Recent years, national laws and government policies were published as series to encourage the development of group standardizations. The updated Standardization Law of the People's Republic of China, implemented on January 1^st, 2018, stipulates that group standard is a part of the Chinese standard system. Under the current supportive circumstances, more institutes and organizations have joined in the writing and releasing procedures of group standards’. Despite the rapid development of group standardization to publish, we are still at the phase of exploring and regulating group standardizations. This review summarizes the development and practice on the development group standardization in the Chinese Preventive Medicine Association and analyzes current condition and deficiency of the work in China, in order to develop suggestions and strategies to improve and regulate group standardization.

Adipose tissue is the energy storage organ of the body, and excess energy is stored in adipocytes in the form of lipid droplets. The homeostasis of adipose tissue is the basis for the body to maintain normal metabolic activity. Prostaglandin E (PGE) is an important lipid mediator in the body. It is synthesized in almost all tissues and participates in the regulation of many physiological processes such as blood pressure, glucose and lipid metabolism, and inflammation. PGE is abundant in white adipose tissue, where it is involved in the regulation of fat metabolism. PGE plays its biological role through binding to four G protein coupled receptors (prostaglandin E receptors), including EP-1, -2, -3, and -4. The EP4 subtype has been proved to play an important role in adipogenesis and adipose metabolism: it could inhibit adipogenesis while it was activated, whereas its knockout could promote lipolysis. This review summarized the relationship between EP4 and adipose metabolism, hoping to identify new targets of drug development for metabolic disorders.
Adipocytes ; Adipogenesis ; Adipose Tissue ; metabolism ; Humans ; Receptors, Prostaglandin E, EP4 Subtype ; physiology

OBJECTIVE:To explore the effects of extracts from Siegesbeckiae herba (HS) on doxorubicin (DOX)-induced chronic myocardial injury in mice. METHODS:48 mice were randomly divided into 3 groups. Mice in blank control(Con)group received distilled water once every day,ig,and normal saline(2 mL/100 g)once every day,ip,for 8 weeks;mice in DOX mice received distilled water(2 mL/100 g)once every day,ig,and DOX(3 mg/kg)once every week,ip,for 8 weeks;mice in DOX+HS group received HS(340 mg/kg)once every day,ig,and DOX(3 mg/kg)once every week,ip,for 8 weeks. After administra-tion,body mass,heart coefficient,cardiac function changes,serum biochemical index levels [alanine aminotransferase(ALT),as-partate aminotransferase (AST), creatine phosphokinase (CK), creatine kinase isoenzyme (CK-MB), lactate dehydrogenase (LDH)and total cholesterol(TC)] of mice were determined. RESULTS:Compared with Con group,body mass of mice in DOX group was decreased(P<0.01);heart coefficient was increased(P<0.05);heart rate slowed down,R-wave was increased(P<0.05 or P<0.01);serum biochemical indexed were increased,there was significant difference in AST(P<0.01). Compared with DOX group,heart coefficient of mice in DOX+HS group was decreased (P<0.01);heart rate was increased (P<0.01);serum biochemical indexes were decreased,there was significant differences in CK,LDH,TC(P<0.01). CONCLUSIONS:HS has cer-tain protective effects on DOX-induced chronic myocardial injury in mice.

Aim To explore the changes of Apelin/APJ system in LPS-induced injury of rat pulmonary mi-crovascular endothelial cells( PMVECs) , and the effect and mechanism of Apelin. Methods PMVECs were cultured with the explant technique, and the identifica-tion of rat PMVECs was carried out by immunocyto-chemical staining of factorⅧrelated antigen. MTT as-say was used to evaluate the viability of PMVECs. The mRNA expression of Apelin and APJ was detected by RT-PCR. The protein expression of PCNA and the phosphorylation of Akt was analyzed by Western blot. Results The mRNA expression of Apelin and APJ showed a compensatory increase after LPS treatment for a short period of time ( P<0. 01 ) , but with the exten-sion of time, which was significantly inhibited, even lower than the control group ( P<0. 05 or P<0. 01 ) , suggesting that Apelin/ APJ system might be involved in LPS-induced PMVECs injury. MTT results showed that 10 -6 ~10 -9 mol · L-1 Apelin obviously promoted the proliferation of rat PMVECs ( P <0. 05 or P <0. 01 ) , and with certain concentration and time de-pendence. Moreover, Apelin also improved the LPS-induced PMVECs injury in different degrees ( P<0. 05 or P < 0. 01 ) . In addition, Western blot analysis showed that Apelin significantly reversed the decrease of the protein expression of PCNA and the Akt phos-phorylation level induced by LPS ( P <0. 05 or P <0. 01 ) . Conclusions The Apelin/APJ system is in-volved in LPS-induced PMVECs injury. Apelin plays an important role in protecting the pulmonary microvas-cular endothelial function and reversing the LPS-in-duced PMVECs injury, which might be related to the activation of Akt phosphorylation pathway.

This paper is to report the exploration of the activation of Rho/ROCK signal pathway in 5-HT-induced proliferation of rat pulmonary artery smooth muscle cells (PASMCs) and the inhibitory effect of m-Nis on this pathway. PASMCs were cultured with the explant technique. MTT assay was used to explore the proliferation of PASMCs after 5-HT treated for different time and the intervening effect of m-Nis. RT-PCR and Western blot were used respectively to explore the mRNA expression of RhoA, ROCK1 and the protein expression of p-MYPT1 in 5-HT-treated PASMCs and intervening effect of m-Nis. The results of MTT assay suggested that 5-HT (1 µmol · L(-1)) treatment for 12-72 h significantly induced the proliferation of rat PASMCs (P<0.05 or P < 0.01), which were inhibited by m-Nis (1 x 10(-5), 1 x 10(-6), l x 10(-7), 1 x10(-8) mol · L(-1)) in dose-dependent manners (P < 0.05 or P < 0.01). Similarly, the mRNA expression of RhoA, ROCK1 and the protein expression of p-MYPT1 were also inhibited by m-Nis in different degrees (P < 0.05 or P < 0.01). Thus, the results of this study suggested that Rho/ROCK pathway played an important role in 5-HT-induced proliferation of rat PASMCs, m-Nis inhibited 5-HT-induced proliferation obviously, which may be related to the blockage of Rho/ROCK signal pathway.

AIM To investigate effect of dipfluzine on sodium current (INa+) in isolated single guinea-pig ventricular myocytes. METHODS INa+ was measured by whole cell patch-clamp technique in single isolated guinea-pig ventricular myocytes which were prepared by enzymatic dissociation method. RESULTSCardiac INa+ was elicited by 50-ms pulses to +50 mV from holding potential at -80 mV with a step of +10 mV, which could be blocked completely by tetrodotoxin 10 μmol·L-1. The peak INa+ occurred at about -20 mV and the reversal potential for INa+ was about +30 mV. Dipfluzine inhibited cardiac INa+ in a concentration-dependent manner. The blocking effect of dipfluzine on INa+ was reversible. Dipfluzine suppressed cardiac INa+, without modifying maximum activation potential and reversal potential. The peak of INa+ was decreased by about 46% at -20 mV and shape of I-V curve was not altered by dipfluzine 40 μmol·L-1. Dipfluzine shifted the steady-state inactivation curve of INa+ towards more negative without changing the slope factor and produced very little change in the steady-state activation curve towards more positive. The mean half activation voltage was (-34.9±5.1) mV and slope factor was (6.0±4.8) mV under control condition and (-33.7±3.6) mV and (5.6±2.4) mV following exposure to dipfluzine 40 μmol·L-1. The half inactivation voltage was (-73.0±4.6)mV and slope factor was (4.8±1.8)mV under control condition and (-82.8±7.2)mV and (4.8±1.8)mV following dipfluzine 40 μmol·L-1 treatment. Dipfluzine delayed recovery of cardiac INa+ from inactivation state. The time course of recovery was (36±11) ms in control group and (79±28) ms in dipfluzine 40 μmol·L-1 group. CONCLUSION Dipfluzine inhi- bits cardiac INa+ in a concentration-dependent manner and has higher affinity for the inactivated state than that for resting state of Na+ channels.

Objective To investigate the basic data of risk estimation of lung cancer among non-uranium miners in China.Methods 2836 workers from 24 mines in 9 provinces/regions were face-to-face interviewed to collect information including age at exposure,exposure duration,cigarette smoking among others.Results Age of the investigated non-uranium miners ranged from 17 to 72(36.9±8.0)years.The miners received low and poor education,3% of them were illiterate,58% with primary and middle school education,only 7% with junior college and higher education.Seventy-five percent of the uranium miners are migrant rural workers.Ethnic minority miners accoungted for 16% of all the investigated miners.Among the migrant rural workers age at initial exposure was estimated to be 29.6±8.0 years.By the time of the investigation,46.7% of the miners had worked in the mine for five years and longer,working years in the mine was 6.7±6.8 years with a median of 4.1years.3.4% of the non-uranium miners began the initial radon exposure in mines before their 18 years of old.17.5% of the investigated miners reported working more than 8 h every working day.Among the males,58.0% were current smokers with a median of 16 cigarettes per day.Age to begin the cigarette smoking was 20 years on average.Current smoking rate was age-dependent,the rate as high as 69.2% for the males aged 15-19 years.Current smoking rate was significantly statistically lower in coal mines than that in other mines,49.0% vs 62.5%.Compared with other miners,more frequent mechanical ventilations were reported by coal miners,Conclusions In China non-uranium mines,75% were migrant rural workers,by the time of the investigation about half of them had worked in the mines for at least five years.Non-uranium miners began their mining at 30 years on average,with a very small percentage of 3%,exposed to the mining radon before their 18 years.Current cigarette smoking rate in non-uranium male miners was the same as the general male population in China.

Effect of strophanthidin (Str) on intracellular calcium concentration ([Ca2+]i) was investigated on isolated ventricular myocytes of guinea pig. Single ventricular myocytes were obtained by enzymatic dissociation technique. Fluorescent signal of [Ca2+]i was detected with confocal microscopy after incubation of cardiomycytes in Tyrode's solution with Fluo3-AM. The result showed that Str increased [Ca2+]i in a concentration-dependent manner. The ventricular myocytes began to round-up into a contracture state once the peak level of [Ca2+]i was achieved in the presence of Str (10 μmol·L-1), but remained no change in the presence of Str (1 and 100 nmol·L-1). Tetrodotoxin (TTX), nisodipine, and high concentration of extracellular Ca2+ changed the response of cardiomycytes to Str (1 and 100 nmol·L-1), but had no obvious effects on the action of Str (10 μmol·L-1). The elevation of [Ca2+]i caused by Str at all of the detected concentrations was partially antagonized by rynodine (10 μmol·L-1) or the removal of Ca2+ from Tyrode's solution. In Na+, K+-free Tyrode's solution, the response of cardiomycytes in [Ca2+]i elevation to Str (10 μmol·L-1) was attenuated, while remained no change to Str (1 and 100 nmol·L-1). TTX, nisodipine, and high concentration of extracellular Ca2+ changed the response of cardiomycytes to Str at all of the detected concentrations in Na+, K+-free Tyrode's solution. The study suggests that the elevation of [Ca2+]i by Str at the low (nomomolar) concentrations is partially mediated by the extracellular calcium influx through Ca2+ channel or a "slip mode conductance" of TTX sensitive Na+ channel. While the effect of Str at high (micromolar) concentrations was mainly due to the inhibition of Na+, K+-ATPase. Directly triggering the release of intracellular Ca2+ from sarcoplasmic reticulum (SR) by Str may be also involved in the mechanism of [Ca2+]i elevation.

AIM To investigate whether dipfluzine (Dip) possesses antiarrhythmic effect on experimental arrhythmias and effect on cytosolic calcium in ventricular myocytes of guinea-pig. METHODS Experimental arrhythmias were induced by strophanthin G infusion through jugular vein in guinea-pigs and by myocardial ischemia-reperfusion (I-R) in rats respectively. Cytosolic calcium concentration ([Ca2+]i) of isolated guinea-pig ventricular myocytes was examined with laser confocal scanning microscope. RESULTSIn guinea-pigs pretreatment with Dip 20 mg·kg-1 increased the dosages of strophanthin G required to induce ventricular premature contraction (VP), ventricular tachycardia (VT), ventricular fibrillation (VF) and cardiac arrest (CA), pretreatment with Dip 10 mg·kg-1 increased the dosages of strophanthin G required to induce VP. In the I-R-induced arrhythmic model of rats, Dip 20 mg·kg-1 decreased the number of rats exhibiting VT, VF and CA, and the number of rats exhibiting VF and CA was decreased by Dip 10 mg·kg-1. Both Dip and verapamil (Ver) decreased [Ca2+]i of the ventricular myocytes in normal Tyrode′s solution. The Ca2+ overload evoked by high extracellular Ca2+ levels was inhibited by Dip and Ver, and the prophylactic effect of Dip was less than that of Ver, while the curative effect of Dip was more obvious than that of Ver. CONCLUSION Dip has antiarrhythmic effect, which is likely related to the modulation on the intracellular calcium homeostasis.

AIM To study the effects of strophanthidin (Str) on cardiac function and Na +,K +-ATPase activity in isolated guinea pig heart failure model. METHODS Langendorff isolated heart failure models made by perfusing heart with K-H solution containing sodium pentobarbital. Eight-channel physiological recording instrument was used to determine cardiac function. Colorimetry method was used to determine cardiac sarcolemmal Na +,K +-ATPase activity. RESULTS Str increased the heart rate, left ventricular systolic pressure and the maximum rise or decline rate of left ventricular pressure in a concentration-dependent manner at 1?10 -9～1?10 -7 mol?L -1. But Str caused first a rise, then a reduction of contractility and arrhythmia accompanied by inhibition of Na +,K +-ATPase when the concentration of Str was higher than 1?10 -6 mol?L -1. Str had no obvious effect on Na +,K +-ATPase activity at 1?10 -7 mol?L -1, but increased cardiac activity at 1?10 -10～1?10 -8 mol?L -1. CONCLUSION The inotropic effect and heart toxicity of Str at higher concentration is due to inhibition of Na +,K +-ATPase, but the inotropic effect of Str at lower concentration is not the result of inhibition of Na +,K +-ATPase activity.