how cystic fibrosis is controlled by arecessive gene?
825223
I don't understand your use of the word controlled.\nIf you mean what is the relationship of recessive genes to Cystic Fibrosis?\nBecause the trait for CF is attached to a recessive gene it means that when that gene is passed on to a child it is harmless on its own.  The disease only occurs when one woman with the recessive linked gene mates with a male with the same recessive gene. Two recessives result in the disease happening in the child.\nThe two parents who only have half the material each on their genes are ''carriers'' of the disease.\nMost cystic fibrosis children are blond and blue eyed because these too are thought to be part of recessive genes.  \nIs that what you want to know?
684058
COPD is generally one of two related conditions, either chronic bronchitis or emphysema, although in some cases asthma can become a form of COPD if there is permanent damage to the airways from chronic inflammation. And sometimes there can be overlap - patients with chronic bronchitis may also have symptoms of emphysema, for example.\n\nYes, in rare cases (less than 1%) COPD can be hereditary. If it is due to asthma, then again it can be hereditary, since asthma does tend to run in families.\n\nAs you probably already know, smoking accounts for the majority of COPD (like 90%). \n\n"Another well-established cause of COPD is a deficiency of alpha-1 antitrypsin (AAT). AAT deficiency is a rare genetic (inherited) disorder that accounts for less than 1% of the COPD in the United States.\n\nAs discussed previously, normal function of the lung is dependent on elastic fibers surrounding the airways and in the alveolar walls. Elastic fibers are composed of a protein called elastin. An enzyme called elastase that is found even in normal lungs (and is increased in cigarette smokers) can break down the elastin and damage the airways and alveoli. Another protein called alpha-1 antitrypsin (AAT) (produced by the liver and released into the blood) is present in normal lungs and can block the damaging effects of elastase on elastin.\n\nThe manufacture of AAT by the liver is controlled by genes which are contained in DNA-containing chromosomes that are inherited. Each person has two AAT genes, one inherited from each parent. Individuals who inherit two defective AAT genes (one from each parent) have either low amounts of AAT in the blood or AAT that does not function properly. The reduced action of AAT in these individuals allows the destruction of tissue in the lungs by elastase to continue unopposed. This causes emphysema by age 30 or 40. Cigarette smoking accelerates the destruction and results in an even earlier onset of COPD.\n\nIndividuals with one normal and one defective AAT gene have AAT levels that are lower than normal but higher than individuals with two defective genes. These individuals are not believed to have an increased risk of developing COPD if they do not smoke cigarettes; however, their risk of COPD probably is higher than normal if they smoke." from \nhttp://www.medicinenet.com/chronic_obstructive_pulmonary_disease_copd/page4.htm
297162
The above answer pretty much says it...plus, they are under the control of a constitutive promoter, instead of an induced promoter. An induced promoter is that which is induced by the presence of an inducer that binds to the promoter region when there is need for the gene product of the gene that the promoter is controlling. A constitutively expressed gene is one that is expressed everytime the genes of the rest of the genome are expressed. So such a gene product is required in a higher quantity in the body, and that is why it is under the control of a constitutive promoter.
83652
A hereditary disease of the exocrine glands, usually developing during early childhood and affecting mainly the pancreas, respiratory system, and sweat glands. It is characterized by the production of abnormally viscous mucus by the affected glands, usually resulting in chronic respiratory infections and impaired pancreatic function. Also called mucoviscidosis.\n\nCystic Fibrosis At A Glance\n\n*Cystic fibrosis (CF) is one of the most commonserious genetic (inherited) diseases. \n*CF gene is carried by 1/20 persons (in *Caucasianpopulations) and 1 in 400 couples is at risk for having childrenwith CF.\n*CF is characterized by the production of abnormalsecretions leading to mucous build-up.\n*CF mucous build-up can impair the pancreas and,secondarily, the intestine.\n*CF mucous build-up in lungs can impair respiration.\n*Early diagnosis of CF is of great importance.\n*Early and continuing treatment of CF is valuable.\n\nFor more information try:  http://www.cff.org/home/
1020295
I have read that the vas defrens are not normal in men with cystic fibrosis. I know women with the disease can get pregnant, but don't know any men who have the illness.
655113
Cf is a genetic disorder affecting the CFTR gene. Causes a fault in trans-membrane conductance. Chlorine is not excreted from the cells correctly, this causes sodium to be absorbed, water follows the sodium due to osmosis.\nThe result is the bodies mucus becomes too sticky. This has serious multi organ effects. For example the lugs become congested and bacterial infections occur.
226864
Height controlled by genes.  Just feed healthy foods and check with pediatrician about vitamins.
581242
Control of gene expression through a complex myriad of regulatory genes and regulatory proteins.
626941
transcriptional control\n\ntranscription factors are the key regulators of which genes are expressed in cells. transcriptional control in the various differentiated cell types allows each type of cell like epithelial, muscle or neuron to express different amounts of the possible proteins. thus, eventually developing into specialized organs with specific roles and functions.
532088
There is no particular way, because this is due to so many variables.  Besides our own inheritance and then circumstances, there are some things in control.  For example, the number of times a guy makes demands does influence the production count.  The body needs time to recoup.  So the most efficient way is to relax, give yourself time to get it together again.\n\nOtherwise, two things are definitely within your control, eating right and the exercise that you do every day to stay healthy and strong.
384762
Restriction Enzymes are used to 'chop' a DNA molecule in a specific pattern in a specifically indentified place on the DNA Molecule. The effect of this is, when the same Restriction Enzyme is used on another DNA molecule (say a Bacterial Plasmid Vector), it will cut in exactly the same place and way.\n\nThis is useful because healthy genes can be incorporated into healthy genes once they have been 'reformed' by an Enzyme called DNA Ligase. An example of this would be placing the cysistic fibrosis gene into a bacterial plasmid, which can then be placed into the lungs via a retrovirus/lipid molecule and the DNA transferred to form the correct Protein required to treat the problem!\n\nI hope that helps,\nTom
1149383
well since the cells are from your own body... you're going to continue to be susceptible to genetic conditions.\n\ni guess, offhand, let's say you have cystic fibrosis and you want to have a lung transplant through therapeutic cloning.\n\nthe defect in the lungs is caused by a mutant gene that is present in your cells. because this gene is still present in the cloned cells, the cloned lung will have the same defect as the one you're looking to replace. so that's one problem.\n\nsince this hasn't been done yet, we can't tell for sure what complications could occur during the process of organ development and how that would impact the health of the transplantee.
135811
gene I think is what you are looking for. Not sure the question makes sence.
394440
chk out these sites these should help\n\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14512027&dopt=Abstract\n\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12080092&dopt=Abstract\n\nhttp://www.genesdev.org/cgi/content/abstract/16/12/1540\n\nhttp://www.genesdev.org/cgi/content/full/16/12/1540\n\nhttp://users.rcn.com/jkimball.ma.ultranet/BiologyPages/P/Promoter.html\n\nhttp://72.14.203.104/search?q=cache:iflXFJ1TVFwJ:www.fccc.edu/research/labs/yen/Mustkov.pdf+function+of+an+Insulator+gene&hl=en&ct=clnk&cd=7\n\nmng.1432@gmail.com
949412
Yes, try to this!\n\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=3906008
813923
Here is the history of cystic fibrosis:\n\nAlthough the entire clinical spectrum of CF was not recognized until the 1930s, certain aspects of CF were identified much earlier. Indeed, literature from Germany and Switzerland in the 1700s warned "Wehe dem Kind, das beim Kuß auf die Stirn salzig schmekt, er ist verhext und muss bald sterben" which translates to "Woe is the child who tastes salty from a kiss on the brow, for he is cursed, and soon must die," recognizing the association between the salt loss in CF and illness. Carl von Rokitansky described a case of fetal death with meconium peritonitis, a complication of meconium ileus associated with cystic fibrosis. Meconium ileus was first described in 1905 by Karl Landsteiner.  In 1936, Guido Fanconi published a paper describing a connection between celiac disease, cystic fibrosis of the pancreas, and bronchiectasis.\n\nIn 1938, Dorothy Hansine Andersen published an article titled "Cystic fibrosis of the pancreas and its relation to celiac disease: a clinical and pathological study" in the American Journal of Diseases of Children. In her paper, she described the characteristic cystic fibrosis of the pancreas correlated it with the lung and intestinal disease prominent in CF.  She also first hypothesized that CF was a recessive disease and first used pancreatic enzyme replacement to treat affected children. In 1952, Paul di Sant' Agnese discovered abnormalities in sweat electrolytes; the sweat test was developed and improved over the next decade.\nIn 1988, the first mutation for CF, ΔF508, was discovered by Francis Collins, Lap-Chee Tsui and John R. Riordan on the seventh chromosome. Research has subsequently found over 1000 different mutations that cause CF. Lap-Chee Tsui led a team of researchers at the Hospital for Sick Children in Toronto that discovered the gene responsible for CF in 1989. Cystic fibrosis represents the first genetic disorder elucidated strictly by the process of reverse genetics. Because mutations in the CFTR gene are typically small, classical genetics techniques were not able to accurately pinpoint the mutated gene.  Using protein markers, gene linkage studies were able to map the mutation to chromosome 7.  Chromosome walking and jumping techniques were then used to identify and sequence the gene\n\nCF is also widely known as "65 Roses." The phrase came into being when it was used by a young boy who had overheard his mother speaking of his illness. He later informed her that he knew she was working to help with "sixty-five roses".  The term has since been used as a symbol by organizations and families of cystic fibrosis victims. In recent years, the need for funding has increased and entertainers around the world are helping to raise overall awareness for the disease. Notable entertainers include pop singer Celine Dion, rock singer Richard Marx, rock group Paul Collins' Beat, Country music singer Charley Pride, rock singer John Wicks, Country music singer Lee Greenwood and painter Michael Israel, who have each helped to raise awareness for cystic fibrosis through special appearances and events worldwide.
831243
Control of Gene Expression: The lac operon consists of one regulatory gene (the i gene) and three structural genes (z, y, and a). The i gene codes for the repressor of the lac operon. The z gene codes for b-galactosidase (b-gal), which is primarily responsible for the hydrolysis of the disaccharide, lactose into its monomeric units, galactose and glucose. The y gene codes for permease, which increases permeability of the cell to b-galactosides. The a gene encodes a transacetylase. During normal growth on a glucose-based medium, the lac repressor is bound to the operator region of the lac operon, preventing transcription. However, in the presence of an inducer of the lac operon, the repressor protein binds the inducer and is rendered incapable of interacting with the operator region of the operon. RNA polymerase is thus able to bind at the promoter region, and transcription of the operon ensues. The lac operon is repressed, even in the presence of lactose, if glucose is also present. This repression is maintained until the glucose supply is exhausted. The repression of the lac operon under these conditions is termed catabolite repression and is a result of the low levels of cAMP that result from an adequate glucose supply. The repression of the lac operon is relieved in the presence of glucose if excess cAMP is added. As the level of glucose in the medium falls, the level of cAMP increases. Simultaneously there is an increase in inducer binding to the lac repressor. The net result is an increase in transcription from the operon. The ability of cAMP to activate expression from the lac operon results from an interaction of cAMP with a protein termed CRP (for cAMP receptor protein). The protein is also called CAP (for catabolite activator protein). The cAMP-CRP complex binds to a region of the lac operon just upstream of the region bound by RNA polymerase and that somewhat overlaps that of the repressor binding site of the operator region. The binding of the cAMP-CRP complex to the lac operon stimulates RNA polymerase activity 20-to-50-fold.