3 fates of this matter

3 fates of this matter

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When an animal eats something, it obtains matter and energy right? But, what are the 3 possible fates of the matter and 3 possible fates energy. I don't understand what they are even asking. What would be the 3 possible fates of each.

I think the poster wants only a simple answer, so I am going to answer in simple terms. The fates can be -

1 Used in cellular respiration as fuel and some amount can be converted to useful energy which can be used to build other substances and some energy can be lost as heat.

2.The animal can become prey for other animal.

3.The animal throws away some matter as feces.

Maybe this video might help you:

Matter and Energy in Organisms

3.2: Elements and Compounds

  • Contributed by Suzanne Wakim & Mandeep Grewal
  • Professors (Cell Molecular Biology & Plant Science) at Butte College

If you look at your hand, what do you see? Of course, you see skin, which consists of cells. But what are skin cells made of? Like all living cells, they are made of matter. In fact, all things are made of matter. Matter is anything that takes up space and has mass. Matter, in turn, is made up of chemical substances. A chemical substance is a matter that has a definite composition and the same composition throughout. A chemical substance may be either an element or a compound.

Figure (PageIndex<1>): Diversity and Unity

A transient decrease in mitochondrial activity contributes to establish the ganglion cell fate in retina adapted for high acuity vision

Although the plan of the retina is well conserved in vertebrates, there are considerable variations in cell type diversity and number, as well as in the organization and properties of the tissue. The high ratios of retinal ganglion cells (RGCs) to cones in primate fovea and bird retinas favor neural circuits essential for high visual acuity and color vision. The role that cell metabolism could play in cell fate decision during embryonic development of the nervous system is still largely unknown. Here, we describe how subtle changes of mitochondrial activity along the pathway converting uncommitted progenitors into newborn RGCs increase the recruitment of RGC-fated progenitors. ATOH7, a proneural protein dedicated to the production of RGCs in vertebrates, activates transcription of the Hes5.3 gene in pre-committed progenitors. The HES5.3 protein, in turn, regulates a transient decrease in mitochondrial activity via the retinoic acid signaling pathway few hours before cell commitment. This metabolic shift lengthens the progression of the ultimate cell cycle and is a necessary step for upregulating Atoh7 and promoting RGC differentiation.

Keywords: Atoh7 Hes5.3 Metabolism Mitochondria Neurogenesis Retina Retinal ganglion cell Retinoic acid.

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

The most wonderful and dreadful thing about destiny is that we will never know, until the future arrives as the present.

The end points may be fixed, but we don’t know precisely how we’ll reach them. The quality of our life depends on how we deal with this uncertainty. Here are a few thoughts.

The inevitable cannot be avoided

We do make choices every single moment. From the mundane to what appears to be the most life changing decisions, and we feel we have some control. But there are events that we cannot change, or even understand—no matter how hard we try.

Events like serious illness, loss of loved ones, macro economic downturns, financial crises, famine, war, and all the causes that may lead to death or suffering don’t fall under our direct control. We can try and minimize some of the risks, but there are eventualities that will take place.

The sooner we accept this, the better we can cope, and live, with the unknown inevitable.

Even the positive outcomes and achievements that we _think _we’ve earned might’ve been prewritten in our book of destiny.

Accept the things to which fate binds you and love the people with whom fate brings you together, and do so with all your heart.

The duality of life: What fate is and isn’t

Life’s events unfold within two contrasting sides, and all of the possible in-betweens.

We, like other aspects of life, are destined to experience some of these contrasts and a shade or more of the in-between.

A deterministic fate might feel depressing or exciting … limiting or liberating—depending on how you look at it.

Here are a few thoughts about how we might view fate.

  • Unknowable: We can’t know, with accuracy, what will happen the next moment, let alone a year, or a lifetime from now.
  • Unpredictable: Events may unfold in ways that defy common sense and all of our statistics and predictions.
  • Moderate and extreme: Fate can be viewed as a friend bestowing upon us good fortune beyond our wildest dreams, or as an enemy handing us the most painful and shocking of experiences. It can also go unnoticed as it mildly guides our day-to-day life.
  • An excuse to give up: No matter what happens, it’s within our control to choose kindness, to do our best, or to do the right thing. Our tiny actions may not matter much from a cosmic perspective, but we will be at peace with our choices.
  • A weapon to use against others: Fate works on its own terms. And maybe, just maybe, other people’s choices that we find reprehensible are governed by a universal fate that we can’t understand. In this case, we can choose compassion instead of harsh judgment and alienation.
  • Understandable or explainable: We may never know why certain things happen and how fate works.

The more we accept that we may not be in control, as much as we’d like, the more we open up to life … and trust.

The dance of surrender

There is no point in resisting, arguing with, or trying to change the unchangeable and uncontrollable tune of this life.

The unknown future may as well determine significant portions of our life, even in this moment. However, it doesn’t have to stop us from being who we are—living, breathing, and unique contrasts of creation.

Fate may have the final say. But until destiny shows its hand, we do the best we can, accept the consequences of our choices … and trust what will be.

We don’t know—and maybe we’ll never know—the purpose of this life, or the inner workings of fate.

We might be ruled by our biology and cosmic laws beyond our control. But between beginnings and endings, we do have some wiggle room. And this is where free will resides, and where we can make conscious choices.

Life is like a game of cards. The hand you are dealt is determinism the way you play it is free will.


RNA primers are used by living organisms in the initiation of synthesizing a strand of DNA. A class of enzymes called primases add a complementary RNA primer to the reading template de novo on both the leading and lagging strands. Starting from the free 3’-OH of the primer, known as the primer terminus, a DNA polymerase can extend a newly synthesized strand. The leading strand in DNA replication is synthesized in one continuous piece moving with the replication fork, requiring only an initial RNA primer to begin synthesis. In the lagging strand, the template DNA runs in the 5′→3′ direction. Since DNA polymerase cannot add bases in the 3′→5′ direction complementary to the template strand, DNA is synthesized ‘backward’ in short fragments moving away from the replication fork, known as Okazaki fragments. Unlike in the leading strand, this method results in the repeated starting and stopping of DNA synthesis, requiring multiple RNA primers. Along the DNA template, primase intersperses RNA primers that DNA polymerase uses to synthesize DNA from in the 5′→3′ direction. [1]

Another example of primers being used to enable DNA synthesis is reverse transcription. Reverse transcriptase is an enzyme that uses a template strand of RNA to synthesize a complementary strand of DNA. The DNA polymerase component of reverse transcriptase requires an existing 3' end to begin synthesis. [1]

Primer removal Edit

After the insertion of Okazaki fragments, the RNA primers are removed (the mechanism of removal differs between prokaryotes and eukaryotes) and replaced with new deoxyribonucleotides that fill the gaps where the RNA was present. DNA ligase then joins the fragmented strands together, completing the synthesis of the lagging strand. [1]

In prokaryotes, DNA polymerase I synthesizes the Okazaki fragment until it reaches the previous RNA primer. Then the enzyme simultaneously acts as a 5′→3′ exonuclease, removing primer ribonucleotides in front and adding deoxyribonucleotides behind until the region has been replaced by DNA, leaving a small gap in the DNA backbone between Okazaki fragments which is sealed by DNA ligase.

In eukaryotic primer removal, DNA polymerase δ extends the Okazaki fragment in 5′→3′ direction, and upon encountering the RNA primer from the previous Okazaki fragment, it displaces the 5′ end of the primer into a single-stranded RNA flap, which is removed by nuclease cleavage. Cleavage of the RNA flaps involves either flap structure-specific endonuclease 1 (FEN1) cleavage of short flaps, or coating of long flaps by the single-stranded DNA binding protein replication protein A (RPA) and sequential cleavage by Dna2 nuclease and FEN1. [2]

Synthetic primers are chemically synthesized oligonucleotides, usually of DNA, which can be customized to anneal to a specific site on the template DNA. In solution, the primer spontaneously hybridizes with the template through Watson-Crick base pairing before being extended by DNA polymerase. The ability to create and customize synthetic primers has proven an invaluable tool necessary to a variety of molecular biological approaches involving the analysis of DNA. Both the Sanger chain termination method and the “Next-Gen” method of DNA sequencing require primers to initiate the reaction. [1]

PCR primer design Edit

The polymerase chain reaction (PCR) uses a pair of custom primers to direct DNA elongation toward each other at opposite ends of the sequence being amplified. These primers are typically between 18 and 24 bases in length and must code for only the specific upstream and downstream sites of the sequence being amplified. A primer that can bind to multiple regions along the DNA will amplify them all, eliminating the purpose of PCR. [1]

A few criteria must be brought into consideration when designing a pair of PCR primers. Pairs of primers should have similar melting temperatures since annealing during PCR occurs for both strands simultaneously, and this shared melting temperature must not be either too much higher or lower than the reaction's annealing temperature. A primer with a Tm (melting temperature) too much higher than the reaction's annealing temperature may mishybridize and extend at an incorrect location along the DNA sequence. A Tm significantly lower than the annealing temperature may fail to anneal and extend at all.

Additionally, primer sequences need to be chosen to uniquely select for a region of DNA, avoiding the possibility of hybridization to a similar sequence nearby. A commonly used method for selecting a primer site is BLAST search, whereby all the possible regions to which a primer may bind can be seen. Both the nucleotide sequence as well as the primer itself can be BLAST searched. The free NCBI tool Primer-BLAST integrates primer design and BLAST search into one application, [3] as do commercial software products such as ePrime and Beacon Designer. Computer simulations of theoretical PCR results (Electronic PCR) may be performed to assist in primer design by giving melting and annealing temperatures, etc. [4]

As of 2014, many online tools are freely available for primer design, some of which focus on specific applications of PCR. Primers with high specificity for a subset of DNA templates in the presence of many similar variants can be designed using DECIPHER [ citation needed ] .

Selecting a specific region of DNA for primer binding requires some additional considerations. Regions high in mononucleotide and dinucleotide repeats should be avoided, as loop formation can occur and contribute to mishybridization. Primers should not easily anneal with other primers in the mixture this phenomenon can lead to the production of 'primer dimer' products contaminating the end solution. Primers should also not anneal strongly to themselves, as internal hairpins and loops could hinder the annealing with the template DNA.

When designing primers, additional nucleotide bases can be added to the back ends of each primer, resulting in a customized cap sequence on each end of the amplified region. One application for this practice is for use in TA cloning, a special subcloning technique similar to PCR, where efficiency can be increased by adding AG tails to the 5′ and the 3′ ends. [5]

Degenerate primers Edit

Some situations may call for the use of degenerate primers. These are mixtures of primers that are similar, but not identical. These may be convenient when amplifying the same gene from different organisms, as the sequences are probably similar but not identical. This technique is useful because the genetic code itself is degenerate, meaning several different codons can code for the same amino acid. This allows different organisms to have a significantly different genetic sequence that code for a highly similar protein. For this reason, degenerate primers are also used when primer design is based on protein sequence, as the specific sequence of codons are not known. Therefore, primer sequence corresponding to the amino acid isoleucine might be "ATH", where A stands for adenine, T for thymine, and H for adenine, thymine, or cytosine, according to the genetic code for each codon, using the IUPAC symbols for degenerate bases. Degenerate primers may not perfectly hybridize with a target sequence, which can greatly reduce the specificity of the PCR amplification.

Degenerate primers are widely used and extremely useful in the field of microbial ecology. They allow for the amplification of genes from thus far uncultivated microorganisms or allow the recovery of genes from organisms where genomic information is not available. Usually, degenerate primers are designed by aligning gene sequencing found in GenBank. Differences among sequences are accounted for by using IUPAC degeneracies for individual bases. PCR primers are then synthesized as a mixture of primers corresponding to all permutations of the codon sequence.

The Embryo Project Encyclopedia

Early development occurs in a highly organized and orchestrated manner and has long attracted the interest of developmental biologists and embryologists. Cell lineage, or the study of the developmental differentiation of a blastomere, involves tracing a particular cell (blastomere) forward from its position in one of the three germ layers. Labeling individual cells within their germ layers allows for a pictorial interpretation of gastrulation. This chart or graphical representation detailing the fate of each part of an early embryo is referred to as a fate map. In essence, each fate map portrays the developmental history of each cell.

Fate maps were developed as a way of tracing a particular region as it develops from an early embryo into a differentiated body plan. The first fate maps date back to the 1880s and in 1905 the first comprehensive collection of Ascidian (sea squirt) fate maps was published by Edwin Conklin. It is now common to find fate maps in introductory embryology texts. For example, Scott Gilbert’s Developmental Biology (2006) shows fate maps for several different model organisms, including the zebrafish, frog, mouse, and chick embryos. Methods used for fate mapping include, but are not limited to, histological staining, genetic, and genetic inducible fate mapping. The ultimate goal in creating a fate map is to construct a lineage diagram that not only gives spatial information about cell fates, but can also allow the observer to trace the parental lineage of each mitotic division. This type of information can be particularly hard to achieve, but when acquired it can be used to trace the development of complex organ systems such as the central nervous system (a process that involves extensive cell migration).

In the fertilized eggs of many organisms, the progenitor cells are totipotent, meaning that they are capable of expressing every gene in their genome and that each individual cell has the potential to create an identical organism. The commitment of a cell to a specialized developmental pathway is called determination. By removing cells that are already determined and implanting them into a host embryo, one can deduce what the original cells were specified to become. The first visible cell positioning in the embryo of most organisms is during gastrulation, when the embryo rearranges itself into three distinct germ layers: endoderm, ectoderm, and mesoderm. As each cell migrates to its position in the embryo, chemical signals are released, inducing the cell to a particular fate. The developmental fates of the ectoderm, for instance, can be epidermis, central nervous system, sensory organs, and neural crest. Mesoderm cells can become part of the skeleton, muscles, blood vessels, heart, and gonads. The lining of the digestive and respiratory tracts, liver, and pancreas can all derive from the endoderm.

According to Walter Vogt’s research in 1925, the amphibian blastula divides into three regions: animal, marginal, and vegetal. Each of these areas houses progenitors of the cells that will make up the future organs of the organism. For instance, the animal cap of Vogt’s amphibian will differentiate into the nervous system, eyes, and epidermis while the marginal zone will supply material for the notochord, connective tissue, mesodermal lining, and the alimentary canal. The vegetal region is composed of cells that will later be found in the mid- and hindgut. Figure 127 in Balinsky’s An Introduction to Embryology (1981) shows an image of the fate map of the amphibians Discoglossus and Ambystoma similar to those created by Vogt for Xenopus.

More detailed fate maps have been created for the frog Xenopus, such as the one published by Osamu Nakamura and Keiko Kishiyama in 1971. Their fate map of the 32-cell-stage embryo divided the cells into four tiers each containing eight cells, labeled A–D (A and B corresponding to the animal pole, C to the marginal zone, and D to the vegetal pole). The fate map was developed by staining each individual cell and tracing each through gastrulation. An image representation of Nakamura and Kishiyama’s 32-cell-stage Xenopus can be found in most embryology textbooks. Once the cells were stained the scientists were able to photograph and detail the development of the amphibian embryo. More recent illustrations, in Hake and Wilt’s Principles of Developmental Biology (2004) show how a fate map can be made using an amphibian egg.

Some embryos show no increase in size during the early stages of development and no random cell migration, as is the case for the highly studied nematode, Caenorhabditis elegans. The cells of this embryo undergo a simple and regulated pattern of mitosis, making C. elegans a model organism for studying development and for assembling a complete fate map and lineage diagram. Experiments done to complete the fate map of this nematode included removing portions of the embryo and analyzing the resulting organism. For example, if a researcher removed a portion of the organism that was fated to become the gut, then the resulting organism would lack a gut. These experiments were initiated in 1974 by Sydney Brenner, biologist and 2002 Nobel Prize winner in Physiology or Medicine. He chose the nematode worm for study because of its rapid period of embryogenesis and very few cell types. Brenner and his colleagues were able to trace the 959 somatic cells of the organism back through their lineage, creating the very first completed fate map with lineage diagram.

Another example of a fate map is that of Drosophila melanogaster. This fly is known for having comparable larval and adult body segmentation regulated by a series of genetic mechanisms. The fate map of D. melangaster can be seen in many developmental biology texts. Along with the production of a fate map, scientists have also been able to produce a map of developmental potential for the fruit fly. The fate map of this organism has been a key factor in determining the complex genetic network used by the fruit fly. Studies of how the fates of each segment are determined have resulted in the discovery of novel genes such as gurken, which determine axis formation in Drosophila.

Creating a fate map is a valuable part of understanding an organism’s developmental pathway. Understanding the lineage and migration of progenitor cells can lead to the discovery of gene regulatory networks and signaling pathways. Furthermore, determining the structural make up of an organism can possibly lead to determining the function of each specific region. The possibility of new developmental discoveries comes with the creation of each new fate map.

3 fates of this matter - Biology

Animal Diversity Web
An extraordinary site from the University of Michigan

The Ocean Planet
An exhibition about our planet and its oceans, sponsored by NASA

Texas Parks and Wildlife
Extensive information about Texas wildlife and natural regions of the state.

Chapter 3
The Biosphere

In this chapter, students will will read about how the biologists called ecologists study the relationships among organisms in the living part of the Earth's environment, called the biosphere. You will also discover how energy and nutrients flow through the biosphere The links below lead to additional resources to help you with this chapter. These include Hot Links to Web sites related to the topics in this chapter, the Take It to the Net activities referred to in your textbook, a Self-Test you can use to test your knowledge of this chapter, and Teaching Links that instructors may find useful for their students.

Hot Links Take it to the Net
Chapter Self-Test Teaching Links

What are Web Codes?
Web Codes for Chapter 3:
Active Art: The Water Cycle
Miller & Levine: Exploring Ecology from Space
SciLinks: Energy Pyramids
SciLinks: Cycles of Matter

Section 3-1: What Is Ecology?
To understand the various relationships within the biosphere, ecologists ask questions about events and organisms that range in complexity from a single individual to a population, community, ecosystem, or biome, or to the entire biosphere.
Scientists conduct modern ecological research according to three basic approaches: observing, experimenting, and modeling. All of these approaches rely on the application of scientific methods to guide ecological inquiry.

Section 3-2: Energy Flow
Sunlight is the main energy source for life on Earth. In a few ecosystems, some organisms rely on the energy stored in inorganic chemical compounds.
Energy flows through an ecosystem in one direction, from the sun or inorganic compounds to autotrophs (producers) and then to various heterotrophs (consumers).
Only about 10 percent of the energy available within one trophic level is transferred to organisms at the next trophic level.

Section 3-3: Cycles of Matter
Unlike the one-way flow of energy, matter is recycled within and between ecosystems.
Every living organism needs nutrients to build tissues and carry out essential life functions. Like water, nutrients are passed between organisms and the environment through biogeochemical cycles.

A changed atmosphere

Our species arrived at the Industrial Revolution two centuries ago with bodies that had been shaped for millions of years by this highly imperfect process.

Clean water, improved medicines and other innovations drastically reduced deaths from infectious diseases. The average life expectancy shot up. But our exposure to airborne toxins also increased.

“If we compressed the last five million years into a single year, it wouldn’t be until Dec. 31, 11:40 p.m., that the Industrial Revolution begins,” Dr. Trumble said. “We are living in just the tiniest little blip of human existence, yet we think everything around us is what’s normal.”

The Industrial Revolution was powered largely by coal, and people began breathing the fumes. Cars became ubiquitous power plants and oil refineries spread. Tobacco companies made cigarettes on an industrial scale. Today, they sell 6.5 trillion cigarettes every year.

Our bodies responded with defenses honed over hundreds of thousands of years. One of their most potent responses was inflammation. But instead of brief bursts of inflammation, many people began to experience it constantly.

Many studies now suggest that chronic inflammation represents an important link between airborne toxins and disease. In the brain, for example, chronic inflammation may impair our ability to clear up defective proteins. As those proteins accumulate, they may lead to dementia.

Pathogens can hitch a ride on particles of pollutants. When they get in our noses, they can make contact with nerve endings. There, they can trigger even more inflammation.

“They provide this highway that’s a direct route to the brain,” Dr. Fox, of the University of California, Los Angeles, said. “I think that’s what makes this a particularly scary story.”

Some genetic variants that arose in our smoky past may offer some help now. They might allow some people to live long despite smoking, Dr. Finch and Dr. Trumble suggest.

But the researchers have studied another gene for which the opposite seems to be true: a variant that was once helpful has become harmful in an age of rising air pollution.

The variant, ApoE4, first came to light because it drastically raises the risk of developing Alzheimer’s disease. More recently, researchers have also discovered that ApoE4 increases the risk that exposure to air pollution leads to dementia.

But these studies were restricted to industrialized countries. When researchers looked to other societies — such as farmers in poor villages in Ghana, or indigenous forest-dwellers in Bolivia — ApoE4 had a very different effect.

In these societies, infectious diseases remain a major cause of death, especially in children. Researchers have found that in such places, ApoE4 increases the odds that people will survive to adulthood and have children.

Natural selection may have favored ApoE4 for hundreds of thousands of years because of this ability to increase survival. But this gene and others may have had harmful side effects that remained invisible until the sooty, smoky modern age.

Paracrine Signaling

Figure 2. The distance between the presynaptic cell and the postsynaptic cell—called the synaptic gap—is very small and allows for rapid diffusion of the neurotransmitter. Enzymes in the synaptic cleft degrade some types of neurotransmitters to terminate the signal.

Signals that act locally between cells that are close together are called paracrine signals. Paracrine signals move by diffusion through the extracellular matrix. These types of signals usually elicit quick responses that last only a short amount of time. In order to keep the response localized, paracrine ligand molecules are normally quickly degraded by enzymes or removed by neighboring cells. Removing the signals will reestablish the concentration gradient for the signal, allowing them to quickly diffuse through the intracellular space if released again.

One example of paracrine signaling is the transfer of signals across synapses between nerve cells. A nerve cell consists of a cell body, several short, branched extensions called dendrites that receive stimuli, and a long extension called an axon, which transmits signals to other nerve cells or muscle cells. The junction between nerve cells where signal transmission occurs is called a synapse. A synaptic signal is a chemical signal that travels between nerve cells. Signals within the nerve cells are propagated by fast-moving electrical impulses. When these impulses reach the end of the axon, the signal continues on to a dendrite of the next cell by the release of chemical ligands called neurotransmitters by the presynaptic cell (the cell emitting the signal). The neurotransmitters are transported across the very small distances between nerve cells, which are called chemical synapses (Figure 2). The small distance between nerve cells allows the signal to travel quickly this enables an immediate response, such as, Take your hand off the stove!

When the neurotransmitter binds the receptor on the surface of the postsynaptic cell, the electrochemical potential of the target cell changes, and the next electrical impulse is launched. The neurotransmitters that are released into the chemical synapse are degraded quickly or get reabsorbed by the presynaptic cell so that the recipient nerve cell can recover quickly and be prepared to respond rapidly to the next synaptic signal.

Determining the body axes: cytoplasmic determinants (intrinsic information) and induction (extrinsic information)

One of the fundamental principles of animal development in all animals (except sponges) is the establishment of the body axes: animal bodies have lateral-medial (left-right), dorsal-ventral (back-belly), and anterior-posterior (head-feet) axes, illustrated below.

Animals have three body axes: anterior-posterior, dorsal-ventral, and left-right. Image credit: Khan Academy

How are these axes established from a ball of apparently identical cells (the blastula)? The process is different among different lineages of animals, with body axes being heavily influenced by cytoplasmic determinants in protostomes (most invertebrates), by yolk polarity in vertebrates with large amounts of asymmetrically-distributed yolk (many fish, amphibians, reptiles, and birds), and by induction (cell-cell communication) in many mammals:

    Cytoplasmic determinants are mRNAs or proteins found in the egg prior to fertilization (they come from mom’s genome, not the embryo). They are asymmetrically distributed, so that after the first cleavage division, the two different resulting cells have different intrinsicinformation, which will then lead to different cell fates. One of the best understood cytoplasmic determinants is a factor called bicoid, which is present in a concentration gradient across the unfertilized eggs of Drosophila (fruit flies). The region of the egg with the highest concentration of bicoid becomes the anterior (head) portion of the embryo, while the region with the lowest bicoid concentration becomes the posterior (tail) region of the embryo. This future cell identity of anterior vs posterior is set after the very first cleavage division, where one cell gets nearly all the bicoid and the other cell has almost none. Cytoplasmic determinants are a key feature of protostome development and some deuterostomes, but they are not present in mammalian embryos.

CC SA 1.0,

By Catcasillas21 – Own work, CC BY 3.0,

The process of induction is important throughout development, and we will revisit it in the next reading on steps 3 and 4 of early animal development.

Watch the video: БЕЛКОВО-ЗАВАРНОЙ КРЕМ! Итальянская меренга! ПОДРОБНО! Рецепт БЗК. Стабильный и очень вкусный! (May 2022).