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Objective:To analyze the distribution and composition characteristics of jellyfish stings in various coastal baths in Qinhuangdao City from 2017 to 2019, and to provide scientific basis for the prevention, control and early warning of jellyfish stings.Methods:Statistics and analysis of the age, gender, time of stings, location of injury, first symptoms, and playing time in the sea at the time of the sting, etc. of people with jellyfish stings in various bathing beaches along the coast of Qinhuangdao from 2017 to 2019 (July to August) were conducted.Results:The number of jellyfish stings in the coastal bathing beaches of Qinhuangdao City in 2017, 2018, and 2019 was decreasing year by year, with 1 890, 492, and 171 cases respectively. Among them, Qianshuiwan Bathing Beach and Dongshan Bathing Beach had more stings (60.90% and 35.08% respectively in 2017, 24.39% and 64.23% respectively in 2018, 16.96% and 16.42% respectively in 2019). There was no significant change in the gender and age distribution of jellyfish stings each year [57.99% males in 2017, with a median age of 13 (8, 31) years old; 63.21% males in 2018, with a median age of 25 (8, 29) years old; and 59.65% males in 2019, with a median age of 12 (7, 31) years old]. Stings were mainly located at the lower limbs (the proportion of lower limb injuries: 46.54% in 2018, 45.61% in 2019), followed by upper limbs (upper arm, elbow, forearm), trunk, etc. The first symptom was mainly pain (89.43% in 2018, 38.29% in 2019), followed by rash (64.43% in 2018, 59.43% in 2019), numbness, blisters, etc. Sting incidents mainly occurred from 13:00 to 17:59 (the proportion of sting incidents in this time period in 2018 and 2019 were 68.09% and 52.63%, respectively).Conclusions:Jellyfish stings in coastal baths in Qinhuangdao City are mainly distributed in Qianshuiwan Baths and Dongshan Baths. The management of these sea areas should be strengthened, and scientific publicity and medical rescue should be strengthened to prevent jellyfish stings in peak hours and related baths.
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Objective To investigate the relationship between the C-reactive protein (CRP) and nonalcoholic fatty liver disease (NAFLD) prevalence.Methods In this study,63,486 workers who had participated in the Kailuan health examination from July 2012 to October 2013 and without history of drinking,myocardial infarction,stroke and cancer and without data incomplete were recruited.The observation population was divided into three groups according to the levels of CRP at baseline:group 1 (＜ 1 mg/L),group 2 (1-3 mg/ L) and group 3 (＞3 mg/L).The prevalence of NAFLD among three groups was observed.Multiple logistic regression was used to calculated relationship between the CRP and NAFLD prevalence.Results The prevalence of NAFLD in group 1,group 2 and group 3 were 26.9％,42.1％ and 49.3％,respectively,and the differences were significant (x2=2 192.31,P ＜ 0.01).Logistic model showed that after adjustment for age,gender,waist circumference and other confounders,the association between CRP and NAFLD was strong and the OR value (95％ CI) among the group 1,group 2 and group 3 were 1.00,1.49 (1.42-1.56),1.54 (1.45 -1.64),respectively.Conclusion CRP is independently associated with the nonalcoholic fatty liver disease.
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Forty cases of nonbacterial prostatitis were treated by pricking therapy, and another 40 cases were treated by norfloxacin capsul and flavoxate hydrochloride tablets as the control. The result showed the effective rate was 100% in the former and 95% in the latter,and there was a statistical difference in therapeutic effect between two groups(P ＜ 0.05).Pricking therapy had a good effect on the nonbacterial prostatitis.
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<p><b>OBJECTIVE</b>To study the analgesic mechanism of gabapentin, an anticonvulsant, during antinociceptive clinical treatment.</p><p><b>METHODS</b>Whole-cell voltage-clamp recordings were taken from adult rat spinal cord slices to investigate the effect of gabapentin on primary afferent A delta-fiber evoked excitatory postsynaptic currents (EPSCs) to substantia gelatinosa (SG) neurons in normal and inflamed (established by plantar injection of carrageenan) rats.</p><p><b>RESULTS</b>Gabapentin (5 - 20 micro mol/L for 5 min) depressed dorsal root A delta fiber evoked polysynaptic, but not monosynaptic EPSCs to SG experiencing inflammation by about 25% (n = 10, P < 0.01). However, gabapentin did not depress the evoked polysynaptic or monosynaptic EPSCs in normal rats. Gabapentin failed to block a glutamate receptor subtype, N-methyl-D-aspartate (NMDA), -induced slow excitatory currents on SG neurons.</p><p><b>CONCLUSIONS</b>Inflammation, at least in part, unmasks the gabapentin depression on nociception transmission in the dorsal horn, and this depression is not due to the blockade of postsynaptic NMDA receptor.</p>
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Animals , Rats , Acetates , Pharmacology , Amines , Cyclohexanecarboxylic Acids , Nerve Fibers, Myelinated , Physiology , Rats, Sprague-Dawley , Receptors, N-Methyl-D-Aspartate , Physiology , Sodium Channels , Physiology , Substantia Gelatinosa , Physiology , Synaptic Transmission , Tetrodotoxin , Pharmacology , gamma-Aminobutyric AcidABSTRACT
Objective To investigate the effect and mechanism of p38 MAPK inhibition in reducing the damage to rat's hippocampal neurons caused by kainic acid (KA) and observe the three-dimensional morphological changes on the cell surface. Methods The rat's hippocampal neurons cultured primarily for 10 days were pretreated with SB203580 (0.2 ?mol/L, a p38 MAPK inhibitor). Thirty minutes later, the hippocampal neurons were administered with KA at concentrations of 0, 25 and 250 ?mol/L for action for 10 and 100 minutes respectively. The cellular membrane structure was scanned and examined at nano-level by using atomic force microscope. Results Normal neurons displayed smooth membrane surface with homogeneous and regular undulation. In contrast, the neurons treated with KA showed coarse membrane surface with holes. Furthermore, the degree changes increased with the action time and the KA concentrations in a dose-effect dependent fashion. The above-mentioned changes were obviously mitigated by means of pretreatment with SB203580 (200 nmol/L). Conclusions Inhibition of p38 MAPK may, in certain degrees, protect the neurons against the impairments on cytomembrane resulted from the toxic effect of KA.
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AIM: To study signal transduction pathway of nitric oxide-induced PC12 cell death. METHODS: After PC12 cells were incubated with sodium nitroprusside(SNP), caspase-3 inhibitor Ⅱ plus SNP or p38 inhibitor-SB203580 plus SNP, cell survival rate was quantified by MTT assay and caspase-3 activity was measured with caspase-3 assay kits. RESULTS: SNP induced PC12 cell death in a dose- and time-dependent manner, and increased caspase-3 activity gradually. Both caspase-3 inhibitorⅡand SB203580 reduced cell death significantly, but SB203580 reduced caspase-3 activity significantly. CONCLUSION: NO might induce PC12 cell death through the activation of p38 and caspase-3.