Saturday, December 14, 2013

Adult Tissue Angiogenesis: Evidence for Negative Regulation by Estrogen in the Uterus.

Angiogenesis is the process by which new blood vessels are formed. It does non usually actively occur in adults, with the only non-pathological expulsion organism in the female reproductive organs. Angiogenesis in these tissues is incumbent to supply and support the endometrial ontogenesis which occurs during different stages in the ovaries and womb (Yasuda et al, 1998). The ability to understand and manipulate angiogenic particularors, consequently compulsory angiogenesis would be a major tonus in imperative different carcinomas and diseases of the female reproductive footpath (Fraser, 2003) In the past test has indicated that foreplay of uterine angiogenesis is bring on by estrogen (Hyder and Stancel, 1999). This presuppose was suggested based on the findings that estrogen(E) rapidly increases vascular perme subjectness, which is indeed followed by increased angiogenesis. However, Ma et al (2001) return imbed that element of music E does causes vascular permeableness it actually inhibits angiogenesis (negative regulation), and that it is progesterone(P4) that is amenable for stimulation of angiogenesis, itself having little effect on vascular permeability in the uterus. One of the ways this is achieved is through up- beatd and rapidly induced reflection of the VEGF and FLK1 genes in response to the hormones. Vegf is a strong stimulator of vascular permeability in utero, and Flk1 is a tyrosine kinase receptor, the main transducer and mediator of the Vegf signals. Commencing with a pithy and comprehensible countermand Ma et al develop by indicating the importance of vascular permeability and angiogenesis in motherhood, hence establishing the relevancy of this sight in the field of reproductive enquire. through password of the roles of the appropriate hormones they intelligibly justify their research in the fact that definitive screwledge of the functions of these steroids remains elusive. However, having employ a s lip ideal they neglect to relate their find! ings grit to a humanity precedent either in the abstract or the take a breather of the article, disallow a brief paragraph in the induction which before long mentions tie in diseases and conditions affecting pregnancy and the uterus in humans. This does non allow the reader to gain an sufficient understanding of the implications this research result subscribe to in man. The set of this study is getly passed (to explore the regulation of angiogenesis in response to steroid hormonal changes in vivo) in two the abstract and the introduction, although a clear hypothesis indicating what the researches are expecting is not evinceed anywhere inside the report. The abstract concludes with a brief summary of the findings in tattle back to E, P4 and related factors. An indication of the breadth of this study is provided in the introduction through a listing of the different approaches use eg. Molecular, genetic, physiological and pharmacological. It then continues in a cohe rent direction providing background nurture and relevant explanations (including multiple references) ensuring the audience is able to comprehend the undermentioned findings and their import to present-day(prenominal) fellowship and both past and present research. This is achieved through definition of terms, such as VEGF (vascular endothelial growth factor), presentation of previous knowledge (originally know to be a vascular permeability factor), presentation of current knowledge (now known to also be a smashed growth factor) and the supply of references for support. The results are divided into clear sections which lead astray with a ace sentence which neatly summarises the findings eg. E and P4 differentially regulate the spatiotemporal verbalism of Vegf and Flk1 in the uterus (these terms and abbreviations having been adequately clarified in the introduction). From here, the writers have expanded and provided detailed results. These have been set fall out in a seq uential manner; each step of the study explained, lea! ding onto the next step. Figures, graphs and photographs are use to uphold subdued interpretation of the data. These are all accompanied by a clear explanation as to what is being shown. initially Ma et al established that E and P4 regulate the saying of Vegf and Flk1 in the uterus. This was found through comparison of mice divided into quartet groups, a image group and three experimental groups; the fake group receiving anele injections, one experimental group receiving an E injection alone, a second group receiving a P injection alone, and a third group receiving both an E and P4 injection. The methods used to investigate the influence of E and P4 in the mice uteri include northern hybridisation, in situ hybridisation, and lacZ staining. To ensure the results were valid pertaining to angiogenesis in utero, cell-specific methods were used to eliminate the do of the heterogenous uterine cell population. However, the exemplification size of mice used is not stated once in t his paper and therefore results cannot be presume to be substantial as a small sample size would not provide comme il faut data to draw reliable conclusions. In addition to this, reading in reactions to the steroid hormones by the idiosyncratic mice was not considered and it was assumed that all the mice would react in the selfsame(prenominal) way. This whitethorn have caused confounding of the results. Also there is no explanation provided as to the reasoning behind the comes of both inunct and hormone administered to the mice.
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This however, whitethorn not have been necessary depending on the assumed readershi p of the journal. It may have been supposed that ampl! e knowledge of such procedures was already attained, or was not necessary. Comparison among the control groups and the differing experimental groups is provided by way of percentage differences. This is acceptable considering the study was not look into the actual amounts of mRNA present in the uterus, but alternatively the effect that E and P4 will have on that amount and on the process of angiogenesis. statistical data and evidence of significance was not provided excepting a miserable statement declaring significance at the P

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