Imaging of Facial Nerve With 3D-DESS-WE-MRI Before Parotidectomy: Impact on Surgical Outcomes

Objective@#The intra-parotid facial nerve (FN) can be visualized using three-dimensional double-echo steady-state waterexcitation sequence magnetic resonance imaging (3D-DESS-WE-MRI). However, the clinical impact of FN imaging using 3D-DESS-WE-MRI before parotidectomy has not yet been explored. We compared the clinical outcomes of parotidectomy in patients with and without preoperative 3D-DESS-WE-MRI. @*Materials and Methods@#This prospective, non-randomized, single-institution study included 296 adult patients who underwent parotidectomy for parotid tumors, excluding superficial and mobile tumors. Preoperative evaluation with 3D-DESS-WE-MRI was performed in 122 patients, and not performed in 174 patients. FN visibility and tumor location relative to FN on 3D-DESSWE-MRI were evaluated in 120 patients. Rates of FN palsy (FNP) and operation times were compared between patients with and without 3D-DESS-WE-MRI; propensity score matching (PSM) and inverse probability of treatment weighting (IPTW) were used to adjust for surgical and tumor factors. @*Results@#The main trunk, temporofacial branch, and cervicofacial branch of the intra-parotid FN were identified using 3D-DESSWE-MRI in approximately 97.5% (117/120), 44.2% (53/120), and 25.0% (30/120) of cases, respectively. The tumor location relative to FN, as assessed on magnetic resonance imaging, concurred with surgical findings in 90.8% (109/120) of cases. Rates of temporary and permanent FNP did not vary between patients with and without 3D-DESS-WE-MRI according to PSM (odds ratio, 2.29 [95% confidence interval {CI} 0.64–8.25] and 2.02 [95% CI: 0.32–12.90], respectively) and IPTW (odds ratio, 1.76 [95% CI: 0.19–16.75] and 1.94 [95% CI: 0.20–18.49], respectively). Conversely, operation time for surgical identification of FN was significantly shorter with 3D-DESS-WE-MRI (median, 25 vs. 35 min for PSM and 25 vs. 30 min for IPTW, P < 0.001). @*Conclusion@#Preoperative FN imaging with 3D-DESS-WE-MRI facilitated anatomical identification of FN and its relationship to the tumor during parotidectomy. This modality reduced operation time for FN identification, but did not significantly affect postoperative FNP rates.

Serum amyloid A inhibits RANKL-induced osteoclast formation

When mouse bone marrow-derived macrophages were stimulated with serum amyloid A (SAA), which is a major acute-phase protein, there was strong inhibition of osteoclast formation induced by the receptor activator of nuclear factor kappaB ligand. SAA not only markedly blocked the expression of several osteoclast-associated genes (TNF receptor-associated factor 6 and osteoclast-associated receptor) but also strongly induced the expression of negative regulators (MafB and interferon regulatory factor 8). Moreover, SAA decreased c-fms expression on the cell surface via shedding of the c-fms extracellular domain. SAA also restrained the fusion of osteoclast precursors by blocking intracellular ATP release. This inhibitory response of SAA is not mediated by the well-known SAA receptors (formyl peptide receptor 2, Toll-like receptor 2 (TLR2) or TLR4). These findings provide insight into a novel inhibitory role of SAA in osteoclastogenesis and suggest that SAA is an important endogenous modulator that regulates bone homeostasis.

A pertussis toxin sensitive G-protein-independent pathway is involved in serum amyloid A-induced formyl peptide receptor 2-mediated CCL2 production

Serum amyloid A (SAA) induced CCL2 production via a pertussis toxin (PTX)-insensitive pathway in human umbilical vein endothelial cells (HUVECs). SAA induced the activation of three MAPKs (ERK, p38 MAPK, and JNK), which were completely inhibited by knock-down of formyl peptide receptor 2 (FPR2). Inhibition of p38 MAPK and JNK by their specific inhibitors (SB203580 and SP600125), or inhibition by a dominant negative mutant of p38 MAPK dramatically decreased SAA-induced CCL2 production. Inactivation of Gi protein(s) by PTX inhibited the activation of SAA-induced ERK, but not p38 MAPK or JNK. The results indicate that SAA stimulates FPR2-mediated activation of p38 MAPK and JNK, which are independent of a PTX-sensitive G-protein and are essential for SAA-induced CCL2 production.

Association between Smoking Status and Insulin Resistance in Apparently Healthy Korean Men / 가정의학회지

BACKGROUND: Several studies have suggested that smoking may cause insulin resistance. However, the association between smoking and insulin resistance is still controversial. The purpose of this study was to investigate the association between smoking status and insulin resistance in Korean nondiabetic male population. METHODS: A total of 5,969 men, aged > 20 years were recruited from those who visited the Health Promotion Center, Samsung Medical Center between 2005 and 2006. All subjects were divided into three categories: on-smokers (n = 2,594), ex-smokers (n = 1,580), and current-smokers (n = 1,795). Fasting values for glucose and insulin were used to estimate insulin resistance by HOMA (homeostasis model assessment). An independent association between smoking status and HOMA-IR (homeostasis model assessment of insulin resistance) was assessed after adjustment for factors influencing insulin sensitivity such as age, exercise, alcohol, body mass index, abdominal circumference, and blood pressure. RESULTS: HOMA-IR was signifi cantly higher in ex-smokers and current-smokers than in non-smokers (2.09 +/- 0.94 vs. 2.04 +/- 0.90, 1.96 +/- 0.86, P or = 40 pack-years smokers than in non-smokers CONCLUSION: Based on HOMA-IR, previous-smoking and chronic smoking were significantly associated with insulin resistance in apparently healthy Korean nondiabetic men.

Association between Clozapine-Induced Weight Gain and Serotonin 5-HT2C Receptor Gene Polymorphism in Patients with Schizophrenia / 대한정신약물학회지

OBJECTIVE: Weight gain is one of the troublesome adverse reaction to clozapine treatment. This problem can lead to poor adherence to treatment. Clozapine-induced weight gain may be associated with genetic predisposition. Recent studies have shown that a polymorphism of the promoter region of the serotonin 5-HT2C receptor gene is associated with antipsychotic-induced weight gain. This study is to investigate the association of clozapine-induced weight gain with -759C/T polymorphism of serotonin 5-HT2C receptor promoter gene in schizophrenic patients. METHODS: Fifty three patients with schizophrenia were included in this study. The subjects were divided into two groups according to body weight change between the start and 10 weeks of clozapine. The cutoff level of weight change is 5% increase of initial body weight. Genotypes of -759C/T polymorphism were identified from AciI-digested fragments of two-primer products amplified by polymerase chain reaction corresponding to -885 to -634 of the serotonin 5-HT2C receptor gene promoter region on chromosome X. RESULTS: There were no differences of baseline variables between patient groups with and without weight gain. 4 of 32 male patients and 6 of 21 female patients had -759T allele, respectively. The authors found that patients with -759T allele had tendency to show less weight gain than those without this allele. CONCLUSION: These findings suggest that clozapine- induced weight gain may be associated with genetic predisposition in schizophrenic patients.

Echocardiographic Measurement of Systolic Time Intervals in Normal Adults and the Patients with Dilated Cardiomyopathy

The systolic time intervals were measured in 25 normal controls and 23 patients with dilated cardiomyopathy by simultaneous recording of the aortic valve echocardiogram and ECG. These values were compared to corresponding ones obtained from the method using simultaneously recorded phonocardiogram, ECG, and indirect carotid pulse tracings. And we assessed left ventricular function by systolic time intervals in dilated cardiomyopathy. The results were as followings. 1) High degree of correlation(r> or =0.94) was found between the two methods for each intervals, EMS, LVET, PEP, PEP/LVET. 2) In normal controls, PEP/LVET obtained from echocardiographic measurement was 0.31+/-0.02. 3) In the patients with dilated cardiomyopathy, PEP/LVET(0.59+/-0.13) was significantly higher(p<0.001), PEP index was longer(p<0.05), LVET index was shorter(p<0.05) than in normal controls.