Phonon bottleneck in p-type Ge/Si quantum dots

We study the effect of quantum dot size on the mid-infrared photo- and dark current, photoconductive gain, and hole capture probability in ten-period p-type Ge/Si quantum dot heterostructures. The dot dimensions are varied by changing the Ge coverage and the growth temperature during molecular beam epitaxy of Ge/Si(001) system in the Stranski-Krastanov growth mode. In all samples, we observed the general tendency: with decreasing the size of the dots, the dark current and hole capture probability are reduced, while the photoconductive gain and photoresponse are enhanced. Suppression of the hole capture probability in small-sized quantum dots is attributed to a quenched electron-phonon scattering due to phonon bottleneck

ЕФЕКТИВНІСТЬ АНТРАЛЮ У ХВОРИХ НА ХРОНІЧНИЙ ГЕПАТИТ С

У статті проведено оцінку гепатопротекторної дії препарату “Антраль” у хворих на хронічний гепатит С, вивчено безпеку його застосування та суб’єктивне задоволення пацієнта та лікаря результатами лікування. Отримані результати показали, що антраль володіє доведеним гепатопротекторним ефектом, достовірно знижуючи рівень сироваткових трансаміназ у 76,5 % пацієнтів, у тому числі в 61,8 % у вигляді нормалізації АЛТ або зниження його рівня нижче 2 верхніх меж показника в нормі після одного місяця лікування. Найважливішим показником, що впливає на ефективність лікування антралем, було вираження фіброзу: у хворих із відсутністю тяжкого фіброзу/цирозу (за результатами фібротесту) результати лікування в цілому були кращі. Застосування антралю не супроводжувалося розвитком яких-небудь побічних явищ. Прийом препарату сприятливо позначається на самопочутті хворих, достовірно покращуючи його до “доброго” (за 5-бальною шкалою). Прийнятна ефективність, здатність впливати на самопочуття хворих, відсутність побічних ефектів були головними чинниками позитивної оцінки суб’єктивного задоволення лікарів результатами лікування препаратом “Антраль”

Novel Pyoverdine Inhibitors Mitigate Pseudomonas aeruginosa Pathogenesis

Pseudomonas aeruginosa is a clinically important pathogen that causes a variety of infections, including urinary, respiratory, and other soft-tissue infections, particularly in hospitalized patients with immune defects, cystic fibrosis, or significant burns. Antimicrobial resistance is a substantial problem in P. aeruginosa treatment due to the inherent insensitivity of the pathogen to a wide variety of antimicrobial drugs and its rapid acquisition of additional resistance mechanisms. One strategy to circumvent this problem is the use of anti-virulent compounds to disrupt pathogenesis without directly compromising bacterial growth. One of the principle regulatory mechanisms for P. aeruginosa’s virulence is the iron-scavenging siderophore pyoverdine, as it governs in-host acquisition of iron, promotes expression of multiple virulence factors, and is directly toxic. Some combination of these activities renders pyoverdine indispensable for pathogenesis in mammalian models. Here we report identification of a panel of novel small molecules that disrupt pyoverdine function. These molecules directly act on pyoverdine, rather than affecting its biosynthesis. The compounds reduce the pathogenic effect of pyoverdine and improve the survival of Caenorhabditis elegans when challenged with P. aeruginosa by disrupting only this single virulence factor. Finally, these compounds can synergize with conventional antimicrobials, forming a more effective treatment. These compounds may help to identify, or be modified to become, viable drug leads in their own right. Finally, they also serve as useful tool compounds to probe pyoverdine activity

Pseudomonas aeruginosa Disrupts Caenorhabditis elegans Iron Homeostasis, Causing a Hypoxic Response and Death

SummaryThe opportunistic pathogen Pseudomonas aeruginosa causes serious human infections, but effective treatments and the mechanisms mediating pathogenesis remain elusive. Caenorhabditis elegans shares innate immune pathways with humans, making it invaluable to investigate infection. To determine how P. aeruginosa disrupts host biology, we studied how P. aeruginosa kills C. elegans in a liquid-based pathogenesis model. We found that P. aeruginosa-mediated killing does not require quorum-sensing pathways or host colonization. A chemical genetic screen revealed that iron chelators alleviate P. aeruginosa-mediated killing. Consistent with a role for iron in P. aeruginosa pathogenesis, the bacterial siderophore pyoverdin was required for virulence and was sufficient to induce a hypoxic response and death in the absence of bacteria. Loss of the C. elegans hypoxia-inducing factor HIF-1, which regulates iron homeostasis, exacerbated P. aeruginosa pathogenesis, further linking hypoxia and killing. As pyoverdin is indispensable for virulence in mice, pyoverdin-mediated hypoxia is likely to be relevant in human pathogenesis

Assessment of senior medical care majors’ knowledge in antimicrobial chemotherapy

The article represents the results of anonymous prospective surveys within the framework of the KANT multi-centered research project aimed at assessing students’ knowledge of rational antimicrobial prescribing practices also known as "antimicrobial stewardship

Localization of electrons in dome-shaped GeSi/Si islands

We report on intraband photocurrent spectroscopy of dome-shaped GeSi islands embedded in a Si matrix with n+-type bottom and top Si layers. An in-plane polarized photoresponse in the 85–160 meV energy region has been observed and ascribed to the optical excitation of electrons from states confined in the strained Si near the dome apexes to the continuum states of unstrained Si. The electron confinement is caused by a modification of the conduction band alignment induced by inhomogeneous tensile strain in Si around the buried GeSi quantum dots. Sensitivity of the device to the normal incidence radiation proves a zero-dimensional nature of confined electronic wave functions