.

Under the terms of the agreement, Hansa will receive a USD 10 million upfront payment, and is eligible for a total of up to USD 397.5 million in development, regulatory and sales milestone payments. Hansa will book all sales of imlifidase, and earn high single-digit to mid-teens royalties on Sareptas incremental gene therapy sales when treating NAb-positive patients enabled through pre-treatment with imlifidase.

Sren Tulstrup, President & CEO of Hansa Biopharma comments,We see significant potential for our enzyme technology in the gene therapy space overall, and we are excited to partner with Sarepta, a leading player in the field, to use the unique features of imlifidase to potentially enable gene therapy treatment in patients who today arent eligible for these breakthrough therapies due to pre-existing neutralizing antibodies in two conditionswith a very high unmet medical need.

Doug Ingram, President & CEO, Sarepta Therapeutics said,As we expand our leadership position in genetic medicine and build out our gene therapy engine, one of Sareptas central ambitions is to find scientific solutions that bring our potentially life-saving therapies to the greatest number of the rare disease patients we serve. One of the current limitations of gene therapy is the inability to treat patients who have pre-existing neutralizing antibodies to the AAV vector. While our AAVrh74 vector has been associated with a low screen out rate for neutralizing antibodies, even that low rate is inconsistent with our mission.

In pre-clinical and clinical models, Hansas technology has shown the ability to clear the IgG antibodies that prevent dosing AAV-based gene therapies. If successful, this could offer the potential of extending our gene therapy treatments to DMD and LGMD patients who would otherwise have been denied access due to pre-existing antibodies.

Hansa Biopharma will be hosting a conference call with President & CEO Sren Tulstrup, CSO & COO Christian Kjellman and CFO Donato Spota.

Conference Call Partnership agreement with Sarepta TherapeuticsA conference call will take place July 2nd, 2020 at 10:00am CET. The audio cast will be recorded and subsequently be available on the Hansa website https://hansa.eventcdn.net/202007

Participants dial-in numbersSE: + 46 81 241 09 52UK: + 44 203 769 6819US: + 1 646 787 0157

This is information that HansaBiopharma AB is obliged to makepublic pursuant to the EU MarketAbuse Regulation.

About imlifidaseImlifidase is a unique antibody-cleaving enzyme originating from Streptococcus pyogenes that specifically targets IgG and inhibits IgG-mediated immune response. It has a rapid onset of action, cleaving IgG-antibodies and inhibiting their activity within hours after administration. CHMP/EMA has adopted a positive opinion, recommending conditional approval of imlifidase for the desensitization treatment of highly sensitized adult kidney transplant patients with a positive crossmatch against an available deceased donor. Endorsement of the positive opinion by the European Commission is expected in the third quarter of 2020.Hansa has also reached an agreement with the FDA on a regulatory path forward for imlifidase in kidney transplantation of highly sensitized patients in the U.S. and has three ongoing phase 2 trials in autoimmune diseases and post-transplant indications.

About gene therapy and neutralizing antibodiesGene therapy is a growing and revolutionizing treatment technology in which healthy gene sequences are inserted into cells of a patient. The treatments are potentially curative in monogenic diseases like hemophilia and muscular dystrophy through a single dose. Harmless recombinant viruses are used to carry the healthy genes into the cell. Due to the partial viral origin of the gene therapy constructs, a certain subset of patients carry neutralizing anti-AAV antibodies towards gene therapy products, depending on what AAV serotype being used, forming a barrier for treatment eligibility.Antibodies prevent effective transfer of healthy gene sequence and can be a safety concern. Imlifidase as a pre-treatment may have the potential to eliminate neutralizing antibodies prior to gene therapy. Similarly, imlifidase may have the potential to enable any potentially necessary re-dosing of gene therapy for all patients.

About Duchenne Muscular Dystrophy (DMD)Duchenne muscular dystrophy is a rare genetic disease caused by mutation in the DMD gene, encoding for the protein dystrophin. Duchenne is an irreversible, progressive disease that causes the muscles in the body to become weak and damaged over time. It is eventually fatal and there is no cure. DMD affects one in 3,500 to 5,000 males born worldwide (approximately 400-500 annual cases in the US) and causes muscles in the body to become weak and most patients use wheelchair by the age of 12.

About Limb-Girdle Muscular Dystrophy (LGMD)Limb-girdle muscular dystrophy or (LGMD) is a genetically and clinically heterogeneous group of rare muscular dystrophies. It is characterised by progressive muscle wasting which affects predominantly hip and shoulder muscles. LGMD has an autosomal pattern of inheritance and currently has no known cure or treatment. It can be caused by a single gene defect that affects specific proteins within the muscle cell, including those responsible for keeping the muscle membrane intact. LGMD has a global prevalence of approximately 1.63 per 100,000 individuals worldwide.

For further information, please contact:Klaus Sindahl, Head of Investor RelationsHansa Biopharma Mobile: +46 (0) 709-298 269E-mail: klaus.sindahl@hansabiopharma.com

About Hansa BiopharmaHansa Biopharma is leveraging its proprietary immunomodulatory enzyme technology platform to develop treatments for rare immunoglobulin G (IgG)-mediated autoimmune conditions, transplant rejection and cancer.The Companys lead product candidate, imlifidase, is a unique antibody-cleaving enzyme that potentially may enable kidney transplantation in highly sensitized patients with potential for further development in other solid organ transplantation and acute autoimmune indications. CHMP/EMA has adopted a positive opinion, recommending conditional approval of imlifidase for the desensitization treatment of highly sensitized adult kidney transplant patients with a positive crossmatch against an available deceased donor. Endorsement of the positive opinion by the European Commission is expected in the third quarter of 2020. Hansas research and development program is advancing the next generation of the Companys technology to develop novel IgG-cleaving enzymes with lower immunogenicity, suitable for repeat dosing in relapsing autoimmune diseases and oncology.Hansa Biopharma is based in Lund, Sweden and also has operations in Europe and US.

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Hansa Biopharma announces exclusive agreement with Sarepta Therapeutics to develop and promote imlifidase as pre-treatment ahead of gene therapy in se...

AVROBIO: On Monday, clinical-stage gene therapy company AVROBIO, headquartered in Massachusetts, announced the appointment of Kim Raineri as chief manufacturing and technology officer.

I am thrilled to join AVROBIO, a leader in lentiviral gene therapy and a true pioneer in driving manufacturing advances that address the gene therapy fields need for faster, more scalable and more automated production, Raineri said. The AVROBIO team has created a state-of-the-art gene therapy platform and is clearly committed to continuous innovation on behalf of the patient communities they strive to serve. I am excited to contribute to that work.

Raineri will be replacing AVROBIO co-founder Kim Warren in the position, who will be retiring at the end of July. Before joining AVROBIO, Raineri served as the vice president of operations for Nikon CeLL Innovation Co.

Scenic Biotech: On Wednesday, Netherlands-based Scenic Biotech announced the appointment of their new chief executive officer. Newly appointed CEO Oscar Izeboud brings more than 20 years of life sciences and finance industry experience.

Prior to joining Scenic, Izeboud served as managing director at NIBC Bank in Amsterdam, where he led its corporate finance and capital markets team with a focus on innovation and growth companies.

Former acting CEO and scientific co-founder Sebastian Nijman takes on the role of chief scientific officer.

Akari Therapeutics: Biopharmaceutical company Akari Therapeutics on Wednesday announced the appointment of Torsten Hombeck as chief financial officer and a member of the company's executive team.

Torsten brings a deep understanding of financial strategy, the capital markets and business development to Akari. We are delighted to have him as a permanent member of Akaris executive leadership team," said Clive Richardson, Chief Executive Officer of Akari Therapeutics. "His appointment comes at a time of significant company opportunity and growth. His business and financial expertise will be instrumental in helping us to further develop the Company."

Hormbeck joins Akari with over 20 years of biopharmaceutical industry experience in financial and strategic planning.

Sarepta Therapeutics: Earlier this week, Cambridge-based Sarepta Therapeutics announced the retirement of Sandy Mahatme, the company's executive vice president, chief financial officer and chief business officer. Mahatme will be leaving the company effective July 10.

The Sarepta from which Sandy retires is a very different one from the organization he joined as our chief financial officer some eight years ago. And the Sarepta of today a financially solid biotechnology organization with perhaps the industrys deepest and most valuable pipeline of genetic medicine candidates with the potential to extend and improve lives would not have been possible without Sandys business acumen and dedication, said Doug Ingram, president and chief executive officer of Sarepta Therapeutics.

Sarepta has launched a search to identify the future chief financial officer.

BioMarin: On June 29, BioMarin, a global biotechnology company, announced a pair of promotions. Brian Mueller was promoted to executive vice president, chief financial officer and Andrea Acosta was promoted to group vice president, chief accounting officer.

Mueller has been with BioMarin since 2002, during which he has taken on roles of increasing responsibility. Acosta has been with BioMarin since 2017 as vice president, corporate controller.

Theravance Biopharma: Dublin-based Theravance Biopharma on Thursday announced the appointment of Deepika Pakianathan to its Board of Directors. Pakianathan serves as a managing member at Delphi Ventures, a venture capital firm focused on biotechnology and medical device investments.

"We are honored to welcome Dr. Pakianathan to our board of directors," said Rick Winningham, chief executive officer of Theravance. "We believe her vast experience in the biotechnology sector, translating breakthrough science and taking important therapies from pipeline to patients, will further enhance our already talented Board of Directors."

Novavax: On Thursday, Maryland-based Novavax announced the appointment of Frank Czworka as senior vice president, global sales. Czworka will be responsible for leading sales planning and distribution for the company. He brings more than 20 years of biopharmaceutical experience to the company, with his most recent experience being as vice president, global customer enngagement at U.S. Pharmacopeia.

Novavax also announced the promotion of Brian Webb to senior vice president, manufacturing. Webb will be responsible for overseeing antigen manufacturing and supply activities in support of the company's vaccine candidates. Webb has been with Novavax since May 2014.

eGenesis: On Wednesday, Massachusetts-based eGenesis announced that it appointed Peter Hanson as chief operating officer. Hanson will be in charge directing eGenesis' day-to-day organizational and operational activities including production and manufacturing.

Peter is a highly experienced biopharmaceutical executive across multiple disciplines, which will be critical to support our next phase of growth as we integrate production and R&D, said Paul Sekhri, President and Chief Executive Officer of eGenesis. Peters operational leadership and veterinary knowledge will help us accelerate our product development as we move closer to IND filing for human clinical studies. We are very grateful for Kenneth Fans many contributions as our founding COO. I am delighted that he will continue to serve as an advisor to the company.

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Movers & Shakers, July 3 | BioSpace - BioSpace

Integrated Health System is bringing cell and gene therapy to cats, dogs, and horses. Recently IHS Pets has helped a paralyzed dog with a spinal cord injury to walk again after it was treated with experimental PRP and prolotherapy. Click here to see the video.

Telomeres

Aging is the root of virtually every complex noncommunicable disease in humans and animals. Telomeres are the protective end caps on the ends of our chromosomes, they are as important for the health of both humans and our pets, and they play roles in longevity.

One of the contributing factors in the lifespan in dog breeds is telomere length. As in humans researchers have found that telomere length is a strong predictor of average life span among 15 different breeds consistent with telomeres playing a role in life span determination. Dogs lose telomeric DNA ~10-fold faster than humans, which is similar to the ratio of average life spans between these species. As such telomerase therapy may be beneficial to pets as well as their human caretakers.

Telomerase gene therapy has been shown to extend lifespan in animals, this therapy may help to increase bone mineral density, improve motor performance, improve metabolism, and improve brain function.

Follistatin

The loss of muscle mass with age is just as problematic for animals as it is to humans; in cats for instance a study showed that for each 100g loss of lean body mass increased the risk of death by 20%. This is typically accompanied by frailty, and it is a contributing factor to metabolic syndrome, diabetes, heart disease, and overall mortality.

Diet and exercise have been shown to pay key roles in keeping pets healthy, but the loss of muscle mass is unavoidable without an effective intervention. Enter follistatin: myostatin blocks muscle growth, when it is inhibited then follistatin is able to let muscles grow freely to stop them from wasting away.

Follistatin gene therapy has been shown to be safe and effective in animals, this therapy may help to protect against frailty, increase muscle density, increase strength, and increase endurance.

Klotho: The Queen of Anti-Aging Proteins

1 in 3 cats will suffer from renal disease, but these numbers are under scrutiny with some suggesting that estimate may be too conservative. Chronic kidney failure can occur gradually over months or years, and it is one of the most common conditions affecting older cats with most cases progressing over time worsening the disease.

Klotho is known to play a significant role in the development of chronic kidney disease, and researchers are now turning to its broader role in the anging process as a whole; such as induces expression with gene therapy in mice has been shown to extend lifespan by targeting many of the same pathways as caloric restriction. Blocking Klotho has been shown to cause premature aging.

Klotho also helps to protect the brain, and contributes to more differences in intelligence than any one single gene. Research from the University of California has shown it to protect the brains of mice and improve brain function within 4 hours; and this result included young mice, old mice, and those that were models of Alzheimers disease.

In addition Klotho also plays a critical role in the inflammaging process. Inflammaging is the long term result of the chronic physiological stimulation of the innate immune system which can become damaging during the aging process.

Circulating levels of Kloto decreases with age, this decrease is associated with an increased risk of age related disease. Gene therapy with Klotho has been shown to increase lifespan in animal models, and it may improve kidney function, brain function, clear damage caused by oxidative stress, and protect against cardiovascular disease.

With the remarkable progress being made in genetics, gene therapy may play increasingly prominent and transformative roles in medicine for both humans and animals due to the potential to treat diseases and congenital disorders.

Pets can be an important part of life, they calm us, make us laugh, and create a bond of unconditional love. The company does note that all therapies are experimental, they are not approved by any regulatory body, and they make no claims that outcomes will be positive or beneficial.

IHS Pets is the veterinary wing of Integrated Health Systems, BioViva Sciences exclusive partner. IHS connects with doctors and patients who are interested in the power of gene therapy to pave the way to healthy aging and longevity.

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IHS Pets: Bringing Cell And Gene Therapy To Cats, Dogs & Horses - Anti Aging News

There was a time when modern medicine was primitive. There were no antibiotics, so every infection took its own course, leading to decline in health. Hypertension and diabetes were largely untreatable. X-ray was new, and remedies had changed but little from medieval times. No one ever embarked on the goodness of preventative treatment, not to speak of predictive medicine, beyond taking a distasteful cod liver oil capsule.

During the last hundred years, modern medicine has undergone a sea change. Just think of it an ever-expanding repertoire of medicines, high-tech procedures, therapies and reams of clinical data to employ when one gets sick. Yet modern medicine remained (in)complete, notwithstanding the therapeutic advances.

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Things are now changing thanks to the integration of all such advances, from how a persons diet interacts with ones unique genetic profile to how environmental pollutants affect our thinking, not to speak of preventative medical approaches in health and wellness. The bigperestroikahas begun, and it is poised to transform health care for a growing number of people in the near future. Welcome to a whole new world of personalized, bespoke medicine.

Personalized medicine is, in essence, tailored or customized medical treatment. It treats while keeping in mind the unique, individual characteristics of each patient, which are as distinct as ones fingerprint or signature. It also includes scientific breakthroughs in our understanding of how a persons unique molecular and genetic profile makes them susceptible to certain illnesses. Personalized medicine expands our ability to envisage medical treatments that would not only be effective but also safe for each patient while excluding treatments that may not provide useful objectives.

Personalized medicine is, in simple terms, the use of new methods of molecular scrutiny. It is keyed to help better manage a patients illness or their genetic tendency toward a particular illness or a group of diseases. In so doing, it aims to achieve optimal therapeutic outcomes by helping both clinicians and patients choose a disease management approach that is likely to work best in the context of the patients unique genetic and environmental summary. In other words, it allows to accurately diagnose diseases and their sub-types while prescribing the best form and dose of medication most suited to the given patient.

Personalized, or precision, medicine is not rocket science it is, in essence, an extension of certain traditional approaches to understanding and treating disease. What jazzed up the therapeutic fulcrum of personalized medicine are tools that are more precise. This is what also offers clinicians better insights for selecting a treatment protocol based on a patients molecular profile. Such a patient-specific methodology, as has been practiced for long in certain complementary and alternative medical (CAM) or integrative approaches, not only curtails harmful side effects but also leads to more successful outcomes, including reduced costs in comparison to the current trial-and-error approach to treatment, which has distressingly come to the fore during these extraordinary and unprecedented times of COVID-19.

It is still early days, but the fact remains that personalized medicine has changed the old ways of how we all thought about, identified and managed health issues. As personalized medicine increasingly bids fair to an exciting journey in terms of clinical research and patient care, its impact will only further expand our understanding of medical technology.

What personalized medicine has done is bring about a paradigm shift in our thinking about people in general and also specifically. We all vary from one another what we eat, what others eat, how we react to stress or experience health issues when exposed to environmental factors. It is agreed that such variations play a role in health and disease. It is also being incrementally accepted that certain natural variations found in our DNA can influence our risk of developing a certain disease and how well we could respond to a particular medicine.

All of us are unique individuals, perhaps with the exemption of identical twins, albeit the genomes are unique in them, too. While we are genetically similar, there are small differences in our DNA that are unique, which also makes us distinctive in terms of health, disease and our response to certain medicinal treatments.

Personalized medicine is poised to tap natural variations found in our genes that may play a role in our risk of getting or not getting certain illnesses, along with numerous external factors, such as our environment, nutrition and exercise. Variations in DNA can, likewise, lead to differences in how medications are absorbed, metabolized and used by the body. The understanding of such genetic variations and their interactions with environmental factors are elements that will help personalized medicine clinicians to produce better diagnostics and drugs, and select much better treatments and dosages based on individual needs not as just fixing a pill or two, as is the present-day conventional medical practice.

It is established that a majority of genes function precisely as intended. This gives rise to proteins that play a significant role in biological processes while allowing or helping an individual to grow, adapt and live in their environment. It is only in certain unusual situations, such as a single mutated or malfunctioning gene, that our apple cart is disturbed. This leads to distinct genetic diseases or syndromes such as sickle cell anemia and cystic fibrosis. In like manner, multiple genes acting together can impact the development of a host of common and complex diseases, including our response to medications used to treat them.

New advances will revolutionize bespoke medical treatment with the inclusion of drug therapy as well as recommendations for lifestyle changes to manage, delay the onset of disease or reduce its impact. Not surprisingly, the emergence of new diagnostic and prognostic tools has already raised our ability to predict likely outcomes of drug therapy. In like manner, the expanded use of biomarkers biological molecules that are associated with a particular disease state has resulted in more focused and targeted drug development.

Molecular testing is being expansively used today to identify breast cancer and colon cancer patients who are likely to benefit from new treatments and to preempt recurrences. A genetic test for an inherited heart condition is helping clinicians to determine which course of treatment would maximize benefit and minimize serious side effects while bringing about curative outcomes.

Such complexities exist for asthma and other disorders too. This is precisely where molecular analysis of biomarkers can help us to identify sub-types within a disease while enabling the clinician to monitor their progression, select appropriate medication, measure treatment outcomes and patients response. Future advances may make biomarkers and other tools affordable and allow clinicians to screen patients for relevant molecular variations prior to prescribing a particular medication.

It is already clear that personalized medicine promises three strategic benefits. In terms of preventative medicine, personalized medicine will improve the ability to identify which individuals are predisposed to develop a particular condition. A better understanding of genetic variations could also help scientists identify new disease subgroups or their associated molecular pathways and design drugs to target them. This could also help select patients for inclusion, or exclusion, in late-stage clinical trials. Finally, it will allow to work out the best dosage schedule or combination of drugs for each individual patient.

Yet not everything is hunky-dory for personalized medicine. Critics of precision medicine believe that the whole idea is too much of overhyped razzmatazz, among other things. Proponents, however, argue that when it comes to managing our own health, most of us are used to the idea of taking a one-size-fits-all approach be it medicines, supplements, diets and diagnoses. This may be wrong.

What works, as they put it, for one may be a gaffe for another. As the award-winning oncologist and medical technology innovator, Dr. David B. Agus, author of the groundbreaking bookThe End of Illness, puts it, each patients individual risk factors are based on ones DNA, the environment and a preventative lifestyle plan in response. He begins with simple, profound pointers: How is your sense of smell? and Is your ring finger longer than your middle finger? He explains with statistics-backed guidelines that moving and walking regularly is mandatory because exercising and then sitting is equivalent to smoking cigarettes, while eating and sleeping at consistent hours is imperative because irregularity causes inflammation.

The inference is obvious: We should all understand our physiology and quiz doctors with the thorough, exploratory frame of mind of a gadget buyer. This holds the key to making medicine truly personal, more humane, effective and safe while keeping in mind the individual in us all as unique and distinctive, the sum of the whole not just the parts.

The views expressed in this article are the authors own and do not necessarily reflect Fair Observers editorial policy.

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The Future of Medicine Is Bespoke - Fair Observer