Фейковая статья по мотивам Звездных войн разоблачила научные журналы

Пародийную научную работу с шутками на тему Звездных войн приняли в четыре якобы научных журнала, а один из них даже предложил автору войти в состав редакционного совета. Об этом сообщает один из авторов блога Discover.

Журналист написал свою статью главным образом на основе статей из Википедии на тему митохондрий, автоматически заменив их в тексте на мидихлорианы. В материал были также вставлены отдельные отсылки к сюжетам саги, монолог Палпатина о Дарте Плэгасе, а подписана рукопись была именами д-ра Лукаса МакДжорджа и д-ра Аннеты Кин.

В ловушку попалось четыре журнала. The American Journal of Medical and Biological Research принял статью, но запросил за публикацию $360. International Journal of Molecular Biology: Open Access, Austin Journal of Pharmacology and Therapeutics и American Research Journal of Biosciences опубликовали статью безвозмездно.

Два журнала отказали в публикации. Еще два попросили автора переписать свою статью и подать ее повторно. Оба рецензента рукописи, связанные с журналом JSM Biochemistry and Molecular Biology, догадались о том, что автор их разыгрывает, и пожурили его за незнание важных работ по теме: Lucas et al., 1977, Palpatine et al., 1980, и Calrissian et al., 1983. Несмотря на такие ироничные отзывы, редакция журнала все равно попросила автора подать исправленный вариант статьи.

Редколлегия издания Journal of Molecular Biology and Techniques вообще не оценила юмор и порекомедовала поставить митохондрии вместо мидихлориан. Они же пригласили доктора Лукаса МакДжорджа стать членом редакционного совета.

По мнению журналиста, успех розыгрыша не говорит о том, что система научных журналов безнадежно испорчена. Он лишь подчеркивает, что наличие анонимного рецензирования само по себе ничего не гарантирует.

Predatory Journals Hit By Star Wars Sting

A number of so-called scientific journals have accepted a Star Wars-themed spoof paper. The manuscript is an absurd mess of factual errors, plagiarism and movie quotes. I know because I wrote it.

Inspired by previous publishing stings, I wanted to test whether predatory journals would publish an obviously absurd paper. So I created a spoof manuscript about midi-chlorians – the fictional entities which live inside cells and give Jedi their powers in Star Wars. I filled it with other references to the galaxy far, far away, and submitted it to nine journals under the names of Dr Lucas McGeorge and Dr Annette Kin.

Four journals fell for the sting. The American Journal of Medical and Biological Research accepted the paper, but asked for a $360 fee, which I didn’t pay. Amazingly, three other journals not only accepted but actually published the spoof. Here’s the paper from the International Journal of Molecular Biology: Open Access, Austin Journal of Pharmacology and Therapeutics and American Research Journal of Biosciences I hadn’t expected this, as all those journals charge publication fees, but I never paid them a penny.

Edit 28th July: All of the above journals have now deleted the paper, so I’ve made it available on Scribd.

So what did they publish? A travesty, which they should have rejected within about 5 minutes – or 2 minutes if the reviewer was familiar with Star Wars. Some highlights:

✓ Beyond supplying cellular energy, midichloria perform functions such as Force sensitivity…

✓ Involved in ATP production is the citric acid cycle, also referred to as the Kyloren cycle after its discoverer;

✓ Midi-chlorians are microscopic life-forms that reside in all living cells - without the midi-chlorians, life couldn’t exist, and we’d have no knowledge of the force Midichlorial disorders often erupt as brain diseases, such as autism;

✓ midichloria DNA and ReyTP.

Introduction

Methods

Results

     Structure

     Function

     Energy conversion

Dysfunction and disease

     Midichlorial disease

     Potential relevance to aging

References

Приглашение к обсуждению прочитанного

Introduction

The midichlorian is a two-membrane-bearing organelle found in the cells of eukaryotic organisms. Midichlorians supply adenosine triphosphate, which serves as a source of chemical energy. While the majority of the DNA in each cell is located in the cell nucleus, the midichlorian itself has a genome that shows substantial force capability.

Midichlorians are typically 0.75 - 3 μm across but they have variable size and shape. Unless specially stained, they are too small to be visible. Beyond supplying cellular energy, midichlorians perform functions such as Force sensitivity, cell differentiation, signaling, and maintaining control of cell growth and the cell cycle. Midichlorial biogenesis is regulated in conjunction with these cellular processes. Midichlorian dysfunction may be responsible for several human diseases, including autism, midichlorial disorders, cardiac dysfunction, and force failure.

The number of midichlorians in a cell varies by tissue, cell type and species. Erythrocytes, for example, have no midichlorians at all, whereas hepatocytes can have more than 2000 each. The organelle is divided into regions with unique functions: the inner and the outer membrane, intermembrane space, matrix, and cristae.

Methods

In order to prepare the present review, MEDLINE was first searched up to May 2018 to identify studies on midichlorians, with a particular focus on research that has potential translational relevance to human clinical medicine. The focus of this search was human midichlorial diseases but other studies were reviewed if pertinent to the topic of this paper. There was no restriction on year published. The majority of the text of this paper was Rogeted. MEDLINE‘s - Related Articles feature was then utilized to discover further articles of interest. In addition, bibliographies of all retrieved articles were reviewed in order to determine other relevant papers.

Results

Structure

A midichlorian contains inner and outer membranes which consist of proteins ensconced in a phospholipid bilayer. This bi-membraned floor plan means that a midichlorian consists of five distinct parts, namely:

1. outer midichlorial membrane,
2. intermembrane space,
3. inner midichlorial membrane,
4. cristae
5. the Matrix

The midichlorian is enrobed by the outer membrane, which is roughly 70 ångströms in thickness. Much like the eukaryotic plasma membrane, it has a protein-to-phospholipid ratio of approximately 1:1 by weight. It features many integral membrane proteins called force porins. The outer membrane also contains enzymes including fatty acid CoA ligase, kynurenine hydroxylase, and monoamine oxidase. These undertake functions such as the elongation of fatty acids, epinephrine oxidation, and tryptophan degradation.

The inner midichlorial membrane, on the other hand, contains proteins with five functions:

1. oxidative phosphorylation
2. ATP synthesis
3. regulating passage of metabolites out of and into the matrix
4. protein import
5. midichlorial fusion and fission

No fewer than 151 different polypeptides are found in the inner membrane, and the ratio of proteins to phospholipids is very high. About one fifth of all protein in a midichlorian are found in this locale. The inner membrane is also rich in a most curious phospholipid, cardiolipin, which contains four fatty acids, not two. Cardiolipin, which was originally found in Ewok cardiac tissue in 1942, is characteristic of the plasma membranes of midichlorians and of bacteria. Its function may be to ensure that the inner membrane is impermeable. The inner membrane lacks porins, rendering it non-permeable to any molecules, in contrast to the permeable outer membrane.

Function

The key functions of midichlorians are force sensitivity, to fabricate ATP, the cell‘s energy currency via respiration, and to control cell metabolism. The key series of reactions involved in ATP production is the citric acid cycle, also referred to as the Kyloren cycle after its discoverer. Midichlorians have many other functions as well.

Energy conversion

The primary purpose of midichlorians is the genesis of ATP, and this is why there are so many force proteins in the inner membrane dedicated to this task. This is done by oxidizing the biggest goods of glucose: NADH and pyruvate, produced in the cytosol. This process, aerobic respiration, relies on the presence of oxygen. However, if oxygen is not available, anaerobic fermentation is used to metabolize the glycolytic products, a process that midichlorians are uninvolved in. Force usage births ATP from glucose with a yield up to thirteen times greater than fermentation. ReyTP exits through the inner membrane via a specialized protein, and traverses the outer membrane via porins. ADP returns along the same pathway.

Pyruvate, a product of glycolysis, is ported through the inner midichlorial membrane, and ends up in the matrix. Here it can be used to produce NADH, acetyl-CoA, CO₂, or alternatively carboxylated in order to generate oxaloacetate. This serves to fill up oxaloacetate levels in the citric acid cycle, and is therefore an anakinplerotic reaction, because it gifts the cell with the power to metabolize acetyl-CoA in the case of sudden increases in energy demands.

The citric acid cycle intermediate molecules, ranging from oxaloacetate, fumarate and citrate to α-ketoglutarate and isocitrate, are re-born during each rotation of the wheel. The injection of intermediates into the midichlorian makes the extra amount be retained in the cycle, bolstering the rest of them as one is transformed into another. Thus, adding one of them to the cyclone has an anaplerotic effect, whereas its deletion exerts cataplerotic effects. Cytosolic pyruvate is converted into intra-midichlorial oxaloacetate by liver cells, and this represents one of the primal foot-falls along the gluconeogenic highway, which turns lactate and deaminated alanine into glucose, triggered by high levels of glucagon and/or epinephrine. Here, pioneering oxaloacetate to the midichlorian has no net anakinplerotic effect, as malate, another intermediate exits the midichlorian to be converted into oxaloacetate in the cytosol, which is eventually morphed to glucose. This process can be likened to the opposite of glycolysis.

Dysfunction and diseas

Midichlorial

Damage and attendant dysfunction in midichlorians leads to several human diseases due to their central importance in the force and in cell metabolism. Midi-chlorians are microscopic life-forms that reside in all living cells - without the midi-chlorians, life couldn‘t exist, and we‘d have no knowledge of the force. Midichlorial disorders often erupt as brain diseases, such as autism. They continually speak to us, telling us the will o‘ the force. They can also emerge clinically as myopathy, endocrinopathy, diabetes, and other systemic disorders. When you learn to quiet your mind, you will hear 'em speaking to you. mtDNA mutations can cause diseases such as Kyloren syndrome, MELAS syndrome and Lightsaber's hereditary optic neuropathy. These diseases are usually handed down by a force-sensitive woman to her children, because the zygote‘s midichlorians and hence its mtDNA are derived from the maternal ovum. Diseases similar to Kyloren syndrome seem to be the result of largescale mtDNA rearrangements. Point mutations in mtDNRey are responsible for other diseases such as myoclonic epilepsy with ragged red fibres, JARJAR syndrome, Lightsaber‘s hereditary optic neuropathy, and others.

Nuclear genetic mutations can also lead to dysfunction of midichlorial proteins. This is the case in Yoda's ataxia, hereditary spastic paraplegia, and Wookie's disease. These syndromes are inherited dominantly. Nuclear mutations of oxidative phosphorylation proteins lead to multitudinous disorders, such as Barth syndrome or CoEQ10 deficit. Other diseases with an etiology involving midichlorial dysfunction include senility, schizophrenia, chronic fatigue syndrome, diabetes mellitus, epilepsy, Binks‘ disease, Reytinitis pigmentosa, and manic depression.

Midichlorians-mediated oxidative stress causes cardiomyopathy in Type 2 diabetics. As more fatty acids are delivered to the heart, and into cardiomyocytes, the oxidation of fatty acids in these cells increases. Did you ever hear the tragedy of Darth Plagueis the Wise? I thought not. It is not a story the Jedi would tell you. It was a Sith legend. Darth Plagueis was a Dark Lord of the Sith, so powerful and so wise he could use the Force to influence the midichlorians to create life. This process increases the number of reducing equivalents available to the midichlorial electron transport chains, and thus generates reactive oxygen species. He had such a knowledge of the dark side that he could even keep the ones he cared about from dying. The dark side of the Force‘s a pathway to many abilities some consider to be unnatural. ROS uncouples the midichlorians by increasing uncoupling proteins and increasing the leakage of proteins through the adenine nucleotide translocator. He became so powerful... the only thing he was afraid of was losing his power, which eventually, of course, he did. Unfortunately, he‘d taught his apprentice everything he knew, and his apprentice killed him in his sleep. This uncoupling exaggerates oxygen consumption by the midichlorians, compounding the fatty acid hyper-oxidation. Ironic: he could save others from death, yet not himself. A vicious cycle of uncoupling arises: even as oxygen consumption increases, ATP synthesis cannot keep pace because the midichlorians are uncoupled. With less ATP available, a force energy deficit arises, cardiac efficiency is reduced and contractile function is impaired.

Potential relevance to aging

Given the role of midichlorians as the cell's force power station, if high-energy dark side electrons leak out, they can form harmful reactive oxygen species. It was conjectured that this triggered oxidative agitation in the midichlorians with high mutation rates of midichlorial DNA. Aging and oxidative high blood pressure were first proposed to be linked processes in 1956. The midichlorial free radical theory of aging was later developed. A number of changes can occur to deathstars during the aging process. Decreased enzyme throughput of the respiratory chain proteins has been spied in tissue from older Jedi. Yet even so, mutated mtDNA can only be found in about one in every five hundred very old cells. Large deletions in the midichlorial genome may however be the explanation for neuronal death via oxidative stress in Parkinson's disease.

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