ABSTRACT
Ubiquicidin [UBI] 29-41 is a synthetic antimicrobial peptide that binds with the microbial cell membrane at the location of infection. This study was conducted to evaluate its probable efficacy as an infection-imaging agent with potential to differentiate bacterial infection from sterile inflammation in humans. Fifteen diabetic foot patients [10 males and 5 females] with suspected bacterial infection, prior to starting antibiotic treatment, were selected for this study. First a routine three phase bone scan and later a [99m]Tc-UBI scan was performed for all the patients. 555-740 MBq of [99m]Tc-UBI was injected intravenously. A 10 minute dynamic study was followed by spot views of the suspected region of infection and corresponding normal areas [liver and kidneys] at 60 and 120 min. Whole-body anterior and posterior images were also acquired. To interpret the studies as positive or negative, visual score [0 -3] was used, with scores of 0 [minimal or no uptake; equivalent to soft tissue] and 1 [mild; less uptake than in liver] being considered negative and scores of 2 [moderate; uptake equal to or greater than that in liver] and 3 [intense uptake equal to or greater than that in kidneys] being considered positive. Of 15 studies performed with [99m]Tc-UBI, all had positive bacterial cultures. The result of bone scan was positive for osteomyelitis in 12 patients [80%]. [99m]Tc-UBI Scintigraphy was positive in 6 patients, but negative in nine. The sensitivity of [99m]Tc-UBI for detection of infection was therefore 40%. From 12 patients who had positive bone scans, only 6 had a positive [99m]Tc-UBI [50%] indicating the sensitivity of 50% for [99m]Tc-UBI in osteomyelitis cases. 99mTc-UBI was not positive in any patient who had evidence of soft tissue infection in the bone scan. Although [99m]Tc-UBI 29-41 was well tolerated by all the patients without any side effects, considering low sensitivity of this agent, this radiopharmaceutical is not of great value for diabetic foot infection diagnosis
ABSTRACT
Previous studies have shown that different mechanisms are involved in neuropathic pain. Increasing nitric oxide [NO] in the location of injury may be an effective factor in neuropathic pain which, in turn, acts through increasing membrane permeability. The aim of this study was to examine the effects of aminoguanidin, a specific inhibitor of inducible nitric oxide synthetase [iNOS] on neuropathic pain behaviors. Male Wistar rats [200-300 gram] were used. Chronic constriction injury [CCI] in the rats were produced by four loosely ligation that the distance between them is 1 millimeter before the triple branching of sciatic nerve. Two weeks later, the animals were tested for thermal hyperalgesia and mechanical allodynia. Aminoguanidine were injected [I.P] 60 min before test in doses of 75, 150 and 300 mg/kg. Our studies showed CCI induced neuropathic pain in all rats. All doses of aminoguanidin [75, 150, 300 mg/kg] significantly reduced mechanical allodynia and thermal hyperalgesia in compared with CCI group. Moreover, the effect of aminoguanidin on thermal hyperalgesia at dose of 300 mg/kg was significantly higher than two lower doses. According to findings of this and other studies, aminoguanidin has an important influence in reducing neuropathic pain. This effect, at least in part, is mediated through inhibition of iNOS. Additionally, an inhibition of di-aminoxidase or anti oxidative effects may be contributed to inhibitory effects of aminoguanidin on neuropathic pain. Thus, further investigations can determine the mechanism of aminoguanidin effects in neuropathic Pain. Findings of this study open a new window for synthesis of new drugs for management of neuropathic pain in clinic