Engineering Surface Architectures for Improved Durability in III-V Photocathodes.

GaInP has shown promise as the wide bandgap top junction in tandem absorber photoelectrochemical (PEC) water splitting devices. Among previously reported dual-junction PEC devices with a GaInP top cell, those with the highest performance incorporate an AlInP window layer (WL) to reduce surface recombination and a thin GaInP capping layer (CL) to protect the WL from corrosion in electrolytes. However, the stability of these III-V systems is limited, and durability continues to be a major challenge broadly in the field of PEC water splitting.

A Spin Coating Method To Deposit Iridium-Based Catalysts onto Silicon for Water Oxidation Photoanodes.

Silicon has shown promise for use as a small band gap (1.1 eV) absorber material in photoelectrochemical (PEC) water splitting. However, the limited stability of silicon in acidic electrolyte requires the use of protection strategies coupled with catalysts.

A Ratiometric Sensor Using Single Chirality Near-Infrared Fluorescent Carbon Nanotubes: Application to In Vivo Monitoring.

Advances in the separation and functionalization of single walled carbon nanotubes (SWCNT) by their electronic type have enabled the development of ratiometric fluorescent SWCNT sensors for the first time. Herein, single chirality SWCNT are independently functionalized to recognize either nitric oxide (NO), hydrogen peroxide (H(2)O(2)), or no analyte (remaining invariant) to create optical sensor responses from the ratio of distinct emission peaks. This ratiometric approach provides a measure of analyte concentration, invariant to the absolute intensity emitted from the sensors and hence, more stable to external noise and detection geometry.

Effects of oleic acid and macrophage recruitment on cholesterol efflux in cell culture and in vivo.

Background And Aim: Monounsaturated fatty acids in diets are beneficial for the plasma lipoprotein profile, but studies in cell culture point out that they may also be detrimental by inhibiting cholesterol efflux to apo AI.

Methods And Results: In the present study we used mouse peritoneal macrophages, loaded with cholesterol and upregulated by cyclic AMP or by LXR/RXR ligands and compared the effect of oleic acid on cholesterol efflux to 3 different acceptors. Inhibition of cholesterol efflux by oleic acid ranged from 10 to 25% with HDL or 2.

Lower macrophage recruitment and atherosclerosis resistance in FVB mice.

The aim of this study was to compare some aspects of cholesterol accretion and cholesterol efflux in cellular components of the aortic wall derived from mice resistant or susceptible to atherosclerosis, FVB or C57BL, respectively. Cholesterol efflux, from cholesterol loaded smooth muscle cells or elicited macrophages, to apo A-I or HDL was similar in the two strains under basal conditions, and after cAMP or LXR upregulation. Recruitment of peritoneal macrophages, 3 days after thioglycollate injection, was 65% lower in FVB than in C57BL mice, commensurate with a 40% reduction in MCP-1 in peritoneal lavage.

LXR activation and cholesterol efflux from a lipoprotein depot in vivo.

Activation of LXR in cultured cells results in enhancement of cholesterol efflux to apo Al. To study cholesterol efflux, in vivo cationized LDL was injected into the rectus femoris muscle of mice to create a lipoprotein depot. LXR ligand TO901317, 10 mg/kg, was given by gavage for 8 days, starting 4 days after injection of the lipoprotein.

Calorie restriction in mice does not affect LDL reverse cholesterol transport in vivo.

Calorie restriction (CR) prolongs life in animals, but may reduce plasma HDL, important in reverse cholesterol transport (RCT). The effect of CR, 60% of an ad libitum (AL) diet, on cholesterol removal from rectus femoris muscle injected with cationized LDL, was studied in C57BL male mice. RCT in vivo, on CR and AL diet, and cholesterol efflux from macrophages exposed to CR or AL sera, was similar, despite a 22% reduction in plasma HDL-cholesterol (HDL-C).

In CCR2-/- mice monocyte recruitment and egress of LDL cholesterol in vivo is impaired.

Recruitment of macrophages plays an important role in initiation of atheroma, but their involvement in cholesterol clearance during regression is unknown. We developed a mouse model to quantitate cholesterol clearance from a depot of cationized LDL injected into a leg muscle, which evokes a sterile inflammatory reaction. In the CCR2(-/-) mice, cholesterol clearance was significantly slower than in C57BL controls because of decrease in cholesteryl ester (CE) hydrolysis, which is mandatory prior to cholesterol efflux.

Reverse cholesterol transport in mice expressing simian cholesteryl ester transfer protein.

The role of cholesteryl ester transfer protein (CETP) in atherogenesis remains ambiguous, as both pro and antiatherogenic effects have been described. Expression of CETP increases HDL-cholesteryl ester turnover, but there is no direct evidence whether CETP mobilizes cholesterol in vivo. The rate of cholesterol removal injected into a leg muscle as cationized low density lipoprotein (cat-LDL) was compared in CETP transgenic and control mice.

Macrophage cholesterol efflux to free apoprotein A-I in C3H and C57BL/6 mice.

Cholesterol efflux from peritoneal macrophages of mice C57BL/6 susceptible and C3H resistant to atherosclerosis was compared, using apoprotein A-I as acceptor. The elicited macrophages were labeled with 3H-cholesterol and cholesterol enriched by incubation for 24 h with acetylated LDL. After incubation for 6 or 24 h, 3H-cholesterol efflux to free apoA-I (10 microg/ml) was significantly higher with macrophages derived from C3H mice compared to C57BL/6 mice.

Effect of atherogenic diet on reverse cholesterol transport in vivo in atherosclerosis susceptible (C57BL/6) and resistant (C3H) mice.

Mice susceptible (C57BL/6) or resistant (C3H) to atherosclerosis induced by a high cholesterol-cholate containing diet (A-diet) were used to study reverse cholesterol transport (RCT) in vivo as measured by loss of cholesterol from a depot created by injection of cationized LDL into the rectus femoris muscle. Plasma total and HDL-cholesterol (HDL-C), total and HDL phospholipid (HDL-PL) levels in chow fed C3H male and female mice were higher than in C57BL/6 mice. After one month on A-diet, plasma cholesterol more than doubled in both strains and genders.

Macrophage cholesterol metabolism, apolipoprotein E, and scavenger receptor AI/II mRNA in atherosclerosis-susceptible and -resistant mice.

Female mice known to be susceptible (C57BL) and resistant (C3H and BALB/c) to diet-induced atherosclerosis were studied. Feeding of a cholate-containing atherogenic diet for 1 month resulted in an increase in plasma total cholesterol, little or no change in total phospholipids and high density lipoprotein (HDL) cholesterol, and a fall in HDL phospholipid, which was most pronounced in the C57BL strain. In elicited macrophages, cholesterol esterification was lower with acetylated low density lipoprotein (acLDL) and higher with beta-very low density lipoprotein (beta-VLDL) in C57BL than in C3H or BALB/C strains.

Clearance of cationized LDL cholesterol from a muscle depot is not enhanced in human apolipoprotein A-IV transgenic mice.

Human apolipoprotein A-IV (apoA-IV) transgenic mice fed an atherogenic diet were shown previously to develop less atherosclerosis than control mice. The question arose whether the antiatherogenic effect of human apoA-IV is due to enhancement of reverse cholesterol transport despite no increase in plasma high-density lipoprotein (HDL) cholesterol. We studied male and female mice overexpressing human apoA-IV and their wild-type (WT) controls, all of which were fed a chow diet.

High levels of human apolipoprotein A-I and high density lipoproteins in transgenic mice do not enhance efflux of cholesterol from a depot of injected lipoproteins. Relevance to regression of atherosclerosis?

The role of high density lipoprotein (HDL) and apolipoprotein A-I (apo A-I)in promoting cholesterol efflux from cultured cells and attenuation of development of atherosclerosis in transgenic (tg) animals has been well documented. The aim of the present study was to determine whether high levels of human (h) apo A-I will enhance cholesterol removal in vivo. h apo A-I in sera of tg mice was 429 +/- 18 and 308 +/- 10 mg/dl in male and female mice, the ratio of phospholipid (PL) to apo A-I was 0.

Dexamethasone impairs cholesterol egress from a localized lipoprotein depot in vivo.

Plasma high density lipoproteins play a central role in the prevention and regression of atherosclerosis, as they are known to promote egress of cholesterol from cells. Glucocorticoids increase plasma HDL, but enhance esterification of cholesterol in macrophages in vitro. A novel model to measure cholesterol egress from a well defined depot in vivo was used currently to study the effect of dexamethasone on reverse cholesterol transport.

Delayed loss of cholesterol from a localized lipoprotein depot in apolipoprotein A-I-deficient mice.

The anti-atherogenic role of high density lipoprotein is well known even though the mechanism has not been established. In this study, we have used a novel model system to test whether removal of lipoprotein cholesterol from a localized depot will be affected by apolipoprotein A-I (apo A-I) deficiency. We compared the egress of cholesterol injected in the form of cationized low density lipoprotein into the rectus femoris muscle of apo A-I K-O and control mice.

Cholesterol efflux in vivo from a depot of cationized LDL injected into a thigh muscle of small rodents.

We have developed a model system to measure quantitatively removal of cholesterol from a well-defined depot in vivo. To that end, lipoproteins were injected into the rectus femoris muscle of small rodents, using a 25 microliters Hamilton syringe and a 27-gauge needle. In most experiments, the injected volume was 10 microliters containing 200 micrograms of cholesterol.

Scavenger receptor activity and expression of apolipoprotein E mRNA in monocyte-derived macrophages of young and old healthy men.

The aim of this study was to compare some aspects of lipid metabolism in monocyte-derived macrophages isolated from young males, aged 18-24 years, and old males, aged 74-90 years, who were found healthy in accordance with the Senieur protocol. The parameters tested were metabolism of 125I-acetylated low-density lipoproteins (LDL) and oxidized LDL, incorporation of [3H]cholesterol into cholesteryl ester and expression of apolipoprotein E (apo E) mRNA. Cell association and degradation of 125I-acetylated LDL by macrophages of old and young subjects, respectively, was 15,978 +/- 2492 and 9300 +/- 1416 ng/mg cell protein per 24 h.

Effects of interactions of apolipoprotein A-II with apolipoproteins A-I or A-IV on [3H]cholesterol efflux and uptake in cell culture.

Conflicting evidence has accumulated with years regarding the putative negative effect of apolipoprotein A-II on apo A-I mediated cholesterol efflux. In this study, this question was reexamined and in addition to the interaction of apo A-II with apo A-I, its possible effect on apo E and apo A-IV was investigated as well. Free cholesterol (FC) donors were the main components of atheroma, namely, mouse peritoneal macrophages (MP), bovine aortic smooth muscle (SMC) and fibroblasts labeled with [3H]FC.

Effect of transforming growth factor-beta on lipoprotein lipase in rat mesenchymal heart cell cultures.

The effect of recombinant transforming growth factor-beta 2 (rTGF-beta 2) on lipoprotein lipase (LPL) synthesis was studied in mesenchymal rat heart cell cultures. Addition of rTGF-beta 2 to culture medium containing 20% serum resulted in a time-dependent decrease in LPL activity. With 10 ng/ml a 30% fall occurred after 12 h and only 20% of enzyme activity remained after 24 h with 5 or 10 ng/ml.

Murine macrophages secrete factors that enhance uptake of non-lipoprotein [3H]cholesteryl ester by aortic smooth muscle cells.

We have recently demonstrated that macrophage conditioned medium (MP medium) and beta VLDL enhance cholesterol esterification in cultured aortic smooth muscle cells by LDL receptor mediated and other pathways (Stein, O. et al. (1993) Arteroscl.

Macrophage-conditioned medium and beta-VLDLs enhance cholesterol esterification in SMCs and HSFs by LDL receptor-mediated and other pathways.

Thioglycolate-elicited mouse peritoneal macrophages were incubated for 24 hours in serum-free Dulbecco-Vogt medium containing 0.5% fatty acid-poor bovine serum albumin. This conditioned medium, designated MP medium, was used for experiments with bovine aortic smooth muscle cells (SMCs) or human skin fibroblasts (HSFs).

Can lipoprotein lipase be the culprit in cholesteryl ester accretion in smooth muscle cells in atheroma?

Bovine aortic smooth muscle cells and human skin fibroblasts were incubated with beta-very low density lipoprotein (beta VLDL) isolated from cholesterol-fed rabbits and labeled with [3H]cholesteryl oleate. Addition of lipoprotein lipase resulted in a 3.2-4.

Persistence of increased cholesteryl ester in human skin fibroblasts is caused by residual exogenous sphingomyelinase and is reversed by phospholipid liposomes.

Human skin fibroblasts (HSF) were exposed to sphingomyelinase 50 or 5 mU/ml for 60 min, washed with 5 mM EDTA or 20% serum and with phosphate-buffered saline, and postincubated for 24 h in the presence of [14C]16:0 sphingomyelin (SP) liposomes. The recovery of up to 48% of label in the medium in ceramide provided evidence of persistence of sphingomyelinase activity. The rate of hydrolysis of [14C]16:0 SP remained the same irrespective of whether the liposomes were added immediately after the wash, or 3 or 6 h thereafter.