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Assessment of the biological condition and nutritional status of adult patients with cystic fibrosis
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1 Przegląd Antropologiczny Anthropological Review Vol. 68, (2005) Assessment of the biological condition and nutritional status of adult patients with cystic fibrosis Magdalena Kosińska, 1 Anita Szwed, 1 Joachim Cieślik, 1 Joanna Goździk, 2 Karol Karbowy 1 1 Institute of Anthropology, Adam Mickiewicz University, Umultowska 89, Poznań, Poland, 2 Chair and Department of Phtysiopneumonology, Academy of Medical Sciences, Szamarzewskiego 89, Poznań, Poland ABSTRACT The aim of the study was to assess the biological condition and nutritional status of adult cystic fibrosis patients. The study included 55 individuals aged from 18 to 31 years. Their biological condition and nutritional status were determined by somatometric parameters and their pulmonary function by spirometry and a microbiological test. The results show considerable physical retardation and poor nutritional status of the studied adult cystic fibrosis patients. It was also shown that the type of mutation affects body mass and height, as well as thigh and calf circumference values, while the severity of the respiratory system disorder modifies only the body mass value (Kruskal-Wallis test: H (3,55)= 8.505, p < 0.04). The authors have demonstrated a statistically significant relationship between the type of mutation and severity of clinical respiratory symptoms, and nutritional status (respectively: H (2,55) = 9.589, p < 0.01; H (3,55) = , p < 0.005). KEY WORDS Cole index, somatometric traits, cystic fibrosis mutation, pulmonary function, developmental retardation, malnutrition Prz. Antropol. Anthropol. Rev. (2005), vol. 68, pp , Figs. 2, Tables 2. ISBN , ISSN Introduction Cystic fibrosis is the most frequent autosomal recessive monogenic disease. The frequency of this pathology in Poland is estimated at approximately 1:2500 births [BOŻKOWA et al. 1971]. Cystic fibrosis is incurable but owing to more effective treatment of respiratory system infections and an improvement in nutritional behavior over the last 20 years the clinical condition of the patients has improved considerably and mean life expectancy has increased considerably (in 1940 it was one year, in years and in 1995 it was estimated as 30 years) [YANKASKAS et al. 2004].
2 54 M. Kosińska et al. The cystic fibrosis gene (CFTR Cystic Fibrosis Transmembrane Conductance Regulator) was located in the mid 1980s on the long arm of chromosome 7 [KEREM et al. 1990; WITT 1994]. Over 1000 mutations of this gene are currently known [Cystic Fibrosis Genetic Analysis Consortium]. The CFTR gene mutations, among which the F508 mutation (a deletion of three nucleotides (CTT) resulting in the loss of phenylalanine residue at position 508 on the peptide chain) is the most frequent, cause CFTR protein dysfunction, and consequent impaired secretion of chloride ions by glandular epithelium cells [STRAND- VIK 1991]. Exocrine glands produce viscous and thick mucus, with clinical sequelae in the form of recurrent pulmonary inflammations and sinusitis, exocrine pancreatic insufficiency, liver damage, as well as energy balance disorders. Another commonly observed disorder is retarded biological development of the patients manifesting as negative deviations of somatometric traits compared to healthy peer group values [e.g., BYARD 1990; LANDON and ROSENFELD 1984; MÜLLER et al. 1999]. The genesis of this growth retardation has not been unequivocally explained so far. Initially, the diversity of clinical expression and the degree of developmental deviations from the normal biological condition were explained by the fact of occurrence of many mutations of the CFTR gene. However, assuming that in the course of physical development an interaction occurs between the genetic determination and external environmental factors, one should expect the occurrence of developmental differences resulting from genotypic variation and from the modifying effect of the environment. One of the fundamental, though still underestimated, problems in cystic fibrosis treatment is proper nutrition. In the past malnutrition and physical retardation were considered to be an inherent element of the disease process. However, as demonstrated by COREY et al. [1988] and LAI et al. [1999], a properly composed diet has a significant effect on the course of the disease and the patient's physical development. The nutritional status of cystic fibrosis patients is a crucial prognostic of the course of the disease, including also maintenance of respiratory system efficiency [REOSEN- FELD et al. 1997; HAYLLAR et al.1997; COREY and FAREWELL 1995; GRASE- MANN et al. 1995]. The goal of the study was to assess the biological condition and the nutritional status of adult patients with cystic fibrosis. Materials and methods The studied group consisted of 55 adult cystic fibrosis patients (24 males and 31 females), aged from 18 to 31 years (respectively: x = 22 ± 3.64; x = 22 ± 2.10) The diagnosis of CF was established in accordance with the criteria proposed by the Polish Cystic Fibrosis Working Group [Zasady rozpoznawania ] (one or more clinical symptoms of the disease present, family history of cystic fibrosis, positive result of the CF newborn screening test). Confirmation was obtained based on the perspiration test, measurement of transepithelial potential difference and molecular tests of the CFTR gene performed in the Human Genetics Institute of the Polish Academy of Sciences in Poznań.
3 Nutritional status of patients with cystic fibrosis 55 The patients were divided into three groups of subjects according to mutation type. The first group (18%) were people with the F508/ F508 genotype, classified as a severe mutation. The second group (67%) were people having a mutation described as mild, i.e., individuals with the F508/M genotype, where M is the other unspecified mutation, causing a more benign form of the disease. The third group (15%) consisted of individuals with the M/M genotype. No statistically significant differences in the frequency of the specified mutation types were found between sexes (χ 2 df=2 = 0.256; p > 0.05). The assessment of biological condition and nutritional status was performed on the basis of somatometric traits. Measurements were taken according to the techniques introduced by Martin and Saller in 1957 [MALINOW- SKI and BOŻIŁOW 1997]. The measurements were performed using Swiss GPM anthropometric instruments and electronic scales. Circumferences were measured using anthropometric tape with accuracy up to 1 cm. Thickness of skinfolds was measured with a skinfold meter with standard pressure of 10 g/sq. mm and accuracy up to 1 mm. The degree of severity of the bronchopulmonary disease was assessed by spirometry and by the standard microbiological sputum test for the presence of Pseudomonas aeruginosa pathogen. The collected data were analyzed statistically by both parametric and nonparametric methods used in compliance with their assumptions. Deviations of the subjects' physical development status from the healthy population were assessed on the basis of the single mean t-test. The assessment of the effect of mutation type and the degree of severity of clinical respiratory symptoms on the values of somatometric traits and on nutritional status was based on the ANOVA and Kruskal-Wallis ranks test. In the course of further analyses, multiple comparisons of rank means were performed in order to estimate differences between individual groups. All values of the studied somatometric traits were standardized. Values of the traits in healthy male 18-year olds and female18-year olds given in Dziecko Poznańskie [CIEŚLIK et al. 1994] and Dziecko Konińskie [1998] were used as reference. Measurements of skinfolds' thickness were presented in logarithmic form, using logarithmic transformation tables constructed by Edwards et al. [Dziecko Konińskie 1998]: Transformation = 100 [log (skinfold in mm 1.8) +1] Nutritional status of the subjects was determined using the Cole index calculated from the following formula [RYŻ- KO 1997]: Cole index = body mass * (body height at the 50th centile level body mass at the 50th centile level * (body 2 ) * height) The values of the Cole index expressed in percent enable the following classification of nutritional status: > 110 overnutrition normal nutrition slight malnutrition malnutrition 75 emaciation The statistical analysis of the material was performed using software package STATISTICA 7.0 (StatSoft. Inc. 2005).
4 56 M. Kosińska et al. Results The physical development status of the subjects was assessed on the basis of somatometric traits. The results of the single mean t-test demonstrate that the physical development in individuals suffering from cystic fibrosis is considerably retarded compared to healthy individuals. The majority of the mean values of standardized somatometric variables exhibit significant statistical deviations in the negative direction compared to the healthy population (Table 1). However, one should note the high variability of the studied traits, for instance for body mass and height the minimum value exceeds minus 4 standard deviations, and the maximum value indicates that among the subjects there are also individuals whose body height and mass do not deviate from the values obtained for the healthy population (Fig. 1). It was also observed that in the studied group there was a higher percentage of individuals with body mass deficiency exceeding minus 2 SD (42%) compared to individuals with body height deficiency exceeding minus 2 SD (29%). However, the difference between the frequencies is not statistically significant (χ 1 2 = 1.95; p > 0.05). At the same time, it should be noticed that over 70% of the subjects have an extremely low (< -2SD) thigh circumference (Fig. 2). A further analysis demonstrated a significant effect of mutation type on body mass and height values and thigh and calf circumferences (Table 2). In turn, the severity of the respiratory symptoms modifies only body mass values of the subjects (Kruskal-Wallis test: H (3,55) = 8.505, p < 0.04). A crucial aspect of the study was the estimation of nutritional status of individuals with cystic fibrosis. It was observed that almost 60% of the patients showed malnutrition symptoms, ranging from slight malnutrition to symptoms indicating emaciation. However, it should be noted that 4% of the subjects were classified into the excessive nutritional status category (Table 3). Nutritional status may be conditioned by many Table 1. Mean values of standardized somatometric traits and the statistical significance of deviations from healthy population Somatometric trait (N=55) x SD p Birth body weight > 0.05 Body mass < Body height < Triceps skinfold > 0.05 Subscapular skinfold < 0.01 Abdomen skinfold < 0.01 Upperarm cimcurference < Forearm circumference < Thigh circumference < Calf circumference < Chest circumference < 0.03 Transverse chest breadth < 0.02 Sagittal chest depth > 0.05
5 Nutritional status of patients with cystic fibrosis 57 Fig. 1. Physical development of studied persons normogram of the variability of somatometric traits. Fig. 2. Standardized deviations of somatometric traits (p < 0.05) frequency of occurence.
6 58 M. Kosińska et al. Table 2. Effect of mutation type on somatometric traits Somatometric trait (N=55) H (2,55) p Birth body weight > 0.05 Body mass < Body height < 0.02 Triceps skinfold > 0.05 Subscapular skinfold > 0.05 Abdomen skinfold > 0.05 Upperarm cimcurference > 0.05 Forearm circumference < 0.05 Thigh circumference < 0.05 Calf circumference < 0.03 Chest circumference > 0.05 Transverse chest breadth > 0.05 Sagittal chest depth > 0.05 factors. The performed analyses demonstrated a statistically significant relationship between the mutation category and severity of the clinical respiratory symptoms, and nutritional status (respectively: H (2,55) = 9.589, p < 0.01; H (3,55) = , p < 0.005). In the course of further analyses, multiple comparisons indicated that individuals with the severe mutation and individuals with severe respiratory symptoms tended to have more clearly marked physical retardation and worse nutritional status (p < 0.05). Table 3. Estimation of nutritional status of studied persons Nutritional status N % Overnutrition Normal nutrition Slight malnutrition Malnutrition Emaciation Discussion In starting to discuss the obtained results one should point to the small size of the sample, which is typical of clinical studies. This fact results in certain interpretational constraints. The physical development status and nutritional status of cystic fibrosis patients are affected by many factors. The causes of physical development and nutritional status disorders are explained in two ways. The first explanation assumes that deviations in this respect are a secondary consequence of gastrointestinal or respiratory disorders, conditioning negative energy balance and malnutrition. This results in the body's decreased energy output for growth and tissue regeneration at the expense of support of the vital organs' functions, and in a delayed physical development. In cases involving such changes regular therapy and a properly composed diet effectively improve the patients developmental status [GRABOWSKA and ŁUCZAK 1996]. According to the second explanation, the scale of developmental retardation coexistent with the disease is in fact independent of the degree of severity of disease and should not be treated as a secondary consequence of the pathological process complications. In light of this interpretation, developmental retardations are ones of the effects of pleiotrophy at the cystic fibrosis locus which may have an effect on the change of the original expression of the gene defect [SING et al. 1982; MAHANEY, MCCOY 1986]. The results obtained in this study, demonstrating a considerable physical retardation of cystic fibrosis patients
7 Nutritional status of patients with cystic fibrosis 59 compared to the healthy population, are consistent with the results obtained by other authors [SHEPHERD et al. 1980; MEARNS 1983; GRABOWSKA and ŁU- CZAK 1996; SHEPHERD et al. 1986]. A significant shift of the mean values of traits in the negative direction was observed. However, it is worth noticing that within the studied sample includes both individuals with extremely low phenotypic values and individuals with values similar to the healthy population. The biggest deviations were recorded in body mass and height and thigh and calf circumferences. However, suggested by many authors [e.g., COREY et al. 1988; BARKHOUSE et al. 1989; LAI et al. 1999] predominance of body mass deficiency over body height deficiency was not observed. In fact, higher values of body mass deviations in comparison with height deviations are not a steadfast rule, since studies by BORBEL and DOCTTER [1997] and WALKOWIAK [1998] failed to demonstrate a predominance of body mass deficiency. The present results show a higher percentage of individuals with body mass deficiency exceeding minus 2 SD (42%) compared to individuals with body height deficiency exceeding minus 2 SD (29%). Nevertheless, the difference between the observed values is not statistically significant (χ 1 2 = 1.95; p > 0.05). As demonstrated by LAI et al. [1999], similar low values have been observed in recent years only in 10-15% of cystic fibrosis patients. The results obtained in this study approximate those observed in highly developed countries in past decades. This is probably due to the fact that intensive nutritional management in Poland started to be implemented only a few years ago [NOWAKOWSKA et al. 1995]. The presented results indicate a significant shift of the means of standardized values of the studied circumferences in the negative direction, with the exception of the chest circumference. The observed deviations in relation to the healthy population agree with the literature data pertaining to children [GRABOWSKA and ŁUCZAK 1996]. The chest circumference being situated within the normal range for the population results from its barrel-like shape (increased sagittal depth with accompanying decreased transverse breadth) typical of this type of pathology. Mean standardized values of a skinfold thickness in the studied group do not deviate from accepted normal values for the healthy group of individuals, which is in agreement with the result obtained by BENTUR et al. [1996]. On the other hand, studies conducted by RICHARDSON et al. [2000] demonstrated a decreased thickness of skin folds in cystic fibrosis patients. In their studies, LAI et al. [2000] and MEARNS [1983] described birth weight deficiencies in newborns with cystic fibrosis, even after the exclusion of newborns of low gestational age and those with meconium ileus. In turn, BRON- STEIN et al. [1992] demonstrated significant deficiencies in body weight at birth only in girls. The authors suggest that deficient growth may start as early as the gestation period. According to the study by MÜLLER et al. [1999], considerable lowering of the birth body weight in newborns with cystic fibrosis (both girls and boys) may result from intrauterine malnutrition caused by pancreatic insufficiency in the fetus. However, the results obtained in this study demonstrate no statistically significantly low-
8 60 M. Kosińska et al. ered values of body weight at birth in individuals with cystic fibrosis as compared to values obtained for healthy individuals. Similar results were obtained by GREER et al. [1991] who found that birth body weight values in cystic fibrosis patients were within normal range. As expected, the authors observed a significant effect of mutation type on body mass and height values and on thigh and calf circumferences. In patients with a severe mutation, physical retardation is more clearly marked. This mutation causes exacerbation of disease symptoms and, as a result, affects the overall biological condition of the patient. It is worth noticing, that this type of mutation has no differentiating effect on the dimensions of the chest. It transpires from the literature that despite the fact that changes in the chest, most likely caused by functional disorders of the respiratory system, are registered in as many as 95% of cystic fibrosis cases, they are dependent on the type of mutation [KOSTUCH and WOJCIEROWSKI 1995]. The presented analyses also failed to demonstrate a relationship between the formation of skinfolds and the type of mutation. This may mean that these traits are highly ecosensitive. A similar situation is observed with regard to the mean body weight at birth. This would corroborate the thesis that the reasons for the demonstrated differentiating effect of the type of mutation on certain traits (body mass and height, thigh and calf circumferences) should be looked for in a secondary effect of functional disorders of individual genotypically conditioned systems rather than among the direct effects of the genetic determination. From abundant literature on the subject of cystic fibrosis it is known that the biological condition of cystic fibrosis patients is affected by clinical respiratory symptoms. However, the results obtained by the authors demonstrate a relationship only between respiratory manifestations and body mass. Similar results were obtained by other authors, e.g., BYARD [1989] and COLLINS et al. [1999]. According to these researchers, lowered body mass is prognostic of pulmonary disease, and anthropometric parameters correlate more strongly with pulmonary function than with, for instance, parameters indicating pancreatic insufficiency. Research by SPROUL and HUANG [1964] also indicate significant relationships between exacerbation of respiratory symptoms and a lowered body mass. The nutritional status is defined as a complex of somatic and biochemical body traits, being a manifestation of the supply of nutrients to the body, their digestion, absorption and metabolism. Resulting from their assessment of the nutritional status of the subjects, the authors were able to corroborate the state of malnutrition in cystic fibrosis patients as suggested earlier by many authors [KEREM et al. 1990; RYŻKO 1997; HAYLLAR et al. 1997]. In the studied group, this ranged from slight to the level indicating emaciation. The obtained results show unequivocally that despite considerable advancement in the medical sciences and a better than before degree of health consciousness, patients with cystic fibrosis still demonstrate poor nutritional status. However, the existence of considerable differences among subjects in this respect, meaning
9 Nutritional status of patients with cystic fibrosis 61 the presence of adequately nourished, and even overnourished individuals in the studied group, highlights the importance of more appropriate nutritional therapy and more efficacious medical care in the treatment of cystic fibrosis. One cannot, however, neglect the importance of the effect of the type of mutation and severity of the respiratory disease symptoms on the nutritional status. Patients with a severe mutation type and those with an obvious pulmonary dysfunction were observed to have inferior nutritional status. No overnourished individuals were found in either the first or the second group. The correctness of the obtained results is confirmed by the fact that other pulmonary diseases (e.g., chronic obstructive lung disease) also result in malnutrition [SAHEBJAMI 1989]. It needs to be emphasized that there exists a strong relationship between the type of mutation and respiratory symptoms, and the nutritional status of cystic fibrosis patients. The more severe the mutation and respiratory symptoms, the worse is the nutritional status of patients with cystic fibrosis. The observed deviations of the anthropometric traits, in locating the subjects below the norm adopted for the healthy population, may result from both inhibited (delayed) growth and malnutrition. It is difficult to state unequivocally whether retarded development is a result of malnutrition or whether malnutrition is a result of inhibited development. Cystic fibrosis is a disease "with many faces" and it is thus difficult to ascertain cause and effect in the observed disorders. On the basis of various results presented in the literature, one can state that correlations of respiratory system functions with specific CFTR gene mutations are not unequivocal. Patients homozygotic for F508 are more prone to chronic bacterial infections, being mostly Pseudomonas aeruginosa colonization [WITT 1994]. Only patients homozygotic for this allele are diagnosed with meconium ileus of the alimentary system as being a cause of malnutrition. It was also demonstrated that nonsense mutations had more severe negative effects on the gastric system than on the respiratory system, though causes of this phenomenon are still unknown. Further, patients with the same genotype were found to exhibit considerable differences in pulmonary symptoms [KEREM et al. 1990], which may be an argument in favor of the impact of other genetic factors or environmental modification in the expression of the disease. Conclusions The phenomenon of retarded biological development which is reflected in the developmental status of adult individuals is an inseparable element of many pathological processes. On the basis of the results obtained in this study, the authors ascertained that adult cystic fibrosis patients demonstrated considerable retardation in physical development and a poor nutritional status. The type of mutation and severity of respiratory symptoms significantly affect the physical development and nutritional status of cystic fibrosis patients. Acknowledgements We are most grateful to Prof. Michał Witt from the Human Genetics Institute of the Polish Academy of Sciences in
10 62 M. Kosińska et al. Poznań for molecular tests of the CFTR gene. We also thank the referees for their comments on the original manuscript of this paper. This study was supported by interdisciplinary grant founded by Adam Mickiewicz University and Academy of Medical Sciences in Poznań (No. PU-II/10). References BARKHOUSE L.B., J. FAHEY, C.T. GILLESPIE, D.E. COLE, 1989, Quantitating the effect of cystic fibrosis on linear growth by mathematic modelling of longitudinal growth curves, Growth Dev. Aging, 53(4), BENTUR L., D. KALNINS, D. LEVISON, M. COREY, P.R. DURIE, 1996, Dietary intakes of young children with cystic fibrosis: Is there a difference?, J. Pediatr. Gastroenterol. Nutr. 22(3), BORBEL P., G. DOCTTER, 1997, Effect of continuous dietary advice on nutrient intake and nutrition status, 21 European Cystic Fibrosis Conference, Davos, Switzerland, Abstracts, p. 170 BOŻKOWA K., H. SIWIŃSKA-GOŁĘBIOWSKA, J. RUTKOWSKI, A. NOWAKOWSKA, 1971, Epidemiologia mukowiscydozy u dzieci w Polsce, Ped. Pol., 46, BRONSTEIN M.N., R.J. SOKOL, S.H. CHATFIELD, K.B. HAMMOND, K.M. HAMBIDGE, C.D. STALL, F.J. ACCURSO, 1992, Pancreatic insufficiency, growth, and nutrition in infants identified by newborn screening as having cystic fibrosis, J. Pediatr., 120(4), BYARD P., 1990, Early childhood growth in patients with cystic fibrosis, Ann. Hum. Biol, 17(6), BYARD P.J., 1989, Relationship between clinical parameters and linear growth in cystic fibrosis, Am. J. Hum. Biol., 1, CIEŚLIK J., M. KACZMAREK, M.D. KALISZEWSKA- -DROZDOWSKA, 1994, Dziecko poznańskie 90, Wyd. Naukowe Bogucki, Poznań COLLINS C.E., L. MACDONALD-WICKS., S. ROWE, E.V. O LOUGHLIN, R.L. HENRY, 1999, Normal growth in cystic fibrosis associated with a specialised centre, Arch. Dis. Child., 81(3), COREY M., F.J. MCLAUGHLIN, M. WILLIAMS, H. LEVISON, 1988, A comparison of survival, growth, and pulmonary function in patients with cystic fibrosis in Boston and Toronto, J. Clin. Epidemiol., 41(6), COREY M., V. FAREWELL, 1995, Determinants of mortality from cystic fibrosis in Canada , Am. J. Epidemiol., 143, Cystic Fibrosis Genetic Analysis Consortium, Mutation Dziecko konińskie. Rozwój fizyczny dzieci i młodzieży województwa konińskiego, 1998, J. Grabowska (ed.), Wydawnictwo Uniwersytetu Łódzkiego, Łódź GRABOWSKA J., B. ŁUCZAK, 1996, Rozwój biologiczny dzieci i młodzieży chorych na mukowiscydozę, [in:] Antropologia a medycyna i promocja zdrowia, t.1, A. Malinowski (ed.), Łódź, pp GRASEMANN H., H.G. WIESEMANN, F. RATJEN, 1995, The importance of lung functions as a predictor of two year mortality in mucoviscidosis, Pneumonologie, 49, GREER R., R. SHEPERD, G. CLEGHORN, F.G. BOWLING, T. HOLT, 1991, Evaluation of growth in body composition following neonatal diagnosis of cystic fibrosis, J. Pediatr. Gastroenterol. Nutr., 13, HAYLLAR K.M., S.G. WILLIAMS, A.E. WISE, S. POURIA, M. LOMBARD, M.E. HODSON, D. WESTABY, 1997, A prognostic model for the prediction of survival in cystic fibrosis, Thorax, 52(4), KEREM E., M. COREY, B. KEREM, J. ROMMENS, D. MARKIEWICZ, H. LEVISON, P. DURIE, 1990, The relation between genotype and phenotype in cystic fibrosis - analysis of the most common mutation ( F508), New Engl. J. Med., 323(22), KOSTUCH M., J. WOJCIEROWSKI, 1995, Mucoviscidosis, Klinika Pediatryczna, 4(2), LAI H.C., M. COREY, S.C. FITZSIMMONS, M.R. KOSOROK, P.M. FARREL, 1999, Comparison of growth status of patients with cystic fibrosis between the United States and Canada, Amer. J. Clin. Nutr., 69, LAI H.C., M.R. KOSOROK, A. LAXOVA, L.A. DAVIS, S.C. FITZSIMMONS, P.M. FARREL, 2000, Nutritional status of patients with cystic fibrosis with meconium ileus: A comparison with patients without meconium ileus and diagnosed early through neonatal screening, Pediatrics, 150(1), 53-61
11 Nutritional status of patients with cystic fibrosis 63 LANDON C., R.G. ROSENFELD, 1984, Short stature and pubertal delay in male adolescents with cystic fibrosis, Am. J. Dis. Child, 138, MÜLLER A.E., B. THAMM, T. LIETZ, W. HANDRICK, S. WALTER, 1999, Cystic fibrosis: A cause of reduced birth weight?, Eur. J. Pediatr, 158(3), 264 MAHANEY M.C., K.S. MCCOY, 1986, Developmental delays and pulmonary disease severity in cystic fibrosis, Hum. Biol., 58(3), MALINOWSKI A., W. BOŻIŁOW, 1997, Podstawy antropometrii. Metody, techniki, normy, Wyd. Naukowe PWN, Warszawa Łódź MEARNS M.B.,1983, Growth and Development, [in:] Cystic fibrosis, M. Hodson, A.P. Norman, J.C. Batten (eds.), Bailliere Tindall, London, pp NOWAKOWSKA A., J. BAL, E. OBERSZTYN, D. SANDS, D. MACIEJKO, T. MAZURCZAK, 1995, Próba oceny zależności pomiędzy fenotypem a genotypem wśród 65 chorych na mukowiscydozę, Pediatria Polska, LXX(8), RICHARDSON I., I. NYULASI, K CAMERON, M. BALL, J. WILSON, 2000, Nutritional status of an adult cystic fibrosis population, Nutrition, 16(4), ROSENFELD M., R. DAVIS, S. FITZSIMMONS, M. PEPE, B. RAMSEY, 1997, Gender gap in cystic fibrosis mortality, Am. J. Epidemiol., 145, RYŻKO J., 1997, Ocena stanu odżywienia u dzieci, Przegląd Pediatryczny, 27(1), SAHEBJAMI H., 1989, Nutrition and lung function, [in:] Lung Cell Biology, D. Massaro (ed.), Marcel Dekker, New York, pp SHEPHERD R., T.L. HOLT, B.J. THOMAS, L. KAY, A. ISLES, P.J. FRANCIS, L.C. WARD, 1986, Nutritional rehabilitation in cystic fibrosis: Controlled studies of effects on nutritional growth retardation, body protein turnover, and course of pulmonary disease, J. Pediatr., 109(5), SHEPHERD R., W.G.E. COOKSLEY, W.D. DOMVILLE COOKE, 1980, Improved growth and clinical, nutritional, and respiratory changes in response to nutritional therapy in cystic fibrosis, J. Pediatr., 97(3), SING C.F., D.R. RISSER, W.F. HOWATT, R.P. ERICSON, 1982, Phenotypic heterogeneity in cystic fibrosis, Am. J. Genet., 13(2), SPROUL A., N. HUANG, 1964, Growth pattern in children with cystic fibrosis, J. Pediatr., 65(5), STRANDVIK B., 1991, Nutritional management of cystic fibrosis, Annales Nestle, 49, WALKOWIAK J., 1998, Stan odżywienia i rozwój fizyczny dzieci chorych na mukowiscydozę w świetle podstawowych wskaźników wagowych i wzrostowych, Przegląd Pediatryczny, 28(3), WITT M., 1994, Wybrane aspekty zależności genotyp fenotyp w mukowiscydozie, Kosmos, 43(3/4), YANKASKAS J.R., 2004, Cystic fibrosis adult care: Consensus conference report, Chest, 125, 1-39 Zasady rozpoznawania i leczenia mukowiscydozy, 2000, Stanowisko Polskiej Grupy Roboczej Mukowiscydozy przy Zarządzie Głównym Polskiego Towarzystwa Pediatrycznego, Medycyna Praktyczna Pediatria, 3, Streszczenie Mukowiscydoza jest najczęściej występującą autosomalną recesywną chorobą monogenową. Do najczęstszych objawów klinicznych mukowiscydozy zalicza się zapalenia płuc i zatok, niewydolność zewnątrzwydzielniczą trzustki, cholestazę oraz podwyższenie poziomu elektrolitów w pocie. Powszechnie obserwowane jest również opóźnienie rozwoju biologicznego, a w przypadku osób dorosłych niedobory masy i wysokości ciała. Głównym celem badań była ocena stanu biologicznego oraz stopnia odżywienia osób dorosłych chorych na mukowiscydozę. Badaniami objęto 55 osób chorych (24 mężczyzn oraz 31 kobiet), w wieku od lat. Rozpoznanie postawiono zgodnie z kryteriami zaproponowanymi przez Polską Grupę Roboczą Mukowiscydozy [Zasady rozpoznawania ]. Potwierdzenie uzyskano w oparciu o test potowy, test wysokich wartości przeznabłonkowej różnicy potencjałów oraz badania molekularne genu CFTR. Na podstawie rodzaju mutacji
12 64 M. Kosińska et al. wyróżniono trzy grupy badanych: 1) osoby o genotypie F508/ F508 uznawanym za mutację ciężką (N = 10; 18%); 2) osoby o genotypie F508/M, gdzie M to inna mutacja tzw. nieokreślona, powodująca łagodniejszy przebieg choroby (N = 37; 67%); 3) osoby o genotypie M/M (N = 8; 15%). Nie stwierdzono różnic istotnych statystycznie w częstości występowania wyróżnionych kategorii mutacji pomiędzy płciami (χ 2 df=2 = 0,256; p > 0,05). Stan biologiczny oraz stopień odżywienia określono przy pomocy parametrów antropometrycznych, a funkcję płuc w spirometrii oraz w badaniu mikrobiologicznym plwociny na obecność Pseudomonas aeruginosa. Zebrane dane poddano analizie statystycznej obejmującej metody parametryczne i nieparametryczne, zastosowane zgodnie z ich założeniami. Wszystkie wartości badanych cech antropometrycznych zestandaryzowano. Pomiary grubości fałdów skórno-tłuszczowych przedstawiono w postaci logarytmicznej, wykorzystując tablice przekształceń logarytmicznych dla tych pomiarów, skonstruowane przez Edwardsa i wsp. [Dziecko Konińskie 1998]. Uzyskane wyniki wskazują, że rozwój fizyczny osób chorych na mukowiscydozę jest znacznie opóźniony w stosunku do osób zdrowych. Średnie wartości standaryzowanych zmiennych antropometrycznych wykazują istotne statystycznie odchylenia w kierunku ujemnym w stosunku do populacji zdrowej (tab. 1, fig. 1). Typ mutacji wpływa na wartości masy i wysokości ciała oraz obwodów uda i podudzia (tab. 2). Nasilenie dolegliwości ze strony układu oddechowego modyfikuje jedynie wartość masy ciała (test Kruskala-Wallisa: H (3,55) = 8,505; p < 0,04). Osoby dorosłe chore na mukowiscydozę wykazują znaczne opóźnienie rozwoju fizycznego i zły stan odżywienia. Wykazano istotną statystycznie zależność pomiędzy kategorią mutacji i nasileniem objawów klinicznych ze strony układu oddechowego a stanem odżywienia (odpowiednio: H (2,55) = 9,589; p < 0,01; H (3,55) = 13,320; p < 0,005).
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text:
Joel Cooper is wary of a backlash from Glentoran
Joel Cooper admits Glenavon are ready for a Glentoran backlash today.
The fixture at Mourneview Park brings together two sides in very different form. Glenavon are flying, having lost just one of their last 11 league games, while the east Belfast men are on a four-match losing run in the Danske Bank Premiership, and were routed 4-0 on their own ground by bottom of the table Warrenpoint last weekend.
It was a result which shocked Glens boss Alan Kernaghan, who will be demanding a reaction from his side when they make the trip to Mid-Ulster.
And Cooper concedes Glenavon must be wary, although the 19-year-old winger believes they are good enough to win the game.
"They will be looking a reaction to last weekend," he said.
"We have to keep it solid in the first 15 minutes or so, but we are on a good run and we are confident we can win the game.
"We're on our own ground, it's a bigger pitch and we're able to move the ball around. If we can work hard I believe we are good enough to win."
Cooper scored the winner as Glenavon claimed a 1-0 win at Dungannon last weekend.
It was their seventh victory in 10 league games, and took them fourth, but Cooper is not satisfied, adding: "We're into fourth but we always want to better ourselves and now we want into third. We'll just take it game by game and our focus is on Glentoran."
Cooper is reluctant to place a target on what the Lurgan club can achieve this season.
"It's just to win as many games as we can and see where it takes us. We look at each game as it comes and don't get ahead of ourselves," he added.
Glenavon have lost just once in the league since October 24.
Ironically, their only defeat came at the Oval where goals from Jonathan Smith and Steven Gordon gave the Glens a 2-0 win.
Cooper admits confidence is growing by the week. He says: "We expect to win every game, no matter who we're playing against."
Belfast Telegraph

subset: commoncrawl


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CherokeeGene-L ArchivesArchiver > CherokeeGene > 2001-05 > 0989862040
From: Donald Panther-Yates <>
Subject: [Cherokee Genealogy only] Isaac Cooper; Chief Black Fox
Date: Mon, 14 May 2001 13:42:10 -0400
Searching for information ca. 1800 on Henry Cooper, father of Capt. John
Cooper, a Choctaw chief and Isaac Cooper,
who married Nancy Black Fox (Paint Clan); also Huston (perhaps William
Huston Cooper), owner of plantation on Harpeth
River, Tennessee. He was my 5g-grandfather through descendants who
settled at Anawaika (Deerhead Cove)at foot
of Sand Mountain on Ga./Ala. line near Trenton and Rising Fawn, Ga.
Family members were scattered to the four winds during Indian Removal
in the 1820s and 1830s. Another of Black Fox's daughters, Mary Ann
Black, married William Davis, a Chickamauga chief near Creek Path on
Sand Mountain. Black Fox's sister married John Looney and their son was
Chief John Looney. The Looney family also married with the Coopers.
Below is a bare
outline of the Coopers--
Don Panther-Yates
Photos and more info at
Descendants of Henry Cooper
Generation No. 1
1. HENRY2 COOPER (-----1) was born Abt. 1750.
Children of HENRY COOPER are:
2. i. ISAAC3 COOPER, b. Abt. 1775, N.C.; d. Aft. 1840,
Tennessee (?).
3. ii. JOHN COOPER, b. Abt. 1771, N.C.; d. Abt. 1839, Perry
Co., Tenn..
iii. HUSTON COOPER.
Generation No. 2
2. ISAAC3 COOPER (HENRY2, -----1) was born Abt. 1775 in N.C.1, and died
Aft. 1840 in Tennessee (?). He
married NANCY BLACK FOX Abt. 1795 in Tenn. (?), daughter of CHIEF FOX
and DAUGHTER
ATTAKULLAKULLA. She was born Abt. 1775.
Children of ISAAC COOPER and NANCY FOX are:
4. i. JAMES4 COOPER, b. Abt. 1795; d. Bef. 1850.
5. ii. MARY (POLLY) COOPER, b. September 30, 1797,
Kentucky; d. August 17, 1862, Wayne Co.,
6. iii. SARAH COOPER, b. March 09, 1800, Tennessee; d.
November 16, 1874, Buffalo River, Newton
Co., Ark..
7. iv. NANCY COOPER, b. 1803, Wayne Co., Ky.; d. 1880,
Temple, Bell Co., Texas.
8. v. ISAAC COOPER, b. Abt. 1804, Wayne Co., Ky. (?); d.
December 23, 1847, Vera Cruz, Mexico.
9. vi. WILLIAM COOPER, b. 1807, Wayne Co., Ky.; d. October
1859, DeKalb Co., Ala..
10. vii. HARMON COOPER, JR., b. August 24, 1811, Kentucky;
d. July 07, 1886, Tennessee.
3. JOHN3 COOPER (HENRY2, -----1) was born Abt. 1771 in N.C., and died
Abt. 1839 in Perry Co., Tenn.. He
married NANCY ANN PILES 1786 in Tenn. or N.C..
Children of JOHN COOPER and NANCY PILES are:
i. ELIZABETH4 COOPER.
ii. MARY COOPER.
iii. HENRY COOPER.
iv. NARCISSA COOPER.
v. DELITHA COOPER, m. ------ NICHOLS.
11. vi. WILLIAM HUSTON COOPER, b. 1806, Maury Co., Tenn.;
d. 1866, Pope County, Arkansas.
Generation No. 3
4. JAMES4 COOPER (ISAAC3, HENRY2, -----1) was born Abt. 1795, and died
Bef. 1850. He married (1)
--------------- Abt. 1812. He married (2) LUCRETIA BLEVINS March 17,
1814 in Wayne Co., Ky., daughter of
JONATHAN BLEVINS and CHARLOTTE MUSE. She was born in Virginia, and died
in Arkansas.
Child of JAMES COOPER and --------------- is:
i. ISAAC5 COOPER, b. August 22, 1812, Wayne Co., Ky.; d.
September 29, 1872, Limestone, Newton
Co., Arkansas; m. NARCISSA JANE RITCHIE, Abt. 1834; b. March 24, 1814,
S.C.; d. September 09, 1908,
Limestone, Ark..
Children of JAMES COOPER and LUCRETIA BLEVINS are:
ii. EDITH5 COOPER, b. 1833, Rutherford Co., Tenn.; m.
iii. MARTHA G. COOPER, b. Abt. 1836.
iv. JULIA COOPER, b. Abt. 1842.
5. MARY (POLLY)4 COOPER (ISAAC3, HENRY2, -----1) was born September 30,
1797 in Kentucky, and
died August 17, 1862 in Wayne Co., Ky.. She married (1) BENJAMIN
BOOKOUT March 25, 1814 in Wayne
Co., Ky.. He was born Abt. 1793. She married (2) JOHN LOVELACE May 16,
1822 in Wayne Co., Ky.. He was
born March 12, 1801 in N.C. or Va., and died September 16, 1867 in
Wayne Co., Ky..
Children of MARY COOPER and BENJAMIN BOOKOUT are:
i. SERRILDA ANN5 BOOKOUT, b. Abt. 1816; m. JOHN C. COGER,
February 02, 1842, Wayne Co.,
ii. JOHN BOOKOUT, b. 1818.
Children of MARY COOPER and JOHN LOVELACE are:
iii. JAMES HENRY5 LOVELACE, b. October 02, 1829; d. March
01, 1914; m. LUCINDA YOUNG,
June 21, 1852, Wayne Co., Ky..
iv. CHARLES LOVELACE, b. 1831, Kentucky; m. ZERALDA
BURNETT, April 13, 1856, Wayne Co.,
v. JOHN LOVELACE, b. December 27, 1832, Kentucky; d.
December 02, 1888; m. LUCINDA
SCOTT, September 21, 1854, Wayne Co., Ky..
vi. WILLIAM LOVELACE, b. 1835.
vii. HARMON LOVELACE, b. 1836; m. MARY JANE SCOTT, October
12, 1858, Wayne Co., Ky..
viii. MARY JANE (POLLY) LOVELACE, b. 1839; m. (1) ISAAC
BURNETT, September 19, 1857,
Wayne Co., Ky.; m. (2) JOHN CONWAY JEFFERSON SELVIDGE, September 23,
1863; b. March 14, 1838.
6. SARAH4 COOPER (ISAAC3, HENRY2, -----1) was born March 09, 1800 in
Tennessee, and died November
16, 1874 in Buffalo River, Newton Co., Ark.. She married JOHN (JACKIE)
ADAIR III Abt. 1816 in Wayne Co.,
Ky.(?), son of JOHN ADAIR and MARY O'DONNELL. He was born August 13,
1794 in Tennessee, and died
September 06, 1878 in Buffalo River, Newton Co., Ark..
Children of SARAH COOPER and JOHN ADAIR are:
i. MELINDA5 ADAIR, m. OLIVER DAVIS.
ii. JAMES ADAIR, b. 1817, Tenn.; m. MARGARET (PEGGY)
CECIL; b. 1821.
iii. JOHN ADAIR IV, b. 1829, Tenn.; m. REBECCA ANN BRISCO;
b. 1828, Ark..
iv. BARBARA ADAIR, b. 1831, Tennessee; m. HARMON COOPER.
v. ISAAC ADAIR, b. 1832.
vi. WILLIAM HARRISON ADAIR, b. 1837; d. 1864.
vii. SARAH G. ADAIR, b. 1840, Arkansas.
viii. HARRIS ADAIR, b. 1842.
ix. GEORGE W. ADAIR, b. 1844; m. ELIZABETH PARKER.
7. NANCY4 COOPER (ISAAC3, HENRY2, -----1) was born 1803 in Wayne Co.,
Ky., and died 1880 in
Temple, Bell Co., Texas. She married (1) JAMES COOPER. He was born Abt.
1800. She married (2)
JONATHAN BURKE March 31, 1820 in Wayne Co., Ky., son of BENJAMIN BURKE
and ELIZABETH (?).
He was born August 28, 1797 in Pittsylvania Co., Va., and died August
14, 1875 in Station Camp Creek, Oneida,
Children of NANCY COOPER and JONATHAN BURKE are:
i. PETER5 BURKE, b. 1821; m. (1) SUSAN MILLIGAN; b. Abt.
1820; m. (2) ELIZA ANN
ii. ELIZABETH BURKE, b. 1823; m. WILLIAM RILEY HATFIELD.
iii. SUSAN BURKE, b. 1825, Kentucky; d. March 1851,
Deerhead Cove, DeKalb Co., Ala.; m. (1)
WILLIAM COOPER, Abt. 1842; b. Abt. 1820, Kentucky; d. 1847, Ga. (?); m.
(2) JAMES COOPER, Abt.
1850; b. 1822, Alabama.
iv. HAYDEN BURKE, b. May 07, 1828; d. March 1903, Eufala,
Okla.; m. NANCY LEWELLEN, 1862,
Nobusiness Creek, Scott Co., Tenn.; b. February 28, 1845, New River,
Morgan Co., Tenn.; d. February 20, 1879,
McAllister, Oklahoma.
v. JOHN GRANVILLE BURKE, b. May 1830; d. 1900; m. ANNA
(ANNIE) BLEVINS; b. 1843; d.
vi. HARMON BURKE, b. October 1834; d. March 25, 1911,
Oklahoma; m. POLLY ANN SMITH,
April 01, 1867, Scott Co., Tenn.; b. December 1831, Tennessee; d. April
20, 1915, Powell, Okla..
vii. MARY (POLLY) BURKE, b. 1835; m. CYRENOUES CARSON; b.
September 1837.
viii. JONATHAN BURKE, b. January 1837, Wayne Co., Ky.; d.
November 29, 1915, Canadian,
Oklahoma; m. MARY JANE MILLIGAN; b. Abt. 1820.
ix. SARAH (SALLY) BURKE, b. October 13, 1838; m. WILLIAM
x. LEWIS BURKE, b. January 1840; d. 1903; m. SARAH (SALLY)
BLEVINS, June 11, 1868, Scott
Co., Tenn..
xi. WILLIAM BURKE, b. 1849.
8. ISAAC4 COOPER (ISAAC3, HENRY2, -----1) was born Abt. 1804 in Wayne
Co., Ky. (?), and died
December 23, 1847 in Vera Cruz, Mexico. He married MAHALA JANE (JENNY)
BLEVINS January 21, 1823 in
Marion Co., Tenn. (?)2, daughter of JONATHAN BLEVINS and CHARLOTTE
MUSE. She was born Abt. 1801
in Virginia, and died Aft. 1870 in Dekalb Co., Ala. or Marion Co.,
Children of ISAAC COOPER and MAHALA BLEVINS are:
i. WILLIAM5 COOPER, b. Abt. 1820, Kentucky; d. 1847, Ga.
(?); m. SUSAN BURKE, Abt. 1842; b.
1825, Kentucky; d. March 1851, Deerhead Cove, DeKalb Co., Ala..
ii. SALLIE COOPER, b. Abt. 1820.
iii. JAMES COOPER, b. 1822, Alabama; m. (1) UNKNOWN FIRST
WIFE; m. (2) SUSAN BURKE,
Abt. 1850; b. 1825, Kentucky; d. March 1851, Deerhead Cove, DeKalb Co.,
Ala.; m. (3) MARY --------, Abt.
1852; b. Abt. 1839, Alabama.
iv. JACKSON (JACK) COOPER, b. Abt. 1825, Kentucky; m. MARY
ANN SIZEMORE, Abt. 1842,
Dade Co., Georgia, probably; b. Abt. 1828, Ga..
v. SUSAN E. COOPER, b. Abt. 1826; d. April 17, 1901; m.
WILLIAM E. ADKINS, April 20, 1863,
Henry Co., Tenn.; b. Abt. 1828, Kentucky; d. 1863, Arkansas.
vi. JOHN COOPER, b. Abt. 1828, Tennessee; d. Bef. 1870; m.
LOUISA --------; b. Abt. 1828,
vii. HARMON COOPER, b. January 08, 1830, Tennessee; d.
August 21, 1879, South Pittsburg, Marion
Co., Tenn.3; m. MALLIAH (DELIA) FRANCIS, 1849, Marion Co., Tenn.; b.
Abt. 1833, Georgia; d. January 12,
viii. MARY (POLLY) ANN COOPER, b. 1831.
ix. GAINES COOPER, b. 1833, Tennessee; m. LUCRETIA
--------, Abt. 1857; b. Abt. 1843.
x. JEMIMA (MIMA) H. COOPER, b. 1839; d. Abt. 1875,
Shellmound, Marion Co., Tenn.; m. JOHN H.
HOLLOWAY, June 28, 1854, Dekalb Co., Ala.; b. February 1828, Tenn.; d.
Aft. 1900, Indian Territory.
xi. NANCY FRANCES COOPER, b. Abt. 1842.
9. WILLIAM4 COOPER (ISAAC3, HENRY2, -----1) was born 1807 in Wayne Co.,
Ky., and died October
1859 in DeKalb Co., Ala.. He married SUSANNAH (SUSAN) -------. She was
born Abt. 1807 in Kentucky.
Children of WILLIAM COOPER and SUSANNAH ------- are:
i. JAMES5 COOPER, b. October 22, 1824, Kentucky; d. June
15, 1888, Alabama; m. LUCINDA
HAWKINS, May 02, 1847, Dekalb Co., Ala.; b. December 28, 1824, McMinn
Co., Tennessee; d. September 22,
1907, Etowah Co., Ala..
ii. JOHN C. COOPER, b. Abt. 1827.
iii. NANCY COOPER, b. June 28, 1832, Wayne Co., Ky.; m.
(1) ---------------; m. (2) ARCHIBALD
D. BLANSETT, SR., September 03, 1865, Dade Co., Ga..
iv. MARY (POLLY) ANN COOPER, b. Abt. 1837.
v. ELVIRA COOPER, b. Abt. 1838.
vi. THOMAS B. COOPER, b. Abt. 1840.
vii. MALINDA COOPER, b. Abt. 1842.
viii. MANORAH COOPER, b. Abt. 1845.
ix. CAROLINE COOPER, b. Abt. 1847.
x. ADALINE COOPER, b. Abt. 1850.
10. HARMON4 COOPER, JR. (ISAAC3, HENRY2, -----1) was born August 24,
1811 in Kentucky, and died
July 07, 1886 in Tennessee. He married (1) MARY ANN (POLLY) ADKINS May
27, 1830 in Wayne Co., Ky.,
daughter of BENJAMIN ADKINS and CATHERINE STIGALL. She was born Abt.
1814 in Wayne Co., Ky.,
and died August 17, 1868 in Ky.. He married (2) MAHALA JACKSON 1849 in
Tennessee. He married (3)
MARTHA PILE Abt. 1860, daughter of WILLIAM PILE and NARCISSA SABIENS.
She was born September
10, 1841 in Tennessee, and died September 20, 1920.
Children of HARMON COOPER and MARY ADKINS are:
i. MEECIE5 COOPER.
ii. TELITHA LEANNE COOPER, b. April 21, 1831; d. May 18,
1902, Norman, I.T.; m. ANDREW H.
iii. LUIDA (LUCINDA) COOPER, b. 1833.
iv. CATHERINE COOPER, b. Abt. 1834.
v. ISAAC COOPER, b. Abt. 1835.
vi. SON COOPER, b. 1836.
vii. LUCINDA JANE COOPER, b. April 28, 1838, Wayne Co.,
Ky.; d. September 15, 1911, Sumner
Co., Ks.; m. (1) RICHARD GRIFFITH; m. (2) CALVIN KOGER, 1860.
viii. JOHN GRANVILLE COOPER, b. Abt. 1841; m. MARY MARTHA
GRIFFITH, 1863, Wayne Co.,
Ky.; b. 1847.
ix. BENJAMIN TURNER COOPER, b. December 05, 1843,
Kentucky; d. April 20, 1930, Topeka,
Kansas; m. JANE CATHERINE ADKINS, August 25, 1867, Wayne Co., Ky.; b.
March 28, 1846; d. February
23, 1920, Jennings, Decaturn Co., Kansas.
x. NANCY ELLEN COOPER, b. April 03, 1845, Wayne Co., Ky.;
d. February 15, 1915; m.
JEFFERSON KOGER, November 24, 1864; b. 1847; d. 1919.
xi. WILLIAM H. COOPER, b. Abt. 1848.
xii. GEORGE WASHINGTON COOPER, b. May 27, 1848; d. 1941,
Grinnell, Poweshiek Co., Iowa; m.
TELITHA LEGRAND ADKINS, June 08, 1868, Scott Co., Tenn.; b. 1851.
xiii. ARTEMELLIA (ARTIE) COOPER, b. Abt. 1850; m. WILLIAM
xiv. MILLEY COOPER, b. October 30, 1852; m. MERRITT
xv. JAMES COOPER, b. November 30, 1854; d. March 17, 1932;
m. (1) ESTER BERTRAM; m. (2)
ANNA ROSE SLAGLE, July 27, 1876.
xvi. CANSADA COOPER, b. February 03, 1859; d. February 26,
1946; m. MORRIS CULWELL
(CULLOM?) ADKINS; b. August 29, 1854.
Children of HARMON COOPER and MARTHA PILE are:
xvii. ALVIN5 COOPER, b. January 31, 1872; m. (1) WILLIE
WHITE; m. (2) MARTHA SLAGLE,
January 16, 1892, Wayne Co., Ky..
xviii. ALFRED COOPER, b. October 21, 1873; d. October 14,
1944; m. MARTHA HURT, March 17,
1903, Wayne Co., Ky..
xix. VICTORIA COOPER, b. June 21, 1876; d. July 26, 1923;
m. LEROY HOUSTON SMITH, October
01, 1893, Wayne Co., Ky..
xx. SILAS COOPER, b. August 18, 1879; d. February 14,
1965; m. (1) FLORENCE GREGORY; m. (2)
xxi. ROSA COOPER, b. Abt. 1884.
xxii. JOSEPH COOPER, b. Abt. 1885; d. February 05, 1964;
m. MARY (POLLY) BURNETT.
11. WILLIAM HUSTON4 COOPER (JOHN3, HENRY2, -----1) was born 1806 in
Maury Co., Tenn., and died
1866 in Pope County, Arkansas. He married BARTHENIA PARILLA HOLBROOK
1824 in Perry Co., Tenn..
Children of WILLIAM COOPER and BARTHENIA HOLBROOK are:
i. CAROLINE5 COOPER.
ii. CINDA COOPER.
iii. JANE COOPER.
iv. POLLY COOPER.
v. NANCY COOPER, b. 1833, Tenn..
vi. JOHN COOPER, b. 1835.
vii. REBECCA COOPER, b. 1837; m. WILLIAM BUFORD BROWN.
viii. THOMAS COOPER, b. 1842, Ark..
ix. SAMUEL HUSTON COOPER, b. April 04, 1844, Russellville,
Pope Co., Ark.; d. August 02, 1901;
m. KISEY MARION BEAVERT, November 06, 1865; b. February 13, 1847; d.
December 11, 1928.
x. NANCY E. COOPER, b. 1849.
1. His son Harmon Cooper in 1880 census.
2. Affadavit William Blevins and Henry Smith, 1850.
3. Marion Co., Tenn. Mortality Schedule
This thread:
|[Cherokee Genealogy only] Isaac Cooper; Chief Black Fox by Donald Panther-Yates <>


text:
|Shinka, the Bloodsoaked Keep
|Card Type:
|Legendary Land
|Oracle Text:
| : Add to your mana pool.
, : Target legendary creature gains first strike until end of turn.
|Flavor Text:
|The glow from within looks inviting, but woe awaits whomever finds out who stokes the fire or what simmers in the pot.


text: Navy Pier is a premiere Chicago attraction on the lakefront offering an exciting array of unique events and things to do in Chicago all season long. Just watch any of the videos below and see for yourself! Be sure to visit the Calendar of Events or Current & Upcoming Events pages to learn more about events at Navy Pier, including special exhibitions, shows and entertainment. Start planning your visit today!


text:
A Fire Escape Ladder for the Home
When I had my house built, I knew that the fact that there were multiple stories might possibly cause some issues with safety. The most important thing to me is the safety of my family, and the last thing that I would ever want would be for one of my kids to be stuck in their bedroom on the second floor during a fire. This is precisely why I decided to buy a fire escape ladder for each room on the upper floor. The ladders that I bought for each room are portable enough to where they can be stored in a small closet, and that means that they never take up a whole lot of space. In the event of a fire emergency, all anyone would have to do would be to grab the ladder, throw it out a window, and begin climbing down to safety.
This is obviously not the only safety measure that I decided to take with this house, but it is one that was very simple to come up with. I do also have a monitored security system that will contact the authorities in the event of any kind of emergency in my home, including a fire, but knowing that my kids would not have to wait for the fire department to arrive in order to get out of the house is something that helps me sleep a whole lot better at night. These escape ladders are really excellent for home use.
If you have a home with more than one floor, I would definitely suggest getting at least one of these ladders for your upper floors. Just having them available should you ever happen to need them is something that will definitely help you to feel more secure in your home.


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We certainly can't leave out the heavily endowed Joselyn Dumas, who turned up at the 2016 Golden Movie Awards on Saturday night in this glittering purple outfit.
On the night, she took home an award for Golden Actress (TV series).
She later thanked fans on IG as she first stated that she wasn't her parts, and wrote;
"About last night#goldenmovieawards with the 'drama'king himself @oscaryaodoe looking dapper as usual, wondering why we were so serious though 🙈😂😂 and @shirleyfmanso was all giggles 😂 well of course she had every reason to….My biggest winner for the night#msMango 😝😝Thank you for all the opportunities and risks you've taken with me and everyone you've come in contact with Shirley…God just got started with us 😘"
EnterGhana.com | What Joselyn Dumas wore to the Golden Movie Awards 2016 (Photos)


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Access to Sentinel Data
The Sentinel Data Access Infrastructure has been tailored to answer the needs of the different use typologies.
Scientific/Other users
Following a self-registration, all other users may access the Sentinel available data at the Copernicus Open Access Hub.
Copernicus Services
Copernicus Services benefit from a privileged access to Sentinels data via the Copernicus Services Data Hub (CopHub).
Latest News
There will be a major maintenance of the Sentinels Data hub services on Tuesday, 01 August 2017. The maintenance window will start at 06:30 UTC (08:30 CEST) and is expected to finish at 16:00 UTC (18:00 CEST).
Referring to the news of 14 July 2017, users are informed that the dissemination of Sentinel-2B products in the Sentinel-2B PreOps Hub resumed in the morning on Monday 17 July.
As a consequence of a ground segment anomaly, the publication of Sentinel-2B products in the S2B PreOps Hub is temporarily interrupted as of today 14 July, with last available products dated 13 July around 06:30 UTC sensing time. The data dissemination is expected to resume as of Monday 17 July.
Sentinel-1B unavailability
10 July 2017
Sentinel-1B was unavailable on 08 July 2017 between 05:21 UTC and 10:15 UTC, due to a SAR anomaly. No data were generated during this period.


text:
We help you find a Newquay music theory teacher. Music Theory lessons are a brilliant way to begin a fun new hobby, pick up a new skill and attain confidence with music theory. Please use our service to search for Newquay music theory teachers and determine which best suits your requirements so you can start your music theory lessons in Newquay straight away!
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text:
Stamford Grand Adelaide
Moseley Square
Glenelg SA 5045
Phone: 08 8376 1222
Fax: 08 8376 1111
Email: firstname.lastname@example.com
Website: www.stamford.com.au/sga
The Promenade Restaurant is all about using quality, fresh ingredients, always prepared with imagination, flair and attention to detail. Coupled with beautiful ocean views, guests are in for a unique dining experience.
Cuisine: Modern Australian
Hours: Daily 6:30am to 10:30am, noon to 3pm, 6pm to 10pm
Payment accepted: MasterCard, Visa, Diners Club and American Express
Licensed: Licensed. Wine available by the glass.
Bookings: This venue accepts bookings. Essential to book ahead of time. Group bookings accepted.
Vegetarian: Vegetarian dishes available
Disabled Facilities: Wheelchair access
Environment: Seats 180 people, ample parking
Available 7 days
Monday - Friday 6:30am - 10:30am
Saturday & Sunday 6:30am - 11:30am
Available 7 days
Monday - Friday 12:00pm - 3:00pm
Saturday & Sunday 12:30pm - 3:00pm
Available 7 days a week
Monday - Friday 11.00am - 5.00pm
Saturday, Sunday & Public Holidays 2:00pm - 5:00pm
Available 7 days a week
A la carte menu Sunday - Friday 6:00pm - 10:00pm
Seafood Buffet Saturday nights only 6:00pm - 10:00pm
The Promenade Restaurant is smartly casual and welcomes both hotel guests and Adelaidians alike.
Conferences - Promenade Restaurant - The Grand Bar - Horizons Cocktail Lounge


text:
Yoder Collection
Click here to learn more about the Old Order Amish brothers that handcraft this beautiful dining room furniture.
Let the lovely form and the smooth outline of the Amish Parkland Bar Stool contribute to your contemporary decor. This Amish made wooden bar stool brings a beautifully shaped chair back to your kitchen counter or bar. Line your bar area or pub table with these stylish solid wood bar stools and rely on a comfortable seating option for everything from casual dinners to afternoon snacks.
The Parkland is shown here in walnut wood which is a dark wood with a medium grain. Walnut makes an elegant appearance in any room. Customize these counter chairs in the wood and stain you like best.
If you are looking for matching chairs then check out our Parkland Dining Room Chairs and we also offer our Amish handcrafted Parkland Dining Room Table and the Parkland Round Table which is avalable in a 36" or 42" table height.
In the Game Room: Provide casual, comfortable seating as you enjoy a lively pool game or a poker night event.
In the Craft/Hobby Room: Work at a draft table or sewing table easily seated comfortably in a solid wood bar stool.
Please call one of our helpful Furniture Specialists, toll-free at 866-272-6773 with any questions you may have.
© Copyrights 2003 - 2017 DutchCrafters All rights reserved.


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Parent or sister buying me a handgun
In Texas I can own a handgun at 18. I am wondering if my older sister or parents can but one for me as a gift. Im pretty sure this isn't a straw purchase. Just want some clarification. Im looking at the Glock 21sf
I don live in the states, but I don't think it would be any different then buying somebody a gun for Christmas/their birthday up here.
It would probably just have to be transferred over to you after they bought it.
Well in TX we don't need to register so id rather not transfer it lol. Don't want the feds knowing what i got
Michael, I'm no lawyer (and to be sure you'd need an attorney that specializes in Texas gun law) but I kinda doubt your parents or legal age sister would get in trouble giving you a handgun. No doubt it happens all the time in Texas. I wouldn't call that a straw purchase but who knows when you bring the legal system into it. It might be best for everyone concerned for them to keep ownership until you're 18. I doubt there's a law against them loaning it to you, then give it to you on your 18th birthday. As you said in Texas and most states an individual to individual transfer of ownership doesn't require paperwork.
You're a smart guy and pretty mature from what I've seen so I'd just say be 100% safe with the gun and don't do anything stupid to draw attention to yourself and you should be ok. The less said the better if you know what I mean. Also this thread may be locked quickly so I'll say again I'm no lawyer and am clueless to the laws involved. Of course nothing said here is the opinion of Firearms Talk Forums!
If you have to quotation marks around the word, gift, that should answer your question. A gift from a family mamber is legal (as long as you are not prohibited from owning). "Gifting" a gun is a straw purchase and as such can send you and your sister to Federal pokey.
I put this in your other thread (by the way, that's a bit of a no-no), if your sister gives the money to you or one of your parents, and then you get your parent to get the gun for you, that's probably for the best. Especially if your living with them.
If Texas laws are like MS laws, you should be able to buy used from a private seller considering your age, and you'll probably save a few bucks too. Now, I don't even like GLOCK, but buying a used GLOCK is almost just as good as buying a new one, they do have a tendency to great longevity.
I like full sized handguns, even considering my small hands. When it comes to GLOCK, it looks to me like your options are only size and caliber, and some are compensated.
Personally, I'd probably get the G17. I'm not a huge fan of 9MM either, but that's 17+1. I seem to recall that there may be more aftermarket stuff for the G17, although I'm not sure if that's true. I do know there are 30 or 33 round mags on the market for it. That's pretty cool.
Plus, of the handgun calibers, 9MM is some of the cheapest. I assume if your 19 then your probably on a fairly limited budget.
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text:
It's almost over! The end of the school year is upon us — some of my readers' kids have less than a week to go, while my own kids are still going to be going on end of year field
The calendar tells me it's that time again: Time to round up the year with something, before we get to the January meal plan and march boldly ahead into 2016. Last year, I did a roundup of the 14 best
As I enter the final push of preparation for the school year, I'm looking back at my own lunch photos to help get some inspiration. As I do, I'm reminded of the lunches that were popular with RRG readers last
In just 19 days, my kids go back to school — 1st and 3rd grades this year. I know some of my readers in other parts of the country are already back (and to you I say, SORRY, every year
I've never been much in the habit of doing a year-end post here on the blog – I don't know if it's pure laziness or the fact that I tend to be more "unplugged" during the final few weeks of
It's back-to-school season! I know some people around the country already have kids back in school; others are starting this week; and others, like my boys, will be going back in a couple of weeks' time (major jealousy, by the
I'm so excited today to announce the launch of a new project that I've been practically SLAVING over (yes, picture me, back of hand to my forehead) with my friend Bonnie from The Joyful Organizer. The two of us have
This week, my Lunch Logic is all about stretching ingredients. Keeping a whole-food lifestyle viable for a family is sometimes challenging, but it gets easier (and more affordable) if you know how to easily transform things you've already cooked into
This week's Lunch Logic is all about making dinner leftovers and on-hand ingredients work in your favor to make standby lunch favorites. The ideas here are ones I use all the time with my two boys — chicken salad, quick
We're back! I took some time off from Lunch Logic, as I'm sure many of you noticed. Over the summer, a lunch-packing feature doesn't make as much sense as it does during the school year, so once June was done


text:
Our mission at suainlogistics.com is to save both time and money of truckers, transporters and 3PL. We accomplish that mission with the use of an innovative system that allows Transporters, truckers and intermediaries to post and confirm loads and trucks. Transporters can easily line up a reliable truck where and when they need it, and truckers can find loads to haul where and when they need them. The suainlogistics.com allows the delivery of freight easier and more efficient. To know more, visit at http://www.suainlogistics.com
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I go back to this product every winter. It is nice and thick and does a great job. Works even on very dry hands. I typically will not use it during the summer and will switch to a lighter lotion. It has a distinct smell but I do not find it to be overwhelming as some lotions can be.
It doesn't smell the best but it works very well, i use it on my hands after washing dishes. I use it at work as well and everyone is always using it.
These reviews are the subjective opinions of ChickAdvisor members and not of ChickAdvisor Inc.


text:
This family-friendly, city and business hotel has a total of 56 rooms over four storeys.
The hotel is conveniently situated within walking distance of Rosebank Mall and is easily accessible from Jan Smuts Avenue, a main north-to-south route. It is also within walking distance of the new Gautrain Station at Rosebank. Rosebank is an upmarket commercial suburb adjacent to Sandton with a number of large corporate headquarters, including financial houses and commercial banks, Internet and telecommunications giants. Similar to Sandton, although on a small scale, Rosebank is an attractive shopping and entertainment destination for local residents and international travellers, as well as a corporate hub. OR Tambo International Airport is around 20 km away.
The Studio Suites offer an open-plan room with a bed, lounge area, an en suite bathroom and a fully equipped kitchenette, and can accommodate 2 adults. The Bedroom Suites have a separate bedroom, lounge, a private bathroom and a fully equipped kitchenette. A 1-bedroom suite can accommodate 2 people (or a maximum of 4 with an option to add an extra bed). There is a TV set in the bedroom and in the lounge. Standard in-room amenities include a shower/bath, hairdryer, double or king-size beds, a direct dial telephone, satellite/cable TV, a radio, hifi and Internet access. A safe, minibar, fridge, cooker, microwave, tea and coffee making facilities and an ironing set are also provided. Individually regulated air conditioning and heating ensure maximum comfort. A balcony or terrace also features.
A full English or continental breakfast is served in the breakfast room. A room service menu also offers light meals in the evenings.
American Express, Diners Club, MasterCard and VISA are accepted as methods of payment.
From OR Tambo International Airport: take R24 West to Johannesburg, exit onto N3 south towards Durban. Exit onto the M2 West to Johannesburg then exit onto the M1 North towards Sandton. Exit onto the R20 Glenhoveroad, turn left at the traffic lights. Continue straight and cross Oxford Road. Turn right onto Sturdeethen, left onto Tyrwhitt and the hotel will be on the left. From Pretoria: take N1 south to Johannesburg then the M1 south towards JHB. Exit onto the R20 Glenhoveroad, turn right at the traffic lights. Continue straight and cross Oxford Road. Turn right onto Sturdeethen, left onto Tyrwhitt and the hotel will be on the left.
Room Facilities:
Direct dial telephone
Satellite cable TV
HiFi stereo system
Internet access
Mini fridge
Tea Coffee
Iron and board
Double bed
King size bed
Individual airconditioned
Individual heating


text:
Celebrate the 10th Anniversary!!!
Since September 2004, over 10 years AVision has been recognized to the success of a leading Microsoft Dynamics partner in Thailand. We have provided consultation service business with Microsoft Dynamics solutions, expertises, business-to-business services, and stong relationship with customers in Thailand, Laos, and Myanmar.
With successfully reaching the 10-year anniversary, we are really proud of that. We always had a long-term vision for doing business. We continue to extend our thanks to all of our customers, partners and employees for the relationships, dedication, support, trust and share with us their thoughts on this past decade. We are excited to return some values back to our customers such as promotions, special events and much more. In October 2014, there will be a special event "AVision Thank you Day" for our existing customers.
We are excited to celebrate 10-year anniversary and look forward to our next 10 years in business. Thanks again to our customers, employees and partners. "Without you, we would not have reached this milestone."


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Fußball ist wie Kirche
In der Heiliggeist Arena haben wir die Parallelen zwischen Kirche und Fußball zusammengefasst. Viel Spaß beim Entdecken! evangelisch.de
Evangelisch deon 12 June 2014
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General enquiries
+44 (0) 20 7079 4399
Call HCA from 8am-8pm Mon-Fri and 9am-5pm Sat
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Neuroradiology, Brain and Central Nervous System cancers
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Dr Wilhelm is a Consultant Neuroradiologist at The Wellington Hospital with NHS appointments at Barts and the London NHS Trust. He has a special interest in vascular interventional neuroradiology. He is Treating Clinician, the London Gamma Knife Centre and past senior examiner, FRCR, Royal College of Radiologists.
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Registered Name: HCA International Limited; The part of the UK in which it is registered: England and Wales;
Registered Number: 03020522; Registered Office Address: 242 Marylebone Road London NW1 6JL.
£500m has been invested by HCA International in the latest medical technologies and facilities over the last 10 years.
Your hospital will be one of our world-class private hospitals: HCA's world-class hospitals are accredited by The CHKS Accreditation Unit, a leading provider of healthcare intelligence and quality improvement services. The accreditation is a measure of the overall quality of a hospital and hospitals with CHKS accreditation have been shown to provide a better quality of service.
Your safety will be protected because we have more critical care beds than any other private hospital group: HCA hospitals achieved 100% compliance with all Care Quality Commission inspected outcomes of care in 2011.
Your treatment will be undertaken using the most advanced diagnostic and treatment facilities: Oliver Wyman, Corporate Accounts: Driving quality and value, January 2012.


text:
The Cambridge Companion to Adorno (Cambridge Companions to Philosophy)
The great German philosopher and aesthetic theorist Theodor Wiesengrund Adorno (1903-1969) was one of the main philosophers of the first generation of the Frankfurt School of critical theory. As an accomplished musician, Adorno originally focused on the theory of culture and art. He later turned to the problem of the self-defeating dialectic of modern reason and freedom. A distinguished roster of Adorno specialists explores the full range of his contributions to philosophy, history, music theory, aesthetics and sociology in this collection of essays.
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