Hypolimnetic oxygenation 2: oxygen dynamics in a large reservoir with submerged down-flow contact oxygenation (Speece cone)

To unveil the activation of dioxygen on the copper centre (Cu2O2core) of tyrosinase, we performed X-ray crystallograpy with active-form tyrosinase at near atomic resolution. This study provided a novel insight into the catalytic mechanism of the tyrosinase, including the rearrangement of copper-oxygen species as well as the intramolecular migration of copper ion induced by substrate-binding.

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RESERVOIR CONNECTIVITY ASSESSMENT USING NEW FORMATION TESTING PLATFORM AND IMAGE LOG EVALUATION INDICATES CONNECTIVITY ACROSS A LARGE RESERVOIR OFFSHORE MEXICO

10.30632/spwla-5001 ◽

2020 ◽

Author(s):

Rahul Umrani ◽

◽

Joel Speights ◽

David Tett ◽

Alex Obvintsev ◽

...

Keyword(s):

Large Reservoir ◽

Testing Platform ◽

Reservoir Connectivity ◽

New Formation

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Accuracy for the Computation of Water Balance of a Large Reservoir of the Ussr

Man-Made Lakes: Their Problems and Environmental Effects - Geophysical Monograph Series ◽

10.1029/gm017p0283 ◽

2013 ◽

pp. 283-286

Author(s):

Z. A. Vikulina ◽

T. D. Kashinova

Keyword(s):

Water Balance ◽

Large Reservoir

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Exploitation of Marine Molecules to Manage Alzheimer’s Disease

Marine Drugs ◽

10.3390/md19070373 ◽

2021 ◽

Vol 19 (7) ◽

pp. 373

Author(s):

Marisa Silva ◽

Paula Seijas ◽

Paz Otero

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Senile Plaques ◽

Nmda Receptor Antagonists ◽

Average Life ◽

Average Life Expectancy ◽

Large Reservoir ◽

Drug Candidates ◽

Neurodegenerative Process ◽

Main Action

Neurodegenerative diseases are sociosanitary challenges of today, as a result of increased average life expectancy, with Alzheimer’s disease being one of the most prevalent. This pathology is characterized by brain impairment linked to a neurodegenerative process culminating in cognitive decline and behavioral disorders. Though the etiology of this pathology is still unknown, it is usually associated with the appearance of senile plaques and neurofibrillary tangles. The most used prophylaxis relies on anticholinesterase drugs and NMDA receptor antagonists, whose main action is to relieve symptoms and not to treat or prevent the disease. Currently, the scientific community is gathering efforts to disclose new natural compounds effective against Alzheimer’s disease and other neurodegenerative pathologies. Marine natural products have been shown to be promising candidates, and some have been proven to exert a high neuroprotection effect, constituting a large reservoir of potential drugs and nutraceutical agents. The present article attempts to describe the processes of extraction and isolation of bioactive compounds derived from sponges, algae, marine bacteria, invertebrates, crustaceans, and tunicates as drug candidates against AD, with a focus on the success of pharmacological activity in the process of finding new and effective drug compounds.

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Inhibition of atrial peptide secretion at different stages of the secretory process: Ca2+ dependence

AJP Cell Physiology ◽

10.1152/ajpcell.1991.261.6.c1162 ◽

1991 ◽

Vol 261 (6) ◽

pp. C1162-C1172 ◽

Cited By ~ 13

Author(s):

E. Page ◽

J. Upshaw-Earley ◽

G. E. Goings ◽

D. A. Hanck

Keyword(s):

Protein Synthesis ◽

Brefeldin A ◽

Atp Depletion ◽

Secretory Process ◽

Protein Synthesis Inhibitors ◽

Large Reservoir ◽

Secretory Rate ◽

Vesicular Traffic ◽

Dependent Inactivation

We have used a noncontracting in vitro preparation of stretched and unstretched rat atria to estimate contributions of constitutive and regulated pathways to the rates of stretch-augmented and basal secretion of immunoreactive atrial natriuretic peptide (ANP) and to examine effects of inhibition of the secretory sequence by 1) protein synthesis inhibitors, 2) disruption of forward vesicular traffic between endoplasmic reticulum and Golgi with brefeldin A (BFA, and 3) cellular ATP depletion. Protein synthesis inhibition with cycloheximide for 44 min slowed neither basal nor stretch-augmented ANP secretion but instead accelerated stretch-augmented secretion at low (but not at physiological) external Ca2+ concentration, suggesting that the constitutive component does not contribute substantially to either basal or stretch-augmented secretion. BFA, which disassembled Golgi cisternae, increased the stretch-augmented secretory rate via the regulated pathway and prevented Ca(2+)-dependent inactivation with time. Cellular ATP depletion rapidly and completely inhibited stretch-augmented secretion. We conclude that both basal and stretch-augmented utilize the energy-dependent regulated pathway, drawing on a large reservoir of concentrated prohormone stored in granules that is not detectably depleted during 44 min of stretch-augmented secretion at 37 degrees C.

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Continuing Mycobacterium bovis transmission from animals to humans in New Zealand

Epidemiology and Infection ◽

10.1017/s0950268806005930 ◽

2006 ◽

Vol 134 (5) ◽

pp. 1068-1073 ◽

Cited By ~ 33

Author(s):

M. G. BAKER ◽

L. D. LOPEZ ◽

M. C. CANNON ◽

G. W. DE LISLE ◽

D. M. COLLINS

Keyword(s):

New Zealand ◽

Restriction Endonuclease ◽

Mycobacterium Bovis ◽

Restriction Endonuclease Analysis ◽

Domestic Animals ◽

Human Infection ◽

Potential Contribution ◽

Large Reservoir ◽

Animal Reservoirs ◽

Endonuclease Analysis

New Zealand has a large reservoir of Mycobacterium bovis infection in wild and farmed animals. This study aimed to assess the extent of human infection with this organism and the potential contribution of these animal sources. Combined epidemiological and laboratory investigation of human tuberculosis cases over the period 1995–2002 showed that M. bovis accounted for 2·7% (54/1997) of laboratory-confirmed human tuberculosis cases, a rate of 0·2/100000 population. M. bovis isolates from humans (23) were typed using restriction endonuclease analysis (REA) and compared with isolates from wild and domestic animals (2600). Fourteen (61%) of the human isolates had REA patterns that were identical to patterns for isolates from cattle, deer, possums, ferrets, pigs, and occasionally cats. These results suggest a low level of ongoing M. bovis transmission from animal reservoirs to humans in New Zealand.

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Stem cell factor and c-kit are involved in hepatic recovery after acetaminophen-induced liver injury in mice

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00024.2008 ◽

2008 ◽

Vol 295 (1) ◽

pp. G45-G53 ◽

Cited By ~ 35

Author(s):

Bin Hu ◽

Lisa M. Colletti

Keyword(s):

Stem Cell ◽

Liver Injury ◽

Stem Cell Factor ◽

Cellular Proliferation ◽

Hepatocyte Proliferation ◽

Mrna Levels ◽

Wild Type ◽

Hepatocyte Apoptosis ◽

Large Reservoir ◽

A Cell

Stem cell factor (SCF) and its receptor c-kit are important in hematopoiesis and cellular proliferation. c-kit has also been identified as a cell surface marker for progenitor cells. We have previously shown that there is a large reservoir of hepatic SCF, and this molecule plays a significant role in liver regeneration after 70% hepatectomy. In the current study, we further examined the expression of SCF and c-kit in acetaminophen (APAP)-induced liver injury in C57BL/6J mice or SCF-deficient sl-sld mice and their appropriate wild-type controls. Following APAP-induced liver injury, c-kit mRNA expression increased, with peak levels detected 48 h postinjury. Hepatic SCF mRNA levels after APAP injury were also increased, with peak levels seen 16 h post-APAP. The mortality rate in SCF-deficient mice treated with APAP was significantly higher than that of wild-type mice; furthermore, administration of exogenous SCF significantly reduced the mortality of APAP-treated wild-type mice. Bromodeoxyuridine incorporation experiments showed that SCF significantly increased hepatocyte proliferation at 48 and 72 h in APAP-treated mice. SCF inhibited APAP-induced hepatocyte apoptosis and increased Bcl-2 and Bcl-xL expression, suggesting that this decrease in hepatocyte apoptosis is mediated through Bcl-2 and Bcl-xL. In summary, SCF and c-kit expression was increased after APAP-induced liver injury. Administration of exogenous SCF reduces mortality in APAP-treated mice, increases hepatocyte proliferation, and prevents hepatocyte apoptosis induced by APAP, suggesting that these molecules are important in the liver's recovery from these injuries.

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