Photothermal therapy (PTT) is a highly effective anti-tumor method. However, when laser radiation was used to ablate tumors, it usually triggers a series of inflammatory reactions, promoting the further development of tumors and affecting the effect of anti-tumor therapy. Therefore, it is an effective method to improve the anti-tumor effect by suppressing the inflammatory response through the precise targeted delivery of anti-inflammatory drug while realizing the photothermal treatment of tumors. To this end, the redox-responsive linker 3,3'-dithiodipropionic acid was used to bond the classic hydrophobic anti-inflammatory drug 18β-glycyrrhetinic acid (18β-GA) and the hydrophilic fragment methoxy-polyethylene glycol (mPEG-NH₂) to obtain redox-responsive amphiphilic polymer PEG-DA-GA in this study. Then, photothermal agent IR-780 was encapsulated to prepare redox-responsive polymer micelle PDG/IR-780 NPs. The PDG/IR-780 NPs exhibited uniform particle size of 80.2 ± 5.3 nm and the polydispersity index (PDI) was 0.215 ± 0.079. All animal experiments followed the ethical requirements formulated by the Ethics Committee of Sichuan University. The results showed that PDG/IR-780 NPs could respond to the abundant glutathione (GSH) in tumor cells to promote the disintegration of nanoparticle and the release of 18β-GA, thus significantly improved the killing efficiency on 4T1 cells, when compared with the non-redox-responsive control PSG/IR-780 NPs. When the concentration of 18β-GA was 50 μg·mL^-1, the cell viability of 4T1 cells in the PDG/IR-780 NPs group was only (19.29 ± 1.80) %, which was significantly lower than the result of in PSG/IR-780 NPs group (29.30 ± 1.37) %. The results of frozen sections of tumor tissues showed that the designed PDG NPs can promote the tumor-targeted distribution of drugs compared with the free drug group. Eventually, PDG/IR-780 NPs achieved wonderful anti-tumor efficacy on 4T1 triple-negative breast cancer model, revealing the new possibility of the combined therapy strategy of photothermal and anti-inflammatory therapy.

Objective To explore whether metformin preconditioning can protect brain injury after cardiac arrest/cardiopulmonary resuscitation(CA/CPR)and its possible mechanisms and signaling pathways.Methods Constructed a CA model by using electrical stimulation.Rats were randomly divided into the sham group(0.9％NaCl gavage daily for 14 days,without inducing CA),model group(CA model was induced after 0.9％NaCl gavage daily for 14 days),experimental group(CA model was induced after 200 mg·kg-1 Met+0.9％NaCl gavage daily for 14 days),Cc group[200 mg·kg-1 Met+0.9％NaCl gavage daily for 14 days,adenosine 5'-monophosphate kinase-activated protein(AMPK)inhibitor Compoud C(Cc)was injected intraperitoneally at 1 hour before modeling],chloroquine(CQ)group(daily 200 mg·kg-1 Met+0.9％NaCl gavage for 14 days,intraperitoneal injection of autophagy inhibitor CQ at 1 hour before modeling)and AICAR group(continuous daily 200 mg·kg-1 Met+0.9％NaCl gavage for 14 days,intraperitoneal injection of AMPK agonist AICAR at 1 hour before modeling).The 7-day survival rate after CA/CPR via using survival curves was recorded;the neurological function 7-days after CA/CPR was scored by using the neurological disability scale;the protein malondialdehyde(MDA)level were measured using the Coomassie Brilliant Blue method;detection of reactive oxygen species(ROS)levels in brain tissue by using ROS fluorescent probe DHE;Western blotting was used to determine the expression levels of related proteins such as AMPK,p-AMPK,microtubule associated protein 1 light chain 3 Ⅰ(LC3 Ⅰ),LC3 Ⅱ,and p62 in brain tissue.Results The 7-day survival rates of sham,model,experimental,Cc,CQ and AICAR groups rats were 100％,40％,70％,40％,40％and 65％,respectively;the 7-day neurological function scores were 78.35±1.65,46.50±4.41,67.93±4.64,49.50±3.53,52.00±2.83 and 68.33±1.53,respectively;the ROS levels were(417.60±8.37),(748.60±36.05),(575.80±10.73),(713.80±18.85),(668.20±9.58)and(566.00±24.48)U·mg-1,respectively;the MDA levels were(4.38±0.33),(8.06±0.76),(5.50±0.48),(7.18±0.29),(6.82±0.31)and(5.20±0.34)nmol·mg-1,respectively;the brain tissue p-AMPK/AMPK were 0.74±0.04,0.87±0.01,1.61±0.01,0.55±0.05,1.09±0.09 and 1.27±0.07,respectively;the p62 values were 0.42±0.02,0.86±0.05,0.61±0.04,0.98±0.04 and 0.78±0.03,respectively;the LC3 Ⅱ/LC3 1 were 0.29±0.32,0.37±0.26,0.96±0.78,0.58±0.26,0.43±0.03 and 1.40±0.10,respectively.Compared with the model group,the differences of above indexes in the experimental group,AICAR group were statistically significant(all P＜0.05);compared with the experimental group,the differences of above indexes in the Cc group,CQ group were statistically significant(all P＜0.05).Conclusion Metformin preconditioning can play a protective role in brain injury after cardiac arrest/cardiopulmonary resuscitationin in rats by activating the AMPK signaling pathway,regulating mitochondrial energy metabolism and promoting autophagy.

Castleman disease is a rare and complicated disease. A case of Castleman disease (CD) in a 40-year-old woman on the neck was reported and literature review was made to understand the occurrence, clinical characteristics, diagnosis and differential diagnosis, treatment, and prognosis of Castleman disease. Because of the rarity of CD, its occurrence in the general population and the typical clinical manifestations are still lacked. There are two types of CD, namely localized CD and multicentric CD, both of them are not easy to be diagnosised. CT scans in preoperative is helpful for the clinical diagnosis, while histopathological examination and lymph node biopsy are beneficial for the early diagnosis. The treatment result is based on the histopathological examination and lymph node biopsy. The prognosis is different with the type of CD. For the localized CD, the prognosis is usually good, while for the multicentric CD is bad. Both of localized CD and multicentric CD have a certain reoccurrence rate.