Surgical smoke: A hidden killer in the operating room.

Surgical smoke is a byproduct of aerosols containing several components produced by energy equipment. The characteristics of surgical smoke components produced by different types of tissues or using different kinds of energy devices vary. For example, the average diameter of smoke particles produced by electrocautery is smaller, and the possibility of viable cells and pathogens in surgical smoke produced by an ultrasonic knife is higher. According to the characteristics of its composition, surgical smoke may be an important risk factor affecting the health and safety of operating room staff and patients. The use of surgical masks, suction devices and portable smoke evacuation systems can reduce this risk to some extent. However, most operating room staff members do not implement corresponding measures to protect themselves. In this paper, the characteristics of surgical smoke and the research progress in protective measures are briefly reviewed.

Effect of purine-rich box1 on proliferation of fibroblasts.

Fibroblasts are pleomorphic cells that have a multi-directional effect on organ morphogenesis, tissue homeostasis, and immune response. In fibrotic diseases, fibroblasts synthesize large amounts of extracellular matrix (ECM), leading to scarring and organ failure. Purine-rich box1 (PU.1) is a specific transcription factor of hematopoietic cell and belongs to the E26 transformation specificity (ETS) family. Recently, it was found that the transcription factor PU.1 is an important regulatory factor of the profibrotic gene expression program. TGF-ß had been proved to play an important role in many ocular tissue fibrosis diseases, and up-regulated the expression of PU.1 in fibroblasts producing ECM in a Smad-3 dependent manner. We explore the effect of PU.1 on fibrosis of different ocular tissues from this perspective. This article reviews the role of PU.1 and its effects on fibrosis of ocular tissue and other tissues.

Atrial fibrillation increases sympathetic and parasympathetic neurons in the intrinsic cardiac nervous system.

BACKGROUND: Chronic atrial fibrillation (AF) leads to heterogeneous autonomic nerve innervation termed neural remodeling. The quantitative changes in neural density as a function of autonomic remodeling and its association with sustained AF has not been previously determined. METHOD AND RESULTS: Seven dogs (paced group) were chronically paced with electrodes sutured to the epicardium of left atrial appendages. Seven dogs (control animals) were not paced. All paced dogs developed sustained AF by 5 weeks of pacing. The fat pads on the atrial epicardium containing ganglionated plexuses (GP) were separated along with underlying myocardial tissue. Immunocytochemical techniques were used to identify the neurons immunoreactive to anti-tyrosine hydroxylase (TH) and anti-acetylcholine antibodies. After chronic AF, sympathetic and parasympathetic neurons in the atrial intrinsic cardiac ganglia increased significantly. In paced dogs, the density of sympathetic neurons was 3,022 ± 507 µm(2) /mm(2) in the right atrial GP (vs control P < 0.01), 8,571 ± 476 µm(2) /mm(2) in the ventral left atrial GP (vs control P < 0.0001)， 6,422 ± 464 µm(2) /mm(2) in the dorsal atrial GP (vs control P < 0.0001) and 5,392 ± 595 µm(2) /mm(2) in the inferior vena cava-inferior atrial GP (vs control P <0.0001), respectively. The density of parasympathetic neurons was 4,396 ± 877 µm(2) /mm(2) in the right atrial GP, 7,769 ± 465 µm(2) /mm(2) in the ventral left atrial GP， 7,016.47 ± 687 µm(2) /mm(2) in the dorsal atrial GP and 5,485 ± 554 µm(2) /mm(2) in the inferior vena cava-inferior atrial GP, respectively, which was higher than control cohorts in corresponding GP (P < 0.05). CONCLUSIONS: This study provides evidence for the remodeling in atrial intrinsic cardiac ganglia in the dogs with pacing induced AF. A significant increase of sympathetic and parasympathetic neurons was present in atrial intrinsic cardiac ganglia.