During my time at the ole' console, I have grown fond of the trumpet and the tuba stop and developed a taste/preference towards loud and festive pieces on the organ. I know many organ fanfares feature the loud Tuba or Trumpet stop but I am sure that there are many other pieces out there which use the tuba/trumpet stop.
Cs Lang Tuba Tune Pdf 18
Download: https://gohhs.com/2vGztd
And Henry Ley's arrangement of "Two Trumpet Tunes and an Air" seems to be back in fashion if, indeed, it was ever completely out of it. It seems that the first Trumpet Tune ("Cheer, boys, cheer, me mother wants the mangle") is, like Purcell's Trumpet Voluntary, actually by Jeremiah Clark. The second Trumpet Tune is "called the Cebell". I had often wondered what a Cebell was and when I finally got round to looking it up found that it was "a type of trumpet tune", which left me no more enlightened than I was before.
Through the fanfares, I have come to appreciate the works of Whitlock, who shares the same enthusiasn for the tuba stop as myself and Dr Francis Jackson of York Minster. I discovered Fanfare for John Bradley in an old OUP music collecting dust at the loft and went on to discover more of his fantastic works.
In your dusty pile of OUP albums, you may discover a green volume called An Album of Praise. There are three pieces in here which, in my opinion, are worthy of attention and two are not too complicated at all. One is Festal Flourish by Gordon Jacob - a wonderfully arresting start on the Tuba and some great concluding chords where you can couple it up! Another is a piece by Flor Peeters - (it might be called Festal Voluntary or something like that) - he doesn't specify a tuba, but you could use one to solo a few obvious passages. And finally, there is another Paean by Peter Hurford. I feel that this is a piece that has never really caught on, and I confess to finding it a bit tricky, but it's there and anything by Peter Hurford is worthy of respect and attention. (You might like his Two Dialogues - not really Tuba pieces, but the first, though over in a few minutes, is very exciting.)
I do have the old OUP An Album of Praise. I am doing Peeters' work for my examination. Half way through the first page, the repeated section where the right hand plays two chords while a melody is played with the left hand, I was told to use the trumpet stop for the melody. The Tuba stop is very loud and the situation of the stop doesn't really help because it is situated right across the old choir stalls which is on the second floor (more of an elevated platform with the organ/organ console/choir stalls). The tuba stop blares right behind you and towards you from 10 feet away.
Tubal endometriosis. (a) Manifestations of tubal endometriosis. (b) Peritoneal endometriotic lesion on the tubal serosa (1) and hydrosalpinx resulting from endometriosis-induced tubal occlusion (2).
Endosalpingiosis is FT epithelial tissue (lacking stroma) located outside the tube, whilst endometriosis is defined as the presence of both endometrial epithelial and stromal-like cells within the same ectopic lesion. Endosalpingiosis could be responsible for the tubal phenotype, whilst the presence of stroma in endometriotic lesions may allow for endometrial differentiation. A potential caveat here is that stromal endometriosis can also occur, with no glandular elements. Papillary tubal hyperplasia has also been proposed as being responsible for endosalpingiosis [27].
Schematic illustration of the proposed stem cell origins of tubal and pelvic endometriosis. Putative stem cell niches exist in the endometrial basalis (LGR5+, SSEA-1++, SOX9++ and N-cadherin++), lumen (LGR5++, SSEA-1+ and SOX9+) and FT epithelium (LGR5+, PAX8+, CD44+ and ALDH+). Endometrial fragments containing stem cells may be refluxed into the peritoneal cavity via the tubes, giving rise to both tubal and pelvic endometriosis. Analogously, desquamation of the endosalpinx through injury or natural shedding may also deposit fragments within the tubal lumen and out into the peritoneal space, thus establishing endometriotic explants of tubal origin. Once established, lesions arising from either the endometrium or the FT can spread to secondary sites.
Inflammation in tubal endometriosis. Adhesion and proliferation of endometrial tissue at ectopic sites leads to an influx of immune cells, secretion of cytokines/chemokines and initiation of the inflammatory response pathway. High concentrations of nitric oxide (NO) produced by macrophages promotes the inflammatory environment. Coupled with oxidative stress and prostaglandin-induced maintenance of the inflammatory state, tissue fibrosis is favoured at lesion sites. When lesions are present in the tubal serosa or endosalpinx, fibrosis can result in hydrosalpinx/haematosalpinx and adhesion formation.
Endometriosis-induced inflammation is also linked to oxidative stress through increased levels of reactive oxygen species (ROS) and reduced levels of antioxidants to counteract them. Heightened levels of ROS in the tubal fluid of patients with endometriosis may negatively impact both sperm, oocyte and embryo viability, thus perpetuating inflammation-induced subfertility [79,80]. Salpingitis may also be linked to endometriosis; one study found that 33% of patients with ovarian endometriosis had chronic salpingitis [81]. However, whether ovarian endometriosis was in fact a result of salpingitis in those patients presenting with both diseases was not established. Lastly, prostaglandins E2 and F are upregulated in the FT of women with endometriosis, most strikingly in the isthmus and ampulla regions during the proliferative phase [82]. Prostaglandins, specifically prostaglandin E2, are known mediators of the inflammatory response in endometriosis [83].
In the tubal endometriosis subtype, the level of local inflammation contained within the FT is anticipated to be higher than that observed in pelvic endometriosis. Elevation of inflammatory and ischemic markers have been observed in a rat model of FT endometriosis. In this model, interstitial FT telocytes implicated in the maintenance of tissue homeostasis were found to decrease in number and display ultrastructural abnormalities when oviductal lesions were present. This was accompanied by enhanced tissue fibrosis, thus linking the endometriosis-induced inflammatory response to tubal damage and resultant subfunction [84]. These findings have not yet been translated to human subjects. In women suffering from tubal endometriosis, local inflammation and fibrotic tissue are more commonly observed when ectopic lesions are present on the serosa compared to the mucosa [24]. Integrated transcriptomic and proteomic analysis of tubal fluid and epithelial cells from patients with tubal endometriosis has identified the acute phase response as uniquely activated, suggesting a disparate pathological mechanism in this subtype [18].
The FTs control oocyte transport, sperm storage, fertilization, preimplantation embryonic development and embryo transfer to the uterus. Aberration of these key functions is common in those suffering from endometriosis and can cause infertility. Whilst ectopic endometrium can implant in the tubes, tubal endometriosis is rare compared to other subtypes, e.g., ovarian endometriosis [14], albeit since the diagnosis requires salpingectomy, the true incidence is likely to be higher. However, as previously mentioned, normal tubal function is also impaired by pelvic endometriosis in the absence of tubal lesions that do or do not affect patency. Here, we will highlight several key studies relevant to endometriosis-associated FT dysfunction and resultant subfertility.
Endometriosis has been shown to affect cilia beat frequency and muscle contractility in the FT. Peritoneal fluid from women with endometriosis significantly reduces ciliary beat frequency in the endosalpinx compared to fluid from healthy patients, most likely through its proinflammatory effects [95]. In a study of 35 women with pelvic endometriosis, it was found that the beat frequency of ciliated cells in the tubal ampulla was significantly decreased compared to healthy controls. Ciliary beat frequency was further decreased in the ampulla and isthmus segments of a subgroup of patients with tubal endometriosis, when compared to the control group and those with pelvic endometriosis only. The same trend was observed when comparing the percentage of ciliated cells in the ampulla and isthmus segments. A decrease in longitudinal muscular contractility and contraction frequency was also observed in the pelvic and tubal endometriosis groups [33]. These changes suggest that the transport function of the FT is deficient in endometriosis, particularly when lesions are present in the tube itself. Reduction in ciliary function and smooth muscle contraction may result in the stagnation of luminal contents and cause a rapid progression to tubal blockage and consequent infertility. A potential mechanism of tubal dysperistalsis in endometriosis is the loss of pacemaker cajal-like type of tubal interstitial cells, which modulate smooth muscle contractility in the FT. A study of 10 women with early stage endometriosis found that cajal-like type of tubal interstitial cells were more sparse and damaged compared to tubes from healthy patients, thus linking endometriosis and aberrant FT motility function at the cellular level [96].
Pain caused by tubal endometriosis can be widely attributed to nociceptive, inflammatory and neuropathic mechanisms similar to other endometriosis related pain. Endometriotic lesions are themselves innervated [106,107,108,109]; however, there are concerns around the correlation between nerve fiber density and degree of pain experienced [110]. It has been suggested that nerve growth alteration is correlated to endometriosis itself rather than endometriosis-induced pain [111]. On the other hand, numerous studies have demonstrated a relationship between high concentrations of nerve growth factor, neuronal markers, nerve growth and pain symptoms [112,113,114]. No studies have explored innervation of endometriotic lesions in the FT. 2ff7e9595c
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