• Journal of Yeungnam Medical Science
• /
• v.40 no.4
• /
• pp.328-334
• /
• 2023

An aging population and changes in dietary habits have increased the incidence of diabetes, resulting in complications such as diabetic foot ulcers (DFUs). DFUs can lead to serious disabilities, substantial reductions in patient quality of life, and high financial costs for society. By understanding the etiology and pathophysiology of DFUs, their occurrence can be prevented and managed more effectively. The pathophysiology of DFUs involves metabolic dysfunction, diabetic immunopathy, diabetic neuropathy, and angiopathy. The processes by which hyperglycemia causes peripheral nerve damage are related to adenosine triphosphate deficiency, the polyol pathway, oxidative stress, protein kinase C activity, and proinflammatory processes. In the context of hyperglycemia, the suppression of endothelial nitric oxide production leads to microcirculation atherosclerosis, heightened inflammation, and abnormal intimal growth. Diabetic neuropathy involves sensory, motor, and autonomic neuropathies. The interaction between these neuropathies forms a callus that leads to subcutaneous hemorrhage and skin ulcers. Hyperglycemia causes peripheral vascular changes that result in endothelial cell dysfunction and decreased vasodilator secretion, leading to ischemia. The interplay among these four preceding pathophysiological factors fosters the development and progression of infections in individuals with diabetes. Charcot neuroarthropathy is a chronic and progressive degenerative arthropathy characterized by heightened blood flow, increased calcium dissolution, and repeated minor trauma to insensate joints. Directly and comprehensively addressing the pathogenesis of DFUs could pave the way for the development of innovative treatment approaches with the potential to avoid the most serious complications, including major amputations.

• Annals of Clinical Neurophysiology
• /
• v.16 no.2
• /
• pp.74-76
• /
• 2014

Foot drop is usually derived from peroneal nerve injury. Traumatic causes of peroneal nerve injury are more common than insidious causes including metabolic syndromes and mass lesions. We present a case with common peroneal neuropathy due to schwannoma, which is extremely rare. Complete excision of the mass lead to a gradual improvement of the symptoms. Schwannoma should be considered as a cause of common peroneal neuropathy.

• Journal of Oral Medicine and Pain
• /
• v.44 no.1
• /
• pp.40-44
• /
• 2019

Third molar extraction, one of the important surgical treatments commonly practiced in dentistry, presents various symptoms after surgery ranging from temporary or mild symptoms to permanent or severe complications. However, oral burning pain, dysesthesia, parageusia, dry mouth, headache and pain in multiple teeth are not the common symptoms that patients often complain after dental extraction. Here, the authors report two cases who presented acute neuropathic symptoms mentioned above in the orofacial regions following third molar extraction. At the initial examination, the healing of the tooth sockets of two patients was normal. One patient was diagnosed as megaloblastic anemia associated with Vitamin $B_{12}$ deficiency and was referred to the Department of Hematology for assessing the underlying etiology of anemia. The laboratory test for the other patient revealed microcytic anemia related to iron deficiency. The patient with iron deficiency anemia was successfully treated with iron supplement. These two cases suggest that anemia, as an underlying systemic disease, may be a rare etiology explaining acute onset of peripheral neuropathy in the orofacial regions after third molar extraction and should be considered in the assessment of patients who report neuropathic symptoms after dental extraction.

• Journal of Food Hygiene and Safety
• /
• v.34 no.3
• /
• pp.303-308
• /
• 2019

L-carnitine is found in high levels in muscle tissues. It has been developed as a nutrient and dietary supplement, and also used as a therapeutic supplement in various diseases including type II diabetes, osteoporosis and metabolic neuropathies. However, it is not fully understood how it affects cellular mechanisms in colorectal cancer. Therefore, we attempted to determine the effect of L-carnitine in HCT116 human colorectal cancer cells. First, the HCT116 cells were exposed to L-carnitine for 24 hours at 0-40 mM, and then analyzed for cellular proliferation, oxidative stress and related mechanisms. In a MTT assay, L-carnitine inhibited cellular proliferation and induced reactive oxygen species (ROS) in HCT116 by DCF-DA analysis. To analyze the mechanism of L-carnitine in colorectal cancer cells, we performed a western blot analysis for pERK1/2 and pp38 MAP kinase. The western blot showed that L-carnitine significantly increased protein levels of pERK1/2 and pp38 compared with control. Taken together, we found that L-carnitine has anti-proliferative function via increased ROS and activation of ERK1/2 and p38 pathway in HCT116. These findings suggest that L-carnitine may have an anti-proliferative role on colorectal cancer.