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P Kozlowski

Publications and source records attributed to P Kozlowski.

At least 19 recordsLinked to original sources
PubMed2006

Additional performance of nasal bone in first trimester screening.

OBJECTIVE: To evaluate and compare the screening performance for fetal trisomy 21 in the first trimester of pregnancy either with or without inclusion of fetal nasal bone using two separate risk-algorithms of the Fetal Medicine Foundation London (FMF). METHODS: This study included 3174 patients self-referred to our tertiary level prenatal centre for first trimester screening at 11-14 weeks of gestation between December 1, 2002 and November 30, 2004. Fetal risk for trisomy 21 was calculated using either the old FMF-algorithm including maternal age, nuchal translucency (NT), free ss-human chorionic gonadotropin (hCG), pregnancy-associated plasma protein-A (PAPP-A) or the new FMF-algorithm using additionally the presence or absence of fetal nasal bone (NB). All ultrasonographers were certified for measurement of nuchal translucency and nasal bone by the Fetal Medicine Foundation Germany. The detection rate for a fixed risk cut-off (1:300) and a fixed false-positive rate (5 %) was calculated for ultrasound (single NT or NT and NB), serum biochemistry, maternal age and the combination of these components. RESULTS: Pregnancy outcome was obtained in 2973 (93.6 %) cases. Nasal bone was absent in 5 of 18 (27.8 %) cases with fetal trisomy 21 and in 2 of 2961 (0.1 %) normal cases. The estimated risks for trisomy 21 based on maternal age, fetal ultrasound and maternal serum free ss-hCG and PAPP-A was 1 in 300 or greater in (old algorithm without NB/new algorithm including NB) 5.5 % (179 of 2961) and 2.8 % (97 of 2961) normal pregnancies and in 94.4 % (17 of 18) and 77.8 % (14 of 18) of those with trisomy 21. For a fixed false-positive rate of 5 % the respective detection rates of screening for fetal Down's syndrome by maternal age and serum free ss-hCG and PAAP-A, maternal age and fetal ultrasound and by maternal age, fetal ultrasound and maternal serum biochemistry were (old algorithm without NB/new algorithm including NB) 72.2 %/66.7 %, 83.3 %/77.8 % and 88.9 %/83.3 %, respectively. CONCLUSION: Our data show no additional performance of including presence or absence of fetal nasal bone in calculation of risk for fetal Down's syndrome between 11 and 14 weeks of gestation. Individual risk-orientated two-stage screening could be an alternative approach for integration of additional ultrasound markers in first trimester screening.

Algorithms↗
PubMed2006

Qualitative and quantitative effects of APOE genetic variation on plasma C-reactive protein, LDL-cholesterol, and apoE protein.

A genetic link between lipid metabolism and inflammation has been suggested by the association between variation in the APOE gene and plasma C-reactive protein (CRP). This association was confirmed among Caucasians and extended to an African-American population, and the well-known associations of APOE variation with LDL-C and apoE protein were also observed. While eight common variants in APOE were examined, the association with CRP involved primarily the two nonsynonymous SNPs that define the major epsilon2, epsilon3, and epsilon4 alleles. In particular, the strongest link involved lower CRP levels among carriers of the APOE epsilon4 allele that also contributes to the risk of cardiovascular and Alzheimer's diseases as well as to higher lipid levels. A lesser effect was characterized by lower CRP levels among carriers of a subtype of the epsilon3 allele. The magnitude of the association with plasma CRP was at least as great as the effect of variation in the CRP gene itself. Quantitative analysis suggested that the effect on CRP is more likely a consequence of intrinsic functional differences among the E2, E3, and E4 apoE proteins than different levels of apoE protein or LDL-C in the plasma.

Alzheimer Disease↗
PubMed2006

Influence of genetic variation in the C-reactive protein gene on the inflammatory response during and after acute coronary ischemia.

The aim of this research was to assess whether common genetic variants within the C-reactive protein gene (CRP) are related to the degree of acute rise in plasma C-reactive protein (CRP) levels following an acute coronary syndrome (ACS). While polymorphisms within CRP are associated with basal CRP levels in healthy men and women, less is known about the relationship of such genetic variants and the degree of CRP rise during and after acute ischemia. Plasma CRP is associated with increased rates of recurrent coronary events. We evaluated seven common genetic variants within CRP and assessed their relationship to the degree of rise in CRP levels immediately following an acute coronary syndrome in 1827 European American patients. Variants in the putative promoter region, -757T > C and -286C > T > A, were associated with the highest CRP elevations after ACS. Patients with two copies of the A allele of SNP -286C > T > A had median CRP values of 76.6 mg/L, compared to 11.1 mg/L in patients with no copies of the rare variant (p-value <0.0001), post ACS. The lowest CRP values were found for patients with minor alleles of the exonic 1059G > C and the 3'untranslated region 1846G > A SNPs. For example, patients homozygous for the minor allele of 1059G > C had 71% lower median CRP values than those homozygous for the major allele [3.5 vs 12.0 mg/L, p < 0.0001]. These trends persisted in the chronic stable phase after ischemia had resolved, and after adjustment for infarct size by peak creatinine kinase levels and clinical status by Killip class. Assessment of CRP genetic variants identified patients with higher and lower CRP elevation after acute coronary syndrome.

Acute Disease↗
PubMed2006

Quantitative fluorescent polymerase chain reaction versus cytogenetics: risk-related indication and clinical implication of nondetected chromosomal disorders.

BACKGROUND: The rapid detection of aneuploidies by quantitative fluorescent polymerase chain reaction (QF-PCR) allows reliable prenatal diagnosis of trisomies 21, 18, and 13. Discussion has been raised as to whether single QF-PCR could be an alternative to traditional cytogenetic karyotyping for certain referral categories. OBJECTIVE: To evaluate an indication-based classification of cases at risk of missing clinically relevant chromosomal disorders by QF-PCR. METHODS: From October 1999 to November 2003, 4,682 of 14,123 patients referred for amniocentesis decided to have QF-PCR as a rapid adjunct to conventional cytogenetic evaluation. Patients were classified according to the risk of missing chromosomal abnormalities by QF-PCR based on anamnestic risk and ultrasound prior to amniocentesis. The results in these two defined categories were compared in relation to the clinical significance of cytogenetic results. RESULTS: QF-PCR and conventional cytogenetic analysis had concordant results in 4,617 of 4,682 (98.6%) cases. Thirty-six of 110 (32.2%) clinically significant chromosomal abnormalities were missed by QF-PCR. Patients classified not to be at risk of missing chromosomal abnormalities using QF-PCR had a residual risk of 1/166 (0.6%) for chromosomal distortions of clinical significance. CONCLUSION: Classification by anamnestic and sonographic data does not specifically identify patients at risk of structural abnormalities. Clinical relevance of the nondetected anomalies essentially justifies traditional karyotyping regardless of risk classification.

Amniocentesis↗
PubMed2005

Association of common CRP gene variants with CRP levels and cardiovascular events.

C-reactive protein (CRP) is a well-documented marker of atherosclerotic cardiovascular disease risk. We resequenced CRP to identify a comprehensive set of common SNP variants, then studied and replicated their association with baseline CRP level among apparently healthy subjects in the Women's Health Study (WHS; n = 717), Pravastatin Inflammation/CRP Evaluation trial (PRINCE; n = 1,110) and Physicians' Health Study (PHS; n = 509) cohorts. The minor alleles of four SNPs were consistently associated in all three cohorts with higher CRP, while the minor alleles of two SNPs were associated with lower CRP (p < 0.05 for each). Single marker and haplotype analysis in all three cohorts were consistent with functional roles for the 5'-flanking triallelic SNP -286C>T>A and the 3'-UTR SNP 1846G>A. None of the SNPs associated with higher CRP were associated with risk of incident myocardial infarction (MI) or ischemic stroke in a prospective, nested case-control study design from the PHS cohort (610 case-control pairs). One SNP, -717A>G, was unrelated to CRP levels but associated with decreased risk of MI (p = 0.001). Taken together, these data imply significant interactions between both genetic and environmental contributions to the increased CRP levels that predict a greater risk of future atherothrombotic events in epidemiological studies.

Atherosclerosis↗
PubMed2004

Tissue oxygen tension measurements in the Shionogi model of prostate cancer using 19F MRS and MRI.

OBJECTIVES: To investigate changes in tumour tissue oxygenation throughout the tumour growth-regression-relapse cycle in an androgen-dependent animal tumour model. MATERIALS AND METHODS: 19F T1 relaxometry of Perfluoro-15-Crown-5-Ether was used to measure in vivo partial oxygen pressure (pO2) of Shionogi tumours on a 2.35-T MR scanner. Perfluoro-15-Crown-5-Ether was administered as an emulsion injected intravenously or as a neat compound injected directly into the tumour. Non-localized, tumour 19F T1 measurements, made at multiple time points throughout the tumour cycle, were translated into pO2 levels. RESULTS: No correlation between tumour size and pO2 values was found. Values of pO2 for growing tumours (50 +/- 30 torr) were significantly lower than for regressing and relapsing tumours after 9 days post-castration (70 +/- 10 torr, p<0.05). Maximum pO2 values (90 +/- 30 torr) were reached between fifth and eighth day post-castration, when tumour pO2 was significantly higher than both pre-castration (p<0.001) and after 9 days post-castration (p<0.05). CONCLUSION: We demonstrate that longitudinal pO2 measurements in vivo are feasible. Values of pO2 for growing androgen-dependent tumours were significantly lower than for regressing and relapsing androgen-independent tumours. These results have potential clinical importance in optimizing the timing of chemotherapy and/or radiotherapy of hormone dependent tumours.

Algorithms↗
PubMed2004

Molecular-cytogenetic characterization of the origin and the presence of pericentromeric euchromatin on minute supernumerary marker chromosomes (SMCs).

Small supernumerary marker chromosomes (SMCs) in human can be defined as additional centric chromosome fragments smaller than chromosome 20. For most small or minute SMCs a correlation with clinical symptoms is lacking, mostly due to problems in visualizing their euchromatic content. Recently we described two new molecular cytogenetic approaches for the comprehensive characterization of small SMCs, excluding those few cases with neo-centromeres. Minute SMCs, consisting preferentially of alpha-satellite DNA, are characterizable in one step by the centromere-specific multicolor FISH (cenM-FISH) approach. For further characterization of minute SMCs and eventually present euchromatic content, the recently developed centromere-near-specific multicolor FISH (subcenM-FISH) technique can be applied. These two approaches are highly informative and easy to perform, as demonstrated in the present report on the example of a prenatal case with a minute SMC derived from chromosome 3 cytogenetically described as min(3)(:p12.1 --> q11.2:).

Centromere↗
PubMed2004

mBAND: a high resolution multicolor banding technique for the detection of complex intrachromosomal aberrations.

Precise breakpoint definition of chromosomal rearrangements using conventional banding techniques often fails, especially when more than two breakpoints are involved. The classic banding procedure results in a pattern of alternating light and dark bands. Hence, in banded chromosomes a specific chromosomal band is rather identified by the surrounding banding pattern than by its own specific morphology. In chromosomal rearrangements the original pattern is altered and therefore the unequivocal determination of breakpoints is not obvious. The multicolor banding technique (mBAND, see Chudoba et al., 1999) is able to identify breakpoints unambiguously, even in highly complex chromosomal aberrations. The mBAND technique is presented and illustrated in a case of intrachromosomal rearrangement with seven breakpoints all having occurred on one chromosome 16, emphasizing the unique analyzing power of mBAND as compared to conventional banding techniques.

Chromosome Aberrations↗
PubMed2002

Going malignant: the hypoxia-cancer connection in the prostate.

The metabolic organization of both normal and malignant prostate cellular phenotypes involves some unusual and surprising features. In particular, both conditions exhibit ratios of NADH/NAD+ and NADPH/NADP+ characteristic of high oxidative states despite a chronic shortage of O2 in both conditions. In this paper, we observe that, in prostate cancer cells, the oxidizing power of the fatty acid synthesis (FAS) pathway is so large that redox is stabilized more favorably (more oxidized) than in normal prostate cells. This FAS-facilitated redox improvement occurs despite the fact that malignant cells are more O2 limited and therefore express more hypoxia inducible factor 1 (HIF1) and express hypoxia-regulated genes more robustly. This unusual metabolic situation clearly separates direct regulatory effects of redox balance from secondary effects of hypoxia per se. The physiological significance of the FAS pathway is thus the harnessing of its oxidizing power for improving redox balance despite conditions of more extreme hypoxia. Similar hypoxia defense strategies are found in animal species that are unusually tolerant to oxygen lack. Our hypothesis is that the metabolic organization in the "low zinc, low citrate" phenotype reflects an hypoxia-defense adaptation geared toward redox balance, with prostate cancer cells being relatively more oxidized, even if more hypoxic, than normal prostate cells. Recognition and understanding of these redox balancing and hypoxia defense functions may lead to new intervention strategies by developing new intracellular targets for prostate cancer therapy.

Humans↗
PubMed2002

Increased c-Fos protein in the brains of scrapie-infected SAMP8, SAMR1, AKR and C57BL mice.

Scrapie is a neurodegenerative disease that occurs naturally in sheep and goats. The histopathological changes include vacuolation, neuronal apoptosis and astrocytosis. The mechanisms involved in neuronal apoptosis are still unknown. Recently, we observed that activated p38 immunohistostaining was increased in scrapie-infected mice. In many neurodegenerative diseases, activation of the p38 pathway and of the immediate-early gene termed c-Fos appears to be required for the initiation of apoptosis. There are similarities in histopathological changes seen in scrapie-infected mice and in an uninfected senescence-accelerated mouse strain (SAMP8). This led us to investigate c-Fos protein levels in the brains of both uninfected and scrapie-infected SAMP8, SAMR1, AKR and C57BL mice using immunohistochemical methods. The SAMR1 strain served as a control in that it is a mouse strain that does not show accelerated ageing, but has a background that is similar to the SAMP8 strain. AKR was used because it is one of the progenitor strains of both SAM strains and, finally, C57BL is a completely unrelated strain. The results showed a low basal c-Fos expression in controls and a marked increase in c-Fos staining in scrapie-infected mice. In scrapie-positive mice, c-Fos immunoreactivity was observed in neurones in the cortex, hippocampus, thalamus, hypothalamus, medulla, midbrain, brainstem, paraterminal body, internal capsule and cerebellar Purkinje cells. Immunoreactivity of c-Fos was also observed in astrocytes in many brain areas of scrapie-infected mice, particularly in the hippocampus and cortex. Our results show that normal mouse brain (NMB)-injected AKR and SAMP8 mice had more c-Fos production than NMB-injected SAMR1 or C57BL mice; scrapie-infection induces significant increases in c-Fos immunoreactivity in all four mouse strains. Our study suggests that the increase in c-Fos levels may play a role in the neuronal apoptosis observed in scrapie-infected mice.

Aging↗
PubMed2002

[Criteria of dignity in ultrasound mammography using a 10-MHz-transducer, also with regard to tumor size].

AIM: Ongoing technical progress has increased the accuracy of imaging in ultrasound mammography. Using a 10-MHz-transducer, eight different criteria of dignity were evaluated for validity, also with regard to the size of a tumor. MATERIALS AND METHODS: Over a period of three years, 446 breast tumors were ultrasonographically examined by two experienced medical doctors. The study comprised only suspicious lesions detected by mammography and/or manual palpation. Diagnostic validity was quantified by means of sensitivity, specificity, positive and negative predictive value, as well as the ODDS-ratio. RESULTS: Ultrasound mammography demonstrated a sensitivity of 94.0 %, specificity of 91.4 %, positive predictive value of 95.9 %, and a negative predictive value of 99.1 %. Eight different sonographic criteria were validated separately. The most important signs of malignancy were (in descending order): a highly echogenic halo, spikes, jagged contour, posterior acoustic shadowing, and discontinuity of tissue structure. Features of benign disease were: smooth edge, posterior acoustic enhancement, displacement margin, bilateral acoustic shadowing and continuity of tissue structure. Furthermore, it appeared that the size of a tumor only had consequences on posterior shadowing (p = 0.017). All other features did not show significant variation in relation to tumor size. CONCLUSION: We were able to prove that ultrasound mammography is an excellent medium for the differentiation of benign and malignant breast lesions, when precise indication criteria were adhered to, even in cases of small tumor size.

Adolescent↗
PubMed2001

Combined SSCP/duplex analysis by capillary electrophoresis for more efficient mutation detection.

SSCP and heteroduplex analysis (HA) continue to be the most popular methods of mutation detection due to their simplicity, high sensitivity and low cost. The advantages of these methods are most clearly visible when large genes, such as BRCA1 and BRCA2, are scanned for scattered unknown mutations and/or when a large number of DNA samples is screened for specific mutations. Here we describe a novel combined SSCP/duplex analysis adapted to the modern capillary electrophoresis (CE) system, which takes advantage of multicolor labeling of DNA fragments and laser-induced fluorescence detection. In developing this method, we first established the optimum conditions for homoduplex and heteroduplex analysis by CE. These were determined based on comprehensive analysis of representative Tamra-500 markers and BRCA1 fragments at different concentrations of sieving polymer and temperatures in the presence or absence of glycerol. The intrinsic features of DNA duplex structures are discussed in detail to explain differences in the migration rates between various types of duplexes. When combined SSCP/duplex analysis was carried out in single conditions, those found to be optimal for analysis of duplexes, all 31 BRCA1 and BRCA2 mutations, polymorphisms and variants tested were detected. It is worth noting that the panel of analyzed sequence variants was enriched in base substitutions, which are usually more difficult to detect. The sensitivity of mutation detection in the SSCP portion alone was 90%, and that in the duplex portion was 81% in the single conditions of electrophoresis. As is also shown here, the proposed combined SSCP/duplex analysis by CE has the potential of being applied to the analysis of pooled genomic DNA samples, and to multiplex analysis of amplicons from different gene fragments. These modifications may further reduce the costs of analysis, making the method attractive for large scale application in SNP scanning and screening.

BRCA1 Protein↗
PubMed2001

Optimal colored perceptrons.

Ashkin-Teller type perceptron models are introduced. Their maximal capacity per number of couplings is calculated within a first-step replica-symmetry-breaking Gardner approach. The results are compared with extensive numerical simulations using several algorithms.

Algorithms↗
PubMed2001

Protein-tyrosine kinase Pyk2 mediates endothelin-induced p38 MAPK activation in glomerular mesangial cells.

Endothelin-1 (ET-1), a member of a family of 21 amino acid peptides possessing vasoconstrictor properties, is known to stimulate mesangial cell proliferation. In this study, ET-1 (100 nm) induced a rapid activation of p21(ras) in human glomerular mesangial cells (HMC). Inhibition of Src family tyrosine kinase activation with [4-Amino-5-(4-methylphenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine] or chelation of intracellular free calcium with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester significantly decreased ET-1dependent p21(ras) activation and suggested the involvement of the cytoplasmic proline-rich tyrosine kinase Pyk2. We have observed that Pyk2 was expressed in HMC and was tyrosine-phosphorylated within 5 min of ET-1 treatment. ET-1-induced activation of Pyk2 was further confirmed using phospho-specific anti-Pyk2 antibodies. Surprisingly, Src kinase activity was required upstream of ET-1-induced autophosphorylation of Pyk2. To determine whether Pyk2 autophosphorylation mediated ET-1-dependent p21(ras) activation, adenovirus-mediated transfer was employed to express a dominant-negative form of Pyk2 (CRNK). CRNK expression inhibited ET-1-induced endogenous Pyk2 autophosphorylation, but did not abolish ET-1-mediated increases in GTP-bound p21(ras) levels. ET-1-induced activation of the p38 MAPK (but not ERK) pathway was inhibited in HMC and in rat glomerular mesangial cells expressing the dominant-negative form of Pyk2. These findings suggest that the engagement of Pyk2 is important for ET-1-mediated p38 MAPK activation and hence the biological effect of this peptide in mesangial cells.

Adenoviridae↗
PubMed2001

Long-term deficits following cerebral hypoxia-ischemia in four-week-old rats: correspondence between behavioral, histological, and magnetic resonance imaging assessments.

We examined whether following a hypoxic-ischemic insult in young animals there are long-lasting functional deficits that correlate either to histological tissue damage or to potential compensatory plasticity changes. Four-week-old rats were subjected to an episode of cerebral hypoxia-ischemia (right carotid artery occlusion + 30 min of hypoxia) or a sham operation. In hypoxic-ischemic animals there were gross neurological deficits 1, 24, and 48 h postinsult with recovery by 1 week. Behavioral deficits were observed in both the acquisition and the performance of a response duration differentiation test and a fine motor control test (staircase test) 3 months after the hypoxia-ischemia. Functional magnetic resonance imaging studies demonstrated less activation in the sensory-motor cortex of hypoxic-ischemic animals in response to left vs right forepaw stimulation 4 months postinsult. Histological assessment delineated striatal, cortical, and hippocampal damage in the hypoxic-ischemic hemisphere and a reduction in cortical thickness, bilaterally. GFAP immunoreactivity was increased in injured striatum and cortex. Neurofilament heavy chain (NF200) immunoreactivity was normally most intense in white matter and decreased in areas of ipsilateral cortical damage. Synaptophysin immunoreactivity was reduced around areas of infarction and somewhat increased in adjacent undamaged striatum and in layer IV of parietal cortex. The histological damage or chronic degenerative changes could account for much of the variance in functional outcome detected with sensitive behavioral tests so that overall the compensatory or plasticity changes evident within the juvenile brain are rather modest.

Age Factors↗
PubMed2001

Effect of a single embryonic exposure to alcohol on glucose transporter (GLUT-1) distribution in brain vessels of aged mouse.

Distribution of glucose transporter (GLUT-1) in brain microvascular endothelium, representing the anatomic site of the blood-brain barrier (BBB), was studied with electron microscopy in 24-month-old mice, which had been exposed prenatally (on 9th day of gestation) to a single teratogenic dose of ethanol. Offspring of mice that had received an equivalent volume of isocaloric dextrose served as controls. Sections of brain samples embedded at low temperature in hydrophilic resin Lowicryl K4M were exposed to anti-GLUT-1 antiserum followed by gold-labelled secondary antibodies. By using morphometry, the labelling density was recorded over luminal and abluminal plasma membranes of the endothelial cells of blood microvessels supplying four brain regions: cortex, hippocampus, cerebellum and olfactory bulb. We found that the density of immunosignals for GLUT-1, represented by colloidal gold particles, was unchanged in the olfactory bulb and slightly lowered in the abluminal plasmalemma of the vascular endothelium in the cerebral cortex of the ethanol-treated mice. In contrast, statistical analysis using Mann-Whitney U-test revealed that in the hippocampus and cerebellum, the density of immunolabelling of both plasma membranes of microvascular endothelial cells was significantly lowered in the ethanol-treated mice. These findings suggest that prenatally applied ethanol had a different influence on the vasculature supplying different brain regions. In effect, the inefficient supply of glucose to selected brain regions can be one of the factors leading to the previously observed deficit in long-term memory in a similar alcohol-treated group of mice.

Aging↗
PubMed2001

Screening for trisomy 21 by fetal nuchal translucency and maternal age: a multicenter project in Germany, Austria and Switzerland.

OBJECTIVE: To examine the effectiveness of screening for trisomy 21 by a combination of maternal age and fetal nuchal translucency thickness at 10-14 weeks of gestation in Germany, Austria and Switzerland. METHODS: This was a multicenter study of screening for trisomy 21 by a combination of maternal age and fetal nuchal translucency thickness at 10-14 weeks of gestation. All the sonographers involved in the study had received The Fetal Medicine Foundation Certificate of Competence in the 10-14-week scan. Fetal nuchal translucency thickness and crown-rump length were measured in 23 805 singleton pregnancies with live fetuses. In each case the risk for trisomy 21 was estimated on the basis of maternal age and fetal nuchal translucency thickness for crown-rump length with the use of The Fetal Medicine Foundation's software. The distribution of estimated risk was determined and the sensitivity and false-positive rate for a risk cut-off of 1 in 300 was calculated. RESULTS: Fetal nuchal translucency thickness was successfully measured in all 23 805 pregnancies and outcome was available in 21 959. The median maternal age was 33 (range 15-49) years and in 7935 (36.1%) the age was 35 years or greater. The median gestation at screening was 12 (10-14) weeks and the median fetal crown-rump length was 61 (range 38-84) mm. The estimated risk for trisomy 21 based on maternal age and fetal nuchal translucency thickness for crown-rump length was 1 in 300 or greater in 13.0% (2800 of 21 475) normal pregnancies, in 87.6% (184 of 210) of those with trisomy 21 and in 87.2% (239 of 274) with other chromosomal defects. CONCLUSIONS: In Germany, Austria and Switzerland the results of screening for chromosomal defects by measurement of fetal nuchal translucency thickness, in centers with appropriately qualified sonographers and using The Fetal Medicine Foundation's software, are similar to those reported in the UK using the same methodology.

Austria↗