If you’ve only just now discovered what your beliefs are, you can’t be expected to fully understand the pros and cons associated with them. Jasmine fills out an Analyzing Advantages and Disadvantages Form (see Worksheet 3-8) in order to more fully comprehend how her change-blocking beliefs affect her. She starts by writing down the reasons her change-blocking beliefs feel good and advantageous to her. Next, she writes about how each belief gives her problems — in other words, how it stands in her way. She fills out this form for each belief in her Top Three Change-Blocking Beliefs Summary. Advantages of This Belief Disadvantages of This Belief If I don’t try, I don’t have to risk failing. I don’t know why, but change is scary, I miss out on opportunities by clinging and this belief keeps me from dealing to this belief. It’s just possible that even if I do fail, I could end up learning something useful for my life. Change-Blocking Belief #2: I feel guilty asking anyone for help, so I’d rather not. Advantages of This Belief Disadvantages of This Belief I don’t expect anyone to help me, so I I don’t get the chance to share my don’t end up disappointed. People don’t have to worry about me I don’t get as close to people as I leaning on them. I don’t worry anyone because they When I’m really upset I get quiet, and never know when I’m upset. Sometimes, everyone needs a little help from others, and I’m at a disad- vantage when I don’t seek it. After completing her Analyzing Advantages and Disadvantages Form, Jasmine takes some time to reflect. She considers whether the advantages she listed are truly advantages and concludes that her original change-blocking beliefs are causing her more harm than good.
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To turn it around, these low concentrations of trimethoprim could be used for the selection of spontaneous thyA mutants if thymine is supplied in the growth medium. Stylized illus- tration of a gram-negative enterobacterium with its large circular chro- mosome with the gene for dihydrofolate reductase, folA. The depicted plasmid carries a gene, dfr, expressing a trimethoprim-resistant dihydro- folate reductase rescuing the host for survival when the chromosomal dihydrofolate reductase is inactivated by trimethoprim. Plasmid-Borne Resistance to Trimethoprim As mentioned earlier, resistance against trimethoprim is presently common and is increasing in frequency. The most com- mon type of trimethoprim resistance in gram-negative entero- bacteria (common pathogens of the urinary tract) is represented by foreign genes expressing trimethoprim-resistant dihydro- folate reductases that have been able to transfer themselves horizontally, borne on a transferable plasmid, into the bacterium to make it resistant (Fig. These bacteria can then be looked upon as a diploid, of sorts, for folA: that is, the chromosomal gene expressing dihydrofolate reductase in bacteria. The bacterium then becomes resistant since the foreign and resistant dihydrofolate reductase can supply the life-supporting reduction of dihydrofolate to tetrahydrofolate while the normal chromosomal enzyme is inactivated by trimethoprim. The origin is not known for any one of these genes, but it could be surmised that they come from organisms whose dihydrofolate reductases, by a biological coincidence, have no affinity for trimethoprim. These resistance genes must have moved horizontally into pathogenic bacteria selected by the heavy use of trimethoprim in human medicine and also in veterinary practice. This mechanism, with an extra resistance- mediating target enzyme, is highly prevalent in enterobacteria, where dfr1, the first one found, seems to be the most common. One of these is, in turn, borne on transposon Tn7, which has spread very successfully, mainly because of its high-frequency insertion into a preferred site on the chromosome of E. Among the horizontally moving trimethoprim resistance genes there is a subclass of five genes, dfr2a, dfr2b, dfr2c, dfr2d, and dfr2e, which are closely related among themselves, but so different from other trimethoprim resistance genes that they cannot be included in the phylogenetic tree, where the interrelationship between the others could be demonstrated (Fig. Colonies of bacteria carrying these genes can be seen to grow among crystals of trimethoprim on agar plates saturated with the drug. The con- spicuous difference from other known dihydrofolate reductases, and their poor enzymic performance (high Km values and low turnover numbers), make their origin puzzling.
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