Do the downloads!! Share!! The diffusion of very important information and knowledge is essential for the world progress always!! Thanks!!
- – > Mestrado – Dissertation – Tabelas, Figuras e Gráficos – Tables, Figures and Graphics – ´´My´´ Dissertation @ #Innovation #energy #life #health #Countries #Time #Researches #Reference #Graphics #Ages #Age #Mice #People #Person #Mouse #Genetics #PersonalizedMedicine #Diagnosis #Prognosis #Treatment #Disease #UnknownDiseases #Future #VeryEfficientDrugs #VeryEfficientVaccines #VeryEfficientTherapeuticalSubstances #Tests #Laboratories #Investments #Details #HumanLongevity #DNA #Cell #Memory #Physiology #Nanomedicine #Nanotechnology #Biochemistry #NewMedicalDevices #GeneticEngineering #Internet #History #Science #World
The influence of physical activity in the progression of experimental lung cancer in mice
- PMID: 22683274
- DOI: 10.1016/j.prp.2012.04.006
GRUPO_AF1 – GROUP AFA1 – Aerobic Physical Activity – Atividade Física Aeróbia – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto
GRUPO AFAN 1 – GROUP AFAN1 – Anaerobic Physical Activity – Atividade Física Anaeróbia – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto
GRUPO_AF2 – GROUP AFA2 – Aerobic Physical Activity – Atividade Física Aeróbia – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto
GRUPO AFAN 2 – GROUP AFAN 2 – Anaerobic Physical Activity – Atividade Física Anaeróbia – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto
Slides – mestrado – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto
DMBA CARCINOGEN IN EXPERIMENTAL MODELS
Avaliação da influência da atividade física aeróbia e anaeróbia na progressão do câncer de pulmão experimental – Summary – Resumo – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto
Lung cancer is one of the most incident neoplasms in the world, representing the main cause of mortality for cancer. Many epidemiologic studies have suggested that physical activity may reduce the risk of lung cancer, other works evaluate the effectiveness of the use of the physical activity in the suppression, remission and reduction of the recurrence of tumors. The aim of this study was to evaluate the effects of aerobic and anaerobic physical activity in the development and the progression of lung cancer. Lung tumors were induced with a dose of 3mg of urethane/kg, in 67 male Balb – C type mice, divided in three groups: group 1_24 mice treated with urethane and without physical activity; group 2_25 mice with urethane and subjected to aerobic swimming free exercise; group 3_18 mice with urethane, subjected to anaerobic swimming exercise with gradual loading 5-20% of body weight. All the animals were sacrificed after 20 weeks, and lung lesions were analyzed. The median number of lesions (nodules and hyperplasia) was 3.0 for group 1, 2.0 for group 2 and 1.5-3 (p=0.052). When comparing only the presence or absence of lesion, there was a decrease in the number of lesions in group 3 as compared with group 1 (p=0.03) but not in relation to group 2. There were no metastases or other changes in other organs. The anaerobic physical activity, but not aerobic, diminishes the incidence of experimental lung tumors.
Copyright © 2012 Elsevier GmbH. All rights reserved.
Curing HIV just got more complicated. Can CRISPR help?
By Jon CohenMar. 15, 2019 , 3:55 PM
SEATTLE, WASHINGTON—Antiretroviral (ARV) drugs have turned HIV infection from a death sentence to a chronic condition. In most people the drugs routinely tamp HIV levels so low that standard tests find no virus in blood samples. But inexplicably, in about 10% of infected people HIV remains easily detectable in the blood even though they take their daily pills and are not saddled with drug-resistant mutants of the virus.
A study presented last week at the largest annual U.S. HIV/AIDS conference offers a solution to this riddle: “repliclones,” populations of replicating cells with HIV’s genome nestled inside them. “It’s the most interesting presentation I’ve seen here,” says George Pavlakis, a retrovirologist at the National Cancer Institute in Frederick, Maryland.
These repliclones highlight what might be a serious shortcoming in a popular HIV cure strategy. They are also drawing new attention to a radical approach for extirpating persistent virus: using the genome editor CRISPR to cut HIV’s genes out of infected cells. A monkey study of the approach presented at the same meeting showed signs of success, and a biotech company is now hoping to launch a clinical trial.
Sign up for our daily newsletter
Get more great content like this delivered right to you! Country Email
Required fields are indicated by an asterisk (*)
HIV-infected people who still have small amounts of virus in their blood despite being on ARVs frequently leave doctors “exasperated,” says virologist John Mellors of the University of Pittsburgh in Pennsylvania. Assuming that the virus has acquired resistance, they often change their patients’ drug regimens and order many extra tests. “Each of those creates anxiety and new side effects,” Mellors says. Moreover, these people may still have high enough viral loads to infect others.
At the Conference on Retroviruses and Opportunistic Infections here, virologist Elias Halvas, who works in Mellors’s lab, described carefully analyzing viral isolates and blood cells from eight men and one woman who have had mysterious, persistent low-level viremia for an average of 3 years, despite taking ARVs. Halvas and co-workers noticed something curious. Normally, each time HIV infects a cell, the virus copies its RNA genome into a DNA version that integrates at a new spot among the cell’s chromosomes. But in each of these patients, all their infected cells had HIV integrated into the exact same chromosome region—a location that differed from person to person. The sequence of the HIV DNA taken from different cells in the same person was identical, too.
Reearchers have long known that HIV can make new copies of itself in two ways. In the basic replication cycle, the HIV DNA integrated in a chromosome creates new virions that bud from that cell, then infect other cells, acquiring mutations each time. ARVs block multiple steps in that process.
In the second pathway, HIV essentially gets a free ride because it infects an immune cell that clones itself, making more cells that carry the viral genome. ARVs have no impact on that scenario, and the viral DNA ends up at the same chromosomal location in all progeny cells, without acquiring any new mutations. These clones can produce new virions themselves, but the ARVs taken by the patients derail new infections. Mellors’s team showed that this pathway single-handedly explains the low but persistent viral loads in these patients.
Daniel Kuritzkes, an HIV/AIDS clinician at Brigham and Women’s Hospital in Boston, says the new data suggest doctors should not be alarmed by the low levels of virus in patients who say they are adhering to their treatment and have no obvious immune damage occurring. “It’s safe to assume that in the absence of increasing viremia there’s no need to change [ARVs],” says Kuritzkes, whose own lab reported a similar finding in an examination of a single patient.
But the finding does cast doubt on a proposed approach to curing an infection: “kicking” cells that harbor HIV’s DNA in a latent, nonreplicating form so that they pump out new copies of the virus, setting themselves up for destruction. These repliclones are spitting out virions yet, for whatever reasons, they aren’t quickly self-destructing or being eliminated by immune responses, Mellors says. So something extra is needed to kill them. “If we can’t knock those guys out with our therapies, then kick and kill isn’t going to work,” he says.
But another approach might: directly excising the persistent HIV DNA from a person’s chromosomes with the genome editor CRISPR. “It’s a science fiction idea that one day may be possible,” Pavlakis says. Currently, he contends, the risks are too high that CRISPR’s Cas9 enzyme will make cuts in the wrong place and directing the editor to the appropriate cells isn’t simple. “CRISPR right now is not there,” he says.
At the meeting, neurovirologist Tricia Burdo of Temple University in Philadelphia in Pennsylvania described a first step: using the editor to excise at least some of the simian version of the AIDS virus, SIV, from the chromosomes of two monkeys. Earlier work has shown that CRISPR could excise HIV nestled inside the cells of mice engineered to have humanlike immune systems. In the new study, researchers infused a harmless adeno-associated virus carrying the genes for CRISPR’s targeted molecular scissors into the veins of two SIV-infected monkeys. The monkeys were on ARVs and had low levels of SIV.
Necropsies of the treated animals showed that CRISPR had cut the SIV DNA in blood, spleen, lymph node, and lung cells, apparently disabling the virus. Blood from the CRISPR’d monkeys could not infect white blood cells, whereas blood from a control animal could. The group also found Cas9 in all 14 tissues studied, suggesting the delivery virus had spread through the body as intended. “The data show much stronger effects than have been seen before, so that’s a step in the right direction,” says John Coffin, a retrovirologist at a branch of Tufts University in Boston.
Burdo says that in a future experiment, her team will take the CRISPR-treated monkeys off ARVs to see whether the virus rebounds. They also plan to transfer millions of blood cells from the CRISPR-treated monkeys to uninfected animals, another sensitive way to determine whether even trace amounts of intact SIV remain hidden.
Burdo’s collaborator, Temple University neurovirologist Kamel Khalili, hopes to develop a human version of this CRISPR gene therapy. Khalili says his firm, Excision BioTherapeutics in Philadelphia, is seeking approval to launch trials of CRISPR excision of HIV in humans by the end of this year.
Some remain skeptical CRISPR could ever hit all HIV-infected cells. Douglas Richman, a virologist at the University of California, San Diego, notes that even a person who has an undetectable viral load may have as many as 100 million cells harboring HIV DNA. “The problem with all the cure interventions is they’re impacting a few cells,” Richman says. “That still leaves a gigantic amount of virus. And when you’re eliminating something that’s dangerous, you have to get all of them.” Posted in:
Jon is a staff writer for Science.
More from News
- Does a new genetic analysis finally reveal the identity of Jack the Ripper?
- Treatments for childhood cancer can devastate lives years later. Scientists are trying to change that
- Antifungal drug could help cystic fibrosis patients for whom common treatments don’t work
Got a tip?
- Lawmakers seek delay of radio spectrum auction for next-gen cell service, saying 5G plans could hurt weather satellite data By Paul VoosenMar. 13, 2019
- New call to ban gene-edited babies divides biologists By Jon CohenMar. 13, 2019
- In a first, U.S. private sector employs nearly as many Ph.D.s as schools do By Katie LanginMar. 13, 2019
- The planet’s premier health agency has announced drastic reforms. Critics say they aren’t drastic enough By Kai KupferschmidtMar. 12, 2019
- NCI Director Norman Sharpless named acting FDA chief By Jocelyn KaiserMar. 12, 2019
- Massive voltages in thunderclouds can slow down subatomic particles Mar. 14, 2019
- Ancient slaughter of 140 children marks largest child sacrifice in the Americas Mar. 6, 2019
- This is one of the oldest tattooing needles in North America Mar. 1, 2019
- A dead whale makes the ocean’s abyss come alive Feb. 26, 2019
- The physics of why packing tape is such a pain to use Feb. 25, 2019
15 March 2019
Vol 363, Issue 6432
- Ecology Nowhere to hide
- Astronomy Flashes in the scan
- Anthropology Rare diseases prompted care in ancient times
- Education Private sector nears rank of top Ph.D. employer
- Scientific Community WHO is ‘changing its DNA’ in bid to meet new goals
- Epidemiology Giant prevention study has sobering message
Receive a year subscription to Science plus access to exclusive AAAS member resources, opportunities, and benefits.
Get Our Newsletters
Receive emails from Science. See full list
Science Table of Contents
Science Daily News
Science News This Week
Science Editor’s Choice
First Release Notification
Science Careers Job Seeker Country
I agree to receive emails from AAAS/Science and Science advertisers, including information on products, services, and special offers which may include but are not limited to news, career information, & upcoming events.
Sign up today
Required fields are indicated by an asterisk (*)
- About us
- For subscribers
- Stay Connected