AIM: To observe the clinical effects of minimally invasive scleral buckling combined with 25G cannula intra-optical fiber lighting in the treatment of rhegmatogenous retinal detachment with the help of non-contact wide angle lens.

METHODS: We retrospectively analyzed 43 patients with rhegmatogenous retinal detachment from May 2011 to March 2015 in our hospital. The retinal tear locations of these patients analyzed preoperatively by pre-set lens and three-mirror contact-lens were uncertain. We detected the retinal tears intraoperatively by non-contact wide angle lens with the help of 25G cannula intra-optical fiber lighting. The tears were sealed by minimally invasive scleral buckling. The patients were followed up at 1wk, 1mo, 3mo and 6mo postoperatively. The vison and intraocular pressure were recorded with the same equipment and methods as preoperatively did. The retina reattachment and tear sealing status were also observed.

RESULTS: The retina were reattached by one operation in 41 patients and the reattachment rate was 95.3%. One patient suffered from incomplete retina reattachment, effusion under the retina, poor position of compressed retinal area, and succeeded by minimally invasive scleral buckling once again. One patient developed new retina tear and completely reattached by vitrectomy.

CONCLUSION:For those patients with uncertain retinal detachment preoperatively, minimally invasive scleral buckling combined with 25G cannula intra-optical fiber lighting could increase the success rate. The statistical analysis in large samples and the long-term complications should be further investigated.

AIM　To study the roles of non-genomi c mechanism of glucocorticoid in the integration of sympathetic nervous system. METHODS　The spontaneous discharge of the identified cardiovascula r neurons in the rostral ventrolateral medulla (RVLM) were extracellularly recor ded in urethane-anaesthetized rats. The effects of microiontophoresis of cortic ostersone sulfate (CORT) on the discharge of the cardiovascular neurons in the RVLM were observed. The responses of RU 486 (a blocker for cytosolic glucocortic oids) to the effects of CORT on the cardiovascular neurons were investigated. RESULTS　Totally 33 cardiovascular neurons in the RVLM were recorded , the firing rate of 25 (76%) cardiovascular neurons increased by microiontophor esis of CORT. The effects of CORT were also positively correlated with the curre nt. In 8 (24%) cardiovascular neurons, microiontophoresis of CORT had no effect on their spontaneous discharge. In 12 of 33 cardiovascular neurons, which discha rge increased by CORT, microiontophoresis of RU 486 had no responses to the base line discharge of these cardiovascular neurons (P>0.05), but completely (3 neurons) or partially (9 neurons) blocked the excitatory effect induced by CORT. CONCLUSION　CORT had rapid excitatory effects on the cardiovascul ar neurons in the RVLM. RU 486 had no responses to the baseline activity of the cardiovascular neurons, and but completely or partially blocked the effect of CO RT on the cardiovascular neurons.

Objective: To study the role of glucocorticoid i n the integration of sympathetic nervous system and cardiovascular activity. Methods: Neurons in the rostral ventrolateral medulla (RVLM) were extracelluarly recorded and identified as the presympathetic neurons of adult rats. The spontaneous discharge of the presympathetic neurons in the RVLM were observed by bolus intravenous injection of corticosterone (50, 100, 150 μg/kg） . Results: The firing rate of 12 presympathetic neurons was incr eased by intravenous application of corticosterone (P<0.05), and this effect showed a dose-dependent manner. The latency of excitatory effect was (104±2 5) s. Conclusion: Corticosterone can rapidly excite the presym pathetic neurons in the RVLM, this action might be involved in the integration o f sympathetic nervous system through the “rapid membrane effects”.

0.05), but completely (3 neurons) or partially (9 neurons) blocked the excitatory effect induced by CORT. CONCLUSION CORT had rapid excitatory effects on the Caldiovascular neuronsin the RVLM. RU 486 had no responses to the baseline activity of the cardiovascular neurons, and but completely or partially blocked the effect of CORT on the cardiovascular neurons.

Objective: To explore the relevant factors of work-related musculoskeletal disorders (WMSDs) among dentists through Meta analysis, providing a basis for the prevention and control of WMSDs among dentists. Methods: In April 2022, cross-sectional research literatures on the prevalence correlation of WMSDs among Chinese dentists were searched in databases such as China National Knowledge Infrastructure, Wanfang, VIP, PubMed, Web of Science, and Em Base database. The search was conducted from the establishment of the database until April 2022, literatures were selected using keywords such as musculoskeletal disorders and dentists. To extract gender, age, length of service, disease classification and other related influencing factors as indicator, and prevalence was selected as the outcome indicator. After evaluating the quality of the literatures, RevMan 5.3 software was used to calculate the combined RD (95%CI) values of the included literatures. Results: A total of 15 articles were included, with a total sample size of 3646 people. Meta analysis results showed that the prevalence of WMSDs among dentists in China was 80%, and the top three parts of the incidence rates were 65% of the waist, 58% of the neck, and 50% of the back. Gender, age, length of service, region and disease classification all increased the risk of WMSDs, and the combined effect size were 75%, 78%, 71%, 77% and 82% respectively (P<0.05) . Conclusion: The occurrence of WMSDs among dentists in China is related to multiple factors such as gender, age, length of service and disease classification. The above risk factors should be taken into account in the workplace and preventive measures should be actively implemented to prolong the working life of dentists.
Humans ; Prevalence ; Cross-Sectional Studies ; Occupational Diseases/epidemiology* ; Surveys and Questionnaires ; Musculoskeletal Diseases/epidemiology* ; Risk Factors ; China/epidemiology* ; Dentists

OBJECTIVE: To explore the role of P2X7 receptor (P2X7R) in migration and invasion of mouse Lewis lung cancer (LLC) cells and examine the tumorigenic ability of LLC cells in P2X7R-knockout mice. METHODS: RT-PCR was used to examine P2X7R mRNA expression in LLC cells. LLC cells were treated with ATP (as a P2X7R agonist) or 2'- 3'- O- (4-benzoyl- benzoyl)-ATP (BzATP) (a P2X7R agonist) with or without pretreatment with P2X7R antagonist oxATP or A438079. The changes in migration and invasive abilities of the cells were evaluated using wound healing assay and Transwell assay; Western blotting was performed to determine the activation level of the key proteins in the AKT signaling pathway. The effects of BzATP, A438079, and LY294002 (a inhibitor of the PI3K/AKT pathway) on migration and invasion of LLC cells were also examined. In wild-type (WT) and P2X7R knockout (P2X7^-/-) C57BL/6 mice, the growth of subcutaneous LLC cell xenografts were observed by measuring tumor volume and weight. RESULTS: P2X7R expression was detected in LLC cells. Treatment with P2X7R agonist significantly enhanced migration and invasion abilities of LLC cells, and this effect was inhibited by application of P2X7R antagonists (P < 0.001). Western blotting showed that BzATP treatment of LLC cells significantly increased the expression level of p-AKT protein, which was obviously lowered by treatment with P2X7R antagonist (P < 0.01). P2X7R antagonist strongly inhibited BzATP-induced enhancement of LLC cell migration and invasion (P < 0.001). In the tumor- bearing mice, the tumor volume and weight were significantly lower in P2X7^-/- mice than in WT mice (P < 0.05). CONCLUSION P2X7R promotes migration and invasion of LLC cells by activating the AKT signaling pathway, and LLC cells show lowered tumorigenic capacity in P2X7^-/- mice.
Humans ; Mice ; Animals ; Receptors, Purinergic P2X7 ; Proto-Oncogene Proteins c-akt/metabolism* ; Phosphatidylinositol 3-Kinases/metabolism* ; Mice, Inbred C57BL ; Signal Transduction ; Adenosine Triphosphate/metabolism* ; Lung Neoplasms

As the P2X receptor family has become a research hotspot in recent years, the study on P2X₇ receptor has also received extensive attention. P2X₇ receptor (P2X₇R) is a dual-transmembrane cation-channel receptor, which is gated in vivo by adenosine triphosphate (ATP) and can be activated. Activated P2X₇ receptor can produce such effects as cationic channel opening, signal pathway activation, inflammatory mediator release and cell apoptosis. It plays an important role in the development of various tumors and inflammatory diseases. Studies have shown that the abnormal expression of P2X₇ receptor affects the occurrence and development of breast cancer by activating a series of signaling pathways, which is expected to become a new target for designing anti-breast cancer drugs. Other studies have shown that multiple microRNAs can promote the occurrence and development of breast cancer by regulating the expression of P2X₇ receptor gene. In this review, we reviewed the recent research advances of P2X₇ receptor and the relationship between breast cancer and its abnormal expression.

Pancreatic cancer is one of the cancers with poor prognosis at present, which has high resistance to various anti-tumor drugs as a result of the interaction among pancreatic cancer cells, cancer stem cells, and the tumor microenvironment. P2X7 receptors are extracellular adenosine triphosphate(ATP)-gated nonselective cation channels, which have many biological functions including being involved in cell signal transduction and cytokine secretion, mediate cell survival and growth. Studies have shown that P2X7 receptor is highly expressed in pancreatic cancer and promotes the proliferation, migration and invasion of pancreatic cancer cells by supporting proliferation of pancreatic stellate cells and regulating the expressed of the MMP2/MMP9 protein. The paper reviews the recent research advances of P2X7 receptor in pancreatic cancer.

Aim To investigate whether targeted inhibition of fibroblast activation protein (FAP) can inhibit the endothelial-to-mesenchymal transition (EndMT) of vascular endothelial cells by affecting exosomes (Exo) of cancer-associated fibroblasts (CAFs) and explore the underlying mechanisms. Methods Primary CAFs and peri-tumor fibroblasts (PTFs) were obtained from lung cancer and peri-cancer tissues, and CAFs-exo and PTFs-exo were collected from culture medium, respectively. Exosomes from CAFs treated with specific FAP inhibitor (3.3 nmol • L-

OBJECTIVETo construct a plasmid carrying granulysin (GLS) and to study the effect of the GLS on apoptosis, mitochondrial transmembrane potential and cytochrome C release of SMMC-7721 cells.

METHODSThe coding sequence of the GLS was amplified from the total RNA of human CTL cells, and it was inserted into pBudCE4.1 plasmid and then it was used to transfect SMMC-7721 cells. The expression of GLS was detected by RT-PCR and confirmed by immunocytochemistry method. Cell apoptosis was ascertained by Hoechst staining and electron microscopy; mitochondrial transmembrane potential was detected using Mitocapture and cytochrome C release was studied using Western blot.

RESULTSRecombinant pBudCE4.1/GLS plasmid was successfully constructed. GLS protein was successfully expressed in the SMMC-7721 cells and it induced apoptosis of the SMMC-7721 cells, and at the same time, mitochondrial transmembrane potential was reduced and cytochrome C was released from mitochondria into the cytosol.

CONCLUSIONSGLS gene carried by recombinant plasmid could express in SMMC-7721 cells and induce cells apoptosis. The change of mitochondrial transmembrane potential and the release of cytochrome C might be one of the key factors of apoptosis induced by GLS.

Antigens, Differentiation, T-Lymphocyte ; pharmacology ; Apoptosis ; drug effects ; Cell Line, Tumor ; Cytochromes c ; metabolism ; Humans ; Membrane Potential, Mitochondrial ; drug effects ; Mitochondria ; drug effects ; metabolism ; physiology