There is considerable controversy surrounding the biological effects of radiofrequency (RF) fields, as emitted by mobile phones. Previous work from our laboratory has shown no effect related to the exposure of 1.9 GHz pulse-modulated RF fields on the expression of 22,000 genes in a human glioblastoma-derived cell-line (U87MG) at 6 h following a 4 h RF field exposure period. As a follow-up to this study, we have now examined the effect of RF field exposure on the possible expression of late onset genes in U87MG cells after a 24 h RF exposure period. In addition, a human monocyte-derived cell-line (Mono-Mac-6, MM6) was exposed to intermittent (5 min ON, 10 min OFF) RF fields for 6 h and then gene expression was assessed immediately after exposure and at 18 h postexposure. Both cell lines were exposed to 1.9 GHz pulse-modulated RF fields for 6 or 24 h at specific absorption rates (SARs) of 0.1-10.0 W/kg. In support of our previous results, we found no evidence that nonthermal RF field exposure could alter gene expression in either cultured U87MG or MM6 cells, relative to nonirradiated control groups. However, exposure of both cell-lines to heat-shock conditions (43 degrees C for 1 h) caused an alteration in the expression of a number of well-characterized heat-shock proteins.

This study found no evidence that exposure of cells to non-thermalizing levels of 1.9 GHz pulse-modulated RF fields can cause any detectable change in stress-related gene expression.

Myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are hematologic malignancies arising from the bone marrow. Despite recent advances in treating these diseases, patients with higher-risk MDS and AML continue to have a poor prognosis with limited survival. It has long been recognized that there is an immune component to the pathogenesis of MDS and AML, but until recently, immune therapies have played a limited role in treating these diseases. Immune suppressive therapy exhibits durable clinical responses in selected patients with MDS, but the question of which patients are most suitable for this treatment remains unclear. Over the past decade, there has been remarkable progress in identifying genomic features of MDS and AML, which has led to an improved discernment of the molecular pathogenesis of these diseases. An improved understanding of immune and inflammatory molecular mechanisms of MDS and AML have also recently revealed novel therapeutic targets. Emerging treatments for MDS and AML include monoclonal antibodies such as immune checkpoint inhibitors, bispecific T-cell-engaging antibodies, antibody drug conjugates, vaccine therapies, and cellular therapeutics including chimeric antigen receptor T-cells and NK cells. In this review, we provide an overview of the current understanding of immune dysregulation in MDS and AML and an update on novel immune therapies for these bone marrow malignancies.

Venous thromboembolism (VTE) remains the number one preventable cause of hospital acquired mortality and morbidity. Each year, more than 12 million patients are at risk for VTE. The delivery of appropriate and timely VTE prophylaxis is still suboptimal in many healthcare institutions and can lead to increased readmissions, morbidity, as well as costs. To clarify this issue further, we performed a retrospective case control study at our institution to determine if poor adherence to the VTE prophylaxis guidelines could lead to an increase in VTE events. This was a retrospective case control study conducted at Winthrop-University Hospital from January 2007 to December 2011. Exclusion criteria were age < 18 and concurrent use of anticoagulant agents. Out of 322 cases of hospital acquired VTE or readmission with VTE within 30 days of discharge, 289 cases were selected for final analysis and paired with age and sex matched controls. Patients with a hospital acquired VTE or a readmission for VTE within 30 days of discharge had a significantly reduced rate of VTE prophylaxis when compared to the control group (54.0 vs. 79.2 %, p < 0.0001). The VTE risk assessment rate was also lower in the VTE group (77.2 vs. 85.5 %, p = 0.035). No difference was noted in the time to prophylaxis administration between the two groups (34.8 vs. 33.1 h, p = 0.34). Lastly, sequential compression device (SCD) documentation rate was not different: 68/116 (58.6 %) vs. 44/87 (50.6 %), p = 0.32, between the two arms. Low adherence to the American College of Chest Physician (ACCP) guidelines for VTE prophylaxis correlated with an increase in hospital acquired VTE. The decreased adherence may be linked to a lower VTE risk assessment rate, and other barriers including incorrect identification of contraindications to pharmacologic prophylaxis, and poor documentation of mechanical prophylaxis. There was no difference in SCD documentation rate and timeliness to administration of initial thromboprophylaxis between the two groups. Future studies are needed to reassess adherence and documentation rates after system-wide improvements.