ObjectiveThe utilization of assisted reproductive technology to rescue genetically modified mouse strains with reproductive disorders provides a reference for improving techniques to preserve valuable experimental mouse strains. MethodsIn vitro fertilization-embryo transfer (IVF-ET) technology was performed on 28 strains of infertile male mice aged 9-18 months. Several indicators such as sperm density and sperm motility in infertile male mice were assessed to select the most viable sperm for IVF-ET experiments. Fertility rate, abnormal egg rate, and birth rate were recorded after the birth of the pups. An optimized ovarian transplantation procedure was applied to 12 strains of infertile female mice aged 8-18 months. 6-week-old female mice with the same genetic background were selected as recipients. One intact ovary was removed from each recipient mouse, and the contralateral oviduct was ligated. An ovary from a donor mouse was isolated and transplanted orthotopically into the side where the ovary had been removed in the recipient mouse. Twenty-one days post-surgery, recipient mice were co-housed with 8-week-old wild type male mice of the same genetic background for breeding. Data such as the pregnancy rate and live birth rate of the recipients were recorded after the birth of the pups. ResultsIVF-ET successfully rescued 28 mouse strains, with the oldest male mice being 18 months old. The success rate of the first round of IVF-ET experiments was 89.29% (25/28). The average fertility rate of IVF in infertile male mice was (51.01±14.97)%, the abnormal egg rate was (9.03±5.28)%, and the birth rate of offspring mice was (18.60±7.03)%. 39 out of 40 ovarian transplant recipient mice survived, with a pregnancy rate of 33.33% (13/39) for ovarian transplant recipients, and a live birth rate of 17.95% (7/39). Four mouse strains were successfully rescued using optimized ovarian transplantation technology, with the oldest female mice being 18 months old. 8 strains were not rescued as they failed to produce offspring that survived to sexual maturity. ConclusionIVF-ET is an effective approach for rescuing mice with reproductive disorders caused by different reasons, especially for those beyond the optimal breeding age. Ovarian transplantation technology can also be used as an alternative for aged female mice. But its success rate is relatively lower than that of IVF-ET, and carries a higher experimental risk.

AIM To observe the effects of Hugan Tablets on high-fat diet induced non-alcoholic fatty liver disease(NAFLD)in a mouse model,and the autophagy,pyroptosis and the PI3K/Akt/mTOR signaling pathway as well.METHODS The C57BL/6 mice were randomly divided into the normal group,the model group,the Hugan Tablets group(0.7 g/kg)and the Yishanfu group(0.23 g/kg),with 10 mice in each group.The NAFLD mouse model was established by 16 weeks feeding of high-fat diet.From the 13th week,the mice started their corresponding dosing of the drug by gavage followed by killing of the mice at the end of 16th week and collection of their serum and liver tissue samples.The mice had their serum ALT,AST,TG,TC,LDL levels,liver TG,TC,NEFA,MDA levels and activities of SOD and GSH-Px detected;their serum levels of IL-1β,IL-6 and TNF-αdetected by ELISA;their hepatic pathological changes observed using HE staining and oil red O staining;and their hepatic protein expressions of ACC,CPT1A,FAS,p-PI3K,p-Akt,p-mTOR,P62,LC3,NLRP3,GSDMD and Caspase1 detected by Western blot.RESULTS Compared with the model group,the Hugan Tablets group displayed decreased body weight and hepatosmatic index level(P＜0.01);decreased levels of serum ALT,AST,TG,TC,LDL,IL-6,IL-1β and TNF-α(P＜0.05,P＜0.01);increased hepatic levels of TG,TC,NEFA and MDA(P＜0.05);decreased activities of SOD and GSH-Px(P＜0.05);improved pathological changes of hepatic lipid deposition and hepatocytic ballooning and decreased NAS score and oil red O staining area(P＜0.01);decreased hepatic protein expressions of ACC1,FAS,NLRP3,Caspase1,GSDMD,P62,p-PI3K,p-Akt and p-mTOR(P＜0.05,P＜0.01);and increased protein expressions of CPT1A and LC3(P＜0.01).CONCLUSION Hugan Tablets can effectively prevent and control the development of high-fat diet induced NAFLD in mice,and the mechanism may be associated with the promotion of autophagy in hepatocytes and the inhibition of pyroptosis via the inhibition of PI3K/Akt/mTOR signaling pathway.

AIM To observe the effects of Hugan Tablets on high-fat diet induced non-alcoholic fatty liver disease(NAFLD)in a mouse model,and the autophagy,pyroptosis and the PI3K/Akt/mTOR signaling pathway as well.METHODS The C57BL/6 mice were randomly divided into the normal group,the model group,the Hugan Tablets group(0.7 g/kg)and the Yishanfu group(0.23 g/kg),with 10 mice in each group.The NAFLD mouse model was established by 16 weeks feeding of high-fat diet.From the 13th week,the mice started their corresponding dosing of the drug by gavage followed by killing of the mice at the end of 16th week and collection of their serum and liver tissue samples.The mice had their serum ALT,AST,TG,TC,LDL levels,liver TG,TC,NEFA,MDA levels and activities of SOD and GSH-Px detected;their serum levels of IL-1β,IL-6 and TNF-αdetected by ELISA;their hepatic pathological changes observed using HE staining and oil red O staining;and their hepatic protein expressions of ACC,CPT1A,FAS,p-PI3K,p-Akt,p-mTOR,P62,LC3,NLRP3,GSDMD and Caspase1 detected by Western blot.RESULTS Compared with the model group,the Hugan Tablets group displayed decreased body weight and hepatosmatic index level(P＜0.01);decreased levels of serum ALT,AST,TG,TC,LDL,IL-6,IL-1β and TNF-α(P＜0.05,P＜0.01);increased hepatic levels of TG,TC,NEFA and MDA(P＜0.05);decreased activities of SOD and GSH-Px(P＜0.05);improved pathological changes of hepatic lipid deposition and hepatocytic ballooning and decreased NAS score and oil red O staining area(P＜0.01);decreased hepatic protein expressions of ACC1,FAS,NLRP3,Caspase1,GSDMD,P62,p-PI3K,p-Akt and p-mTOR(P＜0.05,P＜0.01);and increased protein expressions of CPT1A and LC3(P＜0.01).CONCLUSION Hugan Tablets can effectively prevent and control the development of high-fat diet induced NAFLD in mice,and the mechanism may be associated with the promotion of autophagy in hepatocytes and the inhibition of pyroptosis via the inhibition of PI3K/Akt/mTOR signaling pathway.

Objective:To explore the clinical characteristics and prognosis of patients with diffuse large B-cell lymphoma(DLBCL)of the breast.Methods:The clinical data of 28 DLBCL patients admitted to Shanxi Provincial Cancer Hospital from January 2013 to January 2023 were retrospectively analysed,including 13 cases of primary breast DLBCL(PB-DLBCL)and 15 cases of secondary breast DLBCL(SB-DLBCL),and the data of their clinical manifestations,laboratory tests,pathological examinations,treatment protocols,and follow-up were statistically analyzed.Results:There were significant differences in IPI score,LDH level and β2-microglobulin between PB-DLBCL and SB-DLBCL patients(P＜0.05).Among the 23 patients with breast DLBCL who received regular treatment,13 patients achieved complete remission(9 patients with PB-DLBCL and 4 patients with SB-DLBCL)after initial treatment.By the end of follow-up,11 patients relapsed or progressed(5 patients with PB-DLBCL and 6 patients with SB-DLBCL)and 9 patients died(3 patients with PB-DLBCL and 6 patients with SB-DLBCL).The 5-year OS rate was(75.0±15.3)％in PB-DLBCL group and(32.3±17.1)％in SB-DLBCL group.The 5-year PFS rate was(59.1±19.8)％in PB-DLBCL and 0％in SB-DLBCL group.The 5-year OS rate and PFS rate of PB-DLBCL patients were higher than those of SB-DLBCL patients(P＜0.05);the 5-year OS rate of the combined central preventive treatment group was higher than that of the chemotherapy group(P＜0.05).Conclusion:Breast DLBCL is divided into two categories:PB-DLBCL and SB-DLBCL.Compared with SB-DLBCL,PB-DLBCL has the characteristics of lower IPI score,LDH,and β2-microglobulin levels.PB-DLBCL patients have a longer survival period.In addition,the prognosis of patients receiving central preventive treatment is more optimistic.

Malignant tumors are currently seriously endangering human health and life， which has become one of the main causes of death in China. In modern Western medicine， they are mainly tackled by surgery， chemotherapy， and radiotherapy， but the death toll continues to rise year by year. At present， most of the anti-tumor chemotherapeutics used in clinical practice have toxic and side effects， affecting the anti-tumor efficacy and the conditions after treatment. Long-term medication will also induce drug resistance， making the good anti-tumor effect difficult to be achieved. With the vigorous development of traditional Chinese medicine （TCM）， it has played a crucial role in the fight against tumors. It is believed in TCM that "heat toxin" is one of the important causes of tumors. Therefore， the methods of clearing away heat and removing toxin are often emphasized in the treatment of tumors， and the resulting outcomes are satisfactory. There are many Chinese herbs and Chinese herbal compounds classified into the heat-clearing and toxin-removing type. Xihuangwan， a classic heat-clearing prescription， is composed of Calculus Bovis， Moschus， Olibanum， and Myrrh and has the effects of clearing away heat， removing toxin， eliminating edema， and dissipating mass， which is mainly used to treat carbuncle， pustule， scrofula， multiple abscess， and cancer caused by heat-toxin obstruction. In modern clinical practice， it has been employed in patients with lung cancer， breast cancer， gastric cancer， liver cancer， colorectal cancer， and other malignant tumors， especially during the advanced stage， as a routine or adjuvant treatment for alleviating their clinical symptoms and improving their quality of life. The main active components of Xihuangwan are pentacyclic triterpenoids （such as masticinic acids）， volatile oils， steroids （like porcine deoxycholic acid）， and bilirubin， which have been proved effective in anti-tumor. This paper reviewed the prescription source， pharmaceutical research， clinical anti-tumor research， and pharmacological mechanisms of Xihuangwan， which has provided reference for further expanding the anti-tumor applications of Xihuangwan and enhancing its secondary development.

Objective:To analyze the long-term trend of viral hepatitis mortality in Jing’an District of Shanghai， and to provide a reference for viral hepatitis prevention and control. Methods:Mortality rate， standard mortality rate， PYLL and potential years of life lost rate （PYLL‰） of viral hepatitis in Jing’an district of Shanghai from 1976 to 2015 were calculated. The annual percent change （APC） of the mortality and PYLL‰ were analyzed by Joinpoint regression analysis. Results:From 1976 to 2015， there were 1 342 viral hepatitis death cases， including 832 males and 510 females. The average crude mortality rate was 8.31/100 000， and the average age-standardized mortality rate was 5.45/100 000. Among the deaths of viral hepatitis， men had a higher mortality rate， age-standardized mortality rate and PYLL% than women （χ2_Pearson=107.34， 112.93， 39.15， all P<0.01）， men were mainly in the age group of 35-64 years （accounted for 62.62%）， while women were mainly in the age group of 65 years and above （accounted for 55.49 %）， and the average death age of men was earlier than that of women （by rank-sum test： Z=-8.879，P<0.01）. After 1990 （except in 2002）， hepatitis B was the main cause of deaths from viral hepatitis， accounting for 75.00%-100%， and the proportion of other and unclassified cases gradually decreased. Overall， the mortality rate of viral hepatitis declined significantly during 1976-2015 （APC=-2.0%，P<0.05）， with the turning point in 2002. The mortality rate of viral hepatitis declined significantly from 2002 to 2015 （APC=-8.1%，P<0.05）. The overall PYLL‰ of viral hepatitis declined significantly during 1976-2015 （APC=-3.7%，P<0.05）， with the turning point in 1992. After 1992， the PYLL‰ of viral hepatitis declined significantly during 1992-2015 （APC=-6.5%，P<0.05）. Conclusion:There has been a significant decline trend of viral hepatitis in the mortality rate in Jing’an District of Shanghai from 2002 to 2015， with hepatitis B as the main cause of death.