Electroacupuncture ameliorates pain in cervical spondylotic radiculopathy rat by inhibiting the CaMKII/CREB/BDNF signaling pathway and regulating spinal synaptic plasticity.

BACKGROUND: Central sensitization is one of the important mechanisms underlying neuropathic and radicular pain due to cervical spondylotic radiculopathy (CSR). Recent studies have shown that the calmodulin-dependent protein kinase II (CaMKII)/cAMP-response element binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling pathway mediates central sensitization through its involvement in spinal cord synaptic plasticity. Our group has previously found that electroacupuncture (EA) has a good analgesic effect on CSR. However, the central analgesic mechanism of EA for CSR is not yet clear. METHODS: The rats were randomly divided into Blank group, Sham-operated group, CSR group, and EA group. We prepared the CSR rat model using the fish wire extrusion method. The behavioral and mechanical pain thresholds of the rats in each group were measured 5 days after successful modeling and 7 days after the intervention. The first intervention was started 5 days after successful modeling, and the EA group was treated by acupuncture at the bilateral LI4 and LR3 points on the same side as one group, connected to a G6805-I electroacupuncture apparatus with continuous waves at 1.5 Hz. The remaining groups were not subjected to EA intervention. The treatment was administered once a day for 7 consecutive days and then executed. We used WB, immunofluorescence, and qRT-PCR to detect the expression of CaMKII/CREB/BDNF signaling pathway-related factors in the synaptic of rat spinal cord in each group. RESULTS: EA improved pain threshold and motor function in CSR rats, inhibited the expression of BDNF, P-TrkB, CAMKII, and P-CREB in spinal cord synapses, reduced the expression of pain factor c-fos and postsynaptic membrane protein molecule neuroligin2, exerted a modulating effect on spinal cord synaptic plasticity in CSR rats, and suppressed the overactive synaptic efficacy. CONCLUSION: EA mediates central sensitization and exerts analgesic effects on CSR by modulating spinal synaptic plasticity, which may be related to the inhibition of CaMKII/CREB/BDNF signaling pathway.

Electroacupuncture Attenuates Neuropathic Pain in a Rat Model of Cervical Spondylotic Radiculopathy: Involvement of Spinal Cord Synaptic Plasticity.

Purpose: Cervical spondylotic radiculopathy (CSR) is a common neurologic condition that causes chronic neck pain and motor functions, with neuropathic pain (NP) being the primary symptom. Although it has been established that electroacupuncture (EA) can yield an analgesic effect in clinics and synaptic plasticity plays a critical role in the development and maintenance of NP, the underlying mechanisms have not been fully elucidated. In this study, we explored the potential mechanisms underlying EA's effect on synaptic plasticity in CSR rat models. Materials and Methods: The CSR rat model was established by spinal cord compression (SCC). Electroacupuncture stimulation was applied to LI4 (Hegu) and LR3 (Taichong) acupoints for 20 min once a day for 7 days. Pressure pain threshold (PPT) and mechanical pain threshold (MPT) were utilized to detect the pain response of rats. A gait score was used to evaluate the motor function of rats. Enzyme-linked immunosorbent assay (ELISA), Western blot (WB), immunohistochemistry (IHC), immunofluorescence (IF), and transmission electron microscopy (TEM) were performed to investigate the effects of EA. Results: Our results showed that EA alleviated SCC-induced spontaneous pain and gait disturbance. ELISA showed that EA could decrease the concentration of pain mediators in the cervical nerve root. WB, IHC, and IF results showed that EA could downregulate the expression of synaptic proteins in spinal cord tissues and promote synaptic plasticity. TEM revealed that the EA could reverse the synaptic ultrastructural changes induced by CSR. Conclusion: Our findings reveal that EA can inhibit SCC-induced NP by modulating the synaptic plasticity in the spinal cord and provide the foothold for the clinical treatment of CSR with EA.

[Progress of research on mechanisms of acupuncture and moxibustion in the treatment of rheumatoid arthritis].

In the present paper, we summarize the literature about mechanisms of acupuncture and moxibustion ï¼»including ordinary acupuncture, electroacupuncture, fire needling, warm acupuncture (acupuncture with the needle warmed by burning moxa), cheek acupuncture, wheat-sized moxibustion, suspension moxibustion, etc.ï¼½ treatments of rheumatoid arthritis (RA) both domestically and abroad in recent years. Results indicate that the role of acupuncture and moxibustion therapies in improving RA involves multi-targets and multi-levels. These targets and levels include 1) improving joint and synovial inflammatory response by regulating inflammatory cytokines, inhibiting cell adhesion factor and interferon expression, 2) directly or indirectly regulating immune cell balance, 3) regulating peripheral and central neurotransmitters (plasma CCK-8 and ß-endorphin, hypothalamic prodynorphin, etc.), 4) regulating related signaling pathways (suppressing nuclear factor-kB/vascular endothelial growth factor, Janus tyrosine kinase-signal transducer and activator of transcription, transient receptor potential vanilloid and canonical Wnt/ß-catenin pathways), and activating cholinergic anti-inflammatory pathway, 5) regulating histocyte energy metabolism (improving amino acid supply and reducing negative nitrogen balance to improve immune regulation function), 6) maintaining the balance of bone cells and articular cartilage (by regulating the balance between synthesis and degradation of articular cartilage matrix, and the balance of bone cells and osteoclasts), 7) up-regulating energy metabolism gene (Atp50, Atp6V1B2) expression and regulating biological rhythm gene (clock, Per2, Rev-erb) expression, 8) regulating miRNAs-mediated chondrocyte apoptosis. All these provide experimental basis for acupuncture and moxibustion treatments of RA.

Effects of amino acids on the formation and distribution of glycerol core aldehydes during deep frying.

Glyceryl core aldehyde (GCAs) are hazard factors produced during the frying process using oils and fats, and GCAs control and mitigation research is very important. This study investigated the effects of adding amino acids (methionine, glycine, and histidine) at 2.5, 5, and 10 mM on the formation and distribution of four GCAs during frying. High oleic sunflower oil (HOSO) was selected as frying oil for French fries. After 12 h of frying, the content of GCAs in the tert-butylhydroquinone-treated group (0.02 wt%, 1.1 mM) decreased by 29 % compared with the control group. The addition of methionine, glycine, and histidine decreased the total GCAs by 51 %, 28 %, and 27 %, respectively. The total GCAs content was best inhibited by methionine, while glycine and histidine were not significantly different from TBHQ. Methionine addition significantly reduced GCAs (9-oxo), GCAs (10-oxo-8), and GCAs (11-oxo-9) by 39 %, 78 %, and 80 %, respectively, while histidine was the most potent inhibitor of GCAs (8-oxo), which decreased by 40 %. Methionine also proved effective in slowing degradation of frying oil quality. These results provide a new direction for decreasing GCAs in frying systems.

Associations of selenium exposure with blood lipids: Exploring mediating DNA methylation sites in general Chinese urban non-smokers.

Selenium (Se) is widely distributed in the total environment and people are commonly exposed to Se, while the potential effects and mechanisms of Se exposure on blood lipids have not been well established. This study aimed to assess the associations of urinary Se (SeU) with blood lipids and explore the potential mediating DNA methylation sites. We included 2844 non-smoke participants from the second follow-up (2017-2018) of the Wuhan-Zhuhai cohort (WHZH) in this study. SeU and blood lipids [i.e., total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL), and high-density lipoprotein cholesterol (HDL)] for all participants were determined. The associations of SeU with blood lipids were analyzed by generalized linear models. Then, we conducted the blood lipids related epigenome-wide association studies (EWAS) among 221 never smokers, and the mediation analysis was conducted to explore the potential mediating cytosine-phosphoguanine (CpG) sites in the above associations. In this study, the SeU concentration of the participants in this study was 1.40 (0.94, 2.08) µg/mmol Cr. The SeU was positively associated with TC and LDL, and not associated with TG and HDL. We found 131, 3, and 1 new CpG sites related to TC, HDL, and LDL, respectively. Mediation analyses found that the methylation of cg06964030 (within MIR1306) and cg15824094 (within PLCH2) significantly mediated the positive association between SeU and TC. In conclusion, high levels of Se exposure were associated with increased TC and LDL among non-smokers, and the methylation of MIR1306 and PLCH2 partly mediated Se-associated TC increase. These findings provide new insights into the effects and mechanisms of Se exposure on lipids metabolism and highlight the importance of controlling Se exposure and intake for preventing high blood lipids.

Vitamin D status, genetic factors, and risks of cardiovascular disease among individuals with type 2 diabetes: a prospective study.

BACKGROUND: The presence of a threshold effect has been proposed, suggesting that beneficial effects from vitamin D supplementation may only be present when the vitamin D concentration is below a particular threshold. OBJECTIVES: We investigated the associations of serum 25-hydroxyvitamin D [25(OH)D] concentrations and genetic factors with risks of total and subtypes of cardiovascular disease (CVD) in individuals with type 2 diabetes (T2D), among whom vitamin D deficiency or insufficiency is particularly common. METHODS: This prospective study included 15,103 individuals with T2D who were initially free of CVD and had serum 25(OH)D measurements in the UK Biobank. Incidences of total and subtypes of CVD, including ischemic heart disease (IHD) and stroke, were ascertained via electronic health records. Weighted genetic risk scores (GRSs) were constructed for IHD and stroke. RESULTS: The mean serum 25(OH)D concentration was 43.4 nmol/L (SD: 20.4 nmol/L), and 65.7% of participants had a vitamin D concentration below 50 nmol/L. During a median of 11.2 years of follow-up, 3534 incident CVD events were documented. Compared with individuals with 25(OH)D concentrations <25 nmol/L, participants with 25(OH)D concentrations ≥75 nmol/L had HRs (95% CIs) of 0.75 (0.64, 0.88) for CVD, 0.69 (0.56, 0.84) for IHD, and 0.74 (0.52, 1.06) for stroke. Participants with 25(OH)D concentrations ≥50 nmol/L and low GRSs, as compared with individuals with 25(OH)D concentrations <25 nmol/L and high GRSs, had a 50% (39%, 65%) lower risk of IHD. No significant interactions were demonstrated between serum 25(OH)D concentrations and the GRSs and genetic variants in vitamin D receptors (VDR). CONCLUSIONS: Higher serum 25(OH)D concentrations were significantly associated with lower risks of total CVD and IHD among patients with T2D, regardless of their genetic susceptibility and the genetic variants in VDR. Risk reductions tended to plateau at serum 25(OH)D levels around 50 nmol/L. These findings suggest that maintaining an adequate vitamin D status and avoiding deficiency may help to prevent CVD complications among patients with T2D.

Effects of temperature and ferric ion on the formation of glycerol core aldehydes during simulated frying.

Glycerol core aldehydes (GCAs) are toxins widely formed in oils at high temperature. This study investigated the effects of frying time, temperature, and Fe3+ content on the GCAs formation in high-oleic sunflower oil. The results showed that the GCAs (8-oxo, 9-oxo, 10-oxo-8, 11-oxo-9) concentrations increased with time following the pseudo-first-order kinetics. Frying at 160 °C without Fe3+ and at 180 °C with 0.0005 mol·L-1 Fe3+ yielded the lowest and highest total GCA content. The concentrations of GCAs (8-oxo) and GCAs (9-oxo) or GCAs (10-oxo-8) and GCAs (11-oxo-9) changed similarly with different frying temperature and Fe3+ concentration. The major GCAs was GCAs (9-oxo) (40-70%), which also had the highest formation rate (5.42 × 10-4 mg·g-1·h-1). However, GCA (10-oxo-8) and GCAs (11-oxo-9) with similar proportion (ca. 10-20%) and GCAs (8-oxo) made up the least proportions (<10%).

Insight into COVID-2019 for pediatricians.

Since December 2019, patients with unexplained pneumonia have been found in Wuhan City, Hubei Province, China. The pathogen in these cases is a new type of coronavirus. The World Health Organization confirmed this diagnosis and named the pathogen SARSCoV-2. The disease caused by SARSCoV-2 is called Corona Virus Disease (COVID-2019). The virus is highly infectious and pathogenic, causing human-to-human transmission. At present, SARSCoV-2 is still rampant in the world. Zhengzhou City in Henan Province serves as an example, 102 people have been confirmed to be infected with SARSCoV-2 (at 24:00 on February 5th, 2020), including three children, the youngest is 4 years old. From the perspective of clinical pediatricians as the first line fighting the epidemic, this paper will discuss the clinical characteristics, prevention and control measures, outcomes, diagnosis, and treatment of pediatric cases.

Effects of epigallocatechin-3-gallate on the HMGB1/RAGE pathway in PM2.5-exposed asthmatic rats.

Current studies have shown that long-term exposure to fine particulate matter (PM2.5) can aggravate lung injury in asthmatic children. The HMGB1/RAGE pathway may play an important role, but few studies on the HMGB1/RAGE signaling pathway in PM2.5-induced asthma have been performed. Epigallocatechin-3-gallate (EGCG), which has antioxidant, anti-inflammatory and immunomodulatory effects, has not been examined in studies at home and abroad. In this study, we established an animal model of asthma and observed that the lung tissue was damaged, inflammatory cells infiltrated, bronchial wall thickness (WTt) and bronchial smooth muscle thickness (WTm) increased and the HMGB1 and RAGE mRNA and protein expression increased. The asthmatic rats exposed to PM2.5 showed significantly increased lung injury and inflammatory cell infiltration, WTt and WTm further increased, and HMGB1 and RAGE mRNA and protein levels were higher than those in the asthma group. The asthmatic rats exposed to PM2.5 were treated with EGCG, which alleviated the lung injury, reduced the number of inflammatory cells, decreased WTt and WTm, and reduced the expression of HMGB1 and RAGE mRNA and protein. The high-dose group showed more significant effects than the other groups. In conclusion, our results suggest that HMGB1 and RAGE are involved in the pathogenesis of asthma. PM2.5 exposure significantly aggravated airway inflammation injury in asthmatic rats. EGCG can reduce lung injury and airway remodeling in PM2.5-exposed asthmatic rats and has lung protective effects. The mechanism may be related to regulation of the HMGB1/RAGE signaling pathway. Our results may provide new ideas and methods for the prevention and treatment of PM2.5-induced asthma.

Anti-Depressant-Like Effect of Sinomenine on Chronic Unpredictable Mild Stress-Induced Depression in a Mouse Model.

BACKGROUND Sinomenine (SIN) is an extract of the Chinese medicinal herb Sinomenium acutum; it has various pharmacological properties, including immunosuppression and anti-inflammation. The present study aimed to investigate whether SIN has an anti-depressant-like effect in a mouse model of depression induced by chronic unpredictable mild stress (CUMS), and to explore the underlying molecular mechanisms. MATERIAL AND METHODS A mouse model of depression was established and treated with different concentrations of SIN (30, 100, or 300 mg/kg). Then, behavioral tests, including sucrose preference test (SPT), forced swimming test (FST), and the tail suspension test (TST), were performed. The levels of norepinephrine (NE), 5-hydroxytryptamine (5-HT), and proinflammatory cytokines (interleukin-1ß [IL-1ß] interleukin-6 [IL-6], and tumor necrosis factor-α [TNF-α]) in the hippocampus of mice were detected by ELISA assay. The levels of p-p38, p-p65, NLRP3, ASC, and caspase-1 were measured by Western blot or/and qRT-PCR. RESULTS The results showed that SIN significantly relieved CUMSinduced depressive-like behaviors. Compared with the model mice, SIN treatment significantly increased the sucrose preference of the mice, and the immobility time in the forced swimming and the tail suspension test were shortened. In addition, SIN decreased CUMS-induced reduction in the concentrations of NE and 5-HT in the hippocampus of mice. SIN reduced CUMS-induced increases in the levels of IL-1ß, IL-6, and TNF-α in the hippocampus of mice. Furthermore, activation of the p38MAPK-NF-κB pathway and the nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome induced by CUMS were inhibited by SIN treatment. CONCLUSIONS In conclusion, our results indicate the antidepressantlike effects of SIN on chronic unpredictable mild stress-induced depression in a mouse model.

[Effects of L-carnitine on serum levels of brain natriuretic peptide and N-terminal pro-brain natriuretic peptide and cardiac function in children with severe hand-foot-mouth disease].

OBJECTIVE: To observe the effects of L-carnitine treatment on serum levels of brain natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) and cardiac function in children with heart dysfunction and severe hand-foot-mouth disease (HFMD). METHODS: A total of 120 children with severe HFMD were enrolled and randomly and equally divided into routine treatment group and L-carnitine treatment group. Thirty healthy children served as the control group. HFMD patients were given anti-fever and antiviral treatment as the basic treatment, while the patients in the L-carnitine treatment group were given L-carnitine as an adjuvant treatment to the basic treatment. Treatment outcomes were observed in the two groups. For all the subjects, serum levels of BNP and NT-proBNP and cardiac function parameters including left ventricular ejection fraction (LVEF), fractional shortening (FS), and cardiac index (CI) were measured at different time points before and after treatment. RESULTS: Before treatment, HFMD patients had significantly higher serum levels of BNP and NT-proBNP and heart rate but significantly lower LVEF, FS, and CI compared with the control group (P<0.05). After treatment, the L-carnitine treatment group had a significantly higher response rate than the routine treatment group (P<0.05). After 3 days of treatment, the serum levels of BNP and NT-proBNP, LVEF, FS, and CI were significantly reduced in the L-carnitine group (P<0.05); the L-carnitine group had significantly lower serum levels of BNP and NT-proBNP, LVEF, FS, and CI than the routine treatment group (P<0.05); there were no significant differences in the serum levels of BNP and NT-proBNP, LVEF, FS, or CI between the L-carnitine treatment and control groups (P>0.05). After 5 days of treatment, there were no significant differences in the serum levels of BNP and NT-proBNP, LVEF, FS, or CI between the L-carnitine treatment and routine treatment groups (P>0.05). Heart rate recovery was significantly slower in the routine treatment group than in the L-carnitine treatment group (P<0.05). CONCLUSIONS: As an adjuvant therapy for severe HFMD, L-carnitine treatment has satisfactory short-term efficacy in reducing the serum levels of BNP and NT-proBNP and improving cardiac function, thus improving clinical outcomes.

Comparative Analyses of Cuticular Waxes on Various Organs of Potato (Solanum tuberosum L.).

Complex mixtures of cuticular waxes coat plant surfaces to seal them against environmental stresses, with compositions greatly varying between species and possibly organs. This paper reports comprehensive analyses of the waxes on both above- and below-ground organs of potato, where total wax coverages varied between petals (2.6 µg/cm2), leaves, stems, and tubers (1.8-1.9 µg/cm2), and rhizomes (1.1 µg/cm2). The wax mixtures on above-ground organs were dominated by alkanes, occurring in homologous series of isomeric C25-C35 n-alkanes, C25-C35 2-methylalkanes, and C26-C34 3-methylalkanes. In contrast, below-ground organs had waxes rich in monoacylglycerols (C22-C28 acyls) and C18-C30 alkyl ferulates, together with fatty acids (rhizomes) or primary alcohols (tubers). The organ-specific wax coverages, compound class distribution, and chain length profiles suggest highly regulated activities of wax biosynthesis enzymes, likely related to organ-specific ecophysiological functions.

[Value of mixed embolus transarterial chemoembolization in the treatment of hepatocellular carcinoma].

OBJECTIVE: To investigate the value of transarterial chemoembolization (TACE) using mixed emboli for hepatocellular carcinoma (HCC). METHODS: 188 patients with HCC were divided into two groups according to the treatment modality: 103 patients in group A treated by routine iodine embolus agent; 85 patients in group B by mixed iodine embolus agent (ultra-liquified iodinized oil + gelatin sponge + chemotherapeutic agents). The pattern of the arrested iodine deposition in the tumor, response, resectability during follow-up, pathological changes, survival and complications in the two groups were analyzed and compared. RESULTS: The pattern of full-and-dense iodine deposition in the tumor and the response rate (CR + PR) were 59.2% and 32.0% in group A, 89.4% and 56.5% in group B. Surgical resection after TACE was possible in 5.8% (6/103) of group A versus 15.3% (13/85) of group B. Complete tumor necrosis was observed in 1.0% and 4.7% in groups A and B, respectively. 1-, 2- and 3-year actual survival rates were 57.7%, 42.8% and 8.4% in group A, and 79.8%, 55.3%, 38.5% in group B. The difference in results between the two groups was statistically significant, however, the incidence of complication in the two groups was similar. CONCLUSION: Transarterial chemoembolization with mixed iodine emboli is more effective than with the routine iodine emboli in the treatment of bulky or nodular hepatocellular carcinoma rich in blood supply. Mixed iodine emboli is tolerable without increase in severe complications.