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61.
Cusumano M Di Pietro ML Giannetto A Vainiglia PA 《Journal of inorganic biochemistry》2005,99(2):560-565
The non-covalent interaction of the complexes [Pt(bpy)(R,R'NCSNR',R')(2)]Cl(2) (bpy=2,2'-bipyridine; R=R'=R'=R'=H; R=Me, R'=R'=R'=H; R=n-Bu, R'=R'=R'=H; R=p-tolyl, R'=R'=R'=H; R=Et, R'=H, R'=Et, R'=H) with calf thymus DNA has been studied at pH 7 and 25 degrees C. The processes give rise to: (i) reversible bathochromic shifts and strong hypochromicity of the absorption bands of the complexes, (ii) induced circular dichroism and (iii) an increase both in the melting temperature and viscosity of the DNA comparable to that observed for other well known metallointercalators. The binding constants, K(B), have been determined spectrophotometrically using the McGhee von Hippel equation. Plot of logK(B) vs -log[Na(+)] for the complex with unsubstituted thiourea gives a straight line with a slope value close to that expected for a dicationic intercalator. The binding affinity of the various complexes for DNA is independent of the thiourea nature; this suggests that the intercalation occurs through stacking of the bpy moiety while the ancillary ligands lie outside the nucleobases far away from the sugar phosphate backbone. The data show also that the electronic effects of the ligand substituents are not transmitted to the intercalating unit. 相似文献
62.
Increased plasma levels of adrenomedullin, a vasoactive peptide, in patients with end-stage pulmonary disease 总被引:2,自引:0,他引:2
Vizza CD Letizia C Sciomer S Naeije R Della Rocca G Di Roma A Musarò S Quattrucci S Gaudio C Battagliese A Badagliacca R D'Erasmo E Fedele F 《Regulatory peptides》2005,124(1-3):187-193
AIM: To study adrenomedullin (AM) plasma levels in patients with severe lung disease and to analyze the relationship between AM and heart changes, hemodynamics and blood gases. METHODS: Case control study of 56 patients (36 men, 20 women) with severe lung disease and 9 control subjects (7 men, 2 women). Patients with end-stage pulmonary disease, including chronic obstructive pulmonary disease (COPD, n=11), cystic fibrosis (CF, 26), idiopatic pulmonary fibrosis (ILD, n=9), and idiopatic pulmonary arterial hypertension (PAH, n=10), who were evaluated for lung trasplantation between January 1997 and September 2000, and nine patients who underwent lung surgery for a solitary benign nodule. AM plasma levels in pulmonary artery (mixed venous blood, vein) and aorta or femoral artery (arterial, art), art and vein blood gases, pulmonary hemodynamics, systemic hemodynamics, two-dimensional transthoracic echocardiography and echo-Doppler study. RESULTS: Plasma AM (art and ven) levels were higher among patients' group compared to the controls (AMart p<0.02 and AMven p<0.04) for CF, ILD, PAH (AMart, pg ml(-1) Controls 13.7+/-3.6, COPD 22.8+/-6.2, CF 28.1+/-11.4, ILD 34.1+/-14.3, PAH 35.1+/-18.9; AMven, pg ml(-1) Controls 14.2+/-4.8, COPD 28.1+/-12.6, CF 31.7+/-14.1, ILD 38.7+/-16.5, PAH 40.1+/-4.4). We found with a trend towards higher concentration in ILD and PAH patients compared to COPD and CF but no statistical significant differences. Mixed-venous AM was higher than arterial AM in all groups resulting in AM uptake (AMPulmUp pg min(-1) Controls 4.8+/-22.6, COPD 21.1+/-44.9, CF 20.6+/-45.1, ILD 23.7+/-38.5, PAH 29.9+/-49.7). The univariate analysis showed a weak but significant correlation between AMart and mean systemic arterial pressure, heart rate, mean pulmonary arterial pressure and systemic vascular resistance. In the multivariate analysis, four variables emerged as independent factors of AMart including mean pulmonary arterial pressure, heart rate, mean systemic arterial pressure and left ventricular diastolic diameter (F=8.6, p<0.00001, r=0.60, r2=0.32). A similar weak correlation was apparent between AMven, systemic vascular resistance, and mean pulmonary arterial pressure. The results of multivariate analysis identify right atrial enlargement, mean right atrial pressure, heart rate and left ventricular dimensions as the only independent variables related to AMven (F=4.3, p<0.0004 r=0.56, r2=0.26). AM pulmonary uptake was significantly correlated with AMven (r=0.65), but not with hemodynamic, blood gas and echocardiographic variables. CONCLUSIONS: AM plasma levels are elevated in patients with severe lung disease in face of a preserved pulmonary uptake. These results suggest that the high AM plasma levels in patients with severe lung disease are not caused by a reduced pulmonary clearance, instead suggesting a systemic production. 相似文献
63.
Penolazzi L Bianchini E Lambertini E Baraldi PG Romagnoli R Piva R Gambari R 《Journal of biomedical science》2005,12(6):1013-1020
Summary The P2X7 nucleotide receptor is an ATP-gated ion channel that plays an important role in bone cell function. Here, we investigated
the effects of L-tyrosine derivatives 1–3 as potent P2X7 antagonists on human primary osteoclasts. We found that the level of expression of P2X7 receptor increased after treatment with the derivatives 1–3, together with the induction of high levels of apoptosis. This effect is associated with activation of caspase-3 and inhibition
of expression of IL-6. Interestingly, no pro-apoptotic effect of compounds 1–3 was found on human osteoblasts. Our results suggest that the development of specific P2X7 receptor antagonists may be considered a useful tool to modulate apoptosis of human osteoclasts. Since bone loss due to osteoclast-mediated
resorption represents one of the major unsolved problem in osteopenic disorders, the identification of molecules able to induce
apoptosis of osteoclasts is of great interest for the development of novel therapeutic strategies. 相似文献
64.
Pollegioni L Lorenzi S Rosini E Marcone GL Molla G Verga R Cabri W Pilone MS 《Protein science : a publication of the Protein Society》2005,14(12):3064-3076
Semisynthetic cephalosporins are synthesized from 7-amino cephalosporanic acid, which is produced by chemical deacylation or by a two-step enzymatic process of the natural antibiotic cephalosporin C. The known acylases take glutaryl-7-amino cephalosporanic acid as a primary substrate, and their specificity and activity are too low for cephalosporin C. Starting from a known glutaryl-7-amino cephalosporanic acid acylase as the protein scaffold, an acylase gene optimized for expression in Escherichia coli and for molecular biology manipulations was designed. Subsequently we used error-prone PCR mutagenesis, a molecular modeling approach combined with site-saturation mutagenesis, and site-directed mutagenesis to produce enzymes with a cephalosporin C/glutaryl-7-amino cephalosporanic acid catalytic efficiency that was increased up to 100-fold, and with a significant and higher maximal activity on cephalosporin C as compared to glutaryl-7-amino cephalosporanic acid (e.g., 3.8 vs. 2.7 U/mg protein, respectively, for the A215Y-H296S-H309S mutant). Our data in a bioreactor indicate an ~90% conversion of cephalosporin C to 7-amino-cephalosporanic acid in a single deacylation step. The evolved acylase variants we produced are enzymes with a new substrate specificity, not found in nature, and represent a hallmark for industrial production of 7-amino cephalosporanic acid. 相似文献
65.
2- and 8-alkynyl-9-ethyladenines: Synthesis and biological activity at human and rat adenosine receptors 总被引:1,自引:1,他引:0
Volpini R Costanzi S Lambertucci C Vittori S Martini C Trincavelli ML Klotz KN Cristalli G 《Purinergic signalling》2005,1(2):173-181
The synthesis of a series of 9-ethyladenine derivatives bearing alkynyl chains in 2- or 8-position was undertaken, based on the observation that replacement of the sugar moiety in adenosine derivatives with alkyl groups led to adenosine receptor antagonists. All the synthesized compounds were tested for their affinity at human and rat A1, A2A, and A3 adenosine receptors in binding assays; the activity at the human A2B receptor was determined in adenylyl cyclase experiments. Biological data showed that the 2-alkynyl derivatives possess good affinity and are slightly selective for the human A2A receptor. The same compounds tested on the rat A1 and A2A subtypes showed in general lower affinity for both receptors. On the other hand, the affinity of the 8-alkynyl derivatives at the human A1, A2A, and A2B receptors proved to be lower than that of the corresponding 2-alkynyl derivatives. On the contrary, the affinity of the same compounds for the human A3 receptor was improved, resulting in A3 selectivity. As in the case of the 2-alkynyl-substituted compounds, the 8-alkynyl derivatives showed decreased affinity for rat receptors. However, it is worthwhile to note that the 8-phenylethynyl-9-ethyladenine was the most active compound of the two series (Ki in the nanomolar range) at both the human and rat A3 subtype. Docking experiments of the 2- and 8-phenylethynyl-9-ethyladenines, at a rhodopsin-based homology model, gave a rational explanation of the preference of the human A3 receptor for the 8-substituted compound. 相似文献
66.
Denaturing high-performance liquid chromatography in the detection of ABCA1 gene mutations in familial HDL deficiency 总被引:1,自引:0,他引:1
Mutations in the ABCA1 gene are the cause of familial high density lipoprotein deficiency (FHD). Because these mutations are spread over the entire gene, their detection requires the sequencing of all 50 exons. The aim of this study was to validate denaturing high-performance liquid chromatography (DHPLC) in mutation detection as an alternative to systematic sequencing. Exons of the ABCA1 gene were amplified using primers employed for sequencing. Temperatures for DHPLC were deducted from a software and empirically defined for each amplicon. To assess DHPLC reliability, we tested 30 sequence variants found in FHD patients and controls. Combined DHPLC and sequencing was applied to the genotyping of new FHD patients. Most of the amplicons required from two to five temperature conditions to obtain partially denatured DNA over the entire amplicon length. Twenty-nine of the variants found by sequencing were detected by DHPLC (97% sensitivity). The detection of the last variant (in exon 40) required different primers and amplification conditions. DHPLC and sequencing analysis of new FHD patients revealed that all amplicons showing a heteroduplex DHPLC profile contained sequence variants. No variants were detected in amplicons with a homoduplex profile. DHPLC is a sensitive and reliable method for the detection of ABCA1 gene mutations. 相似文献
67.
Wolbachia pipientis is an intracellular endosymbiont producing reproductive alterations in its hosts. This bacterium have been reported in many arthropods and nematodes. By PCR amplification and sequencing of the 16S rDNA and ftsZ genes we have identified a Wolbachia strain in the newly described sand-flea, Tunga trimamillata. Prevalence of this endosymbiont in the 26 individuals screened is equal to 35%. Sympatric and allopatric specimens of the related species Tunga penetrans were also analysed, but in contrast to literature data, Wolbachia appears absent in the presently analysed 24 specimens. Field studies evidence a female-biased sex-ratio in T. trimamillata, suggesting that Wolbachia may cause sex-ratio distortion in this species. By means of BLAST search and phylogenetic analysis we found that the Wolbachia strain from T. trimamillata pertains to the arthropod-infecting Wolbachia; this strain is highly differentiated from the Wolbachia strain of T. penetrans described in literature. 相似文献
68.
Brandi L Marzi S Fabbretti A Fleischer C Hill WE Gualerzi CO Stephen Lodmell J 《Journal of molecular biology》2004,335(4):881-894
Bacterial translation initiation factor IF2 was localized on the ribosome by rRNA cleavage using free Cu(II):1,10-orthophenanthroline. The results indicated proximity of IF2 to helix 89, to the sarcin-ricin loop and to helices 43 and 44, which constitute the "L11/thiostrepton" stem-loops of 23S rRNA. These findings prompted an investigation of the L11 contribution to IF2 activity and a re-examination of the controversial issue of the effect on IF2 functions of thiostrepton, a peptide antibiotic known primarily as a powerful inhibitor of translocation. Ribosomes lacking L11 were found to have wild-type capacity to bind IF2 but a strongly reduced ability to elicit its GTPase activity. We found that thiostrepton caused a faster recycling of this factor on and off the 70S ribosomes and 50S subunits, which in turn resulted in an increased rate of the multiple turnover IF2-dependent GTPase. Although thiostrepton did not inhibit the P-site binding of fMet-tRNA, the A-site binding of the EF-Tu-GTP-Phe-tRNA or the activity of the ribosomal peptidyl transferase center (as measured by the formation of fMet-puromycin), it severely inhibited IF2-dependent initiation dipeptide formation. This inhibition can probably be traced back to a thiostrepton-induced distortion of the ribosomal-binding site of IF2, which leads to a non-productive interaction between the ribosome and the aminoacyl-tRNA substrates of the peptidyl transferase reaction. Overall, our data indicate that the translation initiation function of IF2 is as sensitive as the translocation function of EF-G to thiostrepton inhibition. 相似文献
69.
Pierfrancesco Biagini Claudio Biancalani Alessia Graziano Nicoletta Cesari Maria Paola Giovannoni Agostino Cilibrizzi Vittorio Dal Piaz Claudia Vergelli Letizia Crocetti Maurizio Delcanale Elisabetta Armani Andrea Rizzi Paola Puccini Paola Maria Gallo Daniele Spinabelli Paola Caruso 《Bioorganic & medicinal chemistry》2010,18(10):3506-3517
A series of pyrazoles and pyrazolo[3,4-d]pyridazinones were synthesized and evaluated for their PDE4 inhibitory activity. All the pyrazoles were found devoid of activity, whereas some of the novel pyrazolo[3,4-d]pyridazinones showed good activity as PDE4 inhibitors. The most potent compounds in this series showed an IC50 in the nanomolar range. The ability to inhibit TNF-α release in human PBMCs was determined for two representative compounds, finding values in the sub-micromolar range. SARs studies demonstrated that the best arranged groups around the heterocyclic core are 2-chloro-, 2-methyl- and 3-nitrophenyl at position 2, an ethyl ester at position 4 and a small alkyl group at position 6. Molecular modeling studies performed on a representative compound allowed to define its binding mode to the PDE4B isoform. 相似文献
70.
Fabrizio Maggi Daniele Focosi Melania Albani Letizia Lanini Maria Linda Vatteroni Mario Petrini Luca Ceccherini-Nelli Mauro Pistello Mauro Bendinelli 《Journal of virology》2010,84(13):6891-6893
Many aspects of the life cycle of torquetenoviruses (TTVs) are essentially unexplored. In particular, it is still a matter of speculation which cell type(s) replicates the viruses and maintains the generally high viral loads found in the blood of infected hosts. In this study, we sequentially measured the TTV loads in the plasma of four TTV-positive leukemia patients who were strongly myelosuppressed and then transplanted with haploidentical hematopoietic stem cells. The findings provide clear quantitative evidence for an extremely important role of hematopoietic cells in the maintenance of TTV viremia.Torquetenoviruses (TTVs) are small naked DNA viruses distinguished by a circular single-stranded DNA genome of only 3.8 kb, classified within the newly established family Anelloviridae (7). TTVs have been found in several animal species but do not appear capable of interspecies transmission. Due to their extensive genetic heterogeneity, human TTVs have been operatively subdivided into 5 genogroups and more than 40 genotypes (4). A remarkable feature of these TTVs is their presence in the plasma of nearly all people, regardless of geographical origin, age, and health status, raising many questions about their life cycle and possible pathological implications (2, 5). Plasma loads of TTVs vary extensively in both healthy and diseased individuals, usually ranging between 103 and 107 DNA copies per ml of plasma. However, some patients, including those with selected inflammatory or neoplastic disorders, transplant recipients, and human immunodeficiency virus-infected individuals, have a tendency to carry especially high burdens of TTVs (1, 6, 13, 22-24).By studying the dynamics of TTV viremia in individuals treated with alpha interferon for hepatitis C, the kinetics of virus replication was found to be quite high, with numbers of virions released into plasma and cleared from it daily on the same order of magnitude as other chronic plasma viremia-inducing viruses, such as the hepatitis B, hepatitis C, and human immunodeficiency viruses (16). Yet, due to considerable difficulties encountered in propagating TTVs in culture and in distinguishing the virions passively adsorbed onto the cells from the ones replicating inside cells, the tissue or tissues where these large numbers of TTV virions originate have yet to be established. Given that the amino acid compositions of the capsid protein believed to mediate viral adsorption to cells are quite diverse in different TTVs (2, 3, 9), it is also possible that permissive cells vary depending on the TTV considered. Relevant studies are limited. Short-term cultures of phytohemagglutinin-stimulated peripheral lymphocytes, but not resting lymphocytes were found to permit a measurable level of TTV replication (15, 18), indicative of at least a moderate degree of lymphotropism. On the other hand, the detection of replicative forms of TTV DNA in several tissues, including bone marrow, peripheral blood mononuclear cells, and liver, has suggested that TTVs might be polytropic in nature (2, 21).In 1999, Kanda et al. (10), researching TTV plasma of bone marrow transplant recipients with a qualitative PCR, noticed that 5 out of 6 previously positive patients tested negative in a sampling collected during the myelosuppressed period and became positive again after graft reconstitution, leading them to suggest that TTV might replicate mainly in hematopoietic cells. In the present study, we further developed this observation by measuring the TTV load in sequential plasma samples obtained from four TTV-positive leukemia patients undergoing hematopoietic stem cell transplantation. This procedure basically consists of a myeloablative conditioning regimen (chemotherapy plus radiotherapy) followed by reinfusion of a positively selected CD34+ stem cell population. The findings are of interest because, in addition to confirming the decrease of TTV load observed by Kanda et al., they shed light on the kinetics of the effect, thus providing a better insight onto the role of hematopoietic cells in the maintenance of TTV viremia and on the life cycle of TTV in general.Table Table11 summarizes the main characteristics of the patients selected for the study. They were treated with 10 Gy total-body irradiation (TBI) on day 0 and received 5 mg/kg/day thiotepa on days 2 and 3, 40 mg/m2/day fludarabine on days 3 to 7, and 1.2 mg/kg/day antithymocyte globulin on days 4 to 8, and then, on day 10, they received the indicated numbers of positively selected CD34+ hematopoietic stem cells from HLA-haploidentical donors. Peripheral blood samples were collected for TTV studies immediately before TBI and at selected times for the next 30 days, and plasma was stored in aliquots at −80°C until DNA extraction. The assay used for TTV quantification was a previously described highly sensitive TaqMan real-time PCR having the potential to detect and quantitate all hitherto recognized genetic forms of the virus (15, 16). All samples from each patient were assayed in a single run and in triplicate, and at least two independent DNA extractions for each sample were examined. The DNA extracts obtained at time zero were also typed with a previously described panel of five distinct PCR assays (12), each specific for one of the genogroups into which TTVs are subdivided. At the start of the study, the patients had viral loads ranging from 4.7 to 6.8 log copies per ml of plasma and harbored between 1 and 3 TTV genogroups (Table (Table1).1). In particular, all carried genogroup 1, which is highly represented in our area (12), and two carried one or two further genogroups. Consistent with previous findings (12), the patient who harbored three genogroups was the one with the highest viral load. As shown by Fig. Fig.1,1, in all four patients, TBI was followed by a steady decline of TTV viremia that continued for at least 22 days and progressively brought the virus to levels very close to the detection limit of the detection/quantitation method used, corresponding to values ranging between 0.003 (patient 3) and 0.00009 (patient 1) of the loads present prior to TBI. However, in no instance did the viral loads go below the limit of sensitivity of the assay (2 × 102 TTV DNA copies per ml of plasma). Although the size of the study does not permit firm conclusions on this aspect, it is noteworthy that the extent of decline was unrelated to the type and number of infecting TTV genogroup(s) originally present in the patients.Open in a separate windowFIG. 1.Plasma TTV loads and WBC counts in the peripheral blood of the 4 patients (Pt. 1 to 4) enrolled in the study. The arrow indicates the day the patients were infused with CD34+ hematopoietic stem cells from HLA-haploidentical donors. The horizontal broken line represents the lower limit of sensitivity of the TTV detection method used.
Open in a separate windowaT-ALL, T-cell acute lymphoblastic leukemia; B-ALL, B-cell acute lymphoblastic leukemia; AML, acute myeloid leukemia.bThe day post-TBI when TTV loads and genogroups were determined is shown in parentheses.cND, not determined.The viral loads observed during the phase of maximum decline (days 0 to 12) were then exploited to investigate the dynamics of TTV infection in the patients by using the mathematical model originally developed by Neumann et al. (20). The results of this analysis are shown in Table Table2.2. The mean clearance rate of circulating TTVs was 3.8 days−1. The half-life of plasma TTVs ranged between 3.6 and 4.8 h, with a mean of 4.3 h, which is a little shorter than previously calculated in patients treated with alpha interferon (16), possibly due to the fact that TBI may have led to a more complete block of viral replication. Overall, however, these values coupled with the calculated numbers of virions produced per day (Table (Table2)2) are a further demonstration that TTV infection is highly dynamic.
Open in a separate windowaCalculated by the equation ln (2)/c.bDaily production of plasma virions was calculated from c multiplied by the pre-TBI viremia load value and by extracellular body fluid volume, which was arbitrarily set at 3.0 × 103 ml.One patient died of multiorgan failure a few h after the 30-day sampling point without noticeable changes in either TTV viremia and white blood cell (WBC) counts. The other patients, starting from day 26, showed a generally moderate but consistent increase of TTV viremia, so that by the end of the 30-day observation period their viral loads were still somewhat to considerably lower than at baseline (Fig. (Fig.1).1). Interestingly, the increase paralleled the reappearance of WBCs in peripheral blood, a clear indicator of substantial engraftment. For two patients, we could also examine plasma samples collected at days 50, 80, and 110. As shown by the inserts in Fig. Fig.1,1, at these times both patients exhibited plasma TTV loads higher than at baseline, indicating that TTV shedding into plasma had resumed and was as abundant as or even more abundant than that at the start of the study. Interestingly, the spectrum of TTV genogroups detected in plasma at this time differed substantially from pre-TBI (Table (Table1),1), indicating that the patients were now replicating newly acquired TTVs, most likely transmitted by the graft or blood component transfusions required to sustain the procedure.Collectively, these findings provide solid quantitative evidence that hematopoietic stem cells represent by far the most important, if not the only source of the generally high TTV burdens found in the blood of infected individuals. The alternative explanation that hematopoietic cells or cytokines produced by them might stimulate other cells to replicate TTV seems less likely. Not only did plasma TTV loads fall dramatically during the myelosuppressed period, but also graft reconstitution was accompanied by a parallel return to high TTV loads. That TTVs have a preference for a highly cycling cell compartment is consistent with the well-established notion that single-stranded DNA viruses, including parvoviruses and circoviruses, have a marked preference for or replicate exclusively in DNA-synthesizing cells (14). The minimal levels of viremia that persisted during myelosuppression might suggest that some TTV replication takes place as well outside the hematopoietic compartment. However, since posttransplant the viral genogroups harbored by the patients were at least partly different from the ones harbored pretransplant, it is also possible that such low viral loads were generated by the hematopoietic cells infused into the patients.The viruses that lack an external lipid envelope are usually cytolytic for the cells in which they replicate. Future studies should therefore focus on clarifying which specific cell type or types within the hematopoietic cell compartment support TTV replication. A preferential replication within the lymphoid cell lineage might explain some of the immunomodulating properties attributed to the TTVs (6, 14, 17), while a preference for the erythroid lineage might explain the cases of aplastic anemia that have been associated with TTV infection (8, 11, 19). On the other hand, the circumstance that the great majority of TTV infections do not emerge clinically is most likely explained by the large regenerative potential of the hematopoietic compartment. 相似文献
TABLE 1.
Relevant parameters of the patients enrolledPatient | Age in yr (sex) | Clinical diagnosisa | No. of CD34 cells grafted (106 cells/kg) | Survival (days) | TTV in plasma | |||
---|---|---|---|---|---|---|---|---|
Pre-TBI | Post-TBI | |||||||
No. of copies/ml | Genogroup(s) | No. of copies/mlb | Genogroup(s) | |||||
1 | 54 (male) | T-ALL | 23.60 | 30 | 6.8 | 1, 3, 5 | NDc | ND |
2 | 47 (female) | ALL | 9.41 | 174 | 4.7 | 1, 4 | 5.4 (day 80) | 1, 3, 4, 5 |
3 | 41 (female) | B-ALL | 11.70 | 111 | 5.3 | 1 | 4.2 (day 30) | 3 |
4 | 58 (female) | AML | 5.90 | 267 | 5.0 | 1 | 7.0 (day 110) | 1, 3, 4, 5 |
TABLE 2.
TTV dynamics in the patients enrolledPatient | Viral parameter | ||
---|---|---|---|
Clearance rate (c [days−1]) | Virion half-life (days)a | Minimal input and clearance of plasma virions/dayb | |
1 | 3.8 | 0.18 | 7.8 × 1010 |
2 | 4.5 | 0.15 | 6.7 × 109 |
3 | 3.7 | 0.19 | 2.1 × 109 |
4 | 3.5 | 0.20 | 9.6 × 108 |
Mean ± SE | 3.8 ± 0.2 | 0.18 ± 0.01 | 2.0 × 1010 ± 1.0 × 1010 |