Galanin plays a role in the conditioning lesion effect in sensory neurons

Sensory neurons show enhanced neurite outgrowth in vivo and in vitro following a conditioning lesion. Previous studies have shown that these effects are dependent on two members of the gp130 family of cytokines, leukemia inhibitory factor and interleukin-6. Here, we asked whether galanin, a neuropeptide induced by these cytokines, plays a role in the conditioning lesion response. Following a conditioning lesion, neurite outgrowth in culture was reduced in sensory neurons from galanin -/- mice compared with those from wild type controls. In neurons from wild type mice, the length of the longest neurite was increased 2.4-fold after a conditioning lesion, compared with 1.8-fold in neurons from knockout animals. The results indicate that the induction of galanin plays an important role in triggering the conditioning lesion response.     

膝关节半月板和冠状韧带的解剖学研究及其临床意义

目的：解剖观察膝关节冠状韧带的结构特点,为解除半月板滑动障碍松解膝冠状韧带提供解剖学基础.方法：解剖观察成尸膝关节标本32侧,观测胫骨髁与半月板及膝冠状韧带的形态、长宽和厚度.结果：（1）外侧半月板向前滑动（5.6±1.3）mm,向后滑动（8.7±1.7）mm;内侧半月板向前滑动（5.5±1.4）mm,向后滑动（7.4±1.8）mm.（2）外侧膝冠状韧带周长（87.2±9.6）mm,上下宽（15.4±3.0）mm,韧带厚（0.9±0.3）mm.（3）内侧膝冠状韧带周长（91.9±7.9）mm,上下宽（15.9±3.2）mm,韧带厚（0.8±0.2）mm.（4）外侧膝冠状韧带前外侧微创进刀点,在膝关节外侧中点向前（26.4±3.7）mm范围内,膝关节前正中点向外（20.2±5.8）mm范围内不宜进刀,两者之间为前外侧进刀点.（5）内侧膝冠状韧带前内侧微创进刀点,在膝关节内侧中点处宽（7.0±2.0）mm范围内不宜进刀,由此处向前至髌韧带间为前内侧进刀点.另在膝关节内侧中点之后（29.1±4.5）mm,与半膜肌、半腱肌腱止点间为后内侧微创进刀点.结论：膝冠状韧带位于半月板外周缘连于胫骨内、外侧髁外周缘,从膝关节上述三个点进刀是微创切断松解膝冠状韧带的理想部位.     

Undetected chronic obstructive pulmonary disease and asthma in people over 50 years with persistent cough

Background

Chronic obstructive pulmonary disease (COPD) and asthma are underdiagnosed in primary care.

Aim

To determine how often COPD or asthma are present in middle-aged and older patients who consult their GP for persistent cough.

Design of study

A cross-sectional study in 353 patients older than 50 years, visiting their GP for persistent cough and not known to have COPD or asthma.

Setting

General practice in the Netherlands.

Method

All participants underwent extensive diagnostic work-up, including symptoms, signs, spirometry, and body plethysmography. All results were studied by an expert panel to diagnose or exclude COPD and/or asthma. The reproducibility of the panel diagnosis was assessed by calculation of Cohen''s κ statistic in a sample of 41 participants.

Results

Of the 353 participants, 102 (29%, 95% confidence interval [CI] = 24 to 34%) were diagnosed with COPD. In 14 of these 102 participants, both COPD and asthma were diagnosed (4%, 95% CI = 2 to 7%). Asthma (without COPD) was diagnosed in 23 (7%, 95% CI = 4 to 10%) participants. Mean duration of cough was 93 days (median 40 days). The reproducibility of the expert panel was good (Cohen''s κ = 0.90).

Conclusion

In patients aged over 50 years who consult their GP for persistent cough, undetected COPD or asthma is frequently present.     

Antibody-induced neutrophil activation as a trigger for transfusion-related acute lung injury in an ex vivo rat lung model

Transfusion-related acute lung injury (TRALI) is a hazardous complication of transfusion and has become the leading cause of transfusion-related death in the United States and United Kingdom. Although leukoagglutinating antibodies have been frequently shown to be associated with the syndrome, the mechanism by which they induce TRALI is poorly understood. Therefore, we reproduced TRALI in an ex vivo rat lung model. Our data demonstrate that TRALI induction by antileukocyte antibodies is dependent on the density of the cognate antigen but does not necessarily require leukoagglutinating properties of the antibody or the presence of complement proteins. Rather, antibody-mediated activation of neutrophils seems to initiate TRALI, a process that could be triggered by neutrophil stimulation with fMLP. Antibody-mediated neutrophil activation and subsequent release of reactive oxygen species may thus represent key events in the pathophysiologic cascade that leads to immune TRALI.     

Dual “motion-frozen heart” combining respiration and contraction compensation in clinical myocardial perfusion SPECT imaging

Objectives  This article assesses the effect of a new correction technique (“motion-frozen heart”) which compensates for the previously described nonuniform blurring of myocardial perfusion imaging (MPI) due to respiration motion or cardiac contraction. Methods  Respiratory and ECG-gated one-day ^99mTc-MIBI MPI studies performed in 48 patients were evaluated. MPI scans were acquired on a gamma camera supporting list-mode functionality synchronized with an external respiratory strap and an ECG device. Respiratory and cardiac-gated bins were generated using the acquired list file. Respiratory-gated bins were corrected for respiratory motion, followed by correction for cardiac contraction motion. In addition, cardiac contraction correction was applied to cardiac-gated bins uncorrected for respiratory motion. Bullseye maps were generated for uncorrected MPI studies, as well as following correction for respiratory motion, cardiac contraction, and both. The mean difference between each of the correction vs the uncorrected bullseye was calculated. Visual assessment of image quality, severity, and extent of the uncorrected perfusion images and following each of the corrections was performed. Results  Average motion due respiration was 7.0 ± 2.6 mm in the axial plane. The maximal score difference in segmental uptake greater than 10% was found in 2%, 15%, and 25% following respiratory correction, contraction correction, and dual corrections, respectively. Percent of scans classified with an excellent image quality was 13%, 21%, 42%, and 52% for the uncorrected images and following respiratory correction, contraction correction, and dual corrections, respectively. Conclusions  A technique that compensates for motion of the heart due to respiration and cardiac contraction in MPI-SPECT was evaluated. Compensating for both respiration and cardiac contraction had the greatest effect on perfusion images resulting in significantly improved image quality.