A sub-ppm acetone gas sensor for diabetes detection using 10 nm thick ultrathin InN FETs.

An indium nitride (InN) gas sensor of 10 nm in thickness has achieved detection limit of 0.4 ppm acetone. The sensor has a size of 1 mm by 2.5 mm, while its sensing area is 0.25 mm by 2 mm. Detection of such a low acetone concentration in exhaled breath could enable early diagnosis of diabetes for portable physiological applications. The ultrathin InN epilayer extensively enhances sensing sensitivity due to its strong electron accumulation on roughly 5-10 nm deep layers from the surface. Platinum as catalyst can increase output current signals by 2.5-fold (94 vs. 37.5 µA) as well as reduce response time by 8.4-fold (150 vs. 1,260 s) in comparison with bare InN. More, the effect of 3% oxygen consumption due to breath inhalation and exhalation on 2.4 ppm acetone gas detection was investigated, indicating that such an acetone concentration can be analyzed in air.

Congenital midline nasal mass: cases series and review of the literature.

Encephalocele, glioma and dermoid cyst are the most common midline nasal masses. Given their potential for intracranial extension, prompt treatment is necessary to prevent complications. Herein, we present two cases of midline nasal masses. A comparison was made to delineate the differences between their clinical courses, treatments and outcomes. Case 1 was a baby girl with respiratory distress beginning at birth. Nasal glioma without definite intracranial extension was present. The mass was completely excised with the aid of a video-assisted endoscope without complications. At follow-up two years after surgery, no recurrence was noted. Case 2 was a two-year-old boy with a midline nasal dermoid cyst. Extirpation of the lesion through a vertical-dorsal approach was performed. He was discharged three days after surgery with a satisfactory aesthetic result.

C-C chemokine ligand 2 gene expression in nasal polyp fibroblasts: possible implication in the pathogenesis of nasal polyposis.

OBJECTIVES: Recruitment of macrophages is essential to the pathogenesis of nasal polyps (NP), since this disease is inflammation-related. In this study, the effects of tumor necrosis factor alpha (TNF-alpha) on the expression of C-C chemokine ligand 2 (CCL2) in fibroblasts derived from nasal polyps (NPFs) were investigated. The roles of cyclooxygenase (COX) 2 and prostaglandins in the mediation of TNF-alpha-stimulated CCL2 gene expression were also investigated. METHODS: Northern blot analysis was used to study the expression of CCL2 and c-Fos in cultured NPFs. An electrophoretic mobility shift assay was used to explore the interactions between activator protein 1 (AP- 1) and DNA. Immunohistochemistry was used to explore the in vivo expressions of COX-2, CCL2, and CD68 in NPs. RESULTS: The Northern blot analysis showed that TNF-alpha stimulated the expression of CCL2 and COX-2 genes, and the synthesis of CCL2 messenger RNA was COX-2-dependent. A transient elevation of c-Fos and c-Jun messenger RNAs was induced by TNF-alpha, whereas COX-2 inhibitors NS-398 and meloxicam abolished the up-regulation of c-Fos. The electrophoretic mobility shift assay revealed that TNF-alpha triggered AP-1 and DNA binding and again, NS-398 and meloxicam inhibited this reaction via reducing c-Fos synthesis. Curcumin (AP-1 inhibitor) markedly suppressed the TNF-alpha-induced CCL2 expression. The immunohistochemical staining of NP surgical specimens also revealed an intimate alignment between CCL2-positive fibroblasts and CD-68-positive macrophages. CONCLUSIONS: These data suggest that NPFs may contribute to NP development by synthesizing CCL2 to promote macrophage recruitment. Furthermore, COX-2 facilitates CCL2 transcription in NPFs via a c-Fos and AP-1 signaling pathway.

Increased epithelial cell proliferation in nasal polyps.

BACKGROUND AND PURPOSE: The mucociliary function of the sinonasal mucosa is an innate defense mechanism of the human nasal airway. Epithelial cell proliferation is required for cell renewal and repair of the sinonasal mucosa. In this study, the MIB-1 monoclonal antibody, which can detect the S-phase nuclear protein Ki-67, was used to evaluate the proliferation of the sinonasal mucosa in patients with various inflammatory conditions of the sinonasal mucosa. METHODS: Specimens from the inferior turbinates of patients with nasal allergy (n = 12), vasomotor rhinitis (n = 20), nasal polyps (n = 22), and control subjects undergoing rhinoplasty (n = 5) and mucosa of chronic sinusitis patients [inferior turbinates (n = 10), middle turbinates (n = 10), and maxillary sinus (n = 9)] were fixed in neutral formalin and embedded in paraffin. MIB-1 monoclonal antibody was used to detect proliferation of epithelial cells. RESULTS: Significantly increased epithelial cell proliferation was noted in nasal polyps compared to sinonasal mucosa. There was no difference among various sinonasal inflammatory conditions between patients and controls. CONCLUSIONS: Increased epithelial cell proliferation in nasal polyps may play an important role in covering the epithelial defects caused by the rupture of the epithelium and prolapse of connective tissue in nasal polyps.

Acute transverse myelitis after thoracic epidural anesthesia and analgesia: should anesthesia and analgesia be blamed?

A 63-year-old man developed acute transverse myelitis (ATM) with a rapid progression of sensory and motor deficits and autonomic dysfunction 2 days after chest surgery. Thoracic epidural anesthesia/analgesia (TEA) had been administered in this case. Since the temporal and spatial relationships between TEA and ATM are so close, one may easily mistake the TEA as the cause. Therefore, we discuss here the differential diagnoses for cord damage after TEA and the characteristics of ATM, and suggest that it is unlikely that TEA is the cause of ATM in this case.

Tumor necrosis factor-alpha stimulates the expression of C-C chemokine ligand 2 gene in fibroblasts from the human nasal polyp through the pathways of mitogen-activated protein kinase.

BACKGROUND: Recruitment of macrophages is crucial to the pathogenesis of the nasal polyp (NP) because this disease is believed to be inflammation related. Information regarding the expression of C-C chemokine ligand 2 (CCL2), an essential modulator of monocyte chemotaxis in nasal polyp fibroblasts (NPFs), remains unavailable. In this study, the effects of tumor necrosis factor (TNF)-a on CCL2 expression in NPFs and the signaling pathway involved were investigated. METHODS: Primary cultures of NPFs were established from NPs. The expressions of CCL2, c-Fos, and c-Jun mRNAs in NPF after TNF-a stimulation were detected by Northern blot. Western blot was used to examine the activation of mitogen-activated protein kinase (MAPK) signaling pathways. Activator protein (AP) 1/DNA interactions were evaluated by electrophoretic mobility shift assay (EMSA). RESULTS: Northern blot showed that TNF-alpha stimulated CCL2 gene expression in NPFs. Significant increase of B-Raf, phosphorated MAPK including mitogen-activated ERK-activate kinase (MEK)1/2, extracellular signal-related kinase 1/2, and p38 were detected by Western blot. c-Fos and c-Jun mRNAs were induced by TNF-alpha, and PD98059 (MEK inhibitor) and SB203580 (p38 inhibitor) abolished the up-regulation of c-Fos. EMSA revealed that TNF-a increased AP-1/DNA binding, and PD98059 and SB203580 attenuated this reaction, possibly via reducing c-Fos synthesis. PD98059 and curcunmin (AP-1 inhibitor) markedly suppressed the TNF-alpha-induced CCL2 expression, whereas the effect of SB203580 was less noted. CONCLUSION: TNF-alpha induces CCL2 transcription in NPFs. B-Raf/MEK/ERK signaling cascade and to a less extent the p38 pathway are responsible for c-Fos activation and the subsequent AP-1/DNA interaction leading to CCL2 expression.

A rare complication of functional endoscopic sinus surgery: maxillary atelectasis-induced spontaneous enophthalmos.

BACKGROUND: The first case report of spontaneous enophthalmos due to maxillary atelectasis as a late complication of FESS is presented. METHODS: Chart review of a 24-year-old male who developed a left progressive enophthalmos within three months post bilateral functional endoscopic sinus surgery. RESULTS: The preoperative computed tomography showed a normal left maxillary sinus. The postoperative computed tomography revealed a left maxillary atelectasis with a descending orbital floor. The subject received revised endoscopic sinus surgery and his enophthalmos was stable without further progression after the operation. CONCLUSIONS: This may have been caused by an ostium occlusion with retention of secretions inducing sinus inflammation, osteolytic activity, and osseous remodeling of the sinus walls. A negative pressure may develop. When the pressure gradient exceeds the sinus wall tension, maxillary atelectasis and enophthalmos occur. Prevention of this complication of FESS should include making a patent naso-antral window, minimizing mucosal trauma, and careful postoperative sinoscopic treatment. A "functional" sinus is the goal.