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Biomedical subjects

O Nielsen

Publications and source records attributed to O Nielsen.

At least 19 recordsLinked to original sources
PubMed2002

Characterisation of symbionts of entomopathogenic nematodes by universally primed-PCR (UP-PCR) and UP-PCR product cross-hybridisation.

This work introduces and demonstrates the applicability of universally primed-PCR (UP-PCR) for differentiating bacterial symbionts of entomopathogenic nematodes. Furthermore, typing by UP-PCR product cross-hybridisation was successfully introduced to cluster the bacterial strains. The work was initiated by isolating 10 isolates of Photorhabdus temperata (S172) from the nematode host Heterorhabditis sp. (DK172) and 12 isolates of Xenorhabdus bovienii (S1) from the nematode Steinernema feltiae (DK1). The isolates were compared by UP-PCR using different primers. The two bacterial species (P. temperata and X. bovienii) could be distinguished on the basis of the banding pattern whereas isolates isolated from the same nematode host had identical banding patterns. Three isolates obtained from DK172 and DK1, respectively, were then selected along with a number of reference strains (Hb, HP88, C1, K122, HSH2, HL81, T228, 61, AN6, Q58) and further characterised by UP-PCR product cross-hybridisation. The Xenorhabdus strains (Q58, AN6, 61, T228, S1) represented three species and these species were separated by the hybridisation technique. The Photorhabdus strains (Hb, HP88, C1, K122, HSH2, HL81, S172) represented two species and were also separated according to this in the cross-hybridisation. Within each species of Photorhabdus, two subgroups were formed as a result of intensity of the hybridisation signals. This grouping was in agreement with previous studies in other laboratories.

Animals↗
PubMed2002

The scavenger receptor, cysteine-rich domain-containing molecule gp-340 is differentially regulated in epithelial cell lines by phorbol ester.

Gp-340 is a glycoprotein belonging to the scavenger receptor cysteine rich (SRCR) group B family. It binds to host immune components such as lung surfactant protein D (SP-D). Recent studies found that gp-340 interacts directly with pathogenic microorganisms and induces their aggregation, suggesting its involvement in innate immunity. In order to investigate further its potential immune functions in the appropriate cell lines, the expression of gp-340 in four conventional immune cell lines (U937, HL60, Jurkat, Raji), and two innate immune-related epithelial cell lines (A549 derived from lung and AGS from stomach), was examined by RT-PCR and immunohistochemistry. The resting immune cell lines showed weak or no gp-340 mRNA expression; while the two epithelial cell lines expressed gp-340 at much higher level, which was differentially regulated by phorbol myristate acetate (PMA) treatment. In the A549 cells, gp-340 was up-regulated along with the PMA-induced proinflammatory expression of both IL-6 and IL-8. In AGS cells, PMA down-regulation of gp-340 was seen in parallel with an up-regulation of the two mature gastric epithelial specific proteins TFF1 (trefoil factor 1) and TFF2, which are implicated as markers of terminal differentiation. Analysis of the distribution of gp-340, together with the TFFs and SP-D in normal lung and gastric mucosa, supported further our in vitro data. We conclude that the differential regulation of gp-340 in the two epithelial cell lines by PMA indicates that gp-340 s involvement in mucosal defence and growth of epithelial cells may vary at different body locations and during different stages of epithelial differentiation.

B-Lymphocytes↗
PubMed2002

Frequent alteration of MDM2 and p53 in the molecular progression of recurring non-Hodgkin's lymphoma.

AIMS: Recurrence of non-Hodgkin's lymphoma with or without transformation is often associated with increased clinical drug resistance and poor prognosis indicating molecular progression. The study addresses the currently poorly understood molecular mechanisms underlying relapsing non-Hodgkin's lymphoma. METHODS AND RESULTS: We have analysed sequential biopsies from 42 non-Hodgkin's lymphoma patients immunohistochemically for p53 alterations (based on p53 and p21Waf1 expression), as well as for expression of MDM2, p27Kip1 and cyclin D3. Relapse of follicle centre lymphoma was associated with p53 alterations as 5/6 (83%) follicle centre lymphomas with normal p53 at diagnosis showed p53 alterations at relapse. Of these cases, three showed transformation to diffuse large B-cell lymphoma. p53 alteration was also associated with relapse of de novo diffuse large B-cell lymphoma and T-cell non-Hodgkin's lymphoma, as 2/5 (40%) diffuse large B-cell lymphomas and 3/9 (33%) T-cell non-Hodgkin's lymphomas with normal p53 at diagnosis showed p53 alterations at relapse. No indolent non-Hodgkin's lymphoma case showed MDM2 over-expression at diagnosis, whereas 4/5 (80%) transformed diffuse large B-cell lymphomas developed MDM2 over-expression. CONCLUSION: Our data are consistent with the notion that p53 alterations are important for the histological transformation of follicle centre lymphoma. However, the data also suggest that relapsing follicle centre lymphomas without overt transformation often have p53 alterations and increased risk of transformation, and that relapse of de novo diffuse large B-cell lymphomas and T-cell non-Hodgkin's lymphomas is associated with p53 alterations. Furthermore, our results are consistent with an association of MDM2 over-expression with histological transformation of both follicle centre lymphoma and marginal zone B-cell lymphoma.

Aged↗
PubMed2001

An insight into the epidemiology of dolphin morbillivirus worldwide.

Serum samples from 288 cetaceans representing 25 species and originating from 11 different countries were collected between 1995 and 1999 and examined for the presence of dolphin morbillivirus (DMV)-specific antibodies by an indirect ELISA (iELISA) (N = 267) or a plaque reduction assay (N = 21). A total of 35 odontocetes were seropositive: three harbour porpoises (Phocoena phocoena) and a common dolphin (Delphinus delphis) from the Northeastern (NE) Atlantic, a bottlenose dolphin (Tursiops truncatus) from Kent (England), three striped dolphins (Stenella coeruleoalba), two Risso's dolphins (Grampus griseus) and a bottlenose dolphin from the Mediterranean Sea, one common dolphin from the Southwest (SW) Indian Ocean, three Fraser's dolphins (Lagenodelphis hosei) from the SW Atlantic, 18 long-finned pilot whales (Globicephala melas) and a bottlenose dolphin from the SW Pacific as well as a captive bottlenose dolphin (Tursiops aduncus) originally from Taiwan. The presence of morbillivirus antibodies in 17 of these animals was further examined in other iELISAs and virus neutralization tests. Our results indicate that DMV infects cetaceans worldwide. This is the first report of DMV-seropositive animals from the SW Indian, SW Atlantic and West Pacific Oceans. Prevalence of DMV-seropositives was 85.7% in 21 pilot whales from the SW Pacific and both sexually mature and immature individuals were infected. This indicates that DMV is endemic in these animals. The same situation may occur among Fraser's dolphins from the SW Atlantic. The prevalence of DMV-seropositives was 5.26% and 5.36% in 19 common dolphins and 56 harbour porpoise from the NE Atlantic, respectively, and 18.75% in 16 striped dolphins from the Mediterranean. Prevalence varied significantly with sexual maturity in harbour porpoises and striped dolphins; all DMV-seropositives being mature animals. The prevalence of seropositive harbour porpoise and striped dolphins appeared to have decreased since previous studies. These data suggest that DMV is not endemic within these populations, that they are losing their humoral immunity against the virus and that they may be vulnerable to new epidemics.

Animal Diseases↗
PubMed2001

Cyclin D3 expression in non-Hodgkin lymphoma. Correlation with other cell cycle regulators and clinical features.

Cyclin D3 is the most widely expressed D-type cyclin and can be rate limiting for G1/S transition. To study the expression of cyclin D3 in non-Hodgkin lymphoma, samples from 198 previously untreated patients with lymphoma from a prospectively collected, population-based lymphoma registry were analyzed immunohistochemically for cyclin D3 expression. In 43 lymphomas (21.7%), cyclin D3 was overexpressed. T-cell lymphomas more frequently overexpressed cyclin D3 than B-cell lymphomas. Furthermore, cyclin D3-overexpressing indolent lymphomas were associated with higher proliferation rate, higher p21Waf1 expression, lower p27Kip1 expression, and altered p53. Cyclin D3 overexpression identified a subgroup of patients with indolent B-cell lymphoma with adverse clinical features: patients were older, more frequently had "B" symptoms and extranodal involvement, and were more frequently in the high-intermediate or high-risk International Prognostic Index groups. At univariate analysis of indolent lymphomas, cyclin D3 overexpression was associated significantly with poor overall survival and poor relapse-free survival. The statistical significance was retained on multivariate analysis of overall survival and relapse-free survival. Our results suggest that cyclin D3 is expressed differentially among lymphoma subtypes and that overexpression might identify a subpopulation of patients with indolent lymphoma with adverse clinical features and poor outcome.

Cell Cycle Proteins↗
PubMed2001

Serologic survey of Brucella spp. antibodies in some marine mammals of North America.

A serologic survey of anti-Brucella spp. antibodies was undertaken on 2,470 samples of 14 North American marine mammal species collected between 1984-97. Serum or blood from eight species of cetaceans and six species of pinnipeds was sampled from Pacific, Atlantic, and Arctic oceans. Two competitive enzyme-linked immunosorbent assays (C-ELISA's), using specific monoclonal antibodies to Brucella abortus cell wall components, were used to detect anti-Brucella spp. antibodies in the samples. Sera from 33 cetaceans and 61 pinnipeds gave inhibition values, in one or both of the tests, which exceeded the threshold that indicates Brucella spp. exposure in cattle. Seropositive animals were identified from Pacific, Atlantic, and Arctic oceans. While Brucella spp. was not isolated, differences in the response of seropositive cetacean and pinniped sera in the two assays suggest that two antigenically distinct species or biovars of Brucella spp. are present. No pathology consistent with clinical brucellosis was noted in any of the animals tested although detailed examination was not conducted on all carcasses.

Animal Diseases↗
PubMed2001

Serologic evidence of influenza A infection in marine mammals of arctic Canada.

A serologic survey of influenza A antibodies was undertaken on 1,611 blood samples from five species of marine mammals collected from Arctic Canada from 1984-98. Sampling was done in 24 locations throughout the Canadian Arctic encompassing Sachs Harbor (72 degrees N, 125 degrees W), Northwest Territories in the west to Loks Land (63 degrees N, 64 degrees W), Nunavut in the east, to Eureka (80 degrees N, 86 degrees W), Nunavut in the north to Sanikiluaq (56 degrees N, 79 degrees W), Nunavut in the south. A competitive ELISA using a monoclonal antibody (Mab) against influenza A nucleoprotein (NP) was used. Five of 418 (1.2%) belugas (Delphinapterus leucas) and 23 of 903 (2.5%) ringed seals (Phoca hispida) were serologically positive. None of the 210 walruses (Odobenus rosmarus rosmarus), 76 narwhals (Monodon monoceros) and four bowhead whales (Balaena mysticetus) had detectable antibodies to influenza A. Positive belugas were identified from communities on southeast Baffin Island while positive ringed seals came from communities in the eastern, western and high Arctic. Virus isolation attempts on lung tissue from a seropositive beluga were unsuccessful. We believe that influenza A infection in marine mammals is sporadic, the infection is probably self-limiting, and it may not be able to be maintained in these animals. Although the predominant hemagglutinin (H) type was not determined and therefore the pathogenicity of the strains to humans is unknown, the hunting and consumption of marine mammals by the Inuit, may put them at risk for influenza A infection.

Animals↗
PubMed2000

Sequence-specific high mobility group box factors recognize 10-12-base pair minor groove motifs.

Sequence-specific high mobility group (HMG) box factors bind and bend DNA via interactions in the minor groove. Three-dimensional NMR analyses have provided the structural basis for this interaction. The cognate HMG domain DNA motif is generally believed to span 6-8 bases. However, alignment of promoter elements controlled by the yeast genes ste11 and Rox1 has indicated strict conservation of a larger DNA motif. By site selection, we identify a highly specific 12-base pair motif for Ste11, AGAACAAAGAAA. Similarly, we show that Tcf1, MatMc, and Sox4 bind unique, highly specific DNA motifs of 12, 12, and 10 base pairs, respectively. Footprinting with a deletion mutant of Ste11 reveals a novel interaction between the 3' base pairs of the extended DNA motif and amino acids C-terminal to the HMG domain. The sequence-specific interaction of Ste11 with these 3' base pairs contributes significantly to binding and bending of the DNA motif.

Amino Acid Sequence↗
PubMed2000

Mik1 levels accumulate in S phase and may mediate an intrinsic link between S phase and mitosis.

Two paradigms exist for maintaining order during cell-cycle progression: intrinsic controls, where passage through one part of the cell cycle directly affects the ability to execute another, and checkpoint controls, where external pathways impose order in response to aberrant structures. By studying the mitotic inhibitor Mik1, we have identified evidence for an intrinsic link between unperturbed S phase and mitosis. We propose a model in which S/M linkage can be generated by the production and stabilization of Mik1 protein during S phase. The production of Mik1 during unperturbed S phase is independent of the Rad3- and Cds1-dependent checkpoint controls. In response to perturbed S phase, Rad3-Cds1 checkpoint controls are required to maintain high levels of Mik1, probably indirectly by extending the S phase period, where Mik1 is stable. In addition, we find that Mik1 protein can be moderately induced in response to irradiation of G(2) cells in a Chk1-dependent manner.

Checkpoint Kinase 1↗
PubMed2000

Frequent disruption of the RB1 pathway in diffuse large B cell lymphoma: prognostic significance of E2F-1 and p16INK4A.

In the present study, we analysed 34 de novo diffuse large B cell lymphoma (DLCL) from a population-based lymphoma registry for alterations of the RB1 pathway at the genetic (RB1 and CDK4) and protein (pRb, cyclin D1, cyclin D3, CDK4, and E2F-1) level. The results were correlated with the data from our previous studies of CDKN2A deletion and hypermethylation, other p53 pathway components, p27Kip1 expression, and proliferation, as well as with clinical outcome, including prognosis. We found aberrant pRb expression in four (12%) of 34 DLCLs. One of these had a point mutation in intron 3 10 bp downstream of exon 3 generating a novel splice signal. Seven tumours (21%) showed cyclin D3 overexpression, including all three thyroid lymphomas (P = 0.006). Cyclin D3 overexpression and p16INK4A/pRb aberrations were mutually exclusive, supporting an oncogenic role for cyclin D3 in DLCL. p16INK4A inactivation, cyclin D3 overexpression, or aberrant pRb expression was identified in 18 of 34 DLCLs (53%). Combining these results with our previous p53 pathway studies showed that 82% of the de novo DLCLs had alterations of these pathways, and that both pathways were altered in 13 cases (38%). Low E2F-1 expression was associated with treatment failure (P = 0.020), and multivariate analysis of overall survival identified both low E2F-1 expression (relative risk = 6.9; P = 0.0037) and p16INK4A inactivation (relative risk = 3.3; P = 0.0247) as independent prognostic markers. These data support a role of E2F-1 as tumour suppressor gene in lymphoma and strongly suggest that the RB1 and p53 pathways are important in the development of de novo DLCL. Furthermore, low E2F-1 expression and p16INK4A inactivation may serve as prognostic markers for patients with this type of lymphoma.

Antigens, Nuclear↗
PubMed2000

Does fetal antigen 1 (FA1) identify cells with regenerative, endocrine and neuroendocrine potentials? A study of FA1 in embryonic, fetal, and placental tissue and in maternal circulation.

Fetal antigen 1 (FA1) is a circulating EGF multidomain glycoprotein. FA1 and its membrane-associated precursor is defined by the mRNAs referred to as delta-like (dlk), preadipocyte factor 1 (pref-1) or zona glomerulosa-specific factor (ZOG). Using a polyclonal antibody recognising both forms, the localisation of FA1/dlk was analysed in embryonic and fetal tissues between week 5 to 25 of gestation and related to germinal origin and development. FA1 was observed in endodermally derived hepatocytes, glandular cells of the pancreas anlage, and in respiratory epithelial cells. FA1 was also present in mesodermally derived cells of the renal proximal tubules, adrenal cortex, Leydig and Hilus cells of the testes and ovaries, fetal chondroblasts, and skeletal myotubes. Ectodermally derived neuro- and adenohypophysial cells, cells in the floor of the 3rd ventricle and plexus choroideus were also FA1 positive. The number of cells expressing FA1 decreased during fetal development where the expression became restricted to specific functional cells. Epidermis, gut epithelium, gall bladder, blood cells, spleen, thyroid gland, salivary glands, and smooth muscle cells were FA1 negative. Analysis of extra-embryonic tissues from normal and pathological pregnancies revealed FA1 in stromal cells surrounding the blood islands of the yolk sac as well as in placental fibroblasts where the expression was most pronounced in diploid, androgenic complete hydatidiform moles. However, as measured by ELISA, the circulating maternal FA1 levels in complete moles were not different from normal pregnancies. The results presented suggest that FA1 is a growth and/or differentiation factor extensively expressed in immature cells and down-regulated during fetal development. FA1 down-regulation was associated with a shift in the subcellular localisation indicating differential post-translational/post-transcriptional modifications during fetal development. FA1 may be a new marker of cellular subtypes with a regenerative potential and of specific cells with endocrine or neuroendocrine functions.

Biomarkers↗
PubMed2000

Does plasminogen activator inhibitor-1 (PAI-1) control trophoblast invasion? A study of fetal and maternal tissue in intrauterine, tubal and molar pregnancies.

Urokinase plasminogen activator, its receptor and the inhibitor PAI-1 are believed to control proteolysis and remodelling of maternal tissue during trophoblast invasion. This system appears to be strictly regulated in normal intrauterine pregnancies whereas tubal and molar pregnancies seem to be characterized by an uncontrolled excessive placental invasion. This study evaluates subcellular PAI-1 by immunohistochemistry in the villous placenta, in the basal plate and placental bed, and in the decidual compartments of normal, tubal and molar pregnancies. PAI-1 was present in villous syncytiotrophoblasts and co-localized focally with fibrin-type fibrinoid on the surface of the chorionic villi. Basal plate and placental bed extravillous interstitial trophoblasts, as well as vascular trophoblasts, were also PAI-1 positive. In the decidua parietalis, PAI-1 was observed in the cytoplasm of the non-invaded decidual cells. In the decidua basalis comprising the basal plate, PAI-1 was seen to be membrane-associated or confined to the extracellular matrix (ECM) facing the invasive front of anchoring villi. The ECM of decidua capsularis and chorion laeve displayed the most pronounced PAI-1 expression towards the maternal interface. In contrast, the majority of placental bed decidual cells adjacent to the interstitial and vascular trophoblasts were PAI-1 negative. Only a few stromal cells distant from the implantation site were PAI-1 positive in the tubal pregnancies and decidualization was not present. Likewise, excessive decidual necrosis and fibrinoid deposition devoid of PAI-1 was a common finding in complete molar pregnancies. These results suggest that PAI-1 defines specific extravillous invasive trophoblasts within the maternal decidua. Moreover, maternal cellular lack of PAI-1 in tubal pregnancies and excessive decidual necrosis in molar pregnancies indicate an uncontrolled placental invasion. The present data indicate that trophoblast invasion is primarily regulated by signals from decidual cells.

Chorionic Villi↗
PubMed2000

Localization of E-cadherin in villous, extravillous and vascular trophoblasts during intrauterine, ectopic and molar pregnancy.

Previous reports have described down-regulation of E-cadherin in trophoblasts differentiating to an invasive phenotype. This study shows the localization of E-cadherin in a prospective design with stereological sampling of fetal and maternal first, second and third trimester tissue. E-cadherin was observed in villous cytotrophoblasts, and in non-proliferating, intermediate trophoblasts (IT) within cell columns and islands in intrauterine, ectopic and partial molar placentas. Highly proliferating IT with cytological atypia in complete molar placentas were also E-cadherin-positive. E-cadherin was present in trophoblasts throughout the anchoring cell columns. Trophoblasts undergoing epithelial mesenchymal transformation (EMT) detaching from the distal cell columns and deeper located single extravillous interstitial trophoblasts (EVT) showed E-cadherin-negative breaches in the cell membrane. Prior to the late second trimester, the relative number of E-cadherin-positive single EMT and EVT differed from the total number of cytokeratin-positive trophoblasts. Intraluminal, endovascular and perivascular trophoblasts adjacent to the maternal vessels were also E-cadherin-positive, but a highly varying pattern was observed at different ages of gestation. Our results indicate a temporary shift in E-cadherin expression in extravillous trophoblasts possessing a migrating and invasive potential. Functional E-cadherin may be restored as trophoblasts aggregate in the decidua and the vessel wall after completion of migration.

Antibodies, Monoclonal↗
PubMed2000

A morbillivirus antibody survey of Atlantic walrus, narwhal and beluga in Canada.

A longitudinal serologic survey was conducted for morbillivirus antibodies in Atlantic walruses (Odobenus rosmarus rosmarus), narwhal (Monodon monoceros), and beluga (Delphinapterus leucas) from the Northwest Territories, Nunavut and the St. Lawrence estuary (Canada). Sixty-five of 131 (50%) walruses sampled between 1984 and 1993 had detectable morbillivirus neutralizing antibodies. Positive walrus were identified from four of five Arctic sampling sites, to as far back as 1984. Prevalence of morbillivirus neutralizing antibodies in walruses from Foxe Basin ranged from a high of 76% (n = 21) in 1993 to a low of 22% (n = 28) in 1984. Limitations in sample acquisition may have produced underestimates for the 1984 data. There are no reports of clinical morbillivirus infection in walruses. Our results are consistent with the hypothesis that a morbillivirus similar or identical to phocine distemper virus (PDV) has circulated among walrus populations of the eastern Canadian Arctic, at least since the early 1980s. No narwhal (n = 79) or beluga (n = 445) from Arctic waters were identified as having antibodies to dolphin morbilivirus (DMV) above the threshold serum dilution of log2 4. Also, none of the beach-cast cetacean carcasses (n = 28) from the Gulf of St. Lawrence and the St. Lawrence estuary were positive for antibodies to DMV. This indicates that Gulf of St. Lawrence, St. Lawrence estuary, and Arctic cetaceans either have not been exposed to DMV or an antigenically related morbillivirus, or are not susceptible to infection.

Animals↗
PubMed2000

Brucellosis in ringed seals and harp seals from Canada. lforbes@em.agr.ca.

A novel Brucella sp. was isolated from lymph nodes of four ringed seals (Phoca hispida) collected near Pangnirtung (Baffin Island, Canada) in January and February 1995 and in one harp seal (Phoca groenlandica) collected near the Magdalen Islands (Gulf of St. Lawrence, Canada) in March 1996. Bacteriological characteristics were the same for all five isolates. The colonies were typical of Brucella spp., but took 2 to 5 days longer than the traditional species to appear on primary isolation media. Biotyping results did not match any of the known biovars of Brucella, but were similar to isolates of the genus Brucella previously reported from marine mammals inhabiting other areas of the northern hemisphere. This is the first confirmed report of brucellosis in marine mammals from Canada, and the first report of this organism in ringed and harp seals.

Animals↗
PubMed1999

Localization and significance of urokinase plasminogen activator and its receptor in placental tissue from intrauterine, ectopic and molar pregnancies.

Urokinase plasminogen activator receptor (uPAR) is a membrane-anchored protein with urokinase plasminogen activator (uPA) as the ligand. This complex induces proteolysis and remodelling of maternal decidua during placental implantation. The presence of uPAR on trophoblasts is supposed to promote adhesion, migration and invasion. In cancer tissue, high levels of uPAR are correlated with a poor prognosis. This immunohistochemical study shows the localization of uPA and uPAR in a prospective design with stereological sampling of fetal and maternal tissue from normal, ectopic and hydatidiform molar (HM) pregnancies. Cytokeratin and Ki67 were used as markers for trophoblasts and proliferating cells. Membrane-bound uPAR was observed on villous non-proliferating intermediate trophoblasts (IT) within cell columns in intrauterine and ectopic pregnancies. The corresponding proliferating IT with cytological atypia sprouting from the chorionic villi in HM was uPAR-negative. uPA but not uPAR was observed in anchoring distal IT at the attachment-point to the basal plate. In the placental bed, extravillous interstitial trophoblasts were uPA-positive but uPAR-negative. The trophoblast giant cells were both uPA- and uPAR-negative. In relation to the maternal vessels, a focal distribution for uPA and uPAR was present in the endovascular and perivascular trophoblasts. The intraluminal trophoblasts overlying endothelial cells were uPAR-positive only. In maternal tissue from intrauterine and molar pregnancies, uPAR was seen in the decidual cells in a zone facing the anchoring villi and the fibrinoid lesions with embedded trophoblasts. In contrast, the stromal cells of the fallopian tube without a decidual reaction facing the implanted gestation were uPAR-negative. Non-invaded decidual, myometrial and muscular tissue of the pregnant uterus and fallopian tube was extensively positive for uPA whereas 'pseudodecidual' cells from the intrauterine evacuate in patients with an ectopic pregnancy only showed a focal and scanty reaction for uPA. When trophoblast invasion of the decidua was present, the decidual cells were uPA-negative. A semi-quantitative assessment of the receptor was estimated in villous IT within cell columns in normal and molar pregnancies but, in conclusion, quantitative evaluation of uPAR cannot be used to predict development of post-molar persistent trophoblastic disease (PTD).

Chorionic Villi Sampling↗
PubMed1999

Biological monitoring of sterilizers and sterilization failures in Norwegian dental offices in 1985 and 1996.

It is essential that dental office sterilizers be regularly challenged with biological indicators (BIs) in order to prove that the test spores are being killed during sterilization. The aims of the study were to biologically monitor Norwegian dental office sterilizers and to identify factors contributing to sterilization failure. In 1985, participants received a packet containing: (i) 4 BI units; (ii) a set of instructions; (iii) a questionnaire concerning operation (including biological monitoring) of the office sterilizer(s), and (iv) a return-address envelope. In 1996, offices were sent (i) a survey which included demographic questions and inquiries concerning instrument sterilization processes; (ii) 2 sets of 3 BI units with instructions for their use on 2 different days; (iii) 1 control BI unit that was not to be processed, and (iv) a return-address envelope. Both private and public offices participated. Response rate to the 1996 study was 60%, which was 9.1% of all dental offices in Norway. Testing results indicated a 6.3% overall sterilization failure rate. Three out of 163 steam autoclaves (SAs) (1.8% of total) and 14 out of 109 dry heat (DH) ovens (12.8% of total) failed. DH ovens were over 7 times more likely to fail BI testing than were SAs (chi2, P < 0.01). Demographic or hygiene procedural factors could not be correlated to sterilization performance (chi2, P > 0.05). The failure rate for SAs (n = 216) in 1985 was almost 5 times greater than in 1996 (8.8% vs 1.8%). Improvement in sterilizer performance during the decade may be related to issuance in 1986 of Norway's 1st infection control guidelines for dentistry and greater awareness of infection control practices and/or to increases over the previous 10 years in the number of postgraduate courses offered in infection control. The current Norwegian guidelines on infection control practices in public health services, including dentistry, recommend regular biological monitoring of sterilizers without specifying how often. There is a lack of information among Norwegian dentists as to how frequently dental office sterilizers should be regularly monitored by BI.

Chi-Square Distribution↗