The composition of the fluid phase in inclusions in synthetic HPHT diamonds grown in system Fe-Ni-Ti-C.

Diamonds grown by high pressure high temperature process (HPHT) are usually characterized by yellow color and high contents of nitrogen. Introduction of Ti decreases nitrogen content in diamond. Understanding the formation of nitrogen-poor diamond is very important not for the progress of HPHT process only, but because these diamond varieties represent the rare natural stones, although their crystallization conditions have not been clarified yet.

Diamond-inclusion system recording old deep lithosphere conditions at Udachnaya (Siberia).

Diamonds and their inclusions are unique fragments of deep Earth, which provide rare samples from inaccessible portions of our planet. Inclusion-free diamonds cannot provide information on depth of formation, which could be crucial to understand how the carbon cycle operated in the past. Inclusions in diamonds, which remain uncorrupted over geological times, may instead provide direct records of deep Earth's evolution.

Quantifying hexagonal stacking in diamond.

Diamond is a material of immense technological importance and an ancient signifier for wealth and societal status. In geology, diamond forms as part of the deep carbon cycle and typically displays a highly ordered cubic crystal structure. Impact diamonds, however, often exhibit structural disorder in the form of complex combinations of cubic and hexagonal stacking motifs.

Fused Microknot Optical Resonators in Folded Photonic Tapers for in-Liquid Durable Sensing.

Optical microknot fibers (OMFs) serve as localized devices, where photonic resonances (PRs) enable self-interfering elements sensitive to their environment. However, typical fragility and drifting of the knot severely limit the performance and durability of microknots as sensors in aqueous settings. Herein we present the fabrication, electrical fusing, preparation, and persistent detection of volatile liquids in multiple wetting⁻dewetting cycles of volatile compounds and quantify the persistent phase shifts with a simple model relating to the ambient liquid, enabling durable in-liquid sensing employing OMF PRs.

Dynamical range and stability enhancement in electrically fused microknot optical resonators.

Microknot resonators (MKRs), locally fused using a two-probe technique, have exhibited significantly improved optical performance and mechanical stability. They have been operated with low losses both in situ and as transferred devices. We found consistently more than threefold dynamical range enhancement, which remained stable in time, in electrically fused MKRs.

Anesthetic concerns in patients with known cerebrovascular insufficiency.

This review outlines the perioperative anesthesia considerations of patients with vascular diseases of the central nervous system, including occlusive cerebrovascular diseases with ischemic risks and various cerebrovascular malformations with hemorrhagic potential. The discussion emphasizes perioperative management strategies to prevent complications and minimize their effects if they occur. Planning the anesthetic and perioperative management is predicated on understanding the goals of the therapeutic intervention and anticipating potential problems.

Proteolytic cleavage of ataxin-7 by caspase-7 modulates cellular toxicity and transcriptional dysregulation.

Spinocerebellar ataxia type 7 (SCA7) is a polyglutamine (polyQ) disorder characterized by specific degeneration of cerebellar, brainstem, and retinal neurons. Although they share little sequence homology, proteins implicated in polyQ disorders have common properties beyond their characteristic polyQ tract. These include the production of proteolytic fragments, nuclear accumulation, and processing by caspases.

The rat vanilloid receptor splice variant VR.5'sv blocks TRPV1 activation.

The capsaicin receptor (VR1, TRPV1) is a ligand-gated ion channel predominantly expressed in peripheral nociceptors and activated by multiple noxious stimuli including products of inflammation. A 5'-splice variant (VR.5'sv) of TRPV1 has been previously isolated and found to be insensitive to noxious stimuli.

Reversal of Alzheimer's-like pathology and behavior in human APP transgenic mice by mutation of Asp664.

The deficits characteristic of Alzheimer's disease (AD) are believed to result, at least in part, from the neurotoxic effects of beta-amyloid peptides, a set of 39-43 amino acid fragments derived proteolytically from beta-amyloid precursor protein (APP). APP also is cleaved intracytoplasmically at Asp-664 to generate a second cytotoxic peptide, APP-C31, but whether this C-terminal processing of APP plays a role in the pathogenesis of AD is unknown. Therefore, we compared elements of the Alzheimer's phenotype in transgenic mice modeling AD with vs.

FGF-2 promotes neurogenesis and neuroprotection and prolongs survival in a transgenic mouse model of Huntington's disease.

There is no satisfactory treatment for Huntington's disease (HD), a hereditary neurodegenerative disorder that produces chorea, dementia, and death. One potential treatment strategy involves the replacement of dead neurons by stimulating the proliferation of endogenous neuronal precursors (neurogenesis) and their migration into damaged regions of the brain. Because growth factors are neuroprotective in some settings and can also stimulate neurogenesis, we treated HD transgenic R6/2 mice from 8 weeks of age until death by s.

Comparison of ischemia-directed migration of neural precursor cells after intrastriatal, intraventricular, or intravenous transplantation in the rat.

Cell replacement therapy may have the potential to promote brain repair and recovery after stroke. To compare how focal cerebral ischemia affects the entry, migration, and phenotypic features of neural precursor cells transplanted by different routes, we administered neuronal precursors from embryonic cerebral cortex of green fluorescent protein (GFP)-expressing transgenic mice to rats that had undergone middle cerebral artery occlusion (MCAO) by the intrastriatal, intraventricular, and intravenous routes. MCAO increased the entry of GFP-immunoreactive cells, most of which expressed neuroepithelial (nestin) or neuronal (doublecortin) markers, from the ventricles and bloodstream into the brain, and enhanced their migration when delivered by any of these routes.

Effect of aging on neuroglobin expression in rodent brain.

Neuroglobin (Ngb), a recently discovered O2-binding heme protein related to hemoglobin and myoglobin, protects neurons from hypoxic-ischemic injury in vitro and in vivo. In immunostained mouse brain sections, we found widespread expression of Ngb protein in neurons, but not astrocytes, of several brain regions that are prominently involved in age-related neurodegenerative disorders. Western blots from young adult (3 month), middle-aged (12 month), and aged (24 month) rats showed an age-related decline in Ngb expression in cerebral neocortex, hippocampus, caudate-putamen, and cerebellum.

Immunolocalization of TASK-3 (KCNK9) to a subset of cortical neurons in the rat CNS.

Tandem pore domain (2P) K channels constitute the most diverse family of K channels and are responsible for background (leak or baseline) K currents. Of the 15 human 2P K channels, TASK-1, TASK-2, and TASK-3 are uniquely sensitive to physiologic pH changes as well as being inhibited by local anesthetics and activated by volatile anesthetics. In this study polyclonal antibodies selective for TASK-3 have been used to localize its expression in the rat central nervous system (CNS).

Specific caspase interactions and amplification are involved in selective neuronal vulnerability in Huntington's disease.

Huntington's disease (HD) is an autosomal dominant progressive neurodegenerative disorder resulting in selective neuronal loss and dysfunction in the striatum and cortex. The molecular pathways leading to the selectivity of neuronal cell death in HD are poorly understood. Proteolytic processing of full-length mutant huntingtin (Htt) and subsequent events may play an important role in the selective neuronal cell death found in this disease.

Neurogenesis and aging: FGF-2 and HB-EGF restore neurogenesis in hippocampus and subventricular zone of aged mice.

Neurogenesis, which may contribute to the ability of the adult brain to function normally and adapt to disease, nevertheless declines with advancing age. Adult neurogenesis can be enhanced by administration of growth factors, but whether the aged brain remains responsive to these factors is unknown. We compared the effects of intracerebroventricular fibroblast growth factor (FGF)-2 and heparin-binding epidermal growth factor-like growth factor (HB-EGF) on neurogenesis in the hippocampal dentate subgranular zone (SGZ) and the subventricular zone (SVZ) of young adult (3-month) and aged (20-month) mice.

Cathepsin L in secretory vesicles functions as a prohormone-processing enzyme for production of the enkephalin peptide neurotransmitter.

Multistep proteolytic mechanisms are essential for converting proprotein precursors into active peptide neurotransmitters and hormones. Cysteine proteases have been implicated in the processing of proenkephalin and other neuropeptide precursors. Although the papain family of cysteine proteases has been considered the primary proteases of the lysosomal degradation pathway, more recent studies indicate that functions of these enzymes are linked to specific biological processes.

VEGF-induced neuroprotection, neurogenesis, and angiogenesis after focal cerebral ischemia.

Vascular endothelial growth factor (VEGF) is an angiogenic protein with therapeutic potential in ischemic disorders, including stroke. VEGF confers neuroprotection and promotes neurogenesis and cerebral angiogenesis, but the manner in which these effects may interact in the ischemic brain is poorly understood. We produced focal cerebral ischemia by middle cerebral artery occlusion for 90 minutes in the adult rat brain and measured infarct size, neurological function, BrdU labeling of neuroproliferative zones, and vWF-immunoreactive vascular profiles, without and with intracerebroventricular administration of VEGF on days 1-3 of reperfusion.

Nanotubules formed by highly hydrophobic amphiphilic alpha-helical peptides and natural phospholipids.

We previously reported that the 18-mer amphiphilic alpha-helical peptide, Hel 13-5, consisting of 13 hydrophobic residues and five hydrophilic amino acid residues, can induce neutral liposomes (egg yolk phosphatidylcholine) to adopt long nanotubular structures and that the interaction of specific peptides with specific phospholipid mixtures induces the formation of membrane structures resembling cellular organelles such as the Golgi apparatus. In the present study we focused our attention on the effects of peptide sequence and chain length on the nanotubule formation occurring in mixture systems of Hel 13-5 and various neutral and acidic lipid species by means of turbidity measurements, dynamic light scattering measurements, and electron microscopy. We designed and synthesized two sets of Hel 13-5 related peptides: 1) Five peptides to examine the role of hydrophobic or hydrophilic residues in amphiphilic alpha-helical structures, and 2) Six peptides to examine the role of peptide length, having even number residues from 12 to 24.

Cerebral neurogenesis is induced by intranasal administration of growth factors.

Neurogenesis persists in the adult brain, where it may contribute to repair and recovery after injury, but the lack of methods for noninvasive stimulation of cerebral neurogenesis limits its potential for clinical application. We report that intranasal administration of either fibroblast growth factor-2 or heparin-binding epidermal growth factor-like growth factor increases neurogenesis, measured by the incorporation of bromodeoxyuridine into cells that express the early neuronal marker protein doublecortin in the subventricular zone of mouse brain. These findings indicate that intranasal growth factors may have potential as neurogenesis-promoting therapeutic agents.

Type 1 insulin-like growth factor receptor (IGF-IR) signaling inhibits apoptosis signal-regulating kinase 1 (ASK1).

The type 1 insulin-like growth factor receptor (IGF-IR) is a receptor-tyrosine kinase that plays a critical role in signaling cell survival and proliferation. IGF-IR binding to its ligand, insulin-like growth factor (IGF-I) activates phosphoinositide 3-kinase (PI3K), promotes cell proliferation by activating the mitogen-activated protein kinase (MAPK) cascade, and blocks apoptosis by inducing the phosphorylation and inhibition of proapoptotic proteins such as BAD. Apoptosis signal-regulating kinase 1 (ASK1) is a MAP kinase kinase kinase (MAPKKK) that is required for c-Jun N-terminal kinase (JNK) and p38 activation in response to Fas and tumor necrosis factor (TNF) receptor stimulation, and for oxidative stress- and TNFalpha-induced apoptosis.

The novel serpin endopin 2 demonstrates cross-class inhibition of papain and elastase: localization of endopin 2 to regulated secretory vesicles of neuroendocrine chromaffin cells.

This study demonstrates that endopin 2 is a unique secretory vesicle serpin that displays cross-class inhibition of cysteine and serine proteases, indicated by effective inhibition of papain and elastase, respectively. Homology of the reactive site loop (RSL) domain of endopin 2, notably at P1-P1' residues, with other serpins that inhibit cysteine and serine proteases predicted that endopin 2 may inhibit similar proteases. Recombinant N-His-tagged endopin 2 inhibited papain and elastase with second-order rate constants (k(ass)) of 1.

Caspase cleavage of members of the amyloid precursor family of proteins.

The synapse loss and neuronal cell death characteristic of Alzheimer's disease (AD) are believed to result in large part from the neurotoxic effects of beta-amyloid peptide (Abeta), a 40-42 amino acid peptide(s) derived proteolytically from beta-amyloid precursor protein (APP). However, APP is also cleaved intracellularly to generate a second cytotoxic peptide, C31, and this cleavage event occurs in vivo as well as in vitro and preferentially in the brains of AD patients (Lu et al. 2000).

Coupling endoplasmic reticulum stress to the cell death program: role of the ER chaperone GRP78.

Alterations in Ca(2+) homeostasis and accumulation of unfolded proteins in the endoplasmic reticulum (ER) lead to an ER stress response. Prolonged ER stress may lead to cell death. Glucose-regulated protein (GRP) 78 (Bip) is an ER lumen protein whose expression is induced during ER stress.

Soy-derived antiapoptotic fractions protect gastrointestinal epithelium from damage caused by methotrexate treatment in the rat.

The ability of a previously described soy-derived antiapoptotic fraction (SDAAF), a soy water extract (Lexirin), and raw soy flour to inhibit methotrexate (MTX)-induced gastrointestinal damage was evaluated by histological examination of duodenal/jejunal sections from MTX-treated rats. Male Sprague-Dawley rats were fed diets containing casein as a sole protein source or diets supplemented with fractions isolated from soy (SDAAF or Lexirin) before and after MTX treatment. The soy fractions were also shown to inhibit serum deprivation-induced programmed cell death (apoptosis) in mouse embryonic C3H10T1/2 cells.