Search PubMed⌕ Search

Biomedical subjects

Hong Jiang

Publications and source records attributed to Hong Jiang.

At least 145 records · Page 8Linked to original sources

[Pharmacokinetics and bioequivalence of trimebutine dispersive tablet in healthy subjects].

AIM: To develop an HPLC-ESI-MS assay for determination of trimebutine in human plasma and to investigate the pharmacokinetics and bioequivalence of two trimebutine tablets in human. METHODS: After being made alkaline with saturated sodium bicarbonate, plasma was extracted by cyclohexane and separated by HPLC on a reversed-phase C18 column with a mobile phase of 10 mmol x L(-1) ammonium acetate buffer solution (pH 3.5)-methanol (18:82). HPLC-ESI-MS was performed in the selected ion monitoring (SIM) mode using target ions at m/z 388 for trimebutine and m/z 280 for the internal standard (sibutramine, IS). The fragmentor voltage was 50 V. A randomized cross-over design was performed in 20 healthy volunteers. In the two study periods, a single 100 mg dose of each tablet was administered to each volunteer. RESULTS: Calibration curve was linear over the range of 0.3 - 150 microg x L(-1). The main pharmacokinetic parameters of T1/2, Tmax and Cmax were (9.2 +/- 2.8) h, (1.0 +/- 0.3) h and (40 +/- 20) microg x L(-1) for the reference tablet; (9.2 +/- 2.3) h, (0.9 +/- 0.4) h and (41 +/- 20) microg x L(-1) for the test tablet. The relative bioavalability of the test tablet was (97 +/- 13)%. The results of variance analysis and two one-sided t-test showed that there was no significant difference between the two formulations in the AUC and Cmax. CONCLUSION: The assay was proved to be sensitive, accurate and convenient. The two formulations were bioequivalent.

Adult↗

[Clinical application of linkage analysis for vWD family].

OBJECTIVE: To explore the application of amplified fragment length polymorphism (amp-FLP) of short tandem repeat (STR) within intron 40 of vWF gene in the gene diagnosis and genetic consulting service for von Willebrand disease (vWD). METHODS: We isolated DNA from the blood of members in 8 families with vWD, measured the relative parameters of vWD simultaneously; and amplified the fragment length polymorphism of two loci (nt1890-1990 and nt2215-2380) within intron 40 of vWF gene using PCR. The RCR products were analyzed by means of polyacrylamide gel electrophoresis (PAGE) and silver staining. RESULTS: Five types of amp-FLP were identified on nt1890-1990 and nt2215-2380 respectively. Haplotypes could be identified to link with defective vWF gene in these families. CONCLUSION: Combination of PCR and PAGE is a fast and practical method for carrying out family analysis of inherited disease; nt1980-1990 and nt2215-2380 of vWF gene are two ideal genetic labels in linkage analysis and hereditary consultation of vWD family.

Adult↗

[Development of a new noninvasive blood sugar detector].

The level of blood sugar is an improtant indicator used in the diagnosis and management of diabetes mellitus. In this respect, polarimeter and blood sugar detector were conventionally and generally used in hospitals; However, the former one is already obsolete; the latter one is invasive. In this paper, the development of a novel noninvasive blood-sugar detector is described. The experiment indicate that this detector is nonivasive, safe, fast, and easy to operate, and it can be of wide application.

Blood Glucose↗

Clinical features of hereditary spastic paraplegia with thin corpus callosum: report of 5 Chinese cases.

BACKGROUND: Hereditary spastic paraplegia is a clinically and genetically heterogeneous group of neurodegenerative disorders of the motor system, characterized by slowly progressive spasticity and weakness of the lower extremities. This study was conducted to investigate the clinical features of hereditary spastic paraplegia with thin corpus callosum (HSP-TCC). METHODS: Clinical data from five patients and thirty-five previously published case reports of HSP-TCC were analyzed retrospectively. RESULTS: Most patients were adolescents at the onset of the disease, presenting with spastic paraparesis of the lower limbs and mental impairment. Some patients also had other clinical features, including spasticity of the upper limbs, cerebellar ataxia, and sensory disturbances. Cranial MRIs of the five patients revealed an extremely thin corpus callosum, sometimes with widened cerebral sulci and ventricles, as well as with cerebellar and cerebral atrophy. CONCLUSION: The main clinical features of HSP-TCC include slowly progressive spastic paraplegia, mental impairment during the second decade of life, and an extremely thin corpus callosum as shown on cranial MRIs.

Adolescent↗

[The effect of recombinant human erythropoietin on postoperative anemia in orthognathic patients].

PURPOSE: To observe the effect of rhEPO on postoperative anemia in orthognathic patients. METHODS: 31 patients had 500-1200 ml blood loss during orthognathic operation, who were divided into two groups randomly, the experiment group and the control group. The patients in the experiment group received rhEPO 6000IU subcutaneously for 3 times in a week and Ferrost sulfatis Et vitamini-medtech 1 tablet per day via oral administration for 12 days after operation, while the patients in the control group only received the same dose of Ferrost sulfatis Et vitamini-medtech. The loss of blood of the patients during operation were estimated and recorded. Their Hb and Hct were mensured before operation, and in the first, third, seventh-twelfth day after operation. RESULTS: In the twelfth day after operation, the Hb and Hct of the patients in the experiment group had a significantly higher increase than that in the control group (P<0.05). CONCLUSIONS: rhEPO combined Ferrost sulfatis Et vitamini-medtech are suitable to apply in orthognathic patients with anemia after operation, which may effectively accelerate the recovery of their anemia, and avoid transfusion of blood.

Adolescent↗

[Study of propofol target controlled infusion for blind tracheal intubation in anesthesia of oral and maxillofacial surgery.].

PURPOSE: To observe the clinical effects of propofol target controlled infusion for blind tracheal intubation in anesthesia of oral and maxillofacial surgery. METHODS: 80 cases with difficult airway of oral and maxillofacial surgery were divided into four groups. They were intubated by a new blind tracheal intubation technique.Before intubation,group 1,group 2,group 3 received fentanyl 4 microg/kg by intravenous infusion and propofol TCI 1.0 microg/ml,1.5 microg/ml,2.0 microg/ml, respectively.Group 4 only received fentanyl 4 microg/kg. All patients underwent tracheal topical anesthesia.The effects of anesthesia in the four groups were observed and compared. RESULTS: Ramsay score in group 2 and group 3 was obviously higher after administer propofol TCI (P<0.05).During intubation, group 2 and group 3 kept higher score than the other groups (P<0.05), MAP and HR changed smoothly and steadily in group 2 and group 3. But in group 1 and group 4, MAP and HR increased significantly (P<0.05). During intubation, RR decreased significantly in the four groups, but most serious in group 3 (P<0.05).There were no significant changes of SpO2, P(ET)CO2. After intubation, plasma PRL and plasma A II increased obviously in different degrees in the four groups,the increase in group 4 was higher than in group 3 (P<0.05). CONCLUSION: Propofol target controlled infusion is a good anesthesia method for blind tracheal intubation.It is safe and effective if target blood concentration controlled appropriately.

Anesthesia, General↗

[Successful tracheal intubation in a child with facial multi-clefts and difficult airway: case report.].

A male patient, aged 7 years, was intended to undergo plastic surgery under general anesthesia with tracheal intubation for his severe facial abnormities as a result of 5, 6, 7 combined facial clefts. Because of his severe facial abnormities and preoperative undetected bilateral antiadoncus, during the period of induction, dyspnoea and dysventilation took place, which were relieved by inserting a medium-sized oropharyngeal airway with difficulty; during euthyphoirally exploring his endolarynx with direct laryngoscope, laryngospasm occurred, which was relieved through inserting airway and pressurizing ventilation; repetitively attempted to blindly insert tracheal intubation through nostril, but failed. Finally, his intubation was achieved by blindly intubating through oral cavity under the assistance of direct laryngoscope.

Anesthesia, General↗

[Cloning and expression of hTRF1 in Escherichia coli and preparation of polyclonal antibody].

Human telomeric repeat binding factor 1(TRF1) contains one Myb-type DNA-binding repeat and an amino-terminal acidic domain. It can bind to the duplex array of TTAGGG repeats at chromosome ends and is shown to be important in preserving genomic stability, maintaining cell proliferative capacity, and blocking the activation of DNA-damage cell cycle checkpoints. Interestingly, the double strand DNA breaks sensor ATM interacts with and phosphorylates Pin2/TRF1 and inhibits its function after DNA damage. Are there some proteins else that can interact with TRF1 and influence its function? In order to analysis the interaction between TRF1 and other proteins, we must prepare the antiserum that can recognize the endogenous TRF1 of cell lysates. TRF1 cDNA was amplified using cDNA Library of HeLa cell by PCR and cloned into pUCm-T vector. Sequence analysis reveals identity to the GenBank report. The TRF1 cDNA was subcloned into expression vector pET-28c(+) and expressed in E. coli as a fusion protein of 65 kD. The recombinant TRF1 can express in the supernatant (about 12.3% in total protein) on the induction of 0.5 mmol/L IPTG at 37 degrees C for 3 hours. Western-blot analysis showed the recombinant protein can react with TRF1 polyclonal antibody sc-6165 (from Santa Cruz Company). His6-TRF1 was purified by Ni(2+) -NTA resin affinity chromatography made by ourselves and showed to be homogeneity in SDS-PAGE. Rabbits were immunized for four times to prepare polyclonal antibody. The unpurified antiserum can recognize the overexpressed TRF1 with myc-tag and the endogenous Pin2/TRF1 of cell lysate by Western-blot at 1:1000 dilution. At 1:400 dilution, the antiserum can interact with endogenous TRF1 by Immunofluorescence cell staining analysis. The endogenous TRF1 in different cell lines, such as HepG2, 803, MCF7 and HeLa, locates in the nucleus. The soluble expression TRF1 and preparation of its antibody lay the foundation to study it further.

Animals↗

Direct interaction between alpha-actinin and hepatitis C virus NS5B.

It has been suggested that cellular proteins are involved in hepatitis C virus (HCV) RNA replication. By using the yeast two-hybrid system, we isolated seven cDNA clones encoding proteins interacting with HCV RNA polymerase (NS5B) from a human liver cDNA library. For one of these, alpha-actinin, we confirmed the interaction by coimmunoprecipitation, immunofluorescent staining and confocal microscopic analysis. Experiments with deletion mutants showed that domains NS5B(84-95), NS5B(466-478), and alpha-actinin(621-733) are responsible for the interaction. Studies of the HCV subgenomic replicon system with small interference RNA indicate that alpha-actinin is essential for HCV RNA replication. Our results suggest alpha-actinin may be a component of the HCV replication complex.

Actinin↗

[Increased DMT1 expression and iron content in MPTP-treated C57BL/6 mice].

Iron plays a key role in Parkinson s disease (PD). To illustrate the mechanism underlying the increase of iron in substantia nigra (SN) in PD, changes of the expression of divalent metal transporter 1 (DMT1) and iron content were examined in SN in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treated mice using immunohistochemistry and histochemistry respectively. Following MPTP treatment for 3 d, elevated iron staining was found in SN. A further increase in iron content was observed after 7 d. In these lesioned animals, tyrosine hydroxylase-immunoreactive DA neurons exhibited a decrease in number and morphological changes as well. There were two isoforms of DMT1 expressed in SN of mice. After MPTP treatment, the expression of DMT1 without IRE form increased in either group, whereas DMT1 with IRE form increased only after 7 d of MPTP treatment. These observations suggest that DMT1 is possibly involved in the process of iron accumulation in SN of MPTP-treated mice, which might be responsible for the subsequent death of DA neurons.

Animals↗

Signaling by ephrinB1 and Eph kinases in platelets promotes Rap1 activation, platelet adhesion, and aggregation via effector pathways that do not require phosphorylation of ephrinB1.

We have previously shown that platelets express 2 receptor tyrosine kinases, EphA4 and EphB1, and the Eph kinase ligand, ephrinB1, and proposed that transcellular Eph/ephrin interactions made possible by the onset of platelet aggregation promote the further growth and stability of the hemostatic plug. The present study examines how this might occur. The results show that clustering of either ephrinB1 or EphA4 causes platelets to adhere to immobilized fibrinogen via alpha(IIb)beta(3). Adhesion occurs more slowly than with adenosine diphosphate (ADP) and requires phosphatidylinositol 3 (PI3)-kinase and protein kinase C activity but not ephrinB1 phosphorylation. By itself, Eph and ephrin signaling is insufficient to cause aggregation or the binding of soluble fibrinogen, but it can potentiate aggregation initiated by a Ca(++) ionophore or by agonists for thrombin and thromboxane receptors. It also enhances Rap1 activation without requiring ADP secretion, ephrinB1 phosphorylation, or the activation of PI3-kinase and Src. From this we conclude that (1) Eph/ephrin signaling enhances the ability of platelet agonists to cause aggregation provided that those agonists can increase cytosolic Ca(++); (2) this is accomplished in part by activating Rap1; and (3) these effects require oligomerization of ephrinB1 but not phosphotyrosine-based interactions with the ephrinB1 cytoplasmic domain.

Blood Platelets↗

[Correlation between iron levels and degeneration of dopaminergic neurons in rat nigrostriatal system during the early 6-OHDA lesions in medial forebrain bundle].

In the present study, using fast cyclic voltammetry (FCV), atomic absorption/flame emission spectrophotometry and immunohistochemistry, we investigated the correlation between iron levels and degeneration of dopaminergic neurons in rat nigrostriatal system during the early 6-OHDA lesions in the medial forebrain bundle (MFB). The results showed that 1 d or 3 d after lesions in MFB, there was a 45% or 66% reduction, respectively, in the density of tyrosine hydroxylase (TH) immunoreactive cells in the substantia nigra (SN) of the lesioned side accompanied by an increase in iron staining intensity and iron concentration; while there was no change in dopamine (DA) release in the striatum (Str) of the lesioned side compared with the unlesioned side and the normal rats. There was no difference in the iron staining and concentration of SN and DA release of Str on the lesioned side between one-day group and three-days group. These results suggest that an iron level elevation in SN may be involved at the early stage of degeneration of DA neurons in SN. However, DA release in Str was unchanged due to the immense compensatory mechanism of DA system.

Animals↗

Studies on the extraction of phenol in wastewater.

A novel extraction procedure has been developed for treating phenolic wastewater. Alcohols, amines, and organic acids were applied as extractants in separation of phenol from the wastewater containing 6000 mg/l phenol and 5% salts discharged by chemical plants, >99% phenol was recovered by extracting with octanol. The interactions of phenol with alcohols, amines, and organic acids were studied by a theoretical calculation with GAUSSIAN 98. The extraction efficiency is strongly dependent on the intermolecular interactions between the phenol and extractants. Based on the experimental and theoretical studies, a pilot-scale LLES was set-up and worked well.

Conservation of Natural Resources↗

[Application of ultrasonic angioplasty in treating totally occluded peripheral arteries, a clinical study of 39 cases].

OBJECTIVE: To evaluate the efficacy and safety of intravascular ultrasonic angioplasty in treating atherosclerotic totally occluded peripheral arteries. METHODS: Percutaneous ultrasonic angioplasty was applied on 39 cases with peripheral atherosclerotic total occlusion under fluoroscopic guidance. The recanalization, clinical efficacy and complications were observed. RESULTS: 38 (97.4%) of the 39 cases achieved successful recanalization in (1157 +/- 376) seconds, with a mean residual stenosis of (32 +/- 11)%. The technical successful rate (residual stenosis < 50%) was 82.1% (32/39). Clinical improvement at different degrees was seen in 38 cases after ultrasonic angioplasty. The patency rates 24 hours, 30 days, 90 days and 180 days after the ultrasonic angioplasty were 100%, 94.7%, 89.5% and 81.6% respectively. The complications related to ultrasonic angioplasty included hemoglobinuria in 9 cases and distal embolization in 1 case. CONCLUSION: Ultrasonic angioplasty appears to be safe and effective for the treatment of atherosclerotic totally occluded peripheral arteries.

Adult↗

A peptide from heat shock protein 60 is the dominant peptide bound to Qa-1 in the absence of the MHC class Ia leader sequence peptide Qdm.

The MHC class Ib molecule Qa-1 binds specifically and predominantly to a single 9-aa peptide (AMAPRTLLL) derived from the leader sequence of many MHC class Ia proteins. This peptide is referred to as Qdm. In this study, we report the isolation and sequencing of a heat shock protein 60-derived peptide (GMKFDRGYI) from Qa-1. This peptide is the dominant peptide bound to Qa-1 in the absence of Qdm. A Qa-1-restricted CTL clone recognizes this heat shock protein 60 peptide, further verifying that it binds to Qa-1 and a peptide from the homologous Salmonella typhimurium protein GroEL (GMQFDRGYL). These observations have implications for how Qa-1 can influence NK cell and T cell effector function via the TCR and CD94/NKG2 family members, and how this effect can change under conditions that cause the peptides bound to Qa-1 to change.

Animals↗

Preclinical characterization of the antiglioma activity of a tropism-enhanced adenovirus targeted to the retinoblastoma pathway.

BACKGROUND: Oncolytic adenoviruses are promising therapies for the treatment of gliomas. However, untargeted viral replication and the paucity of coxsackie-adenovirus receptors (CARs) on tumor cells are major stumbling blocks for adenovirus-based treatment. We studied the antiglioma activity of the tumor-selective Delta-24 adenovirus, which encompasses an early 1 A adenoviral (E1A) deletion in the retinoblastoma (Rb) protein-binding region, and of the Delta-24-RGD adenovirus. Delta-24-RGD has an RGD-4C peptide motif inserted into the adenoviral fiber, which allows the adenovirus to anchor directly to integrins. METHODS: CAR and integrin expression were examined by flow cytometry in six glioma cell lines and in normal human astrocytes (NHAs). Adenoviral vectors containing green fluorescent protein (GFP) (AdGFP and AdGFP-RGD) were used to infect glioma cell lines with high or low CAR expression. Viability of glioma cells infected with different adenoviruses was assessed by trypan blue staining. Adenovirus replication was quantified with the infection-dose replication assay. Athymic mice carrying glioma xenografts received intratumoral injections of Delta-24-RGD or Delta-24 and were followed for survival, which was analyzed by the Kaplan-Meier method and the log-rank test. All statistical tests were two-sided. RESULTS: Half the glioma cell lines expressed low levels of CAR (defined as <50% of cells expressing detectable CAR); all lines expressed integrins in more than 50% of cells. Infection of U-87 MG cells (a low-CAR-expressing line) with AdGFP-RGD resulted in approximately six times more GFP-positive cells than infection with AdGFP. Delta-24-RGD was more cytopathic to both low- and high-CAR-expressing glioma lines than Delta-24, and it replicated more efficiently in both cell lines. In the xenografted mice, intratumoral injection of Delta-24-RGD was associated with longer survival than intratumoral injection of Delta-24 (P<.001, log-rank test). Furthermore, 60% of Delta-24-RGD-treated mice but only 15% of Delta-24-treated mice survived more than 4 months (difference = 45%, 95% CI = 21% to 68%). CONCLUSIONS: The antitumor activity of Delta-24-RGD suggests that it has the potential to be an effective agent in the treatment of gliomas.

Adenoviridae↗

Oncolytic adenoviruses for malignant glioma therapy.

Malignant gliomas are devastating diseases that localize within the central nervous system and are notoriously invasive. Despite recent advances in established treatment modalities such as postoperative radiotherapy and chemotherapy for gliomas, no definitive improvement in survival has been observed. However, progress in the understanding of the biology of these tumors allows for the development of translational research projects and new therapeutic approaches such as gene therapy. One of the most recent strategies is based on the use of targeted oncolytic adenoviruses. The progress of the oncolytic adenoviral system relies on the knowledge of the molecular biology of both the adenovirus and cancer. This review outlines the main strategies currently used to improve adenoviral infection, to restrict adenoviral replication to tumor cells, and to optimize the anticancer effect of oncolytic adenoviruses. Specifically, we discuss the concepts of conditionally replicative adenoviruses, tropism modifications used to efficiently redirect infectivity to cancer cells, and the transcription/transduction systems that limit the adenovirus to the target host cell. Mastery of the mechanisms of adenoviral infection and replication will lead to a full realization of the potential for adenoviruses as critical anticancer tools, and may result in the improvement of the prognosis of patients with brain tumors.

Adenoviridae↗

Suppression of experimental autoimmune encephalomyelitis by selective blockade of encephalitogenic T-cell infiltration of the central nervous system.

Multiple sclerosis (MS) is a devastating neuroinflammatory disorder of the central nervous system (CNS) in which T cells that are reactive with major components of myelin sheaths have a central role. The receptor for advanced glycation end products (RAGE) is present on T cells, mononuclear phagocytes and endothelium. Its pro-inflammatory ligands, S100-calgranulins, are upregulated in MS and in the related rodent model, experimental autoimmune encephalomyelitis (EAE). Blockade of RAGE suppressed EAE when disease was induced by myelin basic protein (MBP) peptide or encephalitogenic T cells, or when EAE occurred spontaneously in T-cell receptor (TCR)-transgenic mice devoid of endogenous TCR-alpha and TCR-beta chains. Inhibition of RAGE markedly decreased infiltration of the CNS by immune and inflammatory cells. Transgenic mice with targeted overexpression of dominant-negative RAGE in CD4+ T cells were resistant to MBP-induced EAE. These data reinforce the importance of RAGE-ligand interactions in modulating properties of CD4+ T cells that infiltrate the CNS.

Animals↗