164 research outputs found
Sixty years of Sverdrup : a retrospective of progress in the study of phytoplankton blooms
Author Posting. Β© The Oceanography Society, 2014. This article is posted here by permission of The Oceanography Society for personal use, not for redistribution. The definitive version was published in Oceanography 27, no. 1 (2014): 222β235, doi:10.5670/oceanog.2014.26.One of the most dramatic large-scale features in the ocean is the seasonal greening of the North Atlantic in spring and summer due to the accumulation of phytoplankton biomass in the surface layer. In 1953, Harald Ulrik Sverdrup hypothesized a now canonical mechanism for the development and timing of phytoplankton blooms in the North Atlantic. Over the next 60 years, Sverdrup's Critical Depth Hypothesis spurred progress in understanding of bloom dynamics and offered a valuable theoretical framework on which to build. In reviewing 60 years of literature, the authors trace the development of modern bloom initiation hypotheses, highlighting three case studies that illuminate the complexity, including both catalysts and impediments, of scientific progress in the wake of Sverdrup's hypothesis. Most notably, these cases demonstrate that the evolution of our understanding of phytoplankton blooms was paced by access not only to technology but also to concurrent insights from several disciplines. This exploration of the trajectories and successes in bloom studies highlights the need for expanding interdisciplinary collaborations to address the complexity of phytoplankton bloom dynamics
Antibody response to a T-dependent antigen requires B cell expression of complement receptors.
The effects of brain death and ischemia on tolerance induction are organβspecific
Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/143776/1/ajt14674_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/143776/2/ajt14674.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/143776/3/ajt14674-sup-0001-FigS1-S2.pd
Increasing condom use in heterosexual men: development of a theory-based interactive digital intervention
Increasing condom use to prevent sexually transmitted infections is a key public health goal. Interventions are more likely to be effective if they are theory- and evidence-based. The Behaviour Change Wheel (BCW) provides a framework for intervention development. To provide an example of how the BCW was used to develop an intervention to increase condom use in heterosexual men (the MenSS website), the steps of the BCW intervention development process were followed, incorporating evidence from the research literature and views of experts and the target population. Capability (e.g. knowledge) and motivation (e.g. beliefs about pleasure) were identified as important targets of the intervention. We devised ways to address each intervention target, including selecting interactive features and behaviour change techniques. The BCW provides a useful framework for integrating sources of evidence to inform intervention content and deciding which influences on behaviour to target
ΠΡΠΊΡΡΡΡΠ²Π΅Π½Π½Π°Ρ Π²Π΅Π½ΡΠΈΠ»ΡΡΠΈΡ Π»Π΅Π³ΠΊΠΈΡ Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΌΠΎΡΠ±ΠΈΠ΄Π½ΡΠΌ ΠΎΠΆΠΈΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΏΡΠΈ Π»Π°ΠΏΠ°ΡΠΎΡΠΊΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΡ ΠΎΠΏΠ΅ΡΠ°ΡΠΈΡΡ Π² ΠΏΠΎΠ»ΠΎΠΆΠ΅Π½ΠΈΠΈ Π’ΡΠ΅Π½Π΄Π΅Π»Π΅Π½Π±ΡΡΠ³Π° (ΠΎΠ±Π·ΠΎΡ Π»ΠΈΡΠ΅ΡΠ°ΡΡΡΡ)
Β Β The literature review is devoted to the peculiarities of artificial lung ventilation (ALV) in patients with morbid obesity during laparoscopic oncosurgical interventions in the Trendelenburg position. At present, there are no consensus recommendations on the choice of the optimal ALV mode during anesthesia in this area of oncosurgery. When analyzing data obtained from other types of operations, there was no impression that there were significant advantages of any ALV modes, both with volume and pressure control. However, high values of positive end-expiratory pressure (PEEP) have the most evidence of benefit in this category of patients, and the inversion of the duration of the respiratory cycle phases without creating a high PEEP can help reduce the risk of lung damage when all other ALV techniques do not allow for adequate oxygenation.Β Β ΠΠ±Π·ΠΎΡ Π»ΠΈΡΠ΅ΡΠ°ΡΡΡΡ ΠΏΠΎΡΠ²ΡΡΠ΅Π½ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΡΠΌ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΡ ΠΈΡΠΊΡΡΡΡΠ²Π΅Π½Π½ΠΎΠΉ Π²Π΅Π½ΡΠΈΠ»ΡΡΠΈΠΈ Π»Π΅Π³ΠΊΠΈΡ
(ΠΠΠ) Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΌΠΎΡΠ±ΠΈΠ΄Π½ΡΠΌ ΠΎΠΆΠΈΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΏΡΠΈ Π»Π°ΠΏΠ°ΡΠΎΡΠΊΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΎΠ½ΠΊΠΎΡ
ΠΈΡΡΡΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
Π²ΠΌΠ΅ΡΠ°ΡΠ΅Π»ΡΡΡΠ²Π°Ρ
Π² ΠΏΠΎΠ»ΠΎΠΆΠ΅Π½ΠΈΠΈ Π’ΡΠ΅Π½Π΄Π΅Π»Π΅Π½Π±ΡΡΠ³Π°. Π Π½Π°ΡΡΠΎΡΡΠ΅Π΅ Π²ΡΠ΅ΠΌΡ ΡΠΎΠ³Π»Π°ΡΠΈΡΠ΅Π»ΡΠ½ΡΠ΅ ΡΠ΅ΠΊΠΎΠΌΠ΅Π½Π΄Π°ΡΠΈΠΈ ΠΏΠΎ Π²ΡΠ±ΠΎΡΡ ΠΎΠΏΡΠΈΠΌΠ°Π»ΡΠ½ΠΎΠ³ΠΎ ΡΠ΅ΠΆΠΈΠΌΠ° ΠΠΠ ΠΏΡΠΈ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΠΈ Π°Π½Π΅ΡΡΠ΅Π·ΠΈΠΈ Π² ΡΡΠΎΠΉ ΠΎΠ±Π»Π°ΡΡΠΈ ΠΎΠ½ΠΊΠΎΡ
ΠΈΡΡΡΠ³ΠΈΠΈ ΠΎΡΡΡΡΡΡΠ²ΡΡΡ. ΠΡΠΈ Π°Π½Π°Π»ΠΈΠ·Π΅ Π΄Π°Π½Π½ΡΡ
, ΠΏΠΎΠ»ΡΡΠ΅Π½Π½ΡΡ
ΠΏΡΠΈ Π΄ΡΡΠ³ΠΈΡ
Π²ΠΈΠ΄Π°Ρ
ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΉ, Π½Π΅ ΡΠ»ΠΎΠΆΠΈΠ»ΠΎΡΡ Π²ΠΏΠ΅ΡΠ°ΡΠ»Π΅Π½ΠΈΡ ΠΎ Π½Π°Π»ΠΈΡΠΈΠΈ Π·Π½Π°ΡΠΈΠΌΡΡ
ΠΏΡΠ΅ΠΈΠΌΡΡΠ΅ΡΡΠ² ΠΊΠ°ΠΊΠΈΡ
-Π»ΠΈΠ±ΠΎ ΡΠ΅ΠΆΠΈΠΌΠΎΠ² ΠΠΠ β ΠΊΠ°ΠΊ Ρ ΡΠΏΡΠ°Π²Π»Π΅Π½ΠΈΠ΅ΠΌ ΠΏΠΎ ΠΎΠ±ΡΠ΅ΠΌΡ, ΡΠ°ΠΊ ΠΈ ΠΏΠΎ Π΄Π°Π²Π»Π΅Π½ΠΈΡ. Π’Π΅ΠΌ Π½Π΅ ΠΌΠ΅Π½Π΅Π΅ Π±ΠΎΠ»ΡΡΠ΅ Π²ΡΠ΅Π³ΠΎ Π΄ΠΎΠΊΠ°Π·Π°ΡΠ΅Π»ΡΡΡΠ² Π² ΠΎΡΠ½ΠΎΡΠ΅Π½ΠΈΠΈ ΠΏΠΎΠ»ΡΠ·Ρ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΡ Ρ ΡΠ°ΠΊΠΎΠΉ ΠΊΠ°ΡΠ΅Π³ΠΎΡΠΈΠΈ Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΈΠΌΠ΅ΡΡ Π²ΡΡΠΎΠΊΠΈΠ΅ Π·Π½Π°ΡΠ΅Π½ΠΈΡ ΠΏΠΎΠ»ΠΎΠΆΠΈΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ Π΄Π°Π²Π»Π΅Π½ΠΈΡ Π² ΠΊΠΎΠ½ΡΠ΅ Π²ΡΠ΄ΠΎΡ
Π° (ΠΠΠΠ), ΠΈΠ½Π²Π΅ΡΡΠΈΡ ΠΏΡΠΎΠ΄ΠΎΠ»ΠΆΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΠΈ ΡΠ°Π· Π΄ΡΡ
Π°ΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ ΡΠΈΠΊΠ»Π° Π±Π΅Π· ΡΠΎΠ·Π΄Π°Π½ΠΈΡ Π²ΡΡΠΎΠΊΠΎΠ³ΠΎ ΠΠΠΠ ΠΌΠΎΠΆΠ΅Ρ ΡΠΏΠΎΡΠΎΠ±ΡΡΠ²ΠΎΠ²Π°ΡΡ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΡ ΡΠΈΡΠΊΠ° ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΡ Π»Π΅Π³ΠΊΠΈΡ
Π² ΡΡΠ»ΠΎΠ²ΠΈΡΡ
, ΠΊΠΎΠ³Π΄Π° Π²ΡΠ΅ ΠΎΡΡΠ°Π»ΡΠ½ΡΠ΅ ΠΌΠ΅ΡΠΎΠ΄ΠΈΠΊΠΈ ΠΠΠ Π½Π΅ ΠΏΠΎΠ·Π²ΠΎΠ»ΡΡΡ Π΄ΠΎΠ±ΠΈΡΡΡΡ Π°Π΄ΠΊΠ΅Π²Π°ΡΠ½ΠΎΠΉ ΠΎΠΊΡΠΈΠ³Π΅Π½Π°ΡΠΈΠΈ
The dosage-dependent effect exerted by the NM23-H1/H2 homolog NDK-1 on distal tip cell migration in C. <i>elegans</i>
Elucidating the Role of the Complement Control Protein in Monkeypox Pathogenicity
Monkeypox virus (MPXV) causes a smallpox-like disease in humans. Clinical and epidemiological studies provide evidence of pathogenicity differences between two geographically distinct monkeypox virus clades: the West African and Congo Basin. Genomic analysis of strains from both clades identified a βΌ10 kbp deletion in the less virulent West African isolates sequenced to date. One absent open reading frame encodes the monkeypox virus homologue of the complement control protein (CCP). This modulatory protein prevents the initiation of both the classical and alternative pathways of complement activation. In monkeypox virus, CCP, also known as MOPICE, is a βΌ24 kDa secretory protein with sequence homology to this superfamily of proteins. Here we investigate CCP expression and its role in monkeypox virulence and pathogenesis. CCP was incorporated into the West African strain and removed from the Congo Basin strain by homologous recombination. CCP expression phenotypes were confirmed for both wild type and recombinant monkeypox viruses and CCP activity was confirmed using a C4b binding assay. To characterize the disease, prairie dogs were intranasally infected and disease progression was monitored for 30 days. Removal of CCP from the Congo Basin strain reduced monkeypox disease morbidity and mortality, but did not significantly decrease viral load. The inclusion of CCP in the West African strain produced changes in disease manifestation, but had no apparent effect on disease-associated mortality. This study identifies CCP as an important immuno-modulatory protein in monkeypox pathogenesis but not solely responsible for the increased virulence seen within the Congo Basin clade of monkeypox virus
Surviving Mousepox Infection Requires the Complement System
Poxviruses subvert the host immune response by producing immunomodulatory proteins, including a complement regulatory protein. Ectromelia virus provides a mouse model for smallpox where the virus and the host's immune response have co-evolved. Using this model, our study investigated the role of the complement system during a poxvirus infection. By multiple inoculation routes, ectromelia virus caused increased mortality by 7 to 10 days post-infection in C57BL/6 mice that lack C3, the central component of the complement cascade. In C3β/β mice, ectromelia virus disseminated earlier to target organs and generated higher peak titers compared to the congenic controls. Also, increased hepatic inflammation and necrosis correlated with these higher tissue titers and likely contributed to the morbidity in the C3β/β mice. In vitro, the complement system in naΓ―ve C57BL/6 mouse sera neutralized ectromelia virus, primarily through the recognition of the virion by natural antibody and activation of the classical and alternative pathways. Sera deficient in classical or alternative pathway components or antibody had reduced ability to neutralize viral particles, which likely contributed to increased viral dissemination and disease severity in vivo. The increased mortality of C4β/β or Factor Bβ/β mice also indicates that these two pathways of complement activation are required for survival. In summary, the complement system acts in the first few minutes, hours, and days to control this poxviral infection until the adaptive immune response can react, and loss of this system results in lethal infection
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