1 tryptophan and feed intake Studies have shown that lack of tryptophan will cause a decrease in pig feed intake. A study by Burgoon (1992) on 10-20 kg piglets showed that feed intake of piglets fed the low tryptophan (0.13%) group was 40% lower than that of the 0.205% tryptophan group. The results of Schutte (1988), Wu Xilin (1994), Libal (1995), Lin Yingcai (1999, 2001) Guzik (2002), Wu Xinlian (2003), etc. are similar. Wu Xilin (1994) and Lin Yingcai (1999) showed that pig feed intake and daily gain were positively correlated with tryptophan in feed (r=0.96-0.98, P<0.001). Henry (1992, 1995, 1996) suggested that tryptophan may regulate pig feed intake through the action of neurotransmitters (serotonin, polyamine). Henry (1996) showed a positive correlation between Trp/LNAA in the diet, Trp/LNAA in the blood, tryptophan in the brain, serotonin, and feed intake in pigs. Its possible explanation is that when tryptophan passes through the blood-brain barrier, it shares a transport system with macromolecular neutral amino acids (LNAA, including Ile, Leu, Phe, Tyr, Val), and LNAA competitively inhibits tryptophan into the brain. Concentration (Adlbl & Gray, 1967, Pardrdge, 1977). The Km of tryptophan hydroxylase, a key enzyme for the conversion of tryptophan to 5-HT in the brain, is 50 μM, which is sensitive to changes in tryptophan concentration. Similar reports have been made by Fernstrom & Wurtman (1972), Leathwood, (1987), Yokogoshi et al, (1987). Hery et al, (1992) and Perez-Cruel (1974) reached similar conclusions in rabbits and humans. Wu Xinlian (2003) reported that the 0.20% tryptophan group was 0.14%, the hypothalamic serotonin content was increased by 60.5%, and the feed intake was increased by 61.8%, further confirming the above conclusion. However, more than a physiological dose of 5-HT inhibits feeding, which may be the reason that excess Trp has no additional benefit to feed intake. The Baker (1996) study confirms the above conclusions. In the corn-soybean-type diet with sufficient Lys and Trp deficiency, Trp was added. ADG and G:F increased linearly with the increase of Trp, but when both were sufficient, Trp was added, and ADG and FI decreased linearly. 2 tryptophan and GH-IGF growth axis A large amount of experimental evidence indicates that the GH-IGF axis is the main mechanism for the regulation of growth of hormones and nutrients, and the effect of tryptophan on growth is also related to this growth axis. Phillips (1991) found that tryptophan was removed from hepatocyte culture medium, and IGF-1 mRNA levels and IGF-1 secretion were reduced. Brameld (1999) got the same conclusion. Huang & Phillips (1996) found an amino acid response element on the murine IGF-1 gene whose expression is particularly sensitive to tryptophan (this sensitivity may be interspecies). Ding Yuhua (2003) showed that dietary low tryptophan levels reduced circulating GH and IGF-1 levels in piglets and inhibited the growth-promoting function of endocrine growth axis, which in turn affected piglet growth. Wu Xinlian (2003) reported that serum IGF-1 concentration increased with the increase of dietary tryptophan levels, with the highest concentration of tryptophan 0.22%, and significant difference with 0.20% group. Jacob (1996) showed that IGF-1 may play a more important role in reducing protein in the process of protein synthesis in animals than in reducing amino acids. Cortanira et al. (1991) suggested that tryptophan stimulates the release of insulin after feeding and increases the synthesis of liver and muscle proteins. Based on the above findings, it can be concluded that the pro-protein synthesis of tryptophan may be the result of synergy between the two. Carew (1987) reported that a lack of tryptophan may cause thyroid hyperplasia, resulting in wasted energy. Ding Yuhua (2003) found that tryptophan had no effect on the circulating T3 and T4 levels in piglets, and concluded that tryptophan regulates growth through the GH-IGF growth axis rather than the pituitary-thyroid axis. 3 The effect of tryptophan on the digestive tract Tryptophan is converted to serotonin and melatonin in intestinal chromaffin cells. Qing Xiaohong et al (2003) confirmed that serotonin is a medium for stress diarrhea. Their possible mechanism for analyzing serotonin-induced stress is: 5-phosphate derived from chromaffin cells and serotonergic neurons. HT activates the 5-HT3 receptor in the gastrointestinal tract, stimulates the intestinal plexus, enhances gastrointestinal motility and fluid secretion, leading to diarrhea. Bubenik (1997) suggests that melatonin may be an agonist of 5-HT inhibitory neuroreceptors. Some scholars have now proposed melatonin-serotonin systems to describe their interactions in regulating gastrointestinal motility. Konturek (1994) also described melatonin gastric mucosal protection mechanisms: reducing gastric acid secretion and stimulating gastrin secretion. The effects of tryptophan-induced IGFs on gastrointestinal development and physiological functions in pigs have also received much attention. Colostrum and pre-lactation pig milk contain high IGFs, and recent studies have shown that the small intestine may be the main pathway for IGF-1 in the blood. Xu et al (1996) showed that oral doses of IGF-1 and IGF-2 can stimulate the gastrointestinal tract cell proliferation of newborn piglets, and the intestinal weight, protein and DNA content, and villus height were significantly increased compared with the unadded group. 4 The effect of tryptophan on immunity The effect of tryptophan on immunity may be achieved by its induced IGFs and metabolites serotonin, melatonin and the like. IGFs can accelerate the proliferation of T cells in the early stage of T cell activation. Binz (1990) reported that IGF-1 can atrophy thymocytes in diabetic rats. Wu Xinlian (2003) reported that with the increase of dietary tryptophan levels, the serum protein coefficient of piglets increased continuously, and after the demand was exceeded, it showed a downward trend. This is similar to the results of Wu Xilin (1994). Wei Tao et al (2003) reported that mice immunized with low-dose melatonin increased the proliferation of ConA spleen lymphocytes by 31.1% (P>0.05), NK cell activity by 62.2% (P<0.05), and the number of antibody-producing cells. The increase of 5.3 (P<0.05), serum hemolysin level increased by 17.1% (P<0.05). Thrust Spherical Roller Bearing
A spherical roller thrust bearing is a rolling-element bearing of thrust type that permits rotation with low friction, and permits angular misalignment. The bearing is designed to take radial loads, and heavy axial loads in one direction.
Spherical roller thrust bearings are of separable construction, The shaft washer is assembled with the cage and a number of asymmetrical spherical rollers and has to be used along with a housing washer having sphered raceway. During mounting, the rings are to be fixed on to their respective seats – shaft washer on the shaft and housing washer on to the housing and then they have to be put together carefully They are manufactured in multiple series. Thrust Spherical Roller Bearing,Single Direction Spherical Roller Thrust Bearing,Thrust Ball Bearings For Detector,Hardness Thrust Spherical Roller Bearings Shijiazhuang Longshu Mechanical & Electrical Equipment Trading Co., Ltd. , https://www.longsbearings.com
The raceway of the housing washer is at an angle with it`s ais of rotation, so as to be able to allow the rollers to remain in touch with it. As a result, a spherical roller thrust bearing is capable of carrying both a radial as well as an axial load. Spherical roller thrust bearings – because of their internal geometry – are capable of accommodating certain amount of misalignment. However, they can take axial loads only from one direction, and may need to be used in pairs in Back-to-Back or Face-to-Face arrangement, if thrust load from both the directions are to be carried.
Spherical roller thrust bearings are capable of compensating misalignment and shaft deflection.
The bearings are manufactured in normal accuracy. However, bearings with higher running accuracy can also be supplied.