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Wilhoit’s teeth matched the bitemark 20mg tamoxifen amex menopause long periods, and in addition order 20mg tamoxifen mastercard women's health boutique houston memorial, bacteria from the bitemark were specifcally unique to Mr buy tamoxifen 20mg on line women's health for pregnancy. Tomas Krauss, a board-certifed forensic odontologist, had been hired by the Wilhoit family. Krauss refuted both the bacterial evidence and the matching of the teeth of Wilhoit to the bitemark. Krauss at the trial, relying only on cross-examination of the prosecution’s experts. Krauss worked with the attorneys handling the appeal and sent the bitemark evidence to eleven other board-certifed forensic odontologists. All eleven odontologists independently excluded Wilhoit as the person who inficted the bite. As in all death sentence cases, the new defense attorneys appealed the conviction in part based on Dr. Both of the odontologists for the State of Oklahoma repeated their earlier testimony linking the teeth and the bacteria found in the bitemark to Mr. Wilhoit and the bacterial evidence was fawed, as more than 50% of the general popu- lation would be expected to have the same types of bacteria reportedly found on the victim’s bitemark. Importantly, had the prosecution’s dentists sought independent second opinions (or indeed eleven independent second opinions) and been willing to accept the possibly that their earlier Bitemarks 323 interpretations could be wrong, Mr. Piakis collected dental information from Krone and told them that his teeth were consistent with the bitemark. He was not an experienced forensic dentist, so he consulted his mentor, a well-known San Diego, California, forensic dentist, Dr. Rawson had lectured to the Arizona Homicide Investigators Association and was known to them as experienced in bitemark analysis. Rawson did a comprehensive analysis and developed a videotaped pre- sentation of his analysis and experiments. Rawson reportedly stated, “Te question should not be are bitemarks as good as fngerprints but are fngerprints as good as bitemarks” (transcript of original trial in State v. In 1995 the Supreme Court of Arizona reversed the decision on procedural grounds and remanded the case for a new trial. Rawson, the state’s expert, prior to the second trial and asked him to reconsider his opinion, Dr. When confronted, he obliquely confessed to the crime, reportedly stating that he only remembered strug- gling with the victim then awakening the next morning with blood on his 324 Forensic dentistry Figure 14. Piakis subsequently had the opportunity of compare Phillips’s dentition to the bitemark and stated that Phillips’s teeth were more consistent with the bitemark than Krone’s. Bitemarks 325 Te case of Ray Krone is a tragic indictment of law enforcement and legal prosecution practices and of the faulty application of bitemark analysis. Tis activity included overstating and overdramatizing the results of tests and experiments and failure to follow accepted guidelines by not seeking second opinions and disregarding or discounting the unsolicited opinions received. Te homicide detectives failed to thoroughly investigate and follow all leads, and the prosecutors exhibited tunnel vision and willingness to shop for expert opinions that supported their theory of the crime. During an inter- view by a prosecutor before the retrial, one defense odontologist remarked, “I hope you have other important evidence … the bitemark evidence is bad” and was bluntly told, “Doctor, this is a bitemark case and has always been a bitemark case. Tis triumvirate committed errors that compounded to produce a gross miscarriage of justice. Tis case is described in detail in a book authored by Jim Rix, Ray Krone’s cousin and the sponsor of his defense. One or more second opinions from other competent forensic odontologists should be sought and considered. Te Supreme Court of Michigan ruled that that type of testimony was inadmissible afer several cases in that state in which bitemarks were associated to a suspect with statements of mathematical degrees of certainty. Te 1991 case of the kidnapping, assault, and rape of Maureen Fournier featured the victim’s eyewitness identifcation of the fve men who participated in the attack and the two who allegedly bit her. Both Michael Cristini and Jefrey Moldowan were convicted based on the victim’s identifcations and two forensic odontologists’ testimony that the bitemark associations were posi- tive. Allan Warnick, testifed that one of the marks was made by Moldowan and the odds that someone else made the mark were 3 million to one. In another case he testifed that “the chances of someone else having made the mark would be 4. Homer Campbell and Richard Souviron independently reviewed the evidence and reported that, in their opinion, Moldowan and Cristini could be excluded. Te court ruled that no testimony regarding mathematical degrees of certainty for bitemarks would be heard. Berman, testifed that Cristini made the bitemark with a high degree of certainty, and the defense expert, Dr. In an unusual twist in this trial, one of the original odontologists for the prosecution in the frst trial in 1991, Dr. Hammel, took the stand for the defense and testifed that she had erred in the original trial. She stated further that she originally had doubts about the orientation of the bitemark, and afer gaining more experience and reviewing the evidence, she realized her error. It took a great deal of courage for her to admit the error, but it was absolutely the right thing to do. Cristini had been arrested and charged with eight counts of frst-degree criminal sexual conduct allegedly involving a fve-year-old child. First, that eyewitness testimony may or may not be accurate—here the victim may have been wrong about the identity of the biters. She accused others that were later proven to be else- where at the time of the crime. Second, there is no scientifc basis for math- ematical degree of certainty with bitemark evidence on skin. Tird, unlike in other cases, one of the experts had the courage to take the stand and admit an earlier error. In the above detailed problem cases there was agreement among both the defense and the prosecution experts that these were indeed human bite- marks. Te disagreements were related to features and orientation of the bitemarks and to who could have or who could not have inficted the bites. Te problems were compounded in some cases by the use of mathematical degrees of certainty or overreaching statements of the value and certainty of bitemark evidence. Te most recent and highly publicized of Bitemarks 327 these cases is that of Kennedy Brewer in Mississippi. Brewer was convicted in 1995 of the murder and sexual assault of Christine Jackson. Te body of the three-year-old victim had been found in a nearby creek on a Tuesday morn- ing, the third day afer her Saturday night disappearance. Michael West, examined Christine Jackson on May 9, 1992, and wrote in his May 14, 1992, report that nineteen human bitemarks were found on the body, and that “the bitemarks found on the body of Christina [sic] Jackson are peri-mortem in nature.
Frequ- the probability of the material producing a positive ently this is a more appropriate measure of carcinogenic response in long-term rodent studies buy tamoxifen without prescription menstruation predictor. However order tamoxifen with visa menstruation at age 5, a the last day of dosing tamoxifen 20mg overnight delivery women's health center temecula ca, that is during the last week, fairly standard worked example is provided by of a 90-day toxicity study. For larger non-rodents, the main study animals can usually provide the Pharmacokinetic studies samples. Guidelines have been made available that cover most aspects of collection and analysis In the early stages of drug development, it is impor- of these data (Federal Register, 1 March 1995). Another reason tissue distribution studies suggest drug localiza- why this is important is that it assists the investi- tion, a tissue distribution study following repeated gator in knowing that the appropriate species has dosing may be indicated. The conditions under been selected for the nonclinical toxicology pro- which such studies may be necessary have been gram. Therefore, it is necessary to have pharmacokinetic information early in the program, so that it can be Safety pharmacology compared to the data generated in the early clinical studies. Studies related to safety pharmacology (sometimes Drug metabolism is a highly specialized ﬁeld confusingly termed ‘general pharmacology’studies) and is increasing in sophistication all the time. A tend now to be performed earlier in the drug devel- relatively new technique that is available to the opment process than was previously the case. These procedures involve the cological properties that may be unrelated to the use of liver slices and/or liver hepatocyte homo- intended indication for the drug. An example of genates and can be done in human and animal this would be signiﬁcant effects of a drug on the cultures at the earliest stages of drug development. Australia: ‘Studies should reveal potentially useful and harmful properties of the drug in a quantitative manner, which will permit an assessment of the therapeutic risk... Investigations of the general pharmacological proﬁle should be carried out’ (Guidelines under the Clinical Trial Exemption Scheme, pp. As can be seen from these wish to use this for formal, internal proceedings guidelines, it is not always clear when such to justify the decision to proceed with initial human studies are required. For exam- ple, a diagnostic agent or a drug with a three- to Nonclinical summary documents four-day exposure (such as an anesthetic agent) may require little in the way of additional Prior to the initiation of initial studies in humans, it repeated-dose toxicity studies beyond what is is important that all of the nonclinical information already conducted prior to phase I. This intended for chronic therapy, for example a new information must be included in the clinical inves- antihypertensive agent, may require much more. The regu- gram if toxicology testing is not to introduce delay latory authority and ethics committees are into the development process. This is chronic studies is generally 6 months, although also done in rats and rabbits. In general, three phases of the reproductive pro- Carcinogenicity studies cess are evaluated. These cover the principal aspects of reproductive biology, namely concep- Carcinogenicity studies involve the treatment of tion and implantation, organ formation and terato- rodents for long periods approximating to the com- genesis and ﬁnally the development of offspring of plete life span (18 months to 2 years) to determine exposed maternal animals allowed to proceed to whether the test material possesses the capability to term. The relevance of these models to the human situation has been debated for many years. Carcinogenicity Fertility and implantation studies have been required for all drugs where clinical therapy may extend for six months or The ﬁrst phase (historically referred to as ‘Segment longer. A recent review of the status of carcino- dose (which had been suggested by the National genicity testing (Reno, 1997) addresses the many Toxicology Program; Haseman and Lockhart, factors that should be considered in a carcinogeni- 1994). A subsequent amendment to this Special studies guideline (Federal Register, 4 December 1997) adds a further proviso that the highest dose in a It is not uncommon in drug development programs carcinogenicity study need not exceed 1500 mg for speciﬁc toxicities to be uncovered. In most À1 kg per day when (a) there is no evidence of cases, additional studies are then carried out that genotoxicity and (b) the maximum recommended will attempt to elucidate additional information human dose is no more than 500 mg per day. For basis for species selection, circumstances needing example, the identiﬁcation of a non-speciﬁc beha- mechanistic studies and exploitation of pharmaco- vioral effect (e. The identiﬁcation of an effect on have changed little since they were ﬁrst established reproduction may warrant the performance of in the early 1970s. In recent years, the use of mice detailed studies to identify the speciﬁc mechanism (historically the second of the two required species or phase of the reproductive cycle that is affected. It is rare that (Federal Register, 21 August 1996) allows for the a drug development program does not involve option of using transgenic mice and study designs some type of special study. Of growing importance is the interaction of fac- tors that are critical to a successful toxicology 6. Metabolic and pharmacokinetic data are important to ensure that the selected models handle Although differing in format for each application, and metabolize the drug in a fashion at least reason- an integrated summary that interrelates the phar- ably similar to humans and may vary for the macology, pharmacokinetic and toxicology study same drug according to the toxic effect of interest. Some of the information in this summary direct importance in terms of the limits on doses is also needed for the product’s package insert. These described, it is to be remembered that no individual comparisons are often quantitative and must be drug development case will be typical. The objective of his chapter has been to provide an ‘Extrapolation of animal toxicity to humans: inter- overview of the objectives and philosophy of the species comparisons in drug development’. Equipoise is the concept international law through the Declaration of that the investigator, and those sponsoring the Helsinki, and in response to the atrocities of the trial, are truly uncertain as to the outcome of the Second World War. The principles of informed study; in practical terms, this is a guarantee to consent are under continuous review and dis- the patient that an unreasonable hazard cannot cussion (e. This is to be expected result from unfavorable randomization because when reasonable standards of informed consent are the treatment options are not known to be dependent not only on the design of a particular unequally hazardous. In any case, there should The large majority of clinical trials use a written be an assurance that no patient identity infor- informed consent document. A statement of the circumstances under which the patient will be withdrawn from the 1. A clear statement that participation is volun- draw from the study at any time and for any tary and that there will be no repercussions reason, again without repercussions to his or either in the patient’s relationship with the her relationship with any clinical care giver. A statement that the patient will be required to part in the study; give a full and accurate clinical and treatment history on study entry and periodically there- 3. The possibility of assessment of hazard of study participation placebo treatment and the probability of will be communicated to the patient without being treated with each test therapy should delay. Clear descriptions of alternative therapies or ing part in the study, and a brief summary of standard therapies or procedures (if any), in how many patients in the past have been order that the patient can judge whether to exposed to the test medication. The methods for compensation that may be signed by both the patient and the investigator, available in the case of injury (these often and ideally the patient should sign before an impar- have marked international variations). Informed consent documents should be written in a language that is understandable to the 6. Name and telephone number of persons that patient, and ideally at a level of complexity that the patient may contact in case of any difﬁculty could be understood by a young adolescent of during the study. Also, the identity of person(s) average intelligence from the same community as of whom the patient may ask questions during the patient. There should be adequate time for the the day-to-day conduct of the study and an patient to review the document. All written infor- expression of willingness on the part of the med consent documents should be approved by an investigator to provide answers to any ques- ethics committee or an institutional review board tions that the patient may have. Under these conditions, there is often not even the time Surrogate informed consent to ﬁnd relatives to provide surrogate informed consent. Even if relatives can be found quickly Some patients are incapable of providing informed enough, then their emotional state may not be consent, whether written or not. These patients are suited to becoming truly informed before giving often in demographic subgroups which are medi- consent.
Interestingly order cheapest tamoxifen and tamoxifen menopause 9gag, the relationship to biological mother’s weight was greater than the relationship with the biological father’s weight order tamoxifen online women's health center memphis tn. Research also suggests that the primary distribution of this weight (upper versus lower body) is also inherited (Bouchard et al buy online tamoxifen women's health uw. Metabolic rate, the number of fat cells and appetite regulation may be three factors inﬂuenced by genetics. Metabolic rate theory The body uses energy for exercise and physical activity and to carry out all the chemical and biological processes that are essential to being alive (e. The rate of this energy use is called the ‘resting metabolic rate’, which has been found to be highly heritable (Bouchard et al. It has been argued that lower metabolic rates may be associated with obesity as people with lower metabolic rates burn up less calories when they are resting and therefore require less food intake to carry on living. A group in Phoenix assessed the metabolic rates of 126 Pima Indians by monitoring their breathing for a 40-minute period. The study was carried out using Pima Indians because they have an abnormally high rate of obesity (about 80–85 per cent) and were considered an interesting population. The subjects remained still and the levels of oxygen consumed and carbon dioxide produced was measured. The researchers then followed any changes in weight and metabolic rate for a four-year period and found that the people who gained a substantial amount of weight were the ones with the lowest metabolic rates at the beginning of the study. In a further study, 95 subjects spent 24 hours in a respiratory chamber and the amount of energy used was measured. The subjects were followed up two years later and the researchers found that those who had originally shown a low level of energy use were four times more likely to also show a substantial weight increase (cited in Brownell 1989). These results suggest a relationship between metabolic rate and the tendency for weight gain. If this is the case, then it is possible that some individuals are predisposed to become obese because they require fewer calories to survive than thinner individuals. Therefore, a genetic tendency to be obese may express itself in lowered metabolic rates. However, in apparent contrast to this prediction, there is no evidence to suggest that obese people generally have lower metabolic rates than thin people. To explain these apparently contradictory ﬁndings it has been suggested that obese people may have lower metabolic rates to start with, which results in weight gain and this weight gain itself results in an increase in metabolic rate (Ravussin and Bogardus 1989). Fat cell theory A genetic tendency to be obese may also express itself in terms of the number of fat cells. People of average weight usually have about 25–35 billion fat cells, which are designed for the storage of fat in periods of energy surplus and the mobilization of fat in periods of energy deﬁcit. Mildly obese individuals usually have the same number of fat cells but they are enlarged in size and weight. Severely obese individuals, however, have more fat cells – up to 100–125 billion (Sjostrom 1980). Cell number is mainly determined by genetics; however, when the existing number of cells have been used up, new fat cells are formed from pre-existing preadipocytes. Most of this growth in the number of cells occurs during gestation and early childhood and remains stable once adulthood has been reached. Although the results from studies in this area are unclear, it would seem that if an individual is born with more fat cells then there are more cells immediately available to ﬁll up. In addition, research suggests that once fat cells have been made they can never be lost (Sjostrom 1980). An obese person with a large number of fat cells, may be able to empty these cells but will never be able to get rid of them. Appetite regulation A genetic predisposition may also be related to appetite control. Over recent years researchers have attempted to identify the gene, or collection of genes, responsible for obesity. Although some work using small animals has identiﬁed a single gene that is associated with profound obesity, for humans the work is still unclear. Two children have, however, been identiﬁed with a defect in the ‘ob gene’, which produces leptin which is responsible for telling the brain to stop eating (Montague et al. To support this, researchers have given these two children daily injections of leptin, which has resulted in a decrease in food intake and weight loss at a rate of 1–2 kg per month (Farooqi et al. Despite this, the research exploring the role of genetics on appetite control is still in the very early stages. Behavioural theories Behavioural theories of obesity have examined both physical activity and eating behaviour. Further, at present only 20 per cent of men and 10 per cent of women are employed in active occupations (Allied Dunbar National Fitness Survey 1992) and for many people leisure times are dominated by inactivity (Central Statistical Oﬃce 1994). Although data on changes in activity levels are problematic, there exists a useful database on television viewing which shows that whereas the average viewer in the 1960s watched 13 hours of television per week, in England this has now doubled to 26 hours per week (General Household Survey 1994). This is further exacerbated by the increased use of videos and computer games by both children and adults. In a survey of adolescent boys in Glasgow in 1964 and 1971, whereas daily food diaries indicated a decrease in daily energy intake from 2795 kcals to 2610 kcals, the boys in 1971 showed an increase in body fat from 16. This suggests that decreased physical activity was related to increased body fat (Durnin et al. To examine the role of physical activity in obesity, research has asked ‘Are changes in obesity related to changes in activity? This question can be answered in two ways: ﬁrst using epidemiological data on a population and second using prospective data on individuals. In 1995, Prentice and Jebb presented epidemiological data on changes in physical activity from 1950 to 1990, as measured by car ownership and television viewing, and compared these with changes in the prevalence of obesity. The results from this study suggested a strong association between an increase in both car ownership and televi- sion viewing and an increase in obesity (see Figure 15. They commented that ‘it seems reasonable to conclude that the low levels of physical inactivity now prevalent in Britain must play an important, perhaps dominant role in the development of obesity by greatly reducing energy needs’ (Prentice and Jebb 1995). Therefore, it remains unclear whether obesity and physical activity are related (the third factor problem – some other variable may be determining both obesity and activity) and whether decreases in activity cause increases in obesity or whether, in fact, increases in obesity actually cause decreases in activity. In addition, the data is at the population level and therefore could miss important individual diﬀer- ences (i. In an alternative approach to assessing the relationship between activity and obesity a large Finnish study of 12,000 adults examined the association between levels of physical activity and excess weight gain over a ﬁve-year follow-up period (Rissanen et al. The results showed that lower levels of activity were a greater risk factor for weight gain than any other baseline measures. However, although this data was pro- spective it is still possible that a third factor may explain the relationship (i. Unless experimental data is collected, conclusions about causality remain problematic. Research has also examined the relationship between activity and obesity using a cross-sectional design to examine diﬀerences between the obese and non-obese.
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