We present a comprehensive theoretical study, using a semi-analytical model within the standard LCDM framework, of the photometric properties of the progenitors of present-day early-type galaxies in ...the redshift range $0 < z < 1$. We explore progenitors of all morphologies and study their characteristics as a function of the luminosity and local environment of the early-type remnant at $z = 0$. In agreement with previous studies, we find that, while larger early-types are generally assembled later, their luminosity-weighted stellar ages are typically older. In dense cluster-like environments, ~70 percent of early-type systems are “in place” by $z = 1$ and evolve without interactions thereafter, while in the field the corresponding value is ~30 percent. Averaging across all environments at z ~ 1, less than 50 percent of the stellar mass which ends up in early-types today is actually in early-type progenitors at this redshift, in agreement with recent observational work. The corresponding value is ~65 percent in clusters, due to faster morphological evolution in such dense environments. We develop probabilistic prescriptions which provide a means of including spiral (i.e. non early-type) progenitors at intermediate and high redshifts, based on their luminosity and optical colours. For example, we find that, at intermediate redshifts (z ~ 0.5), large (MV < -21.5), red ($B-V$ > 0.7) spirals have ~75–95 percent chance of being an early-type progenitor, while the corresponding probability for large blue spirals (MB < -21.5, $B-V$ < 0.7) is ~50–75 percent. The prescriptions developed here can be used to address, from the perspective of the standard model, the issue of “progenitor bias”, whereby the exclusion of late-type progenitors in observational studies can lead to inaccurate conclusions regarding the evolution of the early-type population over cosmic time. Finally, we explore the correspondence between the true “progenitor set” of the present-day early-type population – defined as the set of all galaxies that are progenitors of present-day early-types regardless of their morphologies – and the frequently used “red-sequence”, defined as the set of galaxies within the part of the colour–magnitude space which is dominated by early-type objects. We find that, while more massive members (MV ≤ -21) of the “red sequence” trace the progenitor set reasonably well, the relationship breaks down at fainter luminosities (MV ≥ -21). Thus, while the results of recent observational studies which exploit the red sequence are valid (since they are largely restricted to massive galaxies), more care should be taken when deeper observations (which will probe fainter luminosities) become available in the future.
Complexing processing of «red muds» (R.M.) - waste of bauxite reprocessing by the Bayer's method, is one of the important tasks of toxic industrial waste utilization. Studied the possibility of ...aluminum leaching from the R.M. which content reach 14 %, received from Bogoslovsky aluminum plant of JSC «Siberian-Urals Aluminium Company» by aqueous solutions of NaOH. The process was carried out at atmospheric pressure and temperatures near to the boiling point of leaching solutions with the utilization of the residual alkali. The time’s dependence of the aluminum leaching degree from the R.M. by aqueous solutions of NaOH passes through the maximum due to the formation of secondary precipitation of aluminum. The cause of secondary sedimentation is the interaction of silicon with aluminum with formation of insoluble aluminosilicates, for example, Nа2Аl2Si2O8·2Н2O. The conditions of leaching, under which the formation of stable aluminate solutions during the time do not form of secondary precipitations were established. The maximum achieved values of the aluminum leaching degree in autoclave-free conditions was reach 20-25 %. The removal of alkali and part of aluminum under the first stage of complexing processing of R.M. leads to their enrichment in iron. The cakes from aluminum leaching and next carbonate scandium leaching can be used for pyrometallurgical recovery of iron and slag, in which untreated elements are passed, including residual aluminum, scandium, sum of rare earth elements, titanium and zirconium. A significant decrease in the volume of slag opens more opportunities for further isolation their components by acidic methods.
PTEN is a tumor suppressor gene that is frequently mutated or deleted in a variety of human cancers including human gastric cancer. PTEN functions primarily as a lipid phosphatase and plays a key ...role in the regulation of the PI3 kinase/Akt pathway, thereby modulating cell proliferation and cell survival. On the other hand, the IGF system plays an important role in cell proliferation and cell survival via the PI3 kinase/Akt and MAP kinase pathways in many cancer cells. To characterize the impact of PTEN on the IGF-IGFR-IGFBP axis in gastric cancer, we overexpressed PTEN using an adenovirus gene transfer system in human gastric adenocarcinoma cells, SNU-484 and SNU-663, which lack PTEN. Overexpression of PTEN inhibited serum-induced as well as IGF-I-induced cell proliferation as compared to control cells. PTEN overexpression resulted in a significant decrease in the expression of IGF-I, -II, and IGF-IR. Interestingly, amongst the six IGFBPs, only IGFBP-3 was upregulated by PTEN, whereas IGFBP-4 and -6 were reduced. The IGFBP-3 promoter activity assay and Western immunoblotting demonstrate that PTEN regulates IGFBP-3 at the transcriptional level. In addition, the PI3 kinase inhibitor, LY294002, upregulates IGFBP-3 expression but downregulates IGF-I and IGF-II, indicating that PTEN controls IGFBP-3 and IGFs by an Akt-dependent pathway. These findings suggest that PTEN may inhibit antiapoptotic IGF actions not only by blocking the IGF-IGFR-induced Akt activity, but also by regulating expression of components of the IGF system, in particular, upregulation of IGFBP-3, which is known to exert antiproliferative effects through IGF-dependent and IGF-independent mechanisms in cancer cells.
We present the first measurements of the angular correlation function of galaxies selected in the far (1530 AA) and near (2310 AA) ultraviolet from the GALEX survey fields overlapping SDSS DR5 in low ...Galactic extinction regions. The area used covers 120 deg super(2) (GALEX Medium Imaging Survey) down to magnitude AB = 22, yielding a total of 100,000 galaxies. The mean correlation length is similar to 3.7 plus or minus 0.6 Mpc, and no significant trend is seen for this value as a function of the limiting apparent magnitude or between the GALEX bands. This estimate is close to that found from samples of blue galaxies in the local universe selected in the visible and similar to that derived at z unk 3 for LBGs with similar rest frame selection criteria. This result supports models that predict antibiasing of star-forming galaxies at low redshift and brings an additional clue to the downsizing of star formation at z < 1.
Depending on the experimental model, unmethylated CpG motifs in bacterial DNA or synthetic oligodeoxynucleotides (CpG DNA) either augment or antagonize BCR-induced signals in B cells. CpG DNA ...synergizes with BCR-induced proliferation and Ig production of mature B cells, but blocks BCR-mediated apoptosis of immature B cells. Here, we demonstrate using a murine B lymphoma cell line WEHI-231, which is a model for immature B lymphocytes, that CpG DNA augments BCR-mediated signals for the activation of mitogen-activated protein kinase (MAPK) kinase (MKK)3, MKK4 and MKK6, and their subsequent downstream effectors c-Jun N-terminal kinase (JNK) and p38, but does not enhance MEK1/2 or extracellular signal-regulated kinase (ERK) activation. CpG DNA- and BCR-mediated signals also synergize for the activation of transcription factors AP-1, NFAT and NF-kappaB, but not for cAMP-responsive elements binding factor. Synergistic activations of JNK and p38 contribute to the synergistic production of cytokines induced by CpG DNA- and BCR-mediated signals, but have little or no effect on the ability of CpG DNA to protect WEHI-231 cells from anti-IgM-induced growth arrest. In contrast, all three MAPK, JNK, ERK and p38, contribute to the synergistic induction of splenic mature B cell proliferation by CpG DNA and anti-IgM. These results indicate that CpG DNA- and BCR-mediated signals converge at the level of MKK, NF-kappaB and NFAT activation, and that MAPK have differential regulatory roles for CpG DNA-mediated cytokine production versus cell proliferation in splenic mature B cells and WEHI-231 cells.
Purpose: The objective of this study was to evaluate the therapeutic efficacy of the curcumin analogue L6H4 in attenuating liver fibrosis and alleviating insulin resistance in streptozotocin-induced ...diabetic rats. Methods: Male Sprague-Dawley rats were fed a high-fat diet to induce insulin resistance, followed by streptozotocin injection to induce diabetes. The rats were then treated with L6H4 for eight weeks. Body weight, metabolic parameters, liver function, and liver histopathology were evaluated. Immunohistochemistry was performed to assess the expression of TGF-pi, TIMP-2, and MMP-2 in liver tissues. Statistical analysis was conducted using one-way ANOVA and Spearman rank correlation test. Results: L6H4 treatment effectively reversed the weight gain associated with a high-fat diet and improved metabolic parameters in diabetic rats. Liver function markers, such as ALT and AST, were reduced after L6H4 treatment. Histological analysis showed improved liver morphology and reduced fibrosis in L6H4-treated rats. Electron microscopy revealed improved ultrastructural features of hepatocytes. Immunohistochemistry demonstrated downregulation of TGF-pi and TIMP-2 expression and restoration of MMP-2 expression in the liver tissue of L6H4-treated rats. Correlation analysis showed a significant positive correlation between TGF-beta1 and TIMP-2 expression. Conclusion: The findings suggest that L6H4 has therapeutic potential in attenuating liver fibrosis and alleviating insulin resistance in streptozotocin-induced diabetic rats. The hepatoprotective effect of L6H4 may be attributed to its anti-inflammatory properties and its ability to target molecules involved in fibrosis. Further research is warranted to explore the potential of L6H4 as a treatment option for nonalcoholic fatty liver disease and type 2 diabetes. Plain Language Summary: The versatile curcumin, derived from turmeric, has shown potential in treating type 2 diabetes (T2D) and its complications. However, its bioavailability is limited. This study evaluated the efficacy of L6H4, a curcumin analogue, in treating T2D-induced hepatic fibrosis in rats. The rats were fed a high-fat diet and injected with streptozotocin to induce T2D. L6H4 treatment for eight weeks reversed weight gain, abnormal liver function, and histological changes. The analogue reduced markers of T2D severity, including blood glucose, insulin levels, and insulin resistance. L6H4 also decreased liver fibrosis by reducing the expression of TGF-beta1 and TIMP-2 and increasing MMP-2 expression. These changes in protein expression were consistent with previous studies on liver fibrosis. The effects of L6H4 on MMP-2 and TIMP-2 expression in the liver of diabetic rats had not been observed before. Additionally, L6H4 exhibited anti-inflammatory properties and regulated the expression of key fibrosis-related proteins. The study suggests that L6H4 has the potential as a therapeutic candidate for treating diabetic hepatopathy. Further research is needed to elucidate the molecular mechanisms of action of L6H4 and other curcumin analogues in T2D and liver fibrosis. In conclusion, L6H4 shows promise as a curcumin analogue with hepatoprotective effects and the ability to modulate protein expression involved in liver fibrosis in T2D. Keywords: type 2 diabetic rats, curcumin analogue, L6H4, TIMP-2, MMP-2, TGF-beta1
Glycogen syntheis kinase (GSK-3) inhibitors are novel therapeutic agents for treating various types of cancer, such as breast, lung, and gastric cancer. No pathological changes have been found by the ...morphological examination of GSK-3.
This review describes recent procedures using GSK-3 inhibitors, primarily in treating colon carcinoma. Furthermore, it also explains the mechanism of action of different GSK-3 inhibitors in treating various types of cancers and proposes some additional mechanisms may be useful for further research on GSK-3 inhibitors for cancers, including colon carcinoma.
The majority of the cancerous and pre-cancerous lesions are stimulated by the transformation of membrane-bound arachidonic acid (AA) to eicosanoids, a transformation that promotes for the viability, proliferation, and spread of cancer. GSK-3 inhibitors can reinstate hostility to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) responsiveness in gastric adenocarcinoma cells. GSK-3, the final enzyme in glycogen synthesis, is a serine/threonine kinase that phosphorylates varied sequences that are more than a hundred in number, within proteins in an array of heterogeneous pathways. It is an essential module of an exceptionally large number of cellular processes, playing a fundamental role in many metabolic processes and diseases. Many patients diagnosed with colon cancer achieve long-term remission with outstanding survival through the GSK-3 inhibitors.
Prior to the extensive application of these proposed mechanisms of GSK-3 inhibitor, further evaluation and clinical studies are needed. Only after the completion of appropriate clinical studies and morphological examinations, would extensive application be apprpriate.
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