Professor LI Zhidao puts forward the application of "group acupoints" in his clinical practice by imitating the mutual reinforcement and mutual assistance of Chinese herbal medicine. It is based on the theory as "where is the acupoint located, what are the indications of this acupoint"; and consists with the specific actions of ancient needling techniques at acupoints. The distribution of "group acupoints" is in line with the "located by the region division of the head and trunk, and by the meridians on the four extremities", which is recorded in Zhenjiu Jiayi Jing (the Systematic Classic of Acupuncture and Moxibustion). It shows "the importance of the relationship between acupoints and zangfu", and "the emphasis on the distribution of nerves and muscles" respectively. In clinical practice, controlling needling sensation is the essence of this technique at "group acupoints", the integration of acupoints and needling technique is the basic requirement, and the step-by-step needling manipulation is critical for obtaining the therapeutic effect. "Group acupoints" combined with specific needling technique advance the application efficiency and the effect of acupoints.
Acupuncture Points ; Acupuncture Therapy/methods* ; Humans ; China ; History, 20th Century ; Meridians ; Medicine in Literature ; Acupuncture/history*

Objective To investigate the relationship between the expression of serum long non coding RNA nuclear-enriched abundant transcript 1(lncRNA NEAT1)and microRNA-106a-5p(miR-106a-5p)and the severity and prognosis of sepsis patients.Methods A total of 185 patients with sepsis who were diagnosed and treated in this hospital from August 2021 to July 2024 were selected as the study group,and another 215 healthy volunteers who underwent physical examinations in this hospital during the same period were selected as the control group.The research group was divided into the mild group(n=92),the severe group(n=58)and the shock group(n=35)according to the severity of the disease.The research group was divided into the good prognosis group(n=121)and the poor prognosis group(n=64)according to the prognosis.The expres-sions of lncRNA NEAT1 and miR-106a-5p were detected by real-time fluorescence quantitative polymerase chain reaction,and the correlation of the expressions of lncRNA NEAT1 and miR-106a-5p in the study group was analyzed by Pearson correlation analysis.The binding sites of lncRNA NEAT1 and miR-106a-5p were an-alyzed by StarBase,and the influencing factors of poor prognosis in patients were analyzed by multivariate Lo-gistic regression.The receiver operating characteristic curve was used to analyze the diagnostic value of the combination of lncRNA NEAT1 and miR-106a-5p for poor prognosis in patients.Results The expression of lncRNA NEAT1 in the study group was higher than that in the control group,and the expression of miR-106a-5p was lower than that in the control group,the difference was statistically significant(P＜0.05).The expressions of lncRNA NEAT1 and miR-106a-5p in the study group were negatively correlated(r=-0.413,P＜0.001),and there were binding sites between the two.With the increase of the severity of sepsis,the ex-pression of lncRNA NEAT1 increased and the expression of miR-106a-5p decreased,and the difference was statistically significant(P＜0.05).The acute physiology and chronic health evaluation Ⅱ(APACHE Ⅱ)score,sequential organ failure assessment(SOFA)score,tumor necrosis factor-α,C-reactive protein,and ln-cRNA NEAT1 in the poor prognosis group were higher than those in the good prognosis group,while the ex-pression of miR-106a-5p was lower than that in the good prognosis group,the difference was statistically sig-nificant(P＜0.05).Elevated APACHE Ⅱ score,SOFA score and lncRNA NEAT1 were independent risk fac-tors for poor prognosis in patients,and miR-106a-5p was an independent protective factor(P＜0.05).The ar-ea under the curve of the combined diagnosis of the two was 0.918(95％CI:0.868-0.953),which was supe-rior to the separate diagnosis of each(Zcombined with lncRNA NEAT1=4.112,Zcombined with miR-106a-5p=4.023,P＜0.05).Con-clusion With the increase of disease severity in patients with sepsis,the expression of lncRNA NEAT1 in-creases and the expression of miR-106a-5p decreases.The combined diagnosis of the two for poor prognosis in patients has a high clinical value.

Objective:To analyze 12 antithrombins (AT) gene mutations that cause AT deficiency and discuss the relationship between the SERPINC1 gene. mutations and venous thrombotic events.Methods:This study belongs to case series of observational studies. Collected the clinical data of 12 AT deficiency cases in the First Affiliated Hospital of Wenzhou Medical University from April 2014 to April 2021 and collected the blood samples before treatment. The AT activity (AT: A) and AT antigen (AT: Ag) was detected by chromogenic substrate and immunoturbidimetry, respectively. The 7 exons and flanking sequences of the SERPINC1 gene were sequenced directly by PCR, the suspected mutations were validated by reverse sequencing. Analyzed the correlation between the SERPINC1 gene. mutations and venous thrombotic events and figured out the proportion.Results:The AT: A of the 12 patients all decreased significantly, ranging from 30% to 66%, and the AT: Ag of the 7 patients decreased accordingly, showing type Ⅰ AT deficiency, and the AT: Ag of the other 5 patients were normal, presented type Ⅱ AT deficiency. 12 mutations were found including 6 heterozygous mutations which were discovered for the first time: c.456_458delCTT(p.phe121del), c.318_319insT(p.Asn75stop), c.922G>T(p.Gly276Cys), c.938T>C (p.Met281Thr), c.1346T>A(p.Leu417Gln)and c.851T>C(p.Met252Thr). All 12 patients had venous thrombosis, and 3 cases including 2 compound heterozygotes and 1 single heterozygote all suffered from deep venous thrombosis (DVT) when they were younger without obvious triggers. The other 9 patients all combined with the other thrombotic factors including old age, hypertensive, smoking, pregnancy, and prolonged immobilization.Conclusion:Patients with AT deficiency caused by SERPINC1 gene defects are prone to venous thrombosis, especially combined with other thrombotic factors.

Objective:To evaluate the effect of hydrogen on the expression of hippocampal cold-inducible RNA-binding protein (CIRP) after cardiac arrest-resuscitation in rats.Methods:Ninety clean-grade healthy male Sprague-Dawley rats, weighing 280-320 g, were randomly divided into 3 groups: sham group (group Sham, n=20), cardiac arrest-cardiopulmonary resuscitation group (group CPR, n=35), and hydrogen-rich saline group (group H 2, n=35). Cardiac arrest was induced by transoesophageal cardiac pacing followed by CPR in group CPR.Only femoral arteriovenous puncture and tracheal intubation were performed in group Sham.Hydrogen-rich saline 5 ml/kg was intraperitoneally injected immediately after recovery of spontaneous circulation (ROSC) and at 6 and 12 h after ROSC in group H 2 , while the equal volume of normal saline was given instead in the other two groups.Neuro-functional deficit was assessed using neurologic deficit scores (NDS) at 1 and 3 days after ROSC.The animals were sacrificed immediately after intubation in group Sham and at 6 h and 1, 2 and 3 days after ROSC in CPR and H 2 groups, and the hippocampal tissues were obtained to detect the expression of nuclear and cytoplasmic CIRP by Western blot. Results:Compared with group Sham, NDS was significantly decreased at each time point after ROSC in group CPR and group H 2, the expression of nuclear CIRP was significantly down-regulated at 1, 2 and 3 days after ROSC, and the expression of cytoplasmic CIRP was up-regulated at 1 and 2 days after ROSC in group CPR, and the expression of nuclear CIRP was significantly down-regulated at each time point after ROSC, and the expression of cytoplasmic CIRP was down-regulated at 2 and 3 days after ROSC in group H 2 ( P<0.05). Compared with group CPR, NDS was significantly increased at each time point after ROSC, the expression of nuclear CIRP was down-regulated at 6 h after ROSC, and the expression of cytoplasmic CIRP was down-regulated at 1 and 2 days after ROSC in group H 2 ( P<0.05). Conclusion:The nechanism by which hydrogen reduces brain injury after cardiac arrest-resuscitation may be related to down-regulating hippocampal CIRP expression in rats.

Objective To evaluate the effect of mild hypothermia combined with hydrogen-rich saline on cerebral injury after cardiac arrest and resuscitation in rats.Methods Healthy male Sprague-Dawley rats,aged 7-8 weeks,weighing 280-320 g,were divided into 5 groups (n=33 each) using a random number table method:sham operation group (group S),cardiac arrest and resuscitation group (group CAR),hydrogen-rich saline group (group H2),mild hypothermia group (group MH),and mild hypothermia plus hydrogen-rich saline group (group MH+H2).Cardiac arrest was induced with transoesophageal cardiac pacing followed by cardiopulmonary resuscitation to establish the cerebral injury model.Hydrogen-rich saline 5 ml/kg was intraperitoneally injected immediately after return of spontaneous circulation (ROSC) in H2 and MH+H2 groups,while the equal volume of normal saline was given instead in the other groups.The body temperature of rats was cooled down to 32-34℃ within 15 min starting from the time point immediately after ROSC and maintained for 4 h in MH and MH+H2 groups.Fifteen rats were selected at 24 h after ROSC to assess the neurological function score (NDS).Eighteen rats in each group were sacrificed at 24 h after ROSC,and brains were removed for microscopic examination of the pathological changes in hippocampal CA1 region after hematoxylin and eosin staining and for determination of pyramidal cell count and expression of glucose-regulated protein 78 (GRP78),C/EBP-homologous protein (CHOP),caspase-12,caspase-3,Bcl-2 and Bax in hippocampal CA1 region (by Western blot).Results Compared with group S,the NDS was significantly decreased,the pyramidal cell count was reduced,the expression of GRP78,CHOP,caspase-12,caspase-3 and Bax was up-regulated,and the expression of Bcl-2 was down-regulated in the other four groups (P＜0.05).Compared with group CA-R,the NDS and pyramidal cell count were significantly increased,the expression of GRP78 and Bcl-2 was up-regulated,and the expression of CHOP,caspase-12,caspase-3 and Bax was down-regulated in H2,MH and MH+H2 groups (P＜0.05).Compared with group H2 or group MH,the NDS and pyramidal cell count were significantly increased,the expression of caspase-3 and Bax was down-regulated,the expression of Bcl-2 was up-regulated (P＜0.05),and no significant change was found in the expression of GRP78,CHOP and caspase-12 in group MH+H2 (P＞ 0.05).Conclusion Combination of mild hypothermia and hydrogen-rich saline offers enhanced efficacy in reducing cerebral injury after cardiac arrest and resuscitation over mild hypothermia or hydrogen-rich saline alone in rats.

Objective To observe the effect of continuous incision infusion different concentra-tion of ropivacaine for postoperative analgesia after radical mastectomy.Methods One hundred pa-tients under radical mastectomy,aged 40-70 years,ASA Ⅰ or Ⅱ,were randomly divided into four groups (n =25 each):0.2% (group R1),0.3% (group R2),0.4% (group R3)ropivacaine incision continued infiltration group and patient-controlled intravenous analgesia (group PCIA)as control group.VAS pain scores,sedation Ramsay score and side effects were recorded at each time point in rest and turning over 90°,2 h (T1 ),4 h (T2 ),8 h (T3 ),12 h (T4 ),24 h (T5 ),48 h (T6 )after the operation.Results VAS scores in group R1 at T1-T6 in rest and turn over 90°were significantly high-er than that of group PCIA (P <0.05).There were no significant differences among the group PCIA, group R2 and group R3.Sedation score in PCIA group was significantly higher than that in the other three groups (P <0.05),and the adverse reactions,such as nausea and vomiting,in group PCIA (2 cases)were more serious than that in the other groups (0 cases ).There were no significant differences among the other groups.Conclusion Ropivacaine plays an effective role in infiltration an-algesia when its concentration reaches 0.3% subcutaneous after radical mastectomy.

Objective To observe different behavior of proliferation,migration and invasion of SGC-7901 cells when exposured to dexrnedetomidine of different concentrations.Methods Human gastric cancer cells SGC-7901 were inoculated on culture plate for 24 h,then were randomly divided into 5 groups:control group (group C),dexmedetomidine 312.5μg/ml group (group D1),dexme detomidine 625μg/ml group (group D2),dexmedetomidine 1 250 μg/ml group (group D3),dexmedetomidine 2 500 μg/ml group (group D4).Each group was medicated and incubated for 48 h,then the cell proliferation,migration and invasion immediately were detected by CCK-8 and Transwell.Results SGC-7901 cell viability of groups D1,D2,D3 和 D4 had no significant difference compared with that of group C.The invasion ability and migration ability of SGC-7901 cells in groups D1,D2,D3 and D4 were significantly higher than those in group C (P ＜ 0.05 or P ＜ 0.01).Conclusion Dexmedetomidine can promote migration and invasion of SGC-7901 cells.

Objective To evaluate the effect of hydrogen sulfide on hippocampal endoplasmic reticulum stress during global cerebral ischemia-reperfusion (I/R) in rats.Methods Seventy-two pathogen-free healthy male Sprague-Dawley rats,weighing 280-320 g,aged 8-10 weeks,were divided into 3 groups (n=24 each) using a random number table:sham operation group (group Sham),global cerebral I/R group (group I/R) and global cerebral I/R plus sodium hydrosulfide group (group I/R+NaHS).Cardiac arrest was induced with transoesophageal cardiac pacing followed by cardiopulmonary resuscitation to establish the global cerebral I/R model.Immediately after recovery of spontaneous circulation,sodium hydrosulfide 2.5 mg/kg was intraperitoneally injected in group I/R+NaHS,and normal saline 5 ml/kg was given in group I/R.The hippocampi were immediately removed at 24 h of reperfusion for determination of the expression of glucose-regulated protein 78 (GRP78),C/EBP-homologous protein (CHOP) and caspase-12 in hippocampal tissues (by Western blot).At 1,3 and 7 days of reperfusion,the hippocampal tissues were obtained and stained with haematoxylin and eosin for examination of the pathological changes in hippocampal CA1 region (under a light microscope) and for determination of apoptosis in hippocampal cells (using TUNEL staining),and the apoptosis rate was calculated.Results Compared with group Sham,the apoptosis rate of hippocampal tissues at 1,3 and 7 days of reperfusion in group I/R and at 3 and 7 days of reperfusion in group I/R+NaHS were significantly increased,and the expression of GRP78,CHOP and caspase-12 in hippocampal tissues was significantly up-regulated in I/R and I/R+NaHS groups (P＜0.05).Compared with group I/R,the apoptosis rate of hippocampal tissues was significantly decreased,and the expression of GRP78,CHOP and caspase-12 was down-regulated at 1,3 and 7 days of reperfusion (P＜0.05),and the pathological changes were significantly attenuated in group I/R+NaHS.Conclusion The mechanism by which hydrogen sulfide reduces apoptosis in hippocampal cells is related to inhibition of endoplasmic reticulum stress during global cerebral I/R in rats.

Objective To investigate the effect of mild hypothermia combined with mitochondrial divison inhibitor 1 in mitochondrial after cerebral ischemia-reperfusion (IR).Methods Fourty male healthy Sprague-Dawley (SD) rats, weighing 280-320 g, were randomly divided into 5 groups (n=8 each): group Sham, group IR, hypothermia group (group H), Mdivi-1 group (group M) and hypothermia+Mdivi-1 group (group HM).Animal models of global cerebral IR were established by transoesophageal cardiac pacing inducing cardiac arrest followed by cardiopulmonary resuscitation (ischemia 4 min and reperfusion 6 h).The group Sham was similarly treated to group IR except the cardiac arrest and cardiopulmonary resuscitation.In groups H and HM, the core temperature was cooled down to 32-34℃ within 15 min starting from the beginning of reperfusion, and maintained for 6 h.In the other groups, the core temperature was maintained at the normal temperature.In groups M and HM, the animals were given Mdivi-1 (1.2 mg/kg) intravenously at the beginning of the reperfusion and the other groups were given the same Volume of dimethylsnlfone (DMSO).After 6 h of reperfusion, the rats were sacrificed, and bilateral hippocampi were immediately removed for determination the protein level of dynamin-related proten 1 (Drp1) and cytochrome C (Cyt-C) expression by Western blot and obsevation of the mitochondrial structure of pyramidal cell in hippocampal CA1 under electronic microscope.Results Compared with group Sham, the expression of Drp1 and Cyt-C was up-regulated in groups IR, H, M and HM (P＜0.05).Compared with group IR, the expression of Drp1 and Cyt-C was down-regulated in groups H, M and HM (P＜0.05).Compared with groups H and M, the expression of Drp1 and Cyt-C was down-regulated in group HM (P＜0.05).There was no significant difference in the expression of Drp1 and Cyt-C between groups H and M.The mitochondria were rod-shaped with clear and sound structure in group Sham, while mitochondria showed various degree of fission, swollen structures, matrix deposit, vacuoles formation and cristae collapse in other groups.The changes of group HM were relatively slight.Conclusion Mild hypothermia combined with mitochondrial divison inhibitor 1 alleviate mitochondrial damage after global cerebral IR of rats.The combined effect is better than that of any individual application.

Objective To explore a scientific and reasonable fiscal input mechanism for public hospitals, in order to fully leverage the policy guidance and efficiency of such funding.Methods With literature review, expert consultation and demonstration, a basic subsidy model for public hospitals was established.According to the past operation data of 4 public hospitals in Baoshan district of Shanghai, the study figured out specific subsidy standards.Results The basic subsidy for public hospitals should be determined according to the number of approved beds, the number of outpatients and emergency visits, hospital bed days, surgeries, key services, and the quality and efficiency of work.In Baoshan district, the standard reference value of subsidy for each approved bed, each outpatient and emergency visit, each bed-day, each surgical operation is 42 096 yuan, 27.9 yuan, 104.9 yuan and 244 yuan respectively.The standard value of subsidy is 100 yuan per bed for critically ill inpatients.For patients under clinical pathway management, the subsidy is 300 yuan per case, and for hospital maternal care, it is 150 yuan per person.Conclusions The basic subsidy model for public hospitals has overcome the shortcomings of fiscal input based on hospital scale or hospital workload, and established an incentive mechanism to promote the implementation of key services.These measures can improve the operation mechanism of public hospitals and encourage them to play their role of public welfare as designed.