ABSTRACT
INTRODUCTION: The etiology of calf pain varies widely; therefore, it is difficult to diagnose and requires careful history taking and physical examination by primary care unit physicians. Because ultrasonography is easy to perform, cheap, and readily available to physicians during a routine consultation, it is the first choice of modality for the evaluation of calf pain. However, simple inflammation around the nerve should also be considered as a possible etiology. Here we describe a 35-year-old man with chronic pain in the right calf that was actually caused by fibroma-induced chronic inflammation around the tibial and peroneal nerves but misdiagnosed as centralized neuropathic pain. CASE REPORT: The patient presented with chronic pain and a tingling sensation in the right calf. He had a slowly growing tibial nerve neurilemmoma that was excised at 28 years of age; however, the pain and tingling sensation persisted. He visited several hospitals for 7 years and was misdiagnosed with peripheral nerve injury-induced neuropathic pain. At 35 years of age, he visited our hospital for further evaluation. Ultrasonography revealed a mass in the popliteal region, which was excised and confirmed to be a fibroma via histopathological analysis. Severe inflammation was observed in the operative field. His symptoms finally ameliorated after this surgery. CONCLUSION: The findings from this case suggest that ultrasonography should be used as the primary modality for the evaluation of calf pain. Although the features of unresolved calf pain are similar to those of neuropathic pain, more curable etiologies should be considered.
Subject(s)
Fibroma/complications , Inflammation/etiology , Peroneal Nerve , Tibial Nerve , Adult , Chronic Pain/etiology , Diagnostic Errors , Humans , Leg , Male , Neuralgia/diagnosis , Neuralgia/etiology , Peripheral Nerve Injuries/diagnosis , UltrasonographyABSTRACT
Type 2 diabetes is caused by both insulin resistance and relative insulin deficiency. To investigate age-related changes in glucose metabolism and development of type 2 diabetes, we compared glucose homeostasis in different groups of C57BL/6J mice ranging in age from 4 months to 20 months (4, 8, 12, 16 and 20 months). Interestingly, we observed that non-fasting glucose levels were not significantly changed, but glucose tolerance gradually increased by 20 months of age, whereas insulin sensitivity declined with age. We found that the size of islets and glucose-stimulated insulin secretion increased with aging. However, mRNA expression of pancreatic and duodenal homeobox 1 and granuphilin was decreased in islets of older mice compared with that of 4-month-old mice. Serum calcium (Ca2+) levels were significantly decreased at 12, 20 and 28 months of age compared with 4 months and calcium sensing receptor (CaSR) mRNA expression in the islets significantly increased with age. An extracellular calcium depletion agent upregulated CaSR mRNA expression and consequently enhanced insulin secretion in INS-1 cells and mouse islets. In conclusion, we suggest that decreased Ca2+ levels and increased CaSR expression might be involved in increased insulin secretion to compensate for insulin resistance in aged mice.
Subject(s)
Aging/metabolism , Insulin/metabolism , Receptors, Calcium-Sensing/metabolism , Aging/genetics , Animals , Blood Glucose/metabolism , Body Weight , Calcium/blood , Cell Line , Fasting , Gene Expression , Glucose Tolerance Test , Immunohistochemistry , Insulin Resistance , Insulin Secretion , Islets of Langerhans/metabolism , Male , Mice , RNA, Messenger , Receptors, Calcium-Sensing/geneticsABSTRACT
Inhibition of epithelial-mesenchymal transition (EMT)-inducing transcription factors Twist and Snail prevents tumor metastasis but enhances metastatic growth. Here, we report an unexpected role of a tumor suppressor tristetraprolin (TTP) in inhibiting Twist and Snail without enhancing cellular proliferation. TTP bound to the AU-rich element (ARE) within the mRNA 3'UTRs of Twist1 and Snail1, enhanced the decay of their mRNAs and inhibited the EMT of cancer cells. The ectopic expression of Twist1 or Snail1 without their 3'UTRs blocked the inhibitory effects of TTP on the EMT. We also observed that TTP overexpression suppressed the growth of cancer cells. Our data propose a new model whereby TTP down-regulates Twist1 and Snail1 and inhibits both the EMT and the proliferation of cancer cells.
