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Biomedical subjects

F Liu

Publications and source records attributed to F Liu.

At least 415 records · Page 23Linked to original sources

[Clinical and experimental study on the Houpu Mahuang oral liquid in treating bronchial asthma].

OBJECTIVE: To probe into the curative effect and mechanism of action of the Houpu Mahuang oral liquid (HPMH) in treating bronchial asthma. METHODS: The pulmonary function and level of serum IgE of the patients were determined before and after HPMH treatment. The anti-allergic reaction and relieving spasm effect of HPMH in animal were also observed. RESULTS: HPMH is not only effective in improving clinical symptoms and pulmonary function (P < 0.05), so as to lower the abnormal raising of IgE (P < 0.01), but also has a notable inhibitory effect for passive allergic reaction of rat's skin, it can relieve spasm. CONCLUSIONS: HPMH is effective in relieving spasm, antiallergic reaction, it can improve the symptoms of bronchial asthma.

Adult↗

[Clinical study on effect of Fuzheng Kangbai Granule on long-term survival of patients with acute leukemia].

OBJECTIVE: To observe the effect of Fuzheng Kangbai Granule (FZKBG) on event free interval (EFI) and over survival (OS) of patients with acute leukemia, and to study the mechanism of FZKBG. METHODS: FZKBG was used in 90 cases of completely remitted acute leukemia, immune functions of patients before and after using FZKBG were measured. RESULTS: Five year EFI and OS were 64.2% and 77.2% of 90 cases of completely remitted acute leukemia, and the immune functions after using FZKBG have improved significantly. CONCLUSIONS: FZKBG could increase the EFI and OS of patients with acute leukemia, and the improved immune functions may play a role in increasing 5 year EFI and OS.

Adolescent↗

[Bile salt induces apoptosis of hepatocytes: the mechanism of hepatic function injury during obstructive jaundice].

OBJECTIVE: To determine if the bile salt induces hepatocyte apoptosis in vitro. METHOD: Hepatocytes were isolated by in situ collagenase perfusion and plated in 6 well flat bottom with DMEM/F12, 0.5 micro/ml insulin. Two hours later, glycochenodeoxcholate (GCDC) 25, 50, 100, 200, 300 micromol was added and cells evaluated by DNA-PI staining FACS and terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) 3, 6, 9, 12, 18, 20, 24 hours later. Agarose gel electrophoresis of DNA extracted from hepatocytes after incubation with GCDC using various experimental conditions. RESULT: The hepatocytes treated with GCDC have a high apoptotic rate as compared with the controls. 100 micromol GCDC treated 24 hours, nearly 61.81% of hepatocytes were apoptotic by FACS evaluation. The TUNEL showed that apoptotic hepatocytes had less cell volume and stained with brown by Biotin-11-dUTP. DNA ladder of bile-salt treated hepatocytes were shown in agarose gel electrophoresis. CONCLUSION: The mechanism of hepatic injury during obstructive jaundice is related to bile salt caused hepatocyte apoptosis.

Animals↗

[Study on the analytical method of s-triazine herbicide residues in soil and maize].

The sample was extracted with a mixture of V(acetonitrile): V(methanol) = 1:1. After filtration, the extract was defatted with petroleum ether and then it was passed through a short C18 column for pretreatment and analysed by Nova-Pak C18 column, 150 mm x 3.9 mm i.d., with V(MeOH): V(H2O) = 55:45 as mobile phase. The recoveries were 82.4%-99.8% for cyanazine, 85.6%-102.3% for atrazine and 89.1%-108.4% for simetryne.

Atrazine↗

[The structures elucidation of isodopharicin D and F].

Two new compounds were isolated from Isodon pharicus (Prain) Murata. Their structures were determined to be 3 alpha, 11 beta, 13 alpha-trihydroxy-entkaur-16-en-15-one (1), named isodopharicin D, and 11 beta, 13 alpha, 15 alpha-trihydroxy-entkaur-16-en-3 alpha-beta-D-glucoside (2), named isodopharicin F by chemical and spectral evidence.

Diterpenes↗

[The time-frequency analysis of the exercise ECG signal].

Exercise ECG indicates information about the heart load status in the exercise test. It is very significant to represent the characteristics of the exercise ECG for evaluating the exercise load test. This article introduces the principle of Winger-Ville Distribution time-frequency analysis and its implementation. By applying this method to analyse exercise ECG, some results were acquired. It is a promising method to do research of the exercise ECG in the time-frequency plane.

Algorithms↗

[The design of a fiber optic hygrometer using in patient monitor].

Fiber optic sensor is a kind of newly developed sensory technology in recent ten years. With intrinsic security and wide application, it is superior to the traditional point sensors. This paper presents the design of a kind of fiber optic hygrometer using in patient monitor.

Equipment Design↗

[Effects of sex hormones on the expression of placenta form glutathione S-transferase (GST-P) in rat induced hepatocarcinoma].

Using Solt-Farber method for the induction of rat hepatocarcinoma, the changes of the activity of glutathione S-transferase (GST) and the content of placenta form GST (GST-P) were studied during hepatocarcinogenesis, then the effects of sex hormones on the hepatic expression of GST-P were observed using immunohistochemical method. The results showed that both GST activity and GST-P content began to increase at the 3rd week, and reached the highest level at the 5th week (Table 1). Therefore, the 5th week was selected for the study of GST-P expression in the livers of rats treated with different protocol (Fig. 1). It was found that GST-P was highly expressed in the livers of sham-castrated male rats after chemically induced hepatocarcinoma (PLATE I, Fig. 1A, Table 2). When estradiol was administrated to these rats, both the number and area of GST-P positive(+) foci decreased significantly (PLATE I, Fig. 1B, Table 2). While testosterone was administrated instead of estradiol, the decrease of the area but slight increase of the number of GST-P positive foci were found (PLATE I, Fig. 1C, Table 2). After orchiectomy, the areas of GST-P (+) foci in carcinogen treated liver of male rats were smaller than those in rats with sham-orchiectomy and same carcinogen treatment (PLATE I, Fig. 2A, B, Table 3). When the orchiectomized male rats were administrated with estradiol, the areas of GST-P (+) foci decreased further (PLATE I, Fig. 2C, Table 3). In contrast, after ovariectomy of the female rats, the areas of GST-P (+) foci in carcinogen treated livers were slightly increased as compared with those in the rats with sham-ovariectomy and same carcinogen treatment (PLATE I, Fig. 2D, E, Table 3). While the ovariectomized female rats were administrated with testosterone, the areas of GST-P (+) foci increased further (PLATE I, Fig. 2F, Table 3). Regardless of whether castrations were done or not, GST-P expression in livers of male rats induced hepatocarcinoma was higher than in livers of female rats (PLATE I, Fig. 2A, B, D, E, Table 3). These results indicated that estrogen may inhibit but androgen may promote the GST-P expression in the rat liver during hepatocarcinogenesis. This may be related to the higher incidence of liver carcinoma in male than in female.

2-Acetylaminofluorene↗

Binding of SH2 containing proteins to the insulin receptor: a new way for modulating insulin signalling.

Prior studies have established a role in insulin action for the tyrosine phosphorylation of substrates and their subsequent complexing with SH2 containing proteins. More recently, SH2 proteins have been identified which can tightly bind to the tyrosine phosphorylated insulin receptor. The major protein identified so far (called Grb-IR or Grb10) of this type appears to be present in at least 3 isoforms, varying in the presence of a pleckstrin homology domain and in the sequence of its amino terminus. The binding of this protein to the insulin receptor appears to inhibit signalling by the receptor. The present review will discuss the current knowledge of the structure and function of this protein.

Amino Acid Sequence↗

Dual role of the Smad4/DPC4 tumor suppressor in TGFbeta-inducible transcriptional complexes.

Upon ligand binding, the receptors of the TGFbeta family phosphorylate Smad proteins, which then move into the nucleus where they activate transcription. To carry out this function, the receptor-activated Smads 1 and 2 require association with the product of deleted in pancreatic carcinoma, locus 4 (DPC4), Smad4. We investigated the step at which Smad4 is required for transcriptional activation. Smad4 is not required for nuclear translocation of Smads 1 or 2, or for association of Smad2 with a DNA binding partner, the winged helix protein FAST-1. Receptor-activated Smad2 takes Smad4 into the nucleus where they form a complex with FAST-1 that requires these three components to activate transcription. Smad4 contributes two functions: Through its amino-terminal domain, Smad4 promotes binding of the Smad2/Smad4/FAST-1 complex to DNA; through its carboxy-terminal domain, Smad4 provides an activation function required for Smad1 or Smad2 to stimulate transcription. The dual function of Smad4 in transcriptional activation underscores its central role in TGFbeta signaling.

Activin Receptors, Type I↗

Cloning, chromosome localization, expression, and characterization of an Src homology 2 and pleckstrin homology domain-containing insulin receptor binding protein hGrb10gamma.

hGrb10alpha (previously named Grb-IR) is a Src-homology 2 domain-containing protein that binds with high affinity to the tyrosine-phosphorylated insulin receptor and insulin-like growth factor-1 receptor. At least two isoforms of human Grb10, (hGrb10alpha and hGrb10beta), which differ in the pleckstrin homology (PH) domain and the N-terminal sequence, have previously been identified in insulin target tissues such as human skeletal muscle and fat cells. Here we report the cloning of the third isoform of the hGrb10 family (hGrb10gamma) from human skeletal muscle and its localization to human chromosome 7. We have also determined the human chromosome localization of Grb7 to 17q21-q22 and Grb14 to chromosome 2. hGrb10gamma contains an intact PH domain and an N-terminal sequence that is present in hGrb10alpha but absent in hGrb10beta. RNase protection assays and Western blot analysis showed that hGrb10alpha and hGrb10gamma are differentially expressed in insulin target cells including skeletal muscle, liver, and adipocyte cells. hGrb10gamma is also expressed in HeLa cells and various breast cancer cell lines. The protein bound with high affinity to the insulin receptor in cells, and the interaction was dependent on the tyrosine phosphorylation of the receptor. hGrb10gamma also underwent insulin-stimulated membrane translocation and serine phosphorylation. hGrb10gamma phosphorylation was inhibited by PD98059, a specific inhibitor of mitogen-activated protein kinase kinase, and wortmannin, a specific inhibitor of phosphatidylinositol 3-kinase. Taken together, our data suggest that hGrb10 isoforms are potential downstream signaling components of the insulin receptor tyrosine kinase and that the PH domain may play an important role in the involvement of these isoforms in signal transduction pathways initiated by insulin and other growth factors.

Amino Acid Sequence↗

Protein tyrosine phosphatase 1B interacts with and is tyrosine phosphorylated by the epidermal growth factor receptor.

We used a substrate-trapping technique to search for substrates of protein tyrosine phosphatase (PTP) 1B. A catalytically inactive form of this enzyme forms a stable, phosphotyrosine-dependent complex with epidermal growth factor receptor (EGFR) both in vitro and in cells. PTP1B also interacts with activated platelet-derived growth factor receptor (PDGFR) but not with colony-stimulating factor 1 receptor (CSF-1R). After binding to EGFR, PTP1B becomes tyrosine-phosphorylated at Tyr-66, a site that conforms to the consensus binding sequence for the Src homology 2 (SH2) domains of the adapter protein Grb2. This tyrosine phosphorylation is correlated with a 3-fold increase in PTP catalytic activity. These findings suggest that PTP1B selectively regulates specific activated receptor protein tyrosine kinases (RPTKs) in vivo and might itself be regulated by such receptors.

Animals↗

The granulocyte colony-stimulating factor receptor is required for the mobilization of murine hematopoietic progenitors into peripheral blood by cyclophosphamide or interleukin-8 but not flt-3 ligand.

Hematopoietic progenitor cells (HPC) can be mobilized from the bone marrow into the peripheral circulation in response to a number of stimuli including hematopoietic growth factors, cytotoxic agents, and certain chemokines. Despite significant differences in their biological activities, these stimuli result in the mobilization of HPC with a similar phenotype, suggesting that a common mechanism for mobilization may exist. In this study, the role of granulocyte colony-stimulating factor (G-CSF) in progenitor mobilization was examined using G-CSF receptor (G-CSFR)-deficient mice. In contrast to wild-type mice, no increase in circulating colony-forming cells (CFU-C), CD34+ lineage- progenitors, or day 12 colony-forming unit-spleen progenitors (CFU-S) was detected in G-CSFR-deficient mice after cyclophosphamide administration. This defect was not due to a failure to regenerate HPC following cyclophosphamide administration as the number of CFU-C in the bone marrow of G-CSFR-deficient mice was increased relative to wild-type mice. Likewise, no increase in circulating CFU-C was detected in G-CSFR-deficient mice following interleukin-8 (IL-8) administration. In contrast, mobilization of HPC in response to flt-3 ligand was nearly normal. These results show that the G-CSFR is required for mobilization in response to cyclophosphamide or IL-8 but not flt-3 ligand and suggest that the G-CSFR may play an important and previously unexpected role in HPC migration.

Animals↗

Interleukin-6 and the granulocyte colony-stimulating factor receptor are major independent regulators of granulopoiesis in vivo but are not required for lineage commitment or terminal differentiation.

Multiple hematopoietic cytokines can stimulate granulopoiesis; however, their relative importance in vivo and mechanisms of action remain unclear. We recently reported that granulocyte colony-stimulating factor receptor (G-CSFR)-deficient mice have a severe quantitative defect in granulopoiesis despite which phenotypically normal neutrophils were still detected. These results confirmed a role for the G-CSFR as a major regulator of granulopoiesis in vivo, but also indicated that G-CSFR independent mechanisms of granulopoiesis must exist. To explore the role of interleukin-6 (IL-6) in granulopoiesis, we generated IL-6 x G-CSFR doubly deficient mice. The additional loss of IL-6 significantly worsened the neutropenia present in young adult G-CSFR-deficient mice; moreover, exogenous IL-6 stimulated granulopoiesis in vivo in the absence of G-CSFR signals. Near normal numbers of myeloid progenitors were detected in the bone marrow of IL-6 x G-CSFR-deficient mice and their ability to terminally differentiate into mature neutrophils was observed. These results indicate that IL-6 is an independent regulator of granulopoiesis in vivo and show that neither G-CSFR or IL-6 signals are required for the commitment of multipotential progenitors to the myeloid lineage or for their terminal differentiation.

Animals↗