Embryology

Should Fertility Patients Be Given What They Want, or What They Need? – BioNews

20 January 2020

The final session of the Progress Educational Trust (PET)'s annual conference 'Reality Check: A Realistic Look at Assisted Reproduction' asked: 'Should Fertility Patients Be Given What They Want, or What They Need?'

Sally Cheshire, Chair of the Human Fertilisation and Embryology Authority (HFEA), said that what fertility patients want most of all is a baby, or at least the chance to have a baby. She explained that many patients will do anything to achieve their aim, and that the regulator's job is to help them achieve this in the best way possible, as part of good care. She went on to explain that many patients won't (at least initially) get what they want, raising the point that 60 percent of patients self-fund their treatment, so the HFEA must help ensure that all patients get what they need.

As part of what patients need, Cheshire spoke about the information available to patients and the fact that honest, unbiased opinion about what might work needs to be published and transparent. She explained that it is difficult to regulate new and emerging treatments (not least the 'add-ons' discussed in earlier conference sessions), and that many of these treatments are not, in fact, currently regulated by the HFEA. However, the HFEA can offer information allowing patients to make informed choices about potential treatments, especially when it is sometimes hard for patients to find uncontradictory and unbiased information for themselves.

Overall, Cheshire's message was that the HFEA does not support patients spending money on (often unnecessary) 'add-on' treatments, citing an HFEA survey from last year, showing that three-quarters of patients had at least one add-on with their treatment. The HFEA rates 11 add-ons using a traffic light system. The green rating is reserved for procedures or techniques that have been shown to be effective and safe by at least one good-quality, randomised clinical trial. It was reported in the survey that none of the most common add-ons used were rated green.

Cheshire argued that clinicians selling add-ons without evidence do the fertility sector, and patients, a disservice. The HFEA will continue, as part of the inspections process, to look at information available on clinics' websites and at claims made by these clinics, as well as keeping an eye on some advice coming from the non-regulated sector.

In the next presentation, Dr Jane Stewart, chair of the British Fertility Society (BFS), asked what was difficult about taking medical advice. She said that the role of 'Dr Google' and events like the Fertility Show has both good and bad aspects. It is good that there is much up-to-date information available that can usefully stimulate debate, but this is mixed with out-of-date and commercially influenced information. How might patients tell the difference?

Dr Stewart went on to explain how the doctor-patient relationship has evolved over time, towards a spirit of mutual co-operation and patient-centred care, describing the doctor as a 'bridge between the world of medicine and the expectations and needs of patients'. She pondered whether reproductive medicine had redefined patients as consumers (she insisted on using the word 'patient') and asked what the harm is in giving all patients what they want. The harm, she said, can come from the fact that many patients are vulnerable, some are ill-informed, and most will do anything (including pay) to have the chance of having a child. Thus, the doctor has a duty to help the patient come to the right decisions for them, even if that means challenging their expectations and assumptions. 'It's OK to say no', she argued.

Professor Bobbie Farsides then told us about the power of words, explaining that 'wants' are something that we feel we would like to have, do or be. Simply, a preference. By contrast, 'needs' are things we require, because they are essential or important, not just desirable. She explained that it is easier to claim support for needs as they have more societal endorsement, whereas some wants are not seen as acceptable (though some individual assertions of needs are also deemed unacceptable). 'What starts as a dream becomes a project that's all-consuming', she said, adding 'for example the desire to become a mother turns into a need'.

Structural issues shape expectations in this domain, including the way society thinks and talks about parenthood and about what women are expected to do. Professor Farsides said that given these significant pressures, we (including the fertility sector) must ask whether there is a particular form of vulnerability in patients wanting what others want them to want. She argued that professionals must present a 'fair offer', for patients to consider and maybe accept, that is not against the patients' interests.

PET's head of communications Dr Catherine Hill then gave a personal response to the wants-versus-needs question, telling her story of infertility and the phone call, when she was 21, that changed the course of her life. What she wanted was a large family, though what she needed after that call was help and support, but she was offered none. She described this time as traumatic, leaving her needing to try to forge a new identity as a potential fertility patient.

On starting fertility treatment at 37years of age, she was shocked to find that she was not eligible forIVF on the NHS, but pleased to be told she 'had the eggs of a 30-year old'. This turned out not to be true the test she was given only measured quantity, not quality. A new clinic told her to use an egg donor, and, when she used her own eggs, the clinicsuggested preimplantation genetic screening (PGS) (itself a contentious 'add-on'). This resulted in two embryos, and led to her having a daughter.

Dr Hill said she wished she had been better informed throughout this process. She argued that fertility patients' needs include emotional support, fair access to NHS-funded IVF, fertility education (which becomes more pressing as more and more procedures are offered), and better fertility preservation options. She added that funding of NHS fertility services, as well as monitoring of the funding situation, is incredibly important.

In the discussion chaired by Fiona Fox, chief executive of the Science Media Centre, there was generally much agreement with the speakers. Cheshire, responding to a point from the audience, said that fertility education was not a key responsibility of the HFEA but that they try to do it anyway. She added that the BFS has an ongoing education project, and suggested that perhaps the HFEA could be a conduit for information in new ways in future. Dr Hill added that it was hard to fathom why fertility educationand the Fertility Fairness campaign lacks funding, when the fertility industry is worth so much.

Professor Farsides said that the old-fashioned view that the regulator was something to push against no longer holds true. She argued that clinics, and the fertility industry more widely, should work with the regulator to ensure that patients get both what they want and what they need.

The Progress Educational Trust (PET) would like to thank the sponsors of its conference - the Anne McLaren Memorial Trust Fund, Edwards and Steptoe Research Trust Fund, CooperSurgical, the European Sperm Bank, Ferring Pharmaceuticals, the London Women's Clinic, NGA Law and the Institute of Medical Ethics.

PET's next public events will be:

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Should Fertility Patients Be Given What They Want, or What They Need? - BioNews

Embryology

Amy Hart tells Loose Women she will be freezing her eggs due to early menopause concerns – Worthing Herald

Former Love Island contestant Amy Hart from Worthing said she will be freezing her eggs due to fears she may be facing early menopause.

The 27-year-old appeared on Loose Women this afternoon (January 17) to raise awareness about her situation, which many women in the UK face, and the fertility options open to them as part of the show's fertility week.

Amy said she recently went for a fertility 'MOT', in which the doctor did an internal scan of her ovaries and a blood test to check her Anti-Mllerian hormone, or AMH, levels. While her ovaries were normal, her hormone levels came back at 8.5 - with 20 being the optimum level.

Read more:

Love Island: Amy Hart cheers on fellow Worthing contestant Connor Durman

As her mother Sue went through the menopause aged 44, and her grandmother and aunt at 42 - all classified as early menopause by the NHS - Amy decided she will have her eggs frozen in the coming months, despite saying she had never had any problems with her periods.

She said the intensive treatment involved ten days of injections 'to make your hormones go into overdrive' and being put under general anaesthetic for them to be harvested.

She said: "I did always think I could do whatever I want, my 20s are for me and my 30s are for having kids. Lovely. And then you go, 'oh actually, that isn't my decision, that is my body's decision'.

"I would love to meet someone, get married, have kids naturally, fine. That is my dream idea. But if that doesn't happen, I have got my insurance policy."

According to the Human Fertilisation and Embryology Authority, the whole process for egg freezing and thawing costs an average of 7,000 to 8,000, and it has a fairly low level of success; in 2017, 19 per cent of IVF treatments using a patients own frozen eggs resulted in a baby being born.

Loose Women anchor Kaye Adams questioned Amy's decision. She said: "The NHS doesn't provide this service and they don't particularly recommend it. Look: you are 27, maybe you just need to chill out and let things go a little bit."

But fellow panellist Stacey Solomon, who also had a family history of early menopause, supported Amy's decision. She said she had considered having the treatment herself, and that there was an argument that the NHS should provide egg freezing treatments to women with a proven family history of early menopause.

According to the NHS website, early menopause happens when a woman's periods stop before the age of 45.

If you are experiencing symptoms of the menopause, such as hot flushes or night sweats, it recommended seeing a GP. For further advice, click here.

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Amy Hart tells Loose Women she will be freezing her eggs due to early menopause concerns - Worthing Herald

Cell Biology

Biomedical Applications of Zeolitic Nanoparticles, with an Emphasis on | IJN – Dove Medical Press

Hossein Derakhshankhah, 1, 2,* Samira Jafari, 1, 2,* Sajad Sarvari, 3 Ebrahim Barzegari, 4 Faezeh Moakedi, 5 Milad Ghorbani, 6 Behrang Shiri Varnamkhasti, 1 Mehdi Jaymand, 7 Zhila Izadi, 1, 8 Lobat Tayebi 9

1Pharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran; 2Zistmavad Pharmed Co., Tehran, Iran; 3Department of Pharmaceutical and Pharmacological Science, School of Medicine, West Virginia University, Morgantown, WV, USA; 4Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran; 5Department of Biochemistry and Molecular Biology, School of Medicine, West Virginia University, Morgantown, WV, USA; 6Department of Chemical Engineering, College of Engineering, University of Tehran, Tehran, Iran; 7Nano Drug Delivery Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran; 8Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran; 9Marquette University School of Dentistry, Milwaukee, WI 53201, USA

*These authors contributed equally to this work

Correspondence: Zhila Izadi; Lobat Tayebi Email izadi_zh@razi.tums.ac.ir; lobat.tayebi@marquette.edu

Abstract: The advent of porous materials, in particular zeolitic nanoparticles, has opened up unprecedented putative research avenues in nanomedicine. Zeolites with intracrystal mesopores are low framework density aluminosilicates possessing a regular porous structure along with intricate channels. Their unique physiochemical as well as physiological parameters necessitate a comprehensive overview on their classifications, fabrication platforms, cellular/macromolecular interactions, and eventually their prospective biomedical applications through illustrating the challenges and opportunities in different integrative medical and pharmaceutical fields. More particularly, an update on recent advances in zeolite-accommodated drug delivery and the prevalent challenges regarding these molecular sieves is to be presented. In conclusion, strategies to accelerate the translation of these porous materials from bench to bedside along with common overlooked physiological and pharmacological factors of zeolite nanoparticles are discussed and debated. Furthermore, for zeolite nanoparticles, it is a matter of crucial importance, in terms of biosafety and nanotoxicology, to appreciate the zeolite-bio interface once the zeolite nanoparticles are exposed to the bio-macromolecules in biological media. We specifically shed light on interactions of zeolite nanoparticles with fibrinogen and amyloid beta which had been comprehensively investigated in our recent reports. Given the significance of zeolite nanoparticles interactions with serum or interstitial proteins conferring them new biological identity, the preliminary approaches for deeper understanding of administration, distribution, metabolism and excretion of zeolite nanoparticles are elucidated.

Keywords: zeolite, mesoporous, nanostructure, biosafety, biomedical applications

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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Cell Biology

A Protein At the Center of Cell Division: Researchers Discover the Wonders TPX2 Can Do During Cell Division – Science Times

(Photo : Natanel Mansilla on Flickr)

Cell division is a relatively familiar concept for everyone since it is one of the recurring topics in biology -- mitosis and meiosis, and all.Cell division is importantfor the reproduction, and repair of the tissues and over-all growth of the organism. However, rapid cell division leads to the formation of tumors which, most of than not,leads to cancer. Recently, a team of researchers from Princeton University successfully recreated an important process in cell division in a test tube. This experiment helped them uncover the vital role of a protein that is elevated in over 25% of all cancers.

The findings, which arepublished in Nature Communications, describes a key step towards the recreation of the entire cell division machinery that can lead to new therapies with the primary goal of preventing the growth of cancer cells. Usually, when cells undergo division, themicrotubules (those spindle-shaped structures composed of thousand of filaments)attaches itself to the chromosomes then pulls each chromosome into each newly-forming cell. Each of these microtubules is assembled from tubulin molecules and because the chromosomes must assemble intro these microtubules at the right moment, an error in segregation can lead to cancer. To be able to complete this process correctly, another process called branching microtubule nucleation is necessary. The branching microtubule nucleation is crucial because it allows the cells to form a huge amount of microtubules enabling the capture of the chromosomes.

READ:Laser Can Detect Cancer Cells and Kill It

The crucial process of the branching microtubule nucleation is depending largely on several pieces of "molecular machinery". For instance, the gamma-tubulin ring complex is the one responsible for initiating the assembly of tubulin molecules into microtubules. Meanwhile, theaugmin complexis the one responsible for engaging the gamma-tubulin ring complex to the existing microtubules. The Targeting Protein for Xklp2 or TPX2 is also involved in this process, however, researchers identified that this is protein is elevated in over 25% in all forms of cancer.

The elevated TPX2 levels can lead to the abnormal assembly of microtubules in cells. Sabine Petry, an assistant professor of molecular biology, explains that to be able to better understand branching microtubule nucleation, the researchers had to do the process outside of the cell using putrified proteins. The researchers found out thatlike the augmin complex, TPX2 can bind microtubules and recruit gamma-tubulin ring complexto initiate the process of branching microtubule nucleation. They were also surprised to discover that TPX2 is also responsible for recruiting augmin to microtubules.

According to graduate student Raymundo Alfaro-Aco, the process of branching microtubule nucleation occurs most efficiently when the three molecular pieces are all present. "Surprisingly, TPX2 is at the heart of controlling this process even though it is a single protein." He said. In the published paper, Petry and her graduate student Matthew King further explains that TPX2 forms a liquid layer on the surface of existing microtubules to promote branching microtubule nucleation. These liquid layers will bead up into droplets containing tubulin. The team was also able to discover that TPX2 and tubulin can condense together to form droplets through a phase-separation mechanism (kind of similar to the mechanism that makes oil droplets form in water).

A new batch of microtubules can be formed from these droplets and can result in the formation of branched microtubule structures by condensing on the surface of the existing microtubules. King explains that the condensation of TPX2 and tubulin creates a reservoir of tubulin in a pre-existing microtubule. "It may be necessary to efficiently promote the process of branching microtubule nucleation." He said.

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A Protein At the Center of Cell Division: Researchers Discover the Wonders TPX2 Can Do During Cell Division - Science Times

Cell Biology

The biology of coffee, the world’s most popular drink – The Conversation AU

Youre reading this with a cup of coffee in your hand, arent you? Coffee is the most popular drink in the world. Americans drink more coffee than soda, juice and tea combined.

How popular is coffee? When news first broke that Prince Harry and Meghan were considering Canada as their new home, Canadian coffee giant Tim Hortons offered free coffee for life as an extra enticement.

Given coffees popularity, its surprising how much confusion surrounds how this hot, dark, nectar of the gods affects our biology.

The main biologically active ingredients in coffee are caffeine (a stimulant) and a suite of antioxidants. What do we know about how caffeine and antioxidants affect our bodies? The fundamentals are pretty simple, but the devil is in the details and the speculation around how coffee could either help or harm us runs a bit wild.

The stimulant properties of caffeine mean that you can count on a cup of coffee to wake you up. In fact, coffee, or at least the caffeine it contains, is the most commonly used psychoactive drug in the world. It seems to work as a stimulant, at least in part, by blocking adenosine, which promotes sleep, from binding to its receptor.

Caffeine and adenosine have similar ring structures. Caffeine acts as a molecular mimic, filling and blocking the adenosine receptor, preventing the bodys natural ability to be able a rest when its tired.

This blocking is also the reason why too much coffee can leave you feeling jittery or sleepless. You can only postpone fatigue for so long before the bodys regulatory systems begin to fail, leading to simple things like the jitters, but also more serious effects like anxiety or insomnia. Complications may be common; a possible link between coffee drinking and insomnia was identified more than 100 years ago.

Different people respond to caffeine differently. At least some of this variation is from having different forms of that adenosine receptor, the molecule that caffeine binds to and blocks. There are likely other sites of genetic variation as well.

There are individuals who dont process caffeine and to whom drinks like coffee could pose medical danger. Even away from those extremes, however, there is variation in how we respond to that cup of coffee. And, like much of biology, that variation is a function of environment, our past coffee consumption, genetics and, honestly, just random chance.

We may be interested in coffee because of the oh-so-joyous caffeine buzz, but that doesnt mean that caffeine is the most biologically interesting aspect of a good cup of coffee.

In one study using rats, caffeine triggered smooth muscle contraction, so it is possible that caffeine directly promotes bowel activity. Other studies, though, have shown that decaffeinated coffee can have as strong an effect on bowel activity as regular coffee, suggesting a more complex mechanism involving some of the other molecules in coffee.

What about the antioxidants in coffee and the buzz that surrounds them? Things actually start out pretty straightforward. Metabolic processes produce the energy necessary for life, but they also create waste, often in the form of oxidized molecules that can be harmful in themselves or in damaging other molecules.

Antioxidants are a broad group of molecules that can scrub up dangerous waste; all organisms produce antioxidants as part of their metabolic balance. It is unclear if supplementing our diet with additional antioxidants can augment these natural defences, but that hasnt stopped speculation.

Antioxidants have been linked to almost everything, including premature ejaculation.

Are any of the claims of positive effects substantiated? Surprisingly, the answer is again a resounding maybe.

Coffee wont cure cancer, but it may help to prevent it and possibly other diseases as well. Part of answering the question of coffees connection to cancer lies in asking another: what is cancer? At its simplest, cancer is uncontrolled cell growth, which is fundamentally about regulating when genes are, or are not, actively expressed.

My research group studies gene regulation and I can tell you that even a good cup of coffee, or boost of caffeine, wont cause genes that are turned off or on at the wrong time to suddenly start playing by the rules.

The antioxidants in coffee may actually have a cancer-fighting effect. Remember that antioxidants fight cellular damage. One type of damage that they may help reduce is mutations to DNA, and cancer is caused by mutations that lead to the misregulation of genes.

Studies have shown that consuming coffee fights cancer in rats. Other studies in humans have shown that coffee consumption is associated with lower rates of some cancers.

Interestingly, coffee consumption has also been linked to reduced rates of other diseases as well. Higher coffee consumption is linked to lower rates of Parkinsons disease and some other forms of dementia. Strikingly, at least one experimental study in mice and cell culture shows that protection is a function of a combination of caffeine and antioxidants in coffee.

Higher coffee consumption has also been linked to lower rates of Type 2 diabetes. Complexity, combined effects and variation between individuals seems to be the theme across all the diseases.

At the end of the day, where does all this leave us on the biology of coffee? Well, as I tell my students, its complicated. But as most reading this already know, coffee will definitely wake you up in the morning.

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The biology of coffee, the world's most popular drink - The Conversation AU

Cell Biology

Body Clock Biologists Find That Beauty Sleep Is Real Discovery May Unlock the Mysteries of Aging – SciTechDaily

Biologists from The University of Manchester have explained for the first time why having a good nights sleep really could prepare us for the rigors of the day ahead.

The study in mice and published in Nature Cell Biology, shows how the body clock mechanism boosts our ability to maintain our bodies when we are most active. And because we know the body clock is less precise as we age, the discovery, argues lead author Professor Karl Kadler, may one day help unlock some of the mysteries of aging.

The discovery throws fascinating light on the bodys extracellular matrix which provides structural and biochemical support to cells in the form of connective tissue such as bone, skin, tendon, and cartilage. Over half our body weight is matrix, and half of this is collagen and scientists have long understood it is fully formed by the time we reach the age of 17.

But now the researchers have discovered there are two types of fibrils the rope-like structures of collagen that are woven by the cells to form tissues.

Thicker fibrils measuring about 200 nanometers in diameter a million million times smaller than a pinhead are permanent and stay with us throughout our lives, unchanged from the age of 17.

Colorful video showing cross-sections of different collagen fibrils and the effect of the body clock on the fibrils.

But thinner fibrils measuring 50 nanometers, they find, are sacrificial, breaking as we subject the body to the rigors of the day but replenishing when we rest at night.

The collagen was observed by mass spectrometry and the mouse fibrils were observed using state of the art volumetric electron microscopy funded by the Wellcome Trust every 4 hours over 2 days.

When the body clock genes were knocked out in mice, the thin and thick fibrils were amalgamated randomly.

Collagen provides the body with structure and is our most abundant protein, ensuring the integrity, elasticity, and strength of the bodys connective tissue, said Professor Kadler.

Its intuitive to think our matrix should be worn down by wear and tear, but it isnt and now we know why: our body clock makes an element which is sacrificial and can be replenished, protecting the permanent parts of the matrix.

He added: So if you imagine the bricks in the walls of a room as the permanent part, the paint on the walls could be seen as the sacrificial part which needs to be replenished every so often. And just like you need to oil a car and keep its radiator topped up with water, these thin fibrils help maintain the bodys matrix.

Knowing this could have implications on understanding our biology at its most fundamental level. It might, for example, give us some deeper insight into how wounds heal, or how we age.

Reference: Circadian control of the secretory pathway maintains collagen homeostasis by Joan Chang, Richa Garva, Adam Pickard, Ching-Yan Chlo Yeung, Venkatesh Mallikarjun, Joe Swift, David F. Holmes, Ben Calverley, Yinhui Lu, Antony Adamson, Helena Raymond-Hayling, Oliver Jensen, Tom Shearer, Qing Jun Meng and Karl E. Kadler, 6 January 2020, Nature Cell Biology.DOI: 10.1038/s41556-019-0441-z

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Body Clock Biologists Find That Beauty Sleep Is Real Discovery May Unlock the Mysteries of Aging - SciTechDaily

Cell Biology

Dr. Garrett Wirth Giving hope to patients with personalized care and innovation – MENAFN.COM

(MENAFN - America News Hour) Globally, medical technology is progressing at a rapid pace and itcertainly comes as no surprise to see doctors offer people a new lease on life.Any life-threatening, daunting, or psychological problems patients may face,the healthcare professionals are trying their best to help people understand,accept, and tackle the situation. Dr. Garrett Wirth is one such doctor, who isgiving hope to trauma patients from all walks of life through his ability as a PlasticSurgeon.

Dr. Wirth, of Wirth Plastic Surgery in Newport Beach California is aBoard-Certified Plastic Surgeon who has performed over 20,000 procedures overthe illustrious course of his nearly 15 years of experience. With the help ofhis cosmetic and reconstructive skill set, he has given hope to patientsdiagnosed with cancer, burns, deformities, trauma, and much more. He strives tomake this transformation a positive experience by combining art and science.

Born in Albany, New York, Dr. Wirth completed his Bachelor's atMuhlenberg College in Allentown Pennsylvania with a Biology and a PoliticalScience minor. Towards the end of his time at Muhlenberg College, Dr. Wirth wasintrigued by the idea of pursuing high-quality research and chose to attendGraduate School at the Albany Medical College where he completed his Master'sDegree in Physiology and Cell Biology.

Armed with an impressive resume, he honed his skills further byjoining Doctor of Medicine program also at Albany Medical College where hepursued his MD degree. He started as a and then physician researching andplanning a career in Vascular Surgery before becoming acquainted with plasticsurgery.

Along with his successful training at the Albany Medical Center inGeneral Surgery, where he won the resident teaching award and was recognizedfor his leadership and teaching skills, Dr. Wirth also went on to furthertraining in Plastic Surgery at the University of California Irvine MedicalCenter. Upon completion of thistraining, he was asked, and accepted the honor to serve as a faculty member servingas a Professor of Plastic Surgery at the Aesthetic and Plastic SurgeryInstitute, University of California-Irvine Medical Center. There, he had thehonor of training and educating many healthcare professionals and students. Additionally,he has published his works in severalreputed national and international medical journals.

In 2017, Dr. Wirth established his private practice with the dream tooffer his expertise to 'one patient at a time'. At Wirth Plastic Surgery, hehelps people rediscover their confidence and achieve their aesthetic goals. Dr.Wirth firmly believes in working with his patients and truly understandingtheir needs - a philosophy that is implemented by his team as well. It is forthis reason that he is selective and works only with those patients with whomhe has a mutual understanding of the procedure and its outcome. 'It's about being a high quality team member with each person', says Dr. Wirth.

Through his private practice, his unique career path experience andhis patient-centric approach, he has become a pioneer in breast reconstruction,breast augmentation, and rhinoplasty. Dr. Wirth is committed to helping womenget through breast diseases and reconstruction by following a completelypatient centered approach, covering all the major aspects of the problems andsolutions. In fact, he is leading the way to develop and create a new breastconstruction invention known as Flex HD PliableMAX.He is pursuing further research in this, and many other areas to help improveas many lives as possible.

Dr. Wirth has also published a book, titled 'Personalized Breast Care- A Guide for Cosmetic Surgery, Breast Cancer, and Reconstruction' to helppeople going through breast surgery. Ithelps individuals understand anatomy, surgical and non-surgical options, howfamilyl and friends can help the person through the journey and empowers thereader with information and even questions to ask when setting up the medicaland surgical teams. In two years ofestablishing his practice in Newport Beach, his reputation as a top plasticsurgeon has only amplified, leading him to change more lives in the process. Asa leader, teacher, and a doctor, he has been able to impact lives in ways thattruly matters.

John Wilson is a freelance writer and a professional working with America News Hour as an editor. He enjoys writing about current trends and improvements in Technology & Science, Business Entertainment, Lifestyle and Sports.

MENAFN20012020007010068ID1099577643

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Dr. Garrett Wirth Giving hope to patients with personalized care and innovation - MENAFN.COM

Cell Biology

Refining pathological classification of breast cancer using multiplexed imaging – News-Medical.net

Breast cancer progression can vary significantly between patients. Even within the same tumor, different areas may be composed of different types of cells and characterized by different tumor structures. This heterogeneity makes it challenging to ascertain the severity of a tumor and assess its molecular subtype, thereby affecting the precision of diagnosis and the choice of the most effective treatment approach. More detailed characterization of a breast cancer tissue could help improve a treatment's chances of success and may decrease the risk of relapse.

The research group headed by Bernd Bodenmiller, professor of quantitative biology at UZH, has been able to refine the pathological classification of breast cancer using imaging mass cytometry. This method enables scientists to simultaneously visualize and analyze multiple biomarkers to generate information-rich digital images of tissue sections. In their study, the researchers quantified 35 protein biomarkers in breast cancer patients. "This created an unprecedented view of a tumor's cellular landscape and the surrounding tissue, which enabled us to determine whether more complex biomarkers exist for clinical outcome," explains Jana Fischer, co-first author of the study.

The team of researchers analyzed hundreds of tissue sections from 350 breast cancer patients and categorized the many cell components and how they are organized in cellular communities and form tumor tissues.

Four categories of breast cancer are routinely classified in the clinic, but our new analysis allows us to go further and identify multiple detailed subcategories of breast cancer. The danger from these diverse tumors can be very different, and each type could respond to therapy in its own way."

Hartland Jackson, co-first author

This finding has the potential to change clinical practice. The new subgroups of breast cancer patients vary in their molecular profiles. Bernd Bodenmiller and his research team are now working on finding out which drugs are best able to combat tumor cells with a specific molecular profile. "By improving our ability to describe cellular features and categories as well as our ability to precisely identify patients that have high or low risk breast cancer, we're opening up new possibilities for precision medicine," says Bodenmiller.

Source:

Journal reference:

Jackson, H. W., et al. (2020) The single-cell pathology landscape of breast cancer. Nature. doi.org/10.1038/s41586-019-1876-x.

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Refining pathological classification of breast cancer using multiplexed imaging - News-Medical.net

Cell Biology

Enzymes that cannibalize each other and promote cancer – News-Medical.net

A new study to be published this week in the journal The Proceedings of the National Academy of Sciences in the week of January 20, 2020. shows that certain human enzymes play dual roles in health and disease. Not only do they promote the occurrence of cancer and some other illnesses, they also eliminate one another rather like cannibals. The researchers hope this behaviour can be exploited to prevent these enzymes from causing human disease.

These enzymes are called cathepsins and are intended to break down unnecessary protein in the cells. When exposed to certain environments, however, they bring about a higher risk of cancer, atherosclerosis and other conditions. In an effort to stop them from playing this role, they have been blocked using various experimental drugs. The problem is that these drugs are also toxic, with novel and poorly understood side effects.

The cathepsins in the study were cysteine cathepsins and are best known for their work in the lysosome, a cell organelle, where they break down unneeded proteins into amino acids. Image Credit: National Institutes of Health

The scientists first attempted to study one cathepsin at a time but could not because of mysterious variations in the outcome. This made them suspect that there could be another reason for this behaviour. Even more, they wondered if this was the same cause for some unexplained drug treatment failures.

In an attempt to better characterize the function of the cathepsins, and the reasons for these unexpected adverse reactions, the researchers chose to look at a model of a biological system that includes three of the enzymes working together, rather than examining them singly.

Using both calculations and experimental observations, they built a computational model that reveals the way a change in one parameter affects everything else.

Cathepsins eat away at collagen and elastin in Manu Platt's Georgia Tech lab. Image Credit: Georgia Tech / Allison Carter

The study shows that the three cathepsins investigated, namely, K, L and S, are powerful degrading chemicals, breaking down unwanted structural scaffolding material outside the cell. In addition, they also target each other for degradation, offer alternative sites of action rather than the physiological target, and block each other.

The reason why they cannibalize themselves is explained by researcher Manu Platt, Auto-digestion is my personal favorite. Think about it: You take a group of cathepsin Ks, and they eat each other. Why? Because they're just closer to each other than to what they would otherwise eat. In other words, this happens because they are designed to break down proteins, including themselves. And this is precisely what happens in a disease condition.

Another important aspect is that the three cathepsins in the study depend on each other to achieve this destructive activity. In normal health the cathepsins used in the current study work within lysosomes, the garbage digesters of the cell, cutting proteins into tiny molecules called amino acids. In certain specialized cells such as the immune cells, cathepsin S helps with antigen recognition, priming the cell to distinguish friend from foe.

However, when these enzymes are present at too high levels, they appear at the wrong sites, going berserk and breaking up even the proteins which build the structure of the body. These include elastin and collagen, the proteins that make up the whole framework of every solid body tissue, from tendons and arteries to the fibrous structure at the core of all solid tissues.

This overactivity is simply an overzealous expression of the normal function of cathepsin K, for instance, which is in charge of degrading bone tissue to retrieve and reuse the calcium. However, in a cancer, the picture changes. As Platt puts it, When breast cancer comes, those cancerous cells make cathepsin K to destroy collagen around the tumor. And that allows the cells to escape and metastasize to the bone.

If the researchers can develop a drug to prevent the tumor-promoting activity of cathepsins, it would be a very beneficial step, since these enzymes play a major role in tendon inflammation, endometriosis, cancer, sickle cell disease and atherosclerosis. Platt continues, Many cathepsin inhibitor drugs that have failed clinical trials were very finely targeted but caused big side effects, and some of those cathepsin inhibitor drugs did not even cross-react with other cathepsins they were not targeting - which is usually a good thing - so the cause of the side effects was a mystery," Platt said. "By modeling a system of cathepsins, we think we have a good start toward uncovering that mystery."

What he means is that knowing more about how they work in our bodies will be essential to developing an inhibitor to these enzymes where they are unnecessarily active. The researchers also feel they have helped come up with new approaches to this process by their systems model. One example they posit is increasing the activity of cathepsin S specifically where it could break down the other two, namely, cathepsin K and L.

The systems model is available online in the hope that other scientists can also play with these three cathepsins in a group model, varying their levels, the levels of their target enzymes and the amount of inhibitor in the model.

The researchers say they have paved the way for others to carry out further experiments and test the role of inhibitors in different ways. Platt says, They can set up their own experiments and make predictions, including what inhibitors will do, so they can test inhibitors at varying strengths in this system. They can ask questions that they can't answer yet experimentally then test the model's predictions in the lab. This is because the systems biology setup allows different inputs to be processed in the form of the final effect on the levels of the cathepsin, and on the amount of degradation. It also shows whether the other cathepsins are active or have been broken down or their activity blocked. The final result will appear in the form of a spreadsheet as well as a report for easy understanding.

Source:

While promoting diseases like cancer, these enzymes also cannibalize each other - https://www.eurekalert.org/pub_releases/2020-01/giot-wpd011720.php

Read more from the original source:
Enzymes that cannibalize each other and promote cancer - News-Medical.net

Physiology

Physiology & Breeding Collection Review, 2020 – ResearchAndMarkets.com – Business Wire

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