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Biomedical subjects

R Liu

Publications and source records attributed to R Liu.

At least 271 records · Page 15Linked to original sources

[A study of the thermosensitivity determination for the normal value of the twelve well-point (or jing-point)].

Under certain temperature and humidity, the thermosensitivity values of the twelve Well-point, on 209 healthy young people, selected at random/and aged from 20 to 24, were measured in the morning and in the afternoon respectively. The statistical results show that there is no significance (P > 0.05), when the value of one Well-point on upper limbs of the male is compared with that of the female, except very few well-point. The value of one Well-point on both the left side and the right side measured at the time are almost the same. The value of one Well-point on the lower limbs of the male is higher than that of the female, and the difference is significant (P < 0.05). This study indicates that the normal values of every Well-point exist in human beings, which will assist clinical diagnosis.

Acupuncture Points↗

[Regulation on ACTH, beta-EP and immune function by moxibustion on different acupoints].

The experimental results displayed that the cellular immune functions of tumor-bearing mice in control group were significantly lower than that the normal control group. The cellular immune functions of those groups accepting moxibustion treatment were maintained at a relatively higher level. Among them the Guanyuan group seemed to be best in immune regulation. The data further demonstrated that an instant elevation of serum ACTH and beta-EP could be caused by moxibustion. But the bariations of serum ACTH and beta-EP are not paralleled. A remarkable increase of serum beta-EP was seen in Guanyuan group but not of serum ACTH. The experimental results hinted that the regulation of beta-EP and ACTH was related to the immune regulation induced by moxibustion.

Acupuncture Points↗

[Pathology of endothelium, extracellular matrix and smooth muscle in gastric coronary vein of cirrhotic patients].

Immunohistochemical stain was used to observe the pathology of endothelium, extracellular matrix (ECM), vascular smooth muscle cell (VSMC) in gastric coronary vein of 30 cirrhotic patients and 10 controls. There was widespread destruction to endothelium, intravenous thrombosis, aggregation of pericyte, smooth muscle hyperplasia, and increased FN, LN, collagen IV and smooth muscle actin in the wall of the coronary vein in cirrhotic patients. The thickness of the wall and its smooth muscle were 3.07 +/- 1.03 mm and 2.31 +/- 0.76 mm respectively in cirrhotic patients, and 1.65 +/- 0.49 mm and 0.88 +/- 0.20 mm in non-cirrhotic patients (P < 0.01). Based on these observations a new concept of portal hypertensive vasculopathy was put forward.

Adult↗

[Application of nasal endoscopy and cryosurgery in transsphenoidal removal of pituitary tumors].

In order to sum up the experience of transsphenoidal resection of pituitary tumors, 60 cases operated between 1984 and 1995 were reviewed. The operation was performed via a columella nasi "V" incision and transseptal-sphenoidal approach. 0 degree and 30 degrees endoscopes were used in 16 cases and the cryotherapy was used to destroy the remnant tumor cells in 51 cases. The duration of freezing was only one minute each time and it was repeated once again after thawing. The advantages of this method were as follows: (1) wider operative field and better illumination; (2) magnified operative pictures and TV monitoring; (3) wide and changeable visual angle; (4) lack of complications such as hemorrhage, optic nerve injury, permanent diabetes insipidus. The proper applications of endoscopy and cryosurgery were recommended for transsphenoidal removal of pituitary tumors.

Adenoma↗

Enzymatic synthesis of polymers containing nicotinamide mononucleotide.

Nicotinamide mononucleoside 5'-diphosphate in its reduced form is an excellent substrate for polynucleotide phosphorylase from Micrococcus luteus both in de novo polymerization reactions and in primer extension reactions. The oxidized form of the diphosphate is a much less efficient substrate; it can be used to extend primers but does not oligomerize in the absence of a primer. The cyanide adduct of the oxidized substrate, like the reduced substrate, polymerizes efficiently. Loss of cyanide yields high molecular weight polymers of the oxidized form. Terminal transferase from calf thymus accepts nicotinamide mononucleoside 5'-triphosphate as a substrate and efficiently adds one residue to the 3'-end of an oligodeoxynucleotide. T4 polynucleotide kinase accepts oligomers of nicotinamide mononucleotide as substrates. However, RNA polymerases do not incorporate nicotinamide mononucleoside 5'-triphosphate into products on any of the templates that we used.

Animals↗

Effects of sphingosine derivatives on MC3T3-E1 pre-osteoblasts: psychosine elicits release of calcium from intracellualr stores.

Sphingosine, sphingosine-1-phosphate (SPP) and sphingosylphosphorylcholine (SPC) each elicited transient elevations in intracellular free Ca2+ ([Ca2+]i) as a result of Ca2+ release from an intracellular store in MC3T3-E1 pre-osteoblasts. No elevation in [Ca2+]i was detected in response to the application of N-acetyl sphingosine. Psychosine (1-galactosyl sphingosine) also caused Ca2+ release from intracellular stores, which suggests that phosphorylation of the 1-carbon of sphingosine is not required for its action as a Ca2+ release agonist in MC3T3-E1 cells. Sequential additions of combinations of sphingosine, SPP, SPC and psychosine revealed Ca2+ transients only after the application of the first sphingolipid, despite the fact that the intracellular Ca2+ stores refilled. This indicates that each agent desensitized the MC3T3-E1 cells to the action of the others and suggests that all of the sphingolipids tested employ the same receptor or a common intracellular messenger.

3T3 Cells↗

Synthesis of novel imidazobenzodiazepines as probes of the pharmacophore for "diazepam-insensitive" GABAA receptors.

The syntheses of a series of novel imidazobenzodiazepines and their affinities for diazepam sensitive (DS) and diazepam insensitive (DI) GABAA receptors are described. Imidazobenzodiazepines belong to one of the very few chemical families which exhibit high to moderate potency for DI GABAA receptors. Although imidazobenzodiazepines such as Ro 15-4513, 20, are the most potent DI GABAA receptor ligands described to date, their selectivity for DI versus DS GABAA receptors is only marginal. Previous structure-activity relationship (SAR) studies of imidazobenzodiazepines have indicated that the 3- and 8-positions are critical for high-affinity binding to DI GABAA receptors (J. Med. Chem. 1993, 36, 479-490. J. Med. Chem. 1993, 36, 1001-1006. J. Med. Chem. 1993, 36, 1820-1830). In order to determine why the ester function is critical to high affinity at the DI site, we have synthesized several derivatives which have substituents other than an ester at the C(3) position including 3-alkyl-, 3-alkylketo-, 3-alkyl ether, and 3-dialkylamino-substituted imidazobenzodiazepines. The SAR analysis of these compounds when combined with that of several pyrazoloquinolinones indicates that interactions at H1 and L1 as well as interactions at H2 anti to the imidazole N(2) and at a lipophilic pocket (labeled LDi) about the 3-position are required in order for imidazobenzodiazepines to exhibit selectivity and high affinity for DI GABAA receptors. Furthermore, the imidazobenzodiazepines substituted with an electron-donating group (alkoxy function) at position 8 revealed that the change of the substituent at C(8) from an electron-withdrawing to a donating function did not substantially alter either ligand affinity or selectivity for DI GABAA receptors. Thus, a pharmacophore is proposed for DI GABAA receptor ligands, which is characterized by the requirement of a lipophilic pocket LDi about the C(3) position of imidazobenzodiazepines. Using this model, two pyrazoloquinolinone derivatives were designed and synthesized. Their affinities and selectivities for DI GABAA receptors are consistent with those predicted by the DI GABAA receptor pharmacophore. In addition, examination of the in vitro binding data of 3-alkyl ether analogs confirms that the anti conformation of the ester group at the C(3) position of imidazobenzodiazepines (Ro15-4513, 20 series) is preferred at both DI and DS GABAA receptors. This constitutes the first evidence (other than molecular modeling) to support the auxillary involvement of H2 at the DI site and is important with regard to the synthesis of other DI GABAA receptor selective ligands in the future.(ABSTRACT TRUNCATED AT 400 WORDS)

Affinity Labels↗

Antagonists of phosphatidylinositol 3-kinase block activation of several novel protein kinases in neutrophils.

Several novel protein kinases are known to be rapidly activated in neutrophils stimulated with the chemoattractant fMet-Leu-Phe (fMLP). These kinases include a histone H4 protein kinase and several renaturable kinases with molecular masses of about 69, 63, 49, and 40 kDa. The renaturable kinases can catalyze the phosphorylation of a peptide that corresponds to residues 297-331 of the 47-kDa subunit of the NADPH-oxidase system (p47-phox). Previous studies have indicated that the activation of all of these protein kinases involves an uncharacterized stimulatory pathway and/or novel second messenger. The studies reported herein were undertaken to determine if phosphatidylinositol 3-kinase (PI3-K) is a component of this pathway. We report that certain chromosome derivatives (e.g. 2-(4-morpholinyl)-8-phenylchromone (LY294002)) and wortmannin, which inhibit PI3-K by distinct mechanisms, blocked activation of all of these novel kinases. These antagonists also inhibited the phosphorylation of p47-phox (about 50%) and O2.- release (about 80%) in cells stimulated with fMLP, but not with 4 beta-phorbol 12-myristate 13-acetate. A strong correlation exists between the amounts of these antagonists required to produce 50% inhibition of PI3-K in vitro and O2.- release in vivo. In contrast, a single atom substitution of LY294002 produced a compound (LY303511) that did not inhibit PI3-K. Compound LY303511 did not appreciably inhibit the activation of the novel protein kinases or O2.- generation. These data strongly suggest that PI3-K is involved in the activation of several novel protein kinases in neutrophils, one or more of which may be involved in O2.- release.

Androstadienes↗

Protective effect of peptide leukotriene antagonist on renal failure induced by a tourniquet in rabbits.

We studied the effects of a selective antagonist of peptide leukotriene D4/E4 (LY-171883) and 5-lipoxygenase inhibitor diethylcarbamazine (DEC) in renal failure induced by a tourniquet, because peptide leukotrienes (LTs) were suggested to play a key role in our previous study. The hind limbs of anesthetized rabbits were fastened for 5 h and then released for 6 h. LY171883 (4 mg/kg/h) and DEC (40 mg/kg/h) were administered via the aural vein from 30 min before the tourniquet and during the experiment in each tourniquet group. The tourniquet induced renal injuries represented by increases in serum BUN and creatinine, and the injuries in the fastened muscles represented increases in serum CPK and edema index of the fastened site. LY171883 and DEC significantly attenuated the aggravation of the renal functions induced by a tourniquet when compared with the vehicle-treated group. LY171883 did not affect the injuries in the fastened muscles, but DEC attenuated it significantly when compared with the vehicle-treated group. The protection of peptide LT antagonist and 5-lipoxygenase inhibitor in the tourniquet-induced renal failure elucidate that peptide LTs trigger renal failure induced by a tourniquet.

Acetophenones↗

Insulin regulates transcription of the CCAAT/enhancer binding protein (C/EBP) alpha, beta, and delta genes in fully-differentiated 3T3-L1 adipocytes.

The effect of insulin on expression of CCAAT/enhancer binding protein (C/EBP) alpha, beta, and delta was investigated in fully-differentiated 3T3-L1 adipocytes. Treatment of adipocytes with insulin stimulated rapid dephosphorylation of C/EBP alpha, and repressed the expression of C/EBP alpha within 2-4 h, with > 90% suppression occurring at 24 h. While insulin induced expression of C/EBP beta and C/EBP delta within 1 h and caused a > 20-fold increase by 4 h, expression returned to nearly pretreatment levels by 24 h. The insulin concentration dependence of these effects was consistent with involvement of the insulin receptor. Gel shift analysis revealed that 6 h of insulin treatment decreased the binding of nuclear C/EBP alpha while increasing binding of nuclear C/EBP beta and C/EBP delta. The reciprocal effects of insulin on the steady-state levels of C/EBP transcription factors can be accounted for kinetically and quantitatively by changes in their mRNA levels, which can be accounted for by effects on gene transcription. The effects of insulin on adipocyte gene transcription (e.g. GLUT4) may be mediated, at least in part, by down-regulation of C/EBP alpha and/or its dephosphorylation.

3T3 Cells↗

Deletion of lysine 121 creates a temperature-sensitive alteration in insulin binding by the insulin receptor.

Recently we reported the deletion of Lys-121 in one allele of the insulin receptor gene from a child with severe insulin resistance. In the present work, this mutant receptor (M121) was shown to have an abnormal sensitivity to temperature and an alteration in "negative cooperativity." In contrast to the wild-type receptor (HIRC), insulin binding by the M121 receptor was rapidly and irreversibly lost at temperatures above 30 degrees C with the phosphorylated form of the receptor being more temperature-sensitive than the nonphosphorylated form. Although insulin binding activity was lost, Western analysis and other studies showed that the mutant receptor remained intact. Measurements of 125I-insulin dissociation at 21 degrees C in the presence of native insulin (an estimate of negative cooperativity) demonstrated a difference between the mutant and wild-type receptor. Insulin dissociation from the mutant receptor was not as pronounced as that found with the wild-type receptor. Thus, an abnormality in insulin binding by the mutation was evident at lower "permissive" temperatures. The results of these and other studies argue that Lys-121 occupies an important position for the regulation of insulin receptor conformation. This regulation apparently influences negative cooperative interactions with insulin and modulates signal transduction.

Alkylating Agents↗

High-density lipoprotein and apolipoprotein A-I deficiency induced by combination therapy with probucol and bezafibrate.

The effects of the administration of slow-release bezafibrate to hypercholesterolaemic patients who were already receiving long-term probucol treatment (mean 865 days, 500-1000 mg.day-1) were investigated. Bezafibrate was administered at either 200 mg.day-1 (13 males, 13 females, mean age 55.2 years) or 400 mg.day-1 (11 males, 14 females, mean age 57.2 years), and blood was taken at 0, 3, 6 and 12 months after the beginning of combination therapy. Overall, serum total cholesterol (TC), triglyceride (TG), very low density lipoprotein (VLDL)-TC, high-density lipoprotein (HDL)-TG, VLDL-TG, VLDL-phospholipid (PL), lipoprotein (a) [Lp(a)], apolipoprotein (apo) C-III, apo E levels and LCAT activity decreased significantly with this combination therapy, while HDL cholesterol (C), HDL3-C, HDL-PL, apo A-I and apo A-II levels significantly increased, as assessed by analysis of variance (ANOVA). Five patients (one receiving 200 mg.day-1, four receiving 400 mg.day-1 bezafibrate) showed drastic reductions in HDL-C (HDL-C levels were reduced by a mean of 46.2%, 59.3% and 61.6% at 3, 6 and 12 months, respectively) after beginning combination therapy. These HDL-C reductions were maintained for the 1 year of combination therapy, but then returned to pre-combination treatment levels 1 month after discontinuation of bezafibrate. Serum probucol concentrations and cholesteryl ester transfer protein (CETP) mass were assayed at 6 months, and the probucol concentration was higher in the HDL-deficient group (56.2 vs 26.5 micrograms/ml). In contrast, CETP mass was significantly lower in HDL-deficient patients than in non-HDL-deficient patients (2.08 vs 2.87 mg.1-1)(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗