Is your Neck and Shoulder Pain serious? Most shoulder and neck pain causes are not a serious condition. The reason your shoulder is sore is that the neck and upper back are just not working correctly. If you have had a fall or injury and suddenly develop shoulder and neck pain - seek help. Any injury may affect the many sensitive structures in your neck and upper back. Shoulder and neck pain if they occur together may relate to disc injuries. This is more likely if you are having neck and arm pain, rather than shoulder pain. Pain that travels down the arm to any extent may indicate more severe problems. But as in all pain conditions - if you have had a fall, injury or pain is not easing quickly - seek help from a health professional. The first step to remove your pain The majority of neck and shoulder pain will ease quickly and easily. Even faster if you perform a few simple stretches and techniques to help get those areas moving again. The joints and muscles in the area are smaller than the lower back areas. They cause more pain because they are more sensitive. Not good when pain is there. The good news is - they also respond quicker to certain techniques and exercises. Neck and shoulder pain will ease quickly if you:
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Hypoxia-inducible factor-1 (HIF-1) regulates many pathways potentially important for tumor growth, including angiogenesis and glycolysis. Most attention has focused on its role in the response to hypoxia, but HIF-1 is also constitutively expressed in many tumors. To analyze the role of this pathway in vivo, we used magnetic resonance (MR) methods and complementary techniques to monitor metabolic changes in tumors derived from HEPA-1 mouse hepatoma lines that were either wild type (WT) or deficient in hypoxia-inducible transcription factor HIF-1beta (c4). The c4 tumors grew significantly more slowly than the WT tumors (P < ), but were examined at a similar size (- g). At the tumor size used in these studies, no differences in vascularity were observed, and MR parameters measured that related to tumor blood flow, vascularity, and oxygenation demonstrated no significant differences between the two tumor types. Unexpectedly, the ATP content of the c4 tumor was approximately 5 times less than in the WT tumor [measured in tumor extracts (P < ) and by metabolic imaging (P < )]. Noninvasive (31)P MR spectroscopy showed that the nucleoside triphosphate/P(i) ratio of the two tumor types was similar, so the low ATP content of the c4 tumors was not caused by (or a cause of) impaired cellular bioenergetics. Rather, glycine, an essential precursor for de novo purine formation, was significantly lower in the c4 tumors (P < ), suggesting that ATP synthesis was impaired in the mutant tumor cells. Supporting evidence for this hypothesis came from the significantly lower concentrations of betaine, phosphocholine, and choline in the c4 tumors (P < ); these are intermediates in an alternative pathway for glycine synthesis. No significant differences were seen in lactate or glucose content. MR resonances from phosphodiesters, which relate to the metabolic turnover of phospholipid membranes, were significantly lower in the WT tumors than in the c4 tumors, both in vivo (P < ) and in extracts (P < ). We propose that loss of up-regulation of expression of the genes for glucose transporters and glycolytic enzymes in the c4 tumors decreased formation of glycine, an essential precursor of ATP synthesis, and thus caused the low ATP content of the c4 tumors. In summary, these data suggest that disruption of the HIF-1 pathway in these tumor cells impairs the supply of anabolic precursors required for cell synthesis. They suggest potential biochemical targets that may be modified by therapy blocking HIF-1 function.