HOMOEOPATHIC MEDICINES FOR THE ILL EFFECTS OF ANTIBIOTICS

Antibiotics are a group of medicines that are used to treat infections caused by germs (bacteria and certain parasites). A parasite is a type of germ that needs to live on or in another living being (host). Antibiotics are sometimes called antibacterials or antimicrobials. Antibiotics can be taken by mouth as liquids, tablets, or capsules, or they can be given by injection. Usually, people who need to have an antibiotic by injection are in hospital because they have a severe infection. Antibiotics are also available as creams, ointments, or lotions to apply to the skin to treat certain skin infections.

It is important to remember that antibiotics only work against infections that are caused by bacteria and certain parasites. They do not work against infections that are caused by viruses (for example, the common cold or flu), or fungi (for example, thrush in the mouth or vagina), or fungal infections of the skin.

More or less every drug has side effects because their use disturbs the normal function of the organs of the body and the composition of the blood. The patient may develop disturbances in digestion , discomfort, unsteadiness , diarrhea, sore throat, fever etc. The following medicines may be prescribed  to remove the ill effects of antibiotics. The antibiotics should be stopped when ill effects is noticed

HOMOEOPATHIC MEDICINES

ACIDUM PHOS. 30- For general debility after use of antibiotics

ANTIMONIUM TART. 30- When there is rattling of mucus but little comes up on coughing

BORAX 30—For thrush of tongue and mouth or vagina

BRYONIA ALB 30- Bronchitis with lot of thirst . The patient drinks often and in large quantities. Cough is worse in a warm room and chest is sore.

IPECAUANHA 30-For constant nausea

NITRIC ACID  30—Diarrhea is a very common side effect and it is cured by this remedy

PULSATILLA NIG. 30—Persistent catarrh of the throat and nose

SULPHUR 200-One dose , usually to overcome the so called drug rash

THUJA OCCIDENTALIS 200- It has specific antibacterial action

FALLING ASLEEP REVEALING THE POINT OF TRANSITION

How can we tell when someone has fallen asleep? To answer this question, scientists at Massachusetts General Hospital have developed a new statistical method and behavioural task to track the dynamic process of falling asleep

Dr Michael Prerau, Dr Patrick Purdon, and their colleagues used the evolution of brain activity, behaviour, and other physiological signals during the sleep onset process to automatically track the continuous changes in wakefulness experienced as a subject falls asleep.

The study, publishing today in PLOS Computational Biology, suggests that it is not when one falls asleep, but how one falls asleep that matters. Using these methods, the authors quantified a subset of healthy subjects who behaved as though they were awake even though their brains, by current clinical definitions, were asleep.

Understanding the process of falling asleep is an important problem in neuroscience and sleep medicine. Given that current clinical methods are time-consuming, subjective, and simplify the sleep onset process in ways that limit the accuracy, the authors combine the state-of-the-art in neuroscience and signal processing to design an accurate and efficient way to characterise sleep.

The researchers replaced a standard measure, the behavioural response task, which uses sounds that can disturb sleep, with a new task centred on a subject's focused natural breathing -- an act which may even promote sleep. They modeled the physiological and behavioural changes occurring during sleep onset as a continuum that can develop gradually over time.

The identification of some subjects who continued to perform the task even though current clinical measures would say they were asleep suggests a natural variation in the way cortical and thalamic networks interact in these people.

"Ultimately, such methods could greatly improve clinicians' ability to diagnose sleep disorders and to more precisely measure the effects of sleep drugs and other medications," remarked Dr Prerau.

Future work will look to improve the understanding of the mechanisms underlying neural dynamics during sleep, as well as the development of more sophisticated diagnostic and monitoring tools.

HIV LESSONS FROM THE MISSISSIPPI BABY

The news in July that HIV had returned in a Mississippi toddler after a two-year treatment-free remission dashed the hopes of clinicians, HIV researchers and the public at large tantalized by the possibility of a cure.

But a new commentary by two leading HIV experts at Johns Hopkins argues that despite its disappointing outcome, the Mississippi case and two other recent HIV "rebounds" in adults, have yielded critical lessons about the virus' most perplexing -- and maddening -- feature: its ability to form cure-defying viral hideouts.

Writing in the Aug. 28 issue of the journal Science, HIV research duo Robert Siliciano, M.D., Ph.D., and Janet Siliciano, Ph.D., note that such "failures" are in fact stepping stones to new understanding of what "cure" may look like and new therapies that tame the virus into long-term remission.

"Heartbreaking as these three cases are clinically, they provide a dramatic illustration of the real barrier to an HIV cure and illuminate important therapeutic strategies," says Robert Siliciano. "This is not the end of the story but the beginning of a new chapter."

The 27-month off-treatment remission experienced by the Mississippi toddler is, in and of itself, a laudable therapeutic goal, the Silicianos write, and is what cure of HIV may look like in the foreseeable future. Finding ways to induce long-term remission and to closely monitor its course will be the next frontier in HIV treatment, they write.

The ability to put the virus in remission and go off treatment for months or years at a time is an important goal, because it can spare HIV-infected people from a lifetime of daily antiviral regimens, which can be difficult to tolerate and hard to follow. Failure to comply with the strict treatment protocol, which occurs often, can lead to viral mutations that make HIV resistant to drugs.

All three cases, the Silicianos write, also reaffirm that the single most important hurdle to eradicating HIV is a tiny but extremely stable pool of virus tucked away in a handful of immune cells known as memory CD4+ T cells.

Memory T cells are the immune system's combat-trained sentinels, responsible for fighting invaders they have encountered in the past. Much of the time, memory T cells lie dormant and become active only when the body is invaded by old foes they are specifically trained to recognize. HIV invades memory T cells early in the infection, and as long as the T cells lie quiet, so does HIV inside them.However, as soon as memory T cells get stirred up by an invader, the HIV DNA inside them wakes up, cranks out new virus and reignites infection. Because antiviral drugs work only against actively replicating virus, such silent viral hideouts remain out of therapy's reach. Thus, reducing the number of latently infected cells or precluding their formation altogether is an important and -- as the three recent cases suggest -- realistic strategy, the Silicianos say.

"These cases paint several clinical scenarios where a substantial reduction of viral reservoirs would allow some patients to come off treatment for prolonged yet uncertain periods of time, but they also raise the critical question of how to best monitor them for relapse so they can resume therapy swiftly when the virus rebounds," says Janet Siliciano.

In the widely reported case of the Mississippi baby, a child born to an HIV-infected mother received a full-treatment regimen of antiviral drugs within hours of birth, instead of the customary prophylactic regimen typically used in suspected but unconfirmed newborn infections. The baby's HIV infection was subsequently confirmed. The child was lost to follow-up and went off treatment but later returned to clinic. A series of standard and ultrasensitive tests failed to detect HIV in the child's blood. In total, the child remained free of HIV infection -- with undetectable viral loads and free of HIV antibodies -- for 27 months despite receiving no treatment. By contrast, most HIV-infected people experience dramatic viral rebound within a few weeks of treatment cessation.

Described as the first documented instance of HIV remission in a child, the Mississippi case suggested that very early treatment with antiretroviral drugs quashed the formation of viral reservoirs. The child was followed by a University of Mississippi pediatrician, a University of Massachusetts immunologist and a Johns Hopkins pediatric HIV expert, Deborah Persaud, M.D., who was also the lead author on case report published Nov. 7, 2013, in The New England Journal of Medicine.

In two other "remission" cases reported in 2013, HIV ultimately rebounded in two adults after months without antiviral therapy and following bone marrow transplantation for cancer. Both patients received antiviral drugs while undergoing transplantation to prevent the donors' immune cells from becoming infected with HIV. The patients' own HIV-infected immune cells were killed off by chemotherapy and by graft-versus-host disease, a common post-transplant phenomenon in which the donor's immune cells attack and destroy the recipient's organs, tissues and cells. When antiretroviral treatment was stopped, the patients went into remission for several months, but the virus came roaring back later on, according to published reports.

"Clearly, neither approach managed to eradicate all latently infected cells, and what these cases underscore is the ability of even a few such cells to rekindle infection after prolonged remission," Robert Siliciano says.

The three cases also lend urgency to the search for better ways to monitor the presence of and measure the number of such dormant HIV reservoirs, which could be used as a rough gauge of how long remission might last. Latently infected cells can evade detection by even the most sophisticated tests, which are so exquisitely sensitive that they can sniff the presence of a single HIV-infected cell. The problem is not lack of test sensitivity, the Silicianos explain, but the size of the blood sample tested. Latent HIV reservoirs exist in a few out of millions of immune cells, but a mere 2 percent of memory T cells that harbor such reservoirs are circulating in the blood at any given time. Thus, even large blood samples may not capture the few infected cells harboring dormant virus -- a feat that becomes even more challenging as the number of reservoirs is reduced.

Even though research indicates that remission duration is linked to the amount of latently infected cells, the Silicianos caution remission time is bound to vary widely from patient to patient. Its length would depend on individual biologic factors and the occurrence of other infections that might coax latently infected immune cells out of dormancy and trigger a rebound.

A few patients may never relapse, the Silicianos say, but no patient is safe from rebound as long as he or she harbors even a single latently infected T cell. The unpredictable nature of remission and rebound will therefore require frequent blood monitoring to detect the earliest signs of viral reactivation.

"It is not too soon to begin planning for this type of 'cure' scenario," the authors conclude.

IVF THE NEXT STEP IN LIVE DONOR UTERUS TRANSPLANT PROJECT

In the spring of 2013, a team of researchers and doctors at the University of Gothenburg performed the last of nine planned uterus transplants. The six-month follow up shows that live-donor uterus transplantation has a low risk despite extended surgery duration. In the next phase of the world-unique research project researchers will help seven of the women become pregnant through IVF treatment.

In Sweden alone, an estimated 2,000 young women of fertile age cannot become pregnant either because they were born without a womb or lost it later due to disease.

Professor Mats Brännström, researcher at the University of Gothenburg and chief physician, is leading a unique research project aiming to make it possible for these women to have a uterus transplant and then get pregnant.

A decade of research 

After more than a decade of research that has been evaluated in almost 40 scientific articles, in May 2012 the research team received permission from the Regional Ethical Review Board in Gothenburg to perform uterus transplants on ten Swedish women -- the first in the world with living donors.

The first transplant was completed 15 September 2012, and the ninth and final in the spring of 2013. The tenth woman involved in the project had to be denied at an early stage for medical reasons. Five of the donors are mothers of the receivers; the remaining four a close relative.

Scientific and medical importance In two of the nine cases, the transplanted uterus had to be removed. In one cases due to blood clots in the transplanted blood vessels, in the other because of a local infection that was not fully treatable with antibiotics.

'In a scientific and medical perspective, the transplants have been successful, especially in comparison with other types of transplants that have been introduced and where far fewer initial operations have been successful.'

'The women who had to have their transplanted wombs removed were of course very disappointed, but both of them have recovered well,' says Professor Brännström.

Next phase

The first transplant patients have now had their new uterus for 16 months. During 2014 the second phase of the research project will continue, and the seven transplant patients' own embryos -- produced via IVF prior to the transplant -- will be placed in their uterus with the aim of starting a pregnancy.

`We have made the first attempts at this, but with respect to the women´s integrity we will not comment on the results in the specific cases´, says Brännström.

'The prospects for success are good. On average, the women started menstruating about two months after the transplant, and we followed up on the women twice a week during the first month after the procedure, then once a week for two months and after that every other week. We found and treated a few mild cases of transplant rejection, but after six months, the immunosuppression could be reduced to relatively low levels in most cases and today all women are doing well and have returned to work,' says Brännström.

International interest 

The project is the world's first systematic and research-based attempt to find a treatment for women with uterine infertility. Several medical, psychological and quality of life-related parameters are monitored among the women, which will be of great help for further progress in the field.

A number of research groups around the world are awaiting the results of the Gothenburg study in order to launch similar observational studies.

The article The first clinical uterus transplantation trial: a six-month report was published in Fertility and Sterility on 28 February. In summary, this study shows that a live-donor UTx procedure has a low risk despite extended surgery duration.

GENETICISTS SOLVE 40 YEAR OLD DILEMMA TO EXPLAIN WHY DUPLICATE GENES REMAIN IN THE GENOME

Geneticists at Trinity College Dublin have made a major breakthrough with important implications for understanding the evolution of genomes in a variety of organisms.

They found a mechanism sought for more than four decades that explains how gene duplication leads to novel functions in individuals.

Gene duplication is a biological phenomenon that leads to the sudden emergence of new genetic material. 'Sister' genes -- the products of gene duplication -- can survive across long evolutionary timescales, and allow organisms to tolerate otherwise lethal mutations.

The Trinity geneticists have now identified and described the mechanism underlying this increased tolerance, which is known as 'mutational robustness'.

By experimentally demonstrating that this robustness is important for yeast cells to adapt to novel conditions, including those that are stressful to the cells, they have underlined the likely reason for the existence of gene duplication.

"Natural selection -- a process that keeps essential things in the cell -- also removes genes that are redundant from the genome," said Dr Mario A Fares, Assistant Professor in Genetics at Trinity, and leading author of the study.

"The mechanism resolving the conflict between sister genes and their apparent evolutionary instability had remained a mystery for decades, but we have now cracked this latest part of the genetic code."

Gene duplication is a frequent phenomenon in eukaryotic organisms (which safeguard their genetic material within cell membranes), including yeast, plants, and animals. But understanding how duplication leads to biological innovation is difficult because evolution cannot be easily traced seeing as it occurs on timescales in the order of millions of years.

Despite their apparently redundant nature, duplicate genes that originated 100 million years ago can still be found in today's organisms. This phenomenon has always suggested the existence of a mechanism maintaining them in the genomes. The researchers in this study chose to work with yeast -- an organism whose entire genome has been duplicated over time -- to join up the dots.

They 'evolved' yeast cells in the laboratory under conditions that allowed the spread of mutations rejected by natural selection, by simply reducing the effect that natural selection had on these 'maladapted' cells. They found that duplicate genes tolerated the maladaptive mutations to a greater degree than non-duplicate genes.

The geneticists' simple experimental approach revealed that these genes, duplicated 100 million years ago, were still able to respond to different environments as they changed, as well as highlighting their potential to generate new adaptations that might give them an advantage in new environments.

"Discovering the mechanism of innovation through gene duplication marks an exciting beginning for a new era of research in which evolution can be conducted in the laboratory and theories hitherto speculative tested," added Dr Fares.

"Our discovery also has implications for explaining the importance of redundancy in the human society as well. The role of increased redundancies in a fashioned job market in lenient economical conditions could lead, in crisis times, to the emergence of new companies, specialized workforces, and the optimization of individual capabilities, for example, although this requires a profound investigation."

The research, recently published online in the international journal, Genome Research, was supported by Science Foundation Ireland (SFI).

FROM THE NOSE TO KNEE ENGINEERED CARTILAGE REGENERATES JOINTS

Human articular cartilage defects can be treated with nasal septum cells. Researchers at the University and the University Hospital of Basel report that cells taken from the nasal septum are able to adapt to the environment of the knee joint and can thus repair articular cartilage defects. The nasal cartilage cells' ability to self-renew and adapt to the joint environment is associated with the expression of so-called HOX genes. The scientific journal Science Translational Medicine has published the research results together with the report of the first treated patients.

Cartilage lesions in joints often appear in older people as a result of degenerative processes. However, they also regularly affect younger people after injuries and accidents. Such defects are difficult to repair and often require complicated surgery and long rehabilitation times. A new treatment option has now been presented by a research team lead by Prof. Ivan Martin, professor for tissue engineering, and Prof. Marcel Jakob, Head of Traumatology, from the Department of Biomedicine at the University and the University Hospital of Basel: Nasal cartilage cells can replace cartilage cells in joints.

Cartilage cells from the nasal septum (nasal chondrocytes) have a distinct capacity to generate a new cartilage tissue after their expansion in culture. In an ongoing clinical study, the researchers have so far taken small biopsies (6 millimeters in diameter) from the nasal septum from seven out of 25 patients below the age of 55 years and then isolated the cartilage cells. They cultured and multiplied the cells and then applied them to a scaffold in order to engineer a cartilage graft the size of 30 x 40 millimeters. A few weeks later they removed the damaged cartilage tissue of the patients' knees and replaced it with the engineered and tailored tissue from the nose. In a previous clinical study conducted in cooperation with plastic surgeons and using the same method, the researchers from Basel recently already successfully reconstructed nasal wings affected by tumors.

Surprising Adaption

The scientists around first author Dr. Karoliina Pelttari were especially surprised by the fact that in the animal model with goats, the implanted nasal cartilage cells were compatible with the knee joint profile; even though, the two cell types have different origins. During the embryonic development, nasal septum cells develop from the neuroectodermal germ layer, which also forms the nervous system; their self-renewal capacity is attributed to their lack of expression of some homeobox (HOX) genes. In contrast, these HOX genes are expressed in articular cartilage cells that are formed in the mesodermal germ layer of the embryo.

"The findings from the basic research and the preclinical studies on the properties of nasal cartilage cells and the resulting engineered transplants have opened up the possibility to investigate an innovative clinical treatment of cartilage damage," says Prof. Ivan Martin about the results. It has already previously been shown that the human nasal cells' capacity to grow and form new cartilage is conserved with age. Meaning, that also older people could benefit from this new method, as well as patients with large cartilage defects. While the primary target of the ongoing clinical study at the University Hospital of Basel is to confirm the safety and feasibility of cartilage grafts engineered from nasal cells when transplanted into joint, the clinical effectiveness assessed until now is highly promising.

MEDITATION MUST SLOW THE AGE RELATED LOSS OF GRAY MATTER IN THE BRAIN

Since 1970, life expectancy around the world has risen dramatically, with people living more than 10 years longer. That's the good news.

The bad news is that starting when people are in their mid-to-late-20s, the brain begins to wither -- its volume and weight begin to decrease. As this occurs, the brain can begin to lose some of its functional abilities.

So although people might be living longer, the years they gain often come with increased risks for mental illness and neurodegenerative disease. Fortunately, a new study shows meditation could be one way to minimize those risks.

Building on their earlier work that suggested people who meditate have less age-related atrophy in the brain's white matter, a new study by UCLA researchers found that meditation appeared to help preserve the brain's gray matter, the tissue that contains neurons.

The scientists looked specifically at the association between age and gray matter. They compared 50 people who had mediated for years and 50 who didn't. People in both groups showed a loss of gray matter as they aged. But the researchers found among those who meditated, the volume of gray matter did not decline as much as it did among those who didn't.

The article appears in the current online edition of the journal Frontiers in Psychology.

Dr. Florian Kurth, a co-author of the study and postdoctoral fellow at the UCLA Brain Mapping Center, said the researchers were surprised by the magnitude of the difference.

"We expected rather small and distinct effects located in some of the regions that had previously been associated with meditating," he said. "Instead, what we actually observed was a widespread effect of meditation that encompassed regions throughout the entire brain."

As baby boomers have aged and the elderly population has grown, the incidence of cognitive decline and dementia has increased substantially as the brain ages.

"In that light, it seems essential that longer life expectancies do not come at the cost of a reduced quality of life," said Dr. Eileen Luders, first author and assistant professor of neurology at the David Geffen School of Medicine at UCLA. "While much research has focused on identifying factors that increase the risk of mental illness and neurodegenerative decline, relatively less attention has been turned to approaches aimed at enhancing cerebral health."

Each group in the study was made up of 28 men and 22 women ranging in age from 24 to 77. Those who meditated had been doing so for four to 46 years, with an average of 20 years.

The participants' brains were scanned using high-resolution magnetic resonance imaging. Although the researchers found a negative correlation between gray matter and age in both groups of people -- suggesting a loss of brain tissue with increasing age -- they also found that large parts of the gray matter in the brains of those who meditated seemed to be better preserved, Kurth said.

The researchers cautioned that they cannot draw a direct, causal connection between meditation and preserving gray matter in the brain. Too many other factors may come into play, including lifestyle choices, personality traits, and genetic brain differences.

"Still, our results are promising," Luders said. "Hopefully they will stimulate other studies exploring the potential of meditation to better preserve our aging brains and minds. Accumulating scientific evidence that meditation has brain-altering capabilities might ultimately allow for an effective translation from research to practice, not only in the framework of healthy aging but also pathological aging."

MEIOSIS CUTTING THE TIES THAT BIND

The development of a new organism from the joining of two single cells is a carefully orchestrated endeavor. But even before sperm meets egg, an equally elaborate set of choreographed steps must occur to ensure successful sexual reproduction. Those steps, known as reproductive cell division or meiosis, split the original number of chromosomes in half so that offspring will inherit half their genetic material from one parent and half from the other.

During meiosis, each set of homologous chromosomes pair up in a kind of chromosomal square dance, chromosome 1 with chromosome 1, 2 with 2, and so on down the line. The partners stick together, dancing through the phases of meiosis, until it is time to segregate or separate to opposite ends of the dividing cell. When the dancers don't pair or part appropriately it can result in eggs and sperm with the wrong number of chromosomes, a major cause of miscarriage and birth defects.

To avoid these mistakes, most chromosomes use a process known as crossing over, looping their arms with their partners and even swapping pieces of genetic material to stick together until the dance is over. A few chromosomes, like chromosome 4 in the fruit fly Drosophila melanogaster, are too short to make these crossovers. Yet somehow, they have figured out another way to stay connected to their partners.

Previously, Stacie E. Hughes, Ph.D., a research specialist II at the Stowers Institute for Medical Research, identified thin threads of DNA that seemed to tie these other homologous chromosomes together. Yet a major question remained: once these chromosomes are roped into pairs, how do they manage to come apart again?

Now, Hughes and R. Scott Hawley, Ph.D., have shown that an enzyme called Topoisomerase II is required for resolving these threads so homologous chromosomes can part ways. The finding, published in the October 23, 2014 issue of PLoS Genetics, underscores the complexity of the meiotic process.

"It is not surprising there are many ways to segregate chromosomes because there are also many ways to control other molecular events, like gene expression," says Hawley, a Stowers Institute investigator and American Cancer Society research professor. "This method of segregating shorter chromosomes may be clunky, odd, crazy, and as noncanonical as it gets, but that doesn't matter, because the cells survive. In the end, these processes don't have to be elegant, they just have to work."

Ever since Hughes' initial discovery of DNA threads, she and Hawley have been looking for the molecular scissors responsible for cutting entangled chromosomes free. The most prominent candidate to emerge from their search was Topoisomerase II, an enzyme known to cut and untwist tangled strands of the double helix.

Previous research had shown that Topisomerase II was involved in earlier cellular processes like DNA replication, and the enzyme was still detectable even during later phases of meiosis. The researchers thought that Topoisomerase II might be waiting around to do yet another job, cutting DNA threads to allow homologous chromosomes to segregate.

Testing their hypothesis seemed relatively straightforward. The researchers simply needed to "knock out" Topoisomerase II in their model organism of choice -- the female fruit fly -- and then look to see whether meiosis was able to proceed normally without it. However, because the enzyme was involved in so many critical cellular processes, the researchers knew that such an approach would yield nothing more than dead fruit flies.

Instead, they adapted a sophisticated method known as RNA interference -- which uses small pieces of DNA's chemical cousin RNA to silence genes -- and eliminated Topoisomerase II at a specific time point late in meiosis. Hughes then isolated the oocytes from the fruit flies and analyzed them using fluorescent tags that illuminate the DNA threads connecting the chromosomes. Their findings were dramatic.

"Without this enzyme the chromosomes can't come apart, they are stuck together like glue," says Hughes. "There are large regions of the chromosomes that are tethered together by these threads, while the rest is stretched out like a slinky as the chromosomes are pulled in opposite directions. It is just a mess. Because the chromosomes are just stuck there, they can't finish meiosis."

As a result, the mutant flies are essentially sterile. A separate study published in the same journal shows that male mutants experience a similar fate, their spermatocytes permanently locked in an immature state. Without Topoisomerase II, the oocytes and spermatocytes are locked in meiosis, unable to complete the next steps -- fertilization, cell division and differentiation -- needed to create a new organism.

The work was funded in part by the Stowers Institute for Medical Research and the American Cancer Society (award number RP-05-086-06-DDC).

Summary of Findings

During the formation of eggs and sperm, the cell's chromosomes must pair up and part in an elaborate sequence that results in sex cells with exactly half the number of chromosomes as the parent cell. A single misstep can cause infertility, miscarriage, and birth defects. Recent research has shown that some chromosomes avoid these mistakes by using thin threads of DNA to tether themselves together, but how they come untied again has not been clear. In the current issue of the scientific journalPLoS Genetics, Stowers Institute scientists report that an enzyme called Topoisomerase II is required for these entangled chromosomes to be set free. Stowers Research Associate II Stacie E. Hughes, Ph.D., who led the study, explains that without the enzyme, female fruit flies were unable to complete meiosis and were rendered completely sterile. Topoisomerase II likely resolves the DNA entanglements by cutting and untwisting tangled DNA, as in other processes like DNA replication.