Fifteen morphologically and structurally complete sacrum specimens of normotrophic adult females were choosen. Distances between posterior sacral foramina and median sacral crest,and between the cores of adjacent posterior sacral foramina were measured. Then statistical analysis was done so as to provide objective anatomical evidence for the surface localization of Baliao points. The average distance between Shangliao (BL 31) and median sacral crest was (2.08 ± 0.19) cm; and the average distance between Ciliao (BL 32) and median sacral crest was (1.75 ± 0.12) cm; Zhongliao (BL 33), (1.59 ± 0.15) cm; Xialiao (BL 34), (1.56 ± 0.15) cm. And the distance of S₁-S₂ was (2.36 ± 0.31) cm averagely; S₂-S₃, (1.98 ± 0.23) cm; S₃-S₄, (1.71 ± 0.18) cm. It is considered that to locate Baliao points, Ciliao (BL 32) needs to be ascertained firstly.
Acupuncture Points ; Adult ; Female ; Humans ; Meridians ; Sacrum ; anatomy & histology

High mobility group protein B1 (HMGB1) is the most representative substance in the alarmins family, it is actively or passively release to extracellular by the activation of monocyte/macrophage and the dead cells, and then it stimulates the production of a variety of inflammatory mediators, and increases the organism's inflammatory response through relevant receptors signaling pathways. In recent years, its concentration can reflect the severity of inflammation and injury and was related to the prognosis, HMGB1 has won more and more attention in the development of sepsis. By reviewing the study of HMGB1 in sepsis pathogenesis, signal pathway and reversal measures, it was found that HMGB1 was considered as an important inflammatory mediators and warning signal involved in the pathogenesis of sepsis, and was become a new target in the treatment of sepsis. Further research on the role of HMGB1 in the pathogenesis of sepsis is needed in the future, and the development of new drugs combined with HMGB1 will be used in the study of HMGB1 in animal experiments.

The Change in interleukin-2 (IL-2) production of splenocyte and its relationship with suppressor T cell (Ts) were studied in mice after trauma. The results showed that IL-2 production was reduced, number of Ts was increased and activity of Ts correlated with reduced IL-2 production. Removal of Ts from splenocyte improved IL-2 production in traumatized mice. It is suggested that Ts is activated after trauma, resulting in impaired IL-2 production.

Over the past two decades, multiple drug-resistant infections have escalated globally with the significantly increased morbidity and mortality due to the unreasonable uses of antimicrobial agents in areas such as animal husbandry, industry and medicine. As the situation of drug resistance has been progressively serious, anti-drug-resistant clinical strategies have attracted widely social concerns. This review will report the current status of antibiotic resistance and the mechanism of antibiotic-resistance all over the world. The anti-drug resistance strategies are the emphasis of our report, including the new indication of old antibiotics, the combination of existing antibiotics, the development of new antibiotics, nano-antibiotics, and non-infection treatment with immunomodulators and phage. This review aims to further understand the current situation of drug resistance, which optimizes the strategies of drug-resistant bacteria and clinical services.

Objective To explore the operation indication of fracture of rib with fracture internal-fixation.Methods The clinical data of 103 cases with Fracture of rib,treated by fracture internal-fixation(n =49)and conservative treatment (n =54) respectively,were retrospectively analyzed.Results The hospital stay time,VAS scores and the healing time of surgical group were lower than that of non-surgical group.Fracture internal-fixation could significantly reduce the incidence of lung infection,deformities of chest and delayed hemathorax.Conclusions Internal fixation of fracture is much better than other routine therapies for fracture of ribs.The patients with indication of operation should operate actively.

Objective To investigate the protective effect of agmatine (AGM) against peritoneal inflammatory response and neutrophil (PMN) infiltration induced by zymosan (ZYM) in mice. Methods Thirty-six adult male C57BL/6 mice were randomly divided into sham group, model group, and AGM treatment group. Peritonitis model was reproduced by intra-peritoneal injection of 1 mg/mL ZYM (0.5 mL), while equivalent phosphate buffer saline (PBS) was given to sham group. 200 mg/kg AGM was injected into peritoneal cavity after ZYM challenge in AGM treatment group. Six mice in each group were sacrificed at 2 hours and 6 hours, respectively, after reproduction of the model. Blood sample and peritoneal lavage fluid (PLF) were collected. The levels of keratinocyte-derived chemokine (KC), macrophage inflammatory protein 2 (MIP-2), tumor necrosis factor-α (TNF-α), interleukins-6 (IL-6) in serum and PLF were determined by enzyme linked immunosorbent assay (ELISA). The number of leukocytes and PMN in PLF were determined by hemocytometer and flow cytometry, respectively. Results Compared with sham group, all serum and PLF levels of KC, MIP-2, TNF-α and IL-6 were greatly elevated at 2 hours after ZYM injection in model group, while AGM treatment could dramatically reduce the levels of the above-mentioned cytokines in serum and PLF as compared with those of the model group [serum KC (ng/L): 990.7±137.9 vs. 2 053.2±262.7, MIP-2 (ng/L): 642.2±124.4 vs. 1 369.7±146.5, TNF-α (ng/L): 608.6±38.1 vs. 1 044.7±101.0, IL-6 (ng/L): 1 058.2±129.1 vs. 1 443.3±190.1; PLF KC (ng/L): 7 462.3±839.6 vs. 12 723.5±1 515.7, MIP-2 (ng/L): 1 570.8±193.4 vs. 3 471.4±384.7, TNF-α (ng/L): 1 115.8±156.7 vs. 1 499.2±231.2, IL-6 (ng/L): 2 646.5±223.2 vs. 3 126.7±291.4; all P < 0.05]. The expressions of KC, MIP-2 and TNF-α at 6 hours were significantly lower than those at 2 hours in model group and AGM treatment group, but IL-6 levels were further increased. The levels of KC and MIP-2 in serum and PLF at 6 hours were decreased to the levels of sham group. At 6 hours after the reproduction of the model, the number of total inflammatory cells and PMN of PLF in the model group was significantly higher than those of the sham group. In contrast, AGM notably lowered the number of inflammatory cells and PMN in peritoneal fluid after ZYM attack [total inflammatory cells (×109/L): 14.7±1.1 vs. 2.0±0.4, 10.1±1.2 vs. 14.7±1.1; PMN (×109/L): 11.37±1.22 vs. 0.18±0.05, 7.69±0.57 vs. 11.37±1.22, all P < 0.05]. Conclusion AGM can effectively alleviate acute peritoneal inflammatory injury induced by ZYM, mainly through reducing the secretion of inflammatory mediators and chemokines, and inhibiting the infiltration of leukocytes and neutrophils.

Objective:To explore the influences of neutrophilic granule protein (NGP) on nitric oxide (NO) production in lipopolysaccharide (LPS)-induced macrophages and the regulatory mechanism.Methods:NGP highexpression RAW264.7 cells (NGP/RAW) and negative control empty vector cells (NC/RAW), NGP knockout RAW264.7 cells (NGP KO/RAW) and wild-type cells (WT/RAW) were cultured in vitro. Cells in logarithmic phase were stimulated with 10 mg/L LPS (LPS group) or phosphate buffered saline (PBS group) respectively. The content of NO in the supernatant was detected by Griess method. The mRNA expression of inducible nitric oxide synthase (iNOS) was detected by quantitative reverse transcription-polymerase chain reaction (RT-qPCR). The protein expressions of iNOS and phosphorylated signal transducer and activator of transcription 1 (p-STAT1) were detected by Western blotting.Results:Compared with PBS group, iNOS mRNA and NO expression were significantly increased at different time after LPS stimulation, the mRNA expression of iNOS peaked at 12 hours after LPS stimulation (2 -ΔΔCt: 38.45±1.34 vs. 1.00±0.00 in NC/RAW cells, 56.24±2.41 vs. 1.45±0.30 in NGP/RAW cells, 37.84±1.52 vs. 1.00±0.00 in WT/RAW cells, 5.47±0.62 vs. 0.98±0.40 in NGP KO/RAW cells, all P < 0.05), and the production of NO peaked at 24 hours after LPS stimulation (μmol/L: 24.15±1.26 vs. 0.15±0.04 in NC/RAW cells, 58.80±2.11 vs. 0.18±0.02 in NGP/RAW cells, 25.04±1.80 vs. 0.16±0.02 in WT/RAW cells, 2.42±0.38 vs. 0.12±0.03 in NGP KO/RAW cells, all P < 0.05). After being stimulated by LPS, the expression of iNOS mRNA and NO in NGP/RAW cells were increased significantly compared with NC/RAW cells [iNOS mRNA (2 -ΔΔCt): 8.42±0.59 vs. 4.63±0.37 at 2 hours, 27.16±1.60 vs. 14.25±1.02 at 6 hours, 56.24±2.41 vs. 38.45±1.34 at 12 hours; NO (μmol/L): 4.12±0.25 vs. 2.23±0.17 at 6 hours, 16.50±1.52 vs. 6.35±0.39 at 12 hours, 58.80±2.11 vs. 24.15±1.26 at 24 hours, all P < 0.05]. At the same time, the protein expressions of p-STAT1 and iNOS were also significantly enhanced (p-STAT1/GAPDH: 4.26±1.84 vs. 1.00±0.32 at 0 hours, 20.59±4.97 vs. 0.93±0.21 at 2 hours, 141.99±10.99 vs. 11.17±2.11 at 6 hours; iNOS/GAPDH: 1.27±0.86 vs. 1.00±0.22 at 0 hours, 7.94±1.94 vs. 2.01±0.92 at 2 hours, 24.24±4.88 vs. 3.72±1.11 at 6 hours, all P < 0.05), indicating that NGP might increase the expression of iNOS by promoting the phosphorylation of the signal transducer and activator of transcription 1 (STAT1) pathway, thereby increasing the production of NO. After being stimulated by LPS, the expression of iNOS mRNA and NO in NGP KO/RAW cells were significantly lower than that of WT/RAW cells [iNOS mRNA (2 -ΔΔCt): 2.46±0.31 vs. 4.22±0.18 at 2 hours, 3.61±0.44 vs. 13.02±1.34 at 6 hours, 5.47±0.62 vs. 37.84±1.52 at 12 hours; NO (μmol/L): 1.22±0.19 vs. 2.01±0.12 at 6 hours, 1.60±0.44 vs. 5.15±0.62 at 12 hours, 2.42±0.38 vs. 25.04±1.80 at 24 hours, all P < 0.05]. It showed that iNOS activation was reduced after NGP knockout, which in turn reduced NO production. Conclusion:NGP can positively regulate NO production in activated macrophages by activating the STAT1/iNOS pathway.

Objective:To evaluate the effect of early mobilization on mortality in intensive care unit (ICU) patients with mechanical ventilation after discharge by Meta-analysis.Methods:Databases including SinoMed, China National Knowledge Infrastructure (CNKI), Wanfang data, PubMed, the Cochrane Library, Web of Science, and Embase were searched from inception to September 17th, 2020, to collect randomized controlled trials (RCT) about early mobilization on mortality of patients with mechanical ventilation in ICU after discharge, the references included in the literature were traced. The control group was given routine care, the experimental group was given early mobilization on the basis of the control group, including passive or active mobilization on the bed, sitting on the bed, standing by the bed, transferring to the bedside chair and assisting walking. The literature screening, data extracting, and the bias risk assessment of included studies were conducted independently by two reviewers. Stata 12.0 software was then used to perform Meta-analysis. Funnel plot was used to test publication bias.Results:A total of 10 RCT studies involving 1 323 patients were included, with 660 patients in the control group and 663 patients in the experimental group. The results of literature quality evaluation showed that 7 studies were grade A and 3 studies were grade B, indicating that the overall quality of included literatures was high. The Meta-analysis results showed that early mobilization did not increase the mortality of patients with mechanical ventilation in ICU after discharge [odds ratio ( OR) = 0.92, 95% confidence interval (95% CI) was 0.75-1.13, P = 0.449]. Subgroup analysis results showed that early mobilization had a tendency to reduce the mortality of ICU patients with mechanical ventilation at 3, 6 and 12 months after discharge, but the difference was not statistically significant (3-month mortality: OR = 1.02, 95% CI was 0.74-1.40, P = 0.927; 6-month mortality: OR = 0.95, 95% CI was 0.70-1.27, P = 0.712; 12-month mortality: OR = 0.60, 95% CI was 0.33-1.10, P = 0.101). Funnel plot showed that the distribution of included literatures was not completely symmetrical, suggesting that publication bias might exist. Conclusions:Early mobilization does not increase the mortality of ICU patients with mechanical ventilation after discharge. Although it tends to have a favorable outcome in reducing mortality, and has a trend to reduce the mortality. However, due to the small number of included literatures, small sample size and differences in the specific implementation of early mobilization among various studies, a large number of high-quality RCT studies are still needed for further verification.

Objective To determine the inhibitory effects of Ellipticine (ELL) on inflammation in lipopolysaccharide (LPS)-induced RAW264.7 cells of mouse and explore its molecular mechanism.Methods The RAW264.7 cells in log phase were challenged by LPS (10 mg/L) to induce inflammation and then treated with ELL (0.05, 0.5, 5μmol/L). At the same time the cells treated with ELL (5μmol/L) were considered as ELL control group while without any stimulation as control group. After 12 hours intervention, the content of inflammatory factors in cell supernatant was detected by enzyme linked immunosorbent assay (ELISA), and then confirmed the most suitable concentration for the next experiment. After LPS of 10 mg/L was used to challenged RAW264.7 cells to cause inflammation, 5μmol/L ELL was used for intervention, and the mRNA expressions of inflammatory cytokines were detected by reverse transcription-polymerase chain reaction (RT-PCR) after 2, 4, 6 and 12 hours; the nuclear translocation of nuclear factor-κB p65 (NF-κB p65) as well as the phosphorylation levels of extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinases (p38MAPK), c-Jun N-terminal kinase (JNK), c-jun, c-fos were detected by Western Blot after 15 minutes, 30 minutes, 1 hour and 2 hours.Results ① The different proliferative potential of RAW264.7 treated with LPS (10 mg/L) and ELL (0.05, 0.5, 5μmol/L) had no significant difference comparing with control group, which indicated that ELL had no cytotoxicity with experimental concentration and had no effect on the cell proliferative potential as the result of drug interaction. The levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in supernatant were significantly increased after induced by LPS comparing with control group. However, the different concentrations of ELL could dose-dependently reverse the production of inflammatory factors, and 5μmol/L was the optimum concentration of anti-inflammatory. ② Compared with control group, the mRNA expressions of TNF-α, IL-6 were significantly increased, the nuclear translocation level of NF-κB p65 increased as well as the phosphorylation levels of ERK, p38MAPK, JNK, c-fos, c-jun after stimulated by LPS. While, the different concentration of ELL could reverse the mRNA of TNF-α, IL-6 and phosphorylation levels of JNK, c-fos, c-jun [TNF-αmRNA (2-ΔCt): 2.45± 0.19 vs. 3.41±0.32 after 2 hours, 1.20±0.11 vs. 2.11±0.21 after 4 hours, 1.68±0.09 vs. 2.51±0.31 after 6 hours;IL-6 mRNA (2-ΔCt): 3.41±0.52 vs. 4.10±0.38 after 6 hours, 1.61±0.08 vs. 3.91±0.25 after 12 hours; p-JNK/GAPDH:0.557±0.034 vs. 1.049±0.056 after 1 hour, 0.439±0.040 vs. 0.855±0.038 after 2 hours; p-c-fos/GAPDH: 0.158± 0.030 vs. 0.741±0.035 after 1 hour, 0.156±0.015 vs. 0.932±0.030 after 2 hours; p-c-jun/GAPDH: 0.425±0.036 vs. 0.802±0.059 after 1 hour, 0.345±0.075 vs. 0.952±0.068 after 2 hours; allP < 0.05]. However, it had no significant effect on the nuclear translocation level of NF-κB p65 and the phosphorylation level of ERK and p38MAPK. Conclusion ELL inhibited the production of IL-6, TNF-α inflammatory factors in LPS-induced RAW264.7 cells through suppression the phosphorylation of JNK and activator protein-1 (AP-1).

Objective:To determine the effects of cytochrome P450 1A1 (CYP1A1) on nitric oxide (NO) production in lipopolysaccharide (LPS)-induced macrophages and the underlying mechanism.Methods:The peritoneal macrophages (PMs) were isolated from healthy C57BL/6 mice and stimulated with 10 mg/L LPS to establish inflammatory response model. The CYP1A1 mRNA and protein expressions in the cells were determined. The mouse macrophages RAW264.7 cell line with CYP1A1 overexpression (CYP1A1/RAW) were cultured in vitro, and they were stimulated by 10 mg/L LPS at logarithmic phase. The negative control-expressed RAW264.7 cells (NC/RAW) were established. The protein and mRNA expressions of activator protein-1 (AP-1) and inducible nitric oxide synthase (iNOS) in the cells as well as the content of NO in the cell supernatant were determined. The RAW264.7 cells were cultured in vitro, and they were stimulated by 10 mg/L LPS and 100 nmol/L 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE] only or in combination at logarithmic phase. The blank control group was set up. The expression of iNOS mRNA in the cells and NO content in the cell supernatant were determined to observe whether the effect of CYP1A1 on LPS induced NO production in macrophages was related to 12(S)-HETE produced by metabolism. The RAW264.7 cells with CYP1A1 overexpression and hydroxylase activity mutation (CYP1A1m/RAW) were cultured in vitro, and they were stimulated by 10 mg/L LPS at logarithmic phase. The CYP1A1/RAW cell control group was set up. The iNOS mRNA expression in the cells and NO content in the cell supernatant were determined to observe the effect of hydroxylase activity of CYP1A1 in regulating NO production in macrophages. Results:Compared with the phosphate buffered saline (PBS) control group, the CYP1A1 mRNA expressions were elevated significantly from 2 hours after LPS stimulation and reached a peak at 12 hours [CYP1A1 mRNA (2 -ΔΔCt): 6.41±0.98 vs. 1.00±0.00, P < 0.05], while CYP1A1 protein expressions were increased from 6 hours after LPS stimulation and reached a peak at 24 hours, suggesting that CYP1A1 expression might be involved in LPS-induced macrophage over-activation. Compared with NC/RAW+LPS group, the iNOS mRNA expressions and NO contents both increased in CYP1A1/RAW+LPS group and reached a peak after 12 hours and 24 hours, respectively [12-hour iNOS mRNA (2 -ΔΔCt): 54.42±8.21 vs. 24.22±3.89, 24-hour NO (μmol/L): 66.52±4.09 vs. 41.42±2.09, both P < 0.05], while the iNOS protein expression and AP-1 phosphorylation also enhanced, suggesting that CYP1A1 might increase NO production by promoting AP-1 activation and iNOS expression. LPS and 12(S)-HETE stimulation only or in combination had no effect on iNOS mRNA expression and NO production, and no significant difference was found between the 12 (S)-HETE+LPS group and LPS group [12-hour iNOS mRNA (2 -ΔΔCt): 34.24±4.07 vs. 34.35±4.01, 24-hour NO (μmol/L): 44.02±3.14 vs. 44.56±3.21, both P > 0.05], suggesting that the regulation of CYP1A1 on NO production might not be induced by 12 (S)-HETE. There was no significant difference in the iNOS mRNA expressions or NO content between the CYP1A1m/RAW+LPS group and CYP1A1/RAW+LPS group [12-hour iNOS mRNA (2 -ΔΔCt): 52.11±6.84 vs. 50.21±5.19, 24-hour NO (μmol/L): 60.42±4.14 vs. 52.01±5.12, both P > 0.05], suggesting that CYP1A1 hydroxylase activity deficiency showed no effect on NO production. Conclusions:LPS stimulation significantly increases CYP1A1 expression in macrophages. CYP1A1 overexpression promotes NO production by activated macrophages through AP-1/iNOS pathway, while hydroxylase-deficiency or 12(S)-HETE has no effect on this regulation.