47 research outputs found
Anticancer properties of trichoderma asperellum 302 from buried soils
Melanoma is one of the most malignant tumors, which leaves no chance of survival in the case of the «bang». There are various ways to treat tumors, however, recently in the field of cancer research, there are studies in which fungal metabolites have been used as antitumor agents. In this study we examined the effect of the culture fluid of the fungus Trichoderma asperellum 302 on the growth and development of melanoma B16. We have shown that these culture fluid has anticancer properties, causing destruction of tumor tissue. Obtained data open new possibilities and prospects for the use of active substances derived from fungi in the complex therapy of cancer
Influence of Trichoderma asperellum metabolites on tissue regeneration against pyrene
We studied the influence of the culture fluid of fungi of the genus Trichoderma on Swiss Webster CFW mice after exposure to pyrene - polycyclic aromatic hydrocarbons, which can cause pathological changes in the body. Beneficial effect of Trichoderma metabolites on haematological parameters, the functioning of liver and nephros was shown, the trend toward regeneration of the structure of skin and liver after the damages, caused by the introduction of pyrene, was identified
Apical hypertrophic cardiomyopathy as a mask of acute coronary syndrome: a case series
Apical hypertrophic cardiomyopathy (HCM) or Yamaguchi syndrome is a relatively rare subtype of HCM characterized by a left ventricular apex localization of the hypertrophy. In this case, chest pain can be erroneously interpreted as a manifestation of coronary artery disease. This article presents two cases of apical HCM in patients admitted with a diagnosis of acute coronary syndrome. Electrocardiogram revealed repolarization disorder and giant T wave inversion (up to 10 mm) in the precordial leads. Transthoracic echocardiography revealed local symmetric hypertrophy of the left ventricular apex, which made it possible to diagnose apical HCM. The coronary arteries in both patients were intact. The presented cases demonstrate a variant of apical HCM with chest pain as the leading clinical syndrome, which can often be the cause of overdiagnosis of acute coronary syndrome
Analysis of 3800-year-old Yersinia pestis genomes suggests Bronze Age origin for bubonic plague
© 2018 The Author(s). The origin of Yersinia pestis and the early stages of its evolution are fundamental subjects of investigation given its high virulence and mortality that resulted from past pandemics. Although the earliest evidence of Y. pestis infections in humans has been identified in Late Neolithic/Bronze Age Eurasia (LNBA 5000-3500y BP), these strains lack key genetic components required for flea adaptation, thus making their mode of transmission and disease presentation in humans unclear. Here, we reconstruct ancient Y. pestis genomes from individuals associated with the Late Bronze Age period (~3800 BP) in the Samara region of modern-day Russia. We show clear distinctions between our new strains and the LNBA lineage, and suggest that the full ability for flea-mediated transmission causing bubonic plague evolved more than 1000 years earlier than previously suggested. Finally, we propose that several Y. pestis lineages were established during the Bronze Age, some of which persist to the present day
Analysis of 3800-year-old Yersinia pestis genomes suggests Bronze Age origin for bubonic plague
该论文通过对青铜器时代的两个鼠疫杆菌分离株进行测序,深入剖析了鼠疫杆菌的历史。德国、俄罗斯、中国和瑞士等多国研究员共同参与了研究。这篇论文的第一作者是德国马克斯-普朗克研究所的考古遗传学专家Maria Spyrou。她和同事从俄罗斯墓穴中埋葬的九名古代人的牙齿样本入手,发现有两人感染鼠疫杆菌。之后,他们从这些个体中分离出距今约3800年的病原菌。在这项新研究中,研究人员利用液相捕获和Illumina鸟枪法测序技术,对青铜器时代的一名男子(RT5)的鼠疫杆菌和人类宿主序列进行测序,其中鼠疫杆菌基因组的平均覆盖度达到32倍。同时,他们还对另一名感染个体(RT6)的分离株进行测序,平均覆盖度为1.9倍。系统发育分析表明,RT5和RT6分离株是共同谱系的一部分,这个谱系的祖先是史上三次瘟疫大流行的罪魁祸首。除了众所周知的中世纪欧洲瘟疫大流行,鼠疫杆菌还曾造成公元6世纪的查士丁尼瘟疫和19世纪的中国大规模鼠疫。
马克斯-普朗克人类历史科学研究所的古病理学专家Kirsten Bos表示,这些结果表明“具有传播潜力的瘟疫存在的时间比我们想象得更久。”Bos是这篇论文的通讯作者之一。【Abstract】The origin of Yersinia pestis and the early stages of its evolution are fundamental subjects of investigation given its high virulence and mortality that resulted from past pandemics. Although the earliest evidence of Y. pestis infections in humans has been identified in Late Neolithic/Bronze Age Eurasia (LNBA 5000–3500y BP), these strains lack key genetic components required for flea adaptation, thus making their mode of transmission and disease presentation in humans unclear. Here, we reconstruct ancient Y. pestis genomes from individuals associated with the Late Bronze Age period (~3800 BP) in the Samara region of modern-day Russia. We show clear distinctions between our new strains and the LNBA lineage, and suggest that the full ability for flea-mediated transmission causing bubonic plague evolved more than 1000 years earlier than previously suggested. Finally, we propose that several Y. pestis lineages were established during the Bronze Age, some of which persist to the present day.We thank Cosimo Posth, Marcel Keller, Michal Feldman and Wolfgang Haak for useful insights to the manuscript, as well as Alexander Immel and Stephen Clayton for computational support. In addition, we are thankful to Guido Brandt, Antje Wissgott and Cäcilia Freund for laboratory support. M.A.S., A.H., K.I.B. and J.K. were supported by the ERC starting grant APGREID, and by the Max Planck Society. C.C.W. was supported by the Max Planck Society and the Nanqiang Outstanding Young Talents Program of Xiamen University. D.K. was supported by a Marie Heim-Vögtlin grant from the Swiss National Science Foundation
Stone Age Yersinia pestis genomes shed light on the early evolution, diversity, and ecology of plague
The bacterial pathogenYersinia pestisgave rise to devastating outbreaks throughouthuman history, and ancient DNA evidence has shown it afflicted human populations asfar back as the Neolithic.Y. pestisgenomes recovered from the Eurasian Late Neolithic/Early Bronze Age (LNBA) period have uncovered key evolutionary steps that led to itsemergence from aYersinia pseudotuberculosis-like progenitor; however, the number ofreconstructed LNBA genomes are too few to explore its diversity during this criticalperiod of development. Here, we present 17Y. pestisgenomes dating to 5,000 to 2,500y BP from a wide geographic expanse across Eurasia. This increased dataset enabled usto explore correlations between temporal, geographical, and genetic distance. Ourresults suggest a nonflea-adapted and potentially extinct single lineage that persistedover millennia without significant parallel diversification, accompanied by rapid dis-persal across continents throughout this period, a trend not observed in other pathogensfor which ancient genomes are available. A stepwise pattern of gene loss provides fur-ther clues on its early evolution and potential adaptation. We also discover the presenceof theflea-adapted form ofY. pestisin Bronze Age Iberia, previously only identified inin the Caucasus and the Volga regions, suggesting a much wider geographic spread ofthis form ofY. pestis. Together, these data reveal the dynamic nature of plague’s forma-tive years in terms of its early evolution and ecology
Mycobacterium leprae diversity and population dynamics in medieval Europe from novel ancient genomes
Hansen’s disease (leprosy), widespread in medieval Europe, is today mainly prevalent in tropical and subtropical regions with around 200,000 new cases reported annually. Despite its long history and appearance in historical records, its origins and past dissemination patterns are still widely unknown. Applying ancient DNA approaches to its major causative agent, Mycobacterium leprae, can significantly improve our understanding of the disease’s complex history. Previous studies have identified a high genetic continuity of the pathogen over the last 1500 years and the existence of at least four M. leprae lineages in some parts of Europe since the Early Medieval period
Historical Y. pestis Genomes Reveal the European Black Death as the Source of Ancient and Modern Plague Pandemics
© 2016 Elsevier Inc.Ancient DNA analysis has revealed an involvement of the bacterial pathogen Yersinia pestis in several historical pandemics, including the second plague pandemic (Europe, mid-14th century Black Death until the mid-18th century AD). Here we present reconstructed Y. pestis genomes from plague victims of the Black Death and two subsequent historical outbreaks spanning Europe and its vicinity, namely Barcelona, Spain (1300-1420 cal AD), Bolgar City, Russia (1362-1400 AD), and Ellwangen, Germany (1485-1627 cal AD). Our results provide support for (1) a single entry of Y. pestis in Europe during the Black Death, (2) a wave of plague that traveled toward Asia to later become the source population for contemporary worldwide epidemics, and (3) the presence of an historical European plague focus involved in post-Black Death outbreaks that is now likely extinct
Phylogeography of the second plague pandemic revealed through analysis of historical Yersinia pestis genomes
The second plague pandemic, caused by Yersinia pestis, devastated Europe and the nearby regions between the 14th and 18th centuries AD. Here we analyse human remains from ten European archaeological sites spanning this period and reconstruct 34 ancient Y. pestis genomes. Our data support an initial entry of the bacterium through eastern Europe, the absence of genetic diversity during the Black Death, and low within-outbreak diversity thereafter. Analysis of post-Black Death genomes shows the diversification of a Y. pestis lineage into multiple genetically distinct clades that may have given rise to more than one disease reservoir in, or close to, Europe. In addition, we show the loss of a genomic region that includes virulence-related genes in strains associated with late stages of the pandemic. The deletion was also identified in genomes connected with the first plague pandemic (541–750 AD), suggesting a comparable evolutionary trajectory of Y. pestis during both events
Ten millennia of hepatitis B virus evolution
Hepatitis B virus (HBV) has been infecting humans for millennia and remains a global health problem, but its past diversity and dispersal routes are largely unknown. We generated HBV genomic data from 137 Eurasians and Native Americans dated between ~10,500 and ~400 years ago. We date the most recent common ancestor of all HBV lineages to between ~20,000 and 12,000 years ago, with the virus present in European and South American hunter-gatherers during the early Holocene. After the European Neolithic transition, Mesolithic HBV strains were replaced by a lineage likely disseminated by early farmers that prevailed throughout western Eurasia for ~4000 years, declining around the end of the 2nd millennium BCE. The only remnant of this prehistoric HBV diversity is the rare genotype G, which appears to have reemerged during the HIV pandemic