[Objective] To explore the influencing factors of quality monitoring index on the nucleic acid pooling detection mode and continuously improve the detection quality of nucleic acid laboratory. [Methods] The quality monitoring indicators (NAT reactive rate, NAT resolution reactive rate, NAT invalid batch rate, NAT invalid result rate, equipment failure rate) and causes of invalidity in our laboratory from January 1, 2020 to December 31, 2022 were retrospectively analyzed. The quality monitoring indicators of the laboratory during 2020 to 2022 were compared longitudinally. The quality monitoring indicators of the laboratory in 2022 were compared horizontally with the overall level in Shandong for the same period to find the differences. [Results] From 2020 to 2022, a total of 218 686 samples were detected, the NAT reactive rate was 0.15‰ (32 samples in total), the resolution reactive rate was 39.02%, the invalid batch rate was 1.06%, the invalid result rate was 1.18%, and the equipment failure rate was 3.58%. There were no differences in the NAT reactive rate, NAT resolution reactive rate and NAT invalid batch rate among different years (P>0.05), but there were differences in the invalid result rate (P<0.05). Equipment failure was the main cause of invalid results (56.53%). Compared with other laboratories in Shandong, there were differences in the NAT reactive rate and invalid result rate (P<0.05). There were differences in the reaction rate, resolution rate and invalid result rate among different reagents (P<0.05). Compared with other two laboratories using the same manufacturer's reagent, there were differences in the reactive rate and invalid result rate (P<0.05), but no difference in the resolution rate and invalid batch rate (P>0.05). [Conclusion] Establishing quality indexes for process control and regular analysis can timely detect potential risks in laboratory operation. The use of quality indicators to implement self-comparison and inter-laboratory comparison can help the laboratory systematically and scientifically evaluate its own operating status and formulate corresponding quality management strategies, thereby improving the laboratory's testing capacity and ensure the safety of blood use.

The purpose of this study was to investigate the anti-injury effect and protective mechanism of hydrogen-enriched water in a rat model of acute liver injury induced by aflatoxin B (AFB). Healthy male Sprague-Dawley (SD) rats were randomly divided into control group, model group (AFB group) and hydrogen-enriched water treatment group (AFB+H group). The rat model of acute liver injury induced by AFB was established by single intragastric administration of AFB (2.0 mg/kg), and then the rats were treated with hydrogen-enriched water intragastrically. HE staining was used to observe the pathological changes of liver tissue. Blood samples were taken from vena cava to measure serum liver function indexes. Live tissue was sampled to detect malondialdehyde (MDA) and reduced glutathione (GSH) contents. Western blot was used to detect phosphorylation levels of MAPK signaling pathway proteins (ERK, JNK and p38 MAPK). The results showed that, compared with the AFB group, the AFB+H group exhibited increased body weights, alleviated acute liver injury, decreased activities of serum glutamic-pyruvic transaminase and glutamic oxaloacetic transaminase, as well as total bilirubin level in the serum. Meanwhile, hydrogen-enriched water decreased MDA content and increased GSH content in liver tissue. AFB-increased phosphorylation levels of ERK, JNK and p38 MAPK in liver tissue were down-regulated significantly by hydrogen-enriched water treatment. These results suggest that hydrogen-enriched water can alleviate liver injury induced by AFB, and its mechanism may be related to the reduction of oxidative stress and the inhibition of MAPK signal transduction pathway activation.
Aflatoxin B1 ; Animals ; Chemical and Drug Induced Liver Injury ; pathology ; prevention & control ; Deuterium Oxide ; therapeutic use ; Liver ; pathology ; MAP Kinase Signaling System ; Male ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley

【Objective:】 To understand the real psychological feelings of cancer patients after withdrawing from drug clinical trials, and provide reference for clinical healthcare professionals to serve personalized care for patients in the transitional period after withdrawing from drug clinical trials. 【Methods:】 With the descriptive phenomenology method, 11 subjects who withdrew from drug clinical trials in the oncology department of a tertiary hospital in Shandong Province were selected by intentional sampling method to conduct semi-structured in-depth interviews. Colaizzi seven-step analysis method was used to analyze and sort out records, and refine themes. 【Results:】 The psychological experiences of cancer patients after withdrawing from drug clinical trials were summarized into four themes: benefits of participating in clinical trials, losses of withdrawing from clinical trials, attitudes towards future treatment, and expectations of receiving help. 【Conclusion:】 Cancer patients face great psychological pressure after withdrawing from drug clinical trials and require deep emotional support and humanistic care. Nursing staff should take personalized care measures to meet the special problems of patients’ psychological needs, so as to help patients smoothly pass through the withdrawal stage and enter subsequent treatment.

BACKGROUND: Lung adenocarcinoma (LUAD) is the most common type of non-small cell lung cancer, and any change of miRNAs expression will affect the degree of target regulation, thus affecting intracellular homeostasis. This study verified that miR-186-5p could inhibit the proliferation, migration and invasion of LUAD cells by regulating PRKAA2. METHODS: Previous investigations found that the expression of miR-186-5p was markedly suppressed in LUAD. Bioinformatics method is used to predict the target protein related to ferroptosis downstream and inquire about its expression level in LUAD and its influence on the survival of patients. Double luciferase verified the binding site of PRKAA2 and miR-186-5p. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to detect the expression of PRKAA2. The effects of miR-186-5p of LUAD cells as well as the mechanism by which miR-186-5p inhibits Fer-1's sensitivity to ferroptosis were confirmed by EdU, Transwell, and scratch assays. The effect of miR-186-5p on the amount of reactive oxygen species (ROS) in LUAD cells was discovered using ROS experiment. Malondialdehyde (MDA) and glutathione (GSH) experiments were used to detect the effects of miR-186-5p and PRKAA2 on ferroptosis index of LUAD cells. The concentration of lipid ROS (L-ROS) in LUAD cells were measured using the L-ROS tests to determine the effects of miR-186-5p and PRKAA2. RESULTS: The expression of PRKAA2 is up-regulated, and a high level of PRKAA2 expression was associated with a poor prognosis for patients with LUAD. Overexpression of miR-186-5p decreased the gene and protein expression of PRKAA2. By promoting ferroptosis, miR-186-5p overexpression prevented lung cancer cells from proliferating, invading, and migrating. ROS could be produced in higher amounts in LUAD cells due to miR-186-5p. Overexpression of miR-186-5p and knockdown PRKAA2 up-regulated MDA content and reduced GSH content in LUAD cells, respectively. miR-186-5p could increase the content of L-ROS and promote the ferroptosis sensitivity of LUAD cells by targeting PRKAA2. CONCLUSIONS miR-186-5p promotes ferroptosis of LUAD cells through targeted regulation of PRKAA2, thus inhibiting the proliferation, invasion and migration of LUAD.
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Humans ; Lung Neoplasms/genetics* ; Carcinoma, Non-Small-Cell Lung ; Ferroptosis/genetics* ; Reactive Oxygen Species ; Adenocarcinoma of Lung/genetics* ; MicroRNAs/genetics* ; 3,4-Methylenedioxyamphetamine ; Cell Proliferation/genetics* ; Cell Movement/genetics* ; Gene Expression Regulation, Neoplastic ; Cell Line, Tumor ; AMP-Activated Protein Kinases

Humans ; Bayes Theorem ; Age Factors ; Age Distribution ; Mouth Neoplasms/epidemiology* ; China/epidemiology* ; Mortality

OBJECTIVE To establish a rat model of pulmonary infection by inoculating Pseudomonas aeruginosa to Sprague-Dawley(SD) rats and evaluate it.METHODS Two hundred SD rats were divided into 2 groups: the P.aeruginosa group and the control group,P.aeruginosa was embedded in minute seaweed alginate beads by an ejection set with an acuminate hole.Then the beads were inoculated into the rats′ lung through tracheal intubation.RESULTS The bacteriological values: P.aeruginosa was detected from rats of infected groups.Bacterial number was higher than 105CFU/g 3 and 7 days after infection and higher than 103CFU/g 14 and 28 days after infection.The pathological changes showed: 3 and 7 days after infection,lung abscess,edema,and consolidation could be seen from lungs of infected groups.At optical microscopy,alginateP.aeruginosa caused a pronounced inflammatory reaction with polymorphonuclear cells surrounding a bead.Fourteen and 28 days after infection,fibrinous adhesions and granulomas became the major pathological changes.CONCLUSIONS The animal model of pulmonary infection can be established by inoculating P.aeruginosa embedded in minute seaweed alginate beads made by an ejection set with an acuminate hole to SD rats.

Objective To establish a rat model of chronic pulmonary infection by inoculating Pseudomonas aeruginosa to Sprague-Dawley (SD) rats, and to evaluate the animal model with bacteriological and pathological stndies. Methods 240 healthy, clean SD rats were randomly divided into 2 groups: the infected group and the control group. Pseudomonas aeruginosa were embedded in minute seaweed alginate beads using an ejection set with an acuminate hole. Then the beads were inoculated into the rats′ lung through tracheal intubation. The bacteria number in the lung and pathological scores were determined 3, 7, 14 and 35 days after inoculation. The control group was treated with the same method using the sterile normal saline instead of the bacteria suspension. Results Bacteriological values: no bacterium was detected in the control group. Pseudomonas aeruginosa was detected from the rats of infected group in which the bacterial number was up over 105cfu/g at 3 and 7 days after infection, and up over 103cfu/g at 14 and 35 days after infection. Pathological changes: at 3 and 7 days after infection, lung edema, consolidation and hemorrhage could be seen in rat lungs of the infected group. Under the optical microscope, alginate-Pseudomonas aeruginosa caused a pronounced inflammatory reaction with polymorphonuclear cells surrounding beads, and microcolonies formed at the periphery of beads were also seen. Atelectasis and fibrosis and granalation were the major pathological changes at 14 and 35 days after infection. While in the control group, there were little changes after the inoculation except mild congestion and inflammatory reaction in the lungs 3 days after inoculation. Conclusion The rat model of chronic pulmonary infection can be reproduced by inoculating Pseudomonas aeruginosa embedded in minute seaweed alginate beads.

Objective To study the mutants of pre C/C gene and the base core premotor (BCP) in chronic hepatitis B patients carrying or not carrying hepatitis B e antigen (HBeAg). Method The HBV DNA of BCP and PreC/C ware amplified by PCR from serum samples of patients with chronic hepatitis B, and the products were cloned into T vector and sequenced. Results Of BCP variants, the double mutations of T1762/ A1764 were found in 20 of 42 patients with chronic hepatitis, and the prevalence was significantly lower in HBeAg positive patients (7/20) than in HBeAg negative patients (13/22) (P