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Articles list which use McKinnon Complementary Hypothesis keyword

A System Test of McKinnon's Complementarity Hypothesis With An ..

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Application to Turkey This paper is the first to employ the multivariate cointegration and vector error correction models (VECM) to test McKinnon’s complementarity hypothesis between money and capital. We find that for the Turkish economy over the sample period 1980-1995 money and capital are complementary, suggesting that higher real interest rates will raise the demand for money and lead to higher levels of investment. It is also the case that government investment is complementarity to private sector investment so that there is no crowding out of private investment as a result of increased public investment. The policy implication is that further financial liberalisation in Turkey will enhance investment and lead to, at least temporarily, a higher rate of economic growth. Keywords:

A Critical Appraisal of McKinnon’s Complementarity Hypothesis: ..
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If the Meissner corpuscle is selectively inactivated by the injection of a local anaesthetic through the skin, the sense of flutter or low-frequency vibration is lost. This suggests that it functionally complements the high frequency capacity of the pacinian corpuscles. Together, these two receptors provide neural signals sufficient to account for human sensibility to a full range of vibrations (Mountcastle et al. 1967).

Articles list which use McKinnon Complementary Hypothesis keyword ..

17/02/2007 · In this paper, two models have been used to test the relevance of McKinnon's complementarity hypothesis in Kenya. In …
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In higher organisms, hereditary information is organized in chromosomes. Chromosomes consist of tightly condensed strands of protein-associated DNA. Within a single chromosome, each DNA molecule exists as a pair of long, unbranched chains of nucleotide subunits linked together by phosphodiester bonds that join the 5 carbon of one deoxyribose moiety to the 3 carbon of the next (). In addition, one of four different nucleotide bases (adenine, cytosine, guanine or thymine) is attached to each deoxyribose subunit like beads on a string. Three-dimensionally, each pair of DNA strands forms a double helix with all of the bases oriented toward the inside of the spiral. Within the helix, each base is associated with its complementary base on the opposite DNA strand; hydrogen bonding dictates strong, noncovalent pairing of adenine with thymine and guanine with cytosine (). Since the sequence of nucleotide bases is complementary throughout the entire length of the duplex DNA molecule, both strands carry essentially the same genetic information. In fact, during DNA replication each strand serves as a template for the production of a new partner strand.

In the case of lethal injuries, the most common initial interactions resulting in injury leading to cell death are interference with energy metabolism, such as anoxia, ischaemia or inhibitors of respiration, and glycolysis such as potassium cyanide, carbon monoxide, iodo-acetate, and so on. As mentioned above, high doses of compounds that inhibit energy metabolism typically result in oncosis. The other common type of initial injury resulting in acute cell death is modification of the function of the plasma membrane (Trump and Arstila 1971; Trump, Berezesky and Osornio-Vargas 1981). This can either be direct damage and permeabilization, as in the case of trauma or activation of the C5b-C9 complex of complement, mechanical damage to the cell membrane or inhibition of the sodium-potassium (Na+-K+) pump with glycosides such as ouabain. Calcium ionophores such as ionomycin or A23187, which rapidly carry [Ca2+] down the gradient into the cell, also cause acute lethal injury. In some cases, the pattern in the prelethal change is apoptosis; in others, it is oncosis.

farah's blog: McKinnon’s Complementary Theory

McKinnon’s (1973) complementarityy hypothesis predicts that money and investment are complementary due to self-financed investment, so that a real deposit rate
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The audiogram is the standard test to detect and evaluate hearing loss. Specialized studies to complement the audiogram may be necessary in some patients. These include: tympanometry, word discrimination tests, evaluation of the attenuation reflex, electrophysical studies (electrocochleogram, auditory evoked potentials) and radiological studies (routine skull x rays complemented by CAT scan, MRI).

This crucial component of the medical evaluation uses a device known as an audiometer to determine the auditory threshold of individuals to pure tones of 250-8,000 Hz and sound levels between -10 dB (the hearing threshold of intact ears) and 110 dB (maximal damage). To eliminate the effects of TTSs, patients should not have been exposed to noise during the previous 16 hours. Air conduction is measured by earphones placed on the ears, while bone conduction is measured by placing a vibrator in contact with the skull behind the ear. Each ear's hearing is measured separately and test results are reported on a graph known as an audiogram (). The threshold of intelligibility, that is. the sound intensity at which speech becomes intelligible, is determined by a complementary test method known as vocal audiometry, based on the ability to understand words composed of two syllables of equal intensity (for instance, shepherd, dinner, stunning).

A Critical Appraisal of McKinnon’s Complementarity Hypothesis: Does the Real Rate of Return on Money Matter for Investment in Developing Countries?
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  • 2009/09/01 · Summary McKinnon's [McKinnon, R

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  • Money and capital in economic development

    CORE - COnnecting REpositories

  • Brunel University Research Archive (BURA)

    Makale » DergiPark

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Financial development and economic growth: Some …

Genetic differences in the metabolism of various drugs and environmental chemicals have been known for more than four decades (Kalow 1962 and 1992). These differences are frequently referred to as pharmacogenetic or, more broadly, ecogenetic polymorphisms. These polymorphisms represent variant alleles that occur at a relatively high frequency in the population and are generally associated with aberrations in enzyme expression or function. Historically, polymorphisms were usually identified following unexpected responses to therapeutic agents. More recently, recombinant DNA technology has enabled scientists to identify the precise alterations in genes that are responsible for some of these polymorphisms. Polymorphisms have now been characterized in many drug-metabolizing enzymes—including both Phase I and Phase II enzymes. As more and more polymorphisms are identified, it is becoming increasingly apparent that each individual may possess a distinct complement of drug-metabolizing enzymes. This diversity might be described as a “metabolic fingerprint”. It is the complex interplay of the various drug- metabolizing enzyme superfamilies within any individual that will ultimately determine his or her particular response to a given chemical (Kalow 1962 and 1992; Nebert 1988; Gonzalez and Nebert 1990; Nebert and Weber 1990).

The Primary Outcome Fails — What Next? — NEJM

It has long been recognized that each person’s response to environmental chemicals is different. The recent explosion in molecular biology and genetics has brought a clearer understanding about the molecular basis of such variability. Major determinants of individual response to chemicals include important differences among more than a dozen superfamilies of enzymes, collectively termed xenobiotic- (foreign to the body) or drug-metabolizing enzymes. Although the role of these enzymes has classically been regarded as detoxification, these same enzymes also convert a number of inert compounds to highly toxic intermediates. Recently, many subtle as well as gross differences in the genes encoding these enzymes have been identified, which have been shown to result in marked variations in enzyme activity. It is now clear that each individual possesses a distinct complement of xenobiotic-metabolizing enzyme activities; this diversity might be thought of as a “metabolic fingerprint”. It is the complex interplay of these many different enzyme superfamilies which ultimately determines not only the fate and the potential for toxicity of a chemical in any given individual, but also assessment of exposure. In this article we have chosen to use the cytochrome P450 enzyme superfamily to illustrate the remarkable progress made in understanding individual response to chemicals. The development of relatively simple DNA-based tests designed to identify specific gene alterations in these enzymes, is now providing more accurate predictions of individual response to chemical exposure. We hope the result will be preventive toxicology. In other words, each individual might learn about those chemicals to which he or she is particularly sensitive, thereby avoiding previously unpredictable toxicity or cancer.

The Acid-Alkaline Myth: Part 1 - Chris Kresser

Many classes of toxic chemicals are capable of inducing acute cell injury followed by death. These include anoxia and ischaemia and their chemical analogues such as potassium cyanide; chemical carcinogens, which form electrophiles that covalently bind to proteins in nucleic acids; oxidant chemicals, resulting in free radical formation and oxidant injury; activation of complement; and a variety of calcium ionophores. Cell death is also an important component of chemical carcinogenesis; many complete chemical carcinogens, at carcinogenic doses, produce acute necrosis and inflammation followed by regeneration and preneoplasia.

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