[Efficacy and safety of prophylactic intravenous administration of tranexamic acid in abdominal aorta balloon-assisted pelvic tumor surgery].

Objective: To investigate the efficacy and safety of prophylactic intravenous (IV) administration of tranexamic acid (TXA) in abdominal aorta balloon-assisted pelvic tumor surgery. Methods: The data of patients who underwent abdominal aorta balloon-assisted pelvic tumor surgery in Peking University People's Hospital from January 1, 2015 to December 31, 2019 were retrospectively collected. According to whether receiving the prophylactic use of TXA, the patients were divided into two groups: TXA group and control group. After propensity score matching based on age, gender and surgeon, 51 patients in TXA group and 51 patients in control group were allocated. The baseline, intraoperative and postoperative clinical data of the two groups were compared to explore the efficacy and safety of TXA. Results: A total of 525 cases undergoing abdominal aorta balloon-assisted pelvic surgery were enrolled from 2015 to 2019, of which 51 cases received prophylactic use of TXA, with a utilization rate of 9.7%. There were no significant differences in age [(40.7±15.1) years vs (38.2±14.5) years, P=0.393], gender (male: 51.0% vs 49.0%, P=0.843), body weight, body mass index (BMI), complications, American Society of Anesthesiologists (ASA) classification, hemoglobin, hemocrit (Hct), platelet, coagulation function-related indexes and tumor pathological types between the two groups (all P>0.05). Likewise, there were no significant differences in operation time, anesthesia time, cumulative time of balloon occlusion, intraoperative blood loss, intravenous fluid volume and blood transfusion volume between the two groups (all P>0.05). Additionally, there were no significant differences in postoperative ICU admission rate and length of hospital stay between the two groups (all P>0.05), and no venous thromboembolism (VTE) or death was reported. Compared with the control group, the rate of blood transfusion at 24 hours after operation in the TXA group was lower (41.2% vs 70.6%, P=0.003). The level of fibrinogen degradation products was lower [10.4 (6.1, 22.6) mg/L vs 13.2 (7.0, 24.7) mg/L], but the difference was not statistically significant (P=0.326). Conclusions: Prophylactic IV use of TXA does not reduce intraoperative bleeding in abdominal aorta balloon-assisted pelvic tumor surgery, but can decrease the rate of postoperative blood transfusion. No increased risk of postoperative TXA-related VTE was observed.

[Risk factors for hypothermia in patients undergoing general anesthesia in the postanesthesia care unit].

Objective: To investigate the incidence of hypothermia and its risk factors in patients after general anesthesia in the post anesthesia recovery unit (PACU). Methods: A total of 10 341 patients after general anesthesia in the PACU of Peking University People's Hospital from January to December 2019 were retrospectively reviewed. According to whether hypothermia occurred in the PACU, the patients were divided into hypothermia group and non-hypothermia group. After propensity score matching based on age and gender, 336 cases in hypothermia group and 336 cases in non-hypothermia group were finally included. The clinical characteristics of the two groups were compared, and the potential risk factors of hypothermia in the PACU were analyzed by multivariate logistic regression model. Results: The incidence of hypothermia in PACU was 3.3% (339/10 341). The age of hypothermia group was (54.1±17.1) years, with 156 males and 180 females; the age of non-hypothermia group was (53.1±16.0) years, with 156 males and 180 females. There was no statistically significant difference in age, gender, American Society of Anesthesiologists (ASA) classification and operation type between the two groups (all P>0.05). Compared with the non-hypothermia group, the body mass index (BMI) [(22.8±3.5) kg/m2 vs (24.7±4.2) kg/m2] and baseline body temperature [(36.3±0.5)℃ vs (36.5±0.5)℃] were lower, and anesthesia time [(4.4±1.6) h vs (3.2±1.5) h] and operation time [(3.1±1.4) h vs (2.1±1.3) h] were longer in hypothermia group. The amount of intraoperative bleeding, blood transfusion and intravenous fluid was larger in hypothermia group (all P<0.001). Multivariate logistic regression analysis showed that larger amount of blood loss (L) (OR=5.361, 95%CI: 2.863-10.037, P<0.001), prone position operation (OR=3.653, 95%CI: 2.104-6.342, P<0.001), longer anesthesia time (h) (OR=1.421, 95%CI: 1.227-1.646, P<0.001), and general anesthesia combined with regional nerve block (OR=1.708, 95%CI: 1.026-2.843, P=0.039) were independent risk factors of hypothermia in the PACU, and higher BMI (OR=0.849, 95%CI: 0.801-0.900, P<0.001) was an independent protective factor. Conclusions: The incidence of hypothermia in patients after general anesthesia in the PACU remains relatively high. Therefore, more attention should be paid to identify high-risk patients, and active preventive measures should be taken for the risk factors of hypothermia.

[Effects of stomatin protein expression on proliferation and apoptosis of lung cancer cells].

Objective: To investigate the effect of stomatin protein expression on the proliferation and apoptosis of lung cancer cells. Methods: The expressions of stomatin mRNA in human bronchial epithelial cells (HBE) and lung cancer cells (H520, A549, 95D, H460, Glc-82, 973 and H1299) were detected by Real-time PCR. Immunohistochemistry (IHC) was used to detect stomatin protein expression in 4 lung cancer tissue microarrays with 259 cases of lung cancer and adjacent normal tissues. After knocking down the expression of stomatin in A549 cells, the proliferation was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, the apoptosis was detected by flow cytometry, the expression levels of total protein kinase B (AKT) and phosphorylated AKT at Ser473 were detected by Western blot. BALB/c nude mice were used to detect the tumorigenic ability of stomatin downregulated A549 cells (3 mice) and control cells (3 mice), and the protein expressions of stomatin, Ki67 and CD31 in tumor tissues were detected by IHC. Results: The M (range) of stomatin mRNA expression level in H520, A549, 95D, H460, Glc-82, 973, H1299 and HBE cells were 2.71 (2.66), 3.55 (3.16), 0.26 (0.22), 2.08 (1.98), 0.87 (0.35), 1.72 (2.53), 1.10 (1.82) and 0.01 (0.02), respectively. The mRNA expression levels of stomatin in H520, A549 and H460 cells were higher than that of HBE cells (all P<0.05), whereas there was no statistical difference among 95D, Glc-82, 973, H1299 and HBE cells (all P>0.05). IHC of lung tissue microarrays showed that the positive rate of stomatin expression in human lung cancer tissues was 34.7% (90/259), which was significantly higher than that in adjacent normal tissues [1.9% (5/259)] (P<0.05). In stomatin positive lung cancer tissues, the M (IQR) of tumor size for lower stomatin expression tissues (67 cases) was [41.22 (2 761.50) cm], which was smaller than that of higher stomatin expression tissues [(23 cases, 57.98(1 333.50) cm) (P<0.05). After knocking down stomatin expression, the fourth day absorbance value of stomatin-downregulated A549 cells was 0.55±0.07, which was lower than that of control cells (0.79±0.16) (P=0.012). The proportion of early apoptotic cells of stomatin-downregulated A549 cells [8.83 (53.00)] was higher than that of control cells [4.17 (25.00)] (P=0.026). The Ser473 phosphorylated AKT protein expression level in stomatin-downregulated A549 cells was 0.68±0.16, which was decreased compared with control cells (1.16±0.39) (P<0.05). The M (IQR) of total AKT expression level in stomatin-downregulated A549 cells was 4.25 (17.00), without statistically significant difference from control cells [4.75 (19.00)] (P>0.05). After inoculation of stomatin-downregulated A549 cells in nude mice for 43 days, the tumor volume was (37.93±3.12) mm(3), which was significantly smaller than that of the control group [(454.04±32.39) mm(3)] (P<0.001). And the expression levels of stomatin, nuclear proliferation antigen Ki67, and platelet-endothelial cell adhesion molecule CD31 were 1.78±0.69, 5.19±3.84, and 10.77±1.67, respectively, which were all decreased compared with control group (17.52±8.76, 54.14±41.02, and 19.72±6.97, respectively) (all P<0.05). Conclusion: Stomatin promotes lung cancer cell proliferation and inhibits cell early apoptosis by regulating AKT signaling pathway.

Organotypic Spheroid Culture to Mimic Radiation-Induced Salivary Hypofunction.

Radiation treatment often leads to irreversible damage to normal salivary glands (SGs) because of their proximity to head and neck cancers. Optimization of the in vitro model of irradiation (IR)-induced SG damage is warranted to investigate pathophysiology and monitor treatment outcome. Here, we present an organotypic spheroid culture model to investigate the impact of IR on SGs and the mechanisms underlying IR-induced structural and functional changes. Human parotid epithelial cells were obtained from human parotid glands and plated on either plastic plates or Matrigel. A number of 3-dimensional (3D) spheroids were assembled on Matrigel. After IR at 10 and 20 Gy, morphologic changes in cells in 2D monolayers and 3D spheroids were observed. As the structural integrity of the 3D spheroids was destroyed by IR, the expression levels of salivary epithelial and structural proteins and genes decreased proportionally with radiation dosage. Furthermore, the spheroid culture allowed better measurement of functional alterations following IR relative to the monolayer culture, in which IR-inflicted spheroids exhibited a loss of acinar-specific cellular functions that enable Ca2+ influx or secretion of α-amylase in response to cholinergic or ß-adrenergic agonists. p53-mediated apoptotic cell death was observed under both culture conditions, and its downstream signals increased, such as p53 upregulated modulator of apoptosis (PUMA), Bax, cytochrome c, caspase 9, and caspase 3. These results suggest that the organotypic spheroid culture could provide a useful alternative model for exploration of radiobiology and mode of action of new therapies for prevention of radiation-induced salivary hypofunction.