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The results may have applications of drug design for colon targeting. A series of novel chiral 14 urea, thiourea and squaramide stereoisomers possessing carbohydrate backbones as well as amide functional groups was synthesized and characterized by their, 1H NMR, 13C NMR, FT-IR, HRMS, optical rotation, and melting points. Their antiproliferative activities were investigated against HeLa and PC3 cell lines. The compounds 9, 11 and 12 showed better activities at 25 μM against PC3 cell line with respect to the standard 5-fluorouracil (5-FU). Especially, the compounds 9 and 11 showed higher activities than the standard 5-FU even at low concentration (5 μM) against HeLa cell line. IC50 results also confirm these activities. The compounds 9, 10 and 11 have the IC50 values of 1.10 μM, 1.51 μM and 1.02 μM, respectively while 5-FU has 2.51 μM. Moreover, their cytotoxicity tests have proven that their viabilities were in between 50% and 100%. Chitosan is an organic compound widely used in biomedical and agricultural fields due to its medicinal values. Chitosan is the largest biopolymer after cellulose and it is used as a food supplement as well as a primary health care product. The focus of the present study is to optimize the method for isolation and characterization of chitosan from Omani shrimp shell. The chitosan was isolated chemically from shrimp waste through the chemical processes of demineralization, deproteinization, discoloration and deacetylation. Chitosan isolation was done using hydrochloric acid (HCl), sodium hydroxide (NaOH) and hydrogen peroxide (H2O2) at various concentrations and temperatures during the demineralization, the deproteinization, and the deacetylation processes. A total of twenty-seven samples were run in triplicate and used to isolate chitin from shrimp shell and then different methods of deacetylation were done to extract chitosan. The research was conducted by changing three variables such as the concentration of acid and base and temperature. The coarse powder shrimp waste samples were demineralized by varying the concentrations ranging from 3 to 9% of HCl and at the temperature range between 25 and 55 °C. The demineralized samples were treated with different concentrations of NaOH ranging from 20 to 60% and at the temperature range from 85 to 110 °C to deproteinize the samples. The optimal method for chitin isolation was selected by using FT-NIR spectroscopy. The optimal experimental conditions according to the present study were 3% HCl at 25 °C for an hour demineralization and 50% NaOH at 110 °C for 3 h deproteinization with a yield of 53.313%. Finally, the isolated chitin was decolorized by treatment with 30% H2O2 for 3 h then deacetylatised with 50% NaOH for 15 min. The weight loss was 0.29 gm/5 gm. In conclusion, shrimp waste could be a natural alternative source for the production of chitin. Furthermore, it could be used in medical, pharmaceutical, and biotechnology sectors. Hypoxia, a common characteristic in solid tumors, is found in phenotypically aggressive cancers that display resistance to typical cancer interventions. Due to its important role in tumor progression, tumor hypoxia has been considered as a primary target for cancer diagnosis and treatment. An advantage of hypoxia-activated nanomedicines is that they are inactive in normoxic cells. In hypoxic tumor tissues and cells, these nanomedicines undergo reduction by activated enzymes (usually through 1 or 2 electron oxidoreductases) to produce cytotoxic substances. In this review, we will focus on approaches to design nanomedicines that take advantage of tumor hypoxia. These approaches include i) inhibitors of hypoxia-associated signaling pathways; ii) prodrugs activated by hypoxia; iii) nanocarriers responsive to hypoxia, and iv) bacteria mediated hypoxia targeting therapy. These strategies have guided and will continue to guide nanoparticle design in the near future. These strategies have the potential to overcome tumor heterogeneity to improve the efficiency of radiotherapy, chemotherapy and diagnosis. Neuroinflammation plays an active role in the pathogenesis of several neurodegenerative diseases, including Parkinson's disease (PD). Earlier studies from this laboratory showed that glia maturation factor (GMF), a proinflammatory mediator; is up-regulated in the brain in neurodegenerative diseases and that deficiency of GMF showed decreased production of IL-1β and improved behavioral abnormalities in mouse model of PD. However, the mechanisms linking GMF and dopaminergic neuronal death have not been completely explored. In the present study, we have investigated the expression of NLRP3 inflammasome and caspase-1 in the substantia nigra (SN) of human PD and non-PD brains by immunohistochemistry. Wild-type (WT) and GMF-/- (GMF knock-out) mice were treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydro pyridine (MPTP) and the brains were isolated for neurochemical and morphological examinations. NLRP3 and caspase-1 positive cells were found significantly increased in PD when compared to non-PD control brains. selleck Moreover, GMF co-localized with α-Synuclein within reactive astrocytes in the midbrain of PD. Mice treated with MPTP exhibit glial activation-induced inflammation, and nigrostriatal dopaminergic neurodegeneration. Interestingly, increased expression of the inflammasome components in astrocytes and microglia observed in the SN of MPTP-treated WT mice were significantly reduced in GMF-/- mice. Additionally, we show that NLRP3 activation in microglia leads to translocation of GMF and NLRP3 to the mitochondria. We conclude that downregulation of GMF may have beneficial effects in prevention of PD by modulating the cytotoxic functions of microglia and astrocytes through reduced activation of the NLRP3 inflammasome; a major contributor of neuroinflammation in the CNS. Follistatin-like protein 1 (FSTL1) showed overexpression in the inflammatory synovial pannus, serum, and synovial tissues of osteoarthritis (OA) patients. However, FSTL1 knock out (KO) embryos exhibited reduced vertebral cartilage cellularity, extensive skeleton defects and reduced MSCs proliferation. Thus, the role of FSTL1 in chondrocyte proliferation is not completely understood. In vitro studies revealed that Human recombinant FSTL1 (hFSTL1) promoted chondrogenic signals in the MSCs and cell viability only at low concentrations. Recent reports suggest that high levels of FSTL-1 are proposed to enhance inflammatory signals which suppress chondrogenesis leading to cartilage destruction. Altogether, FSTL1 has the potential to promote MSC proliferation and chondrogenic differentiation in a low concentration-dependent manner. However, the mechanism by which FSTL-1 affects MSCs chondrogenic differentiation and chondrogenesis remains unknown. Therefore, this review introduces a deep discussion of FSTL1's molecular functions in the OA pathophysiology, which will contribute to the deep understanding of FSTL1 molecular activity in the OA pathogenesis.
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