Численный анализ распространения и усиления волн цунами на северо-западном шельфе Черного моря

Выполнен численный анализ распространения длинных волн в северо-западной части Черного моря. Рассмотрено 10 возможных зон сейсмической генерации цунами. Расчеты выполнены на сетке с шагом 500 м. Показано, что положение очага цунами существенно влияет на распределение высот волн вдоль побережья. Как правило, наиболее интенсивные волны формируются у ближайшего участка берега. Землетрясения в Южнобережной сейсмической зоне не могут привести к цунамиопасности в западной части моря. Только сильные землетрясения в северо-западной части способны вызывать заметные колебания уровня Черного моря. Период цунами в районе Одессы составляет около 1 ч и зависит от магнитуды землетрясения, в районе Севастополя он в 2 – 3 раза меньше. В большинстве пунктов побережья экстремальные подъемы и понижения уровня моря не превышают по абсолютной величине начального смещения поверхности моря в очаге цунами. Для отдельных участков побережья Румынии и западного побережья Крыма наблюдается некоторое усиление волн, излученных из зон генерации, расположенных в более глубоководной части исследуемого района. С ростом магнитуды землетрясения усиление волн у берега становится более значительным.Виконаний чисельний аналіз розповсюдження довгих хвиль у північно-західній частині Чорного моря. Розглянуто 10 можливих зон сейсмічної генерації цунамі. Розрахунки виконані на сітці з кроком 500 м. Показано, що положення осередку цунамі суттєво впливає на розподіл висот хвиль уздовж побережжя. Як правило, найінтенсивніші хвилі формуються близько найближчої ділянки берега. Землетруси в південнобережній сейсмічній зоні не можуть призвести до цунамонебезпеки в західній частині моря. Лише сильні землетруси в північнозахідній частині здатні викликати помітні коливання рівня Чорного моря. Період цунамі в районі Одеси складає близько 1 години і залежить від магнітуди землетрусу, в районі Севастополя він в 2 – 3 рази менший. У більшості пунктів побережжя екстремальні підйоми і пониження рівня моря не перевищують за абсолютною величиною початкового зсуву поверхні моря в осередку цунамі. Для окремих ділянок побережжя Румунії і західного побережжя Криму спостерігається деяке посилення хвиль, які випромінюють із зон генерації, розташованих в більш глибоководній частині досліджуваного району. Із зростанням магнітуди землетрусу посилення хвиль біля берега стає значнішим.Numerical analysis of long wave propagation in the Black Sea northwestern part is carried out. Ten possible zones of tsunami seismic generation are considered. The calculation are performed on the grid with a step 500 m. It is shown that location of tsunami source effects essentially the distribution of waves’ heights along the coast. As a rule, the most intensive waves are formed in the part closest to the coast. Earthquakes in the South coast seismic zone can not result in tsunami threat in the western part of the sea. Only strong earthquakes in the Black Sea northwestern part can generate noticeable sea level oscillations. Tsunami period near Odessa is about one hour and it depends on the earthquake magnitude. In the Sevastopol region it is 2 – 3 times lower. In the majority of coastal points extreme rises and falls of the sea level do not exceed the absolute value of the initial sea surface elevation in the tsunami source. Some intensification of the waves generated in deeper regions of the area under study is possible in certain parts of the Romanian coast and the Crimean western coast. The wave intensification near the coast grows with the increase of the earthquake magnitude

Growth of <i>E. faecium</i> on starch, maltotetraose, maltose and glucose.

<p>Growth curves of <i>E. faecium</i> E1162 wild-type (black), its isogenic mutants Δ<i>mdxR</i> (red) and Δ<i>mdxABCD-pulA</i> (blue), and the <i>in trans</i> complemented strain Δ<i>mdxR+mdxR</i> (green) on starch (panel A), maltotetraose (panel B), maltose (panel C) and glucose (panel D) are shown. The growth curve of E1162 wild-type in M1 was shown in grey as a negative control. Overnight cultures were inoculated at an initial OD₆₆₀ of 0.0025 into 300 µl semi-defined minimal medium M1 [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0072285#B9" target="_blank">9</a>], M1 supplemented with 2.5 g/l of starch, maltotetraoise, maltose or glucose as sole carbon source, respectively, and then incubated in the Bioscreen C system at 37° C with continuous shaking. The absorbance of 600nm (A₆₀₀) was recorded every 15 min for 12 hours. Growth curves are mean data of three independent experiments. Note that A₆₀₀ at the start of the experiment is higher in M1 + starch than in the other conditions, due to increased turbidity of the medium containing starch.</p

Schematic representation of the gene clusters involved in maltodextrin and maltose utilization of <i>E. faecium</i> E1162.

<p>Genes are represented by arrows (drawn to scale). Genes putatively encoding proteins involved in maltodextrin transport and/or metabolism are indicated in blue or in red. Genes predicted to be involved in the uptake and/or metabolism of maltose are indicated in green or in purple. The genes that encode putative transcriptional regulators are indicated in red or purple. The grey arrows represent the adjacent genes that are not predicted to be involved in maltodextrin or maltose utilization. Gene names, without the EfmE1162-prefix (omitted for reasons of space), are indicated in the arrows and the gene locus tags are indicated above or below the arrows. The homologs in <i>L. monocytogenes</i> EGD-e or in <i>E. faecalis</i> V583 are shown with corresponding colors above or below the gene clusters of <i>E. faecium</i>. The gene locus tags of the homologs are indicated in the arrows. Lines link the homologous genes with corresponding genes in <i>E. faecium</i> and amino acid identities are indicated.</p

Growth curves of <i>E. faecium</i> E1162 and <i>pbp5</i> mutants in BHI with 20 µg ml⁻¹ ampicillin.

<p>Overnight cultures of wild-type <i>E. faecium</i> E1162, the insertional <i>pbp5</i> mutant (<i>pbp5</i>::pWS3), the markerless deletion mutant Δ<i>pbp5</i> and the <i>in trans</i> complemented deletion mutant (Δ<i>pbp5</i>+<i>pbp5</i>) were inoculated at an initial cell density of OD₆₆₀ 0.0025 in BHI with 20 µg ml⁻¹ ampicillin. Growth curves are mean data of three independent experiments.</p

Footprinting analysis of the transposon mutant library.

<p>(A) Schematic overview of the transposon footprinting strategy. PCR is performed using a gene specific primer and a primer corresponding to the transposon sequence. (B) Agarose gel electrophoresis of transposon footprinting on the essential gene <i>ddl</i> (lane 1), and the non-essential genes <i>nox</i> and <i>esp</i> (lane 2 and 3, respectively). Each band represents a PCR product of a different size, corresponding to a transposon insertion in a different position. The red box represents the product size range expected for transposon insertions within the essential <i>ddl</i> gene.</p

Percentage survival of <i>E. faecium</i> cells following a lysozyme challenge.

<p>Survival of the indicated wild-type, mutant strains and <i>in trans</i> complemented strains following a 30-minute incubation in PBS containing 0.5 mg ml⁻¹ lysozyme relative to the survival of the strains after a 30-minute incubation in PBS without lysozyme. Bars represent the standard deviation of the mean of three independent experiments. Asterisks represent significant differences (<i>P</i><0.005 as determined by a two-tailed Student's <i>t</i>-test) between the indicated mutants and the wild-type strain.</p

<i>E. faecium</i> genes involved in ampicillin resistance as determined by M-TraM analysis.

a<p>Indicates the gene containing the transposon insertion.</p>b<p>Indicates the fold-change derived from the ratio of the unselected control library to the ampicillin competitively selected library. <i>e.g.</i> the value 32.5 means that the relative quantity of mutants of EfmE1162_0447 in the ampicillin-selected library was 32.5-fold less than in the control library grown without selective pressure. This indicates that mutants in EfmE1162_0447 have a lower relative fitness in the presence of ampicillin than wild type cells. The value of −7.5 for EfmE1162_2487 indicates that mutants in this gene outgrow the other mutants in the ampicillin-selected library by 7.5-fold, indicating that mutants of EfmE1162_2487 have higher relative fitness in the presence of ampicillin.</p

D,D-carboxypeptidase activity in <i>E. faecium</i> membrane fractions.

<p>Membrane extracts were isolated from the indicated strains grown in BHI medium (with or without the addition 20 µg ml⁻¹ ampicillin) until an OD₆₀₀ of 0.7. The D,D-carboxypeptidase activity (nmol min⁻¹ mg⁻¹) was defined as the number of nmoles of D-Ala released from pentapeptide (7.5 mM) per min and per mg of protein in the membrane fractions. D-Ala was assayed using D-amino acid oxidase coupled to peroxidase. Bars represent the standard deviation of the mean of three independent experiments. Asterisks represent significant difference (^*<i>P</i><0.05, ^**<i>P</i><0.005 as determined by a two-tailed Student's <i>t</i>-test) between the different strains and conditions.</p

Cytokine levels 6 hours after induction <i>P. aeruginosa</i> pneumonia.

<p>TNF-α (A and D), IL-6 (B and E) and IL-10 (C and F) levels in lung and plasma of mice, 6 hours after intranasal inoculation with <i>P. aeruginosa</i>. Two groups of mice were treated with vancomycin for 19 days; in one of these VRE was administered by gastric inoculation (10⁷ CFU) 5 days after the initiation of vancomycin treatment (VRE colonized mice), while in the other group no VRE was administered (Vancomycin controls). A third group of mice did not receive vancomycin or VRE (Naïve controls). Data are mean±SEM of 8 mice per group; * <i>p</i><0.05 versus mice without vancomycin treatment or VRE colonization.</p

Total enterococcal and aerobic gram-negative count in fecal pellets.

<p>Two groups of mice were treated with vancomycin for 19 days; in one of these, VRE was administered by gastric inoculation (10⁷ CFU) 5 days after the initiation of vancomycin treatment. A third group of mice did not receive vancomycin or VRE. Enterococci, isolated from untreated mice and from mice treated with vancomycin only, were identified as <i>E. faecalis</i> (i.e. normal inhabitants of the intestines).</p>***<p>p<0.001 compared to untreated mice, †p<0.001 compared to only vancomycin treated mice (without VRE). Data are means±SE of 8 mice per group.</p