Apart from the phenotypical difference, our HHV8-positive neoplasms were not distinct from the HHV8-negative group. Literature review of 256 cases, including our cases, revealed that HHV8-positive cases were associated more frequently with HIV and EBV infection, with rare MYC rearrangement, and a poorer prognosis than HHV8-negative cases. We propose to name the HHV8-positive cases as 'classical' or 'type I PEL' and the HHV8-negative cases as 'type II PEL', stressing the similarities and the distinctive features between these two groups.

Decoy receptor 3 (DcR3) is a soluble decoy receptor belonging to the tumor necrosis factor receptor superfamily that is overexpressed in various malignant tumor types. DcR3 has been implicated in tumor cell survival by inhibiting apoptosis and by interfering with immune surveillance. A previous study showed that DcR3 expression is associated with Epstein-Barr virus (EBV)-positive lymphomas but rarely with non-EBVpositive B-cell lymphomas, suggesting that the presence of EBV may affect DcR3 expression. Here, we demonstrated enhanced DcR3 expression upon EBV reactivation in P3HR1 cells and in EBV-infected 293 cells. This enhancement, however, could not be detected in 293 cells infected with EBV with BRLF1 deleted. We found that EBV transactivator, Rta, could upregulate DcR3 expression by direct binding to an Rta-responsive element (RRE) located in the DcR3 promoter region and that this RRE is important for Rta-mediated DcR3 expression. Overexpressing CREB-binding protein (CBP) further enhanced Rta-dependent DcR3 expression, suggesting Rta-dependent DcR3 transcription activity is mediated by CBP. Previously, Rta was shown to enhance phosphatidylinositol-3 kinase (PI3-K) activity. However, Rta-transduced PI 3-K activity plays a minor role in DcR3 expression. This is the first report to demonstrate that Rta upregulates a cellular gene by direct binding to an RRE.Decoy receptor 3 (DcR3)/TR6/M68 is a soluble decoy receptor belonging to the tumor necrosis factor receptor (TNFR) superfamily. Unlike most of the other members of the TNFR family, DcR3 does not contain a transmembrane domain and can be secreted (35). DcR3 is overexpressed in various malignant tumor types arising from the lung, colon, glia, and gastrointestinal tract (4,17,35,44,52,54); in normal tissues, however, its expression can be detected only weakly in colon epithelial cells (35) and the placenta (18). DcR3 overexpression in tumor cells can be dependent on (34, 35) or independent of (4, 34) its gene amplification. DcR3 has been postulated to help tumor cells to gain survival advantage by inhibiting apoptosis and by interfering with immune surveillance by neutralizing the cytotoxic and immunomodulatory effects of Fas ligand, LIGHT (homologous to lymphotoxins, shows inducible expression, and competes with HSV glycoprotein D for herpesvirus entry mediator, a receptor expressed by T lymphocytes), and TNF-like molecule 1A (TL1A) (32,35,63). By neutralization of TL1A, DcR3 overexpression induces angiogenesis in human umbilical vein endothelial cells, suggesting another important role of DcR3 in tumorigenesis (57, 59). Recently, the DcR3.Fc fusion protein was found to modulate CD14 ϩ monocyte differentiation into macrophages and the functions of dendritic cells (8). Incubation of DcR3.Fctreated dendritic cells skews naïve T cells toward a T helper cell type 2 phenotype (8, 21), and DcR3 is able to induce actin reorganization and enhance the adhesion of monocytes via cross-linking heparan sulfate proteoglycan to increase ICAM-1 and VCAM-1 expression of endothe...

Background: Health behavior (HB) is an action taken by a person who pursues good health and prevents illness. Health behavior, thus, reflects a person's health beliefs and attracts, particularly, on published papers in academics. However, who is the most influential author (MIA) with highly-cited papers on HB remains unknown. Objective: The purpose of this study is to apply the authorship-weighted scheme (AWS) developed by authors to select the MIA on HB using the visual displays on Google Maps. Methods: We obtained 1,116 abstracts published between 2012 and 2016 from Medline based on the keywords of (health [Title]) and (behavior [Title] or behavior [Title]) on September 22, 2018. The author names, countries/areas, and Pubmed paper IDs were recorded. The AWS was applied to (1) select the most productive authors (MPA) using social network analysis (SNA); (2) discover the MIA using h-indexes and author impact factors (AIF) dispersed on Google Maps, and (3) display the countries/areas distributed for the x-index in geography. Pajek software was performed to determine the partition categories of clusters. Results: We found that the MPA and MIA are Matthew K Nock (US) and Erika A Waters (US) for the MPA and MIA, respectively. All visual representations that are the form of a dashboard can be easily displayed on Google Maps. The most influential countries are the US (=19.03) and Australia (=6.46) with the highest x-indexes. Readers are suggested to manipulate them on their own on Google Maps. Conclusion: Many individual researchers achievements (IRA) were determined using h-index, AIF, x-index, or other bibliometric indices without quantifying author contributions. We demonstrated visualized representations on Google Maps using the AWS developed by authors to measure authors influences in a specific discipline. The research approach using the AWS to quantify the authors contributions can be applied to measure IRA in the future.

Case Report OJGH (2020) 3:28 Kayexalate or Kalimate crystals: are they the culprits or the bystanders? Sodium polystyrene sulfonate (Kayexalate) or its analog calcium polystyrene sulfonate (Kalimate) has long been used to treat hyperkalemia in patients with chronic kidney disease (CKD). Although the side effect was rare, there were many case reports in the literature. Its etiology remains unclear. Lillemoe et al., on five uremic patients who developed catastrophic colonic necrosis that was temporally associated with the use of Kayexalate in sorbitol, contributed to death in four of their patients. They further provided experimental evidence implicating sorbitol as the agent responsible for colonic necrosis in a rat model. In contrast to the results of aforementioned animal study, Ayoub et al., published another experimental study in rats, they demonstrated that sodium polystyrene sulfonate (SPS), not sorbitol, was the main culprit for colonic necrosis. Recently, we encountered three patients who had hyperkalemia and were on Kalimate in water. They underwent colonic and gastric biopsy because of developing gastrointestinal symptoms. Kalimate crystals were found in all biopsy specimen, admixed with inflammatory exudate, or standing along on the mucosa surface, without provoking inflammatory reaction. We reviewed the photographs in the published case reports, they were similar to ours. Therefore, we felt that those crystals were bystanders, not the culprits. We fell that SPS ion-exchange resins, if given in water, appears to be clinically effective and reasonably safe to treat hyperkalemia in patients with CKD.