Finally, while reimbursement rate data were difficult to obtain, the data available suggested that reimbursement rates for pre-emptive PGx testing remain low.
 
  These findings should inform the establishment of future implementation efforts at institutions considering a pre-emptive PGx testing program.
 These findings should inform the establishment of future implementation efforts at institutions considering a pre-emptive PGx testing program.
  Social media may be particularly valuable in research in rare genetic diseases because of the low numbers of patients and the rare disease community's robust online presence. The goal of this systematic review was to understand how social media is currently used in rare disease research and the characteristics of the participants in these studies.
 
  We conducted a systematic review of six databases to identify studies published in English between January 2004 and November 2020, of which 120 met inclusion criteria.
 
  Most studies were observational (n = 114, 95.0%) and cross-sectional (n = 107, 89.2%), and more than half (n = 69, 57.5%) utilized only surveys. Only 101 rare diseases were included across all studies. Participant demographics, when reported, were predominantly female (70.1% ± 22.5%) and white (85.0% ± 11.0%) adult patients and caregivers.
 
  Despite its potential benefits in rare disease research, the use of social media is still methodologically limited and the participants reached may not be representative of the rare disease population by gender, race, age, or rare disease type. As scholars explore using social media for rare disease research, careful attention should be paid to representativeness when studying this diverse patient community.
 Despite its potential benefits in rare disease research, the use of social media is still methodologically limited and the participants reached may not be representative of the rare disease population by gender, race, age, or rare disease type. As scholars explore using social media for rare disease research, careful attention should be paid to representativeness when studying this diverse patient community.
  To provide a detailed clinical and cytogenomic summary of individuals with chromosome 8p rearrangements of invdupdel(8p), del(8p), and dup(8p).
 
  We enrolled 97 individuals with invdupdel(8p), del(8p), and dup(8p). Clinical and molecular data were collected to delineate and compare the clinical findings and rearrangement breakpoints. We included additional 5 individuals with dup(8p) from the literature for a total of 102 individuals.
 
  Eighty-one individuals had recurrent rearrangements of invdupdel(8p) (n = 49), del(8p)_distal (n = 4), del(8p)_proximal (n = 9), del(8p)_proximal&distal (n = 12), and dup(8p)_proximal (n = 7). Twenty-one individuals had nonrecurrent rearrangements. While all individuals had neurodevelopmental features, the frequency and severity of clinical findings were higher in individuals with invdupdel(8p), and with larger duplications. All individuals with GATA4 deletion had structural congenital heart defects; however, the presence of structural heart defects in some individuals with normal GATA4 copy number suggests there are other potentially contributing gene(s) on 8p.
 
  Our study may inform families and health-care providers about the associated clinical findings and severity in individuals with chromosome 8p rearrangements, and guide researchers in investigating the underlying molecular and biological mechanisms by providing detailed clinical and cytogenomic information about individuals with distinct 8p rearrangements.
 Our study may inform families and health-care providers about the associated clinical findings and severity in individuals with chromosome 8p rearrangements, and guide researchers in investigating the underlying molecular and biological mechanisms by providing detailed clinical and cytogenomic information about individuals with distinct 8p rearrangements.Kupffer cells (KCs), which are liver-resident macrophages, originate from the fetal yolk sac and represent one of the largest macrophage populations in the body. However, the current data on the origin of the cells that restore macrophages during liver injury and regeneration remain controversial. Here, we address the question of whether liver macrophage restoration results from circulating monocyte infiltration or local KC proliferation in regenerating livers after partial hepatectomy (PHx) and uncover the underlying mechanisms. By using several strains of genetically modified mice and performing immunohistochemical analyses, we demonstrated that local KC proliferation mainly contributed to the restoration of liver macrophages after PHx. Peak KC proliferation was impaired in Il6-knockout (KO) mice and restored after the administration of IL-6 protein, whereas KC proliferation was not affected in Il4-KO or Csf2-KO mice. The source of IL-6 was identified using hepatocyte- and myeloid-specific Il6-KO mice and the results revealed that both hepatocytes and myeloid cells contribute to IL-6 production after PHx. Moreover, peak KC proliferation was also impaired in myeloid-specific Il6 receptor-KO mice after PHx, suggesting that IL-6 signaling directly promotes KC proliferation.  https://www.selleckchem.com/products/apilimod.html  Studies using several inhibitors to block the IL-6 signaling pathway revealed that sirtuin 1 (SIRT1) contributed to IL-6-mediated KC proliferation in vitro. Genetic deletion of the Sirt1 gene in myeloid cells, including KCs, impaired KC proliferation after PHx. In conclusion, our data suggest that KC repopulation after PHx is mainly driven by local KC proliferation, which is dependent on IL-6 and SIRT1 activation in KCs.The substantial advances attained by checkpoint blockade immunotherapies have driven an expansion in the approaches used to promote T cell access to the tumor microenvironment to provide targets for checkpoint immunotherapy. Inherent in any T cell response to a tumor antigen is the capacity of dendritic cells to initiate and support such responses. Here, the rationale and early immunobiology of CD40 as a master regulator of dendritic cell activation is reviewed, with further contextualization and appreciation for the role of CD40 stimulation not only in cancer vaccines but also in other contemporary immune-oncology approaches.