Expression of properdin in complete and incomplete deficiency: normal in vitro synthesis by monocytes in two cases with properdin deficiency type II due to distinct mutations.
Molecular characterization of properdin deficiency type III: dysfunction produced by a single point mutation in exon 9 of the structural gene causing a tyrosine to aspartic acid interchange.
Molecular characterization of properdin deficiency type III: dysfunction produced by a single point mutation in exon 9 of the structural gene causing a tyrosine to aspartic acid interchange.
Outcomes of interest include the ratio of studies adhering to the ACS NSQIP/AGS guidelines and evidence for frailty assessments versus usual care for women with PFDs.
Outcomes of interest include the ratio of studies adhering to the ACS NSQIP/AGS guidelines and evidence for frailty assessments versus usual care for women with PFDs.
This study seeks to describe studies among women with PFD and the associated frailty assessments as recommended in the American College of Surgeons National Surgical Quality Improvement Program/American Geriatric Society (ACS NSQIP/AGS) guidelines.
CDK2 protein expression was clearly decreased in PFD-treated LNCaP and PC-3 cells, whereas p21 protein expression was increased in only PFD-treated LNCaP cells.
Outcomes of interest include the ratio of studies adhering to the ACS NSQIP/AGS guidelines and evidence for frailty assessments versus usual care for women with PFDs.
Treatment with PFD significantly reduced ConA-induced expression of type II and IV collagens, α-SMA mRNA expression, and HP content and decreased inflammatory cells infiltration in hepatic tissues.
Treatment with PFD significantly reduced ConA-induced expression of type II and IV collagens, α-SMA mRNA expression, and HP content and decreased inflammatory cells infiltration in hepatic tissues.
In vitro, the experiments revealed that PFD significantly suppressed LPS/ATP-induced production of reactive oxygen species (ROS) and decreased caspase-1 activation and the level of IL-1β in J774 A.1 cells.
In vitro, the experiments revealed that PFD significantly suppressed LPS/ATP-induced production of reactive oxygen species (ROS) and decreased caspase-1 activation and the level of IL-1β in J774 A.1 cells.