Polycrystalline Transparent Al-Doped ZnO Thin Films for Photosensitivity and Optoelectronic Applications.

Thin nanocrystalline transparent Al-doped ZnO (1-10 at.% Al) films were synthesized by solid-phase pyrolysis at 700 °C. Synthesized Al-doped ZnO films were investigated by X-ray diffraction (XRD), scanning and transmission electron microscopy (SEM, TEM). All obtained materials were crystallized into the wurtzite structure, which was confirmed by XRD. The material crystallinity decreases with the introduction of aluminum. SEM and TEM showed that the films are continuous and have a uniform distribution of nanoparticles with an average size of 15-20 nm. TEM confirmed the production of Al-doped ZnO films. The transmittance of Al-doped ZnO films in the range of 400-1000 nm is more than 94%. The introduction of 1% Al into ZnO leads to a narrowing of the band gap compared to ZnO to a minimum value of 3.26 eV and a sharp decrease in the response time to the radiation exposure with a wavelength of 400 nm. An increase in aluminum concentration leads to a slight increase in the band gap, which is associated with the Burstein-Moss effect. The minimum response time (8 s) was shown for film containing 10% Al, which is explained by the shortest average lifetime of charge carriers (4 s).

Nanocomposite Co3O4-ZnO Thin Films for Photoconductivity Sensors.

Thin nanocomposite films based on zinc oxide (ZnO) added with cobalt oxide (Co3O4) were synthesized by solid-phase pyrolysis. According to XRD, the films consist of a ZnO wurtzite phase and a cubic structure of Co3O4 spinel. The crystallite sizes in the films increased from 18 nm to 24 nm with growing annealing temperature and Co3O4 concentration. Optical and X-ray photoelectron spectroscopy data revealed that enhancing the Co3O4 concentration leads to a change in the optical absorption spectrum and the appearance of allowed transitions in the material. Electrophysical measurements showed that Co3O4-ZnO films have a resistivity up to 3 × 104 Ohm∙cm and a semiconductor conductivity close to intrinsic. With advancing the Co3O4 concentration, the mobility of the charge carriers was found to increase by almost four times. The photosensors based on the 10Co-90Zn film exhibited a maximum normalized photoresponse when exposed to radiation with wavelengths of 400 nm and 660 nm. It was found that the same film has a minimum response time of ca. 26.2 ms upon exposure to radiation of 660 nm wavelength. The photosensors based on the 3Co-97Zn film have a minimum response time of ca. 58.3 ms versus the radiation of 400 nm wavelength. Thus, the Co3O4 content was found to be an effective impurity to tune the photosensitivity of radiation sensors based on Co3O4-ZnO films in the wavelength range of 400-660 nm.

Recycling of Epoxy/Fiberglass Composite Using Supercritical Ethanol with (2,3,5-Triphenyltetrazolium)2[CuCl4] Complex.

The widespread use of polymer composite materials (PCM) leads to an increase in non-recyclable waste. This paper discusses the feasibility of recycling fiberglass with an epoxy matrix by solvolysis in ethanol under supercritical conditions. The solvolysis process completes successfully within four hours in an environment of a pure solvent containing 10% water at a temperature of 280 °C when the solvent passes into the supercritical state. The treatment time increases up to 10 h at a process temperature of 250 °C. When using a coordination compound of copper(II) chloride with organic chloride salt having 2,3,5-triphenyltetrazolium as the counterion, having the composition of (2,3,5-triphenyltetrazolium)2[CuCl4], the treatment time is reduced. The addition of the complex of 5% by weight makes it possible to completely remove the epoxy matrix at a temperature of 250 °C for two hours. The products separated from the solvolysis liquid were studied by infrared spectroscopy. The resulting fibers were examined by thermogravimetric analysis and scanning electron microscopy. The residual strength of the recovered fibers is 98%. Thus, the resulting fibers can be reused in the composite industry. Including both for the production of decorative products and for the production of structural products made of polymer composite materials.

High Gas Sensitivity to Nitrogen Dioxide of Nanocomposite ZnO-SnO2 Films Activated by a Surface Electric Field.

Gas sensors based on the multi-sensor platform MSP 632, with thin nanocomposite films based on tin dioxide with a low content of zinc oxide (0.5-5 mol.%), were synthesized using a solid-phase low-temperature pyrolysis technique. The resulting gas-sensitive ZnO-SnO2 films were comprehensively studied by atomic force microscopy, Kelvin probe force microscopy, X-ray diffraction, scanning electron microscopy, transmission electron microscopy, scanning transmission electron microscopy, energy dispersive X-ray spectrometry, and X-ray photoelectron spectroscopy. The obtained films are up to 200 nm thick and consist of ZnO-SnO2 nanocomposites, with ZnO and SnO2 crystallite sizes of 4-30 nm. Measurements of ZnO-SnO2 films containing 0.5 mol.% ZnO showed the existence of large values of surface potential, up to 1800 mV, leading to the formation of a strong surface electric field with a strength of up to 2 × 107 V/cm. The presence of a strong surface electric field leads to the best gas-sensitive properties: the sensor's responsivity is between two and nine times higher than that of sensors based on ZnO-SnO2 films of other compositions. A study of characteristics sensitive to NO2 (0.1-50 ppm) showed that gas sensors based on the ZnO-SnO2 film demonstrated a high sensitivity to NO2 with a concentration of 0.1 ppm at an operating temperature of 200 °C.

Reversible and irreversible differentiation of cardiac fibroblasts.

AIMS: Differentiation of cardiac fibroblasts (Fbs) into myofibroblasts (MyoFbs) is responsible for connective tissue build-up in myocardial remodelling. We examined MyoFb differentiation and reversibility. METHODS AND RESULTS: Adult rat cardiac Fbs were cultured on a plastic substratum providing mechanical stress, with conditions to obtain different levels of Fb differentiation. Fb spontaneously differentiated to proliferating MyoFb (p-MyoFb) with stress fibre formation decorated with alpha-smooth muscle actin (α-SMA). Transforming growth factor-ß1 (TGF-ß1) promoted differentiation into α-SMA-positive MyoFb showing near the absence of proliferation, i.e. non-p-MyoFb. SD-208, a TGF-ß-receptor-I (TGF-ß-RI) kinase blocker, inhibited p-MyoFb differentiation as shown by stress fibre absence, low α-SMA expression, and high proliferation levels. Fb seeded in collagen matrices induced no contraction, whereas p-MyoFb and non-p-MyoFb induced 2.5- and four-fold contraction. Fb produced little collagen but high levels of interleukin-10. Non-p-MyoFb had high collagen production and high monocyte chemoattractant protein-1 and tissue inhibitor of metalloproteinases-1 levels. Transcriptome analysis indicated differential activation of gene networks related to differentiation of MyoFb (e.g. paxilin and PAK) and reduced proliferation of non-p-MyoFb (e.g. cyclins and cell cycle regulation). Dedifferentiation of p-MyoFb with stress fibre de-polymerization, but not of non-p-MyoFb, was induced by SD-208 despite maintained stress. Stress fibre de-polymerization could also be induced by mechanical strain release in p-MyoFb and non-p-MyoFb (2-day cultures in unrestrained 3-D collagen matrices). Only p-MyoFb showed true dedifferentiation after long-term 3-D cultures. CONCLUSIONS: Fb, p-MyoFb, and non-p-MyoFb have a distinct gene expression, ultrastructural, and functional profile. Both reduction in mechanical strain and TGF-ß-RI kinase inhibition can reverse p-MyoFb differentiation but not non-p-MyoFb.

TGF-beta1-induced cardiac myofibroblasts are nonproliferating functional cells carrying DNA damages.

TGF-beta1 induces differentiation and total inhibition of cardiac MyoFb cell division and DNA synthesis. These effects of TGF-beta1 are irreversible. Inhibition of MyoFb proliferation is accompanied with the expression of Smad1, Mad1, p15Ink4B and total inhibition of telomerase activity. Surprisingly, TGF-beta1-activated MyoFbs are growth-arrested not only at G1-phase but also at S-phase of the cell cycle. Staining with TUNEL indicates that these cells carry DNA damages. However, the absolute majority of MyoFbs are non-apoptotic cells as established with two apoptosis-specific methods, flow cytometry and caspase-dependent cleavage of cytokeratin 18. Expression in MyoFbs of proliferative cell nuclear antigen even in the absence of serum confirms that these MyoFbs perform repair of DNA damages. These results suggest that TGF-beta1-activated MyoFbs can be growth-arrested by two checkpoints, the G1/S checkpoint, which prevents cells from entering S-phase and the intra-S checkpoint, which is activated by encountering DNA damage during the S phase or by unrepaired damage that escapes the G1/S checkpoint. Despite carrying of the DNA damages TGF-beta1-activated MyoFbs are highly functional cells producing lysyl oxidase and contracting the collagen matrix.

Collagen production in cardiac fibroblasts during inhibition of aminopeptidase B.

OBJECTIVE: To determine whether the aminopeptidase B inhibitor, arphamenine A, could affect collagen production and expression in control and TGF-ss1-treated cardiac fibroblasts. DESIGN AND METHODS: Cardiac fibroblasts from passage 2 from normal male adult rats were cultured to confluency and incubated with and without 600 pmol/l TGF-ss1 for 2 days in serum-free Dulbecco's modified Eagle's medium and then incubated with 100 mol/l arphamenine A for 1 day in this medium with added ascorbic acid, ss-aminopropionitrile and titriated proline. Soluble collagen was measured in the conditioned medium and non-soluble collagen in the cell layer. Aminopeptidase activity was estimated by spectrophotometric determination of the liberation of p-nitroaniline from alanine- or arginine-p-nitroanilide. Matrix metalloproteinase (MMP) and lysyl oxidase activity were assayed in the conditioned medium. A semi-quantitative reverse transcriptase- polymerase chain reaction was used to examine the expression of lysyl oxidase and collagen type I and III. RESULTS: Arphamenine A dose-dependently inhibited basal and TGF-ss1-stimulated aminopeptidase activity. Arphamenine A reduced soluble and non-soluble collagen production in control and TGF-ss1-treated cardiac fibroblasts, while it decreased collagen type I and III expression only in TGF-ss1-treated fibroblasts. Lysyl oxidase, MMP-1 and MMP-2 activity were inhibited by arphamenine A in the conditioned media of control and TGF-ss1-treated cardiac fibroblasts. CONCLUSIONS: Our data show that the specific aminopeptidase B inhibitor, arphamenine A, reduces collagen production in cardiac fibroblasts and that this reduction is accompanied by a pronounced inhibition of lysyl oxidase.

Reversal of angiotensin II-stimulated collagen gel contraction in cardiac fibroblasts by aminopeptidase inhibition.

The purpose of this investigation was to determine whether aminopeptidase inhibition could affect the angiotensin II-stimulated collagen gel contraction in basal (control) and TGF-beta1-treated cardiac fibroblasts (or myofibroblasts). The tested aminopeptidase inhibitors were the broad range aminopeptidase inhibitor bestatin, the specific inhibitor of alanine aminopeptidase leuhistin, and the specific inhibitor of arginine aminopeptidase arphamenine A. Cardiac fibroblasts (from normal male adult rats) from passage 2 were cultured to confluency and incubated with(out) 400 pmol/L TGF-beta1 in Dulbecco Modified Eagle Medium (DMEM) with 10% fetal bovine serum (FBS). These fibroblasts were then further incubated in a floating collagen gel lattice with the tested products (angiotensin II, bestatin, leuhistin, or arphamenine A) for 3 days in DMEM without FBS. The contraction of the collagen gel lattice by cardiac fibroblasts was determined by measuring the gel volume with tritiated water. Aminopeptidase activity was estimated by spectrophotometric determination of the liberation of p-nitroaniline from alanine- or arginine-p-nitroanilide. Angiotensin II (100 nmol/L) reduced the gel volume in control and TGF-beta1-treated cardiac fibroblasts. The angiotensin II-stimulated collagen gel contraction in control and TGF-beta1-treated fibroblasts was almost completely reversed by leuhistin and arphamenine A (100 micromol/L). Bestatin (100 micromol/L) only partially inhibited the angiotensin II-stimulated collagen gel contraction in control fibroblasts, although it did not affect the angiotensin II-induced contraction in TGF-beta1-treated fibroblasts. In control and TGF-beta1-treated cardiac fibroblasts, 100 micromol/L leuhistin or arphamenine A only partially inhibited alanine aminopeptidase activity, whereas bestatin (100 micromol/L) completely inhibited the alanine aminopeptidase activity. Arginine aminopeptidase activity was only partially inhibited by leuhistin and arphamenine A at 100 micromol/L in control and TGF-beta1-treated fibroblasts. Bestatin, however, completely blocked the arginine aminopeptidase activity in control fibroblasts and only partially in TGF-beta1-treated fibroblasts at 100 micromol/L. Our data suggest that both alanine and arginine aminopeptidases are involved in the reversal of the angiotensin II-stimulated collagen gel contraction in control and TGF-beta1-treated cardiac fibroblasts or myofibroblasts.

Collagen production in cardiac fibroblasts during inhibition of angiotensin-converting enzyme and aminopeptidases.

OBJECTIVE: To determine whether lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, and bestatin, an aminopeptidase inhibitor with broad specificity, could affect collagen production in control and transforming growth factor (TGF)-beta1-treated cardiac fibroblasts. DESIGN AND METHODS: Cardiac fibroblasts from passage 2 from normal male adult rats were cultured to confluency, incubated with or without 600 pmol/l TGF-beta1 for 2 days in serum-free Dulbecco's modified Eagle's medium and then incubated with the test products (lisinopril or bestatin) for 1 day in this medium with added ascorbic acid, beta-aminoproprionitrile and tritiated proline. Soluble collagen was measured in the conditioned medium and non-soluble collagen in the cell layer. ACE activity was measured fluorimetrically with hippuryl-histidyl-leucine as substrate, and DNA with the bisbenzimide dye, Hoechst 33,258. Aminopeptidase activity was estimated by spectrophotometric determination of the liberation of p-nitroaniline from alanine-p-nitroanilide. RESULTS: Lisinopril dose-dependently reduced ACE activity in control and TGF-beta1-treated cardiac fibroblasts. Bestatin inhibited the basal and TGF-beta1-stimulated aminopeptidase activity in a concentration-dependent manner. Lisinopril (10 micromol/l) decreased (P < 0.05) the production of soluble and non-soluble collagen in control cardiac fibroblasts. TGF-beta1 (600 pmol/l) increased (P < 0.05) the production of soluble and non-soluble collagen, and this effect was decreased (P < 0.05) by lisinopril. Bestatin (100 micromol/l) reduced (P < 0.01) the production of soluble collagen in control and TGF-beta1-treated cardiac fibroblasts, but did not affect the production of non-soluble collagen in these cells. CONCLUSIONS: Our data suggest that ACE and aminopeptidases are involved in the basal and TGF-beta1-stimulated production of collagen in adult rat cardiac fibroblasts in culture.

Association between transforming growth factor-beta and hypertension.

Discordant findings are reported on the left ventricular transforming growth factor-beta(1) (TGF-beta(1)) mRNA levels in various rat models. Left ventricular TGF-beta(1) mRNA levels did not differ between spontaneously hypertensive rats (SHR) and normal rats, between deoxycorticosterone (DOCA)-salt and sham-operated hypertensive rats, but were increased in stroke-prone spontaneously hypertensive rats (SHRSP) and in post-myocardial infarction (MI) rats. Renal cortical TGF-beta(1) mRNA levels were, however, higher in DOCA-salt hypertensive rats. Angiotensin II subtype 1 receptor antagonism (AT(1)R) and angiotensin converting enzyme inhibition (ACEI) decreased left ventricular and vascular smooth muscle TGF-beta(1) mRNA levels in SHR and renal TGF-beta(1) mRNA in DOCA-salt hypertensive rats and in SHRSP. In post-MI rats ventricular TGF-beta(1) mRNA decreased by AT(1)R antagonism. In essential hypertensive patients, TGF-beta(1) protein as well as TGF-beta(1) mRNA levels are hyperexpressed. The TGF-beta(1) overproduction in hypertension can be attributed to various factors such as elevated angiotensin II, increased systemic blood pressure (BP) per se, increased fluid shear stress and a differential expression of TGF-beta(1) linked to DNA polymorphism in the promoter. The Arg(25) polymorphism in the TGF-beta(1) gene is associated with higher BP. A higher plasma TGF-beta(1) concentration is found in hypertensive patients with microalbuminuria and left ventricle hypertrophy. In these patients, AT(1)R antagonism and ACEI reduced these plasma TGF-beta(1) levels significantly.

Stimulation of collagen production by transforming growth factor-beta1 during differentiation of cardiac fibroblasts to myofibroblasts.

The aim of the present study was to elucidate how transforming growth factor-beta(1) (TGF-beta(1)) can stimulate collagen deposition in cardiac tissue by interstitial cells via stimulation of fibroblasts, via myofibroblasts, or via differentiation of fibroblasts to myofibroblasts. The dose- and time-dependent stimulation of collagen production and of expression of alpha-smooth muscle actin (alpha-SMA), a marker of myofibroblasts, was studied in cultures of second-passage adult rat cardiac fibroblasts. The TGF-beta(1)-stimulated collagen production is positively correlated (r=0.68, P<0.001) with the appearance of alpha-SMA. Only at high concentrations (40 to 600 pmol/L) and after a long time (24 to 48 hours) of incubation, TGF-beta(1) increases the collagen production and stimulates the differentiation of fibroblasts to myofibroblasts. The maximal stimulation of the collagen production (2-fold, P<0.001) observed after incubation of cultures of fibroblasts with 600 pmol/L TGF-beta(1) for 48 hours is accompanied by a maximal stimulation of alpha-SMA expression (3.5-fold, P<0.001), when cultures consist mainly of myofibroblasts. The stimulation of collagen production cannot be reversed either after additional incubation of TGF-beta(1)-stimulated second-passage cultures for 2 days or in their offspring in the next third passage after incubation for 7 days without TGF-beta(1). The increased collagen production in these third-passage cultures cannot be further stimulated by TGF-beta(1). Our data suggest that TGF-beta(1)-stimulated collagen production in cultures of adult rat cardiac ventricular fibroblasts cannot be explained by a direct stimulation of the collagen production either in fibroblasts or in myofibroblasts. Instead, TGF-beta(1) induces the differentiation of fibroblasts to myofibroblasts, which have a higher activity for collagen production than fibroblasts.