Frictional Melting in Hydrothermal Fluid-Rich Faults: Field and Experimental Evidence From the Bolfín Fault Zone (Chile).

Tectonic pseudotachylytes are thought to be unique to certain water-deficient seismogenic environments and their presence is considered to be rare in the geological record. Here, we present field and experimental evidence that frictional melting can occur in hydrothermal fluid-rich faults hosted in the continental crust. Pseudotachylytes were found in the >40 km-long Bolfín Fault Zone of the Atacama Fault System, within two ca. 1 m-thick (ultra)cataclastic strands hosted in a damage-zone made of chlorite-epidote-rich hydrothermally altered tonalite. This alteration state indicates that hydrothermal fluids were active during the fault development. Pseudotachylytes, characterized by presenting amygdales, cut and are cut by chlorite-, epidote- and calcite-bearing veins. In turn, crosscutting relationship with the hydrothermal veins indicates pseudotachylytes were formed during this period of fluid activity. Rotary shear experiments conducted on bare surfaces of hydrothermally altered rocks at seismic slip velocities (3 m s-1) resulted in the production of vesiculated pseudotachylytes both at dry and water-pressurized conditions, with melt lubrication as the primary mechanism for fault dynamic weakening. The presented evidence challenges the common hypothesis that pseudotachylytes are limited to fluid-deficient environments, and gives insights into the ancient seismic activity of the system. Both field observations and experimental evidence, indicate that pseudotachylytes may easily be produced in hydrothermal environments, and could be a common co-seismic fault product. Consequently, melt lubrication could be considered one of the most efficient seismic dynamic weakening mechanisms in crystalline basement rocks of the continental crust.

Simultaneous analysis of saturated and unsaturated oxylipins in 'ex vivo' cultured peripheral blood mononuclear cells and neutrophils.

Oxylipins are a family of saturated and unsaturated fatty acids peroxidation products with bioactive properties. We have developed an improved method for the measurement of ex vivo oxylipin production by peripheral blood mononuclear cells (PBMCs) and neutrophils. We aimed to develop an analytical method to determine the production rates of polyunsaturated fatty acids (PUFAs), PUFA-oxylipin, and saturated-oxylipins by stimulated PBMCs and neutrophils based on solid phase extraction and HPLC-MS/MS technology. A UHPLC system coupled to a Q-Exactive Hybrid Quadrupole-Orbitrap mass spectrometer was used to identify and quantify oxylipin production. For each oxylipin and PUFA their differential response was calculated with respect to a deuterated internal standard factor (ISF). To calculate oxylipin and PUFAs in the culture samples, the individual ISF was used for each oxylipin and PUFA with respect to the deuterated internal standard. PBMCs and neutrophils showed a different pattern of oxylipin production and fatty acid secretion. Lipopolysaccharide (LPS) did not stimulate oxylipin production or fatty acids secretion in PBMCs, whereas phorbol myristate acetate (PMA) stimulation increased the production rate of 5-HETE, 15-HETE, 15-HEPE, 17-DoHE, PGE2, AA, and DHA. LPS stimulation decreased 16-hydroxyl-palmitatte (16-OHPAL) production and DHA secretion in neutrophils, while PMA stimulation increased the production rate of AA and its derivate oxylipins, 5-HETE, 15-HETE, and PGE2. In conclusion, we have developed a new method to determine oxylipins derived from both saturated and unsaturated fatty acids in culture cell media. This method has enough sensitivity, and accuracy, to determine oxylipin production and fatty acid secretion by PBMCs and neutrophils.

Intake of myo-inositol hexaphosphate and urinary excretion of inositol phosphates in Wistar rats: Gavage vs. oral administration with sugar.

OBJECTIVE: To evaluate the urinary levels of inositol phosphates (InsPs) in rats that received different salts of myo-inositol hexaphosphate (InsP6) by gavage or by oral administration. METHODS: Thirty rats received AIN-76A diet (in which InsPs are undetectable) for 15 days. Then, 12 rats received InsP6 by gavage as a Na salt or a Ca/Mg salt; after 4 days, the Na or Ca/Mg InsP6 was administered with water containing 15 g/L sucrose and urine samples were collected. The other 18 rats received oral InsP6, in which 0.5 g of sugar was combined with InsP6 as a Na salt, a Ca/Mg salt, or a Na salt with CaCO3; daily urine samples were collected. Urine levels of InsPs were determined using a nonspecific method and a specific method (polyacrylamide gel electrophoresis, PAGE), and different InsPs were identified by mass spectroscopy (MS). RESULTS: After 15 days of the InsP6-free diet, the non-specific method detected no urinary InsPs, and MS detected only InsP2. After administration of Na-InsP6 by gavage, the non-specific method indicated more urinary InsPs than the amount of InsP6 determined by PAGE. MS indicated the presence of urinary InsP2, InsP3, InsP4, InsP5, and InsP6 in these rats, with notable variations among animals. Use of the same treatment to administer Ca/Mg-InsP6 led to a lower overall content of urinary InsPs and a lower level of InsP6. Oral administration of InsP6 as a sugar pill led to lower urinary levels of InsPs than administration of InsP6 by gavage, and administration as a Ca/Mg pill or a Ca/Mg pill with CaCO3 led to lower levels than administration as a Na pill. CONCLUSION: Administration of InsP6 to rats leads to the excretion of a mixture of different InsPs. Rats more effectively absorb InsP6 when supplied without dietary components that interfere with its uptake, such as the Ca ion and sugar.

Evaluation of inositol phosphates in urine after topical administration of myo-inositol hexaphosphate to female Wistar rats.

AIMS: Previous studies demonstrated a remarkable increase of urinary InsP6 by topical administration. However, the methodology used for InsP6 analysis was not specific. The aim of this paper is to measure urinary inositol phosphates InsPs using more advanced methodologies and to compare the results with those obtained by the non-specific method. MATERIALS AND METHODS: We fed 12 female rats with a diet without InsP6 for 16days. Then, we administered a topical InsP6 gel at high doses for 7days (50mgInsP6/day) or at low doses for 28days (20mgInsP6/day). We measured urine levels InsPs using a nonspecific method (based on the ability of InsPs to complex Al3+) and levels of InsP6 by a specific method (using polyacrylamide gel electrophoresis). Identification of different InsPs was performed by MS. KEY FINDINGS: At baseline, after dietary deprivation of InsP6, rats only excreted InsP2 in their urine, and there was no detectable InsP6 or other InsPs. Rats given the high dose treatment for 7days had abundant urinary InsP6, but also had other InsPs in their urine; cessation of InsP6 administration led to decreased levels of urinary InsPs. Rats given the low dose treatment for 28days had increasing levels of urinary InsPs over time. The maximum urinary InsP6 was at 21days, after which InsPs excretion decreased. SIGNIFICANCE: We conclude that the skin can absorb InsP6 from a topical gel, and that InsP6 is excreted in the urine, along with other InsPs (InsP5, InsP4, InsP3, and InsP2).

Selective binding of cis-1,3,5-cyclohexane tricarboxylic acid vs its epimeric trans isomer by a tripodal amidopyridine receptor; crystal structures of the 1:1 complexes.

[figure: see text] A tripodal tris-amidopyridine receptor forms a 1:1 complex with trans-1,3,5-cyclohexane tricarboxylic acid that is 1 order of magnitude less stable than the one formed with the corresponding cis-triacid epimer. The X-ray crystal structures of the complexes have been determined, confirming the binding geometry derived from NMR data in solution and force-field calculations, and its geometrical features are used to explain the observed selectivity.

Splenosis and the gynecologic patient: a case report and review of literature.

A 23-year-old woman with pelvic pain and a preoperative assessment of endometriosis eventually diagnosed as splenosis is presented. Hysterectomy, removal of the ovaries and of the splenic pelvic mass resolved her complaint. The pelvic mass in this patient was clinically mistaken for endometriosis. Use of more specific diagnostic techniques can more clearly guide therapy.

Envelope glycoprotein determinants of increased fusogenicity in a pathogenic simian-human immunodeficiency virus (SHIV-KB9) passaged in vivo.

Changes in the envelope glycoprotein ectodomains of a nonpathogenic simian-human immunodeficiency virus (SHIV-89.6) that was serially passaged in vivo have been shown to be responsible for the increased pathogenicity of the resulting virus, SHIV-KB9 (G. B. Karlsson, et al., J. Exp. Med. 188:1159-1171, 1998). The 12 amino acid changes in the envelope glycoprotein ectodomains resulted in increased chemokine receptor-binding and syncytium-forming abilities. Here we identify the envelope glycoprotein determinants of these properties. A single amino acid change in the gp120 third variable (V3) loop was both necessary and sufficient for the observed increase in the binding of the SHIV-KB9 gp120 glycoprotein to the CCR5 chemokine receptor. The increased syncytium-forming ability of SHIV-KB9 involved, in addition to the V3 loop change, changes in the second conserved (C2) region of gp120 (residue 225) and in the gp41 ectodomain (residues 564 and 567). The C2 and gp41 ectodomain changes influenced syncytium formation in a cooperative manner. Changes in the V1/V2 gp120 variable loops exerted a negative effect on syncytium formation and chemokine receptor binding, supporting a previously described role of these changes in immune evasion. The definition of the passage-associated changes that determine the efficiency of chemokine receptor binding and membrane fusogenicity will allow evaluation of the contribution of these properties to in vivo CD4-positive lymphocyte depletion.

Update and review of blastomycosis.

Blastomycosis has a wide spectrum of clinical presentations. When a patient presents with chronic pneumonia, especially coexisting with cutaneous lesions, blastomycosis infection needs to be considered in the differential diagnosis. Erythema nodosum can rarely be associated with pulmonary blastomycosis. A positive culture is the gold standard of diagnosis; occasionally, the organism can be identified by its typical "shoe print" morphology with periodic acid-Schiff (PAS) stain. The Gen-Probe technique may be required to confirm the uncertain culture results. The preferred treatment for blastomycosis in less severe cases is oral itraconazole, with amphotericin B in disseminated cases.

Characterization of molecularly cloned simian-human immunodeficiency viruses causing rapid CD4+ lymphocyte depletion in rhesus monkeys.

In vivo passage of a chimeric simian-human immunodeficiency virus (SHIV-89.6) expressing the human immunodeficiency virus type 1 (HIV-1) tat, rev, vpu, and env genes generated pathogenic viruses (SHIV-89.6P) inducing rapid CD4+ lymphocyte depletion and AIDS-like illness in rhesus monkeys (K. Reimann, J. T. Li, R. Veazey, M. Halloran, I.-W. Park, G. B. Karlsson, J. Sodroski, and N. L. Letvin, J. Virol. 70:6922-6928, 1996). To characterize the molecular changes responsible for this increase in virulence, infectious proviral clones of SHIV-89.6P isolates were derived. Viruses generated from some of these clones caused a rapid and profound decline of CD4+ lymphocytes in a high percentage of inoculated monkeys. Nucleotide changes potentially responsible for the increased virulence of SHIV-89.6P were limited to the env, tat, or long terminal repeat sequences, with most of the observed changes in env. Nucleotide changes in env altered 12 amino acids in the gp120 and gp41 exterior domains, and a 140-bp deletion in env resulted in the substitution of the carboxyl terminus of the SIVmac gp41 glycoprotein for that of the HIV-1 gp41 glycoprotein. The availability of pathogenic proviral clones should facilitate dissection of the molecular determinants of SHIV-89.6P virulence.

Strain differences in tissue repair response to 1,2-dichlorobenzene.

Fischer 344 (F344) rats are reportedly 75-fold more sensitive than Sprague Dawley (S-D) rats to 1,2-dichlorobenzene (o-DCB) hepatotoxicity. Lethality studies were conducted since no information was available regarding the ultimate consequence of this sensitivity in terms of animal survival in the two strains. LD50S for o-DCB (1.66 ml/kg and 1.76 ml/kg in male F344 and S-D rats, respectively) did not differ. Several studies have shown the importance of tissue repair on animal survival following exposure to toxic chemicals. The objective of this study was to investigate if differential rates of cell division and tissue repair might explain the lack of difference in LD50 dose between the two strains despite higher hepatotoxic injury in F344 rats. Age-matched male S-D and F344 rats were administered o-DCB (0.2, 0.6, 1.2 ml/kg, i.p.); injury and tissue repair occurring as two dynamic but opposing events were measured over time. Liver injury was assessed by measuring plasma alanine aminotransferase (ALT) and sorbitol dehydrogenase (SDH) activities and by liver histopathology. Higher plasma ALT elevations were observed in F344 rats following administration of 0.2 and 0.6 ml o-DCB/kg. Using SDH as a marker of liver injury, the strain difference was evident only at 0.2 ml o-DCB/kg. Liver regeneration was estimated by 3H-thymidine incorporation into hepatonuclear DNA and via proliferating cell nuclear antigen (PCNA) assay. Prompt and significantly higher hepatocellular regeneration beginning at 36 h was evident in F344 rats following administration of 0.2 and 0.6 ml o-DCB/kg. The significantly higher depletion of hepatic glycogen observed in F344 rats following administration of 0.2 and 0.6 ml o-DCB/kg occurred without significant changes in plasma glucose and is consistent with highly stimulated tissue repair seen in these rats at the corresponding doses. However, increasing the dose further to 1.2 ml o-DCB/kg results in a delayed (S-phase synthesis begins at 48 h) and diminished response to o-DCB. These findings suggest that a significantly higher rate of tissue repair in F344 rats helps them overcome higher liver injury inflicted by o-DCB. This differential in tissue repair in the two strains may play a vital role in equalizing the ultimate outcome of toxicity in the two strains.