Serum Deoxyribonuclease Research Articles

Serum DNase1, sTNFR1 and sTNFR2 as Risk Factors for Lupus Nephritis in Systemic Lupus Erythematosus Patients

BACKGROUND: Early detection and management of lupus nephritis (LN) in systemic lupus erythematosus (SLE) are essential to prevent irreversible kidney damage and improve patient outcomes; therefore, identifying reliable biomarkers to predict LN is paramount. However, there are still relatively few studies examining the potential biomarkers for LN in SLE patients. This study was conducted to investigate serum deoxyribonuclease I (DNase), soluble tumor necrosing factor 1 (sTNFR1) and soluble tumor necrosing factor 2 (sTNFR2) as a risk factor for LN in SLE patients.METHODS: A case-control study involving SLE patients aged 20-60 years was conducted. Blood was withdrawn from each subject for the measurement of serum level of DNase1, sTNFR1, and sTNFR2 that was performed using enzyme-linked immunoassay (ELISA) methods. Data was then analyzed using Chi-Square test and logistic regression tests.RESULTS: A total of 22 patients with LN and 22 without LN were included. The cut-off value for DNase1, sTNFR1, and sTNFR2 were 5.05 ng/mL, 6.52 ng/mL, and 7.02 ng/mL, respectively. The risk factors of LN in SLE patients were the low level of serum DNase1 (aOR=6.64; 95%CI: 1.25-35.29; p=0.026), low level of serum sTNFR1 (aOR=8.12; 95% CI: 1.56-42.10; p=0.013), and low level of serum sTNFR2 (aOR=5.57; 95%CI: 1.03-30.11; p=0.046).CONCLUSION: Serum DNase1 lower than 5.05 ng/mL, sTNFR1 lower than 6.52 ng/mL, and sTNFR2 lower than 7.02 ng/mL were risk factors for lupus nephritis in SLE patients. Hence, serum DNase1, sTNFR1 and sTNFR2 could be used as risk factors predictors for LN in SLE patients.KEYWORDS: DNase1, sTNFR1, sTNFR2, SLE, lupus nephritis

Blood neutrophil extracellular traps: a novel target for the assessment of mammary health in transition dairy cows

BackgroundMammary health is important for transition dairy cows and has been well recognized to exert decisive effects on animal welfare. However, the factors influencing mammary health are still unclear. Differential somatic cell count (DSCC) could reflect the mastitis risk since it is the percentage of neutrophils plus lymphocytes in total somatic cells and could be reflective of mammary health of dairy cows. This work aimed to investigate the assessment and prognosis of the health of transition cows based on blood neutrophil extracellular traps (NETs).ResultsEighty-four transition Holstein dairy cows were selected. The serum was sampled in all the animals at week 1 pre- and postpartum, and milk was sampled at week 1 postpartum. Based on the DSCC in milk at week 1, cows with lower (7.4% ± 4.07%, n = 15) and higher (83.3% ± 1.21%, n = 15) DSCCs were selected. High DSCC cows had higher levels of red blood cell counts (P < 0.05), hemoglobin (P = 0.07), and hematocrit (P = 0.05), higher concentrations of serum oxidative variables [(reactive oxygen species (P < 0.05), malondialdehyde (P < 0.05), protein carbonyl (P < 0.05), and 8-hydroxy-2-deoxyguanosine (P = 0.07)], higher levels of serum and milk NETs (P < 0.05) and blood-milk barrier indicators, including serum β-casein (P = 0.05) and milk immunoglobulin G2 (P = 0.09), than those of low DSCC cows. In addition, lower concentrations of serum nutrient metabolites (cholesterol and albumin) (P < 0.05) and a lower level of serum deoxyribonuclease I (P = 0.09) were observed in high DSCC cows than in low DSCC cows. Among the assessments performed using levels of the three prepartum serum parameters (NETs, deoxyribonuclease I and β-casein), the area under the curve (0.973) of NETs was the highest. In addition, the sensitivity (1.00) and specificity (0.93) were observed for the discrimination of these cows using NETs levels with a critical value of 32.2 ng/mL (P < 0.05).ConclusionsThe formation of NETs in blood in transition dairy cows may damage the integrity of the blood-milk barrier and thereby increase the risk for mastitis in postpartum cows.

Assessment of Deoxyribonuclease Activity Using DNA Molecules Immobilized Between Microelectrodes

Serum deoxyribonuclease I (DNase I) can serve as a functional biomarker for the therapeutic monitoring of acute myocardial infarction and other diseases. Here, we demonstrate that the electrical properties of DNA molecules can be exploited to monitor enzymatic activity. A label-free DNA biosensor for the detection of DNase I activity was devised based on electrochemical impedance spectroscopy (EIS). Multiple lambda phage DNA molecules were immobilized between two electrodes in a polydimethylsiloxane reservoir. An equivalent circuit estimated from the EIS measurement was used to calculate the impedance of DNA molecules between the electrodes. DNase detection was then achieved by measuring the increase in impedance, after DNA cleavage by DNase I. This was assessed by the impedance-increase ratio, defined as Rafter/Rbefore (where Rbefore and Rafter represent the resistance between the electrode-immobilized DNA molecules before and after DNase I treatment, respectively). After treatment with DNase I at a concentration 10−2 unit/μL, a reproducible impedance-increase ratio of approximately 3.3 times was obtained, with a standard deviation of less than 20%. When DNase solutions of various concentrations were introduced, we succeeded in obtaining a definite correlation between DNase concentration and impedance-increase rate, within the range of 10−4 unit/μL to 10−1 unit/μL.

Serum Deoxyribonuclease 1-like 3 is a potential biomarker for diagnosis of ankylosing spondylitis

BackgroundAnkylosing spondylitis (AS) is an autoimmune disease with high disability rate, and it is sometimes difficult to distinguish from generalized osteoarthritis (GOA). Deoxyribonuclease 1-like 3 (DNASE1L3) was associated with a variety of autoimmune diseases. However, the serum DNASE1L3 level in AS and GOA remain unreported. Herein, this study was designed to gauge serum DNASE1L3 level in patients with AS and GOA, and to discern the utility of serum DNASE1L3 as a biomarker for assessing the severity of patients with AS. MethodsThe study population consisted of 60 patients with AS, 60 patients with GOA and 60 control subjects. Serum DNASE1L3 levels were measured using enzyme-linked immunosorbent assay (ELISA) assay. Disease activity were assessed with Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) in AS patients. ResultsOur data showed that serum DNASE1L3 levels were significantly higher in patients with AS than that of the healthy controls and patients with GOA. Serum DNASE1L3 levels in patients with AS were positively correlated with BASDAI scores, C3 and C-reactive protein (CRP). Furthermore, serum DNASE1L3 showed higher discriminatory accuracy in the diagnosis of AS from GOA (AUC = 0.851, sensitivity = 78.33% and specificity = 81.67%). ConclusionsElevated Serum DNASE1L3 levels in patients with AS were significantly associated with the clinic features and disease activity. DNASE1L3 could be a serum biomarker with a positive diagnostic value in patients with AS, and which could be used as a differential diagnostic indicator for GOA and AS.

Serum deoxyribonuclease activity and anti-nuclear antibodies in ankylosing spondilitis during longterm infliximab therapy

Serum deoxyribonuclease activity and anti-nuclear antibodies in ankylosing spondilitis during longterm infliximab therapy

SAT0252 DNASE serum and polyclonal IGG activity in patients with axial and peripheral spondyloarthritides

BackgroundCatalytic deoxyribonuclease (DNAse) autoantibodies have been demonstrated in patients with autoimmune and infectious diseases, but conclusive data about DNAse activity of antibodies in patients with spondyloarthritides (SpA) are lacking. Recently...

Serum deoxyribonuclease I activity can be a useful diagnostic marker for the early diagnosis of unstable angina pectoris or non–ST-segment elevation myocardial infarction

Recently, serum deoxyribonuclease I (DNase I) activity has been highlighted as a potential diagnostic marker for transient myocardial ischemia. To evaluate whether serum DNase I activity can be a useful biomarker for diagnosing unstable angina pectoris (UAP) or non-ST-segment elevation myocardial infarction (NSTEMI), we investigated serial changes in DNase I levels after chest pain in UAP and NSTEMI (UAP/NSTEMI) patients. Thirty-three and ten patients classified into the UAP/NSTEMI and the chest pain syndrome (CPS) group, respectively, were enrolled. The serum DNase I activity levels within 3h after chest pain and the absolute median value of percentage differences in serum DNase I activity levels from admission to 3h after hospitalization in the UAP/NSTEMI patients was significantly higher than those in the CPS patients. We evaluated the patients to show positive results for DNase I activity if the serum levels or percentage differences exceeded the corresponding cut-off values. The sensitivity and specificity of DNase I within 6h after chest pain in the UAP/NSTEMI patients without elevated levels of cardiac troponin T and the MB isoenzyme of creatine kinase were 89% and 88%, respectively. Serum DNase I activity can be a useful marker for the early diagnosis of UAP/NSTEMI after the onset of chest pain, irrespective of the evidence of myocardial injury.

Development of a sensitive enzyme-linked immunosorbent assay for measurement of DNase I in human serum

Background Serum deoxyribonuclease I (DNase I) activity was reported to increase in the early phase after onset of acute myocardial infarction (AMI). Up to now, DNase I activity has been quantified by the single radial enzyme diffusion (SRED) method, which unfortunately requires a long incubation time. Therefore it is necessary to develop another assay suitable for measurement of serum DNase I concentrations in a clinical setting. Methods A sandwich ELISA was established for measurement of DNase I protein using a polyclonal antibody directed against DNase I protein and a biotinylated monoclonal for subsequent detection. Concentrations of serum DNase I protein were measured in healthy individuals and patients with AMI. Results This method was as precise as SRED, and took less time than SRED. A significant correlation was observed between DNase I concentration and enzyme activity ( r = 0.839; P < 0.001). The average of serum DNase I in AMI patients within 0–12 h of chest pain was significantly higher than that in healthy individuals ( P < 0.001), and decreased with time. Conclusions We have developed a sensitive ELISA capable of measuring DNase I protein concentrations. This method may be a useful alternative to SRED as an aid to diagnosis of AMI based on the serum DNase I level.

Serum deoxyribonuclease I can be used as a useful marker for diagnosis of death due to ischemic heart disease

We recently reported abrupt elevation of serum deoxyribonuclease I (DNase I) activity in the early stage of acute myocardial infarction (AMI). The aim of this study was to evaluate whether serum DNase I could be used as a marker for detection of myocardial ischemia that accompanies AMI. In consecutive patients with stable angina pectoris undergoing elective percutaneous coronary intervention (PCI) or the vasospastic angina pectoris (VSAP) provocation test, together with patients undergoing coronary angiography (CAG), serum samples were tested for DNase I activity. Serum DNase I activity was found to rise significantly within 3 h after PCI, and also after the provocation test in the VSAP-positive group. In all of the CAG and VSAP-negative patients, DNase I activity levels remained unchanged. Transient myocardial ischemia resulting from PCI or VSAP induces a significant elevation of serum DNase I activity, indicating that serum DNase I may be applicable as a novel and specific marker for detection of myocardial ischemia. Similarly, it is suggested that serum DNase I could be potentially useful as a biochemical marker for diagnosis of death due to ischemic heart disease.

Levels of serum deoxyribonuclease I activity on admission in patients with acute myocardial infarction can be useful in predicting left ventricular enlargement due to remodeling

Serum deoxyribonuclease I (DNase I) activity has recently been highlighted as a potential diagnostic marker for the early detection of an acute myocardial infarction (AMI). We evaluated whether the serum DNase I activity was associated with the parameters of the left ventricular (LV) remodeling after an AMI. We measured the serum DNase I activity in 45 patients with an AMI who were admitted to our hospital within approximately 4 h of the onset of their chest pain. We also evaluated the LV ejection fraction (LVEF), LV end-diastolic volume (LVEDV), and LV end-systolic volume (LVESV) of each patient by echocardiography at the time of admission and at 6 months after the onset of the AMI. The serum DNase I activity peaked at 3.5+/-2.0 h after the onset of the symptoms in the patients with an AMI, thereafter exhibiting a time-dependent decline within 12 h, and a return to the basal level within 24 h in almost all cases. Neither the LVEF, LVEDV, nor LVESV in each patient on admission exhibited a significant correlation to the peak levels of the serum DNase I activity. Although there was no correlation between the peak DNase I activity and LVEF at 6 months after the onset, a significant positive correlation of the peak DNase I activity with LVEDV and LVESV (r=0.48, p<0.001 and r=0.34, p=0.02, respectively) was found. Furthermore, the LVEDV at 6 months after the onset in the high DNase I activity group (> 17.9 U/L) were significantly higher than those in the low DNase I activity group (< or = 17.9 U/L) (118.0+/-28.2 ml vs 89.3+/-25.4 ml, p=0.026). The serum DNase I activity level may predict LV enlargement associated with remodeling after an AMI.

Murine serum deoxyribonuclease 1 (Dnase1) activity partly originates from the liver

Reduction of serum DNASE1 (DNase I) activity is supposed to aggravate anti-nuclear autoimmunity, i.e. Systemic Lupus Erythematosus (SLE) in man and mice. To evaluate the etiology of this reduction, more information is needed about the source(s) and regulation of serum DNASE1. In this work we used male C57BL/6 wild-type (WT) mice to verify that serum Dnase1 activity partly depends on hepatic Dnase1 gene expression. Thus serum and liver Dnase1 activity showed a parallel oscillatory course during 24h, which was accompanied by a phase-shifted fluctuation of the hepatic Dnase1 mRNA content. Performing native PAGE zymography (NPZ) we detected a presumably premature non-sialylated and a mature sialylated hepatic Dnase1 isoform, which both show a parallel circadian fluctuation, indicating continuous secretion of Dnase1. The sialylated form was also detectable in serum. By immunostaining the hepatocytes were identified as the source of hepatic Dnase1 gene expression. After 70% hepatectomy, the serum Dnase1 activity increased markedly due to the occurrence of ischemic hepatocellular necrosis in the vicinity of the surgical suture. Similarly, hepatocellular necrosis induced by injection of streptolysin-O (SLO) into the liver led to a rapid parallel increase of Dnase1 and of aspartate- and alanine aminotransferase (AST/ALT) in serum. Subsequent to hepatectomy, Dnase1 gene expression was up-regulated in the regenerating liver most likely leading to an enhanced serum Dnase1 level until complete regeneration. These data demonstrate that serum Dnase1 at least partly originates from the liver and hint to the possibility that natural as well as pathological hepatic conditions influence its activity.

Serum deoxyribonuclease I activity can be used as a novel marker of transient myocardial ischaemia: results in vasospastic angina pectoris induced by provocation test

Serum deoxyribonuclease I (DNase I) activity has recently been highlighted as a potential diagnostic marker for detection of acute myocardial infarction. To evaluate whether serum DNase I activity is useful for detection of myocardial ischaemia, we investigated alteration of its levels after onset of vasospastic angina pectoris (VSAP), resulting in transient myocardial ischaemia, induced by the intracoronary ergonovine provocation test. Twenty-nine consecutive patients with suspected VSAP were subjected to the test. Patients were categorized as VSAP-positive (n = 13) or -negative (n = 16) based on development of angina. Serum samples were examined for DNase I activity before, immediately after, and 3, 6, and 24 h after the provocation tests. The serum DNase I activity increased significantly from the baseline 3 h after the provocation test in 11 patients of the VSAP-positive group whose levels of troponin T were within the normal range. Median of the percentage differences from the baseline in serum DNase I activity 3 h after the test was 32.1% (25th and 75th percentile: 28.6 and 42.0%, respectively; P = 0.000012). In the VSAP-negative group, levels of DNase I activity remained unchanged at any point of time after the provocation test. Transient myocardial ischaemia resulting from VSAP induces a significant elevation of serum DNase I activity. Therefore, serum DNase I activity may be applicable as a useful marker for detecting transient myocardial ischaemia.

Hypoxia induces upregulation of the deoxyribonuclease I gene in the human pancreatic cancer cell line QGP-1

We have previously demonstrated that ischemia caused by acute myocardial infarction induces an abrupt increase of serum deoxyribonuclease I (DNase I) activity. In this study, we examined whether hypoxia can affect the levels of DNase I activity and/or its transcripts in vitro. We first exposed the human pancreatic cancer cell line QGP-1, which is the first documented DNase-I-producing cell line, to hypoxia (2% O 2), and found that this induced a significant increase in both the activity and transcripts of DNase I. This response was mediated by increased transcription only from exon 1a of the two alternative transcription-initiating exons utilized simultaneously in the human DNase I gene ( DNASE1); exposure of QGP-1 cells to hypoxia for 24 h resulted in a 15-fold increase of DNASE1 transcripts starting from exon 1a compared with the expression level under normoxic conditions. Promoter, electrophoretic mobility shift, and chromatin immunoprecipitation assays with QGP-1 cells exposed to hypoxia or normoxia showed that the region just upstream from exon 1a was involved in this response in a hypoxia-induced factor-1-independent, but at least in a Sp1 transcription factor-dependent manner possibly through enhanced binding of Sp1 protein to the promoter. These results indicate that DNASE1 expression is upregulated by hypoxia in the cells.

Association of Gln222Arg polymorphism in the deoxyribonuclease I (DNase I) gene with myocardial infarction in Japanese patients

We have recently reported that serum deoxyribonuclease I (DNase I) activity, which may be involved in apoptosis, increases abruptly in the early phase of acute myocardial infarction (MI) [Kawai Y, Yoshida M, Arakawa K, Kumamoto T, Morikawa N, Masamura K, Tada H, Ito S, Hoshizaki H, Oshima S, Taniguchi K, Terasawa H, Miyamori I, Kishi K, Yasuda T. Diagnostic use of serum deoxyribonuclease I activity as a novel early-phase marker in acute myocardial infarction. Circulation 2004;109:2398-2400]. Death of vascular smooth muscle cells, in part because of apoptosis, is postulated to heighten susceptibility to disruption of vulnerable plaque, resulting in onset of MI. The present study evaluated the possibility that Gln222Arg polymorphism of the DNase I gene may be one of the factors involved in predisposition to MI. We assessed 611 Japanese patients: 311 with MI and 300 with stable angina pectoris (AP). Three common phenotypes determined by two common codominant alleles, DNASE1*1 and *2, whose corresponding gene products exhibit different properties, were found in these patient groups. The prevalence of DNASE1*2 was significantly higher in patients with MI than in those with AP (0.543 vs. 0.428, P < 0.001), being confirmed by phenotyping of the second study population. Multiple logistic regression analysis showed that the odds ratio of DNASE1*2 was 1.51 [95% confidence interval (CI) 1.04-2.18]. The association of the DNASE1*2 allele with MI was statistically significant, being independent of other conventional risk factors. Our data demonstrate that Gln222Arg polymorphism in the DNase I gene is associated with MI in the Japanese patients.

Mirror, mirror on the wall: the quest for the earliest marker of myocardial ischaemiaThe opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.

This editorial refers to ‘Serum deoxyribonuclease I activity can be used as a sensitive marker for detection of transient myocardial ischaemia induced by percutaneous coronary intervention'† by K. Arakawa et al., on page 2375 In patients with acute ST-segment elevation myocardial infarction (STEMI), the diagnosis and immediate initiation of reperfusion therapy is based on the standard 12-lead ECG. Owing to the fact that cardiac markers appear in the blood a substantial time after the onset of symptoms, cardiac markers are neither helpful for early diagnosis of patients with STEMI nor should results be awaited before initiation of recanalization therapy. Unfortunately, at least 40% of all patients with confirmed acute myocardial infarction (AMI) show no diagnostic ECG changes on admission.1 In these patients with suspected acute coronary syndrome (ACS), cardiac troponins have become the biochemical gold standard for classification, risk stratification, and guidance of therapy.1 Cardiac troponins owe their exclusive superiority to their cardiospecificity, which indicates myocardial necrosis, and to their higher sensitivity compared with creatine kinase. However, obviously myocardial necrosis is a prerequisite for appearance of troponins in the blood, and the inflicting event needs to have occurred a few hours earlier.2 Novel cardiac markers ideally should improve these limitations by appearing earlier in the blood in case of an AMI, or by allowing identification of myocardial ischaemia in advance, or even in the absence … *Corresponding author. Tel: +49 6221 56 8670. E-mail address : hugo_katus{at}med.uni-heidelberg.de

Serum deoxyribonuclease I activity can be used as a sensitive marker for detection of transient myocardial ischaemia induced by percutaneous coronary intervention

Cardiac markers such as troponin T (c-TnT) have proven unsuitable for the detection of early and transient myocardial ischaemia. We recently reported that abrupt elevation of serum deoxyribonuclease I (DNase I) activity in the early stage of acute myocardial infarction could be used as a diagnostic marker. To evaluate whether serum DNase I could be used as a marker of early myocardial ischaemia, we investigated alterations in its levels after transient ischaemia induced during percutaneous coronary intervention (PCI). In 24 consecutive patients with stable angina undergoing elective PCI and 12 patients undergoing coronary angiography (CAG), serum samples were tested for DNase I, creatine kinase isoenzyme MB (CK-MB), and c-TnT before, soon after, and 3 and 12-24 h after completion of the procedures. Serum DNase I activity had risen significantly from baseline by 3 h after PCI in 21 of the 24 PCI patients. The mean per cent difference from baseline in serum DNase I activity 3 h after PCI was 35.9+/-37.5%. Even among the 16 PCI patients whose levels of CK-MB and c-TnT were within the normal range, 13 showed elevation of serum DNase I activity from baseline after PCI. In the CAG patient group, DNase I activity levels remained unchanged at all times after CAG. Elevation of serum DNase I activity can be used as a sensitive marker for detection of transient myocardial ischaemia.

Diagnostic use of serum deoxyribonuclease I activity as a novel early-phase marker in acute myocardial infarction.

The delayed release of serum cardiac markers such as creatine kinase isoenzyme MB and equivocal early electrocardiographic changes have hampered a diagnosis of acute myocardial infarction (AMI) in the early phase after its onset. Therefore, a reliable serum biochemical marker for the diagnosis of AMI in the very early phase is desirable. Serum samples were collected from the patients with AMI, unstable angina pectoris, stable angina pectoris, and other diseases. Levels of serum deoxyribonuclease I (DNase I) activity in the patients were determined. An abrupt elevation of serum DNase I activity was observed within approximately 3 hours of the onset of symptoms in patients with AMI, with significantly higher activity levels (21.7+/-5.10 U/L) in this group compared with the other groups with unstable angina pectoris (10.4+/-4.41 U/L), angina pectoris (10.8+/-3.70 U/L), and other diseases (9.22+/-4.16 U/L). Levels of the DNase I activity in serum then exhibited a marked time-dependent decline within 12 hours and had returned to basal levels within 24 hours. We suggest that serum DNase I activity could be used as a new diagnostic marker for the early detection of AMI.

A molecular analysis of the low serum deoxyribonuclease activity in lupus patients.

A molecular analysis of the low serum deoxyribonuclease activity in lupus patients.

Deoxyribonuclease activity in Echinococcus granulosus protoscoleces and hydatid fluid

Deoxyribonuclease activity was detected in E. granulosus protoscoleces from sheep hydatid cysts by electrophoresis in agarose gels of DNA fragments obtained after incubation of integral DNA with a protoscoleces preparation. Preliminary characterization showed that deoxyribonuclease activity was optimal at neutral-alkaline pH, magnesium ions were required, and it was able to digest different types of DNA, making random cuts. Electrophoresis in DNA-containing sodium dodecylsulfate (SDS)-polyacrylamide gels indicated a relative molecular mass, under non-reducing conditions, of 32 kDa. Deoxyribonuclease activity was also found in sheep hydatid fluid. It shared optimal pH, ionic and substrate requirements with the enzyme from protoscoleces but had a higher relative molecular mass (40 kDa), the same as that of normal sheep serum deoxyribonuclease.

Measurement of deoxyribonuclease I activity in human tissues and body fluids by a single radial enzyme-diffusion method

In the single radial enzyme-diffusion (SRED) method for assay of deoxyribonuclease I, a precisely measured volume of the enzyme solution is dispensed into a circular well in an agarose gel layer in which DNA and ethidium bromide are uniformly distributed. A circular dark zone is formed as the enzyme diffuses from the well radially into the gel and digests substrate DNA. The diameter of the dark circle of hydrolyzed DNA increases in size with time and correlates linearly with the amount of enzyme applied to the well. Thus, the SRED can be used for quantitation of deoxyribonuclease I with a limit of detection of 2 x 10(-6) unit. This corresponds to 1 pg of purified urine deoxyribonuclease I. We measured the deoxyribonuclease I activity of 17 different human tissues and body fluids from healthy donors. Urine samples showed the greatest activity, 6.0 +/- 2.2 kilo-units/g protein (mean +/- SD). Serum deoxyribonuclease I activity was 4.4 +/- 1.8 units/L.