Objedctive To study the mechanism of GnRH agalogus(Alarelin)on[ Ca2 + ]; mobilization in stomach smooth muscle cells (SSMc)of rats. Methods Cells were cutured and loaded with Fluo-3-AM. [Ca2 + ]; was measured by nuomeent intensity(FL) in each cell with confocal micoopy. Results (1 ) In Hanks solution. l0-7, l0-6, l0 - 5mol L- 1 Alarelin can elevate[ Ca2 + ], its peak - resting values reached 6. 00 ?0. 50 .9. 23 ?0. 62. l8. 97 ?2. 42 respectively, which indicate that the level of [Ca2+ ]; act in an deede- pendent and time - dependent. (2) thntredly. when Alarelin was 10 4mol?Ｌ－１, its peak - resting value only reached 6. 32 ?0 .67, conpared with Alarelin l0 5m.l L－1 which was sigificantly lower(P 0. 05 ). (5 )When pertreatment with Lacidipine in Hanks solution, the effect of Alarelin l0 5mol L-1.as partly inhibited(P

OBJECTIVETo investigate the expression of methionine sulfoxide reductase (MsrA) in colorectal cancer stem cells and its association with the tumorigenesis and progression of colorectal cancer.

METHODSThe CD133⁺/CD44⁺/ESA⁺ subpopulation of colorectal cancer cell line SW480 was obtained by magnetic activated cell sorting (MACS). The expression of MsrA, VEGF, MMP-13 and CXCR4 in the cancer cells, cancer stem cells and normal colon mucosa cells were detected using RT-PCR. The proliferation of colorectal cancer stem cells was evaluated with MTT assay.

RESULTSThe expression of MsrA was significantly higher in cancer stem cells than in the cancer cells and normal mucosa cells. Overexpression of MsrA inhibited the proliferation of colorectal cancer stem cells and down-regulated the expression of VEGF, MMP-13 and CXCR4.

CONCLUSIONSMsrA suppresses the tumorigenesis and progression of colorectal cancer cells possibly by inhibiting cell proliferation and down-regulating VEGF, MMP-13 and CXCR4.

Cell Line, Tumor ; Cell Proliferation ; Colorectal Neoplasms ; enzymology ; Down-Regulation ; Humans ; Matrix Metalloproteinase 13 ; metabolism ; Methionine Sulfoxide Reductases ; metabolism ; Neoplastic Stem Cells ; enzymology ; Receptors, CXCR4 ; metabolism ; Vascular Endothelial Growth Factor A ; metabolism

Objective To investigate the expression of methionine sulfoxide reductase (MsrA) in colorectal cancer stem cells and its association with the tumorigenesis and progression of colorectal cancer. Methods The CD133+/CD44+/ESA+subpopulation of colorectal cancer cell line SW480 was obtained by magnetic activated cell sorting (MACS). The expression of MsrA, VEGF, MMP-13 and CXCR4 in the cancer cells, cancer stem cells and normal colon mucosa cells were detected using RT-PCR. The proliferation of colorectal cancer stem cells was evaluated with MTT assay. Results The expression of MsrA was significantly higher in cancer stem cells than in the cancer cells and normal mucosa cells. Overexpression of MsrA inhibited the proliferation of colorectal cancer stem cells and down-regulated the expression of VEGF, MMP-13 and CXCR4. Conclusions MsrA suppresses the tumorigenesis and progression of colorectal cancer cells possibly by inhibiting cell proliferation and down-regulating VEGF, MMP-13 and CXCR4.

Objective To investigate the expression of methionine sulfoxide reductase (MsrA) in colorectal cancer stem cells and its association with the tumorigenesis and progression of colorectal cancer. Methods The CD133+/CD44+/ESA+subpopulation of colorectal cancer cell line SW480 was obtained by magnetic activated cell sorting (MACS). The expression of MsrA, VEGF, MMP-13 and CXCR4 in the cancer cells, cancer stem cells and normal colon mucosa cells were detected using RT-PCR. The proliferation of colorectal cancer stem cells was evaluated with MTT assay. Results The expression of MsrA was significantly higher in cancer stem cells than in the cancer cells and normal mucosa cells. Overexpression of MsrA inhibited the proliferation of colorectal cancer stem cells and down-regulated the expression of VEGF, MMP-13 and CXCR4. Conclusions MsrA suppresses the tumorigenesis and progression of colorectal cancer cells possibly by inhibiting cell proliferation and down-regulating VEGF, MMP-13 and CXCR4.

Objective:To elucidate the quasispecies variation of 3′ half-length genome in HIV-1 CRF103_01B-infected patients in Beijing using single genome amplification (SGA).Methods:This study enrolled six CRF103_01B-infected patients who were diagnosed during a drug resistance monitoring for newly diagnosed cases or newly treated cases with antiviral therapy in Beijing from 2017 to 2020. RNA was extracted from their plasma samples, and 3′ end of cDNA was diluted by serial dilution method after reverse transcription. Nested PCR was used to amplify the 3′ half-length genome sequences of HIV-1 quasispecies. MEGA 11 was used to construct Neighbor-Joining (NJ) tree and calculate the intrahost genetic distance. Genetic variation in HIV-1 quasispecies was visualized by online Highlighter tool. BootScan analysis was performed using Simplot 3.5 software to analyze inter-quasispecies recombination. Virus tropism was predicted by online Geno2pheno tool.Results:Among the six CRF103_01B-infected patients, five were men who have sex with men. A total of 144 3′ half-length genome SGA sequences (19-36 sequences/case) were obtained. The NJ tree based on the 3′ half-length genome of HIV-1 quasispecies revealed different degrees of genetic diversity. The HIV-1 quasispecies in BL4748-00 case of acute infection has the least variation with the intrahost distance of 0.002±0.000, showing genetic homogeneity. The quasispecies sequences from BL4981-00, BL3150-00 and BL3558-00 cases formed at least three subclusters, respectively, with different evolutionary directions, and their intrahost distance ranked from 0.031±0.004 to 0.016±0.002 (BL3150-00>BL3558-00>BL4981-00). The quasispecies sequences from the couple BL3022-00 (female) and BL3023-00 clustered into a large monophyletic cluster (bootstrap value=100%), and the intrahost distance of the latter (0.025±0.003) was higher than that of the former (0.019±0.002). Inter-quasispecies recombination was observed in BL3558-00 case. The quasispecies from the six patients were CCR5-tropic viruses.Conclusions:The diversity of quasispecies variation in CRF103_01B-infected patients is related to disease progress. Genetic homogeneity is observed in acute HIV infection, while multiple evolutionary directions are detected in chronic infection. Co-infection or superinfection cases are not found, but there are recombination events among quasispecies in some cases.

Objective:To explore the characteristics of HIV-1 genotypic drug resistance for protease-reverse transcriptase (PR-RT) and integrase (IN) among antiretroviral therapy (ART)-naive individuals in Beijing, and provide evidence for clinical diagnosis and treatment.Methods:Newly diagnosed individuals or cases initiating ART were recruited in Beijing covering 2019 to 2020, then pol gene fragments and integrase gene were synchronously amplified and sequenced. Phylogenetic analyses were performed to determine subtypes, and the pol gene and integrase gene sequences were submitted to Stanford University HIV drug resistance database for the interpretation of mutations and drug resistance. Results:Among 168 ART-naive individuals, 93.6% were infected via men who have sex with men (MSM). The top two subtypes were CRF01_AE (41.0%) and CRF07_BC (30.3%), and unique recombinant forms accounted for 16.1% infections. Six individuals carried surveillance drug resistance mutations in PR-RT, with a prevalence of transmitted drug resistance (TDR) at 3.7%. And one case carried nucleoside reverse transcriptase inhibitor mutation of K65R, accompanied with major integrase mutation of T66I (0.6%), conveying resistance to elvitegravir and raltegravir at high and low levels, respectively.Conclusions:The prevalence of transmitted drug resistance was considerably low among ART-naive individuals in Beijing, and the surveillance of genotypic drug resistance should be strengthened, including integrase drug resistance.

People as third-party observers, without direct self-interest, may punish norm violators to maintain social norms. However, third-party judgment and the follow-up punishment might be susceptible to the way we frame (i.e., verbally describe) a norm violation. We conducted a behavioral and a neuroimaging experiment to investigate the above phenomenon, which we call the "third-party framing effect". In these experiments, participants observed an anonymous perpetrator deciding whether to keep her/his economic benefit while exposing a victim to a risk of physical pain (described as "harming others" in one condition and "not helping others" in the other condition), then they had a chance to punish that perpetrator at their own cost. Our results showed that the participants were more willing to execute third-party punishment under the harm frame compared to the help frame, manifesting a framing effect. Self-reported anger toward perpetrators mediated the relationship between empathy toward victims and the framing effect. Meanwhile, activation of the insula mediated the relationship between mid-cingulate cortex activation and the framing effect; the functional connectivity between these regions significantly predicted the size of the framing effect. These findings shed light on the psychological and neural mechanisms of the third-party framing effect.
Empathy ; Female ; Gyrus Cinguli ; Humans ; Neuroimaging ; Pain ; Punishment/psychology*