Macrophages are innate immune cells connected with the development of inflammation. Retinoic acid has previously been proved to have anti-inflammatory and anti-arthritic properties. However, the exact mechanism through which retinoic acid modulates arthritis remains unclear. This study aimed to investigate whether retinoic acid ameliorates rheumatoid arthritis by modulating macrophage polarization. This study used retinoic acid to treat mice with adjuvant arthritis and evaluated anti-inflammatory effects by arthritis score, thermal nociceptive sensitization test, histopathologic examination and immunofluorescence assays. In addition, its specific anti-arthritic mechanism was investigated by flow cytometry, cell transfection and inflammatory signaling pathway assays in RAW264.7 macrophages in vitro. Retinoic acid significantly relieved joint pain and attenuated inflammatory cell infiltration in mice. Furthermore, this treatment modulated peritoneal macrophage polarization, increased levels of arginase 1, as well as decreased inducible nitric oxide synthase expression. In vitro, we verified that retinoic acid promotes macrophage transition from the M1 to M2 type by upregulating mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1) expression and inhibiting P38, JNK and ERK phosphorylation in lipopolysaccharide-stimulated RAW264.7 cells. Notably, the therapeutic effects of retinoic acid were inhibited by MKP-1 knockdown. Retinoic acid exerts a significant therapeutic effect on adjuvant arthritis in mice by regulating macrophage polarization through the MKP-1/MAPK pathway, and play an important role in the treatment of rheumatic diseases.

Macrophages are innate immune cells connected with the development of inflammation. Retinoic acid has previously been proved to have anti-inflammatory and anti-arthritic properties. However, the exact mechanism through which retinoic acid modulates arthritis remains unclear. This study aimed to investigate whether retinoic acid ameliorates rheumatoid arthritis by modulating macrophage polarization. This study used retinoic acid to treat mice with adjuvant arthritis and evaluated anti-inflammatory effects by arthritis score, thermal nociceptive sensitization test, histopathologic examination and immunofluorescence assays. In addition, its specific anti-arthritic mechanism was investigated by flow cytometry, cell transfection and inflammatory signaling pathway assays in RAW264.7 macrophages in vitro. Retinoic acid significantly relieved joint pain and attenuated inflammatory cell infiltration in mice. Furthermore, this treatment modulated peritoneal macrophage polarization, increased levels of arginase 1, as well as decreased inducible nitric oxide synthase expression. In vitro, we verified that retinoic acid promotes macrophage transition from the M1 to M2 type by upregulating mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1) expression and inhibiting P38, JNK and ERK phosphorylation in lipopolysaccharide-stimulated RAW264.7 cells. Notably, the therapeutic effects of retinoic acid were inhibited by MKP-1 knockdown. Retinoic acid exerts a significant therapeutic effect on adjuvant arthritis in mice by regulating macrophage polarization through the MKP-1/MAPK pathway, and play an important role in the treatment of rheumatic diseases.

Macrophages are innate immune cells connected with the development of inflammation. Retinoic acid has previously been proved to have anti-inflammatory and anti-arthritic properties. However, the exact mechanism through which retinoic acid modulates arthritis remains unclear. This study aimed to investigate whether retinoic acid ameliorates rheumatoid arthritis by modulating macrophage polarization. This study used retinoic acid to treat mice with adjuvant arthritis and evaluated anti-inflammatory effects by arthritis score, thermal nociceptive sensitization test, histopathologic examination and immunofluorescence assays. In addition, its specific anti-arthritic mechanism was investigated by flow cytometry, cell transfection and inflammatory signaling pathway assays in RAW264.7 macrophages in vitro. Retinoic acid significantly relieved joint pain and attenuated inflammatory cell infiltration in mice. Furthermore, this treatment modulated peritoneal macrophage polarization, increased levels of arginase 1, as well as decreased inducible nitric oxide synthase expression. In vitro, we verified that retinoic acid promotes macrophage transition from the M1 to M2 type by upregulating mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1) expression and inhibiting P38, JNK and ERK phosphorylation in lipopolysaccharide-stimulated RAW264.7 cells. Notably, the therapeutic effects of retinoic acid were inhibited by MKP-1 knockdown. Retinoic acid exerts a significant therapeutic effect on adjuvant arthritis in mice by regulating macrophage polarization through the MKP-1/MAPK pathway, and play an important role in the treatment of rheumatic diseases.

Macrophages are innate immune cells connected with the development of inflammation. Retinoic acid has previously been proved to have anti-inflammatory and anti-arthritic properties. However, the exact mechanism through which retinoic acid modulates arthritis remains unclear. This study aimed to investigate whether retinoic acid ameliorates rheumatoid arthritis by modulating macrophage polarization. This study used retinoic acid to treat mice with adjuvant arthritis and evaluated anti-inflammatory effects by arthritis score, thermal nociceptive sensitization test, histopathologic examination and immunofluorescence assays. In addition, its specific anti-arthritic mechanism was investigated by flow cytometry, cell transfection and inflammatory signaling pathway assays in RAW264.7 macrophages in vitro. Retinoic acid significantly relieved joint pain and attenuated inflammatory cell infiltration in mice. Furthermore, this treatment modulated peritoneal macrophage polarization, increased levels of arginase 1, as well as decreased inducible nitric oxide synthase expression. In vitro, we verified that retinoic acid promotes macrophage transition from the M1 to M2 type by upregulating mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1) expression and inhibiting P38, JNK and ERK phosphorylation in lipopolysaccharide-stimulated RAW264.7 cells. Notably, the therapeutic effects of retinoic acid were inhibited by MKP-1 knockdown. Retinoic acid exerts a significant therapeutic effect on adjuvant arthritis in mice by regulating macrophage polarization through the MKP-1/MAPK pathway, and play an important role in the treatment of rheumatic diseases.

Macrophages are innate immune cells connected with the development of inflammation. Retinoic acid has previously been proved to have anti-inflammatory and anti-arthritic properties. However, the exact mechanism through which retinoic acid modulates arthritis remains unclear. This study aimed to investigate whether retinoic acid ameliorates rheumatoid arthritis by modulating macrophage polarization. This study used retinoic acid to treat mice with adjuvant arthritis and evaluated anti-inflammatory effects by arthritis score, thermal nociceptive sensitization test, histopathologic examination and immunofluorescence assays. In addition, its specific anti-arthritic mechanism was investigated by flow cytometry, cell transfection and inflammatory signaling pathway assays in RAW264.7 macrophages in vitro. Retinoic acid significantly relieved joint pain and attenuated inflammatory cell infiltration in mice. Furthermore, this treatment modulated peritoneal macrophage polarization, increased levels of arginase 1, as well as decreased inducible nitric oxide synthase expression. In vitro, we verified that retinoic acid promotes macrophage transition from the M1 to M2 type by upregulating mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1) expression and inhibiting P38, JNK and ERK phosphorylation in lipopolysaccharide-stimulated RAW264.7 cells. Notably, the therapeutic effects of retinoic acid were inhibited by MKP-1 knockdown. Retinoic acid exerts a significant therapeutic effect on adjuvant arthritis in mice by regulating macrophage polarization through the MKP-1/MAPK pathway, and play an important role in the treatment of rheumatic diseases.

ObjectiveTo evaluate the pharmacodynamic effect of Huangqintang （HQT） on ulcerative colitis （UC） model mice and investigate its protective effect against UC by regulating intestinal flora. MethodMale Balb/c mice were randomly divided into control group，model group， high-， medium-， and low-dose HQT groups （20， 10， 5 g·kg^-1）， flora interference group， flora interference model group， and flora interference-drug treatment group （HQT， 20 g·kg^-1）. The flora interference model was constructed through intragastric administration of antibiotics （200 mg·kg^-1 bacitracin and 200 mg·kg^-1 vancomycin） for 8 d， and the UC model was constructed by allowing mice with free access to 3% dextran sulfate sodium （DSS） solution for 7 d. HQT was administered for 7 d. After the experiments， the mice were sacrificed， and blood， colon， and feces were collected. Hematoxylin-eosin （HE） staining was performed to observe the colonic lesions. The serum levels of interleukin （IL）-4， IL-6， IL-10， and tumor necrosis factor （TNF）-α were detected by enzyme-linked immunosorbent assay （ELISA）. The mRNA and protein expression of Claudin1， MUC1， Occludin， and zonula occludens-1（ZO-1） in colon tissues was detected by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot， respectively. The fecal DNA of mice was extracted and analyzed by high-throughput sequencing. ResultCompared with the normal group， the model group showed increased serum content of IL-4， IL-6， and TNF-α （P<0.05， P<0.01） and decreased IL-10 （P<0.05）. Compared with the model group， the HQT groups displayed decreased serum levels of IL-4， IL-6， and TNF-α （P<0.05， P<0.01）， increased IL-10 content （P<0.01）， increased mRNA and protein expression levels of Claudin1， MUC1， Occludin， and ZO-1 （P<0.05， P<0.01）. After flora interference， the diversity and abundance of intestinal bacteria decreased. To be specific， Proteobacteria increased （P<0.01）， and Firmicutes and Bacteroidetes decreased （P<0.01）. After UC induction by DSS， Bacteroidetes and Tenericutes decreased （P<0.05）. The high-， medium-， and low-dose HQT groups showed increased Bacteroidetes and Tenericutes （P<0.05， P<0.01） and decreased Firmicutes （P<0.05）. Additionally， the abundance of Lactobacillus， Lachnospiraceae NK4A136 group， Escherichia-Shigella， and Helicobacteris was positively proportional to the dose of HQT. ConclusionHQT can inhibit the inflammatory response of UC mice， restore the imbalance of intestinal flora， and repair the damaged intestinal mucosal barrier.

Fetal ECG monitoring is a routine clinical detection method that can reflect the changes of fetal heart in utero in real time. At present, most of the clinical fetal heart rate detection adopts the ultrasonic Doppler method, which is technically difficult and highly specialized in operation and expensive. This study introduces a fetal ECG detection system based on the maternal abdominal electrode method. The weak fetal ECG changes are sensed through the maternal abdominal electrode, and the mixed ECG signal is obtained through the corresponding amplification and filtering circuit. Finally, the obtained signal is passed through WiFi, transmitted to the host computer. The host computer uses the adaptive filtering algorithm to estimate the fetal ECG signal. The system has strong feasibility, low operation expertise, low cost, and is more convenient.

Body temperature is an important physiological parameter of the human body and is used in medicine to reflect the physiological state and health status of the human body. At present, the commonly used clinical thermometers on the market are mainly divided into contact and non-contact types. Most of them are used for rapid body temperature measurement, and it is not easy to monitor body temperature changes in real time. This article introduces a new wearable wireless body temperature monitoring system based on NTC, which senses through NTC. The temperature changes are amplified and filtered, zeroed, and calibrated, and then the temperature data is uploaded to the mobile phone APP via Bluetooth in real time to achieve real-time accurate measurement of body temperature.
Body Temperature ; Cell Phone ; Humans ; Monitoring, Physiologic ; Temperature ; Wearable Electronic Devices ; Wireless Technology

This study introduces a portable multi-channel EEG signal acquisition system. The system is mainly composed of EEG electrode connector, signal conditioning circuit, EEG acquisition part, main control MCU and power supply part. The low-power EEG acquisition front-end ADS1299 and STM32 are used to form the signal acquisition and data communication part. The collected EEG signal can be transmitted to the PC for real-time display. After relevant tests, the system has small volume, low power consumption, high signal-to-noise ratio, and meets the requirements of portable wearable medical devices.
Electric Power Supplies ; Electrodes ; Electroencephalography ; Signal Processing, Computer-Assisted ; Signal-To-Noise Ratio

Objective:To evaluate the effectiveness of perioperative fasting abbreviation in traumatic patients with orthopaedic trauma and diabetes mellitus undergoing selective surgery.Methods:The patients were selected for this prospective nonrandomized controlled study who had undergone selective surgery from June 2019 to June 2021 at Department of Orthopaedic Trauma, Beijing Jishuitan Hospital. They were divided into an intervention group and a control group according to the wards where they stayed. The intervention group was fasted for solids from 0 o'clock on the surgery day and received oral solution with 6.25% maltodextrin which had been prepared by the nutritional department 3 hours prior to surgery. The control group was fasted for either liquids or solids from the midnight before surgery. All patients were evaluated according to the wake-up score and defensive reflex score after surgery. Once they were awakened, they were allowed slag-free drinks. Normal food was allowed if there was no discomfort after 2 hours. The 2 groups were compared in terms of basic information, actual preoperative fasting time, total amount of preoperative drinking, and postoperative time for initial drinking and eating. The perioperative subjective feelings (anxiety, thirst, hunger, nausea, fatigue, dizziness, sweating, stomach discomfort, etc.), grip strength and blood glucose were observed and compared between the 2 groups. Adverse reactions in the 2 groups were also observed.Results:A total of 135 patients were included, including 52 in the intervention group and 83 in the control group. The intervention group consisted of 22 males and 30 females aged from 30 to 84 years; the control group consisted of 39 males and 44 females aged from 29 to 81 years. There was no significant difference in the basic information between the 2 groups, showing comparability ( P>0.05). The intervention group had significantly shorter preoperative fasting time [3.5 (2.5, 6.3) h versus 12.0 (9.0, 16.0) h], significantly higher water intake before surgery [300 (200, 300) mL versus 100 (100, 200) mL], significantly shorter postoperative fasting time [0.08 (0, 1.25) h versus 2.00(0, 6.00) h], and significantly reduced time to return to normal diet [2.0 (2.0, 2.3) h versus 3.0(2.0, 6.0) h] than the control group (all P<0.05). The symptoms of anxiety, fatigue, sweating, and stomach discomfort in the intervention group were significantly fewer than those in the control group throughout the evaluation period. The thirst in the intervention group was significantly alleviated than that in the control group immediately after returning to the ward after surgery, and the dizziness and hunger were significantly alleviated than those in the control group when the patients left the ward to the operation room before surgery and immediately after returning to the ward. The symptom of nausea after returning to normal diet in the intervention group was significantly relieved compared with the control group. All the comparisons above showed statistically significant differences ( P<0.05). The blood glucose in the intervention group 2 hours after taking slag-free drinks was significantly higher than that in the control group ( Z=-2.108, P=0.035). There was no significant difference in the blood glucose between the 2 groups during other measurement periods ( P>0.05). There were no serious adverse reactions in either of the 2 groups. Conclusion:The protocol of perioperative fasting abbreviation may be safe and feasible for the patients with orthopaedic trauma and diabetes mellitus undergoing selective surgery, because it shows benefits of improving the patients' subjective feelings and stabilizing the blood glucose perioperatively.