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Purpose. The research aims to address the challenges posed by the integration of diverse methods, focusing on data collection techniques and level of detail (LoD) considerations, which facilitates the creation of detailed 3D models. The CityGML standard is employed for its ability to represent complex urban features, adapted here for mining environments. Methodology. Combining Unmanned Aerial Vehicle (UAV) and Terrestrial Laser Scanning (TLS) technologies to collect data for open-pit and underground coal mines. These data are processed to generate point clouds, which are then used to create 3D models of mining structures using Sketchup and REVIT. Finally, these models are converted into the CityGML standard using FME SAFE software. Findings. Through the use of Unmanned Aerial Vehicle and Terrestrial Laser Scanning technologies, precise point cloud data for open-pit and underground structures are acquired. CityGML serves as a suitable framework for digital mine representation, offering standardized data organization and exchange. The proposed methodology optimizes data collection and processing procedures, ensuring accuracy and efficiency in model creation. Notably, the study introduces a nuanced approach to LoD selection, considering the complexity and specific requirements of different mining structures. Originality. The article innovatively combines UAV and TLS technologies with the CityGML standard to create comprehensive 3D GIS models for coal mines operating with both open-pit and underground methods, addressing the unique challenges of modeling diverse mining structures and terrain features. Practical value. The practical value of the article lies in its provision of a systematic approach using UAV and TLS technologies, coupled with the CityGML standard, to create accurate 3D GIS models for coal mines employing both open-pit and underground methods. This methodology enhances mine management efficiency, resource estimation accuracy, and safety assessment capabilities. [ABSTRACT FROM AUTHOR]

Dragon fruit branches are an abundant and underutilized waste released from the annual pruning of dragon fruit. In this study, dragon fruit branches were used for the first time as a raw material for producing magnetic biochar through one-pot pyrolysis. The results showed that zero-valent iron and magnetite particles were generated in the carbon matrix, providing a saturation magnetization of 5.92 emu/g. Due to FeCl3 activation, magnetic biochar possessed a total pore volume of 0.15 cm³/g and a specific surface area of 203 m²/g. Subsequently, magnetic biochar was explored as a catalyst for enhanced ozonation of sunset yellow. 95% of sunset yellow (50 ppm) was treated within 80 min at pH 7.0. From the calculation results using pseudo-first-order kinetics, the sunset yellow decolorization constant was improved by 79% by using the magnetic biochar catalyst compared to ozone alone. Overall, dragon fruit branch-derived magnetic biochar is a promising material, especially as a green catalyst, because of its magnetic separability and potential catalytic activity for the treatment of sunset yellow by ozone. [ABSTRACT FROM AUTHOR]

To establish the relationships between the fatty acid composition of adipose tissue in growing pigs and the intake of fatty acids, we performed a feeding trial and did a literature survey. Six groups of pigs were fed diets with variable combinations of corn, linseed and fish oil. After 38 days, biopsies of adipose tissue were analyzed for their contents of linoleic, α-linolenic, eicosapentaenoic and docosahexaenoic acid. For the four fatty acids, intake data and adipose tissue levels were also collected from the literature. Linear correlations were computed for the intake of each polyunsaturated fatty acid and its level in adipose tissue, the data set consisting of either the original results only or combined with literature figures. The observed strong correlations between dietary and fat tissue polyunsaturated fatty acids indicate that the fatty acid composition of the diet may be used as an index of the fatty acid composition of the diet, and vice versa. The regression equations presented can be used to steer the fatty acid composition of adipose tissue of growing pigs by the fatty acid composition of their diet.

Congenital hypothyroidism associated with thyroid hypoplasia can be caused by several genetic defects, including mutations in the TSHbeta-subunit, the TSH receptor, the G(s)alpha-subunit, and the transcription factor PAX8. Four girls with sporadic congenital hypothyroidism and hypoplastic thyroid glands were analyzed for mutations in PAX8 and TTF2 (FKHL15). Mutations in the coding region of the TSHbeta-subunit gene, the TSH receptor gene, and exons 8 and 9 of G(s)alpha had been excluded previously. Serum TSH concentrations were 150 mU/liter or more, TG levels were within normal limits, and thyroid autoantibodies were absent. Technetium scintigraphies did not reveal the presence of thyroid tissue, but ultrasonography documented hypoplastic, normally located glands. One patient was found to harbor a heterozygous transversion 119A-->C in exon 3 of PAX8 replacing a conserved glutamine by proline in the paired box domain (Q40P). Analysis of her family members revealed that her mother, who has a thyroid gland of normal size and mild, adult-onset autoimmune hypothyroidism, is also heterozygous for this mutation. Functional analyses of the PAX8 Q40P mutation showed impaired binding to a PAX8 response element and absent trans-activation of a thyroid peroxidase promoter luciferase reporter gene. These findings confirm the important role of PAX8 in the development of the thyroid, but they indicate that PAX8 gene mutations may have a variable penetrance or expressivity. The absence of mutations in the coding sequences of the analyzed genes in the three other patients supports the concept that the pathogenesis of congenital hypothyroidism associated with thyroid hypoplasia is diverse.

Objective: To determine the effects of synovial fluids (SF) on DNA binding activity of transcription factor nuclear factor-kappaB (NF-kappaB) in the Mono Mac 6 monocytic/macrophage cell line as a model for the interaction between SF and synovial tissue macrophages in arthritis., Methods: Mono Mac 6 cells were incubated with SF from the knee joints of human subjects with rheumatoid arthritis (RA), undifferentiated seronegative oligoarthritis, and osteoarthritis (OA). Nuclear extracts prepared from the Mono Mac 6 cells and RA synovial tissue were analyzed by electrophoretic mobility shift analysis (EMSA) for NF-kappaB DNA binding proteins., Results: Induction of NF-kappaB DNA binding by the p65(RelA)/p50 heterodimer was observed in response to incubation of Mono Mac 6 cells with SF (20% in culture medium) from 5 of 8 subjects with RA, 4 of 5 with OA, and none of 3 with undifferentiated seronegative oligoarthritis. Incubation of SF with neutralizing antibodies against tumor necrosis factor-alpha (TNF-alpha), but not antibodies against interleukin 6 (IL-6), significantly reduced the induction of p65/p50 binding activity in SF from subjects with RA and OA. Unexpectedly, a slowly migrating SF inducible NF-kappaB-binding complex was observed in EMSA of Mono Mac 6 cells after incubation with SF from 5 of 8 RA and 2 of 5 OA subjects. The induction of this complex by SF was not affected by neutralization of TNF-alpha or IL-6 in SF, and the complex was not inducible by TNF-alpha, IL-1beta, TNF-alpha/IL-1beta, IL-6, platelet derived growth factor, lipopolysaccharide, or tetradecanoyl phorbol acetate. The slowly migrating complex could not be supershifted with antibodies against NF-kappaB, Jun, or the transcriptional coactivators p300 or CBP. A NF-kappaB-binding complex with similar slow mobility was observed in nuclear extracts prepared from fresh human RA synovial tissue., Conclusion: Biological activity of TNF-alpha in SF from RA and OA subjects is capable of inducing p65/p50 NF-kappaB DNA binding activity in macrophages. A property of SF that is independent of TNF-alpha and other cytokines is responsible for the induction of a novel slowly migrating NF-kappaB-binding complex. Soluble mediators in SF of subjects with RA and OA can therefore modulate binding of nuclear proteins to the NF-kappaB binding site in macrophages and may play a role in inflammatory gene expression in arthritis.

cAMP mediates the effects of TSH by regulating thyroid follicular cell proliferation, differentiation, and function. To assess the functional importance of the cAMP response element binding protein (CREB) in thyroid follicular cell regulation in vivo, we targeted the expression of a dominant negative (DN) CREB isoform to the thyroid glands of transgenic mice using a tissue-specific promoter. Transgenic mice exhibited severe growth retardation and primary hypothyroidism. Serum levels of TSH were elevated 8-fold above normal levels, and T4 and T3 levels were low. Histologically, the mutant thyroid glands were characterized by poorly developed follicles that were heterogeneous in size with diminished colloid. Ciliated thyroid epithelial cells were observed in the transgenic thyroid glands, suggesting a failure of follicular cell differentiation. Consistent with this hypothesis, the DN CREB transgene inhibited the expression of an array of genes including thyroglobulin, thyroperoxidase, and the TSH receptor in semiquantitative RT-PCR experiments. Altered expression of the thyroid transcription factors Pax-8, TTF-1, and TTF-2 was also observed. These results demonstrate a critical role for CREB in thyroid growth, differentiation, and function in vivo.

1. The drugs used in the treatment of rheumatoid arthritis (RA) form a diverse group with unpredictable adverse effects, mostly weak efficacy and variable responses. Despite their differences, a common feature of many anti-inflammatory and disease-modifying anti-rheumatic drugs (DMARD) is inhibition of pro-inflammatory transcription factors, particularly nuclear factor (NF)-kappaB and activator protein (AP)-1. 2. The present brief review identifies those drugs capable of inhibiting transcription factors, particularly steroids, gold salts, D-penicillamine, cyclosporine A and possibly salicylates. 3. The newer biological inhibitors of tumour necrosis factor (TNF)-alpha and interleukin (IL)-1beta are capable of indirect inhibition of NF-kappaB activation, although even with these potent agents the problem of variability in response has not disappeared. 4. The development of selective inhibitors of the transcription factor NF-kappaB should have the benefit of the anti-inflammatory drugs and DMARD, both new and old. 5. It is hypothesized that this strategy will overcome much of the variability in the therapeutic response and adverse effects that limit the usefulness of the existing drugs in the treatment of RA.

Goiter (increased thyroid gland size) is more prevalent in women than men, even in areas where iodine levels in the diet are sufficient. We investigated a possible role of estrogen on thyroid follicular cell growth using rat FRTL-5 thyroid follicular cells as a model. Estrogen receptor-alpha (ERalpha) messenger RNA was present in FRTL-5 cells using a RT-PCR assay and was confirmed by Western blot analysis. An estrogen-responsive reporter gene was transfected into FRTL-5 cells to test the functionality of the endogenous ERs. Estradiol increased the activity of the reporter gene, and the antagonist, ICI182780, inhibited ER-dependent transcription. To extend this analysis, we examined the effect of estradiol on FRTL-5 cell growth. Estradiol increased FRTL-5 cell growth in a time- and concentration-dependent manner in either the absence or presence of TSH. Because iodine is known to inhibit thyroid cell growth, the effect of estradiol on the expression of the sodium/iodide symporter (NIS) was assessed as a potential target of estrogen action. Estradiol blocked TSH-induced NIS expression, and treatment of cells with estradiol and ICI182780 restored TSH-induced NIS expression to normal levels. These data demonstrate that FRTL-5 cells contain functional ERs that enhance cell growth and inhibit expression of the NIS. The demonstration of a direct effect of estradiol on thyroid follicular cells raises the possibility that it may play a role in the sexually dimorphic prevalence of goiter.

Sporadic congenital hypothyroidism is most commonly caused by developmental abnormalities of the thyroid gland. More rarely, it is due to defects in gene products involved in the regulation of the hypothalamic-pituitary-thyroid axis or thyroid hormone synthesis. Loss of function mutations in the thyrotropin (TSH) receptor have been shown to result in resistance to biologically active TSH. In complete resistance to TSH, the thyroid gland is hypoplastic and unable to synthesize and secrete sufficient amounts of thyroid hormones. In partial resistance, referred to as euthyroid hyperthyrotropinemia, the size of the gland and the thyroid hormone levels are normal at the expense of an elevated TSH. Four patients with sporadic congenital hypothyroidism and properly located hypoplastic thyroid glands were included in this study. Serum TSH concentrations were 150 mU/L or higher, serum thyroglobulin levels were within normal limits (6.1 to 8.2 ng/mL; normal range: 2.1 to 32 ng/mL), and thyroid autoantibodies were absent. The coding region of the TSHbeta subunit gene, the TSH receptor gene, and exons 8 and 9 of Gsalpha were analyzed by direct sequencing and found to be normal in all patients. One patient was heterozygous for a G to A transition in the TSHbeta gene resulting in a substitution of alanine by threonine at position -7 of the signal peptide. This substitution was also found in her euthyroid father. In addition, Southern analysis of the TSH receptor gene excluded major structural alterations. These findings support previous reports that indicate that TSH resistance is genetically heterogeneous. In addition to mutations in the TSH receptor or the Gsalpha genes, other genetic defects can lead to an identical phenotype. These observations also suggest that TSH receptor mutations might be a relatively rare cause of congenital thyroid hypoplasia.

The validation of a procedure designed to clean glass and stainless steel surfaces after exposure to the experimental anticancer drug losoxantrone is described. The cleaning procedure, using water and hypochlorite bleach, was validated using a wipe test and a high-performance liquid chromatography (HPLC) method developed to quantitate low levels of losoxantrone. The HPLC method is shown to be linear and reproducible (relative standard deviation (RSD): 7.1% or less), with a detection limit of 2 ng/ml. Recoveries of 71.0%, 50.1%, and 57.6% were reproducibly obtained from the wipe pads, glass plates, and stainless steel plates, respectively, at levels of 70-140 ng per 100 cm2. The cleaning procedure is shown to clean glass and stainless steel plates to less than 20 ng and 17 ng losoxantrone per 100 cm2, respectively. These results demonstrate the need to fully characterize the recovery of drugs from surfaces and swabs in order to properly validate cleaning procedures.

A fifty-three year old woman presented with pyoderma gangrenosum on the right buttock. She had associated intestinal symptoms, but repeated roentgenologic studies revealed no abnormalities. Local treatment with benzoyl peroxide (20 percent) lotion produced clearing of the cutaneous lesion in about six weeks.

Concomitant allergic reactions to manganese and cadmium sulfide developed in a patient in tattooed areas. Although the reaction to cadmium was elicited by sunlight, attempts to reproduce it with artificial long-wave ultraviolet light were unsuccessful.