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A phylogenetic tree is a tree showing the interrelationships among various or other entities that are believed to have a .

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A phylogenetic tree is similar in form to a . In a phylogenetic tree, each node with descendants represents the most recent common ancestor of the descendants, and edge lengths correspond to estimates. Each node in a phylogenetic tree is called a taxonomic unit. Internal nodes are generally referred to as Hypothetical Taxonomic Units (HTUs) as they cannot be directly observed.

Fig. 1: A speculatively rooted tree for rRNA genes

A rooted phylogenetic tree is a tree with a unique node corresponding to the (usually ) most recent common ancestor of all the entities at the leaves of the tree. Figure 1 depicts a rooted phylogenetic tree, which has been colored according to the (ref }}. 1998. The Universal Ancestor. Proceedings of the National Academy of Sciences 95: 6854-6859.). The most common method for rooting trees is the use of an uncontroversial outgroup - close enough to allow inference from sequence or trait data, but far enough to be a clear outgroup.

While unrooted phylogenetic trees can be generated from rooted ones by omitting the root from a rooted tree, a root cannot be inferred on an unrooted tree without either an outgroup or additional assumptions (for instance, about relative rates of divergence). Links some pictures are given in the subsection below.

There are three main methods of constructing phylogenetic trees: distance-based methods such as , -based methods such as , and character-based methods such as or .

Tree-building methods can be assessed on the basis of several criteria (ref Penny, D., Hendy, M. D. & M. A. Steel}}. 1992. Progress with methods for constructing evolutionary trees. Trends in Ecology and Evolution 7: 73-79. ):

  • efficiency (how long does it take to compute the answer, how much memory does it need?)
  • power (does it make good use of the data, or is information being wasted?)
  • consistency (will it converge on the same answer repeatedly, if each time given different data for the same model problem?)
  • robustness (does it cope well with violations of the assumptions of the underlying model?)
  • falsifiability (does it alert us when it is not good to use, i.e. when assumptions are violated?)

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  • By their very nature, phylogenetic trees cannot represent actual evolutionary patterns and are in fact distorted by any (ref Woese, C. R. 2002. On the evolution of cells. Proceedings of the National Academy of Sciences 99: 8742-8747.) or between species that are not nearest neighbors on the tree before hybridisation takes place. For these reasons, the proposed (see external links below) does not assume a tree structure.
  • The phylogenetic tree of a single or taken from a group of species often differs from similar trees for the same group of , and therefore great care is needed in inferring phylogenetic relationships amongst species. This is most true of genetic material that is subject to lateral gene transfer and , where different blocks can have different histories.
  • When extinct species are included in a tree, they should always be terminal nodes, as it is unlikely that they are direct ancestors of any extant species. Scepticism must apply when extinct species are included in trees that are wholly or partly based on DNA sequence data, due to evidence that DNA is not preserved intact for longer than 100,000 years (see .)

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An interesting conundrum is posed by organisms that have originated by symbiosis, since their phylogeny cannot be easily fit into a treelike topology. Lichens are the symbiosis of a fungus and an alga, which gives lichens that problem. But the fungus is more choosy about which alga than the alga about which fungus, meaning that lichen taxonomy follows that of their component fungi.

Related to this conundrum is organisms that have performed much lateral gene transfer, and sometimes even lateral genome transfer (), as many one-celled organisms have done. In particular, the taxonomy of has traditionally been descriptive, because it has been difficult to work out their phylogeny without using molecular sequences. And if their molecules are all scrambled, as has been suggested, then one may be stuck with descriptive taxonomy. But the "average" molecular phylogeny approximates that of information-system macromolecules like often-used ribosomal RNA. So as with lichens, a treelike phylogeny-based taxonomy remains reasonable when one uses some reasonable subset of the organism.


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Credits: This article is licensed under the . It uses material from the ; copied to Palaeos org MAK061004. The section "Always Treelike"? is from This page incorporates material from and so is licensed under the ). EvoWiki url:

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Drugstore Erectile Dysfunction (ED or "male impotence") is a sexual dysfunction characterized by the inability to develop or maintain an erection of the penis.An erection occurs due to blood entering and being retained in sponge-like bodies within the penis. Current research on erectile dysfunction is aimed at understanding the causes of erectile dysfunction and the diseases that impair normal function at the cellular and molecular levels, including diabetes and high blood pressure. Erectile dysfunction research is also being done to discover treatments that reverse the effects of this condition. The following health professionals can evaluate symptoms of erection problems: (NaturalNews) A press release by the American College of Cardiology (ACC) reveals that erectile dysfunction may mean more than a troubled romance. According to two new studies of men with type-2 diabetes, erectile dysfunction is a very strong indicator of heart disease. Published in the Journal of the American College of Cardiology (JACC) in May, the research makes clear the need for men with erectile dysfunction to not only get treatment to surmount their sexual difficulties but also for the related cardiovascular issues. Stroke Some types of prostate or bladder surgery How Does It Work? Evidence of an immune-mediated, antitumor effect of PDE5 inhibition is further shown by tetramer analysis on splenocytes obtained from sildenafil-treated, CT26WT tumor- bearing mice, which revealed a higher number of CTLs specific for AH-1 (unpublished data), a CT26 tumor-associated antigen, as compared with their untreated counterparts (19). To confirm immune-mediated antitumor activity in the sildenafil-treated groups, we performed an in vivo cytotoxicity assay. BALB/c mice were injected with PBS (naive), vaccinated with -irradiated CT26WT or C26GM, or challenged with CT26WT or C26GM tumors on day 0. On day 12 (CT26WT) or day 5 (C26GM), all mice received carboxyfluorescein diacetate succinimidyl ester (CFSE)–labeled splenocytes pulsed with the MHC class I–restricted AH-1 peptide (CFSEhigh), admixed with CFSE-labeled splenocytes pulsed with the irrelevant hemagglutinin (HA)-peptide (CFSElow). In vivo T cell cytotoxicity was determined 40 h later (Fig. 2). These time points were chosen based on the kinetics of tumor outgrowth observed in Fig. 1 A and Fig. 1 B, respectively, when tumor size significantly differed between untreated and sildenafil-treated mice. As expected, an endogenous AH1-specific immune response was observed in the vaccinated mice as compared with their tumor-bearing counterparts. PDE5 inhibition in the vaccine-primed mice failed to augment antigen-specific CD8 responsiveness compared with no treatment. In contrast, tumor-bearing mice treated with sildenafil early after tumor challenge generated antigen-specific immunity that was significantly greater then that observed in their untreated counterparts and similar, or even superior, to that induced by vaccination. Collectively, this is the first indication that PDE5 inhibitors can modulate antitumor immunity. Because the sildenafil-mediated antitumor immune response does not completely eradicate tumors, tumor escape mechanisms may be associated with their outgrowth. To test this hypothesis, the parental CT26WT cell line, as well as the CT26 tumor removed on day 24 from sildenafil-treated mice (either AH-1 pulsed or unpulsed), and BALB/c splenocytes were incubated with either AH-1 peptide-primed (Fig. S1 C) or tumor-primed (Fig. S1 D) effector T cells. Although effector T cells recognized the parental CT26WT line and released IFN- in the assay, they failed to recognize the sildenafil-derived tumor. Its recognition, however, was restored by loading the sildenafil-derived tumor with the AH-1 peptide. (Fig. S1, C and D). These results suggest that the immune response in sildenafil-treated mice does not result in complete tumor eradication but rather in the selection of antigen-escape variants. Erectile Dysfunction At A Glance Related Health News The vaccine consisted of 106 -irradiated CT26 or C26GM cells injected s.c. For ACT experiments, mice were vaccinated on days –14 and –7 before ACT in all four limbs with 106 -irradiated C26GM. The CD8+ T cells were negatively purified using the CD8+ isolation kit (Miltenyi Biotec), and 3 x 106 CD8+ T cells were transferred per mouse. In the 4T1-HA experiments, HA-specific CD8+ naive T cells were isolated from spleens and lymph nodes of pCL4-TCR mice. Related Health News By E.J. Mundell HealthDay Reporter Of the men surveyed, 395 reported having restless legs at least 15 times a month. They were more likely than the other men to use antidepressants and more likely to smoke. Your doctor will probably start by asking you some questions and doing a physical exam. Samples of your blood and urine may be tested for diseases and disorders. Other tests may also be needed. Your doctor will determine which tests are right for you. The Dutch researchers noted that pulmonary hypertension is typically mild to moderate among COPD patients but is particularly aggravated while exercising. Vardenafil (Levitra) What Are the Side Effects?

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