[Serum interleukin-2 receptor α as a clinical biomarker in patients with systemic lupus erythematosus].

OBJECTIVE: To investigate the clinical relevance of serum interleukin-2 receptor α (IL-2Rα) in patients with systemic lupus erythematosus (SLE). METHODS: One hundred and seven SLE patients and 39 healthy controls with comparable age and gender were recruited at Peking University People's Hospital from January 2019 to December 2020. Complete clinical data in 107 SLE patients at baseline and follow-up were collected. SLE disease activity index 2000 (SLEDAI-2K) was used to assess the disease activity of the SLE patients. The serum level of IL-2Rα in the SLE patients and healthy controls was measured using enzyme-linked immunosorbent assay (ELISA). The association between serum IL-2Rα and clinical and laboratory parameters was investigated. Mann-Whitney U test or t test, Chi-square test and Spearman correlation were used for statistical analysis. RESULTS: The serum IL-2Rα levels were significantly higher in the SLE patients [830.82 (104.2-8 940.48) ng/L], compared with those in the healthy controls [505.1 (78.65-1 711.52) ng/L] (P < 0.001). Association analysis showed that the increased serum IL-2Rα was positively associated with SLEDAI-2K scores and anti-nucleosome antibody (r=0.357, P < 0.001; r=0.25, P=0.027, respectively). Thirty-six of 107 (33.6%) SLE patients had lupus nephritis. Serum IL-2Rα levels were significantly higher in the patients accompanied with lupus nephritis [1 102.14 (126.52-8 940.48) ng/L] than in the patients without lupus nephritis [743.89 (104.19-4 872.06) ng/L] (P=0.032). The patients in the high IL-2Rα group had more lupus nephritis compared with those in the low IL-2Rα group (40.8% vs. 19.4%, P=0.031). Meanwhile, SLEDAI-2K scores were found significantly higher in the high IL-2Rα group than in the low IL-2Rα group [10 (3-21) vs. 7 (3-16), P=0.001]. With the improvement of disease activity in the SLE patients after conventional treatments, serum levels of IL-2Rα [1 119.1 (372.25-2 608.86) ng/L] in the week 12 decreased significantly compared with the baseline [1 556.73 (373.08-8 940.48) ng/L] (P=0.042). CONCLUSION: Serum IL-2Rα may be used as a biomarker of disease activity in patients with SLE. There is certain correlation between serum IL-2Rα and renal involvement in SLE.

[A case of hyperlacticemia caused by linezolid in severely burned patient].

On October 3rd, 2017, one male patient, aged 27 years, was admitted to our hospital 6 hours after hydrothermal scald of torso, buttocks, and limbs. The total area of burn was about 60% total body surface area, and the depth was from deep partial-thickness burn to full-thickness burn. Immediately after admission, the patient was given symptomatic support treatments, such as anti-shock, fluid replacement, and anti-infection, etc. After being treated by debridement and xenogenic (porcine) skin grafting for 2 times, the wounds were healed well. On the 12th day of admission, linezolid was used to prevent infection according to the results of microbial culture and drug sensitivity test, since when the level of his blood lactate continued to increase. After 8 days, linezolid was discontinued and vitamin B1 was given orally for 1 week, and the level of lactic acid gradually decreased to normal in result. This case was used mainly to analyze whether linezolid could directly cause hyperlacticemia and its important mechanism, aiming at reminding clinicians of being alert to the risk of hyperlacticemia when using linezolid. If hyperlacticemia occurs, linezolid should be discontinued immediately and vitamin B1 should be taken orally to correct the high lactic acid value, and the treatment plan should be adjusted if necessary.

[A comparative study of the short-term efficacy and long-term efficacy of systematic lymph node dissection and elective lymph node dissection in patients with early esophageal cancer].

Objective: To investigate the feasibility, safety, short-term efficacy and long-term efficacy of elective lymph node dissection in patients with early esophageal cancer. Methods: The study retrospectively evaluated 405 patients with cT1N0M0 esophageal carcinoma who received minimally invasive esophagectomy in the First Affiliated Hospital of University of Science and Technology of China between March 2007 and March 2013. Of those patients, 208 patients underwent systematic lymph node dissection (SLND) and 197 patients underwent elective lymph node dissection (ELND). The clinicopathologic factors, operational factors, postoperative complications, lymph node dissection and prognosis of patients were compared by independent sample t test, χ(2) test, or Mann-Whitney rank test. The 5-year overall survival was calculated by the Kaplan-Meier estimation method using the Log-rank test. Results: There was no significant difference in clinicopathological data between the SLND group and the ELND group. The incidence of pulmonary infection (8.2% vs. 2.9%, P=0.04) and arrhythmia (6.2% vs. 2.0%, P=0.03) of the minor postoperative complications in the SLND group were higher than the ELND group. The incidence of pulmonary infection (6.2% vs. 2.0%, P=0.03), Chylothorax (5.8% vs.1.5%, P=0.02), anastomotic or pleural hemorrhage requiring reoperation (2.9% vs.0.5%, P=0.04) of major postoperative complications in the SLND group were higher than the ELND group, the difference was statistically significant. In the perioperative data of two groups, the incidence of total postoperative complications, total pulmonary complications, operation time, intraoperative blood loss, postoperative hospitalization, postoperative thoracic drainage duration and postoperative thoracic drainage fluid volume of the SLND group were higher than the ELND group, the difference was statistically significant. The mean numbers and stations of dissected lymph node in the SLND were 30.2±4.2 and 12.1±2.7, the mean numbers and stations of dissected lymph node in the ELND were 25.7±3.8 and 8.4±3.6. The survival rates of 1, 3, 5 years of all patients were 100%, 95.9% and 82.5%, respectively. The median survival time was 87.4 months. Further analysis showed that the 1, 3 and 5 years survival rate of patients with stage Ⅰ esophageal cancer was 100%, 97.1% and 88.9%, respectively. The median survival time was 89.3 months. The 1, 3 and 5 years survival rate of patients with stage Ⅱa esophageal cancer was 100%, 93.2% and 76.8%, respectively. The median survival time was 77.2 months. There was no significant difference in survival rate between the SLND group and the ELND group in 1, 3 and 5 years. When taking a further analysis of stage Ⅰ esophageal cancer, the survival rates between 188 patients in the SLND group and 180 patients in the ELND group were no significant difference. When focus on the stage Ⅱa esophageal cancer, the 1, 3 and 5 years survival rate were higher in the SLND group than that in the ELND group (100%, 94.5%, 83.2% vs. 100%, 91.3%, 72.1%, P=0.047), the difference was statistically significant. Conclusion: ELND can be safely and effectively performed for early esophageal cancer with favorable short-term efficacy and long-term efficacy.

[The application of 3D reconstruction in investigating the frontal sinus drainage pathway based on computer tomography data].

Objective:The aim of this study is to explore the value of 3D reconstruction technology based on computer tomography data in understanding the frontal sinus drainage pathway. Method:Three-dimensional reconstruction of DICOM data from 100 cases of sinus CT was performed by using Mimics 19.0 software. The 3D models were used to study types, the relative locations of frontal sinus and recess cells as well as the influence of the frontal sinus drainage pathway. Result:The 3D model of frontal sinus, frontal recess cells and frontal sinus drainage pathway were reconstructed successfully. Among them, the incidence of nasal cavity was 95.5% (191/200), nasal cavity was 31.5% (63/200), nasal cavity on the frontal air room was 24.5% (49/200) supra bulla cells were 54% (108/200), supra bulla frontal cells were 14.5% (29/200), supraorbital ethmoid cells were 20.5% (41/200), and the rate of frontal septal cells were 4% (8/200). It visually demonstrated the relationship between the frontal recess and the frontal sinus drainage channel. Conclusion:The 3D reconstruction technology based on computer tomography data not only helps us to understand the anatomy of the frontal sinus, the relative position of the frontal crypt and the effect on the frontal sinus drainage channel, but also provides a new method for preoperative planning and intraoperative guidance to endoscopic frontal sinus surgery.

Complementary DNA sequences of the constant regions of T-cell antigen receptors α, ß and γ in mandarin fish, Siniperca chuatsi Basilewsky, and their transcriptional changes after stimulation with Flavobacterium columnare.

In this study, the constant-region genes (Cα, Cß and Cγ) that encode the T-cell antigen receptor (TCR) α, ß and γ chains were cloned from mandarin fish, Siniperca chuatsi Basilewsky, an important freshwater fish species in China. The complementary DNA sequences of Cα, Cß and Cγ were 843, 716 and 906 base pairs (bp) in length and had a 465-, 289- and 360-bp 3' untranslated region, encoding 125, 142 and 182 amino acids, respectively. The amino-acid sequences of the constant regions of mandarin fish TCR α, ß and γ chains (encoded by Cα, Cß and Cγ, respectively) were most similar to those of their teleost counterparts, showing 60% similarity with pufferfish, 48% similarity with Atlantic salmon and 57% similarity with flounder, respectively. The phylogenetic analysis revealed that the mandarin fish Cα, Cß and Cγ were clustered, respectively, with their vertebrate counterparts. The mandarin fish Cα, Cß and Cγ could also be separated into four domains: immunoglobulin; connecting peptide (CP); transmembrane (TM); and cytoplasmic tail. Several conserved features in mammalian TCRs were also found in those of mandarin fish, such as a conserved cysteine residue in the CP domain of Cα, necessary for creating an interchain disulphide bond with the TCR ß chain, and a conserved antigen receptor TM motif in Cα and Cß. Meanwhile, transcripts of Cα, Cß and Cγ were detectable in all examined organs, with a stronger signal observed in lymphoid organs. In addition, the temporal transcriptional changes for Cα and Cγ were investigated, 1, 2, 3, 4, 5, 6 and 8 weeks after stimulation with Flavobacterium columnare, in head kidney, spleen, blood, thymus, gill and intestine, using real-time polymerase chain reaction. The results demonstrated stimulation-dependent up-regulations in almost all tissues examined, which indicates that T cells may play important roles in preventing mandarin fish from bacterial invasion. In particular, apart from thymus, T cells were distributed mainly in gill and intestine, where striking up-regulation of Cγ was also observed. These results will facilitate functional studies of teleost TCRs and T cells.

Comparison of biological activated carbon (BAC) and membrane bioreactor (MBR) for pollutants removal in drinking water treatment.

Biological activated carbon (BAC) and membrane bioreactor (MBR) were systematically compared for the drinking water treatment from slightly polluted raw water under the same hydraulic retention time (HRT) of 0.5 h. MBR exhibited excellent turbidity removal capacity due to the separation of the membrane; while only 60% of influent turbidity was intercepted by BAC. Perfect nitrification was achieved by MBR with the 89% reduction in ammonia; by contrast, BAC only eliminated a moderate amount of influent ammonia (by 54.5%). However, BAC was able to remove more dissolved organic matter (DOM, especially for organic molecules of 3,000 approximately 500 Daltons) and corresponding disinfection by-product formation potential (DBPFP) in raw water than MBR. Unfortunately, particulate organic matter (POM) was detected in the BAC effluent. On the other hand, BAC and MBR displayed essentially the same capacity for biodegradable organic matter (BOM) removal. Fractionation of DOM showed that the removal efficiencies of hydrophobic neutrals, hydrophobic acids, weakly hydrophobic acids and hydrophilic organic matter through BAC treatment were 11.7%, 8.8%, 13.9% and 4.8% higher than that through MBR; while MBR achieved 13.8% higher hydrophobic bases removal as compared with BAC.

Ontogeny of IgM-producing cells in the mandarin fish Siniperca chuatsi identified by in situ hybridisation.

The ontogeny of IgM-producing cells was studied in juvenile mandarin fish Siniperca chuatsi, an important fish in China's aquaculture sector. The IgM-producing cells were localised through in situ hybridisation with a probe complementary to the Ig mu-chain in lymphoid-related tissues, including head kidney, spleen, thymus, intestine and gills. In head kidney, transcripts of Ig mu were first detected at 20days post-hatching (dph) with a few positive signals, and the number of IgM-producing cells increased obviously from 39dph onwards. At 136dph, a large amount of positive cells were observed in the entire organ with clusters of these cells located around the blood vessels. In spleen, IgM-producing cells were found from 26dph onwards, followed by an increase until 67dph; clusters of positive cells were also detected around blood vessels at 102dph. In thymus, IgM-producing cells were first observed at 39dph; thereafter, no obvious increase was detected until 78dph. The positive cells in thymus were distributed mainly in the outer zone of thymus. A few IgM-producing cells were still observed in thymus of 1-year-old mandarin fish. IgM-producing cells were not detected in the intestine until 87dph, with several discrete positively stained cells distributed in the lamina propria. IgM-producing cells, scattered mainly in primary gill filaments around blood vessels, were detected in gills from 90dph. As in other teleosts, these results indicated that the head kidney appears to be the primary organ for IgM production in mandarin fish, and IgM-producing cells exist in all organs examined in the present study, implying their lymphoid role in fish. In addition, it is suggested that vaccination after 20dph may be much more effective in mandarin fish.

[Establishment of Z-HL16C cell line.].

BACKGROUND: To establish and study the nature and the application of Z-HL16C cell line. METHODS: The cell line was continuously passed, frozen stored and recovered. Its application was expanded and the cell type was identified. RESULTS: The cell line had an epithelial-cell-like shape, the size appeared uniform, the cell boundary was distinct. It has been continuously passed, frozen stored and recovered for ten years. Its recovery rate was about 90%. It has been proved to be sensitive to the tested viruses which were enteroviruses (Polio, Cox, Echo), influenza viruses, parainfluenzaviruses, adenoviruses, measles virus. This cell line has been identified as a cancerization cell. CONCLUSION: The cell line Z-HL16C has been stably established, it has a broad spectrum in sensitivity for culturing viruses.

Automated Sleep Staging by a Hybrid System Comprising Neural Network and Fuzzy Rule-based Reasoning.

A hybrid system for automated EEG sleep staging is presented in this article. By combining a self-organizing feature map (SOFM) with a fuzzy reasoning-based classifier (FRBC) and utilizing both temporal and spectrum features of the EEG signal, the system provides a reliable tool for automatic EEG sleep staging. Conceptually, the system is divided into four passes: artifact detection, rough staging, stage refinement and post processing. The artifact detection module is firstly employed to exclude stage movement from other stages. Then, the SOFM with features as its inputs derived from the power spectrum divides sleep into three "extreme" stages: Wake, Light/REM and Deep stage. In stage refinement pass, the FRBC, which takes characteristic waveforms' activities as inputs, subdivides the extreme stages into the exact stages (i.e., stage 1, stage 2) defined by R&K standard. At last, in post processing pass, a stage-smoothing method that mainly utilizes the temporal context information is used to correct unexpected stage transitions, thus to improve the system's performance. The system was tested with eight whole night sleep records with an average man-machine agreement of 85.3%. Compared with the high inter-scorer disagreement, the performance is desirable.

Chronic treatments with tacrine and (-)-nicotine induce different changes of nicotinic and muscarinic acetylcholine receptors in the brain of aged rat.

The present study evaluated effects of chronic treatment with tacrine and (-)-nicotine for 21 days on nicotinic and muscarinic acetylcholine receptors in the brains of old rats (24-25 months) by receptor autoradiography. The nicotinic receptor (nAChR) binding sites were measured by (-)-[3H]nicotine and [3H]epibatidine, and the muscarinic receptor (mAChR) binding sites by [3H]pirenzepine and [3H]AFDX 384. No change in (-)-[3H]nicotine binding was observed in all of the brain regions analysed following chroinic treatment with tacrine (10 mg/kg). Similarly, the [3H]epibatidine binding was not changed in most of the brain regions analysed except for a few brain regions where a decrease was observed in tacrine treated animals compared to control animals. Chronic treatment with (-)-nicotine (0.45 mg base/kg) significantly increased both (-)-[3H]nicotine and [3H]epibatidine bindings in every brain regions analysed except for the hippocampus when measured by (-)-[3H]nicotine. A significant decrease in [3H]AFDX 384 binding, but not in [3H]pirenzepine binding was observed in all of the brain regions analysed following the treatment with tacrine. These data suggest that chronic treatments with tacrine and (-)-nicotine differentially interfere and regulate the subtypes of nAChRs and mAChRs in the brain of aged rat. These data differ from what have been earlier observed in the brain of young adult rat following tacrine treatment, revealing some dynamic changes in receptor properties in the brain during aging.

Reduced expression of neuronal nicotinic acetylcholine receptors during the early stages of damage by oxidative stress in PC12 cells.

The mechanism for a large loss of neuronal nicotinic acetylcholine receptors (nAChRs) in brains with neurodegenerative diseases remains unclear. Based on our previous results of [(3)H]epibatidine binding influenced by lipid peroxidation, we suggest that nAChR deficit in neurodegenerative diseases might be related to the neurons attacked by free radicals. To further understand how free radicals influence the expression of nAChRs, we detected [(125)I]alpha-bungarotoxin binding, nAChR subunit protein and mRNA during the early stage of damage by oxidative stress in PC12 cells in the present study. The results showed that free radical insult (FeSO(4)) within the concentration range (1 -100 microM) used in the study induced dose-dependent increases in lipid peroxidation and toxicity to PC12 cells, but did not result in apoptosis or necrosis. Significant reductions in [(125)I]alpha-bungarotoxin binding site, protein level for the alpha3 and alpha7 subunits, and mRNA level for the alpha7 subunit were observed in PC12 cells treated by FeSO(4) at the concentrations without inducing cell death compared to control. Pretreatment of cultural cells with antioxidant such as Vitamin E and reduced glutathione prevented the inhibiting effect of free radicals on [(125)I]alpha-bungarotoxin and [(3)H]epibatidine bindings. The present results further demonstrate that oxidative stress might reduce the number of [(125)I]alpha-bungarotoxin binding site and selectively suppress the expression of the nAChR subunits at protein and mRNA levels during the early stages of damage in PC12 cells.

Suppressed expression of nicotinic acetylcholine receptors by nanomolar beta-amyloid peptides in PC12 cells.

A line of evidence has shown that a link between the common pathological features of beta-amyloid peptide (Abeta) deposition and cholinergic degeneration observed in Alzheimer's disease (AD) may exist, however, no experimental evidence has shown that exposure to Abeta can decrease expression of nicotinic acetylcholine receptors (nAChRs), which have been shown to play roles in brain cognitive functions. Here, we report that treatment with Abeta1-40 and Abeta25-35 at nanomolar concentrations significantly decreased the [3H]epibatidine and [125I]alpha-bungarotoxin binding sites, the protein and mRNA levels of nAChR alpha3, alpha7 and beta2 subunits in PC12 cells. Abeta1-40 and Abeta25-35 at the concentrations used in the treatment study neither bound to nAChRs nor induced apoptosis, but significantly inhibited the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5,diphenyl tetrazolium bromide) reduction. These data suggest that the decreased biosynthesis of nAChRs induced by Abeta may be attributable partially to perturbances of some intracellular signal transduction pathways. The results presented in this study lead to a hypothesis that Abeta can degenerate nAChRs early in the course of AD before the formation of abundant Abeta fibrils.

Regulation of no synthesis induced by inflammatory mediators in RAW264.7 cells: collagen prevents inhibition by osteopontin.

Osteopontin has been shown to inhibit the induction of inducible nitric oxide synthase (iNOS, or NOS2) by lipopolysaccharide and interferon-gamma in the RAW264.7 mouse monocyte/macrophage line and in primary mouse proximal tubule epithelial cells. However, the RAW264.7 cells become refractory to the action of OPN after several subcultures or under dilute culture conditions, possibly because of changes in the composition of the extracellular matrix. We make this suggestion because if the cells are plated on a collagen type I or collagen type IV substrate the inhibitory action of OPN is completely suppressed; this is not the case on substrates consisting of laminin, fibronectin, poly-D-lysine, or poly-(2-hydroxyethylmethylacrylate). These observations imply that macrophages are sensitive to regulation by OPN only in certain physiological contexts. Both hyaluronate, which binds CD44, and rat IgGs are also able to inhibit the induction of NO synthesis by the inflammatory mediators. The similar actions of HA and OPN are consistent with the possibility that CD44 may be a receptor for OPN.

[Antithrombotic and antiplatelet effects of rosmarinic acid, a water-soluble component isolated from radix Salviae miltiorrhizae (danshen)].

Wistar rats of both sex were used. Ros A was intravenously injected 5-10 min before blood collection or the ligation of vena cava. 1. Stasis-induced venous thrombosis: A tight ligature was applied to inferior vena cava below the left renal vein in anesthetized rats. The abdominal walls were closed and then reopened two hours later. The vena cava was clamped 2 cm below the ligature. This segment was cut to remove the thrombus. The dry weight of the thrombus was determined. 2. Platelet aggregation: Using Born's method the platelet aggregation induced by collagen or ADP was studied. 3. Blood coagulation times: Blood recalcium time (RT), kaolin partial thromboplastin time (KPTT) and prothrombin time (PT) were estimated. 4. Plasma fibrinolytic activity was observed by the determination of euglobulinolytic time (ELT). Plasma fibrinogen content was estimated based on the biuret reaction. The venous thrombosis was inhibited by 41.9% and 54.8% (P < 0.05) when Ros A was injected at the dosages of 50 and 100 mg/kg. The blood platelet aggregation elicited by collagen was suppressed by 30.4% (P < 0.05) and 46.4% (P < 0.01) after the injection of Ros A at doses of 100 and 150 mg/kg respectively. The ELT was shortened after the injection of Ros A (100 and 150 mg/kg) as compared with the control value (P < 0.05), while the plasma fibrinogen content remained unchanged. The results that Ros A showed mild antithrombotic effect. The mechanism of this effect might be related to its inhibition of platelet aggregation and promotion of fibrinolytic activity.

[Effect of sodium ferulate on arachidonic acid metabolism].

Sodium ferulate (SF) is one of the antiplatelet ingredients in Radix Angleica sinensis. The effect of SF on 14C-arachidonic acid metabolism in washed intact rabbit platelets was studied with radiochromatography and radioautography. SF (0.1-3.2 mmol/L) inhibited the generation of platelet thromboxane B2 in a dose-dependent manner (reduced by 16.7-93.8%) and the IC50 was shown to be 0.762 mmol/L. Simultaneously with the reduction of TXB2 generation, the formation of PGE2 and PGF2 alpha was also reduced significantly after treatment with SF. Using radioimmunoassay SF (0.145-2.32 mmol/L) was found to inhibit rabbit platelet TXB2 formation in a dose-dependent manner. SF (0.58-2.32 mmol/L) also suppressed aortic tissue 6-keto-PGF1 alpha generation in rabbits. At the same concentrations the inhibitory effect of SF on platelet TXB2 formation was greater than that on aortic tissue 6-keto-PGF1 alpha generation. These results indicate that the cyclo-oxygenase activity may be inhibited by SF.