<AbstractText>The purpose of this investigation was to evaluate the impact of print layer thickness and post-curing method on the degree of conversion (DC) of a three-dimensional (3D) print material for temporary restorations.</AbstractText><AbstractText>120 specimens of the resin material NextDent C&<em>B</em> were additively manufactured in three different print layer thicknesses (25 µm, 50 µm, and 100 µm) using a DLP printer, and post-cured by either Labolight DUO (LL), Otoflash G171 (OF), LC-3DPrint <em>B</em>ox (P<em>B</em>) or PCU LED (PCU). Each subgroup contained 10 specimens. Raman spectra were measured for the liquid state of the resin (n = 10), directly after printing (Rprint) and after post-curing (Rcured). DC and ΔDC were calculated. The data were statistically analyzed using the Kolmogorov-Smirnov test, the general linear model analysis together with partial eta-squared (<em>ηP</em>²), Kruskal-Wallis, and Mann-Whitney U tests (P < 0.05).</AbstractText><AbstractText>Specimens post-cured by OF showed the highest ΔDC, followed by specimens post-cured by P<em>B</em>, PCU, and LL (P < 0.001). Post-curing by P<em>B</em>, PCU, and LL resulted in the same ΔDC value range (P = 0.076 to 0.209). The print layer thicknesses of 100 µm and 50 µm (P = 0.931) showed higher ΔDC than the print layer thickness of 25 µm (P < 0.001).</AbstractText><AbstractText>The choice of the post-curing method has a high impact on the DC of the tested 3D print material followed by the specific print layer thickness. Overall, specimens post-cured by OF showed the highest DC and ΔDC values. <em>B</em>rands Technology Duration Wavelength Manufacturer LC-3DPrint <em>B</em>ox (P<em>B</em>) Ultraviolet light (UV) 30 min Range 315 to 550 nm, peaks at approximately 360 and 435 nm NextDent (Soesterberg, Netherlands) Otoflash G171 (OF) Flashlight, nitrogen atmosphere Two processes of 2000 flashes Range 300 to 700 nm, peaks at approximately 480 and 530 nm NK Optik (<em>B</em>aierbrunn, Germany) Labolight DUO (LL) Light-emitting diode (LED) Two processes of 3 min Range 380 to 510 nm, peaks at approximately 395 and 475 nm GC Europe (Leuven, <em>B</em>elgium) PCU LED (PCU) Light-emitting diode (LED), vacuum 5 min Peaks at approximately 410 nm Dreve (Unna, Germany).</AbstractText>

Lineage B.1.617+, also known as G/452R.V3 and now denoted by WHO with the Greek letters δ and κ, is a recently described SARS-CoV-2 variant under investigation first identified in October 2020 in India. As of May 2021, three sublineages labeled as B.1.617.1 (κ), B.1.617.2 (δ), and B.1.617.3 have been already identified, and their potential impact on the current pandemic is being studied. This variant has 13 amino acid changes, three in its spike protein, which are currently of particular concern: E484Q, L452R, and P681R. Here, we report a major effect of the mutations characterizing this lineage, represented by a marked alteration of the surface electrostatic potential (EP) of the receptor-binding domain (RBD) of the spike protein. Enhanced RBD-EP is particularly noticeable in the B.1.617.2 (δ) sublineage, which shows multiple replacements of neutral or negatively charged amino acids with positively charged amino acids. We here hypothesize that this EP change can favor the interaction between the B.1.617+ RBD and the negatively charged ACE2, thus conferring a potential increase in the virus transmission.

Keywords: B.1.617 δ and κ variants; SARS-CoV-2; electrostatics potential changes.

CLSM and fluorescent probes were applied to assess the structure, composition, metabolic activity and gradients within naturally occurring β-proteobacteria microcolonies. Extracellular polymeric substances (EPS) as defined by lectin-binding analyses had three regions: (i) cell associated, (ii) intercellular and (iii) an outer layer covering the entire colony. We assessed structural, microenvironmental and metabolic implications of this complex EPS structure. Permeability studies indicated that the outer two layers were permeable to 20 nm beads, intercellular EPS to <40 nm beads and the outer layer was permeable to <100 nm beads. Phosphatase activity occurred at the cell surface and associated polymer. Glucose oxidase activity was only detected inside the cells and the cell-associated polymer. Rhodamine 123 suggested that activity was highest near the cell surface. The potential sensitive dye JC-1 concentrated within the outer EPS layer and the gradient was responsive to inhibition by KCN, dispersion using KCl and enhanced by addition of nutrients (nutrient broth). pH gradients occurred from the cell interior (pH 7) to the microcolony interior (pH 4+) with a gradient of increasing pH (pH 7+) to the colony exterior. The EPS provides a physical and chemical structuring mechanism forming microdomains that segregate extracellular activities at the microscale, possibly resulting in a microcolony with unitary structure and function.

To investigate the pathophysiology of infantile spasms (IS), we measured the cerebrospinal fluid (CSF) levels of beta-endorphin (beta-EP), adrenocorticotropic hormone (ACTH), and corticotropin-releasing hormone (CRH) in 20 patients with IS, including 11 with the secondary form and 9 with the cryptogenic form of the disease. The findings were compared with those obtained in age-matched controls without neurologic disease. The CSF levels of beta-EP and ACTH were significantly lower in patients with IS than those in the controls. The CSF levels of CRH in patients with IS were lower, although, this trend was not significant. These reductions in the CSF levels of these neuropeptides could explain the impairment of the brain-adrenal axis in such patients. These results might support the hypothesis that, instead of originating from an increased abundance of CRH, which can act as a rapid and potent convulsant, some infantile seizures could be caused by an ACTH deficiency.

OBJECTIVE

To determine whether MR images with motion-probing gradients (MPGs) usefully improve lesion detection in comparison with MR images without MPGs.

METHODS

Echo planar (EP) images without MPGs and with small and intermediate MPGs (gradient factor b = 2, 18, and 188 second/mm(2), respectively) were acquired for 61 hepatic lesions (21 hepatocellular carcinomas (HCCs), 19 metastases, eight hemangiomas, and 13 cysts). The lesion-to-liver signal intensity ratios (SIRs) of these lesions were calculated using EP images with and without MPGs. Qualitative analysis for detection of HCCs and metastases were also performed between the images without MPGs and with small MPGs.

RESULTS

The SIRs of HCCs and metastases for the images with small MPGs were significantly higher than the values for the images without MPGs (P < 0.05), although no significant differences were found in the case of hemangiomas and cysts. In comparison to images without MPGs, images with small MPGs improved lesion detection of three metastases and six HCCs, and worsened lesion detection of two HCCs.

CONCLUSIONS

Images with small MPGs may improve HCC and metastasis detection over images without MPGs.

This study is carried out on single (not averaged) recordings combining the spontaneous activity preceding the stimulus onset and the EP recorded upon acoustical stimulation. These recordings, which we call EEG-EPograms, are measured simultaneously from different subdural brain structures, such as the auditory cortex, medial geniculate nucleus, inferior colliculus, reticular formation and the hippocampus of awake cats. Using a combined analysis procedure (C.A.P.), the relevant frequency components of spontaneous EEG and EPs, recorded simultaneously from these brain nuclei, are analyzed according to the consistent selectivity bands depicted by the determined amplitude-frequency characteristics. These analyses provide us the following information: (1) there is an important congruency in the time courses of simultaneous response components in common frequency bands, especially in the alpha and beta frequency ranges; (2) there exist significant coupling and synchrony between the evoked amplitude enhancements in the simultaneously recorded single response components; (3) the inter-nuclei coherency in the brain's electrical activity is enormously increased upon stimulation; (4) the evoked response magnitude can be predicted, with reasonable accuracy, from the spontaneous activity preceding the stimulation. The strong dependence of the response magnitude on the stimulus-preceding EEG is explained by means of a model network consisting of a population of relaxation oscillators, which can be brought to different states of synchrony and asynchrony. Some suggestions and comments are also made for investigators working toward theories of signal transmission in the brain.

IL-3 is one of the primary factors capable of supporting the growth and development of hematopoietic cells in culture. In comparison with the other hematopoietic growth factors, IL-3 preferentially supports the proliferation of early multilineage progenitors or progenitors at early stages of development within the different lineages. Subsequently, the developing cells lose responsiveness to IL-3 while acquiring dependence on the later acting factors: GM-CSF, G-CSF, M-CSF, or Ep. In addition, IL-3 has been demonstrated to exert biologic effects with other target cell populations. These activities include the potentiation of the IL-2-dependent growth of normal T cells; the potentiation of the IL-2-dependent secretion of IgG by activated B cells; and the potentiation of the activities of eosinophils, basophils, and monocytes. The importance of any of these activities of IL-3 in vivo in either normal or stressed animals remains to be determined. Initial experiments in primates with IL-3 have yielded results consistent with its role as a regulator of early hematopoietic cell development. Although administration of IL-3 alone has relatively little effect on the levels of circulating blood cells, this treatment primes the animals to become hyper-responsive to subsequent administration of the later acting factors GM-CSF and Ep. Thus combinations of factors, at least in some situations, can provide a more potent stimulation of hematopoiesis than provided by the individual molecules, a finding that should greatly expand the utility of the different hematopoietins to more indications in the clinic.

Circulatory levels of ACTH, beta-endorphin (beta-Ep), prolactin (PRL), growth hormone (GH) and cortisol were evaluated in 19 volunteers athletes 48 h, 1 h before and soon after an international marathon (Romaratona 1988) and a national half-marathon. ACTH, beta-Ep and cortisol levels 48 h and 1 h before the half-marathon were similar, whereas 1 h before the marathon they were significantly elevated (p less than 0.01). Presumably the stress produced by the expectancy of the race induce a significant increase of the hormones of the hypothalamus-pituitary-adrenal axis in the very competitive marathon (Romaratona 1988). Moreover a remarkable increase of ACTH, beta-Ep, GH, PRL and cortisol circulating levels has been observed in the athletes after both runs, but in a different extend in relation not only to the duration and intensity of the muscular work but also to the agonistic effort: thus the hormonal increase was higher after the international marathon run than after the national half-marathon.

Eddy current induced geometric distortions can only be accurately corrected in brain diffusion-weighted echo-planar (DW-EP) images for b-values less than approximately 300 s mm(-2) using the iterative cross-correlation (ICC) algorithm. This is due to the difference in signal intensity of the cerebrospinal fluid (CSF) compartment in the diffusion-weighted and baseline T(2)-weighted echo-planar (T2W-EP) images. At larger values of b, image misalignment artefacts can, however, be removed by directly correlating CSF-suppressed T2W-EP images with non-CSF-suppressed and CSF-suppressed DW-EP images. Separate phantom experiments can also be performed to provide eddy current calibration data. Here the ability of these methods to remove eddy current induced artefacts from DW-EP images collected in volunteer diffusion tensor imaging (DTI) experiments is investigated. Monte Carlo simulations show that in order for the ICC algorithm to produce accurate estimates of the eddy current induced distortions at b-values greater than 1000 s mm(-2), the degree of CSF suppression should be greater than approximately 80%. This condition is typically met for FLAIR inversion times between 0.5 and 0.8 of the spin-lattice relaxation time of CSF. In volunteer studies the most complete image realignment was provided by direct correlation of CSF-suppressed T2W-EP and DW-EP images acquired in the FLAIR DTI experiment. These results indicate that although calibration data obtained from brain or phantom images can significantly reduce eddy current induced distortions, the optimum image realignment achievable using post-processing methods is likely to be that obtained by direct image warping techniques.

This study examined the misdiagnosis and delayed diagnosis factors for ectopic pregnancy (EP) and heterotopic pregnancy (HP) after in vitro fertilization and embryo transfer (IVF-ET) in an attempt to reduce the diagnostic error. Clinical data of patients who underwent IVF-ET treatment and had clinical pregnancy from 12463 cycles were retrospectively analyzed. Their findings of serum β-hCG test and transvaginal ultrasonography were also obtained during follow-up. These patients were divided into two groups according to the diagnosis accuracy of EP/HP: early diagnosis and misdiagnosis/delayed diagnosis. The results showed that the incidence of EP and HP was 3.8% (125/3286) and 0.8% (27/3286) respectively for IVF/ICSI-ET cycle, and 3.8% (55/1431) and 0.7% (10/1431) respectively for frozen- thawed embryo transfer (FET) cycle. Ruptured EP occurred in 28 patients due to initial misdiagnosis or delayed diagnosis. Related factors fell in 3 categories: (1) clinician factors: misunderstanding of patients' medical history, insufficient training in ultrasonography and unawareness of EP and HP; (2) patient factors: noncompliance with medical orders and lack of communication with clinicians; (3) complicated conditions of EP: atypical symptoms, delayed elevation of serum β-hCG level, early rupture of cornual EP, asymptomatic in early gestation and pregnancy of unknown location. All the factors were interwoven, contributing to the occurrence of EP and HP. It was concluded that complicated conditions are more likely to affect the diagnosis accuracy of EP/HP after IVF-ET. Transvaginal ultrasonography should be performed at 5 weeks of gestation. Intensive follow-up including repeated ultrasonography and serial serum β-hCG tests should be performed in patients with a suspicious diagnosis at admission.

The Scatchard plot, [X]b/[E]t[X] versus [X]b/[EP]t where [X]b denotes the concentration of bound ligand, [E]t the total concentration of the binding protein and [X] the free ligand concentration, was designed originally for plotting data of ligand binding to a macromolecule possessing identical non-interacting ligand binding sites. However, the plot is used for describing cooperative binding processes. In such cases, the slope of the Scatchard plot is not then equal to minus the intrinsic association constant any more. The meaning of the slope in such cases is a complex function of the binding parameters and its exact interpretation depends on the particular model used to analyze the binding data. In this communication, the meaning of the slope of the Scatchard plot is analyzed in terms of the different allosteric models.

Perturbation of adhesion mediated by cadherins was achieved by over-expressing truncated forms of E- and EP-cadherins (in which the extracellular domain was deleted) in different blastomeres of stage 6 Xenopus laevis embryos. Injections of mRNA encoding truncated E- and EP-cadherins into A1A2 blastomeres resulted in inhibition of cell adhesion and, at later stages, in morphogenetic defects in the anterior neural tissues to which they mainly contribute. In addition, truncated EP-cadherin mRNA produced a duplication of the dorso-posterior axis in a significant number of cases. The expression of truncated E- and EP-cadherins in blastomeres involved in gastrulation and neural induction (B1B2 and C1), led to the duplication of the dorso-posterior axis as well as to defects in anterior structures. Morphogenetic defects obtained with truncated EP-cadherin were more severe than those induced with truncated E-cadherin. Cells derived from blastomeres injected with truncated EP-cadherin mRNA, dispersed more readily at the blastula and gastrula stages than the cells derived from the blastomeres expressing truncated E-cadherin. Presumptive mesodermal cells expressing truncated cadherins did not engage in coherent directional migration. The alteration of cadherin-mediated cell adhesion led directly to the perturbation of the convergent-extension movements during gastrulation as shown in the animal cap assays and indirectly to perturbation of neural induction. Although the cytoplasmic domains of type I cadherins share a high degree of sequence identity, the over-expression of their cytoplasmic domains induces a distinct pattern of perturbations, strongly suggesting that in vivo, each cadherin may transduce a specific adhesive signal. These graded perturbations may in part result from the relative ability of each cadherin cytoplasmic domain to titer the beta-catenin.

A place preference conditioning procedure was used to characterize the motivational effects of beta-endorphin-(1-27), a naturally occurring fragment of beta-endorphin (beta-EP). The intracerebroventricular (ICV) administration of beta-EP, selective mu-(DAGO) or delta-(DPDPE) opioid receptor agonists to rats produced marked preferences for the drug-associated place, whereas the selective kappa-opioid receptor agonist, U-50488H produced conditioned aversions. ICV injections of the beta-EP-(1-27) (5-20 micrograms), however, resulted in no preference for either the drug- or vehicle-associated place. Pretreatment with beta-EP-(1-27) (10 micrograms) eliminated the place preference produced by beta-EP. It abolished the place preferences induced by both DAGO and DPDPE but did not modify the effects of either U-50488H or the psychostimulant d-amphetamine. These data demonstrate that beta-EP-(1-27) selectively antagonizes the motivational effects of mu- and delta-opioid agonists and suggest that this fragment may function as an endogenous antagonist of the reinforcing effects of opioid agonists in vivo.

To identify the effects of acute starvation on endogenous opioids in man, plasma beta-endorphin (beta-EP) was measured in 17 patients before, during and after fasting. Patients were assigned a posteriori into two groups: group A, comprised of 11 patients able to tolerate 5-7 days of fasting, and group B, comprised of 6 patients able to tolerate 10 days of fasting. Changes in plasma beta-EP, serum cortisol, circulating nutritional markers, and their relative levels were assessed on the 5th and 10th days of fasting, and on the 5th and 10th days of the refeeding period. Beta-EP had increased by the 5th day (group A: 4.74 +/- 0.42 to 6.91 +/- 0.65 pmol/l, p less than 0.01; group B: 3.60 +/- 0.48 to 5.14 +/- 0.22 pmol/l, p less than 0.05, and remained at 5.05 +/- 0.65 pmol/l on the 10th day (group B: 0.05 less than p less than 0.1) during fasting. Group B had lower levels of plasma beta-EP on the 5th day of fasting than group A (p less than 0.05). However, serum cortisol levels changed similarly in both groups. Plasma beta-EP showed no significant correlation with either the percentage of body weight lost or the body mass index (kg/m2) over this study period. These findings indicate that plasma beta-EP is elevated in the early phase of fasting, while not directly being associated with body weight changes. Plasma beta-EP is lower and less activated in subjects who are able to tolerate fasting for longer periods.

The effects of chronic treatment with methadone, a long-acting opiate agonist, and naltrexone, a long-acting opiate antagonist on brain immunoreactive beta-endorphin (IR-beta-EP) concentrations were studied in the rat. Male rats were treated for 30 days with either methadone, 2.5 mg/kg/day; naltrexone 2 mg/kg/day, or saline. In a repeat experiment, rats were treated for 36 days with either methadone 2.5 mg/kg/day; naltrexone 4 mg/kg/day, or saline. Brain regions were homogenized in 0.2 N HCl and assayed for IR-beta-EP by RIA. No change in the IR-beta-EP content of the hypothalamus, thalamus, midbrain, or amygdala was measured in either experiment after methadone treatment. Naltrexone, however, significantly lowered brain IR-beta-EP in both experiments. In the first study hypothalamic IR-beta-EP fell from 189 +/- 17 (SEM) to 132 +/- 7.0 ng/g wet weight of tissue after naltrexone treatment (p less than 0.01). In the second experiment naltrexone lowered IR-beta-EP in the hypothalamus from 23.4 +/- 3.6 to 15.5 +/- 1.2 ng/mg protein (p less than 0.005). Similar decreases in the IR-beta-EP content of the thalamus (from 6.74 +/- 0.59 to 4.59 +/- 0.38 ng/mg protein) and amygdala (from 1.31 +/- 0.08 to 0.90 +/- 0.10) were also measured (p less than 0.01). We conclude that occupancy of opiate receptors by an opiate antagonist reduces brain levels of IR-beta-EP and suggests that chronic opiate receptor blockade may result in a compensatory increase in brain beta-EP release.

One hundred-twenty nine HIV-1 seropositive patients (39 females, 90 males) were studied by means of pattern visual evoked potential (VEP) and brainstem auditory evoked potential (BAEP) recording. Utilizing the criteria of the Centers for Disease Control the patients were clinically defined and then subdivided into four groups: group A included patients of category II (n:11); group B patients of category III (n:29); group C patients of category IVa and IVc2 (n:55) and group D patients belonging to the other subgroups of category IV (n:34). EP were altered in 26.35% of the entire group with a marked prevalence of BAEP alterations (21.7%) rather than of VEP (4.65%). A considerable amount of BAEP abnormalities (24.13%) were found in patients with persistent generalized lymphadenopathy (group B). A significant increase of BAEP mean interpeak latencies were observed in group B, C, D patients when compared with those of the control group. On the whole, EP were altered in 20.65% of the neurologically asymptomatic patients. EP alterations may precede any clinical manifestation and can be found during the earlier phases of HIV-1 infection.

Endogenous opioid peptides have a role in the regulation of the hypothalamic-pituitary-adrenal axis. Recently, beta-endorphin (EP) has been thought to inhibit CRF release in vivo and in vitro. In the present study we examined the effects of central administration of EP on ACTH secretion and gene expression of both CRF in the hypothalamus and POMC in the anterior pituitary gland (AP) during basal and insulin-induced hypoglycemia in pentobarbital-anesthetized rats. Administration of EP in the lateral ventricle decreased basal CRF levels in the median eminence and inhibited basal and hypoglycemia-induced ACTH secretion in a dose-dependent manner. Hypoglycemia-induced POMC mRNA levels in the AP and CRF mRNA levels in the hypothalamus were also dose-dependently inhibited by the administration of EP. The inhibitory effect of EP was reversed by naloxone. These results suggest that 1) central administration of EP acts through the opioid receptor to inhibit hypoglycemia-induced CRF gene expression in the hypothalamus and CRF release, which results in a decrease in ACTH secretion and POMC mRNA levels in the AP; and 2) the active site of EP is the CRF neuron in the paraventricular nucleus.

We explored in the duck hepatitis B virus (DHBV) model the impact of electroporation (EP)-mediated DNA vaccine delivery on the neutralizing humoral response to viral preS/S large envelope protein. EP enhanced the kinetics and magnitude of anti-preS response compared to the standard needle DNA injection (SI). Importantly, EP dramatically enhanced the neutralizing potency of the humoral response, since antibodies induced by low DNA dose (10 μg) were able to highly neutralize DHBV and to recognize ten antigenic regions, including four neutralization epitopes. Whereas, SI-induced antibodies by the same low DNA dose were not neutralizing and the epitope pattern was extremely narrow, since it was limited to only one epitope. Thus, EP-based delivery was able to improve the dose efficiency of DNA vaccine and to maintain a highly neutralizing, multi-specific B-cell response, suggesting that it may be an effective approach for chronic hepatitis B therapy at clinically feasible DNA dose.

We previously demonstrated that MIBP1 and RFX1 polypeptides associate in vivo to form a complex that binds to the MIF-1 element in the c-myc gene and the major histocompatibility complex class II X-box recognition sequence. We now show that the EP element, a key regulatory sequence within hepatitis B virus enhancer I, also associates with MIBP1 and RFX1. Using polyclonal antisera directed against either oligonucleotide-purified MIBP1 or a peptide derived from the major histocompatibility complex class II promoter-binding protein RFX1, we showed that MIBP1 and RFX1 are both present in the DNA-protein complexes at the EP site. In addition, while the EP element can act cooperatively with several adjacent elements to transactivate hepatitis B virus expression, we demonstrated that the EP site alone can repress transcription of simian virus 40 promoter in a position- and orientation-independent manner, suggesting a silencer function in hepatocarcinoma cells.

CRF, a hypothalamic peptide, is a potent stimulator of POMC synthesis and secretion in the pituitary. POMC biosynthesis has been documented in the testis, specifically in Leydig cells, and recent studies suggest that CRF is synthesized locally in the testis. A reverse hemolytic plaque assay and immunocytochemistry with Leydig cell-specific antibodies were used to study the effect of CRF on secretion of the POMC peptide beta-endorphin (beta EP) from normal rat primary Leydig cell cultures. In enriched Leydig cell preparations incubated with beta EP antiserum (diluted 1:50) then with complement (diluted 1:25), approximately 15% of immunocytochemically identified Leydig cells formed plaques. Preabsorption of the antiserum with beta EP (2 micrograms/microliters antiserum) overnight at 4 C abolished the formation of plaques. Increasing concentrations of CRF (from 10(-1) to 10(-7) M) resulted in an approximately 80% increase in both the percentage of plaque-forming cells and the mean plaque size. When the CRF antagonist CRF-(9-41) (10(-6) M) was added in the presence of CRF, the increases in plaque number and average size did not occur. These results demonstrate that Leydig cells have functional CRF receptors and that beta EP secretion from these cells is stimulated by CRF.

We observe an enormous spontaneous exchange bias (~300-600 Oe)--measured in an unmagnetized state following zero-field cooling--in a nanocomposite of BiFeO(3) (~94%)-Bi(2)Fe(4)O(9) (~6%) over a temperature range 5-300 K. Depending on the path followed in tracing the hysteresis loop--positive (p) or negative (n)--as well as the maximum field applied, the exchange bias (H(E)) varies significantly with | - H(Ep) |>> | H(En) |. The temperature dependence of H(E) is nonmonotonic. It increases, initially, till ~150 K and then decreases as the blocking temperature T(B) is approached. All these rich features appear to be originating from the spontaneous symmetry breaking and consequent onset of unidirectional anisotropy driven by "superinteraction bias coupling" between the ferromagnetic core of Bi(2)Fe(4)O(9) (of average size ~19 nm) and the canted antiferromagnetic structure of BiFeO(3) (of average size ~112 nm) via superspin glass moments at the shell.

Activin A as a predictor of pregnancy failure has been the focus of heated debate, but the value of a combined activin A and follistatin (FS) measurement in serum to predict pregnancy failure has not been reported yet. We assessed whether a single serum measurement of the two physiological antagonists at 6-8 weeks gestation could differentiate ectopic pregnancies (EP) or missed abortions (MA) from healthy intrauterine pregnancies (IUP). activin A concentrations were significantly lower in women with EP (n = 30, median value of 264 pg/mL) and women with MA (n = 30, median value of 350 pg/mL) compared to IUP (n = 33, median value of 788 pg/mL); P < 0.001. At a threshold value of 505 pg/mL, activin A had 87.9% sensitivity and 100% specificity and negative predictive value of 0.974 for discriminating an ectopic pregnancy from viable pregnancies. FS was able to discriminate IUP from EP (ROC curve P < 0.001) as was their ratio (ROC curve P = 0.008), but was unable to discriminate a MA from an EP. In EP, activin A did not correlate with beta HCG levels. The present findings support the thesis that activin A or FS could be considered promising biomarkers for the discrimination between an IUP and a failed pregnancy (MA or EP).

OBJECTIVE

We investigated genotoxic effects of occupational exposure to lead acetate in pottery-glaze ceramic workers.

METHODS

The study was carried out in 30 exposed workers and 30 matched controls, to whom several biochemical parameters-the blood lead (B-Pb; range: exposed, 41.68-404.77; controls, 12-52) and cadmium (B-Cd) level, the activity of delta-aminolevulinic acid dehydratase (ALAD), erythrocyte protoporphyrin (EP), the level of vitamin B(12) and folate in serum-were measured. The genotoxic effects were evaluated by the alkaline comet assay, the DNA diffusion assay and micronucleus test in peripheral blood lymphocytes.

RESULTS

Subjects exposed to lead had significantly higher B-Pb level and, consequently, increased values of tail intensity (TI), frequency of apoptotic and necrotic cells, and frequency of micronuclei (MN). In contrast, their activity of ALAD, the level of vitamin B(12) and folate in serum were significantly lower compared to controls. Poisson regression analysis showed a significant correlation of profession, duration of exposure, smoking, level of cadmium in blood, ALAD and EP with primary DNA damage. A majority of primary damage repairs in a short period after exposure to a genotoxic agent. In addition, the influence of gender and level of vitamin B(12) and folate in serum MN frequency in exposed group was observed.

CONCLUSIONS

In this study, DNA diffusion and micronucleus test showed higher influence of tested parameters to DNA damage. The results indicate a need for concomitant use of at least two different biomarkers of exposure when estimating a genetic risk of lead exposure.

The reason for the particularly increased risk for cardiovascular complications in diabetic women is still unclear. We have previously found decreased distensibility of elastic arteries in type I diabetic women, indicating increased cardiac load, not seen in type I diabetic men, which might be one contributing factor. Whether the effect of gender is different in muscular arteries in type I diabetic patients has not been assessed. As estimates of arterial distensibility we measured stiffness (beta) and pressure strain elastic modulus (Ep) in the muscular common femoral artery using echo-tracking sonography in 30 women (mean age 34 years, range 20-61) and 26 men (mean age 38 years, range 22-56) with type I diabetes. The results were compared with those of 89 healthy individuals of corresponding age and gender and with previously published results from elastic arteries in these patients obtained at the same occasion. The internal common femoral diameter was significantly decreased in both diabetic men and women. In sharp contrast to the highly significant decreased distensibility of the elastic abdominal aorta and common carotid artery in the type I diabetic women, the distensibility of the common femoral artery did not clearly differ between patients and controls, neither for women nor for men. Thus, the gender difference in changes of arterial distensibility found in elastic arteries was absent or far less obvious in the femoral artery. In conclusion, female gender seems to affect the mechanical properties of elastic, but not of large muscular arteries in type I diabetic patients. Thus, putative gender differences in arterial changes in type I diabetes are to be sought in elastic rather than muscular arteries.