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In general, these reviews were very brief, uninformative, and written in extremely poor English. In this context, it must be noted that several of our trusted referees got extremely exhausted by the large number of review requests and, accordingly and understandably, declined. In fact, we received several complaints by referees for the high workload. We can only apologize to our referees. We were simply not aware of the problem.

Thus, paper mill authors intentionally exploit and exhaust honest and trusted referees as a most valuable resource of a scientific journal so that desperate editors, as last-resort, use the author-suggested fake reviewers. Same paper, different authors: In one particularly egregious case, a paper administratively withdrawn from our files because of suspected fraud was submitted shortly thereafter to another pharmacological journal, the only major difference being that the list of authors was totally different.

It is very likely that this example is not an isolated case because there is no generally accessible data base of rejected fake papers. Thus, paper mills can aggressively exploit this lack of data base on rejected fake papers and the fundamental assumption of author honesty for their business model.

This type of fraud can only be detected by chance. As a minimalistic precaution against detection of this type of fraud, paper mills slightly change the paper title, barely disguising the identity of the content. Geographical origin of fake papers: The retraction notes published in this issue Table 1 and the additionally forthcoming retraction notes are all from one country. It cannot be excluded that paper mills operate in other countries as well. Therefore, in our revised editorial guidelines, the request for original data concerns authors from all countries.

We deeply regret that we had to implement this rule globally, but we did not want to convey the impression of discrimination of a specific country. These strategies complement each other to lead to the desired result. At the same time, the portfolio of strategies minimizes the risk of the fraud authors to be identified, minimizing the risk of negative professional consequences. Only authors providing original data as electronic supplement to their papers were allowed to proceed to online and final publications.

This first emergency measure prevented the online and final publication of another 10 fraudulent papers. Moreover, the Editor-in-Chief immediately interrupted the peer review process of all papers under consideration. Peer review was only allowed to continue when authors provided raw data. This second emergency intervention resulted in the drop-out of another 30 papers from the peer review and publication pipeline.

In virtually all cases, authors never responded to the request of original data and ignored up to 10! The respective papers were then all administratively withdrawn by the Editor-in-Chief prior to acceptance or rejection. All authors from fraudulent papers were flagged to prevent future submissions to the journal. A total number of 10 paper retractions in a single journal within 1 year is quite a large. Probably, this high percentage is related to the fact that the journal traditionally publishes many papers on natural compound pharmacology and that career incentives to publish in this field in the target country and in this journal must be very substantial.

We may have stopped the fraud wave at the beginning of an exponential growth phase. Quantitative comparisons of the fraud extent with other journals are impossible because of the lack of data, but at least one journal Molecular Brain in a somewhat different scientific field reports a substantial quantitative problem with fake submissions as well Miyakawa Lists of journals tentatively affected by paper mills posted on science blog sites corroborate the assumption that the problem does not only concern the field of natural compound pharmacology.

The respective text of the editorial guidelines is shown below:. Since the journal has experienced a rather extensive wave of fraud submissions of papers from paper mills and papers including fake data from external service laboratories, we had to extend the submission prerequisites to the following requests as stated in our Instructions for Authors:.

Request of institutional email addresses. At the minimum, at least the corresponding author should provide an institutional email address.

Request of supplemental original source data raw data, original data, individual data points presented in tables and figures in a generally readable format.

This action is similar to fi-neurotoxins such as attributed to differences in the phospholipid compo- fi-bungarotoxin which have previously been shown to sition of the nerve terminal between species Radvanyi bind irreversibly to the presynaptic terminal Kelly and et al. The increase in M E P P frequency would Brown and may reflect a requirement for inter- therefore appear to be sensitive to the phospholipid nalisation of the toxin into the prejunctional terminal content of the terminal, and thus could be primarily Kamenskaya and Thesleff Further experiments to assess the effects of tex- In the present study, the M E P P frequency stayed tilotoxin on evoked and spontaneous acetylcholine re- elevated for the duration of most experiments using lease were performed to determine the mechanisms textilotoxin in the toad muscle preparations.

In one underlying the triphasic changes in muscle twitch ten- experiment where the muscle was successfully impaled sion. Alterations in the amplitude of the EPP closely for longer than 3 h the frequency fell again after paralleled the previously observed changes in twitch min.

This fall in M E P P frequency has been noted tension. The EPP amplitude decreased after an initial previously Brazil and Excell and has been sug- slight delay, indicating a delayed effect after the addi- gested to be a result of a decrease in the number of tion of textilotoxin, perhaps due to a slow binding or vesicles in the terminal.

This decrease in vesicle number internalisation step. Even given the large safety factor at the end of the intoxication has been reported in of neuromuscular transmission this reduction in EPP a number of ultrastructural studies conducted with amplitude would probably be sufficient to prevent textilotoxin Nicholson et al. This was Chang et al. It may also reflect a general and com- the first mins of muscle tension experiments de- plete destruction of the integrity of the membrane or of scribed above see Fig.

There followed a period of the release mechanism in the active zone such as a com- increased EPP amplitude, and then a decrease of the plete depolarisation of the terminal by this stage, or mean EPP amplitude until eventual development of some other loss of sensitivity to the depolarisation complete neuromuscular blockade. The variability of Chang and Lee Successive quency, textilotoxin did not alter the modal M E P P EPPs varied widely in amplitude, and the proportion of amplitude consistent with a presynaptic mode of action failures increased dramatically.

This is indicative of an to alter EPP amplitude and therefore rfi. It is impossible effect either on the release process or on the continued to distinguish by this method, however, a change in the availability of vesicle-stored acetylcholine for release. This seems unlikely, tude of MEPPs. Firstly marked changes in the fre- as it would be highly improbable that the acetylcholine quency of MEPPs were observed.

Immediately after sensitivity and the M E P P acetylcholine content would the addition of textilotoxin, there was a tendency for always both change at the exact rate required to show the frequency of MEPPs to decrease slightly, and al- no change in M E P P amplitude, as different mecha- though this reduction in M E P P frequency was dra- nisms would be responsible for the pre- and postsynap- matic in some preparations, the average decrease was tic effects.

This initial fall of M E P P frequency is charac- population in the presence of textilotoxin. Despite indi- teristic of other phospholipase A2 toxins such as vidual MEPPs becoming more variable in size and crotoxin Hawgood et al. Naunyn-Schmiedeberg'sArch Pharmacol the amount of acetylcholine released ie. If tex- ties of a high molecular weight neurotoxin from the Eastern tilotoxin disrupts a regulatory machinery that controls brown snake Pseudonaja textilis. This conclusion would sup- the common or Eastern Australian brown snake Pseudonaja port the view of Vautrin that transmitter release textilis.

Neuroscience 1: acetylcholine concentrative and storage device, rather Datyner ME, Gage PW Presynaptic and postsynaptic effects than the prime determinant of quantal size as originally of the venom of the Australian tiger snake at the neuromuscular proposed by del Castillo and Katz and elabor- junction.

J Physiol In summary the present study characterises the Del Castillo J, Katz B Quantal components of the end-plate actions of textilotoxin at the amphibian neuromuscular potential. J Physiol junction. These were confirmed to be presynaptic in Hamilton RC, Broad AJ, Sutherland SK a Effects of Austra- lian Eastern brown snake Pseudonaja textilis venom on the nature, leading to a triphasic alteration of acetylcholine ultrastructure of nerve terminals on the rat diaphragm.

Neurosci release from the terminal, and an eventual complete Lett 50 neuromuscular blockade. An analysis of MEPP ampli- Hamilton RC, Broad AJ, Sutherland SK b Ultrastructural tude showed no change in the postsynaptic sensitivity, effects of the venom of the small-scaled snake Parademansia but demonstrated clear disruptions in the presynaptic microlepidotus on the motor terminal of the rat diaphragm.

These features are characteristic of the actions the mammalian neuromuscular junction. These included the triphasic nature of the development of neuromuscular blockade, Hawgood BJ, Smith J The presynaptic action of crotoxin at the murine neuromuscular junction. The authors would tials that occur after prolonged transmitter release at frog neuro- also like to thank Dr Ian Spence for many helpful discussions.

Alkadhi KA Giant miniature end-plate potentials at the Toxicon 81 untreated and emetine-treated frog neuromuscular junction. J Physiol skeletal muscle. Toxicon of Bungarus multicinctus and their modes of neuromuscular Liley AW An investigation of spontaneous activity at the blocking action. Arch Int Pharmacodyn neuromuscular junction of the rat.

Biochim Biophys Acta tially blocks one class of miniature endplate potentials. A comparison with non- textilotoxin in vivo. Toxicon neurotoxic snake venom phospholipase Az.

Toxicon snake Pseudonaja textilis. J Physiol Lond — Brain Res — Br J Pharmacol P. John Willey, Chichester, pp — Am J Physiol HH Naunyn-Schmiedeberg's Arch Pharmacol — Dietl H, Eisert A, Kraus A, Philippu A The release of endogenous catecholamines in the cat hypothalamus is affected by spinal transection and drugs which change the arterial blood pressure.

J Auton Pharmacol — Experentia — Dropp JJ Mast cells in the central nervous system of several rodents. Anat Rec — Dubocovich M, Langer S Dopamine and alpha adrenoceptor agonists inhibit neurotransmission in the cat spleen through different presynaptic receptors.

J Pharmacol Exp Ther — Neurology — In vivo dopamine release from the anterior hypothalamus of the rat. Eur J Pharmacol — J Neurochem — Juskevich J, Lovenberg W Neuronal regulation of blood pressure. Academic Press, New York. Kant G, Meyerhoff J Release of endogenous norepinephrine from rat hypothalamus in vitro. Life Sci — Lithium modulates multiple tau kinases with distinct effects in cortical and hippocampal neurons according to concentration ranges Authors V.

De-Paula O. Would carvacrol be a supporting treatment option effective in minimizing the deleterious effects of COVID? This journal has open access articles. View all articles.