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Q. Pedar, M.B. B.CH. B.A.O., M.B.B.Ch., Ph.D.
Medical Instructor, University of Houston
Evidence of low molecular weight components in the organic matrix of the reef building coral, Stylophora pistillata. Comparative Biochemistry and Physiology - Part A: Molecular & Integrative Physiology 147: 850-856. Antibodies against the organic matrix in scleractinians: a new tool to study coral biomineralization. Coral Reef Targeted Research and Capacity Building for Management Program, University of Queensland. Getting bigger faster: Mediation of size-specific mortality via fusion in juvenile coral transplants. Porites ulcerative white spot disease: description, prevalence, and host range of a new coral disease affecting IndoPacific reefs. In vivo light-microscopic documentation for primary calcification processes in the hermatypic coral Stylophora pistillata. Discrete Bands of Petroleum Hydrocarbons and Molecular Organic Markers Identified Within Massive Coral Skeletons. Effect of light on skeletal delta 13C and delta 18O, and interaction with photosynthesis, respiration and calcification in two zooxanthellate scleractinian corals. Effect of light and temperature on calcification and strontium uptake in the scleractinian coral Acropora verweyi. Preliminary investigations into the chemical nature of mucus from the staghorn coral (Acropora formosa). Characterization of superoxide dismutases in anoxia- and hyperoxia-tolerant symbiotic cnidarians. Energetics, Competence, and Long-Distance Dispersal of Planula Larvae of the Coral Pocillopora damicornis. Coral-Reefs - Present Problems and Future Concerns Resulting from Anthropogenic Disturbance. Laboratory experiments on the effects of crude oil on the Red Sea coral Stylophora pistillata. Temporal and spatial infection dynamics indicate recognition events in the early hours of a dinoflagellate/coral symbiosis. Alteration of normal cellular profiles in the scleractinian coral (Pocillopora damicornis) following laboratory exposure to fuel oil. Quantitative assessment of coral diseases in the Florida Keys: strategy and methodology. Late Larval Development and Onset of Symbiosis in the Scleractinian Coral Fungia scutaria. Asexual reproduction does not produce clonal populations of the brooding coral Pocillopora damicornis on the Great Barrier Reef, Australia. A single cyanobacterial ribotype is associated with both red and black bands on diseased corals from Palau. Observations of the tissue-skeleton interface in the scleractinian coral Stylophora pistillata. Widespread occurrence of mycosporine-like amino acid compounds in scleractinians from French Polynesia. Maintenance of ancestral complexity and non-metazoan genes in two basal cnidarians. Patterns of formation and the ultrastructure of the larval skeleton of Pocillopora damicornis. Interaction between benthic algae (Lyngbya bouillonii, Dictyota dichotoma) and scleractinian coral Porites lutea in direct contact. Posterior expression of nanos orthologs during embryonic and larval development of the anthozoan Nematostella vectensis. Effects of spatial variability and colony size on the reproductive output and gonadal development cycle of the Mediterranean red coral (Corallium rubrum L.
No pre-existing fault had been detected at this location, suggesting that small "pre-existing fractures or smalloffset (sub-seismic) faults may have focused the energy of hydraulic fractures on certain areas. The injection well operator, American Water Management Services, had recently received permission to increase pressures at the site of the wells. In 2012, Governor John Kasich had halted disposal of fracking wastewater surrounding a well site in the same region after a series of earthquakes were tied to a deep-injection well. The state placed seismic-monitoring devices in the Warren area under protocols adopted after the series of earthquakes in nearby Youngstown. An evaluation of fracture growth and gas/fluid migration as horizontal Marcellus Shale gas wells are hydraulically fractured in Greene County, Pennsylvania. The 2001-present induced earthquake sequence in the Raton Basin of Northern New Mexico and Southern Colorado [abstract]. Seismic movement can be caused if the rate of injection is too fast or if there is a geological feature, such as a fault or fracture in nearby areas. Although Albertans in rural areas have been reporting for years that they can feel tremors under their feet near oil and gas activity, especially around areas of fracking, the Alberta Energy Regulator noted that deep well injections have been shown to create more of an earthquake hazard than hydraulic fracturing. In comparison, Saskatchewan recorded 13 in the same time period and British Columbia recorded more than 1,200 earthquakes in 2007 alone. There are currently 24 seismic monitors in Alberta, which are tied into other networks, such as those belonging to Environment Canada, University of Calgary, and University of Alberta. In addition, residents of Oklahoma, where a sharp spike in earthquake activity has been noted over the past decade, are showing an increased interest in obtaining earthquake insurance. Moreover, injected fluids in high volume wells triggered earthquakes over 30 kilometers (over 18 miles) away. Similar mechanisms may function in other states with high volumes of underground injection of wastewater from unconventional oil and gas production. Earthquake hazard linked with deep well injection in Alberta: Deep well disposal of oilfield waste over time leads to increased earthquake risk. Sharp increase in central Oklahoma seismicity since 2008 induced by massive wastewater injection. The surges of natural gas that caused the explosive tremors (earthquakes) may have weakened an adjacent salt cavern and caused its collapse. Alternatively, part of the salt cavern may have collapsed, causing a nearby gas pocket to give off surges of gas, later followed by the complete collapse of the salt cavern. These findings help illuminate the role of pressurized fluids in triggering seismic events. Monitoring by a team of seismologists from the University of Colorado had picked up evidence of continuing lowlevel seismic activity near the injection site, including a magnitude 2. The advisory stated that this dramatic increase in the frequency of small earthquakes "significantly increases the chance for a damaging quake in central Oklahoma. During the first four months of 2014, Oklahoma had experienced 109 earthquakes of magnitude 3 or higher on the Richter 803 Schmall, E. Moment tensor inversion of seismic events associated with the sinkhole at Napoleonville Salt Dome, Louisiana. Colorado drilling regulators halt injection-well activity in reaction to Greeley quake. Colorado regulators halt fracking wastewater injection operation after earthquake strikes area for second time in a month. By mid-June, the number of earthquakes had topped 200, exceeding the frequency of earthquakes in California. They also noted a statistical correlation between seismic activity and fracking, particularly in the border state of Nuevo Leon, which registered at least 31 quakes between magnitude 3. An investigation of seismicity clustered near the Cordel Field, west central Alberta, and its relation to a nearby disposal well. As the New York Times noted, "Oklahoma has never been known as earthquake country, with a yearly average of about 50 tremors, almost all of them minor.
Astrocytes, star-shaped neuronal cells, encapsulate the capillaries, forming a "blood-brain barrier" and controlling many important neurologic functions. Because the amount of intracellular water affects the concentration of intracellular contents and cell size, changes in osmolality can disturb the complex signaling network that orchestrates cell function. Given the complexity of brain function, even minor changes in neuron ionic composition and size can have profound effects on the processing and transmission of neuronal signals. Consequently, the brain has developed complex osmoregulatory mechanisms to defend against changes in plasma osmolality. Penetrating capillaries descend through the subarachnoid space into the parenchyma, and are encased by astrocytes, which in addition to controlling important neurologic functions, form the blood-brain barrier. In the setting of hypotonicity, as shown in Figure 2, the rapid swelling of the cell activates quiescent cell membrane channels and leads to immediate Cl2, K1, and attendant water loss, a process termed regulatory volume decrease. Over the subsequent 24 hours, the cells lose further organic solutes, such as myo-inositol, and amino acids, such as glutamine, glutamate, and taurine. With hyperosmolar-induced cell shrinkage, brain cells respond with immediate uptake of surrounding Na1, K1, and Cl2, correcting cell volume in a process termed regulatory volume increase (12). With more prolonged exposure, organic solute concentrations within the cells rise, replacing the high levels of ions. Despite these important cell protective mechanisms, alterations in plasma osmolality can have disastrous consequences. The classic neurologic symptoms of hypo-osmolality, including headache, nausea, vomiting, and if severe enough, seizures, are generally thought to occur at a serum sodium 854 Clinical Journal of the American Society of Nephrology Figure 2. In this figure, a normal cell is challenged by either a hyperosmolar (left) or hypo-osmolar (right) milieu. In the setting of hyperosmolar stress, whereby the cell shrinks with water egress, neurons then respond by rapidly accumulating Na1, K1, and Cl2 ions, followed by the production of intracellular organic solutes. The increase of intracellular solute content then draws water in to normalize the concentrations across the cell membrane, thereby restoring cell size. More mild changes of plasma osmolality are also associated with neurologic symptoms, including gait instability, memory impairment, and cognitive decline. Children are considered at increased risk of hypo-osmolar encephalopathy, possibly because of the relatively larger brain to intracranial volume compared with adults (13). Conversely, because the brain begins to atrophy in the sixth decade, elderly individuals may be at a lower risk of severe complications from acute hyponatremia. In addition to age, sex is also considered an important determinant of neurologic sensitivity. The vast majority of reported cases of postoperative hyponatremia resulting in fatal outcomes have been in women (14), including postpartum and postmenopausal women (15). Unlike the brain swelling associated with hypo-osmolality, the brain shrinks in hypertonic conditions. The protective reflex of intense thirst may disappear as hypertonicity worsens, replaced by somnolence, confusion, and muscle weakness (16). If severe enough, the shrinking brain will pull away from the calvarium, tearing the rich capillary plexus, and causing subarachnoid hemorrhage, cerebral bleeding, and death. The highest reported serum sodium in the adult literature remains 255 mEq/L, a consequence of drinking salty water as part of a fatal exorcism ritual (17). Presumably due to the use of table salt as a common antiemetic, fatal salt ingestion, either accidentally or voluntarily, is well reported (18), as is accidental iatrogenic administration (19). In summary, despite internal cellular mechanisms to protect cell volume, cells remain at risk with alterations of water balance; consequently, preventing significant changes in plasma osmolality is critical for survival. Sensing Changes in Body Concentration: the Osmoreceptor the ability to internally sense plasma osmolality is fundamental to the process of water homeostasis. Much progress in explaining the mechanisms of the "osmoreceptor" has been made, as reviewed by Sharif-Naeini et al. Electrophysiologic recordings from supraoptic nuclei of the hypothalamus in rats show an increasing rate of cellular depolarization in response to water deprivation (26), and a decreasing rate with water administration (27). More recent studies have shown that hyperosmolality causes osmoreceptor membrane depolarization via activation of nonselective calcium-permeable cation channels.
For every 1 liter of water change, approximately 666 ml affect the cellular space, with only about 110 ml affecting the vascular space. The amount of body water remains remarkably stable despite a huge range of water intake and a multitude of routes for water loss, including the respiratory and gastrointestinal tract, skin, and the kidneys. Maintaining Brain Cell Size With a plethora of capillaries descending through the subarachnoid space into the parenchyma, the brain is remarkably vascular. It remains somewhat unresolved whether the exact stimulus is change of specific intracellular solutes associated with cell dehydration or a mechanical effect linked to cell membrane shrinkage. The importance of cell volume in neuronal activation would explain why ineffective osmoles that cross the cell membrane, such as urea and glucose (in the presence of insulin), do not activate the osmoreceptor. The osmoreceptor, likely because of its role in orchestrating the pathways of water retention, has a blunted regulatory volume decrease response, whereby its own shrinkage due to hyperosmolality is maintained, allowing sustained stimulation of thirst and vasopressin release until the plasma osmolality can be corrected (30). In the following sections, we discuss how the osmoreceptor regulates thirst and vasopressin (synonymously known as antidiuretic hormone) release. Thirst the sensation of thirst is the experiential component of the complex physiologic drive to drink. Neuroimaging studies have localized the anatomic origin of thirst, with hyperosmolality stimulating activity in the anterior wall of the third ventricle, the anterior cingulate, parahippocampal gyrus, insula, and the cerebellum (31). These brain regions are also associated with complex functions, including emotional behavior and thought, perhaps explaining why the perception of thirst, in addition to its physiologic basis, is so connected to social and behavioral mores. The osmolar threshold for thirst has traditionally been considered to be approximately 5 mOsm/kg above the threshold for vasopressin release, although some suggest similar set points (32). A higher thirst threshold allows vasopressin titration of urinary water excretion without the need to be constantly drinking. Upon drinking, the sensation of thirst is quenched almost immediately, suggesting that a direct satiating effect of water on the tongue and buccal membrane as well as cognitive awareness of fluid intake might explain the resolution of thirst. In addition, the recent recognition of peripheral osmoreceptors located within the gastrointestinal tract and portal venous system suggest a local mechanism that directly senses gastric water absorption (34). Whether these peripheral osmoreceptors might contribute to the disorders of osmolality frequently seen in patients with cirrhosis remains unknown. Thirst on the battlefield is legendary, with exsanguinating soldiers asking for water. Conversely, hypo-osmolar cell swelling deactivates these channels, leading to cell hyperpolarization, extinguishing thirst and vasopressin release. Thirst is a common complaint for patients with congestive heart failure (43,44), frequently plagues dialysis patients, and likely contributes to the prevalence of hyponatremia in these populations. Pharmacologic blockade of the renin-angiotensin axis, although theoretically attractive, does not seem to reduce thirst (45). In addition to disorders of fluid volume, thirst is also frequently encountered in patients with psychiatric disorders, reported in up to 25% of hospitalized patients with schizophrenia. Although this might be in part due to compulsive behavior or the anticholinergic side effects of psychotropic medications, studies have suggested an alteration of the sensation of thirst in patients with mental illness, with a lower osmolar threshold (46). It is synthesized as a prohormone in the magnocellular cell bodies of the paraventricular and supraoptic nuclei of the posterior hypothalamus, and by binding to the carrier protein neurohypophysin, it is transported along the supraoptic hypophyseal tract to the axonal terminals of magnocellular neurons in the posterior pituitary. The most sensitive stimulus for vasopressin release is increasing plasma osmolality. The presence of stored vasopressin in the pituitary guarantees a rapid and effective mechanism of water regulation. As water is retained and the plasma osmolality returns to normal, the stimuli for vasopressin release is extinguished. Such high concentrations rapidly exhaust the pituitary vasopressin stores, and given the time-consuming nature of vasopressin production, vasopressin depletion is thought contributory to shock physiology (53). Subtle changes in body fluid volume modify the responsiveness of vasopressin release to osmolality. Early physiologic experiments on dogs using either hemorrhage or transfusion illustrated that circulatory blood volume modified the association between plasma osmolality and vasopressin (54). For any given plasma osmolality, hemorrhage was associated with a higher vasopressin concentration, whereas transfusion was associated with a lower vasopressin concentration. Although myriad terms, such as intravascular volume, effective arterial volume, or circulatory volume, have been used to describe the component of body fluid that effectively perfuses critical organs, these terms imply that the vascular compartment is readily measurable, a feat that is difficult in the laboratory and impossible at the bedside.
