We have investigated the change of atomic and electronic structures of fluorinated single-walled carbon nanotubes (SWCNTs) using x-ray photoemission spectroscopy (XPS), electrical resistivity measurements, and transmission electron microscopy (TEM). The fluorine content increases with increasing reaction temperature up to 300 °C. XPS indicated that the fluorinated SWCNT reveals an ionic-bonding character at low concentration and covalent-bonding character at high concentration. The resistivity increases with reaction temperatures, resulting from the band gap enlargement at high fluorine concentration. It is also observed from TEM that the fluorination at reaction temperature above 250 °C leads to the disintegration of the CNT structures and formation of various phases such as multiwall-like and turbostratic morphologies.

MUC5B is a major mucin of the human respiratory tract, and it is not clear how MUC5B expression is regulated in various airway diseases. The goal of this study was to determine the mechanisms by which 17beta-estradiol induces MUC5B gene expression in airway epithelial cells. It was found that E2, a sex hormone, stimulates MUC5B gene overexpression by interaction with estrogen receptor alpha (ERalpha) and by acting through extracellular signal-regulated kinase 1/2 (ERK1/2)-mitogen-activated protein kinase (MAPK). Pretreatment with ER antagonist ICI 182,780 blocked both E2-induced ERK1/2-MAPK activation and MUC5B gene expression. It was also found that the activation of p90 ribosomal S 6 protein kinase 1 (RSK1), cAMP-response element-binding protein (CREB), and cAMP-response element (CRE) (-956 region of the MUC5B promoter)-responsive signaling cascades via ERK1/2 MAPK are crucial aspects of the intracellular mechanisms that mediate MUC5B gene expression. Taken together, these studies give additional insights into the molecular mechanism of hormone-induced MUC5B gene expression and enhance our understanding of abnormal mucin secretion in response to hormonal imbalances.

We suggest that LL-37 is one of the antimicrobial peptides found in human nasal mucosa and that it participates in the innate immune system of the nasal mucosa.

PurposeThe aim of this study was to determine the diagnostic value of three screening questionnaires in identifying Korean patients at high risk for obstructive sleep apnea (OSA) in a sleep clinic setting in Korea.Materials and MethodsData were collected from 592 adult patients with suspected OSA who visited a sleep center. All patients completed the Sleep Apnea of Sleep Disorder Questionnaire (SA-SDQ), the Berlin questionnaire, and the STOP-Bang questionnaire. Estimated OSA risk was compared to a diagnosis of OSA. The sensitivity, specificity, positive predictive value, and negative predictive value were calculated for each questionnaire.ResultsThe prevalence of OSA was 83.6% using an apnea-hypopnea index (AHI) ≥5/h and 58.4% for an AHI ≥15/h. The STOP-Bang questionnaire had a high sensitivity (97% for AHI ≥5/h, 98% for AHI ≥15/h), but the specificity was low (19% and 11%, respectively). In contrast, the sensitivity of the SA-SDQ was not high enough (68% for AHI ≥5/h, 74% for AHI ≥15/h) to be useful in a clinical setting, whereas the specificity was relatively good (66% and 61%, respectively). The sensitivity and specificity values of the Berlin questionnaire fell between those of the STOP-Bang questionnaire and the SA-SDQ.ConclusionThe STOP-Bang questionnaire may be useful for screening OSA in a sleep clinic setting, but its specificity is lower than the acceptable level for this purpose. A new screening questionnaire with a high sensitivity and acceptable specificity is therefore needed in a sleep clinic setting.

Oxaliplatin is a widely used chemotherapy agent, but induces serious peripheral neuropathy. Duloxetine is a dual reuptake inhibitor of serotonin and norepinephrine, and is shown to be effective against pain. However, whether and how duloxetine can attenuate oxaliplatin-induced allodynia in rodents is not clearly understood. A single injection of oxaliplatin (6 mg/kg, intraperitoneal; i.p.) induced a cold and mechanical allodynia, which was assessed by acetone and von Frey filament tests, respectively. When significant allodynic signs were observed, three different doses of duloxetine (10, 30, and 60 mg/kg, i.p.) were injected. Administration of 30 and 60 mg/kg of duloxetine significantly reduced the allodynia, whereas 10 mg/kg did not. By using an in vivo extracellular recording method, we further confirmed that 30 mg/kg of duloxetine could significantly inhibit the hyperexcitability of spinal wide dynamic range (WDR) cells. The anti-allodynic effect of duloxetine was completely blocked by an intrathecal injection of phentolamine (non-selective α-adrenergic receptor antagonist, 20 μg), or prazosin (α1-adrenergic receptor antagonists, 10 μg); however, idazoxan (α2-adrenergic receptor antagonist, 10 μg) did not block it. In conclusion, we suggest that duloxetine may have an effective protective action against oxaliplatin-induced neuropathic pain and spinal hyperexcitability, which is mediated by spinal α1-adrenergic receptors.

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