Research progress on the mechanism of chronic neuropathic pain.

Chronic neuropathic pain (CNP) refers to pain that lasts for more than three months due to a disease or an injury to the somatosensory nervous system. The incidence of CNP has been increasing in the world, causing it to become a global concern and patients often experience spontaneous pain, hyperalgesia, abnormal pain or even abnormal sensation as some of its main symptoms. In addition to serious pain and poor physical health, CNP also negatively affects patients' mental health, thus impacting the overall quality of their lives. The pathogenesis of CNP is not clear, but some studies have proved that central sensitization, peripheral sensitization, neuroinflammation, dysfunction in descending nociceptive modulatory systems, oxidative stress reaction, activation of glial cells and psychological factors play an important role in the occurrence and development of CNP. In this context, this article summarizes the current research progress on the mechanism of CNP to provide a basis for further research in preventing and treating the disease.

Complete Thoracoscopic Resection of Left Ventricular Myxoma - A Case Report.

Cardiac myxoma is a common cardiac tumor. Most are found in the left cardiac system, of which 75% of myxomas are located in the left atrium [Pinede 2001], and the origin of the left ventricle is relatively rare. Surgical resection is the most effective method for the treatment of myxoma, but because of the complex anatomy of the left ventricle, most of the reported cases are performed through the traditional median thoracotomy through the ascending aorta and vena cava to establish cardiopulmonary bypass. It is rare to establish cardiopulmonary bypass through the femoral artery and femoral vein to remove left ventricular myxoma under complete video-assisted thoracoscopy. This paper reports the surgical process and perioperative echocardiographic, magnetic resonance, radiological and pathological features of a completely thoracoscopic resection of left ventricular myxoma.

Effect of positive end-expiratory pressure ventilation on plasma nitric oxide, endothelin-1 and vascular celladhesion molecule-1 levels in patients undergoing uvulopalatopharyngoplasty.

BACKGROUND: During uvulopalatopharyngoplasty (UPPP), cardiovascular adverse events may occur which can be harmful to patients. OBJECTIVE: To evaluate the effect of the protective ventilation strategy on the function of vascular endothelial cells. METHODS: Forty obstructive apnea syndrome (OSA) patients who underwent uvulopalatopharyngoplasty (UPPP) were enrolled. Patients were randomly divided into the control group (group C, PEEP = 0 cm H2O) and PEEP group (group P, PEEP = 5 cm H2O). Each group (n= 20) received intermittent volume controlled ventilation (VCV) with tidal volume 6 ml/kg of the predicted body weight, I:E 1:2, rate titrated for ETCO2 35-45, FiO2 0.7. Blood from the radial artery was sampled for blood gas analysis at four time points: the fifth minute of inhaling pure oxygen (T0), after tracheal intubation (T1), at the end of the operation (T2), and 20 minutes after extubation (T3). Three ml of arterial blood was retained, preserved at -20∘C after serum isolation, and plasma nitric oxide (NO), endothelin-1 (ET-1) and vascular celladhesion molecule-1 (VCAM-1) levels were determined by enzyme linked immunosorbent assay (ELISA). RESULTS: Compared with group C, plasma ET-1 at T3 decreased in group P, and plasma NO levels at T2 and T3 increased (P< 0.05). Compared with samples collected at T0, plasma VCAM-1 levels at T1, T2 and T3 increased in group C, while plasma VCAM-1 levels at T2 and T3 decreased in group P (P< 0.05). Compared with group C, plasma VCAM-1 levels T2 and T3 decreased in group P (P< 0.05). CONCLUSIONS: Positive end-expiratory pressure (PEEP) ventilation has a protective effect on vascular endothelial cell function in patients during UPPP.

Intravenous acid fibroblast growth factor protects intestinal mucosal cells against ischemia-reperfusion injury via regulating Bcl-2/Bax expression.

AIM: To detect the effect of acid fibroblast growth factor (aFGF) on apoptosis and gene expression of bax and bcl-2 gene in rat intestine after ischemia/reperfusion (I/R) injury, and to explore the protective mechanisms of aFGF. METHODS: One hundred and eight Wistar rats were randomly divided into sham-operated control group (C) (n = 6), intestinal ischemia group (I) (n = 6), aFGF treatment group (A) (n = 48) and intestinal ischemia-reperfusion group (R) (n = 48). In group I, the animals were killed after 45 min of superior mesenteric artery (SMA) occlusion, while in groups R and A, the rats sustained 45 min of SMA occlusion and were then treated with normal saline and aFGF, respectively, sustained 15 min, 30 min, 1, 2, 6, 12, 24, or 48 h of reperfusion, respectively. In group C, SMA was separated, but without occlusion. Apoptosis in intestinal villus was determined with terminal deoxynucleotidyl transferase mediated dUTP-biotin nick-end labeling technique (TUNEL). Intestinal tissue samples were taken not only for detection of bax and bcl-2 gene expression by RT-PCR, but also for detection of bax and bcl-2 protein expression and distribution by immunohistochemical analysis. RESULTS: The rat survival rates in aFGF treated group were higher than group R (P<0.05) and the improvement of intestinal histological structures was observed at 2, 6, and 12 h after the reperfusion in group A compared with group R. The apoptotic rates were (41.17+/-3.49)%, (42.83+/-5.23)% and (53.33+/-6.92)% at 2, 6 and 12 h after reperfusion, respectively in group A, apparently less than those of group R at matched time points (50.67+/-6.95, 54.17+/-7.86, 64.33+/-6.47, respectively) (P<0.05). The bax gene transcription and translation were significantly decreased in group A vs group R, while mRNA and protein contents of Bcl-2 in group A were obviously higher than those in group R during 2-12 h period after reperfusion. CONCLUSION: The changes in histological structure and the increment of apoptotic rate indicated that the intestinal barrier was damaged after intestinal I/R injury, whilst intravenous aFGF could alleviate apoptosis induced by ischemia and reperfusion in rat intestinal tissues, in which genes of bax and bcl-2 might play important roles.