Oxytocin neurons in the paraventricular nucleus and fear empathy among male mice.

BACKGROUND: Recent studies have identified empathy deficit as a core impairment and diagnostic criterion for people with autism spectrum disorders; however, the improvement of empathy focuses primarily on behavioural interventions without the target regulation. We sought to compare brain regions associated with empathy-like behaviours of fear and pain, and to explore the role of the oxytocin-oxytocin receptor system in fear empathy. METHODS: We used C57BL mice to establish 2 models of fear empathy and pain empathy. We employed immunofluorescence histochemical techniques to observe the expression of c-Fos throughout the entire brain and subsequently quantified the number of c-Fos-positive cells in different brain regions. Furthermore, we employed chemogenetic technology to selectively manipulate these neurons in Oxt-Cre-/+ mice to identify the role of oxytocin in this process. RESULTS: The regions activated by fear empathy were the anterior cingulate cortex, basolateral amygdala, nucleus accumbens, paraventricular nucleus (PVN), lateral habenula, and ventral and dorsal hippocampus. The regions activated by pain empathy were the anterior cingulate cortex, basolateral amygdala, nucleus accumbens, and lateral habenula. We found that increasing the activity of oxytocin neurons in the PVN region enhanced the response to fear empathy. This enhancement may be mediated through oxytocin receptors. LIMITATIONS: This study included only male animals, which restricts the broader interpretation of the findings. Further investigations on circuit function need to be conducted. CONCLUSION: The brain regions implicated in the regulation of fear and pain empathy exhibit distinctions; the activity of PVN neurons was positively correlated with empathic behaviour in mice. These findings highlight the role of the PVN oxytocin pathway in regulating fear empathy and suggest the importance of oxytocin signalling in mediating empathetic responses.

Primary pulmonary lymphoepithelioma-like carcinoma misdiagnosed as lung squamous cell carcinoma: A case report.

BACKGROUND: Primary pulmonary lymphoepithelioma-like carcinoma (PPLELC) is an uncommon subtype of squamous cell carcinoma (SCC) of the lung, closely associated with Epstein-Barr virus (EBV) infection. The pathological features of PPLELC closely resemble those of SCC, which makes it prone to misdiagnosis. Surgical intervention constitutes the primary treatment approach for PPLELC. CASE SUMMARY: This report describes a 44-year-old woman who was hospitalized for 1 mo due to left chest pain. Computed tomography revealed a mass shadow in the anterior basal segment of the left lower lobe, and a subsequent needle biopsy suggested SCC. The patient underwent radical tumor resection in the lower left lobe of the lung, and postoperative pathological examination indicated lymphoepithelial carcinoma, and the test for EBV encoded small RNA was positive. Following surgery, the patient was scheduled to receive four cycles of adjuvant chemotherapy, using the paclitaxel + carboplatin regimen, but the patient refused further treatment. CONCLUSION: PPLELC is an exceptionally rare subtype of lung SCC and is prone to misdiagnosis.

MicroRNA-1 promotes apoptosis of hepatocarcinoma cells by targeting apoptosis inhibitor-5 (API-5).

Although microRNA-1 (miR-1) is a known liver cancer suppressor, the role of miR-1 in apoptosis of hepatoma cells has remained largely unknown. Our study shows that ectopic miR-1 overexpression induced apoptosis of liver hepatocellular carcinoma (HepG2) cells. Apoptosis inhibitor 5 (API-5) was found to be a potential regulator of miR-1 induced apoptosis, using a bioinformatics approach. Furthermore, an inverse relationship between miR-1 and API-5 expression was observed in human liver cancer tissues and adjacent normal liver tissues. Negative regulation of API-5 expression by miR-1 was demonstrated to promote apoptosis of HepG2 cells. Our study provides a novel regulatory mechanism of miR-1 in the apoptosis of hepatoma cells.

The fern-feeder aphids (Hemiptera: Aphididae) from China: a generic account, descriptions of one new genus, one new species, one new subspecies, and keys.

Fern-feeder aphids (Hemiptera: Aphididae) in China are represented by 13 species in 10 genera, including a new genus, Vietaphis gen nov., a new species, Vietaphis aliquantus sp nov., from Guizhou and Tibet on Plagiogyria japonicum, and a new subspecies, Amphorophora scabripes galba ssp nov., from Guizhou on Pentarhizidium intermedium. Two genera, Amphorophora Buckton and Idiopterus Davis, and four species or subspecies, Amphorophora ampullate ben-galensis Hille Ris Lambers and Basu, Idiopterus nephrelepidis Davis, Micromyzodium polypodii Takahashi, and Myzus filicis Basu, are reported for the first time in China. Apterae and alatae of Myzus filicis are redescribed herein, and with host plant notes. The fern-feeder aphid genus Ne-omacromyzus Lee is considered a junior synonym of Idiopterus. Furthermore, Neomacromyzus cyrtomicola Lee is transferred to the genus Idiopterus, as Idiopterus cyrtomicola (Lee), comb nov., which is herein considered a junior synonym of Idiopterus nephrelepidis Davis. Keys to Chinese fern-feeder species are provided. Morphological figures and biometrical data of Vietaphis aliquantus sp nov., Amphorophora scabripes galba ssp nov., and Myzus filicis are presented.

Aberrant promoter DNA methylation inhibits bone morphogenetic protein 2 expression and contributes to drug resistance in breast cancer.

Bone morphogenetic protein 2 (BMP2) is a growth factor that is involved in the development and progression of various types of cancer. However, the epigenetic regulation of the expression of BMP2 and the association between BMP2 expression and drug resistance in breast cancer remains to be elucidated. The present study reported that the expression of BMP2 was significantly decreased in primary breast cancer samples and the MCF­7/ADR breast cancer mulitdrug resistance cell line, which was closely associated with its promoter DNA methylation status. The expression of BMP2 in MCF­7/ADR cells markedly increased when treated with 5­Aza­2'­deoxycytidine. Knockdown of BMP2 by specific small interfering RNA enhanced the chemoresistance of the MCF­7 breast cancer cell line. These findings indicated that epigenetic silencing of BMP2 in breast cancer may be involved in breast cancer progression and drug resistance, and provided a novel prognostic marker and therapeutic strategy for breast cancer.

Long-term stable expression of antisense cDNA of cyclin B1 profoundly inhibits the proliferation of tumor cells and suppresses tumorigenicity in implanted mice.

BACKGROUND: Cyclin B1 (CLB1) is necessary for mitotic initiation in mammalian cells and plays important roles in cancer development. Therefore, a potential strategy in cancer therapy is to suppress the activity of CLB1 by delivering antisense constructs of CLB1 into tumor cells. In previous CLB1 studies, antisense constructs with a short half life were often used and these constructs might not persistently inhibit CLB1. METHODS: We successfully created a recombinant plasmid encoding the full-length antisense cDNA of mouse cyclin B1 (AS-mCLB1) and transfected this construct to the murine Lewis lung carcinoma (LL/2) and CT-26 colon carcinoma (CT-26) cells. We isolated clones of LL/2 and CT-26 transfectants with stable expression of AS-mCLB1. Reverse transcriptional polymerase chain reaction (RT-PCR) and Western blot were applied to detect the expression of the mRNA and protein levels of CLB1. To further test the efficacy of this strategy in vivo, AS-mCLB1-expressing LL/2 and CT-26 transfectants were implanted into mice. RESULTS: We found the expression of the mRNA and protein levels of CLB1 decrease in these transfectants. The inhibition of CLB1 caused prominent G1 arrest, abnormal morphology, retarded cell growth and an increase in apoptosis. In AS-mCLB1-expressing LL/2 and CT-26 transfectants implanted mice, tumorigenicity was effectively suppressed compared with the controls. In addition, the expression of AS-mCLB1 also significantly increases the survival duration of implanted animals. CONCLUSION: AS-mCLB1 is likely to be useful in future cancer therapy, which may be associated with its ability to down-regulate the expression of CLB1 and then induce G1arrest and apoptosis in tumor cells.

OB glue paste technique for establishing nude mouse human gastric cancer orthotopic transplantation models.

AIM: To establish nude mouse human gastric cancer orthotopic transplantation models using OB glue paste technique. METHODS: Using OB glue paste technique, orthopic transplantation models were established by implanting SGC-7901 and MKN-45 human gastric cancer cell strains into the gastric wall of nude mice. Biological features, growth of the implanted tumors, the success rate of transplantation and the rate of auto-metastasis of the two models were observed. RESULTS: The success rates of orthotopic transplantation of the two models were 94.20% and 96%. The rates of hepatic metastasis, pulmonary metastasis, peritoneal metastasis, lymphocytic metastasis and splenic metastasis were 42.13% and 94.20%, 48.43% and 57.97%, 30.83% and 36.96%, 67.30% and 84.06%, and 59.75% and 10.53%, respectively. The occurrence of ascites was 47.80% and 36.96%. CONCLUSION: OB glue paste technique is easy to follow. The biological behaviors of the nude mouse human gastric cancer orthotopic transplantation models established with this technique are similar to the natural processes of growth and metastasis of human gastric cancer, and, therefore, can be used as an ideal model for experimental research of proliferative metastasis of tumors.

[Nude mouse model of human gastric carcinoma metastasis constructed by orthotopic transplantation using organism glue paste technique].

BACKGROUND & OBJECTIVE: Ideal animal model of tumor metastasis is an important precondition for the research on tumor prevention and treatment. Traditional gastric cancer models were constructed using full tumor tissue block by "subcutaneous transplantation" or "gastric bursa method" with limitations, such as operative complexity, and low survival rate. We tried to construct nude mouse model of human gastric carcinoma metastasis by orthotopic transplantation using organism glue paste technique to solve the problems. METHODS: Transplanted gastric tumor tissue block was constructed through repeatedly subcutaneously inoculating and passaging human gastric carcinoma SGC-7901 cells in nude mouse, and pasted orthotopically on the stomach wall of BALB/c nude mouse with OB biological glue. Tumor growth, successful rate of orthotopic transplantation, and incidence of metastasis in nude mice performed organism glue paste were compared with those in nude mice performed subcutaneous transplantation or gastric bursa method. RESULTS: In nude mice performed organism glue paste, the successful rate of orthotopic transplantation was 100%, the metastasis rate of local lymph node, lung, liver, and peritoneum were 100%, 62.5%, 87.5%, and 87.5%, respectively, while those in nude mice performed gastric bursa method were 100%, 100%, 50.0%, 50.0%, and 33.3%, respectively. The nude mice performed organism glue paste showed a increased metastatic rate of peritoneum (P < 0.05) with a higher survival rate. No local invasion and distance metastasis was observed in nude mice performed subcutaneous transplantation. CONCLUSION: Organism glue paste technique can create gastric cancer metastasis model more easily than traditional methods, and represent clinical metastasis process.