A team approach to a brighter smile.
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It is not uncommon for teeth to still not be attractive, even though they are straight following treatment. Several examples have been given of what can be done to improve the attractiveness of teeth when this occurs. It is the responsibility of the dental team involved in the management of a persons total dental care to advise patients of what dental services are available to them. People should have the opportunity to evaluate what dental services are needed to accomplish a pleasing result that is satisfying to them and to the dental team involved.
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The science of human evolution is confronted with the popular chimpanzee theory and the earlier but largely ignored orangutan theory. The quality and scope of published documentation and verification of morphological features suggests there is very little in morphology to support a unique common ancestor for humans and chimpanzees. A close relationship between humans and African apes is currently supported by only eight unproblematic characters. The orangutan relationship is supported by about 28 well-supported characters, and it is also corroborated by the presence of orangutan-related features in early hominids. The uniquely shared morphology of humans and orangutans raises doubts about the almost universal belief that DNA sequence similarities necessarily demonstrate a closer evolutionary relationship between humans and chimpanzees. A new evolutionary reconstruction is proposed for the soft tissue anatomy, physiology, and behavioral biology of the first hominids that includes concealed ovulation, male beard and mustache, prolonged mating, extended pair-bonding, "house" construction, mechanical "genius," and artistic expression.
A new concept for sequence-specific labeling of DNA by using chemically modified cofactors for DNA methyltransferases is presented. Replacement of the amino acid side chain of the natural cofactor S-adenosyl-L-methionine with an aziridine group leads to a cofactor suitable for DNA methyltransferase-catalyzed sequence-specific coupling with DNA. Sequence-specifically fluorescently labeled plasmid DNA was obtained by using the DNA methyltransferase from Thermus aquaticus (M.TaqI) as catalyst and attaching a fluorophore to the aziridine cofactor. First results suggest that all classes of DNA methyltransferases with different recognition sequences can be used. In addition, this novel method for DNA labeling should be applicable to a wide variety of reporter groups.
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During the last 40 years over 100 patients have been reported with a dysfunctional lower urinary tract associated with a peculiar distortion of the facial expression. This most unusual disorder was initially considered a local observation. Time, however, has proven otherwise, since patients with this syndrome have now been reported from various countries throughout the world. This association of lower urinary tract and bowel dysfunction with an abnormal facial expression was named the urofacial (Ochoa) syndrome. Genetic studies have demonstrated that this condition is inherited as an autosomal recessive trait, and a potential gene has been mapped to chromosome 10q23-q24. There is also enough evidence to suggest that patients with this syndrome as well as those with subclinical neurological bladder, occult neuropathic bladder, non-neurogenic neurogenic bladder or Hinman syndrome, dysfunctional voiding, or dysfunctional elimination may be affected by the same congenital disorder of neurological origin.
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The use of angiotensin-converting enzyme (ACE) inhibitors in acute myocardial infarction (AMI) is based on their capacity to limit ventricular enlargement and dysfunction. To date, the safety profile of administration of ACE inhibitors early in the course of AMI has not been established. In-hospital and long-term consequences of treatment with the ACE inhibitor zofenopril initiated within 24 hours of the onset of symptoms were compared with those of standard treatment in an open-label trial involving 204 patients with AMI who were not undergoing thrombolytic treatment. Zofenopril promptly blocked ACE activation. Blockade was almost complete (91 +/- 6%) after 72 hours and paralleled decreases in systolic blood pressure. Systemic blood pressure was acutely reduced by zofenopril, and severe but reversible hypotension occurred in 15% of hospitalized patients and in 3% of those treated over the long term. No adverse clinical or biochemical events were reported during the course of zofenopril therapy. Overall cardiovascular mortality was not significantly reduced by early zofenopril compared with placebo therapy (7.8% vs 10.7% [difference not significant]). The inhospital incidence of acute left ventricular failure and ventricular arrhythmias decreased by 63% and 39%, respectively, among zofenopril-treated patients, who also reported fewer anginal episodes both acutely (68% reduction) and over the long term (56% reduction) and did not require as much drug treatment (i.e., diuretics, digoxin, and/or anti-ischemic agents) during the follow-up phase. Left ventricular size decreased and ejection fraction (EF) increased in patients who received zofenopril, and the improvement was greater among patients with poorer ventricular function (EF less than 40%). Early administration of ACE inhibitors may therefore constitute a safe form of therapy for patients with AMI, particularly when the event is complicated by clinical signs or evidence of ventricular dysfunction.