dr rongsheng cai manufacturer

Dr. Rongsheng Cai is a Neurosurgery Specialist in Tulsa, Oklahoma. He graduated with honors in 1985. Having more than 38 years of diverse experiences, especially in NEUROSURGERY, Dr. Rongsheng Cai affiliates with no hospital, cooperates with many other doctors and specialists in medical group University Of Arkansas. Call Dr. Rongsheng Cai on phone number (918) 494-1710 for more information and advice or to book an appointment.

This doctor profile was extracted from the dataset publicized on Feb 1st, 2018 by the Centers for Medicare and Medicaid Services (CMS) and from the corresponded NPI record updated on Jun 2nd, 2020 on NPPES website. If you found out anything that is incorrect and want to change it, please follow this Update Dataguide.

Dr. Rongsheng Cai M.D. is a male health care provider in Tulsa with Neurological Surgeon listed as his primary medical specialization. His credentials are: M.D. (Doctor of Medicine). Dr. Rongsheng Cai M.D."s practice location is: 6151 S Yale Ave Ste 2403 Tulsa, OK 74136-1907.

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Last month, authorities began investigating Cai Rongsheng, the head of admissions at Beijing’s elite Renmin University, also for suspected corruption.

There is a star rating of 4/5 for Dr. Rongsheng Cai, MD. Patients say that they trusted the provider"s decisions and the provider explained conditions well. See all patient feedback on Sharecare.

Cai Rongsheng, former head of the university"s admissions office, was detained in Shenzhen, Guangdong province, as he attempted to travel to Canada in November 2013. He was arrested in May last year on charges of taking bribes of over 10 million yuan ($1.6 million) to help secure student enrollments at the university from 2006 to 2013, according to the top anti-graft authority.

Moen O, Morten G, Endresen I (2004). Internationalization of small computer software firms: Entry forms and market selection. European Journal of Marketing, 38: 1236–1251

Correspondence to: Dr Rongsheng Zeng or Dr Lusai Xiang, Guanghua School of Stomatology, Hospital of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, 56 Lingyuanxi Road, Guangzhou, Guangdong 510055, P.R. China, E-mail: moc.361@4270xoag, E-mail: nc.ude.usys.liam@slgnaix

Female Chinese Kunming mice (n=9, 4 weeks old), Chinese Kunming mice (n=20, 7 days old) and 4 male nude mice (n=4, 4 weeks old) were purchased from San Yet-sun University. For all experiments involving isolation of tooth germs, three mice were used for each group. In each experiment, the mice from all groups originated from same pregnant mouse to minimize genetic differences. In total, 6 mice were sacrifice at days E14.5 (25±1.5 g), 3 mice were sacrifice at days E16.5 (25±1.5 g), 20 mice were sacrificed at P7 (6.4 g) and 4 nude mice (20 g) were used for Subrenal capsule assays. All mice were kept at 26–28°C, 40% humidity, and 10-h light and 14-h dark cycle. All mice were fed ad libitum with drinking water filtered and autoclaved before use.

In order to study the influence of various factors on tooth-germ development in a controlled environment, tooth germs of first molars were dissected from the mandibles of embryonic day 14.5 (E14.5) mice and cultured in vitro. The tissue surrounding tooth germs was removed carefully under microscope guidance. The effect of the removal of the dental epithelium on tooth development was analyzed. First, isolated tooth germs were incubated in 1.2 U/ml of dispase II (cat. no. 17105041; Gibco; Thermo Fisher Scientific, Inc.) for 5 min at room temperature, and then the dental mesenchyme was isolated with a fine needle. Tooth germs and the isolated dental mesenchyme were cultured for 7 days on 6-well Transwell™ plates with 1,000 µl/well of Dulbecco"s modified Eagle"s medium (cat. no. 11885092; Gibco; Thermo Fisher Scientific, Inc.) supplemented with 10% fetal bovine serum, 100 µg/ml of ascorbic acid (cat. no. PHR1008; Sigma-Aldrich; Merck KGaA) and 2 mM of L-glutamine (cat. no. 25030081, Gibco; Thermo Fisher Scientific, Inc.). Recombinant mouse osteoprotegerin protein (100 or 200 ng/ml; cat. no. 375-TL; R&D Systems) was added to the culture medium to study its effect on tooth development. Cultures were incubated at 37°C in a humidified atmosphere of 5% CO2. The culture medium was changed every 3 days.

Tissue preparation and histology. To assess osteoprotegerin expression dynamically during tooth development, mice were sacrificed at E14.5, E16.5, post-partum day 1 (P1), P3, P5 and P7. Embryos at E14.5 and E16.5 and mandibles from P1, P3, P5, and P7 were fixed with 4% paraformaldehyde for 72 h at room temperature. Then, the tooth germs from first molars were dissected. Following decalcification with 0.5 M of ethylenediamine tetraacetic acid solution for 2 weeks, samples were dehydrated with graded solutions of alcohol and embedded. Tooth germs from E14.5 mice were dehydrated with graded solutions of alcohol and embedded without decalcification.

Total RNA was extracted from tooth germs or samples of isolated dental mesenchyme using PureLink® RNA Mini Kit (cat. no. 12183018A; Invitrogen; Thermo Fisher Scientific, Inc.) according to manufacturer"s instructions. Complimentary-DNA synthesis was performed with random 6-mer primers using a PrimeScript™ 1st Strand cDNA Synthesis kit (cat. no. 6110A; Takara Bio, Inc.). Messenger-RNA expression was assessed by RT-qPCR using the SYBR®-Green method. The thermocycling conditions were: Initial denaturation for 30 sec at 95°C, followed by 40 cycles of 5 sec at 95°C and 30 sec at 60°C. The relative fold change for expression of the target gene was calculated following the method proposed by of Livak and Schmittgen (14). Glyceraldehyde-3-phosphate dehydrogenase was used as endogenous reference for normalization, and the expression level in tooth germ with no osteoprotegerin treatment as a calibrator. The primers employed are listed in Table SI.

OA is a chronic degenerative articular disease characterized by chronic arthralgia, stiffness, declining locomotor ability, and eventually, disability (20). Accurate details of the pathophysiological mechanisms of the disease remain unknown. A previous study indicated that degenerated articular cartilage is the initial change in the development of OA (21). Subsequently, the complex molecular mechanisms of OA have been observed, including the formation of osteophytes, the remodeling of subchondral bone, the abnormal remodeling of cartilage, changes in the synovium, bone marrow lesion, chondrocyte apoptosis and ECM degradation (22-26). Non-coding RNAs, including miRNAs and circRNAs, were recently confirmed to play a regulatory role in the onset and progression of OA. miRNAs are a group of short non-coding RNAs measuring ~22 nucleotides in length (27). Several miRNAs have been proven to regulate various signaling pathways, apoptosis and chondrocyte functions in OA (28). Some miRNAs are differentially expressed during the onset and development of OA (29-31). A total of 42 circRNAs have also been found to be differentially expressed in OA (32). These circRNAs regulate chondrocyte apoptosis by sponging targeted miRNAs. In the present study, the ceRNA mechanism of the circCSNK1G1/miR-4428/FUT2 that may exist in arthritis was first constructed by referencing and applying the TargetScan (http://www.targetscan.org/vert_72/) and Starbase (http://starbase.sysu.edu.cn/index.php) websites. Furthermore, the role of circCSNK1G1 in aggravating inflammation at the chondrocyte level we confirmed through relevant experiments. Therefore, the function and regulatory mechanisms of circCSNK1G1 were further invesigated in arthritis. The aim of the present study was to examine the regulatory role of the circCSNK1G1/miR-4428/FUT2 axis in arthritis and to determine the cellular/molecular mechanisms of this axis.

Studies have demonstrated that some circRNAs are involved in the progression of arthritis. circRNA-CDR1as has been shown to be upregulated in OA tissue and targets miR-641 to increase MMP-13 and IL-6 expression (33). circ_0136474 has been shown to sponge miR-127-5p to upregulate MMP-13 expression and inhibit chondrocyte proliferation (34). circRNAs, such as hsa_circRNA_0020014 and hsa_circ_0032131, can serve as diagnostic biomarkers and treatment targets for OA (35-37). The present study provided some novel findings. First, circCSNK1G1 expression negatively correlated with miR-4428 expression; specifically, the former was upregulated, whereas the latter was downregulated in OA. Second, the role of circCSNK1G1 in OA was confirmed and it was found that the overexpression of circCSNK1G1 promoted the progression of OA. circCSNK1G1 was upregulated in OA-affected cartilage and induced chondrocyte apoptosis and EMC degradation by sponging the target of miR-4428. miR-4428 conferred protective effects against OA by inhibiting FUT2 expression. FUT2 has been shown to trigger airway inflammation via C3a production and dendritic cell accumulation (38); it has also been shown to promote breast cancer development by regulating cell proliferation, adhesion and migration (39). FUT2 is upregulated in OA-affected tissues, and miR-17-5p targets FUT2 to regulate the Wnt/β-catenin pathway and inhibit OA development (18,40,41). In the present study, FUT2 and circCSNK1G1 were similarly upregulated in OA-affected cartilage. The inhibition of FUT2 expression resulted in beneficial effects against OA development. As a target gene of miR-4428, FUT2 may mediate the role of the circCSNK1G1/miR-4428 axis in promoting OA. However, the pathways downstream of FUT2 were not detected in the present study.

Chondrocytes are the only cells that make up articular cartilage. The balance between chondrocyte apoptosis and proliferation plays a pivotal role in maintaining chondrocyte cell numbers in cartilage. Apoptosis refers to the programmed death of cells triggered by caspases (42). There is evidence to indicate that apoptosis plays a pivotal role in the onset and development of OA (43). The H19/miR-675/COL2A1 axis is activated and induces apoptosis in OA (44). The lncRNA-CIR/miR-27/MMP13 axis regulates chondrocyte apoptosis in OA (45). The DLL1/PI3K/AKT (46), MyD88/NF-kB/p38MAPK (47) and BCL-2/MAPK/JNK (48) pathways have also been reported to regulate chondrocyte apoptosis in OA. Thus, the chondrocyte cell number is the foundation of ECM formation and degradation (49).

In conclusion, the present study, to the best of our knowledge, is the first to report the role of the circC-SNK1G1/miR-4428/FUT2 axis in OA development via the regulation of chondrocyte apoptosis and ECM degradation. The results reveal that the circCSNK1G1/miR-4428/FUT2 axis may present a novel therapeutic target for the treatment of OA.

About 500 papers in this proceeding presented a panorama of the state-of-the-art of the most recent R/D and applications of all techniques and areas of nondestructive and structural testing. The articles were presented in 19 sessions, comprising papers beyond the disciplinary limits of NDT. They included activities such as diagnosis of machinery, structure, welding, life management and quality control. In the field of power generation: hydro-, thermo- and nuclear electricity. In manufacturing: steel making, automotive, aerospace, civil structure. Patrimony and heritage: pieces of art, service and insurance companies, industrial maintenance and inspection. Commercial presentations were also included. In addition to the comprehensive technical program, the conference also featured an exhibition of the latest NDT systems, technical tours and a full social program, including options for accompanying persons.

Members: Dr. Shen Jianzhong, Dr. Geng Rongsheng, Dr.Guo Chengbin, Mr. Yang Jianhong, Mr. Pan Bingxun, Mr. Nardoni, Dr. Farley, Dr. Marshall, Dr. Klyuev, Dr. Vahaviolos, Dr. Link, Dr. Raj