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The Code Is Almost Universal All organisms studied so far use the same genetic code purchase super viagra 160 mg mastercard erectile dysfunction in young males causes, with some rare exceptions generic 160mg super viagra erectile dysfunction commercial. One exception occurs in human mitochondrial mRNA, where UGA codes for tryp- tophan instead of serving as a stop codon, AUA codes for methionine instead of isoleucine, and CUA codes for threonine instead of leucine. The Code Is Nonoverlapping and without Punctuation mRNA does not contain punctuation to separate one codon from the next and the codons do not overlap. Beginning with a start codon (AUG) near the 5 -end of the mRNA, the codons are read sequentially, end- ing with a stop codon (UGA, UAG, or UAA) near the 3 -end of the mRNA. RELATIONSHIP BETWEEN mRNA AND THE PROTEIN PRODUCT The start codon (AUG) sets the reading frame, the order in which the sequence of bases in the mRNA is sorted into codons (Fig. The order of the codons in the mRNA determines the sequence in which amino acids are added to the growing polypeptide chain. Thus, the order of the codons in the mRNA determines the lin- ear sequence of amino acids in the protein. EFFECTS OF MUTATIONS Mutations that result from damage to the nucleotides of DNA molecules or from unrepaired errors during replication (see Chapter 13) can be transcribed into mRNA, and, therefore, can result in the translation of a protein with an abnormal amino acid sequence. Various types of mutations can occur that have different effects on the encoded protein (Table 15. For any given mRNA sequence, there are three pos- sible reading frames (1, 2, and 3). An AUG near the 5 -end of the mRNA (the start codon) sets the reading frame for translation of a protein from the mRNA. The codons are read in linear order, starting with this AUG. They would give proteins with different amino acid sequences. Types of Mutations Type Description Example Point A single base change Silent A change that specifies the same CGA → CGG amino acid Arg → Arg Missense A change that specifies CGA → CCA a different amino acid Arg → Pro Nonsense A change that produces a stop CGA → UGA codon Arg → Stop Insertion An addition of one or more bases Deletion A loss of one or more bases A. Point Mutations Point mutations occur when only one base in DNA is altered, producing a change in a single base of an mRNA codon. There are three basic types of point mutations: silent mutations, missense mutations, and nonsense mutations. Point mutations are Sickle cell anemia is caused by a said to be “silent” when they do not affect the amino acid sequence of the protein. In each of the For example, a codon change from CGA to CGG does not affect the protein because alleles for -globin, Will Sichel’s both of these codons specify arginine (see Table 15. In missense mutations, one DNA has a single base change (see Chapter amino acid in the protein is replaced by a different amino acid. In the sickle cell gene, GTG replaces the change from CGA to CCA causes arginine to be replaced by proline. Thus, in the mRNA, the codon mutation causes the premature termination of a polypeptide chain. For example, a GUG replaces GAG and a valine residue codon change from CGA to UGA causes a codon for arginine to be replaced by a replaces a glutamate residue in the protein. Insertions, Deletions, and Frameshift Mutations One type of thalassemia is caused An insertion occurs when one or more nucleotides are added to DNA. Codon 17 tion does not generate a stop codon, a protein with more amino acids than normal of the -globin chain is changed could be produced. This change results in the When one or more nucleotides are removed from DNA, the mutation is known conversion of a codon for a tryptophan as a deletion. If the deletion does not affect the normal start and stop codons, a pro- residue to a stop codon. Is it likely that Anne Niemick has this mutation in codon 17? A frameshift mutation occurs when the number of inserted or deleted nucleotides is not a multiple of three (Fig. The reading frame shifts at the point where the Some types of thalassemia are insertion or deletion begins. Beyond that point, the amino acid sequence of the pro- caused by deletions in the globin tein translated from the mRNA differs from the normal protein. Patients have been studied who have large deletions in either the 5 or the 3 coding region of the -globin gene, IV.

Very large families of homologous proteins are called a superfamily discount 160 mg super viagra with amex erectile dysfunction causes tiredness, which is subdivided by name into families of proteins with the most similarity in structure discount super viagra 160 mg without a prescription erectile dysfunction treatment devices. The paralogs of a protein family are considered different proteins and have different names because they have different functions. Myoglobin and the different chains of hemoglobin, for example, are paralogs and members of the same globin family that have similar, Homologous families of proteins are proteins that have the same but not identical, structures and functions. Myoglobin, an intracellular heme ancestral protein and arose from protein present in most cells that stores and tranports O2 to mitochondria, is a the same gene. The term homologs includes single polypeptide chain containing one heme oxygen-binding site. Orthologs are hemoglobin is composed of four globin chains, each with a heme oxygen- genes from different species that have binding site that is present in red blood cells and transports O2 from the lungs evolved from a common ancestral gene as to tissues. The gene for myoglobin is assumed to have evolved from gene dupli- different species developed (for example, cation of the -chain for hemoglobin, which evolved from duplication of the - human and pork insulin). Among these three proteins, only 15 invariant the genome of a single species (e. To compare the primary structure of two homologous polypeptide chains, the sequences are written left to right from the amino terminal to the carboxyl ter- minal. The sequences are aligned with computer programs that maximize the identity of amino acids and minimize the differences caused by segments that are pres- ent in one protein and not in the other. The primary structure of human globin proteins 1 5 10 15 Myoglobin gly-----leu-ser-asp-gly-glu-trp-gln-leu-val-leu-asn-val-trp-gly-lys-val- β chain Hemoglobin val-his-leu-thr-pro-glu-glu-lys-ser-ala-val-thr-ala-leu-trp-gly-lys-val- α chain hemoglobin val-----leu-ser-pro-ala-asp-lys-thr-asn-val-lys-ala-ala-trp-gly-lys-val- ζ chain Hemoglobin met-ser-leu-thr-lys-thr-glu-arg-thr-ile-ile-val-ser-met-trp-ala-lys-ile- γ chain Hemoglobin met-gly-his-phe-thr-glu-glu-asp-lys-ala-thr-ile-thr-ser-leu-trp-gly-lys-val- Fig 6. The primary structures of a region in human globin proteins. Gaps in the structure, indicated with dashes, are introduced to maximize the alignment between proteins in structure comparisons. They are assumed to coincide with mutations that caused a deletion. Regions of sequence similarity (identity and conservative substitution) are indicated in blue. Within these regions, there are smaller regions of invariant residues that are exactly the same from protein to protein. Tissue and Developmental Variations The term isozyme was originally defined as meaning enzymes with in Protein Structure a different primary structure, cat- Within the same individual, different isoforms or isozymes of a protein may be syn- alyzing the same reaction, encoded by dif- thesized during different stages of fetal and embryonic development, may be pres- ferent genes. However, the term is now used ent in different tissues, or may reside in different intracellular locations. Some isozymes are now a protein all have the same function. If they are isozymes (isoforms of enzymes), known to arise from alternate splicing of pre- mRNA to form different mRNAs (mRNA is they catalyze the same reactions. However, isoforms have somewhat different prop- the final nucleic acid template used for pro- erties and amino acid structure. DEVELOPMENTAL VARIATION Hemoglobin isoforms provide an example of variation during development. Hemoglobin is expressed as the fetal isozyme HbF during the last trimester of pregnancy until after birth, when it is replaced with HbA. HbF is composed of two hemoglobin and 2 hemoglobin polypeptide chains, in contrast to the adult hemoglobin, hemoglobin A, which is 2 and 2 chains. During the embryonic stages of development, chains with a different amino acid composi- tion, the embryonic and chains, are produced (see Fig. These differ- ences are believed to arise evolutionarily from mutation of a duplicated gene to produce , and mutation of a duplicate gene to produce. The fetal and embryonic forms of hemoglobin have a much higher affinity for O2 than the adult forms, and thus confer an advantage at the low O2 tensions to which the fetus is exposed. At different stages of development, the globin genes specific for that stage are expressed and translated. TISSUE-SPECIFIC ISOFORMS Proteins that differ somewhat in primary structure and properties from tissue to tis- A myocardial infarction (heart sue, but retain essentially the same function, are called tissue-specific isoforms or attack) is caused by an atheroma- isozymes. The enzyme creatine kinase is an example of a protein that exists as tis- tous obstruction or a severe spasm sue-specific isozymes, each composed of two subunits with 60 to 72% sequence in a coronary artery that prevents the flow of homology. Of the two creatine kinases that bind to the muscle sarcomere, the M blood to an area of heart muscle. Thus, heart form is produced in skeletal muscle, and the B polypeptide chains are produced in cells in this region suffer from a lack of oxy- the brain.

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On occasions the athlete’s sport participation is permanently curtailed 160 mg super viagra overnight delivery erectile dysfunction mayo. This anecdotal approach was originally attributed to Quigley in 1945 and subsequently adopted by Thorndike who suggested that if any athlete 66 Concussion suffered “three concussions cheap super viagra 160mg with amex impotence in men symptoms and average age, which involved loss of consciousness for any period of time, the athlete should be removed from contact sports for the remainder of the season”. The unstated fear behind this approach is that an athlete suffering repeated concussions would suffer a gradual cognitive decline similar to the so-called “punch drunk” syndrome or chronic traumatic encephalopathy seen in boxers. In some cases the injuries suffered by such athletes are more severe than the typical sport related concussive injuries, yet in the minds of the public no distinction is made. In such injuries, long term symptoms are not wholly unexpected. In other cases, professional athletes suffer repeated concussions yet are not banned from sport, as may be the advice to lesser athletes. Although professional athletes may be monitored more closely than other sporting participants, nevertheless the variation in management between elite and recreational athletes is often seen as hypocritical. In still other cases, the “post-concussive” symptoms experienced are mostly headache. This symptom is non-specific and can be the result of a variety of causes other than concussion. Much of the concern in relation to the management of repeated concussive injury relates to the absence of a consensus definition and severity grading of concussion and to the lack of scientifically valid management guidelines. Until this central issue is resolved then it is unlikely that a clear answer to the problem of retirement due to chronic symptoms will ensue. Definition of concussion The recent Vienna concussion conference has provided a new consensus definition and understanding of sport related concussion. The new definition incorporates both the historical understanding of concussion as well as emphasising the functional rather than structural nature of the injury. This definition states that: “Concussion is defined as a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces. Several common features that incorporate clinical, pathological, and biomechanical injury constructs that may be used in defining the nature of a concussive head injury include the following. Resolution of the clinical and cognitive symptoms typically follows a sequential course. In the absence of documented objective evidence of brain injury, there is no scientific support for this generalisation. Athletes excluded from competition on such basis may consider a medico-legal appeal that would be impossible to defend in a court of law. There are several anecdotal guidelines available in the literature. As mentioned above, these are not supported by published scientific evidence and should be considered management “options” at best. The main return to sport after repeated concussive injury guidelines are those published by Cantu8,9 and the Colorado Medical Society. It can be seen that there are many superficial similarities between the two scale systems. Although the criteria for injury severity differ, the mandatory requirement is that two Grade 3 injuries or three injuries of any grade result in termination of the athletes season. Given that a Cantu Grade 2 is equivalent to a Colorado Grade 3, it can be seen that the scales give differing recommendations for the same injury. The physiology of concussion The effects of diffuse injury to axons and neurones sustained at the time of head injury may or may not be reversible depending on the magnitude of the blow. Some authors have suggested that strains produced by all head injuries result in axonal injury. Cantu system (adapted from 9) Severity grade 1st concussion 2nd concussion 3rd concussion Grade 1 RTP after 1 week if RTP in 2 weeks if Terminate season. RTP if RTP next season LOC < 5 min, PTA at least 1 week asymptomatic for if asymptomatic > 30 min at least 1 week. Consider terminate season Grade 3 Minimum of 1 month Terminate season.

At this stage these important issues remain unresolved quality super viagra 160mg erectile dysfunction medications generic. In general terms buy cheap super viagra 160mg online erectile dysfunction stress treatment, although minor neuropathological changes may occur following concussive brain injury the clinical symptoms are due to functional disturbance, presumably at the cell membrane level, rather than due to any structural injury. This is supported by experimental evidence demonstrating that mechanical stress can produce a sudden neuronal depolarisation, followed by a period of nerve cell transmission failure in the absence of structural injury. In the handful of case reports of persons dying from other causes following brain injury, scattered neuronal cell death may be demonstrated. The findings however, are generally insufficient to explain the degree of clinical dysfunction, suggesting the clinical symptoms are manifest by additional functional cell impairment. The neuropsychology of concussion It is only in the past few decades that there has been interest in studying the neuropsychological consequences of concussion, particularly those injuries seen in sport. While there is now acceptance of an organic basis to the problems associated with concussion, controversy remains regarding the nature of the cognitive deficits as well as the speed and extent of their recovery. The major areas of deficit include: • Disturbances of new learning and memory19,20,25,29–35 • Planning and the ability to switch mental ‘set’29,32,34,36 • Reduced attention and speed of information processing. While ongoing neuropsychological deficits have been reported by some researchers at one month,30,44,51,52 other workers have reported normal neuropsychological performance20,38,48 or performance at pre-injury levels by this time. MacFlyn et al reported complete recovery at six months44 and Dikmen et al by one year. In the various studies, a wide variation in severity of injury has been included under the rubric of concussion ranging from no LOC or mild stunning of the sensorium for a few seconds32,34,37,40,53,55 to periods of PTA for 24 hours or LOC for 20 minutes29,38,44,46 through to cases with PTA of 6 days,22 4 weeks,57 and 4 months45 and loss of consciousness for at least one week. This heterogeneity may account for some of the differences between studies since the magnitude of the head acceleration forces may differ considerably depending upon the cause. The first proposes that the symptoms associated with PCS are a direct consequence of brain injury,65,66 whilst the second proposes that the symptoms are functional and represent psychological or emotional sequelae of the brain injury. The issue of malingering and compensible litigation is also often proposed as a mechanism for symptom prolongation. Whether this relates to different impact forces as compared to motor vehicle crash studies remains speculative. Whether this may be mediated through alterations in neurotransmitter function rather than structural neuronal damage is unknown. The risk of repeat concussions in sport It has become a widely held belief that having sustained a concussive injury, that one is then more prone to future concussive injury. The evidence for this contention is limited at best. In a widely quoted study by Gerberich et al that involved self reported questionnaires relating the prior history of head injury in high school gridiron footballers, an increased risk of subsequent concussions was reported in players with a past history of concussion. Not least is the fact that the authors included cases of catastrophic brain injury. Furthermore, the reliability of a self diagnosis of concussion is questionable given that only 33% of those with loss of consciousness and 12% of those with other symptoms were medically assessed. The majority of the diagnoses of “concussion” were made by the coach, other team mates or by the players themselves. It would seem obvious that in any collision sport the risk of concussion is directly proportional to the amount of time playing the sport. In other words, the more games played the more chance of an injury occurring. Therefore the likelihood of repeat injury may simply reflect the level of exposure to injury risk. Similar criticisms can also be levelled at another retrospective study where it was reported that once an initial concussion was sustained, the probability of incurring a second concussion greatly increases. Apart from boxing related head injuries, the most widely cited studies of the cumulative effects of concussion have studied patients with injuries sustained in motor vehicle accidents that were severe enough to warrant presentation to hospital. Generally, concussive injuries suffered in collision sports such as football involve lesser degrees of acceleration-deceleration forces than experienced in motor vehicle accidents. For example, some head injuries in the cited studies were retrospectively assessed up to eight years after their occurrence.

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