Mcmanusmeyers4415

In conclusion, HTG stably grafts native and processed celluloses to xyloglucan-oligosaccharides, which may carry valuable 'cargoes', exemplified by sulphorhodamine. We thus demonstrate HTG's biotechnological potential to modify various cellulose-based substrates such as textiles, pulps, papers, packaging, sanitary products and hydrogels.

Marine macroalgae known for its polysaccharides exhibit potent biomedical properties and its potential as an anti-inflammatory agent has increased in the recent past as inflammation is a major pathology noted in many chronic diseases.

The present study investigates the anti-inflammatory potential of a sulfated polysaccharide (PS) isolated from the marine algae Turbinaria ornata collected from the Indian waters on LPS induced inflammation in RAW 264.7 macrophages.

PS isolated from the macroalgae was characterized using ESI(MS) and was screened for its antioxidant and anti-inflammatory potential in RAW 264.7 cells by assessing markers of oxidative stress, and inflammation.

LPS significantly increased the levels of LPO and LDH in RAW 264.7 cells which were significantly reduced in PS pre-treatment groups. Pretreatment significantly increased the antioxidants GSH and SOD and significantly reduced mRNA levels of IL6 and TNFα in vitro confirming its anti-inflammatory potential. NFκB and iNOS were significantly modulated by PS confirming the probable mode of action.

Altogether, it can be concluded that PS isolated from Turbinaria ornata collected from the Southeast Coast of India exhibits antioxidant and anti-inflammatory potential probably mediated by the sulfated polysaccharide containing glucopyranose and fucopyranose moieties.

Altogether, it can be concluded that PS isolated from Turbinaria ornata collected from the Southeast Coast of India exhibits antioxidant and anti-inflammatory potential probably mediated by the sulfated polysaccharide containing glucopyranose and fucopyranose moieties.Biopolymers-based nanoparticles delivery emerged alternatively to improve nutraceuticals and drug bioavailability. The intestinal physiology suggested a prerequisite of lipid moiety for carotenoid absorption. This study aimed to fabricate chitosan-based nanoparticles with phosphatidylcholine (PC) to enhance lutein bioavailability. Lutein encapsulated chitosan nanoparticles with PC (LCNPC) or without PC (LCN) were assessed for bioaccessibility, sustain release, cellular uptake/internalization, and basolateral secretion of lutein in Caco-2 cells. Standard lutein mixed micelles (LMM), and micelles derived through in vitro digestion of green leafy vegetables (GMM) treated as controls. The LCNPC showed reduced particle size, higher colloidal stability, homogeneous dispersion, and suitable for oral administration compared to LCN. The cellular uptake of lutein (20 h) in LCNPC was higher than LCN, LMM, and GMM, respectively. Interestingly, lutein uptake was maximum at 8 h in LMM and gradually decreased against sustain-release response in LCNPC and LCN, whereas considerably low lutein uptake from GMM at all time points. Further, LCNPC significantly increased basolateral secretion of triglyceride (TG) and positively correlated enhanced lutein uptake/internalization process than LCN and micelles. Also, LCNPC demonstrated the upregulation of endocytosis, paracellular, scavenger receptor class B type 1 (SRB-1), and peroxisome proliferator-activated receptor gamma (PPARγ) mediated lutein transport mechanism. These results suggested that fabrication of biopolymer-based nanoparticles with PC could provide greater insight to improve lutein bioavailability at enterocyte levels, to avoid age-related macular degeneration and other chronic diseases.

In 2012, the KDIGO group proposed new definitions for acute kidney injury (AKI), acute kidney disease (AKD) and chronic kidney disease (CKD). According to the definition adapted by the International Club of Ascites, AKI has been extensively investigated in patients with cirrhosis. On the contrary, there are currently no data on the epidemiology and clinical outcomes associated with AKD. The aim of the study was to assess the prevalence and the impact of AKD on the clinical course and survival of patients with cirrhosis.

A total of 272 consecutive patients with cirrhosis attending our outpatient clinic were included in the study. Clinical and laboratory data were collected at inclusion. Patients were followed-up until death, liver transplant or the end of follow-up.

During follow-up, 80 patients developed AKD (29.4%). Forty-two (52.5%) recovered from the first episode of AKD and 26 maintained a normal renal function up to the end of follow-up. Sixteen patients developed a second episode of AKD. Globally, impact on survival.

Renal impairment has a very negative impact on patients with cirrhosis. Renal impairment seems to be characterized by a very dynamic course, which is defined according to renal function and length of the impairment as acute kidney injury, acute kidney disease and chronic kidney disease. The role of acute kidney disease is currently unknown. Our study shows for the first time that acute kidney disease is frequent in patients with cirrhosis and has a very negative impact on survival.

Mutational profiling of patient tumors has suggested that hepatocellular carcinoma (HCC) development is mainly driven by loss-of-function mutations in tumor suppressor genes. selleck kinase inhibitor p90 ribosomal S6 kinase 2 (RSK2) functions as a direct downstream kinase of ERK1/2 and elevated RSK2 expression has been reported to support oncogenic functions in some cancers. We investigated if RSK2 was also dysregulated by inactivating mutations in cancers including HCC.

We performed exome sequencing and targeted DNA sequencing on HBV-associated HCCs to examine recurrent RSK2 mutations. The functional significance and mechanistic consequences of RSK2 mutations were examined in natural RSK2-null HCC cells, and RSK2-knockout HCC cells. The potential downstream pathways underlying RSK2 mutations were investigated by RNA sequencing, qRT-PCR and mass spectrometry.

We detected recurrent somatic RSK2 mutations at a rate of 6.3% in our HCC cohorts and revealed that, among many cancer types, HCC was the cancer most commonly harboring RSK2 mutations.