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                <text>Robert Ahmed Khan, Moshiur Rahman, Amit  Agrawal, Ezequiel Garcia-Ballestas, Luis Rafael  Moscote-Salazar</text>
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                <text>Background. COVID-19 has become an alarming pandemic for our earth. It has created panic not only in China but also in developing countries like Bangladesh. Bangladesh has adequate confinements to constrain the spread of the infection and in this circumstance, overall healthcare workers including neurosurgeons are confronting a ton of difficulties. The purpose of this paper is to depict the proficiency of Global neurosurgery in this COVID-19 time.   Method. Global neurosurgery offers the chance of fusing the best proof-based guidelines of care. This paper demonstrated that, in low to middle-income countries, Global medical procedure has been received to address the issues of residents who lack critical surgical care.   Results. Inappropriate and insufficient asset allotment has been a significant obstacle for the health system for decently giving security to the patients. The fundamental training process has been genuinely hampered in the current circumstance. Worldwide health activities have set to an alternate centre and Global neurosurgery as an assurance is slowed down.   Conclusion. This paper recommended that Global neurosurgical activities need to come forward and increase the workforce to emphasize surgical service.</text>
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                <text>Romanian Neurosurgery</text>
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                <text>Covid-19: End of the beginning?</text>
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                <text>Robert Bergquist, Anna-Sofie Stengaard</text>
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                <text>The limited case cluster of atypical pneumonia detected in central China in December 2019, now known as Coronavirus Disease 2019 (Covid-19), converted into a million confirmed cases worldwide in only 10 weeks. Declared a pandemic by the World Health Organization (WHO) on 11 March 2020 (WHO, 2020) and passing the 3 million mark on 27 April, the world is under formidable strain with respect to public health, economy and personal life. Time and again we are alerted about unforeseen, new effects of this disease, which brings to mind the terms “known unknowns” and “unknown unknowns” used by former U.S. Secretary of Defense Donald Rumsfield when referring to the lack of evidence of weapons of mass destruction in Iraq ahead of the second Gulf war, a fitting vocabulary as we again are faced with mass destruction, though this time of a different kind.</text>
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                <text>DOI: 10.4081/gh.2020.897</text>
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                <text>Covid-19: Pandemonium in our time</text>
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                <text>While pandemonium has come to mean wild and noisy disorder, the reference here is to John Milton's epic poem Paradise Lost and the upheaval following Lucifer's banishment from Heaven and his construction of Pandæmonium as his hub. Today's avalanche of conflicting news on how to deal with the coronavirus disease 2019 (Covid-19) brings to mind the Trinity nuclear bomb test with Enrico Fermi estimating its strength by releasing small pieces of paper into the air and measuring their displacement by the shock wave. Fermi's result, in fact not far from the true value, emphasised his ability to make good approximations with few or no actual data. The current wave of Covid-19 presents just this kind of situation as it engulfs the world from ground zero in Wuhan, China. Much information is indeed missing, but datasets that might lead to useful ideas on how to handle this pandemic are steadily accumulating.</text>
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                <text>DOI: 10.4081/gh.2020.880</text>
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                <text>Role of China in the Quest to Define and Control Severe Acute Respiratory Syndrome</text>
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                <text>Robert F. Breiman, Meirion R. Evans, Wolfgang Preiser, James Maguire, Alan Schnur, Henk Bekedam, John S. Mackenzie</text>
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                <text>China holds the key to solving many questions crucial to global control of severe acute respiratory syndrome (SARS). The disease appears to have originated in Guangdong Province, and the causative agent, SARS coronavirus, is likely to have originated from an animal host, perhaps sold in public markets. Epidemiologic findings, integral to defining an animal-human linkage, may then be confirmed by laboratory studies; once animal host(s) are confirmed, interventions may be needed to prevent further animal-to-human transmission. Community seroprevalence studies may help determine the basis for the decline in disease incidence in Guangdong Province after February 2002. China will also be able to contribute key data about how the causative agent is transmitted and how it is evolving, as well as identifying pivotal factors influencing disease outcome. There must be support for systematically addressing these fundamental questions in China and rapidly disseminating results.</text>
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                <text>Arctic medicine. Tropical medicine, Public aspects of medicine</text>
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                <text>Repeat sequences that are expanded in copy number are the basis for ~20 dominantly inherited neurodegenerative diseases, including Huntington’s Disease. Despite some of the responsible genes being identified as long as 20 years ago, the identity and nature of the disease-causing pathogenic pathway remains a gap in knowledge for these diseases. This understanding is essential for rational approaches to delay onset, slow progression or ultimately effect cure. We have previously hypothesized that an RNA-based pathogenic pathway has a causal role in the dominantly inherited unstable expanded repeat neurodegenerative diseases. In support of this hypothesis we, and others, have characterized rCAG.rCUG100 repeat double-strand RNA (dsRNA) as a previously unidentified agent capable of causing pathogenesis in a Drosophila model of neurodegenerative disease. Dicer, Toll and autophagy pathways have distinct roles in this Drosophila dsRNA pathology. Dicer-dependence is accompanied by cleavage of rCAG.rCUG100 repeat double-strand RNA down to r(CAG)7 21-mers. Among the ‘molecular hallmarks’ of this pathway that have been identified in Drosophila, some [i.e. r(CAG)7 and elevated TNF] correlate with observations in affected people (e.g. HD, ALS) or in related animal models [i.e. autophagy]. The Toll pathway is activated in the presence of repeat-containing double-stranded RNA and toxicity is also dependent on this pathway. How might the endogenously expressed dsRNA mediate Toll-dependent toxicity in neuronal cells? Endogenous RNAs are normally shielded from Toll pathway activation as part of the mechanism to distinguish ‘self’ from ‘non-self’ RNAs. This typically involves post-transcriptional modification of the RNA. Therefore, it is likely that rCAG.rCUG100 repeat double-strand RNA has a characteristic property that interferes with or evades this normal mechanism of shielding. We predict that repeat expansion leads to an alteration in RNA structure and/or form that perturbs RNA mod</text>
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                <text>neurodegeneration, toll-like receptor, RNA pathogenesis, innate inflammation, expanded repeat diseases</text>
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                <text>DOI: 10.1371/journal.pmed.0030411</text>
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                <text>The Inhibitory Effect of Non-Substrate and Substrate DNA on the Ligation and Self-Adenylylation Reactions Catalyzed by T4 DNA Ligase.</text>
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                <text>DNA ligases are essential both to in vivo replication, repair and recombination processes, and in vitro molecular biology protocols. Prior characterization of DNA ligases through gel shift assays has shown the presence of a nick site to be essential for tight binding between the enzyme and its dsDNA substrate, with no interaction evident on dsDNA lacking a nick. In the current study, we observed a significant substrate inhibition effect, as well as the inhibition of both the self-adenylylation and nick-sealing steps of T4 DNA ligase by non-nicked, non-substrate dsDNA. Inhibition by non-substrate DNA was dependent only on the total DNA concentration rather than the structure; with 1 μg/mL of 40-mers, 75-mers, or circular plasmid DNA all inhibiting ligation equally. A &gt;15-fold reduction in T4 DNA ligase self-adenylylation rate when in the presence of high non-nicked dsDNA concentrations was observed. Finally, EMSAs were utilized to demonstrate that non-substrate dsDNA can compete with nicked dsDNA substrates for enzyme binding. Based upon these data, we hypothesize the inhibition of T4 DNA ligase by non-nicked dsDNA is direct evidence for a two-step nick-binding mechanism, with an initial, nick-independent, transient dsDNA-binding event preceding a transition to a stable binding complex in the presence of a nick site.</text>
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                <text>DOI: 10.1371/journal.pone.0150802</text>
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