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|--Yinpanolithus Lu in Lu & Chang 1974 [Trinucleinae]
| |--*Y. yinpanensis Lu in Lu & Chang 1974
| |--Y. guizhouensis Yin in Yin & Li 1978
| |--Y. tenuilimbatus (Zhang in Qui et al. 1983)
| `--Y. wutangensis (Lu in Wang et al. 1962)
|--Salterolithus Bancroft 1929 [incl. Smeathenia Dean 1960]
| |--*S. caractaci (Murchison 1839) (see below for synonymy)
| `--S. harnagensis (see below for synonymy)
`--Broeggerolithus Lamont 1935 (see below for synonymy)
|--*B. broeggeri (Bancroft 1929) [=Cryptolithus broeggeri, *Broeggeria broeggeri]
| |--B. b. broeggeri [incl. B. constrictus Bancroft in Dean 1960]
| |--B. b. globiceps (Bancroft 1929) (see below for synonymy)
| |--B. b. soudleyensis (Bancroft 1929) (see below for synonymy)
| `--B. b. ulrichi (Bancroft 1949) [=Salterolithus (Ulricholithus) ulrichi]
`--+--B. discors (Angelin 1854) [=Trinucleus discors, Cryptolithus dicors (l. c.)]
|--B. nicholsoni (Reed 1910) (see below for synonymy)
`--B. transiens (Bancroft 1929) [=Cryptolithus transiens, Broeggeria transiens]
Salterolithus harnagensis Bancroft 1929 [=Broeggerolithus harnagensis; incl. Salterolithus caractaci var. paucus Cave 1957, Sa. praecursor Dean 1960, Sa. smeathenensis Bancroft in Dean 1958, Smeathenia smeathenensis]
* Type species of genus indicated
Bowdler-Hicks, A., J. K. Ingham & A. W. Owen. 2002. The taxonomy and stratigraphical significance of the Anglo-Welsh Cryptolithinae (Trinucleidae, Trilobita). Palaeontology 45 (6): 1075-1106.
Prothero, D. R. 1998. Bringing Fossils to Life: An introduction to paleobiology. WCB McGraw-Hill: Boston.
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Erectile dysfunction, or ED, can be a total inability to achieve erection, an inconsistent ability to do so, or a tendency to sustain only brief erections. These variations make defining ED and estimating its incidence difficult. Estimates range from 15 million to 30 million, depending on the definition used. According to the National Ambulatory Medical Care Survey (NAMCS), for every 1,000 men in the United States, 7.7 physician office visits were made for ED in 1985. By 1999, that rate had nearly tripled to 22.3. The increase happened gradually, presumably as treatments such as vacuum devices and injectable drugs became more widely available and discussing erectile function became accepted. Perhaps the most publicized advance was the introduction of the oral drug sildenafil citrate (Viagra) in March 1998. NAMCS data on new drugs show an estimated 2.6 million mentions of Viagra at physician office visits in 1999, and one-third of those mentions occurred during visits for a diagnosis other than ED.
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Dr. Peter Chun-Yip Tong who led the study said: "The development of erectile dysfunction should alert both patients and healthcare providers to the future risk of coronary heart disease."
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Learning to overcome ED is like learning any sexual skill; it takes patience, practice, and a partner. Solving erection problems is only a part of regaining a satisfying sex life. You and your partner have a whole world of erotic possibilities to explore. Remember the sexiest word in the language: communication.
For people who are at risk of developing ED, taking active steps to prevent its occurrence will not only help you maintain erectile function, but also help you lead a healthier life overall. Some steps you can take to prevent ED include:
By Amanda Gardner
Excessive stress is cause by the stressful life styles, no time for rest, putting yourself under the extreme conditions, too much of exercise, more exertion of body than body can face, and many other reasons. Excessive stress leads to the injure of entire health and makes you prone to many diseases. Stress activates the fight-or-flight response, where the adrenal glands release the hormones cortical and adrenaline into the blood stream. Cortical stimulate the liver to release sugar into the blood for quick energy. Adrenaline causes the blood vessels to constrict and increases breathing and heart rate, and shuts down the digestive system.
The bottom line: Whatever it takes, experts say don't shut down the line of emotional communication, even if you have to put your physical relationship on hold. And most importantly, listen to your heart.
Other research has linked BPA to an increased risk of diabetes, cancer and heart arrhythmias. Male sexual dysfunction may be an early indicator of BPA-related problems that take longer to develop, Li said.
Better treatments for erectile dysfunction are badly needed, McCullough added. About 35 percent of men don't respond to impotence drugs, including Viagra, Cialis and Levitra. As men age, diabetes, high cholesterol and hypertension -- all conditions that can affect male sexual function -- can worsen, making the drugs less effective.
"We do need more research," she added. "I'm sure it can be a pharmacological tool that may one day be able to help patients who cannot take Viagra."
Metabolism (breakdown) of vardenafil can be slowed by aging, liver disease, and concurrent use of certain medications (such as erythromycin, ketoconazole (Nizoral), and protease inhibitors). Slowed breakdown allows vardenafil to accumulate in the body and potentially increase the risk for side effects. Therefore, in men over age 65, with liver dysfunction, or who are also taking medication(s) that can slow the breakdown of vardenafil, the doctor will initiate vardenafil at low doses to avoid its accumulation. For example:
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.
High cholesterol or blood pressure
Magnetic resonance angiography uses magnetic fields and radio waves to provide detailed images of the blood vessels. This is a painless procedure but may involve an agent injected to make veins stand out more vividly.
A small percentage of men undergo vascular reconstructive surgery to improve blood flow to the penis. Revascularization involves bypassing blocked veins or arteries by transferring a vein from the leg and attaching it so that it creates a path to the penis that bypasses the area of blockage. Young men with only local arterial blockage are the best candidates for this procedure. It may restore function in 50% to 75% of men.
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