Is snoring intensity responsible for the sleep partner’s poor quality of sleep?

Purpose

This study aimed to determine if the intensity of breathing noise (including snoring) and/or the presence of abnormal breathing events (ABE) are factors that trigger arousal/awakening of a snorer??s bed partner.

Methods

We conducted a prospective multicenter study investigating couples where the male had a chronic disturbing snoring. We simultaneously recorded the male??s respiration and snoring and the female?? sleep. We counted the number of arousals and awakenings during N2 sleep and randomly took nine of each. Then, for periods before, during, and after each arousal and awakening, we observed on the respiratory tracings what was happening in terms of breathing noise intensity and presence/absence of snoring and/or ABE.

Results

Thirteen couples were analyzed. The intensity of breathing noise and the presence/absence of snoring and/or ABE were comparable before and at initiation of arousal/awakening and between arousal and awakening. However, breathing volume intensity was lower and the presence of snoring and/or ABE was less frequent when the bed partner returned back to sleep from awakening compared to the other periods (p always <0.001).

Conclusions

The intensity of breathing noise or the presence of ABE does not seem to be essential to trigger an arousal or an awakening. However, the persistence of noise or events may prolong the duration of wakefulness during the sleep period and could be one factor that explains the bothersome snoring.     

The Sequential Relation Between Changes in Catastrophizing and Changes in Posttraumatic Stress Disorder Symptom Severity

Catastrophizing has been discussed as a cognitive precursor to the emergence of posttraumatic stress disorder (PTSD) symptoms following the experience of stressful events. Implicit in cognitive models of PTSD is that treatment-related reductions in catastrophizing should yield reductions in PTSD symptoms. The tenability of this prediction has yet to be tested. The present study investigated the sequential relation between changes in a specific form of catastrophizing—symptom catastrophizing—and changes in PTSD symptom severity in a sample of 73 work-disabled individuals enrolled in a 10-week behavioral activation intervention. Measures of symptom catastrophizing and PTSD symptom severity were completed at pre-, mid-, and posttreatment assessment points. Cross-sectional analyses of pretreatment data revealed that symptom catastrophizing accounted for significant variance in PTSD symptom severity, β = .40, p < .001, sr = .28 (medium effect size), even when controlling for known correlates of symptom catastrophizing, such as pain and depression. Significant reductions in symptom catastrophizing and PTSD symptoms were observed during treatment, with large effect sizes, ds = 1.42 and 0.94, respectively, ps < .001. Cross-lagged analyses revealed that early change in symptom catastrophizing predicted later change in PTSD symptoms; early changes in PTSD symptom severity did not predict later change in symptom catastrophizing. These findings are consistent with the conceptual models that posit a causal relation between catastrophizing and PTSD symptom severity. The clinical implications of the findings are discussed.     

巨噬细胞迁移抑制因子通过CC趋化因子配体2诱导巨噬细胞聚集

巨噬细胞迁移抑制因子最初是由于能抑制体外巨噬细胞随机迁移而被发现,现在它作为一种重要的调节因子参与一系列炎症性疾病过程.我们最近发现,巨噬细胞迁移抑制因子的缺失使一些由炎症介质诱发的白细胞-内皮细胞相互作用减弱,提示巨噬细胞迁移抑制因子在炎症反应中起作用的机制之一是促进白细胞聚集.……     

In vitro killing of neuroblastoma cells by neutrophils derived from granulocyte colony-stimulating factor-treated cancer patients using an anti-disialoganglioside/anti-Fc gamma RI bispecific antibody

Neutrophils isolated from cancer patients treated with granulocyte colony-stimulating factor (G-CSF) express high levels of Fc gamma RI. They exhibited an efficient killing of GD2+ neuroblastoma cells in the presence of an antidisialoganglioside (GD2) mouse monoclonal antibody (MoAb; 7A4, IgG3 kappa). However, this cytotoxicity was totally blocked by human monomeric IgG. In contrast, a bispecific antibody (7A4 bis 22/MDX-260), prepared by chemically linking an F(ab') fragment of 7A4 with an F(ab') fragment of an anti-Fc gamma RI MoAb, 22, which binds outside the Fc binding domain, triggered antibody-dependent cell cytotoxicity, even when neutrophils were preincubated with human monomeric IgG. F(ab')2 22 MoAb abrogated the MDX-260 killing without affecting that of 7A4. The 3G8 MoAb, directed against the Fc gamma RIII binding site, did not inhibit the cytotoxicity induced by either antibody. Thus, these results indicate that G-CSF-activated neutrophils exert their cytotoxic effect against neuroblastoma cells through Fc gamma RI and not Fc gamma RIII, and that the saturation of the high affinity Fc gamma RI by monomeric IgG can be overcome by the use of bispecific antibodies binding epitopes outside the IgG Fc gamma RI binding site. A combined administration of such bispecific antibodies and G-CSF may be, therefore, an efficient therapeutic approach to trigger tumor lysis by cytotoxic neutrophils in vivo.     

Large ventricular aneurysms occurring after myocardial infarction.

We have studied 33 patients with a large ventricular aneurysm complicating an anterior myocardial infarction. The features of myocardial infarction progressing towards an aneurysm were no previous history of coronary disease, severe infarction as shown by the severity of pain and the presence of pericardial rub and heart failure, and large increase in serum levels of cardiac enzymes. A large aneurysm usually follows a large infarction resulting from the total or partial occlusion of the left anterior descending artery, which is involved alone in about half the patients and is associated with lesions of the circumflex and right coronary arteries in the other half. In most cases, standard radiography showed an abnormal cardiac configuration, but in 7 patients (21%) there was no radiological evidence of aneurysm. ST segment elevation (mean 2.7 mm) was reported in all subjects but one. Heart failure was present in most patients and was an indication for surgical treatment in one-third of the patients. A large aneurysm was not a contraindication to operation even when at angiography the aneurysm seemed to occupy almost all the left ventricle. Twenty-one patients were operated upon for resection of the aneurysm with a mortality rate of 14 per cent.