Miracle-dz/UniFAR-FTUs huggingface dataset:
THE EARLY HISTORY OF ATMOSPHERIC OXYGEN : Homage to

■ Abstract This paper reviews the Precambrian history of atmospheric oxygen, beginning with a brief discussion of the possible nature and magnitude of life before the evolution of oxygenic photosynthesis. This is followed by a summary of the various lines of evidence constraining oxygen levels through time, resulting in a suggested history of atmospheric oxygen concentrations. Also reviewed are the various processes regulating oxygen concentrations, and several models of Precambrian oxygen evolution are presented. A sparse geologic record, combined with uncertainties as to its interpretation, yields only a fragmentary and imprecise reading of atmospheric oxygen evolution. Nevertheless, oxygen levels have increased through time, but not monotonically, with major and fascinating swings to both lower and higher levels.
Subchondral bone morphology in the metacarpus of racehorses in training changes with distance from the articular surface but not with age

The repetitive large loads generated during high‐speed training and racing commonly cause subchondral bone injuries in the metacarpal condyles of racehorses. Adaptive bone modelling leads to focal sclerosis at the site of highest loading in the palmar aspect of the metacarpal condyles. Information on whether and how adaptive modelling of subchondral bone changes during the career of a racehorse is sparse. The aim of this cross‐sectional study was to describe the changes in subchondral bone micromorphology in the area of highest loading in the palmar aspect of the metacarpal condyle in thoroughbred racehorses as a function of age and training. Bone morphology parameters derived from micro‐CT images were evaluated using principal component analysis and mixed‐effects linear regression models. The largest differences in micromorphology were observed in untrained horses between the age of 16 and 20 months. Age and duration of a training period had no influence on tissue mineral density, bone volume fraction or number and area of closed pores to a depth of 5.1 mm from the articular surface in 2‐ to 4‐year‐old racehorses in training. Horses with subchondral bone injuries had more pores in cross‐section compared with horses without subchondral bone injuries. Differences in bone volume fraction were due to the volume of less mineralised bone. Tissue mineral density increased and bone volume fraction decreased with increasing distance from the articular surface up to 5.1 mm from the articular surface. Further research is required to elucidate the biomechanical and pathophysiological consequences of these gradients of micromorphological parameters in the subchondral bone.
Vision-based 1D barcode localization method for scale and rotation invariant

In this paper, we use a vision-based image processing technique to propose a method of real-time one-dimensional barcode localization robust for rotation and scale. The proposed method consists of three main steps. The first step generates and analyzes an orientation histogram of input images and removes their background regions and small clutters. The second step analyzes a local entropy-based orientation for the segmentation of a large region that is highly likely to be barcodes. Finally, the third step analyzes and verifies the barcode structures of the selected candidate region. The test results based on the data set available to the public demonstrate the proposed method is more accurate than existing methods by 10% or more.
Mitogenic and metabolic actions of epidermal growth factor on rat articular chondrocytes: modulation by fetal calf serum, transforming growth factor-beta, and tyrphostin.

The effects of human recombinant epidermal growth factor (EGF) on rat articular chondrocytes from humeral and femoral head cartilage of 21-day-old Wistar rats were analyzed. The cells were cultured under standard conditions as monolayers. Cell proliferation was studied by [3H]thymidine incorporation and determination of DNA content, proteoglycan synthesis by [35S]sulfate incorporation, and collagen synthesis by [3H]proline incorporation. The presence of specific receptors was confirmed by [125I]-EGF binding and that of EGF and EGF-receptor (EGF-R) mRNA by reverse transcription and the polymerase chain reaction. EGF (0.5-2.5 ng/ml) stimulated [3H]thymidine incorporation and increased DNA content of cultures. The effect was strongest when serum concentration was low (< or =1%) and was lost at high (> or =7.5%) serum concentrations. The EGF-induced effect on deoxynucleic acid synthesis was inhibited by transforming growth factor-beta and tyrphostin, a tyrosine kinase inhibitor that blocks the phosphorylation of tyrosine residues on EGF-R. Cultured rat articular chondrocytes possess a single class of high-affinity binding sites (Kd 0.18 nM). There were about 4.5 x 10(9) binding sites per microgram of DNA or about 37,800 binding sites per cell with 8.3 pg DNA per cell. Cultured cells contained EGF mRNA and EGF-R mRNA. Incubation of cells with EGF for 24 h decreased the EGF mRNA transcripts and increased the EGF-R mRNA levels. These findings suggest that EGF probably takes part in the regulation of chondrocyte activity under normal and presumably pathological conditions.
Migration ofAntigen-Specific T Cells Away from CXCR4-Binding Human ImmunodeficiencyVirus Type 1gp120

ABSTRACT Cell-mediated immunity depends in part on appropriate migration and localization of cytotoxic T lymphocytes (CTL), a process regulated by chemokines and adhesion molecules. Many viruses, including human immunodeficiency virus type 1 (HIV-1), encode chemotactically active proteins, suggesting that dysregulation of immune cell trafficking may be a strategy for immune evasion. HIV-1 gp120, a retroviral envelope protein, has been shown to act as a T-cell chemoattractant via binding to the chemokine receptor and HIV-1 coreceptor CXCR4. We have previously shown that T cells move away from the chemokine stromal cell-derived factor 1 (SDF-1) in a concentration-dependent and CXCR4 receptor-mediated manner. Here, we demonstrate that CXCR4-binding HIV-1 X4 gp120 causes the movement of T cells, including HIV-specific CTL, away from high concentrations of the viral protein. This migratory response is CD4 independent and inhibited by anti-CXCR4 antibodies and pertussis toxin. Additionally, the expression of X4 gp120 by target cells reduces CTL efficacy in an in vitro system designed to account for the effect of cell migration on the ability of CTL to kill their target cells. Recombinant X4 gp120 also significantly reduced antigen-specific T-cell infiltration at a site of antigen challenge in vivo. The repellant activity of HIV-1 gp120 on immune cells in vitro and in vivo was shown to be dependent on the V2 and V3 loops of HIV-1 gp120. These data suggest that the active movement of T cells away from CXCR4-binding HIV-1 gp120, which we previously termed fugetaxis, may provide a novel mechanism by which HIV-1 evades challenge by immune effector cells in vivo.
Increases in lung tissue expression of intercellular adhesion molecule-1 are associated with hyperoxic lung injury and inflammation in mice.

Lung injury caused by breathing enriched oxygen continues to be a major problem in clinical medicine. Experimentally, hyperoxic lung injury is characterized by pulmonary edema and associated neutrophil accumulation. Although extensively investigated, the mechanisms for neutrophil accumulation and the role of this accumulation in hyperoxic lung injury remain controversial. Intercellular adhesion molecule-1 (ICAM-1) is an adhesion molecule that when increased on endothelium by inflammatory cytokines leads to increased adhesion of neutrophils to the inflamed endothelium and transendothelial migration. The purpose of this study was to examine the role of inflammation in hyperoxia-induced lung injury by investigating ICAM-1 expression in the lungs of mice exposed to > 95% oxygen continuously. Lung tissue from mice exposed to > 95% oxygen was analyzed for ICAM-1 mRNA by slot blot analysis and for ICAM-1 protein expression. We also examined lungs from mice exposed to hyperoxia for up to 96 h by light microscopy to correlate pulmonary inflammation with ICAM-1 expression. We found that mRNA for ICAM-1 increased 56% over baseline after 48 h of exposure to hyperoxia, that ICAM-1 protein increased by more than 5-fold over baseline after 96 h of exposure to hyperoxia, and that lung inflammation and injury were not evident until 96 h of exposure. Our data demonstrate that exposure to hyperoxia causes an increase in ICAM-1 gene transcription and/or mRNA stability in mouse lungs, and that this increase is followed by an increase in ICAM-1 protein. (ABSTRACT TRUNCATED AT 250 WORDS)
Growth of Abused Children

While the identification of a growth-retarded or otherwise undernourished child suggests a diagnosis of child abuse or neglect, it is not certain that abused children from poor communities are less well nourished than children living in similar environments. The setting of this study -day care centers in an urban poor city—provided an opportunity to make this comparison with appropriate community-based controls. Measures of height, weight, and weight/height2 (Body Mass Index (BMI)) were compared for 196 children, 2 to 6 years of age, 53 of whom were victims of physical abuse. The data was adjusted for age, sex, and ethnicity using logistic regression analysis to determine occurence of wasting (weight for height <5th percentile) and stunting (height for age <5th percentile). Significantly more abused children (16.3%) showed wasting as compared to non-abused (0.7%) with abused children 16.6 times more likely to show wasting than non-abused (95% confidence limits on the Odds Ratio 1.9-145.0). While 11.6 percent of abused children showed stunting compared to 5.6 percent of non-abused, this difference was not significant when the data was adjusted for demographic factors. The BMI (15.02 kg/m2) for abused children was significantly less than that (15.9 kg/m2) for non-abused children (F = 8.11; p = 0.0049). In the present study, significant wasting as seen in acute malnutrition was found among abused children at diagnosis, suggesting that within an urban poor community the growth of children so identified does differ from the growth of children who are not abused.
Reversal of ultraviolet radiation‐induced immune suppression by recombinant interleukin‐12: suppression of cytokine production

Exposure to ultraviolet (UV) radiation, a complete carcinogen, suppresses the immune response. Data from a number of laboratories have indicated that one consequence of UV exposure is suppressed T helper type 1 (Th1) cell function with normal Th2 cell activation, resulting in a shift to a Th2‐like phenotype. The reversal of UV‐induced immune suppression and tolerance induction by recombinant interleukin‐12 (rIL‐12) supports this observation. The focus of this study was to determine the mechanism(s) by which rIL‐12 reverses UV‐induced immune suppression. Two possibilities were considered: up‐regulation of interferon‐γ (IFN‐γ) secretion by rIL‐12 and suppression of UV‐induced cytokine secretion by rIL‐12. To our surprise we found that the ability of rIL‐12 to overcome UV‐induced immune suppression was independent of its ability to up‐regulate IFN‐γ secretion. Rather, rIL‐12 suppressed the production of cytokines that are known to be important in UV‐induced immune suppression. Injecting UV‐irradiated mice with rIL‐12, or adding rIL‐12 to UV‐irradiated keratinocyte cultures suppressed IL‐10 secretion, in part by affecting the transcription of the IL‐10 gene. Furthermore, we found that rIL‐12 suppressed UV‐induced tumour necrosis factor‐α (TNF‐α) production. Because IL‐10 is involved in the UV‐induced suppression of delayed‐type hypersensitivity and TNF‐α in the UV‐induced suppression of contact allergy, these findings provide a mechanism to explain how rIL‐12 overcomes UV‐induced immune suppression in these related but different immune reactions. In addition, they suggest a novel mechanism by which rIL‐12 alters immune reactivity, direct suppression of cytokine secretion induced by UV radiation.
Fisp12/Mouse Connective Tissue Growth Factor Mediates Endothelial Cell Adhesion and Migration through Integrin αvβ3, Promotes Endothelial Cell Survival, and Induces Angiogenesis In Vivo

ABSTRACT Fisp12 was first identified as a secreted protein encoded by a growth factor-inducible immediate-early gene in mouse fibroblasts, whereas its human ortholog, CTGF (connective tissue growth factor), was identified as a mitogenic activity in conditioned media of human umbilical vein endothelial cells. Fisp12/CTGF is a member of a family of secreted proteins that includes CYR61, Nov, Elm-1, Cop-1/WISP-2, and WISP-3. Fisp12/CTGF has been shown to promote cell adhesion and mitogenesis in both fibroblasts and endothelial cells and to stimulate cell migration in fibroblasts. These findings, together with the localization of Fisp12/CTGF in angiogenic tissues, as well as in atherosclerotic plaques, suggest a possible role for Fisp12/CTGF in the regulation of vessel growth during development, wound healing, and vascular disease. In this study, we show that purified Fisp12 (mCTGF) protein promotes the adhesion of microvascular endothelial cells through the integrin receptor αvβ3. Furthermore, Fisp12 stimulates the migration of microvascular endothelial cells in culture, also through an integrin-αvβ3-dependent mechanism. In addition, the presence of Fisp12 promotes endothelial cell survival when cells are plated on laminin and deprived of growth factors, a condition that otherwise induces apoptosis. In vivo, Fisp12 induces neovascularization in rat corneal micropocket implants. These results demonstrate that Fisp12 is a novel angiogenic inducer and suggest a direct role for Fisp12 in the adhesion, migration, and survival of endothelial cells during blood vessel growth. Taken together with the recent finding that the related protein CYR61 also induces angiogenesis, we suggest that Fisp12/mCTGF and CYR61 comprise prototypes of a new family of angiogenic regulators that function, at least in part, through integrin-αvβ3-dependent pathways.
Knowledge and attitude toward interdisciplinary team working among obstetricians and gynecologists in teaching hospitals in South East Nigeria

Background Interdisciplinary team working could facilitate the efficient provision and coordination of increasingly diverse health services, thereby improving the quality of patient care. The purpose of this study was to describe knowledge of interdisciplinary team working among obstetricians and gynecologists in two teaching hospitals in South East Nigeria and to determine their attitude toward an interdisciplinary collaborative approach to patient care in these institutions. Methods This was a questionnaire-based cross-sectional study. Data analysis involved descriptive statistics and was carried out using Statistical Package for the Social Sciences software version 17.0 for Windows. Results In total, 116 doctors participated in the study. The mean age of the respondents was 31.9±7.0 (range 22–51) years. Approximately 74% of respondents were aware of the concept of interdisciplinary team working. Approximately 15% of respondents who were aware of the concept of interdisciplinary team working had very good knowledge of it; 52% had good knowledge and 33% had poor knowledge. Twenty-nine percent of knowledgeable respondents reported ever receiving formal teaching/training on interdisciplinary team working in the course of their professional development. About 78% of those aware of team working believed that interdisciplinary teams would be useful in obstetrics and gynecology practice in Nigeria, with 89% stating that it would be very useful. Approximately 77% of those aware of team working would support establishment and implementation of interdisciplinary teams at their centers. Conclusion There was a high degree of knowledge of the concept and a positive attitude toward interdisciplinary team working among obstetricians and gynecologists in the study centers. This suggests that the attitude of physicians may not be an impediment to implementation of a collaborative interdisciplinary approach to clinical care in the study centers.
Prognostic significance of grading in lung adenocarcinoma

Although grading has prognostic significance for many tumor types, a prognostically significant grading system for lung adenocarcinoma has not yet been established. The aim of this study was to evaluate histologic characteristics included in tumor grading systems, establish optimal cutoff values that have the strongest association with overall survival, and develop a grading system incorporating the histopathologic characteristics that the authors found to have prognostic significance in patients with lung adenocarcinoma.
Experimental model in vivo for quantitative assessment of bone resorption inhibition

Quantitative assessment of bone resorption inhibition in vivo is not easily accomplished; methods relying on a count of osteoclasts are questionable, and histomorphometric evaluation of the bone mass presents several technical problems as well. The authors developed a simple method to measure the inhibition of bone resorption by study of the proximal tibial metaphysis of growing rats: the height of the perichondrial bone ring was taken as an index of the balance between osteoblastic and osteoclastic activity because any agent that inhibits osteoclasts (without interference with osteoblasts) produces an increase in the height of this anatomical structure. Since the ring is well demarcated by surrounding tissues, its height can be measured with accuracy and used for quantitative assessment of bone resorption inhibition. This model was tested with salmon calcitonin, and it provides evidence in vivo that this hormone inhibits osteoclastic bone resorption.
Macular edema after cataract surgery in eyes without preoperative central-involved diabetic macular edema.

IMPORTANCE The incidence of development or worsening of macular edema (ME) is variable in eyes without diabetic ME (DME) undergoing cataract surgery. OBJECTIVE To estimate the incidence of central-involved ME 16 weeks following cataract surgery in eyes with diabetic retinopathy without definite central-involved DME preoperatively. DESIGN, SETTING, AND PARTICIPANTS In a multicenter, prospective, observational study, 293 participants with diabetic retinopathy without definite central subfield thickening on optical coherence tomography (OCT) underwent cataract surgery. EXPOSURE Cataract extraction surgery performed within 28 days of enrollment of eyes without DME in individuals with diabetes mellitus. MAIN OUTCOMES AND MEASURES Development of central-involved ME defined as the following: (1) OCT central subfield thickness of 250 μm or greater (time-domain OCT) or 310 μm or greater (spectral-domain OCT) with at least a 1-step increase in logOCT central subfield thickness preoperatively to the 16-week visit; (2) at least a 2-step increase in logOCT central subfield thickness preoperatively to the 16-week visit; or (3) nontopical treatment for ME received before the 16-week visit with either of the OCT criteria met at the time of treatment. RESULTS The median participant age was 65 years. The median visual acuity letter score was 69 letters (Snellen equivalent 20/40). Forty-four percent of eyes had a history of treatment for DME. Sixteen weeks postoperatively, central-involved ME was noted in 0% (95% CI, 0%-20%) of 17 eyes with no preoperative DME. Of eyes with non-central-involved DME, 10% (95% CI, 5%-18%) of 97 eyes without central-involved DME and 12% (95% CI, 7%-19%) of 147 eyes with possible central-involved DME at baseline progressed to central-involved ME. History of DME treatment was significantly associated with central-involved ME development (P < .001). CONCLUSIONS AND RELEVANCE In eyes with diabetic retinopathy without concurrent central-involved DME, presence of non-central-involved DME immediately prior to cataract surgery or history of DME treatment may increase the risk of developing central-involved ME 16 weeks after cataract extraction.
Secretory component mediates Candida albicans binding to epithelial cells.

OBJECTIVES Candida albicans attaches to oral surfaces via a number of mechanisms including adherence mediated by salivary components adsorbed to the C. albicans cell surface. Our goal was to identify the salivary molecules involved. MATERIALS AND METHODS Biotinylated salivary polypeptides that were bound by C. albicans were detected in extracts from washed, saliva-treated yeast cells by polyacrylamide gel electrophoresis and electroblot or immunoblot transfer analysis and purified by electroelution. Purified material was tested for the ability to promote the adherence of radiolabelled C. albicans yeast cells to cultured epithelial monolayers. RESULTS Three of the polypeptides bound by C. albicans cells were identified as components of secretory IgA, including secretory component. Using non-denaturing polyacrylamide gel electrophoresis, we demonstrated that secretory component could be detected in its free form in saliva, and was bound by yeast cells. Secretory component which was purified by electroelution from non-denaturing PAGE-separated saliva, without detectable complete IgA, promoted adherence of yeast cells to cultured epithelial monolayers in a dose-dependent fashion. CONCLUSION These results indicate that despite the inhibitory effect on adherence of IgA specific to C. albicans, IgA components, in particular secretory component, also promote binding to cultured epithelial monolayers.
Topological and Modulation Design of Three-Level Z-Source Inverters

This paper presents the development of two three-level cascaded Z-source inverters, whose output voltage can be stepped down or up unlike a traditional buck three-level inverter. The proposed inverters are designed using two three-phase voltage-source inverter bridges, supplied by two uniquely designed Z-source impedance networks. These three-phase bridges can either be cascaded at their dc sides to form a dc-link-cascaded Z-source inverter or at their ac outputs using single-phase transformers to form a dual Z-source inverter. The dc-link-cascaded inverter has the advantages of not using any clamping diodes and transformers, but does not have redundant switching states within a phase leg for equalizing switching losses among the power devices. This constraint limits the modulation options for the dc-link-cascaded inverter, and indeed, it can only be controlled using the modified carrier disposition technique with appropriate ldquoZ-source shoot-throughrdquo states inserted for achieving balanced voltage boosting and optimal ldquonearest-three-vectorsrdquo switching. On the other hand, the dual Z-source inverter with transformer isolation can be controlled using different modulation approaches due to the presence of redundant switching states within a phase leg. Particularly, using a modified phase-shifted-carrier (PSC) scheme with shoot-through states inserted, it is shown that the dual inverter can be implemented using only a single Z-source network, while still achieving the correct volt-sec average and switching loss equalization. This represents a significant reduction in cost, and can more than compensate for the slightly degraded spectral characteristics of the PSC scheme. To verify the theoretical concepts discussed, experimental testing has been performed with the captured results presented in a later section of the paper.
Tuberculous meningitis in adults – experience from Turkey

Background: The annual incidence of tuberculous meningitis (TM) is unknown. TM is a disease that still often results in residual sequelae, and has a mortality rate ranging between 15 and 51%. Experience of countries such as Turkey where drug‐resistant tuberculosis and TM are prevalent is important.