Effect of pyrite on the treatment of chlorophenolic compounds with zero-valent iron-Fenton process under uncontrolled pH conditions: reaction mechanism and biodegradability.

This current study explored the effect of pyrite on the treatment of chlorophenolic compounds (CP) by Fenton process with micron-sized zero-valent iron (ZVI) as the catalyst. The experiments were conducted in batch reactors with 100 mg L CP, 0-0.02 M HO, and variable pyrite and ZVI doses (0-1 g L).

Role of reactor type on Cr(VI) removal by zero-valent iron in the presence of pyrite: Batch versus sequential batch reactors.

This study was conducted to understand the role of application sequence of pyrite and zero-valent iron (Fe) (simultaneous vs. sequential) on chromium (VI) removal by Fe. In batch experiments, pyrite and Fe were homogeneously mixed in batch reactors maintained at a constant total solids loading of 2 g L.

Ligand enhanced pharmaceutical wastewater treatment with Fenton process using pyrite as the catalyst: Column experiments.

Advanced oxidation processes offer practical and cost effective solutions for the treatment of poorly biodegradable industrial wastewaters. Here, column experiments were performed to understand the role of a complexing agent, citrate, on Fenton-treatment of an actual pharmaceutical wastewater with pyrite as the catalyst under dynamic flow conditions. Our results suggest that the pharmaceutical wastewater treatment with Fenton reaction using pyrite as the catalyst was mainly regulated by the extent of Fe dissolution from pyrite, which, in turn, resulted in formation of hydroxyl radicals in solution.

Role of complexing agents on oxidative degradation of chlorophenolic compounds by pyrite-Fenton process: Batch and column experiments.

This study involves batch reactor and fixed-bed continuous flow experiments to determine the effects of complexing agents (e.g., tartrate and citrate) on the treatment of chlorophenolic (CP) compounds using heterogeneous Fenton system with pyrite mineral as the iron source.

Diclofenac removal by pyrite-Fenton process: Performance in batch and fixed-bed continuous flow systems.

This study provides experimental results from batch and column studies to investigate diclofenac degradation by pyrite-Fenton process under variable chemical conditions (e.g., pyrite loading).

Oxidative degradation of chlorophenolic compounds with pyrite-Fenton process.

Batch experiments, in conjunction with chromatographic and spectroscopic measurements, were performed to comparatively investigate the degradation of various chlorophenolic (CP) compounds (e.g., 2-CP, 4-CP, 2,3-DCP, 2,4-DCP, 2,4,6-TCP, 2,3,4,6-TeCP) by a modified Fenton process using pyrite as the catalyst.

Synthesis, characterization, and biological properties of composites of hydroxyapatite and hexagonal boron nitride.

Hydroxyapatite (HA), obtained from bovine bones, was successfully reinforced with hexagonal boron nitrite (h-BN). h-BN/HA composites, with BN content up to 1.5 wt %, were sintered at various temperatures between 1000 and 1300°C, in air.

Involvement of autophagy in T cell biology.

Autophagy is an essential cellular pathway that sequesters various cytoplasmic components, including accumulated proteins, damaged organelles or invading microorganisms and delivers them to lysosomes for degradation. The function of autophagy has been reported in various tissues and systems, including its role in the regulation of cellular immunity. Autophagy plays a fundamental role at various stages of T cell maturation.

IBMPFD Disease-Causing Mutant VCP/p97 Proteins Are Targets of Autophagic-Lysosomal Degradation.

The ubiquitin-proteasome system (UPS) degrades soluble proteins and small aggregates, whereas macroautophagy (autophagy herein) eliminates larger protein aggregates, tangles and even whole organelles in a lysosome-dependent manner. VCP/p97 was implicated in both pathways. VCP/p97 mutations cause a rare multisystem disease called IBMPFD (Inclusion Body Myopathy with Paget's Disease and Frontotemporal Dementia).

RACK1 Is an Interaction Partner of ATG5 and a Novel Regulator of Autophagy.

Autophagy is biological mechanism allowing recycling of long-lived proteins, abnormal protein aggregates, and damaged organelles under cellular stress conditions. Following sequestration in double- or multimembrane autophagic vesicles, the cargo is delivered to lysosomes for degradation. ATG5 is a key component of an E3-like ATG12-ATG5-ATG16 protein complex that catalyzes conjugation of the MAP1LC3 protein to lipids, thus controlling autophagic vesicle formation and expansion.

Review on Lithotripsy and Cavitation in Urinary Stone Therapy.

Cavitation is the sudden formation of vapor bubbles or voids in liquid media and occurs after rapid changes in pressure as a consequence of mechanical forces. It is mostly an undesirable phenomenon. Although the elimination of cavitation is a major topic in the study of fluid dynamics, its destructive nature could be exploited for therapeutic applications.

Physiological and pathological significance of the molecular cross-talk between autophagy and apoptosis.

Autophagy and apoptosis are two important molecular mechanisms that maintain cellular homeostasis under stress conditions. Autophagy represents an intracellular mechanism responsible for turnover of organelles and long-lived proteins through a lysosome-dependent degradation pathway. Cell death signals or sustained stress might trigger programmed cell death pathways, and among them, apoptosis is the most extensively studied one.

Effect of Varying Magnetic Fields on Targeted Gene Delivery of Nucleic Acid-Based Molecules.

Several physical methods have been developed to introduce nucleic acid expression vectors into mammalian cells. Magnetic transfection (magnetofection) is one such transfection method, and it involves binding of nucleic acids such as DNA, RNA or siRNA to magnetic nanoparticles followed by subsequent exposure to external magnetic fields. However, the challenge between high efficiency of nucleic acid uptake by cells and toxicity was not totally resolved.

Hydrodynamic cavitation kills prostate cells and ablates benign prostatic hyperplasia tissue.

Hydrodynamic cavitation is a physical phenomenon characterized by vaporization and bubble formation in liquids under low local pressures, and their implosion following their release to a higher pressure environment. Collapse of the bubbles releases high energy and may cause damage to exposed surfaces. We recently designed a set-up to exploit the destructive nature of hydrodynamic cavitation for biomedical purposes.

Cleavage of Atg3 protein by caspase-8 regulates autophagy during receptor-activated cell death.

Autophagy is an evolutionarily conserved mechanism contributing to cell survival under stress conditions including nutrient and growth factor deprivation. Connections and cross-talk between cell death mechanisms and autophagy is under investigation. Here, we describe Atg3, an essential regulatory component of autophagosome biogenesis, as a new substrate of caspase-8 during receptor-mediated cell death.

Bubbly cavitating flow generation and investigation of its erosional nature for biomedical applications.

This paper presents a study that investigates the destructive energy output resulting from hydrodynamic bubbly cavitation in microchannels and its potential use in biomedical applications. The research performed in this study includes results from bubbly cavitation experiments and findings showing the destructive effects of bubbly cavitating flow on selected solid specimens and live cells. The bubbles generated by hydrodynamic cavitation are highly destructive at the surfaces of the target medium on which they are carefully focused.

The roles of pericystic cells and Sertoli cells in spermatogonial proliferation stimulated by some growth factors in organ culture of newt (Cynops pyrrhogaster) testis.

We have previously shown FSH promotes spermatogonial proliferation and their differentiation into primary spermatocytes in organ culture of newt testicular fragments. Several growth factors identified in newt testis, such as stem cell factor (SCF), insulin-like growth factor (IGF)-I, and neuregulin (NRG)1, also stimulate spermatogonial proliferation in the organ culture. However, any growth factor added in vitro might not work on spermatogonia directly, but act on somatic cells such as Sertoli cells or pericystic cells, because size-selective barrier exists around a cyst which is enclosed by Sertoli cells.

Promotion of spermatogonial proliferation by neuregulin 1 in newt (Cynops pyrrhogaster) testis.

We have previously shown that mammalian follicle-stimulating hormone (FSH) promotes the proliferation of spermatogonia and their differentiation into primary spermatocytes in organ culture of newt testis. In the current study, we performed microarray analysis to isolate local factors secreted from somatic cells upon FSH treatment and acting on the germ cells. We identified neuregulin 1 (NRG1) as a novel FSH-upregulated clone homologous to mouse NRG1 known to control cell proliferation, differentiation and survival in various tissues.