Cementation scenarios for New Zealand Cenozoic nontropical limestones

Cenozoic limestones are widely distributed in New Zealand, especially in the Oligocene-earliest Miocene in both islands, and the Pliocene-Pleistocene in North Island. A spectrum of limestone types exists, but all are skeletal-dominated (>70%), with usually <20% interparticle cement-matrix and <10% siliciclasts, and they have facies attributes typical of nontropical carbonates. The range of diagenetic features identified within the limestones is the basis for assigning them to a small number of “end-member” cementation classes that are inferred to be associated with four, broad, diagenetic settings

Lithostratigraphy and depositional episodes of the Oligocene carbonate-rich Tikorangi Formation, Taranaki Basin, New Zealand

The subsurface Oligocene Tikorangi Formation is a unique and important oil producer in the onshore Waihapa-Ngaere Field, Taranaki Basin, being the only carbonate and fracture-producing reservoir within the basin. Core sample data from seven onshore wells (foredeep megafacies) and a single offshore well (basinal megafacies) are correlated with a suite of sonic and gamma-ray geophysical well log data to derive interpretative carbonate facies for the Tikorangi Formation. Four mixed siliciclastic-carbonate to carbonate facies have been defined: facies A-calcareous siliciclastite (75% carbonate). Single or interbedded combinations of these facies form the basis for identifying nine major lithostratigraphic units in the Tikorangi Formation that are correlatable between the eight wells in this study.The Tikorangi Formation accumulated across a shelf-slope-basin margin within a tectonically diversified basin setting, notably involving considerable off-shelf redeposition of sediment into a bounding foredeep. Analysis of gamma, sonic, and resistivity well logs identifies five major episodes of sedimentary evolution. Episode I comprises retrogradational siliciclastic-dominated redeposited units associated with foredeep subsidence. Episode II is a continuation of episode I retrogradation, but with increased mass-redeposited carbonate influx during accelerated foredeep subsidence and relative sea-level rise, the top marking the maximum flooding surface. Episode III involves a progradational sequence comprising relatively pure redeposited carbonate units associated with declining subsidence rates and minimal siliciclastic input, with movement of facies belts basinward. Episode IV consists of prograding aggradation involving essentially static facies belts dominated by often thick, periodically mass-emplaced, carbonate-rich units separated by thin background siliciclastic shale-like units. Episode V is a retrogradational sequence marking the reintroduction of siliciclastic material into the basin following uplift of Mesozoic basement associated with accelerated compressional tectonics along the Australia-Pacific plate boundary, initially diluting and ultimately extinguishing carbonate production factories and terminating deposition of the Tikorangi Formation

Petrogenesis of the Tikorangi Formation fracture reservoir, Waihapa-Ngaere Field, Taranaki Basin

The subsurface mid-Tertiary Tikorangi Formation is the sole limestone and the only fracture-producing hydrocarbon reservoir within Taranaki Basin. This study, based on core material from seven wells in the onshore Waihapa/Ngaere Field, uses a range of petrographic (standard, CL, UV, SEM) and geochemical techniques (stable isotope, trace element data, XRD) to unravel a complex diagenetic history for the Tikorangi Formation. A series of eight major geological-diagenetic events for the host rock and fracture systems have been established, ranging from burial cementation through to hydrocarbon emplacement within mineralized fractures. For each diagenetic event a probable temperature field has been identified which, combined with a geohistory plot, has enabled the timing of events to be determined. This study has shown that the Tikorangi Formation comprises a complex mixed siliciclastic-carbonate-rich sequence of rocks that exhibit generally tight, pressure-dissolved, and well cemented fabrics with negligible porosity and permeability other than in fractures. Burial cementation of the host rocks occurred at temperatures of 27-37°C from about 0.5-1.0 km burial depths. Partial replacement dolomitisation occurred during late burial diagenesis at temperatures of 36-50°C and at burial depths of about 1.0 km, without any secondary porosity development. Fracturing occurred after dolomitisation and was associated with compression and thrusting on the Taranaki Fault. The location of more carbonate/dolomite-rich units may have implications for the location of better-developed fracture network systems and for hydrocarbon prospectivity and production. Hydrocarbon productivity has been ultimately determined by original depositional facies, diagenesis, and deformation. Within the fracture systems, a complex suite of vein calcite, dolomite, quartzine, and celestite minerals has been precipitated prior to hydrocarbon emplacement, which have substantially healed and reduced fracture porosities and permeabilities. The occurrence of multiple vein mineral phases, collectively forming a calcite/dolomite-celestite-quartzine mineral assemblage, points to fluid compositions varying both spatially and temporally. The fluids responsible for vein mineralisation in the Tikorangi Formation probably involved waters of diverse origins and compositions. Vein mineralisation records a history of changing pore fluid chemistry and heating during burial, punctuated by changes in the relative input and mixing of downward circulating meteoric and upwelling basinal fluids. A sequence of mineralisation events and their probable burial depth/temperature fields have been defined, ranging from temperatures of 50-80°C and burial depths of 1.0-2.3 km. Hydrocarbon emplacement has occurred over the last 6 m.y. following the vein mineralization events. The Tikorangi Formation must continue to be viewed as a potential fracture reservoir play within Taranaki Basin

Lithostratigraphy and depositional episodes of the Oligocene carbonate-rich Tikorangi Formation, Taranaki Basin, New Zealand

The subsurface Oligocene Tikorangi Formation is a unique and important oil producer in the onshore Waihapa-Ngaere Field, Taranaki Basin, being the only carbonate and fracture-producing reservoir within the basin. Core sample data from seven onshore wells (foredeep megafacies) and a single offshore well (basinal megafacies) are correlated with a suite of sonic and gamma-ray geophysical well log data to derive interpretative carbonate facies for the Tikorangi Formation. Four mixed siliciclastic-carbonate to carbonate facies have been defined: facies A-calcareous siliciclastite (75% carbonate). Single or interbedded combinations of these facies form the basis for identifying nine major lithostratigraphic units in the Tikorangi Formation that are correlatable between the eight wells in this study.The Tikorangi Formation accumulated across a shelf-slope-basin margin within a tectonically diversified basin setting, notably involving considerable off-shelf redeposition of sediment into a bounding foredeep. Analysis of gamma, sonic, and resistivity well logs identifies five major episodes of sedimentary evolution. Episode I comprises retrogradational siliciclastic-dominated redeposited units associated with foredeep subsidence. Episode II is a continuation of episode I retrogradation, but with increased mass-redeposited carbonate influx during accelerated foredeep subsidence and relative sea-level rise, the top marking the maximum flooding surface. Episode III involves a progradational sequence comprising relatively pure redeposited carbonate units associated with declining subsidence rates and minimal siliciclastic input, with movement of facies belts basinward. Episode IV consists of prograding aggradation involving essentially static facies belts dominated by often thick, periodically mass-emplaced, carbonate-rich units separated by thin background siliciclastic shale-like units. Episode V is a retrogradational sequence marking the reintroduction of siliciclastic material into the basin following uplift of Mesozoic basement associated with accelerated compressional tectonics along the Australia-Pacific plate boundary, initially diluting and ultimately extinguishing carbonate production factories and terminating deposition of the Tikorangi Formation

Petrologic evidence for earliest Miocene tectonic mobility on eastern Taranaki Basin margin

At Gibsons Beach on the west coast of central North Island, the earliest Miocene (Waitakian) Otorohanga Limestone, the top-most formation in the Te Kuiti Group, is unconformably overlain on an undulating, locally channelised erosion surface by the Early Miocene (Otaian) Papakura Limestone at the base of the Waitemata Group. The basal facies of the Papakura Limestone is a conglomerate composed exclusively of tightly packed pebble- to cobble-sized clasts of skeletal limestone sourced from the underlying Otorohanga Limestone. This petrographic and geochemical study demonstrates that the Otorohanga Limestone was partially lithified during marine and shallow-burial cementation at subsurface depths down to a few tens of metres prior to uplift, erosion and cannibalisation of the limestone clasts into the Papakura Limestone. Strontium isotope dating of fossils from both the Otorohanga and Papakura Limestones at Gibsons Beach yield comparable ages of about 22 Ma, close to the Waitakian/Otaian boundary, indicating very rapid tectonic inversion and erosion of the section occurred in the earliest Miocene. We envisage the clasts of Otorohanga Limestone were sourced from a proximal shoreline position and redeposited westwards by episodic debris flows onto a shallow-shelf accumulating mixed siliciclastic-skeletal carbonate deposits of the Papakura Limestone. Subsequent burial of both limestones by rapidly accumulating Waitemata Group sandstone and flysch instigated precipitation of widespread burial cements from pressure dissolution of carbonate material at subsurface depths from about 100 m to 1.0 km. The vertical tectonic movements registered at Gibsons Beach can be related to the oblique compression associated with the development of the Australian-Pacific plate boundary through New Zealand at about this time and coincide with overthrusting of basement into Taranaki Basin between mid-Waitakian (earliest Miocene) and Altonian (late Early Miocene) times

Constraints on the evolution of Taranaki Fault from thermochronology and basin analysis: Implications for the Taranaki Fault play

Taranaki Fault is the major structure defining the eastern margin of Taranaki Basin and marks the juxtaposition of basement with the Late Cretaceous-Paleogene succession in the basin. Although the timing of the basement over-thrusting on Taranaki Fault and subsequent marine onlap on to the basement block are well constrained as having occurred during the Early Miocene, the age of formation of this major structure, its character, displacement history and associated regional vertical movement during the Late Cretaceous- Recent are otherwise poorly known. Here we have applied (i) apatite fission track thermochronology to Mesozoic basement encountered in exploration holes and in outcrop to constrain the amount and timing of Late Cretaceous-Eocene exhumation of the eastern side of the fault, (ii) basin analysis of the Oligocene and Miocene succession east of the fault to establish the late-Early Miocene - Early Pliocene subsidence history, and (iii), regional porosity-bulk density trends in Neogene mudstone to establish the late uplift and tilting of eastern Taranaki Basin margin, which may have been associated with the main period of charge of the underlying Taranaki Fault play. We make the following conclusions that may be useful in assessing the viability of the Taranaki Fault play. (1) Mid-Cretaceous Taniwha Formation, intersected in Te Ranga-1 was formerly extensive across the western half of the Kawhia Syncline between Port Waikato and Awakino. (2) Taranaki Fault first formed as a normalfault during the Late Cretaceous around 85±10 Ma, and formed the eastern boundary of the Taranaki Rift-Transform basin. (3) Manganui Fault, located onshore north of Awakino, formed as a steeply east dipping reverse fault and accommodated about four km of displacement during the mid-Cretaceous. (4) Uplift and erosion, involving inversion of Early Oligocene deposits, occurred along the Herangi High during the Late Oligocene. This may have been associated with initial reverse movement on Taranaki Fault. (5) During the Early Miocene (Otaian Stage) the Taranaki and Manganui Faults accommodated the westward transport of Murihiku basement into the eastern margin of Taranaki Basin, but the amount of topography generated over the Herangi High can only have been a few hundred metres in elevation. (6) The Altonian (19-16 Ma) marked the start of the collapse of the eastern margin of Taranaki Basin that lead during the Middle Miocene to the eastward retrogradation of the continental margin wedge into the King Country region. During the Late Miocene, from about 11 Ma, a thick shelf-slope continental margin wedge prograded northward into the King Country region and infilled it (Mt Messenger, Urenui, Kiore and Matemateaonga Formations). (7) During the Pliocene and Pleistocene the whole of central New Zealand, including the eastern margin of Taranaki Basin, became involved in long wavelength up-doming with 1-2 km erosion of much of the Neogene succession in the King Country region. This regionally elevated the Taranaki Fault play into which hydrocarbons may have migrated from the Northern Graben region

Direct comparison of virtual reality and 2D delivery on sense of presence, emotional and physiological outcome measures

Introduction: Virtual-reality (VR) technology has, over the last decade, quickly expanded from gaming into other sectors including training, education, and wellness. One of the most popular justifications for the use of VR over 2D is increased immersion and engagement. However, very little fundamental research has been produced evaluating the comparative impact of immersive VR on the user’s cognitive, physiological, and emotional state.Methods: A within-subject cross-over study design was used to directly compare VR and 2D screen delivery of different subject matter content. Both physiological and self-report data were collected for scenes containing calming nature environments, aggressive social confrontations, and neutral content.Results: Compared to 2D, the VR delivery resulted in a higher sense of presence, higher ratings of engagement, fun, and privacy. Confrontational scenes were rated as more tense whilst calming scenes were rated as more relaxing when presented in VR compared to 2D. Physiological data indicated that the scenes promoted overall states of arousal and relaxation in accordance with the scene subject matter (both VR and 2D). However, heart rate (HR) and galvanic skin response (GSR) were consistently higher throughout the VR delivery condition compared to 2D, including responses during scenes of neutral and calming subject matter.Discussion: This discrepancy between emotional and physiological responses for calming and neutral content in VR suggest an elevated arousal response driven by VR immersion that is independent of the emotional and physiological responses to the subject matter itself. These findings have important implications for those looking to develop and utilize VR technology as a training and educational tool as they provide insights into the impact of immersion on the user

Teratology Primer-2nd Edition (7/9/2010)

Foreword: What is Teratology? “What a piece of work is an embryo!” as Hamlet might have said. “In form and moving how express and admirable! In complexity how infinite!” It starts as a single cell, which by repeated divisions gives rise to many genetically identical cells. These cells receive signals from their surroundings and from one another as to where they are in this ball of cells —front or back, right or left, headwards or tailwards, and what they are destined to become. Each cell commits itself to being one of many types; the cells migrate, combine into tissues, or get out of the way by dying at predetermined times and places. The tissues signal one another to take their own pathways; they bend, twist, and form organs. An organism emerges. This wondrous transformation from single celled simplicity to myriad-celled complexity is programmed by genes that, in the greatest mystery of all, are turned on and off at specified times and places to coordinate the process. It is a wonder that this marvelously emergent operation, where there are so many opportunities for mistakes, ever produces a well-formed and functional organism. And sometimes it doesn’t. Mistakes occur. Defective genes may disturb development in ways that lead to death or to malformations. Extrinsic factors may do the same. “Teratogenic” refers to factors that cause malformations, whether they be genes or environmental agents. The word comes from the Greek “teras,” for “monster,” a term applied in ancient times to babies with severe malformations, which were considered portents or, in the Latin, “monstra.” Malformations can happen in many ways. For example, when the neural plate rolls up to form the neural tube, it may not close completely, resulting in a neural tube defect—anencephaly if the opening is in the head region, or spina bifida if it is lower down. The embryonic processes that form the face may fail to fuse, resulting in a cleft lip. Later, the shelves that will form the palate may fail to move from the vertical to the horizontal, where they should meet in the midline and fuse, resulting in a cleft palate. Or they may meet, but fail to fuse, with the same result. The forebrain may fail to induce the overlying tissue to form the eye, so there is no eye (anophthalmia). The tissues between the toes may fail to break down as they should, and the toes remain webbed. Experimental teratology flourished in the 19th century, and embryologists knew well that the development of bird and frog embryos could be deranged by environmental “insults,” such as lack of oxygen (hypoxia). But the mammalian uterus was thought to be an impregnable barrier that would protect the embryo from such threats. By exclusion, mammalian malformations must be genetic, it was thought. In the early 1940s, several events changed this view. In Australia an astute ophthalmologist, Norman Gregg, established a connection between maternal rubella (German measles) and the triad of cataracts, heart malformations, and deafness. In Cincinnati Josef Warkany, an Austrian pediatrician showed that depriving female rats of vitamin B (riboflavin) could cause malformations in their offspring— one of the early experimental demonstrations of a teratogen. Warkany was trying to produce congenital cretinism by putting the rats on an iodine deficient diet. The diet did indeed cause malformations, but not because of the iodine deficiency; depleting the diet of iodine had also depleted it of riboflavin! Several other teratogens were found in experimental animals, including nitrogen mustard (an anti cancer drug), trypan blue (a dye), and hypoxia (lack of oxygen). The pendulum was swinging back; it seemed that malformations were not genetically, but environmentally caused. In Montreal, in the early 1950s, Clarke Fraser’s group wanted to bring genetics back into the picture. They had found that treating pregnant mice with cortisone caused cleft palate in the offspring, and showed that the frequency was high in some strains and low in others. The only difference was in the genes. So began “teratogenetics,” the study of how genes influence the embryo’s susceptibility to teratogens. The McGill group went on to develop the idea that an embryo’s genetically determined, normal, pattern of development could influence its susceptibility to a teratogen— the multifactorial threshold concept. For instance, an embryo must move its palate shelves from vertical to horizontal before a certain critical point or they will not meet and fuse. A teratogen that causes cleft palate by delaying shelf movement beyond this point is more likely to do so in an embryo whose genes normally move its shelves late. As studies of the basis for abnormal development progressed, patterns began to appear, and the principles of teratology were developed. These stated, in summary, that the probability of a malformation being produced by a teratogen depends on the dose of the agent, the stage at which the embryo is exposed, and the genotype of the embryo and mother. The number of mammalian teratogens grew, and those who worked with them began to meet from time to time, to talk about what they were finding, leading, in 1960, to the formation of the Teratology Society. There were, of course, concerns about whether these experimental teratogens would be a threat to human embryos, but it was thought, by me at least, that they were all “sledgehammer blows,” that would be teratogenic in people only at doses far above those to which human embryos would be exposed. So not to worry, or so we thought. Then came thalidomide, a totally unexpected catastrophe. The discovery that ordinary doses of this supposedly “harmless” sleeping pill and anti-nauseant could cause severe malformations in human babies galvanized this new field of teratology. Scientists who had been quietly working in their laboratories suddenly found themselves spending much of their time in conferences and workshops, sitting on advisory committees, acting as consultants for pharmaceutical companies, regulatory agencies, and lawyers, as well as redesigning their research plans. The field of teratology and developmental toxicology expanded rapidly. The following pages will show how far we have come, and how many important questions still remain to be answered. A lot of effort has gone into developing ways to predict how much of a hazard a particular experimental teratogen would be to the human embryo (chapters 9–19). It was recognized that animal studies might not prove a drug was “safe” for the human embryo (in spite of great pressure from legislators and the public to do so), since species can vary in their responses to teratogenic exposures. A number of human teratogens have been identified, and some, suspected of teratogenicity, have been exonerated—at least of a detectable risk (chapters 21–32). Regulations for testing drugs before market release have greatly improved (chapter 14). Other chapters deal with how much such things as population studies (chapter 11), post-marketing surveillance (chapter 13), and systems biology (chapter 16) add to our understanding. And, in a major advance, the maternal role of folate in preventing neural tube defects and other birth defects is being exploited (chapter 32). Encouraging women to take folic acid supplements and adding folate to flour have produced dramatic falls in the frequency of neural tube defects in many parts of the world. Progress has been made not only in the use of animal studies to predict human risks, but also to illumine how, and under what circumstances, teratogens act to produce malformations (chapters 2–8). These studies have contributed greatly to our knowledge of abnormal and also normal development. Now we are beginning to see exactly when and where the genes turn on and off in the embryo, to appreciate how they guide development and to gain exciting new insights into how genes and teratogens interact. The prospects for progress in the war on birth defects were never brighter. F. Clarke Fraser McGill University (Emeritus) Montreal, Quebec, Canad

Morphological and Functional Changes in the Retina after Chronic Oxygen-Induced Retinopathy

The mouse model of oxygen-induced retinopathy (OIR) has been widely used for studies of retinopathy of prematurity (ROP). This disorder, characterized by abnormal vascularization of the retina, tends to occur in low birth weight neonates after exposure to high supplemental oxygen. Currently, the incidence of ROP is increasing because of increased survival of these infants due to medical progress. However, little is known about changes in the chronic phase after ROP. Therefore, in this study, we examined morphological and functional changes in the retina using a chronic OIR model. Both the a- and b-waves in the OIR model recovered in a time-dependent manner at 4 weeks (w), 6 w, and 8 w, but the oscillatory potential (OP) amplitudes remained depressed following a return to normoxic conditions. Furthermore, decrease in the thicknesses of the inner plexiform layer (IPL) and inner nuclear layer (INL) at postnatal day (P) 17, 4 w, and 8 w and hyperpermeability of blood vessels were observed in conjunction with the decrease in the expression of claudin-5 and occludin at 8 w. The chronic OIR model revealed the following: (1) a decrease in OP amplitudes, (2) morphological abnormalities in the retinal cells (limited to the IPL and INL) and blood vessels, and (3) an increase in retinal vascular permeability via the impairment of the tight junction proteins. These findings suggest that the experimental animal model used in this study is suitable for elucidating the pathogenesis of ROP and may lead to the development of potential therapeutic agents for ROP treatment