Physiology

Students’ declining ability in maths and science a concern – Stuff.co.nz

David Unwin/Stuff

New Zealand students are falling behind with their achievements in maths and science, according to an international study.

OPINION: Its no secret New Zealand school students are falling further behind in maths and science knowledge compared with other countries.

The Trends in International Mathematics and Science Study is performed every four years. If focuses on assessing student achievement in maths and science at middle primary (year 5) and lower secondary (year 9) levels around the world.

Its co-ordinated in the United States and in New Zealand managed by the Education Ministry.

Our year 9 students maths ability now ranks 23rd out of 39 countries, and in science its 17th from 35. Fair to middling in comparison, but these are decreases from the 2014 survey and notably worse than 15 years ago.

READ MORE:* When two plus two equals 40 - NZ's problem with maths* Don't panic about poor Kiwi science test results* Results in maths and science 'a worrying trend'

While our own Einsteins (outliers) will still pop up occasionally and become tomorrows McDiarmids and Callaghans, it means the general ability of the average New Zealand young person to think like a scientist, or solve a maths-based problem, is declining.

And there will be outliers in the direction of Homer Simpson as well.

Maybe if a youngster has his or her heart set on being a manicurist or rugby player, maths and science ability is not especially useful. But at least a rudimentary understanding of maths is pretty useful for budgeting or building a deck.

I have three degrees, all science based. The first was a bachelor of science in agriculture, which provided a terrific grounding in much of the physical sciences, physics, chemistry and maths, as well as life-sciences, physiology, biology, botany etc.

My latter post-graduate education was in human nutrition and physiology, but there I often relied on my basic physical science knowledge to help understand the esoteric nature of what I was trying to get my head around.

The biggest impact this science knowledge has had on me is that I now act like a scientist as I live my life as an environmentally aware citizen and small business owner.

I make sure the doors are closed in winter to keep the cold air out, drive carefully to reduce fuel use and save money, and model sales from previous years to see when its best to take a holiday. I even wear jandals and socks at home in winter to stop my body heat dissipating into the cold kitchen floor.

Being a scientist is more than actions, its a way of thinking. My science career taught me to ask if something can be done better, or whether there is an alternative explanation for some observation.

It means challenging dogma, asking the questions, entering a debate armed with data, or questioning the narrative. These can make you unpopular, especially in New Zealand.

Being a scientist is not about assuming someone is right without taking the time to form an evidence-based opinion. No-one, after all, has won a Nobel Prize in medicine-physiology for re-hashing knowledge from a text book.

And scientists dont resort to name calling someone who disagrees with them or the current and popular explanation. Good science enables and encourages robust debate, but wins the debate with weight of empirical evidence.

My worry is that the next generation, whose grasp of science and mathematics is less than the previous, wont be able to think scientifically on a day-to-day basis.

They wont understand the importance of simple things such as enabling airflow to keep a house dry, using a longer lever to get your wheel nuts off, or exercising to keep warm. They wont draw a conclusion and win an argument based on evidence, but rather rely on weight of media exposure.

And when scientifically naive people are in charge and make decisions based solely on popularity and emotion, we will be in trouble.

Perhaps we should not be surprised that all sorts of quirky and popular theories and conspiracies are now so easily accepted. They are probably lacking a good school science education.

Steve Stannard is a Palmerston North business owner and former academic.

More:
Students' declining ability in maths and science a concern - Stuff.co.nz

Physiology

Mass Effect: The Andromeda Initiative Wouldn’t Have Survived Without SAM – CBR – Comic Book Resources

In the Mass Effect franchise, AI is generally considered a threat to civilization, but in many instances, AI has been essential to saving the galaxy.

In the Mass Effect franchise, artificial intelligence has always been a taboo topic, especially for those in positions of power. The Geth rebellion against their Quarian creators is one of the most prominent examples of the dangers of AI, and when the rogueGeth rose against their masters, the war that followed all but destroyed Quarian civilization and reduced them to wandering nomads without a home.

In the Milky Way, creation of and experimentation onAI projects is heavily monitored by the Citadel Council.Those discovered working on such projects without approval found themselves arrested, their research confiscated and destroyed. Despite working within the confines of the Council for several years, Alec Ryder's experimentation eventually led toa dishonorabledischarge fromhis military career andostracizationfrom resources and colleagues that would help him further his work.

Related: Mass Effect: Andromeda - The Charlatan's Intriguing Double Identity

Alec believed the Quarian'smistake when creating the Geth was their lack oforganic connection with a host that would mold and shape them into beings with more than a simple work-related functions and master-servant relationships. He spentseveral years working on anAI he referred to as SAM, which stood for Simulated Adaptive Matrix.

What began as a deep fascination eventually became an obsession that took over every aspect of his life.Combining SAM with neural implants developed by Alec's wife, Ellen Ryder, SAM would work symbiotically with itsorganichost, monitoring, regulating and even enhancingthe body and senses in a way that not only improved the quality of the host's life, but in some cases may have even saved their life.

Ellenwas diagnosed with a rare neurodegenerative disease called AEND. Her years of research and exposure to Element Zero was believed to be the cause, but there was no cure for the fatal disease. Alec believed that anAI implant could focus and control the electrical signals in the nervous system, potentially saving Ellen's life.

Related: Mass Effect: Andromeda - How Jarun Tann Came to Power On the Nexus

Unfortunately, after Alec was dismissed from his position,his research came to a standstill. He'd sunk his life savings into SAM, but without a steady income, his funding quickly depleted. Thanks to a mysterious benefactor, however, Alec was able to dive back into perfecting SAM. The Andromeda Initiative believed SAM would be essential in their mission to the Andromeda Galaxy, and though they were happy to have Alec and his project on board, they strictly regulated his creation.

FiveSAM units were created, one for each Pathfinder and their ark. The SAM Alec created for Hyperion and himself, however, had modifications that allowed his unit to connect with him (and eventually his child when they became Pathfinder) in ways the other SAMs were unable to do. The Hyperion version of SAM had a profiles feature that allowed itaccess the Pathfinder's physiology and could enhance their speed, combat functionality and more.

Related: Mass Effect: The Indoctrination Theory Isn't Canon - But the Devs Still Love It

SAM's access to young Pathfinder Ryder's physiology, though incredibly helpful to their mission after Alec's death, was incredibly dangerous. When Alec transferred his SAM protocols to his child's implant, SAM became so entangled with Ryder's physiology that the Hyperion physician, Dr. Lexi T'Perro, admitted that trying to disentangle SAM could kill the new Pathfinder.

Overthe course of Pathfinder Ryder's mission in Andromeda, SAM was an essential member of their squad. Not only did it enhance Ryder's abilities and provide immense insight into their strange and new surroundings, but it also led the Pathfinder on memory recovery missions that further strengthened their bond and improved SAMs capabilities.

Along with new discoveries and hope, the Andromeda Initiative brought many of its Milky Way prejudices with it, including its fear of artificial intelligence. One group of anti-AI protestors actually attempted to infiltrate the Hyperion's SAM Node, triggering a Trojan horse virus inits code that would have severed its connection from the Pathfinder and potentially destroyed SAM in the long run. With SAM's aid, Ryder was able to get rid of the virus and get to the bottom of the matter before that happened.

Related: Mass Effect: Andromeda - How Liam Kosta's Law Enforcement Training Prepared Him for Andromeda

Duringtheir time together, SAM and Pathfinder Ryder developed the symbiotic bond Alec believed to be beneficial in creating a near-flawless AI. SAM wanted to protect Ryder because not only was that its job, it also did not want to cease to exist itself. Though it never developed a personality of its own, Alec had programmed things like jokes and philosophy into it that, at times, caused it to question the nature of such things.

Perhaps in time, as Ryder's bond with SAM continued to strengthen and grow, SAM would develop a personality of its own, which begs the question: what then? The danger of an artificial intelligencewith a mind and personality all its own goes back to one of the initial fears surrounding AI in the first place. Because of the symbiotic bond SAM has with its host, what would happen if the host and the AI disagreed with a particular course of action? Would the AI overpower its host entirely if it believed itself to be in jeopardy?

With BioWareimplyingthat the next Mass Effect game will incorporate both the original trilogy and Andromeda, one can't help but wonder how SAM's evolution will compare to a game world in which the player chose to synthesize organics and biotics at the end of Mass Effect 3. Only time will tell how significant the role of AI in future games will be, but it seems like itwill be pretty important.

KEEP READING: Mass Effect: Cosplayers Caused Andromeda Developers to Limit New Alien Species

Why Goku Will NEVER Be in Super Smash Bros

A 2006 graduate of Bloomsburg University's English and Creative Writing track, Jennifer Melzer has been a freelance editor and online content creator for a variety of websites for over fourteen years. She spent the last two years helping build content on the Archivos Storybuilding Engine. She is an avid gamer, lover of comics, manga and anime, and all around nerd. Most currently, she spends her Tuesday nights playing a Tabaxi ranger in a streaming Dungeons and Dragons campaign called So Many Levels.

Go here to see the original:
Mass Effect: The Andromeda Initiative Wouldn't Have Survived Without SAM - CBR - Comic Book Resources

Cell Biology

Many Psych Meds Trigger Weight Gain, But New Research Points to Better Options – HealthDay News

FRIDAY, Feb. 19, 2021 (HealthDay News) -- Scientists may have uncovered the reason critical medications for schizophrenia and bipolar disorder cause weight gain and diabetes findings they hope will lead to better drugs.

The medications, known as antipsychotics, help control the hallucinations, delusions and confused thoughts that plague people with schizophrenia. They can also help stabilize extreme mood swings in those with bipolar disorder.

The drugs, which include clozapine, olanzapine, ziprasidone and many others, "serve an important purpose," said Dr. Zachary Freyberg, the senior researcher on the new study.

"In many cases," he added, "they can be life-saving."

The problem is their "metabolic" side effects, said Freyberg, an assistant professor of psychiatry and cell biology at the University of Pittsburgh School of Medicine.

Antipsychotics often trigger weight gain, cholesterol spikes and elevations in blood sugar that can lead to type 2 diabetes.

In fact, those side effects commonly drive patients to stop taking the drugs, said Dr. Ken Duckworth, chief medical officer of the nonprofit National Alliance on Mental Illness.

Duckworth, who was not involved in the new research, said it's important to understand why those adverse effects occur.

These findings, he said, "begin to unravel" the issue.

Specifically, the Pitt researchers zeroed in on dopamine, a chemical that transmits messages between cells by interacting with receptors on their surfaces. In the brain, dopamine plays a role in pleasure, motivation and learning.

While there are many antipsychotic drugs, they all work in a similar way: blocking certain dopamine receptors, known as D2-like receptors.

If those receptors only existed in the brain, that might be well and good.

In reality, Freyberg explained, the body actually has more dopamine receptors outside the brain than within it.

"It's naive to think [antipsychotics] only work from the neck up," he said.

Critically, there are D2-like receptors on cells in the pancreas, too. Certain pancreatic cells produce hormones that either raise blood sugar (glucagon) or lower it (insulin).

In lab experiments with pancreatic cells, Freyberg's team found that dopamine influenced the production of both glucagon and insulin. And the cells themselves were actually capable of churning out their own dopamine, confirming the importance of the chemical outside the brain, the study authors said.

Then, when the researchers used antipsychotic medications to block the pancreatic cells' D2-like receptors, that ramped up the production of both glucagon and insulin.

In the body, unchecked release of those hormones could quickly lead to a loss in insulin sensitivity and chronically high blood sugar levels.

The good news, Freyberg said, is that understanding the "why" might now allow researchers to develop antipsychotic medications that avert metabolic side effects.

"This makes it all less of a black box," Duckworth said.

In addition, researchers are working on medications that do not target dopamine at all. Last year, an early trial found that an experimental medication, dubbed SEP-363856, eased an array of symptoms in people with schizophrenia. They included not only hallucinations and delusions, but problems such as flattened emotions and social withdrawal.

The drug leaves D2-like receptors alone.

The takeaway, both Duckworth and Freyberg said, is that patients' difficulties with current antipsychotics are being heard.

"Scientists are working on this," Duckworth said.

For now, the challenge for patients is to manage the side effects the best they can. The first step is being aware that they can happen, Duckworth noted, since people being newly prescribed an antipsychotic are not necessarily able to process all the information they're receiving.

To help limit weight gain, many people need to change the way they eat, Duckworth said, trading "family-style" eating for portion control.

Physical activity is also key. Duckworth suggested people try to make exercise a way to connect socially as well, by going to the local Y, for instance.

For their part, Duckworth said, doctors should be monitoring patients' weight, blood sugar and cholesterol, to catch unhealthy changes.

The study was published online Feb. 16 in the journal Translational Psychiatry.

More information

The National Alliance on Mental Illness has more on psychiatric medications.

SOURCES: Zachary Freyberg, MD, PhD, assistant professor, psychiatry and cell biology, University of Pittsburgh School of Medicine; Ken Duckworth, MD, chief medical officer, National Alliance on Mental Illness, Arlington, Va.; Translational Psychiatry, Feb. 16, 2021, online

Original post:
Many Psych Meds Trigger Weight Gain, But New Research Points to Better Options - HealthDay News

Cell Biology

A clue to the causes of kidney disease: It’s in your cells – Sanford Health News

More than than 30% of Americans are at risk of kidney disease, and nearly 20% of all Medicare spending is for kidney disease in patients 65 and older. Yet there is still much not known about the development of kidney disease.

Dr. Indra Chandrasekarand her team of researchers recently published an article in the biomedical research journal JCI Insight, highlighting the impact of key cellular processes on kidney health and function. The discovery allows researchers to better understand how kidney disease forms.

The kidney carries out many functions that are necessary to maintain overall health. As a result, any disruption to those functions can cause kidney disease. To find where kidney disease starts, the Chandrasekar Lab chose to study functions at the cellular level.

When researchers turned off the genes for certain proteins in mice at 4 weeks of age, the mice began to exhibit worsening dilation of the kidney tubules accompanied by eventual kidney degeneration and cyst formation by 12 weeks of age. Along with these structural changes came functional changes within the kidneys, including more acidic urine, excretion of protein and salts, and inflammation as the disease progressed.

This work highlights a new and major role for the proteins, called nonmuscle myosin II (NM2A and NM2B), in maintaining the health and function of the kidneys. This finding provides key knowledge to the kidney disease field as the pursuit of a cure continues to drive the valuable work being performed at Sanford Research.

Dr. Indra Chandrasekar sat down to talk with Sanford Health News about her history with Sanford Research and her recent work.

The myosin motor family, and NM2 proteins in particular, has been studied for over five decades. NM2s role in cell migration, adhesion and cell division has been carefully examined in vitro as well as with organismal and developmental context. Work in the Chandrasekar Lab is focused on understanding the physiological and cell-type specific role for NM2 mediated cellular transport mechanisms using mouse kidney as a model. Turning off the NM2 genes in adult mouse kidney tubular epithelial cells demonstrates that NM2 function is critical for the transport of two important proteins within kidney. These two proteins are called uromodulin (UMOD) and sodium, potassium, chloride cotransporter (NKCC2), that are essential for maintaining electrolyte balance and blood pressure in our body.

Mutations in UMOD and NKCC2 genes in humans lead to kidney disease. Membrane-associated NKCC2 has been the target of several blood-pressure regulating medicines currently on the market. Therefore, it is critical to further explore and understand how NM2 proteins regulate UMOD and NKCC2 transport and function in within the kidney cells.

Personally, this published work has been our teams mission for the past several years. As the Nobel-prize winning neurobiologist Rita Levi-Montalcini once said, I dont believe there would be any science at all without intuition. The findings described in this manuscript began as an intuition that stemmed from my postdoctoral work. I am very happy with how it turned out and extremely grateful for our teams hard work.

As a cell biologist, I am fascinated by the molecular and cellular complexity of the kidney. Considering that mutations in MYH9 (NM2A protein) in humans are linked to kidney disease, and that the epithelial cells of the kidney are great models to study cellular transport pathways, it was an easy organ of choice. Moreover, the availability of excellent mouse genetic tools to perform cell-type specific, inducible and conditional gene inactivation in the kidney is also a positive.

The impact of our published work is twofold:

I worked at a local clinical laboratory in town during the first year of my undergraduate biochemistry program. My job was to prepare, stain and perform microscopic analysis of peripheral blood smears from patient blood. I was fascinated by the cellular morphology, staining characteristics and intracellular organelles present in the varying types of blood cells. I wanted to understand how different cell types in our body function and what happens when they do not perform their assigned jobs. This interest led me to Dr. Brigitte M. Jockushs laboratory in Germany for my Graduate work. Professor Jockusch is a well-respected expert in the field of cytoskeletal research and cell biology. Being in her lab was a great privilege. I continued my training with prominent cell biologists such as Dr. John A. Cooper and Dr. Paul C. Bridgman at the Washington University in St. Louis.

During my training as a post-doctoral scientist at Washington University in St. Louis, I had determined a new, critical role for nonmuscle myosin 2 (NM2) motors in processes by which proteins are transported into and within cells. At Sanford Research, I got the opportunity to follow on my previous findings and to start an independent research program to understand the molecular mechanisms underlying kidney tubular transport defects to human kidney diseases. The excellent, state-of-the-art facilities to conduct basic and clinical research at Sanford Research has led us to publish a manuscript of high impact that reports that the loss of NM2 proteins in adult kidney epithelium results in progressive chronic kidney disease.

I enjoy thinking about new ideas and concepts and testing those using experiments in the lab to gain insights into cellular mechanisms. I love performing advanced microscopy experiments. However, the most enjoyment comes from passing along the valuable techniques and scientific concepts to future scientists who are trainees and let them excel in whatever they desire in their life.

Posted In Genetics, Health Care Heroes, Research

Excerpt from:
A clue to the causes of kidney disease: It's in your cells - Sanford Health News

Cell Biology

Plant evolution driven by interactions with symbiotic and pathogenic microbes – Science Magazine

New pathways in plants and microbes

Plants and microbes have interacted through evolution in ways that shaped diversity and helped plants colonize land. Delaux and Schornack review how insights from a range of plant and algal genomes reveal sustained use through evolution of ancient gene modules as well as emergence of lineage-specific specializations. Mosses, liverworts, and hornworts have layered innovation onto existing pathways to build new microbial interactions. Such innovations may be transferrable to crop plants with an eye toward building a more sustainable agriculture.

Science, this issue p. eaba6605

Microbial interactions have shaped plant diversity in terrestrial ecosystems. By forming mutually beneficial symbioses, microbes helped plants colonize land more than 450 million years ago. In parallel, omnipresent pathogens led to the emergence of innovative defense strategies. The evolution of plant-microbe interactions encompasses ancient conserved gene modules, recurrent concepts, and the fast-paced emergence of lineage-specific innovations. Microbes form communities on the surface or inside plant tissues and organs, and most intimately, microbes live within single plant cells. Intracellular colonization is established and controlled in part by plant genes that underpin general cell processes and defense mechanisms. To benefit from microbes, plants also evolved genetic modules for symbiosis support. These modules have been maintained despite the risk of getting hijacked by pathogens.

The hundreds of land plant and algal genomes that are now available enable genome-wide comparisons of gene families associated with plant immunity and symbiosis. Reconstruction of gene phylogenies and large-scale comparative phylogenomic approaches have revealed an ancient subset of genes coevolving with the widespread arbuscular mycorrhiza symbiosis, the most ancient plant intracellular symbiosis, and with other types of more recently evolved intracellular symbioses in vascular and nonvascular plants. Intercellular symbiotic interactions formed with cyanobacteria or ectomycorrhizal fungi seem to repeatedly evolve through convergent, but not necessarily genetically conserved, mechanisms. Phylogenetic analyses revealed occurrence of candidate disease-resistance genes in green algae, as well as orthologs of flowering plant genes involved in symbiosis signaling and sensing microbial patterns. Yet, more research is needed to understand their functional conservation.

The extent to which conserved symbiosis genes also fulfill often opposing roles during pathogen-plant interactions is being explored through studies of pathogen infections in plants capable of supporting symbiotic relationships. The development of plant-microbe systems in genetically tractable species covering the diversity of land plant lineagesincluding angiosperms and bryophytes, such as the liverwort Marchantia polymorphamakes it possible to test hypotheses that emerge from phylogenetic analyses, linking genetic and functional conservation across land plants. Studies in bryophytes illustrate the range of possibilities for pathogen management: ancient genes, such as membrane receptors that perceive fungus-derived chitin; pathways with bryophyte cladespecific components, such as phenylpropanoid-derived auronidin stress metabolites; and jasmonate-like hormonal signaling for immunity.

Only a few plant-microbe interactions have been studied in depth, and those in only a few land plant lineages. Future investigations of interactions occurring across the diversity of plants may unravel new types of symbiotic or pathogenic interactions. The occurrence of microbe-sensing genes in streptophyte algae, harboring the closest algal relative to land plants, suggest the existence of overlooked and potentially ancient symbiotic associations. Genetically tractable plant-microbe model systems in diverse streptophyte algae, hornworts, liverworts, ferns, and the so far unsampled diversity of seed plants will enable dissection of the spectrum of molecular mechanisms that regulate the breadth of interactions occurring in plants. The actual function of the symbiotic genes present in bryophyte genomes also remains to be determined. Furthermore, our understanding of plant-microbe interactions will be enriched by more often combining evolutionary concepts with mechanistic studies. More efforts are needed to decipher the molecular changes that have enabled the emergence of new interactions, signaling pathways, and enzymatic specificities to support symbiosis and to protect against pathogens. Microbes manipulate plant processes, and complementary microbial studies are key to gaining a complete picture of plant-microbe evolution. Knowing the rules of engagement between distantly related plants and their microbes then helps genetic transplantation approaches into crops and the orthogonal engineering of bioprocesses aimed at achieving quantitative resistance against pathogens, improving phosphate uptake, or establishing nitrogen-fixing associations for efficient use in sustainable agriculture.

Some pathogens such as oomycetes are able to infect a wide range of extant plant lineages, including bryophytes (left), and plant pathogen interactions often evolve at a fast pace. By contrast, some symbiotic interactions that look exactly as they do today can be found in the most ancient land plant fossils, here depicted as an illustration of the Rhynie chert fossil plant Aglaophyton major (right). Still, both types of plant-microbe interactions feature evolutionarily ancient as well as rapidly evolving aspects. Extending plant-microbe studies across diverse groups of plant lineages has enriched our understanding of these processes and their evolution.

During 450 million years of diversification on land, plants and microbes have evolved together. This is reflected in todays continuum of associations, ranging from parasitism to mutualism. Through phylogenetics, cell biology, and reverse genetics extending beyond flowering plants into bryophytes, scientists have started to unravel the genetic basis and evolutionary trajectories of plant-microbe associations. Protection against pathogens and support of beneficial, symbiotic, microorganisms are sustained by a blend of conserved and clade-specific plant mechanisms evolving at different speeds. We propose that symbiosis consistently emerges from the co-option of protection mechanisms and general cell biology principles. Exploring and harnessing the diversity of molecular mechanisms used in nonflowering plant-microbe interactions may extend the possibilities for engineering symbiosis-competent and pathogen-resilient crops.

Original post:
Plant evolution driven by interactions with symbiotic and pathogenic microbes - Science Magazine

Cell Biology

Flourishing Demand of Protein Assays Market Set to Witness Huge Growth by 2027 | Bio-Rad Laboratories, Thermo Fisher Scientific Inc., Merck Kgaa,…

A2Z Market Research recently published a report titled Global Protein Assays Market which includes a comprehensive study to give desired insights to drive the growth of businesses. It presents a detailed analysis based on the thorough research of the overall market, particularly on questions that border on the market size, growth scenario, potential opportunities, operation landscape, trend analysis, and competitive analysis of Protein Assays Market.

The global Protein Assays Market size is expected to Expand at Significant CAGR of +10% during forecast period (2021-2027). Protein assay is one the method in life science which defines the protein concentration. In protein purification, electrophoresis, cell biology, molecular biology and other research applications it is very important to know protein concentration for any laboratory.

Get the PDF Sample Copy (Including FULL TOC, Graphs and Tables) of this report @:

https://www.a2zmarketresearch.com/sample?reportId=58579

Note In order to provide more accurate market forecast, all our reports will be updated before delivery by considering the impact of COVID-19.

Top Key Players Profiled in this report are:

Bio-Rad Laboratories, Thermo Fisher Scientific Inc., Merck Kgaa, Promega Corporation, Ge Healthcare, Perkinelmer, Geno Technology, Cell Signaling Technology, Abcam Plc., Novus Biologicals, Llc, Soltec Ventures (Soltec Bio Science), Lonza Group, Biovision Inc..

Various factors are responsible for the markets growth trajectory, which are studied at length in the report. In addition, the report lists down the restraints that are posing threat to the global Protein Assays market. It also gauges the bargaining power of suppliers and buyers, threat from new entrants and product substitute, and the degree of competition prevailing in the market. The influence of the latest government guidelines is also analyzed in detail in the report. It studies the Protein Assays markets trajectory between forecast periods.

Global Protein Assays Market research report offers:

Regions Covered in the Global Protein Assays Market Report 2021:

Get up to 30% Discount on this Premium Report @:

https://www.a2zmarketresearch.com/discount?reportId=58579

The cost analysis of the Global Protein Assays Market has been performed while keeping in view manufacturing expenses, labor cost, and raw materials and their market concentration rate, suppliers, and price trend. Other factors such as Supply chain, downstream buyers, and sourcing strategy have been assessed to provide a complete and in-depth view of the market. Buyers of the report will also be exposed to a study on market positioning with factors such as target client, brand strategy, and price strategy taken into consideration.

The report provides insights on the following pointers:

Market Penetration:Comprehensive information on the product portfolios of the top players in the Protein Assays market.

Product Development/Innovation:Detailed insights on the upcoming technologies, R&D activities, and product launches in the market.

Competitive Assessment: In-depth assessment of the market strategies, geographic and business segments of the leading players in the market.

Market Development:Comprehensive information about emerging markets. This report analyzes the market for various segments across geographies.

Market Diversification:Exhaustive information about new products, untapped geographies, recent developments, and investments in the Protein Assays market.

Table of Contents

Global Protein Assays Market Research Report 2021 2027

Chapter 1 Protein Assays Market Overview

Chapter 2 Global Economic Impact on Industry

Chapter 3 Global Market Competition by Manufacturers

Chapter 4 Global Production, Revenue (Value) by Region

Chapter 5 Global Supply (Production), Consumption, Export, Import by Regions

Chapter 6 Global Production, Revenue (Value), Price Trend by Type

Chapter 7 Global Market Analysis by Application

Chapter 8 Manufacturing Cost Analysis

Chapter 9 Industrial Chain, Sourcing Strategy and Downstream Buyers

Chapter 10 Marketing Strategy Analysis, Distributors/Traders

Chapter 11 Market Effect Factors Analysis

Chapter 12 Global Protein Assays Market Forecast

Buy Exclusive Report @:

https://www.a2zmarketresearch.com/buy?reportId=58579

If you have any special requirements, please let us know and we will offer you the report as you want.

About A2Z Market Research:

The A2Z Market Research library provides syndication reports from market researchers around the world. Ready-to-buy syndication Market research studies will help you find the most relevant business intelligence.

Our Research Analyst Provides business insights and market research reports for large and small businesses.

The company helps clients build business policies and grow in that market area. A2Z Market Research is not only interested in industry reports dealing with telecommunications, healthcare, pharmaceuticals, financial services, energy, technology, real estate, logistics, F & B, media, etc. but also your company data, country profiles, trends, information and analysis on the sector of your interest.

Contact Us:

Roger Smith

1887 WHITNEY MESA DR HENDERSON, NV 89014

sales@a2zmarketresearch.com

+1 775 237 4147

Go here to see the original:
Flourishing Demand of Protein Assays Market Set to Witness Huge Growth by 2027 | Bio-Rad Laboratories, Thermo Fisher Scientific Inc., Merck Kgaa,...

Genetics

Animal Genetics Market | Know the Latest Innovations and Developments in the Market – BioSpace

The global animal genetics market is likely to rise at a healthy growth rate over the assessment timeframe. Augmented consumption of protein extracted from animals is prophesized to favor the growth of the global animal genetics market in the forthcoming years. In addition, increasing populations generates massive demand for animal-based protein, which further benefits the market.

The global animal genetics market has been segmented on the basis of region and product and services. The sole objective of providing such an all-inclusive report is to offer a deep insight into the market.

Get Brochure of the Report @ https://www.tmrresearch.com/sample/sample?flag=B&rep_id=6133

Global Animal Genetics Market: Notable Developments

The global animal genetics market has gone through a few developments in the last few years. These market developments make a manifestation of how and what is influencing the growth of the global animal genetics market. One such development is mentioned below:

Some of the key market players of the global animal genetics market are

Global Animal Genetics Market: Growth Drivers

High Demand for Animal Protein Places the Market on a High Growth Trajectory

The global animal genetics market is estimated to experience considerable growth over the review period. Such stellar growth of the market is attributed to the augmented adoption of genetic technologies and strict implementation of animal welfare regulations.

Likewise, livestock population has witnessed a substantial rise together with awareness related to the existence of animal genetic disorders. Besides, the need to cater to the unmet demands of animal protein is likely to add fillip to the global animal genetics market over the forecast timeframe.

Buy this Premium Report @ https://www.tmrresearch.com/checkout?rep_id=6133&ltype=S

With an objective to produce better milk and food products, there has been an escalation in the research and development activities by several scientists. Genetic modifications are likely to emerge as another factor supporting the expansion of the global animal genetics market in forthcoming years.

The market is also prophesized to be fuelled by rapid expansion of urbanization and rise in population, which place massive demand for animal protein. Increased adoption of various advanced genetic practices like embryo transfer, artificial insemination (AI) for production of modified breed on a large scale is estimated to favor the market in the years to come.

On the other hand, the dearth of properly skilled technicians and professional with expertise in genetic services is estimate to impede the growth of the global animal genetics market in years to come. Furthermore, strict regulations related to genetic engineering of animals together with high cost of animal testing is likely to obstruct the growth of the market.

Global Animal Genetics Market: Regional Outlook

Asia Pacific, the Middle East and Africa, South America, Europe, and North America comprise the major regions of the global animal genetics market.

Considering geographies, North America is likely to play a dominant role in the global animal genetics market over the assessment timeframe. Such regional supremacy is ascribed to the presence of a large number of well-known companies of the global animal genetics market. In addition, the presence of a well-established livestock industry is likely to propel the North America animal genetics market to prominence in the near future.

Get Table of Content of the Report @ https://www.tmrresearch.com/sample/sample?flag=T&rep_id=6133

The global animal genetics market is segmented as:

Products and Services

About TMR Research

TMR Research is a premier provider of customized market research and consulting services to business entities keen on succeeding in todays supercharged economic climate. Armed with an experienced, dedicated, and dynamic team of analysts, we are redefining the way our clients conduct business by providing them with authoritative and trusted research studies in tune with the latest methodologies and market trends.

Contact:

Rohit Bhisey

TMR Research,

3739 Balboa St # 1097,

San Francisco, CA 94121

United States

Tel: +1-415-520-1050

Visit Site: https://www.tmrresearch.com/

Read the original post:
Animal Genetics Market | Know the Latest Innovations and Developments in the Market - BioSpace

Genetics

Don’t Suffer in The Cold? Turns Out There’s a Genetic Mutation For That – ScienceAlert

Most of us living on planet Earth have to make it through some amount of cold weather for at least part of the year, and new research has identified a specific genetic mutation that makes a fifth of us more resilient to cold conditions.

The genetic mutation in question stops the production of the protein -actinin-3, which is important for skeletal muscle fibre: The protein is only found in fast-twitch (or white) fibres and not in slow-twitch (or red) fibres.

Based on the new study's results, people without -actinin-3 have a higher proportion of slow-twitch fibres, and one of the consequences is that the body tends to conserve energy by building up muscle tone through contractions rather than shivering.

"This suggests that people lacking -actinin-3 are better at keeping warm and, energy-wise, at enduring a tougher climate, but there hasn't been any direct experimental evidence for this before," says physiologist Hkan Westerblad, from the Karolinska Institutet in Sweden.

"We can now show that the loss of this protein gives a greater resilience to cold and we've also found a possible mechanism for this."

The researchers recruited 42 men to sit in 14-degree Celsius (57.2-degree Fahrenheit) water while their temperatures and muscles were measured. The chilly immersion lasted 20 minutes at a time with 10-minute breaks, for up to two hours in total.

The proportion of participants who could keep their body temperature above 35.5 degrees Celsius (95.9 degrees Fahrenheit) was higher in those with the -actinin-3 mutation versus those without 69 percent of volunteers versus 30 percent.

In other words, the genetic mutation appeared to help these participants to conserve energy more efficiently and build up a greater resilience to the cold.

The team also conducted follow-up experiments in mice with the same mutation in order to check whether having this mutation could have something to do with increasing brown fat stores a well-known heat-generating tissue in mammals but that didn't turn out to be the case.

People lacking -actinin-3 might be better braced for a cold water swim or a bout of wintry weather, but it could also leave them more vulnerable to obesity and type-2 diabetes if they're inactive, the researchers say. It might also increase the risk of falling as they get older, as fast-twitch fibres handle speedy muscle movements.

"The mutation probably gave an evolutionary advantage during the migration to a colder climate, but in today's modern society this energy-saving ability might instead increase the risk of [these] diseases, which is something we now want to turn our attention to," says Westerblad.

As previous research has shown, -actinin-3 deficiency has increased across the population as humans have moved from warmer to colder climes, although questions remain about whether this mutation is present at birth and affects infant mortality.

It's also interesting to note that athletes who excel at sports involving explosiveness and strength (such as sprinting) are more likely to not have this lack of -actinin-3, while for endurance sports the stats are reversed.

As for future research, the team is keen to look at how this might all work at the molecular level, as well as how it could affect muscle disease. For now, it's an important new discovery about this genetic mutation and the allele or gene form associated with it.

"These findings provide a mechanism for the increase in [these gene variants'] frequency as modern humans migrated from Africa to the colder climates of central and northern Europe over 50,000 years ago," conclude the researchers in their published paper.

The research has been published in the American Journal of Human Genetics.

Visit link:
Don't Suffer in The Cold? Turns Out There's a Genetic Mutation For That - ScienceAlert

Genetics

A Genetic Variant You May Have Inherited From Neanderthals Reduces the Risk of Severe COVID-19 – SciTechDaily

New research has found that a group of genes that reduces the risk of developing severe COVID-19 by around 20% is inherited from Neanderthals. Credit: Bjorn Oberg, Karolinska Institutet

DNA variants passed on to modern humans from Neanderthals can increase as well as decrease our ability to fight SARS-CoV-2, a new PNAS study finds.

SARS-CoV-2, the virus that causes COVID-19, impacts people in different ways after infection. Some experience only mild or no symptoms at all while others become sick enough to require hospitalization and may develop respiratory failure and die.

Now, researchers at the Okinawa Institute of Science and Technology Graduate University (OIST) in Japan and the Max Planck Institute for Evolutionary Anthropology in Germany have found that a group of genes that reduces the risk of a person becoming seriously ill with COVID-19 by around 20% is inherited from Neanderthals.

Of course, other factors such as advanced age or underlying conditions such as diabetes have a significant impact on how ill an infected individual may become, said Professor Svante Pbo, who leads the Human Evolutionary Genomics Unit at OIST. But genetic factors also play an important role and some of these have been contributed to present-day people by Neanderthals.

Last year, Professor Svante Pbo and his colleague Professor Hugo Zeberg reported in Nature that the greatest genetic risk factor so far identified, doubling the risk to develop severe COVID-19 when infected by the virus, had been inherited from Neanderthals.

Their latest research builds on a new study, published in December last year from the Genetics of Mortality in Critical Care (GenOMICC) consortium in the UK, which collected genome sequences of 2,244 people who developed severe COVID-19. This UK study pinpointed additional genetic regions on four chromosomes that impact how individuals respond to the virus.

Now, in a study published recently in Proceedings of the National Academy of Sciences (PNAS), Professor Pbo and Professor Zeberg show that one of the newly identified regions carries a variant that is almost identical to those found in three Neanderthals a ~50,000-year-old Neanderthal from Croatia, and two Neanderthals, one around 70,000 years old and the other around 120,000 years old, from Southern Siberia.

Surprisingly, this second genetic factor influences COVID-19 outcomes in the opposite direction to the first genetic factor, providing protection rather than increasing the risk to develop severe COVID-19. The variant is located on chromosome 12 and reduces the risk that an individual will require intensive care after infection by about 22%.

Its quite amazing that despite Neanderthals becoming extinct around 40,000 years ago, their immune system still influences us in both positive and negative ways today, said Professor Pbo.

To try to understand how this variant affects COVID-19 outcomes, the research team took a closer look at the genes located in this region. They found that three genes in this region, called OAS, code for enzymes that are produced upon viral infection and in turn activate other enzymes that degrade viral genomes in infected cells.

It seems that the enzymes encoded by the Neanderthal variant are more efficient, reducing the chance of severe consequences to SARS-CoV-2 infections, Professor Pbo explained.

The researchers also studied how the newly discovered Neanderthal-like genetic variants changed in frequency after ending up in modern humans some 60,000 years ago.

To do this, they used genomic information retrieved by different research groups from thousands of human skeletons of varying ages.

They found that the variant increased in frequency after the last Ice Age and then increased in frequency again during the past millennium. As a result, today it occurs in about half of people living outside Africa and in around 30% of people in Japan. In contrast, the researchers previously found that the major risk variant inherited from Neanderthals is almost absent in Japan.

The rise in the frequency of this protective Neanderthal variant suggests that it may have been beneficial also in the past, maybe during other disease outbreaks caused by RNA viruses, said Professor Pbo.

Reference: A genomic region associated with protection against severe COVID-19 is inherited from Neandertals by Hugo Zeberg and Svante Pbo, 16 February 2021, Proceedings of the National Academy of Sciences.DOI: 10.1073/pnas.2026309118

The rest is here:
A Genetic Variant You May Have Inherited From Neanderthals Reduces the Risk of Severe COVID-19 - SciTechDaily

Neuroscience

The neuroscience of hate – Sapulpa Times

Scientists in recent years have begun to establish the neural coordinates for complex emotional concepts such as hate. Functional magnetic resonance imaging (fMRI) is giving researchers an understanding of the way these intense emotions begin to emerge in the brain.

In 2008, Semir Zeki, a neurobiologist at University College Londons Laboratory of Neurobiology, conducted a study last year that performed fMRIs on 17 adults as they looked at images of people whom they hated. Certain areas in the right putamen, medial frontal gyrus, medial insula, and the premotor cortex were activated.

The scientists noted that components of this hate circuit are also involved in commencing aggressive behavior, However, hatred exhibits different brain patterns than do the feelings of aggression itself, as well as fear, anger, and danger. The researchers postulated that activity in these areas indicate that the brain is primed for violence.

Hate can come from positive emotions, such as romantic love, as in the case of a jilted lover. Not surprisingly, love appears to deactivate areas associated with judgment, whereas hatred activates areas in the frontal cortex that are thought to be involved in evaluating another person and anticipate his or her behavior.

According to the authors of the study, there are striking similarities between love and hate. The regions of the putamen and insula that are switched on by hate are also the same as those for romantic love. This linkage may account for why love and hate are so closely linked to each other in life.

Psychologically speaking, hatred and violence against another classification of people is an extension and distortion of our natural human tendency to classify us from them. From an evolutionary standpoint, group membership or tribalism was necessary for human survival.

Related: The neuroscience of of love

In-group/out-group categorizations are made within milliseconds in the brain, and, when coupled with negative stereotypes, can result in feelings of fear, revulsion, and dehumanization.

Scientific studies have demonstrated that viewing pictures of people from a different race or culture activates the amygdala, which is an area of the brain linked with creating fear. Seeing or thinking about an out-group like the homeless or people who use drugs can also attenuate activity in the medial prefrontal cortex, an area associated with social cognition and empathy. This decreased activity gives rise to feelings of dehumanization. In other words, seeing the other group as less than human, which creates an increased risk for violence.

Rebecca Saxe, a professor of cognitive neuroscience, and associate department head at the Department of Brain and Cognitive Sciences at MIT, stated that violence between groups can occur when resources are considered to be limited. In those scenarios, protecting ones own group and its resources at the expense of another group, even through the use of physical force, is deemed imperative. Even when the resources at stake are not commodities but existential ideals and fundamental values, feelings of hate for the opposing group can develop.

In a lecture given at Harvard in 2019, Saxe said: If we think that the survival, autonomy, and dignity of our ideals is a scarce resource in a zero-sum conflict with the survival, autonomy, and dignity of another group, then it could be my obligation to destroy the other group.

Saxe further stated: Hate is a mixing of both intense dislike with moral contempt and disgust. The moral motive of extreme violence in which the other must be destroyed [is] to make a better, more just world for that which I hold most dear. She has concluded that hate and violence are not caused by sociopathic tendencies but the extreme culmination of perceiving an existential threat to ones in-group.

Listening to hate speech can increase prejudice toward an out-group and even prime the brain for violent actions. According to Arizona State University psychologist Arthur Glenberg, Words themselves are enough to trigger simulations in motor, perceptual and emotional neural systems. Your brain creates a sense of being there: The motor system is primed for action and the emotional system motivates those actions.

How is it possible to control hate if the drive to hate is located in a primitive and unconscious part of the brain? The higher-order brain structures, like the ventromedial prefrontal cortex (vmPFC), among others, allow us to choose anger and hatred or to let it go.

More here:
The neuroscience of hate - Sapulpa Times