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BACKGROUND: Sinusitis-derived subperiosteal orbital collection is uncommon and is usually diagnosed as subperiosteal orbital abscess or, rarely, as hematoma. We report a unique and even rarer case of subperiosteal orbital collection, which is actually a complication of hematoma and abscess. CASE SUMMARY: A 26-year-old female presented with left eyeball pain and ipsilateral chemosis. She had no history of head trauma or upper respiratory infection. Her blood cell count showed an increase in leukocytes. Fiberoptic rhinolaryngoscopy revealed only mucosal edema of the left olfactory crest without apparent discharge. The computed tomography scan results showed an opaque left posterior ethmoid cell with a thickened bony shell and fusiform changes in the periosteal elevation of the medial wall of the left orbit. Emergent surgery revealed an ethmoid mucocele complicated with subperiosteal orbital hematoma and abscess. The pathology of the lamina papyracea between the mucocele and subperiosteal collection was necrotic, and the overlying mucosa was de-epithelialized. CONCLUSION: Subperiosteal orbital hematoma with abscess in a patient with sinusitis adds to the current knowledge of orbital complications of sinusitis.
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Nesfatin-1, an 82-amino acid neuropeptide, has been shown to induce anorexia and energy expenditure. Food intake is decreased in ad libitum-fed rats following injections of nesfatin-1 into the lateral, third, or fourth ventricles of the brain. Although the lateral parabrachial nucleus (LPBN) is a key regulator of feeding behavior and thermogenesis, the role of nesfatin-1 in this structure has not yet been delineated. We found that intra-LPBN microinjections of nesfatin-1 significantly reduced nocturnal cumulative food intake and average meal sizes without affecting meal numbers in rats. Because glucose sensitive neurons are involved in glucoprivic feeding and glucose homeostasis, we examined the effect of nesfatin-1 on the excitability of LPBN glucosensing neurons. In vivo electrophysiological recordings from LPBN glucose sensitive neurons showed that nesfatin-1 (1.5 × 10-8 M) excited most of the glucose-inhibited neurons. Chronic administration of nesfatin-1 into the LPBN of rats reduced body weight gain and enhanced the expression of uncoupling protein 1 (UCP1) in brown adipose tissue (BAT) over a 10-day period. Furthermore, the effects of nesfatin-1 on food intake, body weight, and BAT were attenuated by treatment with the melanocortin antagonist SHU9119. These results demonstrate that nesfatin-1 in LPBN inhibited food intake, modulated excitability of glucosensing neurons and enhanced UCP1 expression in BAT via the melanocortin system.
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OBJECTIVE: To investigate the relationship between the drug resistance of Pseudomonas aeruginosa (PA) isolated from burn patients wounds and its mobile genetic elements, including plasmid, transposon, and integron. METHODS: Thirty-two strains of PA were isolated from wounds exudate of hospitalized burn patients in Ningbo No. 2 Hospital. PA drug sensitivity was determined using GNS-448 drug sensitivity card and K-B tests. The genetic markers of plasmid, transposon and integron including traA, traF, tnpA, tnpU, merA, int I 1 were amplified by PCR and verified by gene sequencing. RESULTS: Drug resistant rate of 32 PA strains to gentamicin, amikacin, cefoperazone/sulbactam, ciprofloxacin was 43.7%, 32.0%, 46.8%, 49.9%, respectively. PA drug resistant rates to piperacillin, cefotaxime, ceftazidime, cefepime, aztreonam, piperacillin/tazobactam, levofloxacin, imipenem and meropenem were all above 56.0%. Seventeen out of 32 PA strains were found to carry transposon and (or) integron genetic markers. One strain was positive for both tnpA and merA, 8 strains were positive for both merA and int I 1, 1 strain was only positive for tnpA, 2 strains were only positive for merA, and 5 strains were positive for int I 1 only. CONCLUSIONS: PA isolated from burn wounds of hospitalized patients in Ningbo No. 2 Hospital is seriously drug resistant, which may relate with its high positive rate of mobile genetic elements of transposon and (or) integron.