AIM: To provide a basis for appraising quality standard of Baohe Pill (Fructus Gataegi, Massa medicata fermentata, Rhizoma pinelliae, Pericapium citr reticulatae, Fructus forsythiae, Semen raphani, Fructus Mordei germinatus, Poria) inclusive of its RP-HPLC fingerprint chromatogram. METHODS: The chromatographic column was Kromasil C_ 18 column (4.6 mm?250 mm, i.d, 5-?m particle size). The mobile phase was 0.5% solution of ammonium dihydrogen phosphate (NH_4H_2PO_4), and the flow rate was 0.8 mL/min with UV detector at 214 nm. RESULTS: The RP-HPLC fingerprint chromatogram of Baohe Pill was established. In the experiment, for precision and repeatability, the RSD of each area of common peak was less than 3%. CONCLUSION: This method is simple and reliable.

Objective To investigate patients'cognition of social status of physicians and nurses,and find out the influence factors of it. Methods 286 patients were asked to finish serf-designed scale of social status of physicians and nurses. Results Most patients thought social status of nurses was above the middle level in our country.The majority of patients considered doctors " social status was higher than nurses'(approval rate 75.5% ).The nurses'economic treatment was lower than doctors' (approval rate 62.2% );About 14 items among 15 items on the occupational reputation,doctors" occupation cognition rate was higher than the nurses,the nurses' occupation cognition rate was higher than the doctors' occupation only on the item of labor intensity.The influence factors of the social status differences between physicians and nurses were economic treatment,the important degree of occupation,the professional authority,the requirement of specialized skills for workers. Conclusions To study the influence factors of the social status difference of physicians and nurses is beneficial for us to study the strategy of improving the nurses' social status in order to fulfil the viewpoint of science development,keep nurse troops developing continuously and set up the harmonious physician-nurse relationship.

Objective To investigate the effects of CYP3A5~* 3 genetic polymorphism on analgesia with fentanyl. Methods One hundred and eighty ASA Ⅰ or Ⅱ patients, aged 20-50 yr, Hart nationality, Henan province, scheduled for elective abdominal total hysterectomy or myomectomy under general anesthesia, were enrolled in this study. The polymorphic sites of the CYP3A5~* 3 allele were analyzed by polymerase chain reaction-restriction fragment length polymorphism. The patients were assigned to one of 3 groups according to their genotypes: wild homozygote group, mutation heterozygote group and mutation homozygote group. Midazolam, remifentanyl, propofol and succinylcholine were used for induction of anesthesia. The patients were mechanically ventilated after tracheal intubation. Remifentanyl, propofol and atracurium were given iv for maintenance of anesthesia. The pain was assessed with visual analog scale (VAS) after consciousness was regained. When VAS score > 3, the patients were given fentanyl 20 μg every 5 min until VAS score was decreased to ≤3 and then patient-controlled intravenous analgesia (PCIA) with fentanyl was started. The background infusion rate of fentanyl 1.0 mg and droperidol 5 mg (in 100 ml normal saline) was 0.5 ml/h. The PCIA pump was programmed to give a 2 ml bolus of fentanyl solution with a 5 min lockout interval, 7 time successful delivery per hour and maximum dosage 145 μg/h, and VAS score was maintained less than 3. The amount of fentanyl used within 24 h after surgery was recorded. Results No significant difference was detected in the fentanyl consumption in the 24 h during PCIA among the 3 groups (P> 0.05). Conclusion The genetic polymorphism CYP3 A5~* 3 is not the factor contributing to the individual variation in the patient's response to analgesia with fentanyl.

Objective:The current study aimed to evaluate the possible protective effects of N-acetylcysteine (NAC) against Indum-tin oxide (ITO) nanoparticle (Nano-ITO) -induced pulmonary alveolar proteinosis (PAP) in rats, especially via modulation of nuclear factor kappa B (NF-κB) signaling.Methods:In October 2019, 50 adult male Sprague-Dawley rats were randomly allocated into five groups (10 rats each) as follows: blank control group, saline control group, NAC control group (200 mg/kg), Nano-ITO group (receiving a repeated intratracheal dose of 6 mg/kg Nano-ITO) and NAC intervention group (pre-treated intraperitoneally with 200 mg/kg NAC 1.5 h before the administration of an intratracheal dose of 6 mg/kg Nano-ITO). The rats were exposed twice a week for 12 weeks. Rats were then euthanized under anesthesia, and their lungs were removed for histopathological and immunohistochemical analysis. The comparison of indicators reflecting oxidative stress and pulmonary inflammation among groups was conducted using one-way analysis of variance (ANOVA) and Bonferroni's test. The effect of NAC on Nano-ITO induced NF-κB signaling pathway in rats was analyzed.Results:Histopathological examination of Nano-ITO exposed rats revealed diffuse alveolar damage, including PAP, cholesterol crystals, alveolar fibrosis, pulmonary fibrosis, and alveolar emphysema. Immunohistochemical results of Nano-ITO exposed rats showed strong positive for nuclear factor κB p65 (NF-κB p65) and nuclear factor Kappa B inhibitory factor kinase (IKK-β) and weak positive for nuclear factor κB inhibitory protein α (IκB-α) in the nuclei of bronchiolar and alveolar epithelial cells. Compared with blank control group, saline control group and NAC control group, the level of total protein (TP) in bronchoalveolar lavage fluid of rats in Nano-ITO group was significantly increased ( P<0.05), and the activities of lactate dehydrogenase (LDH), superoxide dismutase (SOD), malondialdehyde (MDA) content and total antioxidant capacity (T-AOC) were significantly increased ( P<0.05), the levels of proinflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) were significantly increased ( P<0.05), and the levels of NF-κB p65, IKK-β, inducible nitric oxide synthase (iNOS) and reactive oxygen species (ROS) in lung tissue were significantly increased ( P<0.05). Compared with Nano-ITO group, the levels of TP, T-AOC, MDA and TNF-α in bronchoalveolar lavage fluid of rats in NAC intervention group were significantly decreased ( P<0.05), and the levels of NF-κB p65 and ROS in lung tissue were significantly decreased (P<0.05). Western blot results showed that compared with the control groups, the protein expressions of NF-κB p65 and IKK-β in the lung tissue of Nano-ITO group were increased, while the protein expression of IκB-α was decreased ( P<0.05). Compared with Nano-ITO group, the protein expressions of NF-κB p65 and IKK-β in lung tissue of rats in NAC intervention group were decreased, while the protein expression of IκB-α was increased ( P<0.05) . Conclusion:The study demonstrated that Nano-ITO might induce pulmonary toxicity through the activation of NF-κB signaling pathway, and NAC could antagonize the pulmonary toxicity of Nano-ITO by inhibiting the NF-κB signaling pathway.

Objective:The current study aimed to evaluate the possible protective effects of N-acetylcysteine (NAC) against Indum-tin oxide (ITO) nanoparticle (Nano-ITO) -induced pulmonary alveolar proteinosis (PAP) in rats, especially via modulation of nuclear factor kappa B (NF-κB) signaling.Methods:In October 2019, 50 adult male Sprague-Dawley rats were randomly allocated into five groups (10 rats each) as follows: blank control group, saline control group, NAC control group (200 mg/kg), Nano-ITO group (receiving a repeated intratracheal dose of 6 mg/kg Nano-ITO) and NAC intervention group (pre-treated intraperitoneally with 200 mg/kg NAC 1.5 h before the administration of an intratracheal dose of 6 mg/kg Nano-ITO). The rats were exposed twice a week for 12 weeks. Rats were then euthanized under anesthesia, and their lungs were removed for histopathological and immunohistochemical analysis. The comparison of indicators reflecting oxidative stress and pulmonary inflammation among groups was conducted using one-way analysis of variance (ANOVA) and Bonferroni's test. The effect of NAC on Nano-ITO induced NF-κB signaling pathway in rats was analyzed.Results:Histopathological examination of Nano-ITO exposed rats revealed diffuse alveolar damage, including PAP, cholesterol crystals, alveolar fibrosis, pulmonary fibrosis, and alveolar emphysema. Immunohistochemical results of Nano-ITO exposed rats showed strong positive for nuclear factor κB p65 (NF-κB p65) and nuclear factor Kappa B inhibitory factor kinase (IKK-β) and weak positive for nuclear factor κB inhibitory protein α (IκB-α) in the nuclei of bronchiolar and alveolar epithelial cells. Compared with blank control group, saline control group and NAC control group, the level of total protein (TP) in bronchoalveolar lavage fluid of rats in Nano-ITO group was significantly increased ( P<0.05), and the activities of lactate dehydrogenase (LDH), superoxide dismutase (SOD), malondialdehyde (MDA) content and total antioxidant capacity (T-AOC) were significantly increased ( P<0.05), the levels of proinflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) were significantly increased ( P<0.05), and the levels of NF-κB p65, IKK-β, inducible nitric oxide synthase (iNOS) and reactive oxygen species (ROS) in lung tissue were significantly increased ( P<0.05). Compared with Nano-ITO group, the levels of TP, T-AOC, MDA and TNF-α in bronchoalveolar lavage fluid of rats in NAC intervention group were significantly decreased ( P<0.05), and the levels of NF-κB p65 and ROS in lung tissue were significantly decreased (P<0.05). Western blot results showed that compared with the control groups, the protein expressions of NF-κB p65 and IKK-β in the lung tissue of Nano-ITO group were increased, while the protein expression of IκB-α was decreased ( P<0.05). Compared with Nano-ITO group, the protein expressions of NF-κB p65 and IKK-β in lung tissue of rats in NAC intervention group were decreased, while the protein expression of IκB-α was increased ( P<0.05) . Conclusion:The study demonstrated that Nano-ITO might induce pulmonary toxicity through the activation of NF-κB signaling pathway, and NAC could antagonize the pulmonary toxicity of Nano-ITO by inhibiting the NF-κB signaling pathway.