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Biomedical subjects

L M Wang

Publications and source records attributed to L M Wang.

At least 127 records · Page 7Linked to original sources
PubMed1990

Macrophage-colony-stimulating factor (CSF-1) induces proliferation, chemotaxis, and reversible monocytic differentiation in myeloid progenitor cells transfected with the human c-fms/CSF-1 receptor cDNA.

The c-fms protooncogene encodes the receptor for macrophage-colony-stimulating factor (CSF-1). Expression vectors containing either normal or oncogenic point-mutated human c-fms genes were transfected into interleukin 3 (IL-3)-dependent 32D cells in order to determine the effects of CSF-1 signaling in this murine clonal myeloid progenitor cell line. CSF-1 was shown to trigger proliferation in association with monocytic differentiation of the 32D-c-fms cells. Monocytic differentiation was reversible upon removal of CSF-1, implying that CSF-1 was required for maintenance of the monocyte phenotype but was not sufficient to induce an irrevocable commitment to differentiation. Human CSF-1 was also shown to be a potent chemoattractant for 32D-c-fms cells, suggesting that CSF-1 may serve to recruit monocytes from the circulation to tissue sites of inflammation or injury. Although c-fms did not release 32D cells from factor dependence, point-mutated c-fms[S301,F969] (Leu-301----Ser, Tyr-969----Phe) was able to abrogate their IL-3 requirement and induce tumorigenicity. IL-3-independent 32D-c-fms[S301,F969] cells also displayed a mature monocyte phenotype, implying that differentiation did not interfere with progression of these cells to the malignant state. All of these findings demonstrate that a single growth factor receptor can specifically couple with multiple intracellular signaling pathways and play a critical role in modulating cell proliferation, differentiation, and migration.

Animals↗
PubMed1990

An in vitro approach to the kinetics of insulin antibodies in diabetic patients.

The purpose of this study is to evaluate the binding behavior of plasma insulin antibodies (Iab) in diabetic patients, by the following parameters: Incubation time, temperature, buffer pH, and Iab titer. We investigated the plasma insulin binding patterns of 12 insulin-treated diabetic patients, and they were separated as higher titer group (Iab = 51.9 +/- 7.28, n = 6) and lower titer group (Iab = 14.88 +/- 4.75, n = 6). The procedure was: (1) plasma samples were deinsulinized by 0.12N HCL, dextran coated charcoal suspension and 0.12N NaOH. (2) I-125 monoiodoinsulin was used to prevent artifacts resulting from variability in ligand binding due to excessive iodination, (3) separation of free and bound insulin was accomplished by rapid precipitation of hormone-antibody complex with polyethylene glycol, and (4) decanting the supernatants and counting the pellets in the automatic gamma counter. The data were obtained as the condition of incubation time, temperature, buffer pH, and Iab titer. The results obtained by the Scatchard analysis indicated that high temperature (39 degrees C vs 37 degrees C) in vitro would increase the free insulin levels and decrease the low affinity binding capacity (Q2-Q1) of Iab in patients with high titer of Iab (greater than 40%), whereas this phenomenon is not observed in patients with low affinity binding sites of Iab in patients with low titers of insulin antibodies (less than 20%).

Antigen-Antibody Reactions↗
PubMed1990

The action of gliclazide on insulin secretion and insulin sensitivity in non-obese non-insulin dependent diabetic patients.

We evaluated the effects of gliclazide on the secretion and action of insulin in 18 non-obese (BMI 24.09 +/- 0.47 Kg/m2, range 20.89-27.52 Kg/m2) non-insulin dependent diabetic patients (mean age 56.9 +/- 1.8 years, range 39-67 years) by the oral glucose tolerance test (OGTT) and insulin suppression test (IST). Most of them were diagnosed recently and thus untreated previously. All subjects were treated with gliclazide or placebo for 3 months in a double blind cross-over design. After gliclazide therapy, fasting and 2 hour post-OGTT plasma glucose significantly decreased (136 vs. 185 mg/dl, P less than 0.005 291 vs. 358 mg/dl, P less than 0.005), 2 hours post-OGTT plasma insulin was significantly increased (79 vs. 59 uU/ml, P less than 0.05) while fasting plasma insulin remained unchanged (21 vs. 19 uU/ml, P greater than 0.1). HbAlc decreased significantly with gliclazide therapy (6.6 vs. 7.6%, P less than 0.005). In addition, oral glucose tolerance, as measured by the mean incremental areas under the plasma glucose curve, were improved significantly (1430.6 +/- 682.4 vs. 16192.5 +/- 608.5 mg.min/dl, P less than 0.005). The mean incremental areas under the plasma insulin curve during OGTT also increased (4482.0 +/- 637.1 vs. 3167.5 +/- 511.9 uU.min/ml, P less than 0.05) after gliclazide therapy. Mean steady state plasma glucose levels (SSPG) showed no remarkable difference during drug and placebo administration (188 vs. 190 mg/dl). Throughout the trial there was no significant change of body weight, nor any side effect as judged from blood counts, urinalysis, and the results of SMA-23 and EKG.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Atrio-ventricular pressure difference associated with mitral valve motion].

Pressure difference (PD) across the mitral valve was analyzed by a computer-aided catheter system in dogs. Positive PD (PPD) was consistently traced in the initial phase of rapid filling. While heart rate (HR) was below 100 beat/min, a negative PD (NPD) followed the above PPD. In the period between the NPD and the 2nd PPD due to atrial contraction, PD was kept at zero, while LA and LV pressures were gradually elevated by pulmonary venous return. As HR exceeded 100, 2 positive peaks of PD merged into M-shaped or mono-peaked PD. Through higher inflow resistance produced by artificial mitral stenosis, PPD peak decayed without NPD. In mitral regurgitation with an acute volume overload, all of the PD amplitudes were exaggerated. Thus the quick reversal of PD suggested the effect in blood filling process across the mitral valve.

Animals↗
PubMed1989

Determination of 3H-labelled cytosine arabinoside and eight metabolites in cell extracts by high-performance liquid chromatography and scintillation spectrometry.

We have developed a method for the separation and quantitation of radiolabeled cytosine arabinoside and its eight metabolites in cell extracts by anion-exchange gradient high-performance liquid chromatography. Baseline separation of cytosine arabinoside and uracil arabinoside and their respective 5'-mono-, di- and triphosphates, as well as cytosine arabinoside diphosphocholine was obtained with the shortest interval between peaks being 3 min. This degree of separation was found to be essential for quantitation of 3H-labeled metabolites by scintillation counting of 1-min fractions. Application of this procedure to the quantitation of [3H] cytosine arabinoside and its metabolites from HL60 human leukemia cells is demonstrated.

Arabinofuranosyluracil↗
PubMed1989

Mouse melanoma growth stimulatory activity gene (Mgsa) is polymorphic and syntenic with the W, patch, rumpwhite, and recessive spotting loci on chromosome 5.

Melanoma growth stimulatory activity (Mgsa) is a polypeptide growth factor originally detected in culture medium of the human malignant melanoma cell line Hs294T and may have an autocrine role in neoplastic growth. Mgsa is a member of the small inducible gene (SIG) family and shares homology with beta-thromboglobulin and platelet factor 4. Mgsa was localized to chromosome 5 using a cDNA probe for mouse Mgsa and somatic cell hybrids and is thus syntenic with Kit (W), Ph, Rw, and rs loci. The results eliminate Mgsa as the product of the Steel locus on chromosome 10, but raise the possibility that Mgsa might be synonymous with a chromosome 5 locus affecting skin pigmentation.

Animals↗
PubMed1989

Effect of habitual physical activity on age-related glucose intolerance.

Plasma glucose and insulin responses to a standard oral glucose challenge and a mixed meal were determined for two groups of male volunteers (office workers and laborers) and a group of female housewives or office workers. Although glucose tolerance declined with age to a certain degree in all three groups, the age-related change varied as a function of both level of habitual physical activity and gender. Specifically, the decline in glucose tolerance was greatest in the male office workers and least in the females. The plasma insulin responses did not increase with age in any of the groups. These results suggest that glucose tolerance decreases with age because there is a decline in insulin action, which is not compensated for by an increase in insulin secretion. Insulin sensitivity appears to be enhanced in females as compared with males. Sensitivity is also enhanced in males habitually engaged in physical labor; thereby accounting for the age-related decline being greatest in the male office workers. Finally, the results showed that although the loss of glucose tolerance with age varied from group to group, the quantitative nature of the change was modest in all three groups. These data further emphasize that very little change in glucose tolerance is associated with aging in generally healthy, nonobese individuals.

Adult↗
PubMed1989

Sigje, a member of the small inducible gene family that includes platelet factor 4 and melanoma growth stimulatory activity, is on mouse chromosome 11.

Stiles and coworkers originally identified a gene they termed JE that is transcriptionally activated in mouse fibroblasts early after treatment with platelet derived growth factor or serum. This gene, now named Sigje, can encode a 148-amino acid secreted, basic polypeptide that belongs to the small inducible gene (SIG) family whose members include, for example, platelet factor 4, melanoma growth stimulatory activity (Mgsa), and interferon inducible protein 10. SIG family members share a conserved array of cysteine and proline residues and a similar predicted secondary structure, and may have evolved from a common ancestral gene. Several members of the SIG family have been assigned to the proximal long arm of human chromosome 4, to a region that has genetic homoeology with a portion of mouse Chromosome 5. We report here that mouse Sigje, in contrast to Mgsa, is on Chromosome 11. Sigje restriction fragment length polymorphisms in Mus spretus DNA were identified with the enzymes TaqI, MspI, BclI, and XbaI, and will be useful in mapping by meiotic recombination.

Animals↗
PubMed1989

[The innervation of the dentine].

The innervation in both human and rat dentine was studied by modified silver stain and anterograde radioautographic neuroanatomical tracing (ARNT). The results showed that very fine nerve fibrils were demonstrated in human and rat dentine. They could be traced in continuity with those in predentine and dental pulp and extended to the dentine enamel junction. These facts show that the innervation in dentine does exist, and the nerve fibrils in dentine originate from dental pulp.

Animals↗
PubMed1989

Limitations in calculating left ventricular volume by two dimensional geometry--an exised canine heart study.

The left ventricle was removed from 76 dogs and was cast in silicone, in vitro, under three fixing pressure levels to simulate various end-diastolic pressures. This cast was designated as a silicone cast. The waxen cast was constructed by adding attachments which protrude inside the LV cavity, such as the papillary muscles and trabeculae carneae to the silicone cast. The cast volumes were compared with the volume calculated by the area-length method, including ellipsoid and paraboloid models, and by Chapman's method in which silhouettes of the silicone casts projected on 4 planes were used. Under a lower fixing pressure, the volume of papillary muscles and trabeculae carneae accounted for about 35% of the LV volume which was independent of either size of heart or weight of the dog. This ratio was reduced at higher fixing pressure levels. The relationship between the cast volume and the volume calculated by the silhouette method was linearly proportional. However, the deviation increased with higher fixing pressure levels and with larger ventricular volumes in all calculation methods, indicating the shape of the left ventricle cannot be represented by any ideal symmetrical spherical model. The calculated volume agreed with its corresponding cast volume with an error of less than 10% if either the fixing pressure level was below 5 mmHg, or the volume was less than 50 ml.

Animals↗
PubMed1989

Immunogenicity of highly purified porcine and human insulins in diabetic patients with high titers of insulin antibody.

Twenty-nine non-insulin-dependent diabetic Chinese subjects previously treated with conventional porcine isophane insulin (NPH) for a period of time, whose titer of serum insulin antibody was greater than 40% were changed to either highly purified pork insulin (Nordisk, Denmark) or human insulin of recombinant DNA origin (Eli Lilly, USA) for 1 year in a double-blind and randomized trial. The human (n = 16) and pork insulin (n = 13) groups were carefully matched for age, sex and measures of metabolic control. In highly purified pork-insulin-treated patients, the glycated hemoglobin and fasting blood sugar values began to fall significantly from a mean of 13.2% to 12.3% (p less than 0.05) and 228 mg/dl to 183 mg/dl (p less than 0.005), respectively, 2 months after the commencement of this study, whereas insulin antibody levels began to fall significantly from a mean of 61.8% to 49.5% (p less than 0.01) 6 months after the start of the study. Also, daily insulin doses increased significantly from a mean of 58 units to 70 units (p less than 0.005) 6 months after the start of the study. In human-insulin-treated patients, there were no significant changes in the glycated hemoglobin values. The fasting blood sugar levels fell significantly (p = 0.0515) at the end of the study period but the insulin antibody levels did not show any significant change during the same study period. Daily insulin dose increased significantly from a mean of 51 units to 57 units (p less than 0.01) 4 months after beginning the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Site-directed deletion mutagenesis using phagemid vectors and genetic selection.

Oligonucleotide-directed mutagenesis was used along with the dut and ung genetic selection method of Kunkel to introduce large site-specific deletions into cDNAs cloned into phagemid vectors. We find that large deletions can be achieved with an efficiency equal to that of single point mutations, with a very low frequency of aberrent clones. To facilitate screening of clones, E. coli strain DH5 alpha was used as the recipient host cell to genetically select for deletion mutants. Comparisons were made to deletion mutagenesis without genetic selection, and to reactions utilizing two oligonucleotide primers simultaneously. The low frequency of deletion mutants observed without genetic selection renders random screening for deletion mutant clones cumbersome. The results provide representative expectations and a useful guide for those contemplating the construction of deletion mutants.

Base Sequence↗
PubMed1989

Insulin resistance in obesity and noninsulin dependent diabetes mellitus.

Insulin clamp studies were carried out on 13 non-diabetics and 12 non-insulin-dependent diabetics (NIDDM). Based upon the body mass index (BMI), they were further divided into obese (BMI greater than or equal to 27 kg/m2) and nonbese groups (BMI less than 27 kg/m2). All received euglycemic insulin clamp study (Humulin-S 40mU/m2/min). Thermoregulated venous samplings were done every five minutes for measurements of plasma glucose (PG) and immunoreactive insulin (IRI). Steady state plasma glucose (SSPG) was obtained 20-80 minutes and kept for 100 more minutes. The data of final 40 minutes of clamp were used for analysis. Variations in SSPG and metabolic clearance rate of glucose (MCRG) instead of glucose infusion rate (M) value were used to assess the insulin sensitivity. The results showed that insulin resistance was noted in obese non-diabetic and diabetic subjects as well as in non-obese diabetic patients, as evidenced by higher basal IRI and lower MCRG than non-obese normal controls. Correlation analysis revealed that there was no correlation between the reduction of MCRG and the BMI in either non-diabetic or diabetic patients. There was a strong negative correlation between MCRG and the ambient fasting plasma glucose in the diabetic group, whereas this correlation was not found in the non-diabetic group. In conclusion, obesity with or without diabetes did have remarkable insulin resistance. In non-diabetic obese subjects the insulin resistance did not go up as the BMI increased further. In diabetic patients, both obesity and hyperglycemia contributed significantly insulin resistance.

Adult↗
PubMed1988

Gene for parathyroid hormone-like peptide is on rat chromosome 2.

Parathyroid hormone-like peptide (PLP) is thought to be a mediator of hypercalcemia in both human and rodent malignancies. A rat PLP cDNA was used as a hybridization probe in Southern blot analysis of DNAs isolated from a panel of rat-mouse somatic cell hybrids. The single-copy gene for PLP was assigned to rat chromosome 2, whereas the rat parathyroid hormone (PTH) gene has previously been assigned to rat chromosome 1. Consequently, despite significant amino-terminal homology between PLP and PTH the genes encoding these peptides in the rat as well as human species have discrete chromosomal localizations.

Animals↗
PubMed1988

Chromosome assignment of mouse insulin, colony stimulating factor 1, and low-density lipoprotein receptors.

Receptors for insulin, low-density lipoprotein, and colony stimulating factor 1 are associated with diabetes, atherosclerosis, and cancer in man. Complementary DNA clones for Insr, Ldlr, and Csfmr were used to chromosomally assign the three genes in mouse. In contrast to their close linkage on the short arm of human Chromosome 19, Insr and Ldlr are asyntenic, residing on mouse Chromosomes 8 and 9, respectively. The genes for CSF1R, CSF1, CSF2, IL-3, and IL-5 form a cluster on the long arm of human Chromosome 5. In mouse, Csfm, Csfgm, and IL-3 are syntenic on Chromosome 11. The Csfmr gene was assigned to mouse Chromosome 18 and is thus unlinked to other members of this gene cluster. These gene assignments provide additional topographical information on conservation of linkage groups in man and mouse and provide a genetic framework for evaluating the possible roles for the three receptor genes in genetic diseases in mouse.

Animals↗