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41.
Sowmya H. Reddy Sumanth K. Kambalimath Rajesh K. Singhal Manjunath K. Chikkakariyappa Raveendran Muthurajan Mavinahalli P. Rajanna Rohini Sreevathsa Amitha M. Sevanthi Trilochan Mohapatra Neelamraju Sarla Viswanathan Chinnusamy Gopala S. Krishnan Ashok K. Singh Nagendra K. Singh Rameshwar P. Sharma Sreeman M. Sheshshayee 《Physiologia plantarum》2019,166(2):596-611
42.
Reddy RE Pan Y Johnson DD Chen YY Datwyler SA Hauptman MS Thottathil JK 《Bioorganic & medicinal chemistry》2005,13(10):3467-3473
An efficient method was developed for the preparation of polyanionic affinity agent (3), a key component in the measurement of glycated hemoglobin (GHb). Glycated hemoglobin is an important clinical marker for diagnosis of patients with diabetes and useful to monitor the management of disease. The affinity agent (3) was prepared based on coupling reaction between poly(acrylic acid) (1) and 3-aminophenylboronic acid (2) in water. The critical features of this polymeric affinity agent (3), such as size, boronic acid incorporation ratio and concentration, on the measurement of glycated hemoglobin were evaluated. It was found that the agent (3) prepared using poly(acrylic acid) (1) with 225 kDa molecular weight gave optimal GHb measurement. The performance test results demonstrated that the boronic acid incorporation ratio and concentration of affinity agent (3) play a critical role in the assay and determines the precision of glycated hemoglobin measurement. 相似文献
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Globoid-cell Leukodystrophy (GLD; Krabbe’s disease) is a rapidly progressing inherited demyelinating disease caused by a deficiency of the lysosomal enzyme Galactosylceramidase (GALC). Deficiency of GALC leads to altered catabolism of galactosylceramide and the cytotoxic lipid, galactosylsphingosine (psychosine). This leads to a rapidly progressive fatal disease with spasticity, cognitive disability and seizures. The murine model of GLD (Twitcher; GALC−/−) lacks the same enzyme and has similar clinical features. The deficiency of GALC leads to oligodendrocyte death, profound neuroinflammation, and the influx of activated macrophages into the CNS. We showed previously that keratinocyte chemoattractant factor (KC) is highly elevated in the CNS of untreated Twitcher mice and significantly decreases after receiving a relatively effective therapy (bone marrow transplantation combined with gene therapy). The action of KC is mediated through the CXCR2 receptor and is a potent chemoattractant for macrophages and microglia. KC is also involved in oligodendrocyte migration and proliferation. Based on the commonalities between the disease presentation and the functions of KC, we hypothesized that KC and/or CXCR2 contribute to the pathogenesis of GLD. Interestingly, the course of the disease is not significantly altered in KC- or CXCR2-deficient Twitcher mice. There is also no alteration in inflammation or demyelination patterns in these mice. Furthermore, transplantation of CXCR2-deficient bone marrow does not alter the progression of the disease as it does in other models of demyelination. This study highlights the role of multiple redundant cytokines and growth factors in the pathogenesis of GLD. 相似文献
46.
Our previous studies have shown that benzyl isothiocyanate (BITC) suppresses pancreatic tumor growth by inhibiting STAT-3; however, the exact mechanism of tumor growth suppression was not clear. Here we evaluated the effects and mechanism of BITC on pancreatic tumor angiogenesis. Our results reveal that BITC significantly inhibits neovasularization on rat aorta and Chicken-Chorioallantoic membrane. Furthermore, BITC blocks the migration and invasion of BxPC-3 and PanC-1 pancreatic cancer cells in a dose dependant manner. Moreover, secretion of VEGF and MMP-2 in normoxic and hypoxic BxPC-3 and PanC-1 cells was significantly suppressed by BITC. Both VEGF and MMP-2 play a critical role in angiogenesis and metastasis. Our results reveal that BITC significantly suppresses the phosphorylation of VEGFR-2 (Tyr-1175), and expression of HIF-α. Rho-GTPases, which are regulated by VEGF play a crucial role in pancreatic cancer progression. BITC treatment reduced the expression of RhoC whereas up-regulated the expression of tumor suppressor RhoB. STAT-3 over-expression or IL-6 treatment significantly induced HIF-1α and VEGF expression; however, BITC substantially suppressed STAT-3 as well as STAT-3-induced HIF-1α and VEGF expression. Finally, in vivo tumor growth and matrigel-plug assay show reduced tumor growth and substantial reduction of hemoglobin content in the matrigel plugs and tumors of mice treated orally with 12 μmol BITC, indicating reduced tumor angiogenesis. Immunoblotting of BITC treated tumors show reduced expression of STAT-3 phosphorylation (Tyr-705), HIF-α, VEGFR-2, VEGF, MMP-2, CD31 and RhoC. Taken together, our results suggest that BITC suppresses pancreatic tumor growth by inhibiting tumor angiogenesis through STAT-3-dependant pathway. 相似文献
47.
M. Bhushana Reddy S. Sailaja K. Vemasevana Raju C. Nageswara Raju P. Giridhar B. Vengala Rao B. Sudhakar Reddy 《Luminescence》2011,26(6):680-684
Rare earth ions (Eu3+ or Tb3+)‐activated Ca3 Ga2 Si3O12 (CaGaSi) phosphors were synthesized by using a sol–gel method. Photoluminescence spectra of Eu3+:CaGaSi phosphors exhibited five emission bands at 578, 592, 612, 652 and 701 nm, which were assigned to the transitions (5D0 → 7F0, 7F1, 7F2, 7F3 and 7F4), respectively, with an excitation wavelength of λexci = 392 nm. Among these, the transition 5D0 → 7F2 (612 nm) displayed bright red emission. In the case of Tb3+:CaGaSi phosphors, four emission bands were observed at 488 (5D4 → 7F6), 543 (5D4 → 7F5), 584 (5D4 → 7F4) and 614 nm (5D4 → 7F3) from the measurement of PL spectra with λexci = 376 nm. Among these, the transition 5D4 → 7F5 at 543 nm displayed bright green emission. The structure and morphology of the phosphors were studied from the measurements of X‐ray diffraction (XRD), scanning electron microscopy (SEM) and energy‐dispersive X‐ray analysis (EDAX) results. Copyright © 2011 John Wiley & Sons, Ltd. 相似文献
48.
A quantitative, atom-based, method is described for comparing protein subunit interfaces in icosahedral virus capsids with quasi-equivalent surface lattices. An integrated, normalized value (between 0 and 1) based on equivalent residue contacts (Q-score) is computed for every pair of subunit interactions and scores that are significantly above zero readily identify interfaces that are quasi-equivalent to each other. The method was applied to all quasi-equivalent capsid structures (T=3, 4, 7 and 13) in the Protein Data Bank and the Q-scores were interpreted in terms of their structural underpinnings. The analysis allowed classification of T=3 structures into three groups with architectures that resemble different polyhedra with icosahedral symmetry. The preference of subunits to form dimers in the T=4 human Hepatitis B virus capsid (HBV) was clearly reflected in high Q-scores of quasi-equivalent dimers. Interesting differences between the classical T=7 capsid and polyoma-like capsids were also identified. Application of the method to the outer-shell of the T=13 Blue tongue virus core (BTVC) highlighted the modest distortion between the interfaces of the general trimers and the strict trimers of VP7 subunits. Furthermore, the method identified the quasi 2-fold symmetry in the inner capsids of the BTV and reovirus cores. The results show that the Q-scores of various quasi-symmetries represent a "fingerprint" for a particular virus capsid architecture allowing particle classification into groups based on their underlying structural and geometric features. 相似文献
49.
Oral pathogens have created a menace in recent years due to biofilm formation and antimicrobial drug resistance. The current treatment strategy works well with antibiotics. However, constant use of antibiotics creates a selective pressure, which increases adaptability of the pathogens. Therefore, it is of interest to analyze the potential targets of genistein in dental pathogens using computer aided prediction tools. 相似文献
50.
K. M. Bhaskara Reddy Dokka Mallikarjunasarma Kamana Bulliraju Vanjivaka Sreelatha Y. Bharathi Kumari Ramesh Dandala Kuppanna Ananda 《International journal of peptide research and therapeutics》2011,17(2):113-121