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A paleohydrothermal giant quartz reef (at least 75 m wide, 40 km long) and abundant hot springs at the Heyuan fault, South China, provide an excellent opportunity to investigate hydrothermal flows from the Mesozoic through to present-day.The giant quartz reef has formed in the extensional regime initiated in the Mesozoic, while a change to compressional stress on the Heyuan in the Cenozoic led to the development of cross-cutting strike-slip faults and associated vertical fracture network. Here, we present multiscale observations and analyses from the earlier long-term extensional phase.Detailed microstructural analyses identified a 'quartz-reef window' of formation occurring between ~200-350˚C, linking in both quasi-static criteria (accommodation space; massive fluid sources; and a cap rock/seal) and dynamic mechanisms (episodic-dynamic permeability; brittle-ductile cycles; and fluid injection though brittle-ductile equivalent of Sibson's 'fault-valve' behaviour.This oscillatory brittle-ductile fault-valve is recorded in the field through its apparent contradiction between idiomorphic 5 cm long quartz crystal growth in mode-I fractures, embedded at large-scale inside far from equilibrium fault zones with mylonitic and cataclastic microstructures. Another characteristic feature is the increasing quartz vein frequency towards the core shown by enrichment of SiO2, with depletion of K2O and Na2O in tectonites during alteration from the host granite; a reaction partly sourcing the SiO2 for the quartz reef.We present a first theoretical model compatible with the observation of oscillatory macroscale far from equilibrium conditions, followed by long periods of micro-scale local equilibrium. The model can in particular describe mechanisms of abundant SiO2 dominated fluid release reaching episodically above hydrostatic pressures followed by long periods of SiO2 precipitation, allowing growth of up to 5 cm long idiomorphic quartz crystals in subparallel open channels, which presumably were held open by high fluid pressures. In this interpretation, the observations instabilities are seen to stem from the multiscale and multiphysics of the mineral reactions at the brittle-ductile transition, promoted by a slow extensional geodynamic driver at the Heyuan fault.The new approach allows interpretation of rock physics properties in terms of recently discovered Thermo-Hydro-Mechanical-Chemical (THMC) multiscale wave-like instabilities. In the model short wavelength chemical dissolution-precipitation reaction waves are bouncing between the phyllonitic cap rock and the mylonitic shear zone below. A resonance phenomenon of constructive interference in a finite width around the future quartz-reef triggers the long-time scale steady-state attractor allowing quartz reef growth over geodynamic time scales. We show that this solitary wave limit forms a standing wave matching the characteristic periodic pattern of mode-I quartz veining around the reef and also explaining the fluid overpressures leading to local hydro-fracturing.

Geothermal energy potential in China is high, and although they currently lead the way in direct heat production, geothermal power generation is still low. Hot spring analysis and surface heat flux data indicate significant potential resources for the major industrial province of Guangdong, South China. This pilot study investigates the Heyuan Fault, Guangdong, as a potential site for a geothermal power plant. Here we line out (i) preferred locations of possible hot spots on fault intersections, (ii) the possible sources of the heat anomalies, (iii) potential pathways for hot fluid circulation in the upper crust, (iv) available hot spring data and (v) the future work plan to investigate the geothermal hot spots. We find that hot springs occur along the NE trending Heyuan Fault, clustering where NNW striking faults crosscut the Heyuan. The increased heat flow can be explained partly by radioactive decay of a large granite pluton beneath the fault, however, additional heat sources may need to be considered to explain the heat flow maxima of above 85 mWm-2. We postulate that advective (topographically driven) and convective (deep fluids ponding at the brittle-ductile transition) processes may be operating to generate these heat anomalies. Expansive quartz reef systems exposed on the Heyuan Fault, are proposed here, to represent uplifted sections of these deep fluid circulation patterns. A detailed systematic analysis of reef structures will reveal (i) the fluid provenance, (ii) precipitation conditions and (iii) deformation mechanisms, which will ultimately help us understand how fault intersection relations control fluid flow; which is of key significance if it can be utilised for targeting geothermal energy.

The South China, Heyuan Fault Zone provides unique crustal exposure to study the meso- macroscale architecture of evolving fracture networks in response to a change in tectonic stress regime and associated changing fluid flow pathways. Multiple generations of fracturing across the fault zone reveal its structural evolution related to the change in stress regime from extensional (since the Mesozoic) to transpressive (in the Cenozoic), which coincides with generations of growth and fracturing on the microscale. Low angle, mode-I fractures, quartz veining, and a giant quartz reef (>75 m wide and 40 km long) were formed due to a combination of chemo-mechanical mechanisms, including a crucial phyllonite ‘cap rock’, during the extensional phase. This evolved through to a predominately sub-vertically aligned, shear fracture network, exhibiting only minor quartz precipitation. These open fractures are attributed to the transpressive regime experienced since the Cenozoic, in which strike-slip faults cross-cut the Heyuan Fault. We propose that this sub-vertical fracture network provides the fluid flow pathway supplying the present-day hot springs by penetrating through the phyllonite seal, which previously enabled SiO2 accumulation. Additionally, further quartz-reef building would likely be reduced due to (i) lack of seal integrity, and (ii) an unfavourable tectonic setting to channel the flow and provide accommodation space.

A long-lived hydrothermal system at the Heyuan fault, South China, has led to the development of a giant quartz reef, now partially exhumed along its length for more than 40 km. Systematic analyses and focused microstructural studies have been undertaken to unravel a complex formation history of repeated fracturing, hydrothermal fluid flow and sealing cycles, resulting in a dynamic permeability across the fault zone. The change in morphology and decreasing grain size with time further indicates the move from slow ductile opening to fast seismic events. Quartz-reef formation has been estimated to occur within a range of ~200–350 °C, based on evaluation of (i) quartz deformation microstructures; (ii) chlorite and mica geothermometry; and (iii) review of comparable quartz-reef studies. Additionally, a set of physico-chemical formation conditions have been identified which compose the ‘quartz-reef window’. These are: (i) significant volume of fluid; (ii) fluid sources from meteoric, metamorphic and/or from mantle origin; (iii) considerable Time-Integrated Fluid Fluxes; (iv) SiO2 oversaturation due to (a) temperature change, (b) sudden pressure drop, or (c) chemical change e.g. fluid mixing; (v) accommodation space to ‘grow’ the reef; (vi) channel permeability; and (vii) cap rock/seal to trap the fluid flow. The mechanism of quartz-reef growth is here interpreted as the brittle-ductile analogue of the brittle fault-valve model.

Background: Proteoglycans, a major component of extracellular matrix in the vascular wall, play a critical role in the development of atherosclerosis due to their ability to bind and retain atherogenic lipoproteins. Of all the vascular proteoglycans, biglycan has been shown to be the one most closely associated with apolipoprotein B. Our previous studies showed that AngII increases vascular biglycan content and predisposes to diet-induced atherosclerosis in Ldlr null mice. Moreover, we demonstrated that TGFβ is required for AngII stimulation of vascular biglycan content in vitro . In this study, we determined whether TGFβ is required for AngII-induced biglycan accumulation and atherosclerosis predisposition in vivo . Methods and Results: Ldlr null mice fed a normal chow diet were infused with AngII or saline for 28 days. TGFβ1 levels in AngII-infused mice peaked at 24h then returned to baseline levels by day 5. A single injection of TGFβ neutralizing antibody 1D11 (2mg/kg) not only prevented the induction of TGFβ1 levels by AngII, but also attenuated AngII-induced accumulation of aortic biglycan content, whereas there was no attenuation of AngII-induced increase in TGFβ or biglycan by a control antibody. To study atherosclerosis, the experiment was repeated but after 28 days of AngII or saline infusions the pumps were removed and the mice were fed Western diet for 6 weeks. TGFβ neutralizing antibody injection had no effect on systolic blood pressure or plasma lipids (triglyceride and cholesterol). However, AngII-infused mice that received TGFβ neutralizing antibody injection showed reduced atherosclerotic lesion area (aorta root, en face and the brachiocephalic artery) compared to AngII-infused mice that received a control antibody injection. Therefore, our study showed that TGFβ inhibition attenuates AngII stimulation of vascular biglycan content in vivo and attenuates AngII-accelerated atherosclerosis.

Serum amyloid A (SAA), along with high sensitivity C- Reactive Protein, is a clinical marker of atherosclerosis, a vascular inflammatory disease responsible for half a million deaths per year in the US. Interestingly, SAA is modestly but chronically elevated in several diseases such as diabetes and obesity that confer greater risk to developing atherosclerosis. Recently SAA has been shown to contribute to the progression of atherosclerosis but its role in initiation of atherosclerosis has yet to be determined. As outlined in the response to retention hypothesis of atherosclerosis, proteoglycan mediated lipoprotein retention is thought to be a key initiating step. We previously demonstrated that mice overexpressing SAA had increased vascular biglycan, a small matrix proteoglycan, which was larger and had greater LDL binding affinity than native biglycan. Here we tested the hypothesis that overexpression of SAA would lead to increased atherosclerosis. ApoE -/- male mice were injected with an adenovirus carrying the gene for SAA (adSAA), a null control (adnull) or saline and maintained on chow for 16 weeks. SAA was elevated immediately after injection of adSAA but returned to baseline by 10 days; there was no elevation of SAA in adnull or saline injected mice. Although the duration of elevation of SAA was short, mice injected with adSAA had significantly increased atherosclerosis at the aortic sinus (p

A novel protein kinase, the Esk kinase, has been isolated from an embryonal carcinoma (EC) cell line by using an expression cloning strategy. Sequence analysis of two independent cDNA clones (2.97 and 2.85 kb) suggested the presence of two Esk isoforms in EC cells. The esk-1 cDNA sequence predicted an 857-amino-acid protein kinase with a putative membrane-spanning domain, while the esk-2 cDNA predicted an 831-amino-acid kinase which lacked this domain. In adult mouse cells, esk mRNA levels were highest in tissues possessing a high proliferation rate or a sizeable stem cell compartment, suggesting that the Esk kinase may play some role in the control of cell proliferation or differentiation. As anticipated from the screening procedure, bacterial expression of the Esk kinase reacted with antiphosphotyrosine antibodies on immunoblots. Furthermore, in in vitro kinase assays, the Esk kinase was shown to phosphorylate both itself and the exogenous substrate myelin basic protein on serine, threonine, and tyrosine residues, confirming that the Esk kinase is a novel member of the serine/threonine/tyrosine family of protein kinases.

A novel protein kinase, the Esk kinase, has been isolated from an embryonal carcinoma (EC) cell line by using an expression cloning strategy. Sequence analysis of two independent cDNA clones (2.97 and 2.85 kb) suggested the presence of two Esk isoforms in EC cells. The esk-1 cDNA sequence predicted an 857-amino-acid protein kinase with a putative membrane-spanning domain, while the esk-2 cDNA predicted an 831-amino-acid kinase which lacked this domain. In adult mouse cells, esk mRNA levels were highest in tissues possessing a high proliferation rate or a sizeable stem cell compartment, suggesting that the Esk kinase may play some role in the control of cell proliferation or differentiation. As anticipated from the screening procedure, bacterial expression of the Esk kinase reacted with antiphosphotyrosine antibodies on immunoblots. Furthermore, in in vitro kinase assays, the Esk kinase was shown to phosphorylate both itself and the exogenous substrate myelin basic protein on serine, threonine, and tyrosine residues, confirming that the Esk kinase is a novel member of the serine/threonine/tyrosine family of protein kinases.

In a screen of mouse erythroleukemia cDNA expression libraries with anti-phosphotyrosine antibodies, designed to isolate tyrosine kinase coding sequences, we identified several cDNAs encoding proteins identical or very similar to known protein-tyrosine kinases. However, two frequently isolated cDNAs, clk and nek, encode proteins which are most closely related to protein kinases involved in regulating progression through the cell cycle, and contain motifs generally considered diagnostic of protein-serine/threonine kinases. The clk gene product contains a C-terminal cdc2-like kinase domain, most similar to the FUS3 catalytic domain. The Clk protein, expressed in bacteria, becomes efficiently phosphorylated in vitro on tyrosine as well as serine/threonine, and phosphorylates the exogenous substrate poly(glu, tyr) on tyrosine. Direct biochemical evidence indicates that both protein-tyrosine and protein-serine/threonine kinase activities are intrinsic to the Clk catalytic domain. These results suggest the existence of a novel class of protein kinases, with an unusual substrate specificity, which may be involved in cell cycle control.