Effective inhibition of lytic development of bacteriophages λ, P1 and T4 by starvation of their host, Escherichia coli

BACKGROUND: Bacteriophage infections of bacterial cultures cause serious problems in genetic engineering and biotechnology. They are dangerous not only because of direct effects on the currently infected cultures, i.e. their devastation, but also due to a high probability of spreading the phage progeny throughout a whole laboratory or plant, which causes a real danger for further cultivations. Therefore, a simple method for quick inhibition of phage development after detection of bacterial culture infection should be very useful. RESULTS: Here, we demonstrate that depletion of a carbon source from the culture medium, which provokes starvation of bacterial cells, results in rapid inhibition of lytic development of three Escherichia coli phages, λ, P1 and T4. Since the effect was similar for three different phages, it seems that it may be a general phenomenon. Moreover, similar effects were observed in flask cultures and in chemostats. CONCLUSION: Bacteriophage lytic development can be inhibited efficiently by carbon source limitation in bacterial cultures. Thus, if bacteriophage contamination is detected, starvation procedures may be recommended to alleviate deleterious effects of phage infection on the culture. We believe that this strategy, in combination with the use of automated and sensitive bacteriophage biosensors, may be employed in the fermentation laboratory practice to control phage outbreaks in bioprocesses more effectively

Influence of the Escherichia coli oxyR gene function on λ prophage maintenance

In Escherichia coli hosts, hydrogen peroxide is one of the factors that may cause induction of λ prophage. Here, we demonstrate that H2O2-mediated λ prophage induction is significantly enhanced in the oxyR mutant host. The mRNA levels for cI gene expression were increased in a λ lysogen in the presence of H2O2. On the other hand, stimulation of the pM promoter by cI857 overproduced from a multicopy plasmid was decreased in the ΔoxyR mutant in the presence of H2O2 but not under normal growth conditions. The purified OxyR protein did bind specifically to the pM promoter region. This binding impaired efficiency of interaction of the cI protein with the OR3 site, while stimulating such a binding to OR2 and OR1 sites, in the regulatory region of the pM promoter. We propose that changes in cI gene expression, perhaps in combination with moderately induced SOS response, may be responsible for enhanced λ prophage induction by hydrogen peroxide in the oxyR mutant. Therefore, OxyR seems to be a factor stimulating λ prophage maintenance under conditions of oxidative stress. This proposal is discussed in the light of efficiency of induction of lambdoid prophages bearing genes coding for Shiga toxins

Atypical microbial infections of digestive tract may contribute to diarrhea in mucopolysaccharidosis patients: a MPS I case study

BACKGROUND: Mucopolysaccharidoses are heritable, metabolic diseases caused by deficiency in an activity of one of specific lysosomal enzymes involved in degradation of mucoplysaccharides (glycosaminoglycans). Among many medical problems of patients with mucopolysaccharidoses, there are frequent episodes of diarrhea of unknown etiology. CASE PRESENTATION: A girl, diagnosed enzymatically for mucopolysaccharidosis type I (deficiency of α-L-iduronidase) at the age of 3 years and 9 months, was investigated until the age of 5 years and 4 months. Frequent loose stools and episodes of diarrhea, often accompanied by vomiting, were encountered. Detailed microbiological analyses were performed and atypical microbial infections (most often enetropathogenic Escherichia coli, but also other species, like Pseudomonas aeruginosa or Staphylococcus aureus, as well as adenoviruses) of the digestive tract were found in most severe diarrhea episodes. Often, isolations of pathogenic bacterial strains from stools of the investigated patient suffering from diarrhea were not obvious during the first screening, and only detailed microbiological studies, including re-isolation of colonies, gave the results of isolation of particular pathogenic strains (especially in the case of enetropathogenic E. coli). CONCLUSION: We conclude that atypical microbial infections of digestive tract may contribute significantly to diarrhea in mucopolysaccaridosis patients. Since isolated strains were not typical and their isolation was often possible only after detailed investigation (not during a standard screening), such atypical microbial infections of digestive tract of mucopolysaccharidosis patients could be usually overlooked to date. Importantly, these atypical infections could be effectively treated with antimicrobial agents

Deer reduce habitat quality for a woodland songbird: evidence from settlement patterns, demographic parameters, and body condition.

Understanding avian responses to ungulate-induced habitat modification is important because deer populations are increasing across much of temperate Europe and North America. Our experimental study examined whether habitat quality for Blackcaps (Sylvia atricapilla) in young woodland in eastern England was affected by deer, by comparing Blackcap behavior, abundance, and condition between paired plots (half of each pair protected from deer). The vegetation in each pair of plots was the same age. The Blackcap is an ideal model species for testing effects of deer on avian habitat quality because it is dependent on dense understory vegetation and is abundant throughout much of Europe. We compared timing of settlement, abundance, age structure (second-year vs. after-second-year), and phenotypic quality (measured as a body condition index, body mass divided by tarsus length) between experimental and control plots. We used point counts to examine Blackcap distribution, and standardized mist netting to collect demographic and biometric data. Incidence of singing Blackcaps was higher in nonbrowsed than in browsed plots, and singing males were recorded in nonbrowsed plots earlier in the season, indicating earlier and preferential territory establishment. Most Blackcaps, both males and females, were captured in vegetation prior to canopy closure (2–4 years of regrowth). Body condition was superior for male Blackcaps captured in nonbrowsed plots; for second-year males this was most marked in vegetation prior to canopy closure. We conclude that deer browsing in young woodland can alter habitat quality for understory-dependent species, with potential consequences for individual fitness and population productivity beyond the more obvious effects on population density

Measurements, Models, Systems and Design

531 s.

Effects of flavonoids on glycosaminoglycan synthesis: implications for substrate reduction therapy in Sanfilippo disease and other mucopolysaccharidoses

Sanfilippo disease (mucopolysaccharidosis type III, MPS III) is a severe metabolic disorder caused by accumulation of heparan sulfate (HS), one of glycosaminoglycans (GAGs), due to a genetic defect resulting in a deficiency of GAG hydrolysis. This disorder is characterized as the most severe neurological form of MPS, revealing rapid deterioration of brain functions. Among therapeutic approaches for MPS III, one of the most promising appears to be the substrate reduction therapy (SRT). Genistein (5, 7-dihydroxy-3- (4-hydroxyphenyl)-4H-1-benzopyran-4-one) is an isoflavone that has been used in SRT for MPS III. In this report, we tested effects of other flavonoids (apigenin, daidzein, kaempferol and naringenin) on GAG synthesis. Their cytotoxicity and anti-proliferation features were also tested. We found that daidzein and kaempferol inhibited GAG synthesis significantly. Moreover, these compounds were able to reduce lysosomal storage in MPS IIIA fibroblasts. Interestingly, although genistein is believed to inhibit GAG synthesis by blocking the tyrosine kinase activity of the epidermal growth factor receptor, we found that effects of other flavonoids were not due to this mechanism. In fact, combinations of various flavonoids resulted in significantly more effective inhibition of GAG synthesis than the use of any of these compounds alone. These results, together with results published recently by others, suggest that combination of flavonoids can be considered as a method for improvement of efficiency of SRT for MPS III

Hyperhomocysteinemia - important risk factor for ischemic stroke

Udary mózgu są trzecią co do częstości przyczyną śmierci oraz najczęstszą przyczyną inwalidztwa w populacji osób dorosłych. Etiologia udarów często pozostaje nieustalona. Wśród licznych czynników etiopatogenetycznych udaru mózgu należy uwzględnić hiperhomocysteinemię, która odgrywa istotną rolę w patogenezie udaru mózgu jako czynnik wywołujący proces miażdżycowy i wpływający na zaburzenia krzepnięcia. Metabolizm homocysteiny zależy od wielu czynników, takich jak: stężenia kwasu foliowego, witamin B6 i B12 lub mutacji genów kodujących metabolizm homocysteiny: reduktazy N5, N10-metylenotetrahydrofolianowej (MTHFR, methylenetetrahydrofolate reductase), β-syntazy cystationinowej (CBS, cystationine β syntase) i syntazy metioninowej (MS, metionine syntase). Ocena stężenia homocysteiny u pacjentów z chorobami naczyniowymi, w tym u chorych z udarem mózgu, nie tylko poszerza wiedzę o etiologii i mechanizmach udarów mózgu, ale w sposób praktyczny wpływa na ich leczenie i zapobieganie im.Hyperhomocysteinemia is emerging as possible risk factor for cardiovascular disease, including cerebral stroke. Stroke is one of the leading causes of mortality and disability in Poland. The etiology of stroke is often unknown; it has been estimated that etiology and pathophysiology in more that 40% of strokes remains unexplained. Hyperhomocysteinemia is considered a modifiable risk factor for stroke, possibly because of atherogenic and prothrombotic mechanism. Both, genetics and environmental (e.g. dietary intake of folic acid and B vitamins) factors affects homocysteine level. One of the most common genetics defects of homocysteine metabolism is a mutation in the enzyme methylenetetrahydrofolate reductase (MTHFR), metionine syntase (MS) and cystationine beta syntase (CBS). Identification of the role of hyperhomocysteinemia as the modifiable risk factor for stroke may lead to more effective prevention of stroke through dietary and pharmacological modification of homocysteine level

Guz łożyska — opis przypadku i przegląd piśmiennictwa

Guzy łożyska zwykle przebiegają bezobjawowo i są wykrywane jedynie podczas rutynowego badania histopatologicznego. Najczęściej występującym guzem jest chorangioma, czyli naczyniak łożyska. Wiąże się on z wystę­powaniem licznych powikłań ciąży, takich jak wielowodzie oraz niedokrwistość, małopłytkowość, kardiomegalia i niewydolność krążenia u płodu. Prezentujemy przypadek guza łożyska z obrazem ultrasonograficznym typowym dla chorangioma z towarzyszącą kardiomegalią u płodu, który rozpoznano ostatecznie w badaniu histopatologicznym jako hamartoma

Hemorrhagic stroke as a complication of fibrynolytic treatment in myocardial infarction

Thromboembolic stroke most often occurs in patients who do not receive fibrynolytic treatment. Intracranial hemorrhage is the most common form of stroke in patients receiving thrombolytic therapy. Majority of thromboembolic stroke occures more than 48 hours after fibrynolytic therapy administration. Hemorrhagic stroke usually occurs in the first 24 hours after fibrynolytic therapy. It is well known that some groups of patients have high risk intracranial hemorrhage as a complication of thrombolytic treatment of myocardial infarction. Fibrynolytic therapy reduces risk of death in myocardial infarction with ST segment elevation and is commonly used in many hospitals. The risk of as serious complication as cerebral hemorrhage, which can cause impaired neurological functions or even death, is very high in patients with recent myocardial infarction and stoke in history, so in this situations primary percutaneous angioplasty should be prefered.Udar zakrzepowo-zatorowy jest najczęstszą formą udaru u chorych nieleczonych fibrynolitycznie, natomiast u pacjentów poddanych terapii fibrynolitycznej najczęściej dochodzi do krwawienia śródczaszkowego. Większość udarów niedokrwiennych występuje ponad 48 godzin od zastosowania tej terapii. Udary krwotoczne powstają najczęściej w ciągu pierwszych 24 godzin. Wiadomo, że niektórzy chorzy są bardziej narażeni na krwawienie śródczaszkowe jako powikłanie leczenia fibrynolitycznego stosowanego w zawale serca. Leczenie takie zmniejsza śmiertelność w zawale serca z uniesieniem odcinka ST i nadal jest powszechnie stosowaną metodą terapeutyczną w wielu ośrodkach. Jednak - ze względu na ryzyko wystąpienia tak poważnego powikłania, jakim jest krwawienie śródczaszkowe, które wiąże się z ryzykiem ciężkiego inwalidztwa, a nawet zgonu - u chorych z zawałem serca i przebytym udarem w wywiadzie oraz towarzyszącymi innymi czynnikami ryzyka krwawienia śródczaszkowego należy preferować pierwotną angioplastykę przed leczeniem fibrynolitycznym