The risk of cardiovascular disease is known to be increased in obstructive sleep apnea syndrome (OSAS). Its mechanism can be explained by the observation that the sympathetic tone increases due to repetitive apneas accompanied by hypoxias and arousals during sleep. Heart rate variability (HRV) representing cardiac autonomic function is mediated by respiratory sinus arrhythmia, baroreflex-related fluctuation, and thermoregulation-related fluctuation. We evaluated the heart rate variability of OSAS patients during night to assess their relationship with the severity of the symptoms. We studied overnight polysomnographies of 59 male untreated OSAS patients with moderate to severe symptoms (mean age 45.4± 11.7 yr, apnea-hypopnea index [AHI]=43.2±23.4 events per hour, and AHI >15). Moderate (mean age 47.1±9.4 yr, AHI=15-30, n=22) and severe (mean age 44.5±12.9 yr, AHI >30, n=37) OSAS patients were compared for the indices derived from time and frequency domain analysis of HRV, AHI, oxygen desaturation event index (ODI), arousal index (ArI), and sleep parameters. As a result, the severe OSAS group showed higher mean powers of total frequency (TF) (p=0.012), very low frequency (VLF) (p= 0.038), and low frequency (LF) (p=0.002) than the moderate OSAS group. The LF/HF ratio (p=0.005) was higher in the severe group compared to that of the moderate group. On the time domain analysis, the HRV triangular index (p=0.026) of severe OSAS group was significantly higher. AHI was correlated best with the LF/HF ratio (rp=0.610, p<0.001) of all the HRV indices. According to the results, the frequency domain indices tended to reveal the difference between the groups better than time domain indices. Especially the LF/HF ratio was thought to be the most useful parameter to estimate the degree of AHI in OSAS patients.

Frontal recess pneumatization patterns differ in the Korean and Caucasian adult populations. Because corresponding differences in skull base length were not identified, these differences seem likely to reflect other factors. Such information has clinical significance for frontal recess surgery in these patient populations.

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Colon and urinary tract involvement in LE patients may be associated with the recurrence of LE.

This study shows good agreement and correlation between SPT with individual specific IgE test and multiple allergen simultaneous test on a majority of the tested allergens for patients with chronic rhinitis. Comparing the two in vitro tests, individual specific IgE test agrees with SPT better than multiple allergen simultaneous test.

Basophils are rare, circulating granulocytes proposed to be involved in T helper (TH) type 2 immunity, mainly through secretion of interleukin (IL)-4. In addition to IL-4, basophils produce IL-6 and tumor necrosis factor (TNF)-α in response to immunoglobulin E (IgE) crosslinking. Differentiation of TH17 cells requires IL-6 and transforming growth factor (TGF)-β, but whether basophils play a significant role in TH17 induction is unknown. Here we show a role for basophils in TH17 cell development by using in vitro T cell differentiation and in vivo TH17-mediated inflammation models. Bone marrow derived-basophils (BMBs) and splenic basophils produce significant amounts of IL-6 as well as IL-4 following stimulation with IgE crosslink or cholera toxin (CT). In addition, through IL-6 secretion, BMBs cooperate with dendritic cells to promote TH17 cell differentiation. In the TH17 lung inflammation model, basophils are recruited to the inflamed lungs following CT challenge, and TH17 responses are significantly reduced in the absence of basophils or IL-6. Furthermore, reconstitution with wild-type, but not IL-6-deficient, basophils restored CT-mediated lung inflammation. Lastly, basophil-deficient mice showed reduced phenotypes of TH17-dependent experimental autoimmune encephalomyelitis. Therefore, our results indicate that basophils are an important inducer of TH17 cell differentiation, which is dependent on IL-6 secretion.

Our results indicate that innate immune responses characterized by the production of IL-33, TSLP, and IL-5 are associated with the development of EPE in PSP by an ILC2-dependent and Th2-independent mechanism.