The neutrophil/lymphocyte ratio is a better addition to C-reactive protein than CD64 index as a marker for infection in COPD.

BACKGROUND: This study investigated the importance of neutrophil/lymphocyte ratio (NLR) and other new inflammatory markers including CD64 expression in patients with chronic obstructive pulmonary disease (COPD) for identifying the severity of inflammation and recognition of acute exacerbation and infection. METHODS: Seventy-two patients with a diagnosis of COPD exacerbation who were admitted to the Department of Internal Medicine B, 13 with stable COPD, and control group of 15 healthy people were enrolled in the study. Complete blood count (CBC), measurement of C-reactive protein (CRP), mean platelet volume (MPV), red blood cell distribution width (RDW) and CD64 expression were determined within 2 hours of hospital admission. RESULTS: NLR and other inflammatory markers, such as RDW, CRP, and CD64 were found to be significantly elevated in exacerbated COPD compared to stable COPD and control participants. There was a significant correlation of NLR with CRP (r=0.309, P<0.001), For an NLR cutoff of 7.3, sensitivity for detecting exacerbation of COPD was 0.768 and specificity was 1-0.269 (AUC=0.793, P=0.001) RDW was significant as NLR. CD64 is statistically significant (P=0.002) the lack of significance was between acute exacerbation of COPD and stable COPD, but indexes were higher in the group of COPD patients with complications. CONCLUSIONS: Elevated NLR can be used as a marker similar to CRP, and RDW, in the determination of increased inflammation in acutely exacerbated COPD. NLR could be beneficial for the early detection of potential acute exacerbations in patients with COPD who have normal levels of traditional markers; CD64 was higher but did not reach statistical significance. MPV was not helpful.

Mitochondrial pro-apoptotic ARTS protein is lost in the majority of acute lymphoblastic leukemia patients.

Acquired resistance towards apoptosis is the hallmark of most if not all types of cancer. We have previously identified and characterized ARTS, a broadly expressed protein localized to mitochondria. ARTS was initially shown to mediate TGF-beta induced apoptosis. Recently, we have found that high levels of ARTS induce apoptosis without additional pro-apoptotic stimuli. Further, ARTS promotes apoptosis in response to a wide variety of pro-apoptotic stimuli. Here, we report that the expression of ARTS is lost in all lymphoblasts of more than 70% of childhood acute lymphoblastic leukemia (ALL) patients. The loss of ARTS is specific, as the related non-apoptotic protein H5, bearing 83% identity to ARTS, is unaffected. During remission, ARTS expression is detected again in almost all patients. Two leukemic cell lines, ALL-1 and HL-60 lacking ARTS, were resistant to apoptotic induction by ara-C. Transfection of ARTS into these cells restored their ability to undergo apoptosis in response to this chemotherapeutic agent. We found that methylation process contributes to the loss of ARTS expression. We conclude that the loss of ARTS may provide a selective advantage for cells to escape apoptosis thereby contributing to their transformation to malignant lymphoblasts. We therefore propose that ARTS can function as a tumor suppressor protein in childhood ALL.