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The FHD-2B proton magnetometer at Wen’an station had large F component noise from 2020 to 2021. There is a high correlation between noise interference and temperature, which is generally characterized by high noise in winter and low noise in summer. The surrounding environment, power supply voltage, grounding resistance, power supply line leakage, probe leakage and power frequency interference of the magnetic room were checked respectively, and no interference sources were found. By studying the principle of FHD proton magnetometer, it is found that the harmonic capacitance capacity of FHD proton magnetometer changes with temperature. The capacity is small at low temperature and large at high temperature. The change of the capacity of the harmonic capacitor will affect the center frequency of the oscillation circuit f0, resulting in increased noise. Since the noise interference of the FHD proton magnetometer at Wen’an station is highly correlated with temperature, it is speculated that the noise interference may be related to the change in the capacity of the harmonic capacitance. We can adjust the inductance L of the probe to correct the influence of the circuit center frequency of the harmonic capacitance capacity transformation. The probe inductance was adjusted several times through experiments, and 34.4 mH was selected as the most appropriate probe inductance value. After the experiment, the noise value of F component decreased, the data curve became smooth, and the noise interference was solved.

Background Themucosal structure of the respiratory tract is similar to that of the gastrointestinal tract in humans, which is the body's first line of defense against the invasion of pathogens through the function of mucosal barrier. When the respiratory tract infection stimulates the airway mucosa to produce a local immune response, it affects the intestinal tract through migration and homing, resulting in the weakening of the local mucosal anti-infection ability, inducing mucosal barrier damage, and further aggravating chronic obstructive pulmonary disease (COPD) . Objective To explore the effects of Bufei Jianpi Formula on the expression levels of inflammatory factors in lung tissue, and the content of lung-gut related peptides in lung and colon tissues in a rat model of stable COPD based on a typical viscera theory of Traditional Chinese Medicine, namely "the lungs and large intestines are interior-exteriorly related" . Methods This experiment was carried out from September 2019 to December 2020. Fifty SPF SD rats were selected, and equally and randomly divided into control, model, Bufei Jianpi, aminophylline and probiotics groups. Except for the control group, the rats in other groups received cigarette smoke exposure combined with intranasal instillation of lipopolysaccharide (LPS) in the first eight weeks of intervention for establishing a COPD model. From the ninth week of intervention, rats in the control and model groups received intragastric administration of 0.9% sodium chloride solution, and those in Bufei Jianpi, aminophylline and probiotics groups received intragastric administration of Bufei Jianpi Formula, aminophylline and probiotics, respectively. The rats were sacrificed after 12 weeks of intervention. The pathological changes of lung and colon tissues were observed under an optical microscope, the expression levels of tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) in lung tissue were detected by immunohistochemistry. The contents of secretory immunoglobulin A (SIgA) in bronchoalveolar lavage fluid (BALF) , substance P (SP) and vasoactive intestinal peptide (VIP) in lung and colon tissues were detected by enzyme-linked immunosorbent assay (ELISA) . Results In terms of morphology, the lung and colon tissue structures of rats in the control group were basically intact. In the model group, the trachea was narrowed and surrounded by a lot of inflammatory cells with thickened bronchial wall. The improvement in histopathology of the lung tissues was the most obvious in Bufei Jianpi group. The colon tissue of rats in the model group was damaged, which was manifested by numerous shed epithelial cells, and crypts in different shapes and sizes. Bufei Jianpi group demonstrated better improvement in histopathology of the colon tissue. There were statistically significant differences in the expression levels of TNF-α, IL-10, SP and VIP in the lung tissue of the five groups of rats (FTNF-α=70.640, FIL-10=8.444, FSP=108.700, FVIP=4.665, P

Objective To investigate the influence of transient receptor potential cation channel 6 (TRPC6) on renal tubulointerstitial inflammation in mice with diabetic kidney disease (DKD) and its mechanism. Methods A total of 36 male C57/BL6J mice, aged 6 weeks, were randomly divided into control group (group A), DKD model group (group B), DKD+normal saline intervention group (group C), DKD+mitophagy activator intervention group (group D), DKD+negative control lentivirus transfection group (group E), and DKD+TRPC6 knockdown lentivirus transfection group (group F), with 6 mice in each group. The mice in groups A and B were respectively given intraperitoneal injection of 0.1 mmol/L citrate buffer and 10 g/L streptozotocin (hereinafter referred to as administration); the mice in groups C and D were respectively given normal saline and 10 mmol/L urolithin A by gavage in addition to the treatment in group B; the mice in groups E and F were respectively injected with negative control lentivirus and TRPC6 knockdown lentivirus via the tail vein in addition to the treatment in group B. The levels of fasting blood glucose (FBG), urinary albumin-to-creatinine ratio (ACR), and blood urea nitrogen (BUN) were measured at week 12 after administration; PAS staining was used for the observation and scoring of renal tubular injury; RT-qPCR was used to measure the mRNA expression levels of inflammatory factors [interleukin-1β (IL-1β), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-α (TNF-α)] in renal tissue; immunohistochemical staining was used to measure the protein expression level of TRPC6 in renal tissue, and Western blotting was used to measure the relative expression levels of TRPC6, LC3B, P62, PINK1, and Parkin in renal tissue; transmission electron microscopy was used to observe the change in the number of mitophagosomes in renal tubular cells of mice. HK-2 cells were divided into high glucose+TRPC6 siRNA transfection+DMSO intervention group (group G, treated with TRPC6 siRNA+35.0 mmol/L glucose+0.06% DMSO) and high glucose+TRPC6 siRNA transfection+mitophagy inhibitor intervention group (group H, treated with TRPC6 siRNA+35.0 mmol/L glucose+12 μmol/L oroxylin A), and then RT-qPCR was used to measure the mRNA expression levels of inflammatory factors (IL-1β, MCP-1, and TNF-α) in cells. Results At week 12 after administration, compared with group A, group B had significantly higher whole blood FBG, ACR, BUN, renal tubular injury score, mRNA expression levels of inflammatory factors, and protein expression levels of TRPC6 and P62 in renal tissue (t=2.77-13.61,P