AIM: To study the efficacy and adverse reactions of carnitine on patients with acute cerebral infarction.　METHODS: One hundred and thirty-five patients with acute cerebral infarction diagnosed by CT or MRI were randomly divided into 2 groups, on the basis of conventional therapy. Sixty-eight patients in carnitine group (M37,F31; age 60 a± s 17 a) received carnitine 2-3g, iv, drip, qd for 28 d. The other 67 patients of control group (M39, F28; age 63 a±17 a) received compound salvia miltirrhiza 20 mL in dextran-40 glucose injection 500 mL, iv, drip, qd for 28 d.　RESULTS: The total effective rates of carnitine group and control group for acute cerebral infarction were 80％ and 55％, respectively (P<0.05). No adverse reactions were found.　CONCLUSION: Carnitine is safe and effective in the treatment of acute cerebral infarction.

Dental Implants, Single-Tooth ; Dental Prosthesis, Implant-Supported ; Esthetics ; Humans ; Maxilla

To observe the effect of autologous stem cell transplantation in diabetic retinopathy.
●METHODS:Totally 58 cases (116 eyes) who underwent autologous stem cell transplantation were confirmed as no diabetic retinopathy (18 eyes), mild non-proliferative diabetic retinopathy (NPDR) (41 eyes), mid-level NPDR (51 eyes); severe NPDR (6 eyes) by ophthalmoscope directly or indirectly and fluorescence fundus angiography (FFA ). Follow - up was 6 - 12mo, the changes of retinopathy were observed.
●RESULTS: The total effective rate of vision and retinopathy was 84. 4%, 76. 7%. The results of severe NPDR was statistically worse than the other groups ( P <0. 05).
●CONCLUSlON: The stable blood glucose level and improved pancreatic function after autologous stem cell transplantation might be helpful in diabetic retinopathy, the long effects need to be researched further.

Hepatocellular carcinoma (HCC) is a serious threat for human health, the incidence of HCC in China accounts for more than 50% worldwide. There is an urgent need to develop novel anticancer agents for the treatment of HCC patients. Here we characterized the inhibitory effect and the molecular mechanism of protopine on HCC cancer cells. The results of a CCK-8 assay indicated that protopine displays anticancer activities on HCC cells. Flow cytometry and JC-1 staining confirmed that treatment with protopine decreased the mitochondrial membrane potential and induced apoptosis in HCC cells. Western blot analysis showed that protopine was able to increase protein expression in the mitochondrial apoptotic pathway; the level of cytochrome C, apoptotic protease activating factor-1 (Apaf-1), Bax, cleaved-poly ADP-ribose polymerase (cleaved-PARP), cleaved-caspase-3, and cleaved-caspase-9 were increased while the expression of Bcl-2 was suppressed significantly. An in vivo study revealed that protopine significantly suppressed the growth of tumors in nude mice bearing HepG2 cells. Administration of protopine intraperitoneally at a concentration of 50 mg·kg^-1 inhibited tumor growth by 72.46%. Animal experiments were carried out according to the Regulation of the Animal Ethics Committee of Southwest Medical University. This study provides preliminary evidence that there is potential to develop protopine as a lead compound for the treatment of HCC.

Child ; Dystonia Musculorum Deformans ; diagnosis ; etiology ; genetics ; Humans ; Magnetic Resonance Imaging ; Male

OBJECTIVETo investigate the relationship between expression of vascular endothelial growth factor (VEGF) and pathogenesis of acute leukemia (AL).

METHODSVEGF mRNA expression was analysed by using semi-quantitative RT-PCR technique. VEGF level of culture supernatant of the bone marrow mononuclear cell (BMMNC) was detected by ELISA. The influence of culture supernatant of the BMMNC on proliferation of human umbilical vein endothelial cell line huECV304 in vitro was determined by MTT assay.

RESULTSThe median VEGF/beta-actin expression level of BMMNC in newly diagnosed untreated AL group was higher (0.86) than that in remission group (0.41) and normal control group (0.39) (P < 0.01, both), but was no difference from the relapse group (1.02, P > 0.05). Among the patients with newly diagnosed untreated AL, VEGF/beta-actin level in AML (1.03) was statistically higher than that in ALL (0.61) (P < 0.05). The VEGF level in 72 h culture supernatant of BMMNC was higher in newly diagnosed untreated AL group (91.48 ng/L) than in remission group (31.91 ng/L) and normal control group (28.71 ng/L) (P < 0.01). In ALL group (32.76 ng/L), the VEGF level of 72 h culture supernatant was much lower than that in AML group (173.49 ng/L) (P < 0.01). The proliferation of huECV304 cells after co-cultured with the 72 h culture supernatant of AML BMMNC with addition of anti-VEGF antibody was inhibited notably compared with culture supernatant alone (P < 0.01). However, no such result was found in ALL group (P > 0.05).

CONCLUSIONThe mRNA expression and secretion of VEGF in AML cells were higher than those in ALL cells. The regulators that participated angiogenesis were different in ALL and AML patients.

Acute Disease ; Adult ; Cell Proliferation ; drug effects ; Cells, Cultured ; Endothelial Cells ; cytology ; drug effects ; Female ; Humans ; Leukemia ; metabolism ; Male ; Monocytes ; metabolism ; RNA, Messenger ; genetics ; Umbilical Veins ; cytology ; Vascular Endothelial Growth Factor A ; genetics ; metabolism ; pharmacology

By reverse transcription-polymerase chain reaction (RT-PCR), an open reading frame of pathogenesis-related protein 1 (PR1) was isolated from Panax notoginseng and named as PnPR1. Molecular and bioinformatic analyses of PnPR1 revealed that an open reading frame of 501 bp was predicted to encode a 166-amino acid protein with a deduced molecular mass of 18.1 kD. Homology analysis showed that the deduced amino acid sequence of PR1 protein of Panax notoginseng had a high similarity with other higher plants had the same conservative structure domain of cysteine-rich secretory protein (CAP). The recombinant expressed plasmid pET28a(+)-PnPR1 was expressed in Escherichia coli BL21. The expression conditions were optimized by induction at different times, different temperatures, different IPTG concentrations and different giving times. The optimum expression condition was 0.4 mmol.L-1 IPTG at 28 degrees C for 20 h. The successful expression of PnPR1 provides some basis for protein purification and preparation of the monoclonal antibody.
Amino Acid Sequence ; Cloning, Molecular ; Escherichia coli ; metabolism ; Molecular Weight ; Open Reading Frames ; genetics ; Panax notoginseng ; chemistry ; Phylogeny ; Plant Proteins ; genetics ; metabolism ; Plants, Medicinal ; chemistry ; Reverse Transcriptase Polymerase Chain Reaction ; Sequence Alignment

OBJECTIVE Cloves(Syzygium aromaticum L.)have been used as both a spice and a traditional Chinese medicinal herb for thousands of years. However, relatively little is known about its potential anticancer activity and mechanisms.In this study,we investigated the in vitro and in vivo anti-tumor effects and mechanisms of water extract of cloves(WEC)against colorectal cancer. METHODS MTS assay and Colony-formation assay were used to detect the anti-tumor activity of WEC on HT-29 cells.The in vivo anti-tumor effect of WEC was detected in a subcutaneous transplantation tumor model of human HT-29 cells.Autophagy was detected by flow cytometry and the expressions of autophagy related proteins(Beclin-1 and LC-3a/b)were determined by western blot. RESULTS MTS result showed that WEC significantly inhibited the viability of HT-29 cells,with the IC50values of 150 μg·mL-1.The colony-formation assay showed that the WEC significantly suppressed colon cancer cells proliferation.WEC also exhibited significant antitumor activity in tumor bearing nude mice. Flow cytometry result showed that WEC significantly induced autophagy, and the averaged relative values of fluorescence intensity were 206,251,341 and 356 in cells treated with 0,100,150 and 200 μg·mL-1WEC for 48 h.Western blot result showed that WEC treatment significantly increased Beclin-1 expression and ratios of LC3-II/LC3-I. CONCLUSION These result showed that WEC inhibited the growth of colon tumor both in vitro and in vivo, which might be related with autophagy induction, and WEC has potential to be developed as a novel anticancer agent for the treatment of colon cancer.

OBJECTIVE Zn-doped CuO nanocomposites (Zn-CuO NPs) are novel nanoparticles synthesized by our research group.In this study,we assessed the in vitro and in vivo antitumor effects of Zn-CuO NPS on pancreatic cancer cells,as well as the potential mechanisms. METHODS MTS assay was used to detect the effects of Zn-CuO NPS on proliferation pancreatic cancer cells(Panc-mia and Aspc-1). The in vivo antitumor effects of Zn-CuO NPs were detected by xenografts model in nude mice. The effects of Zn-CuO NPS on autophagy were detected bytransmission electron microscopy (TEM) andflow cytometry. Autophagy related proteins were detected by Western blotting. RESULTS Zn-CuO NPS significantly inhibited the proliferation of Panc-mia cells and Aspc-1 cells.In vivo experi-ments showed that Zn-CuO NPS significantly inhibited the tumor growth in nude mice without affecting the body weight of the mice. TEM and flow cytometry showed that Zn-CuO NPS induced autophagy, and significantly increased the number of autophagosome.Western Blot showed that Zn-CuO NPS alterd the expression of autophagy related proteins,such as AMPK,mTORand Beclin-1.Also,AMPK inhibitor could significantly reduce Zn-CuO NPS-induced autophagy pathwayas analyzed byWestern blotting. CONCLUSION The findings suggested that Zn-doped CuO nanocomposites inhibited the in vitro and in vivo growth of pancreatic cancer by inducing autophagy through AMPK/mTOR pathway.

OBJECTIVE Granulin A (GRN A), a cytokinesis protein, is derived from proteolysis of progranulin. The previous study in our laboratory has shown that GRN A is able to inhibit cancer cell growth significantly. This study aimed to investigate the effect of combination of GRN A and cisplatin on in vitro and in vivo on the growth of hepatocellular carcinoma. METHODS The in vitro and in vivo antitumor effects of combination of GRN A and Cisplatin were evaluated with MTS assay and subcuta-neous transplantation tumor model.Chou-Talalay method was used to calculate the combination index (CI). Colony formation assay and flow cytometry were used to detect the effects of GRN A on apoptosis. The expression of apoptosis-related proteins were detected by Western blot. RESULTS MTS assay showed that GRN A significantly inhibit hepatocellular carcinoma cells growth with the IC50of 5.6 μmol·L-1, and GRN A combined with cisplatin synergistically inhibit hepatocellular carcinoma proliferation, with the CI<1.The colony-formation assay showed that GRN A significantly enhanced the inhibitory effects of cisplatin on cellular anchorage-independent growth. Flow cytometry showed that GRN A combined with cisplatin synergistically induced apoptosis,with the apoptotic rates of 5.87%,32.74%,35.67% and 67.15% in control, GRN A, Cisplatin, and combination of GRN A and Cisplatin groups, respectively. Western blot confirmed that the two drugs synergistically changed the expressions of proteins related to apoptosis.In vivo experiment indicated that combination of GRN A and cisplatin significantly suppressed tumor growth compared with single drug treatment groups.CONCLUSION The combination of GRN A and cisplatin resulted in synergistic antitumor effects against hepatocellular carcinoma both in vitro and in vivo.