Biomedical subjects

H C Li

Publications and source records attributed to H C Li.

At least 55 records · Page 3Linked to original sources

PubMed1995

In situ polymerization of pyrrole in animal tissue in the formation of hybrid biomaterials.

Porcine pericardium was impregnated with pyrrole or its derivative, sodium 4-(3-pyrrolyl)butanesulphonate (SPBS), by soaking the animal tissue in the monomer. Subsequent in situ chemical polymerization of the monomer-rich tissue using FeCl3 as initiator produced black polypyrrole-tissue hybrid biomaterials. The rate and extent of polymerization was found to be greater in 0.5 M acetic acid than in Hepes-buffered saline (HBS) and also greater for SPBS than for pyrrole. However, better tissue integrity was obtained for polymerization in HBS. Histological examination showed that the monomers do not permeate through the entire tissue, restricting polymerization to the surface layers of the tissue. The samples so formed do not exhibit detectable electrical conductivity.

Acetates↗

PubMed1995

Characterization of the reactive intermediates in laser flash photolysis of adenine, adenosine and dAMP using acetone as photosensitizer.

Transient absorption spectra of adenine, adenosine and 2'-deoxyadenosine 5'-monophosphate (dAMP) arising from 248 nm laser flash photolysis using acetone as a photosensitizer have been observed. The intermediates recorded are assigned to the excited triplet states and dehydrogenated radicals of adenine and its nucleoside and nucleotide. The excited triplet states of adenine and its derivatives are produced via triplet-triplet excitation transfer and observed for the first time, while the dehydrogenated radicals stemming from the interaction of triplet acetone with adenine and its derivatives via electron transfer through a five-member-ring electron donor-acceptor intermediate. The site of dehydrogenation is suggested to be the hydrogen atom on C(8) of the adenine moiety. Moreover, three sets of kinetic parameters of the triplet decay have been determined. The rate constants of the unimolecular decay (k0), the triplet quenching by the ground state (ksq) and by the triplet quencher Mn2+ (kq) are 1.1 x 10(5), 7.9 x 10(4), 3.7 x 10(4) s-1, 6.9 x 10(8), 8.3 x 10(8), 3.6 x 10(8) dm3 mol-1 s-1 and 4.2 x 10(8), 3.5 x 10(8), 6.0 x 10(8) dm3 mol-1 s-1 respectively for adenine, adenosine and dAMP.

Acetone↗

PubMed1995

Variation of growth rate of a rat tumour during a light-dark cycle: correlation with circadian fluctuations in tumour blood flow.

To determine whether tumour growth is influenced by circadian variations in tumour tissue blood flow, we measured changes in area doubling time of tumours (Sato lung carcinoma) within transparent chambers and changes in tissue blood flow of rat subcutaneous tumour during a light-dark cycle. Rats were subjected to an artificial light-dark cycle with light from 7 a.m. to 7 p.m. Tumour doubling times (TDTs) during the dark and the light spans were 33.5 +/- 11.9 h (n = 38, 20 rats) and 70.6 +/- 36.9 h (n = 39, 20 rats) respectively. The former was significantly shorter than the latter (P < 0.001). In addition, the larger the tumour became, the longer was the TDT during the light span (P < 0.05). Tumour tissue blood flow during the night (10 p.m.-4 a.m.) was approximately 1.5 times greater than that during the day (10 a.m.-4 p.m.). The time during which tumours actively grow and that during which tissue blood flow in tumours increases coincided. These results strongly suggest that tumour tissue blood flow is a determining influence on tumour proliferative activity and that tumour growth is influenced by circadian variations in tumour tissue blood flow.

Animals↗

PubMed1995

Induction of the hepatic CYP2B and CYP3A enzymes by the proestrogenic pesticide methoxychlor and by DDT in the rat. Effects on methoxychlor metabolism.

In earlier investigations, methoxychlor treatment did not elicit induction of hepatic P450 monooxygenases in rats, apparently due to the short half-life of methoxychlor in vivo. The current study demonstrates that multiple bidaily doses of methoxychlor to female rats produce a marked induction of the hepatic microsomal P450 2B1/2B2 and 3A proteins. There was no increase in CYP1A1 or CYP2E1 proteins, demonstrating selectivity of induction by methoxychlor. Similarly, treatment with DDT, a methoxychlor analog, increased CYP2B and 3A proteins but had no effect on CYP1A1 and 2E1. Methoxychlor moderately elevated the enzymatic activity corresponding to CYP2B and 3A catalysis. In immature rats, only the higher dose of methoxychlor (300 mg/kg), produced elevation of testosterone hydroxylation at the 16 alpha position (major product) that was statistically significant, indicative of increased catalysis by CYP2B1/2B2. Both the low (150 mg/kg) and high dose (300 mg/kg) of methoxychlor increased the 6 beta hydroxylation (major product) and 2 beta and 15 beta hydroxylation (minor products) of testosterone, indicative of increased catalysis by CYP3A. In mature female rats, both methoxychlor and DDT treatment elevated the 16 alpha and 6 beta hydroxylation and androstenedione formation. Additional indication of methoxychlor- and DDT-mediated induction of CYP2B enzymatic activity in mature and immature rats was evident from increased ring hydroxylation of methoxychlor, an activity attributed to CYP2B. These findings indicate that methoxychlor and DDT belong to the phenobarbital type of inducers and that exposure to methoxychlor can affect its own metabolism. The methoxychlor-mediated increase in CYP2B and 3A proteins was considerably larger than the increase in the corresponding enzymatic activities. The possible reasons for the lack of correlation between P450 levels and their enzymatic activities and the potential relevance of induction by methoxychlor to its metabolism and toxicity are discussed.

Animals↗

PubMed1995

[Correlation between kidney deficiency syndrome and bone density].

In order to study the relationship between Kidney Deficiency Syndrome (KDS)and bone density (BD), the BD of 2068 subjects (40-69 years old)was measured with SPA-IIC type monophoton BD scanning device made in China. The subjects including 1144 cases of KDS (320 males and 824 females); 608 cases without KDS (306 males and 302 females); 164 cases of Lung Deficiency (80 males and 84 females); 152 cases of Spleen Deficiency (76 males and 76 females). Through comparison with the same sex and age group, it was found that BD in KDS patients was significantly lower than that in the normal subjects and those without KDS, also lower than that in the Lung and Spleen Deficiency patients. It indicated that KDS had the corresponding BD changes, which confirmed the TCM classical theory "The Kidney governs the bone". Based on the measuring data, the authors took the lower limit of BD normal value minus two folds of SD as the critical value for KDS diagnosis in 40-49 years age group, i. e., male BD < 0.6 g/cm2, female BD < 0.5 g/cm2. The clinical feedback showed that the male and female related coincident rates were 76% and 80% respectively. Therefore, the critical value could be taken as an objective index for KDS diagnosis after excluding other affecting factors.

Adult↗

PubMed1994

Orientational changes of troponin C associated with thin filament activation.

We have used electron paramagnetic resonance to describe the orientational changes of troponin C (TnC) accompanying muscle activation by Ca2+. Rabbit skeletal TnC was labeled with maleimide spin label (MSL) at Cys-98 and reconstituted into an oriented skinned muscle fiber. About 70% of endogenous troponin C was replaced with labeled TnC, with a concomitant recovery of 80-90% of muscle tension. The nanosecond domain mobility present in solution, as determined from the EPR spectra of randomized samples, is fully inhibited in the reconstituted fibers. The orientational analysis revealed a bimodal orientational distribution of TnC in the absence Ca2+ and attached myosin heads. One of the components is well-ordered with its probe axis inclined at 22 degrees to the fiber axis, while the other is more disordered and inclined at 58 degrees. Ca2+ and/or cross-bridge binding significantly disordered the labeled domain and increased the average probe axis angle by 20-30 degrees away from the fiber axis. The order for the magnitude of angular tilt was Ca2+ < myosin cross-bridges < Ca2+ and cross-bridges. Thus, TnC exists in many different orientational conformations depending on which ligand is bound. We believe that these conformations reflect different activation mechanisms by Ca2+ and cross-bridge binding.

Animals↗

PubMed1994

Changes in vessel pressure and interstitial fluid pressure of normal subcutis and subcutaneous tumor in rats due to angiotensin II.

To elucidate the mechanism of enhancement of transport of anticancer drugs into tumor tissue due to angiotensin II (AII), changes in microvascular pressure (MVP) and interstitial fluid pressure (IFP) due to AII were measured in normal subcutis and subcutaneous tumor in rats. Two different tumor cell lines AH109A and AH272 were used. MVP and IFP were measured using a microocclusion method and a diffusion chamber method, respectively. Insignificant changes in the pressure of normal venous vessels and the IFP of normal subcutis were brought about by AII-induced hypertension. In both AH109A and AH272, the IFP of the same region within the tumor increased with enlargement of tumor volume. The IFP of AH109A tumor (tumor volume = 1.8-2.2 cm3) increased slightly due to AII, but the tumor MVP of AH109A and AH272 increased markedly. Though both tumor IFP and MVP increased significantly due to AII, the increases the hydrostatic pressure difference between tumor vascular and interstitial spaces and leads to enhancement of the efficiency of filtration from tumor vessels to tumor tissue, which is one of the mechanisms of enhancement of drug delivery to tumor tissue due to AII.

Angiotensin II↗

PubMed1994

Effects of intravenous infusion of dopamine on tumor blood flow in rat subcutis.

To determine the effects of intravenous administration of dopamine hydrochloride (DA) on tumor blood flow (TBF), we measured the blood flow of normal subcutaneous tissue and subcutaneous tumor (LY-80, a variant of Yoshida sarcoma) in enflurane-anesthetized male Donryu rats using a hydrogen clearance method. Measurements were made before and during intravenous infusion of DA at a rate of 5 micrograms/kg/min, while recording the mean arterial blood pressure of the rats. Under mild hypertension induced by DA, the blood flow of normal subcutis decreased and TBF increased significantly. SCH-23390, an antagonist of the DA1 receptor, inhibited the enhancement of TBF by DA; while domperidone, an antagonist of the DA2 receptor, did not modify the effects of DA. In experimental chemotherapy against the tumor using adriamycin (ADM) 5 mg/kg i.v., only the combination of DA and ADM significantly inhibited the tumor growth. Moreover, DA reduced the weight loss caused by ADM. These results indicate that DA could have a role in increasing TBF and possibly enhance drug delivery to tumors. Moreover, it appears that the DA1 receptor contributes, at least in part, to the enhanced blood flow in rat subcutaneous tumor following DA administration.

Animals↗

PubMed1994

[Mutation of p53 gene in human cancers of the esophagus and gastric cardia].

p53 gene in human esophageal cancer (EC) and cancer of gastric cardia was analyzed. Southern blotting hybridization revealed that five of 35 of EC sample were found to contain abnormal structure of p53 gene, including 2 deletions and 3 rearrangements; two of 27 adjacent non-tumor tissues also contain abnormal structure of p53 gene (7.4%), among them one case was fragment deletion and another case was rearrangement. PCR-direct sequencing technique was used to detect p53 point mutation within exon and intron 5 through 9. Fifteen of 30(50%) of esophageal squamous cell carcinomas contained mutation of p53 gene. Five of 11(45%) adjacent non-tumor tissues also contained mutation of p53 gene. An esophageal adenocarcinoma showed p53 mutation. Three of 4 carcinoma of gastric cardia showed p53 mutation. Mutation spectrum in EC: 8 of 22 cases (36.4%) of p53 mutation were G:C to A: T transition, 6 of 22 cases (27.3%) of p53 mutation were frameshift mutation, including 13.6% (3/22) insertion and 9.1% (2/22) deletion mutation. Some new sites of p53 mutation in human EC were identified. The results suggest that the p53 gene plays an important role in carcinogenesis of human esophagus and gastric cardia.

Base Sequence↗

PubMed1994

[The multiple tumor suppressor genes in human esophageal cancer].

The mutation and deletion of the multiple tumor suppressor genes, including p53, Rb, APC and MCC in the same tissue of humanesophageal cancer (EC) and adjacent non-tumor were analysed by PCR amplification and direct sequencing. In 10 cases of EC 6 were found mutations of p53 gene, 5 were found abnormality of Rb gene, 3 were found mutation of APC gene, 3 were found mutation of MCC gene, 8 were found atleration abnormality of tumor suppressor genes Rb, p53, APC and MCC, 6 were found two or more abnormality of the tumor suppressor genes. The results indicated that the alterations in multiple of tumor suppressor genes were related to carcinogenesis of human esophageal cancer.

Base Sequence↗

PubMed1994

[Microvascular mechanisms of change in tumor blood flow elicited by vasopressors].

To elucidate the microvascular mechanisms of change in tumor blood flow due to vasopressors (angiotensin II, epinephrine, methoxamine), we analyzed the site of vascular resistance (VR) increased by each vasopressor. Arteriolar vessels within a transparent rat chamber were classified centripetally (a2-a5) according to Strahler's nomenclature. Vessels that feed into the tumor microcirculation were a2 modified by the tumor (starting vessels). Under angiotensin II (A II)-induced hypertension, the pressure of all arteriolar vessels increased roughly in proportion to the increase in mean arterial blood pressure. The greatest pressure drop and hence the most resistance due to A II occurred across the a2. During epinephrine-induced hypertension, there were major pressure drops between a4 and a3, and between a3 and a2. The amount of contraction of arteriolar vessels due to methoxamine was much smaller than that due to epinephrine, and the pressure increase in a4 and a3 was also small. From the facts described above, we may conclude as follows: A II creates greater vascular resistance of a2 vessels to blood flow and also greater perfusion pressure of a5-a3 vessels, resulting in increased blood inflow into a starting vessel which then becomes a passive vessel. Epinephrine causes an increase in the resistance of a3, a4 and probably upstream from a4 arterioles to blood flow. Thus, tissue blood flow in subcutis and tumor almost always decreases together. The fact that tissue blood flow in normal subcutis and tumor did not change significantly under methoxamine-induced hypertension is probably due to the results that methoxamine had little effects on the vascular resistance of smaller arterioles to blood flow.

Angiotensin II↗

PubMed1993

Microvascular mechanisms of change in tumor blood flow due to angiotensin II, epinephrine, and methoxamine: a functional morphometric study.

To elucidate the microvascular mechanisms of change in tumor blood flow elicited by vasopressors, a functional morphometric study of the s.c. microcirculation within a rat transparent chamber was performed. Arteriolar vessels were classified centripetally (a2-a5) according to Strahler's method. Arteriolar pressure in each segment both under normotension and under hypertension induced by angiotensin II, epinephrine, or methoxamine was measured using a microocclusion technique. Vasoconstriction was estimated by changes in vessel diameters. In addition, tissue blood flow of the subcutis and s.c. tumor (LY80, a variant of Yoshida sarcoma) under the same conditions was measured with the hydrogen clearance method. By comparing the sites of the greatest pressure drop and the vasoconstriction induced by each vasopressor, we assessed the sites of vascular resistance (VR) which showed increases due to these vasopressors. The greatest VR increase elicited by angiotensin II occurred across a2 vessels. On the other hand, the sites of VR increase due to epinephrine were in a3 vessels and larger vessels upstream from a3 arterioles. The VR increase induced by methoxamine was much smaller than that induced by epinephrine. We conclude that the fact that the sites of increased VR differ with each vasopressor is the primary reason that various vasopressors have been found to produce different changes in tumor blood flow.

Angiotensin II↗

PubMed1993

Reversible and time-dependent inhibition of the hepatic cytochrome P450 steroidal hydroxylases by the proestrogenic pesticide methoxychlor in rat and human.

Methoxychlor, a currently used pesticide, is demethylated and hydroxylated by several hepatic microsomal cytochrome P450 enzymes. Also, methoxychlor undergoes metabolic activation, yielding a reactive intermediate (M*) that binds irreversibly and apparently covalently to microsomal proteins. The study investigated whether methoxychlor could inhibit or inactivate certain liver microsomal P450 enzymes. The regioselective and stereoselective hydroxylation of testosterone and the 2-hydroxylation of estradiol (E2) were utilized as markers of the P450 enzymes inhibited by methoxychlor. Both reversible and time-dependent inhibition were examined. Coincubation of methoxychlor and testosterone with liver microsomes from phenobarbital treated (PB-microsomes) male rats, yielded marked diminution of 2 alpha- and 16 alpha-testosterone hydroxylation, indicating strong inhibition of P4502C11 (P450h). Methoxychlor moderately inhibited 2 beta-, 7 alpha-, 15 alpha-, 15 beta-, and 16 beta-hydroxylation and androstenedione formation. There was only a weak inhibition of 6 beta-hydroxylation of testosterone. The methoxychlor-mediated inhibition of 6 beta-hydroxylation was competitive. By contrast, when methoxychlor was permitted to be metabolized by PB-microsomes or by liver microsomes from pregnenolone-16 alpha-carbonitrile treated rats (PCN-microsomes) prior to addition of testosterone, a pronounced time-dependent inhibition of 6 beta-hydroxylation was observed, suggesting that methoxychlor inactivates the P450 3A isozyme(s). The di-demethylated methoxychlor (bis-OH-M) and the tris-hydroxy (catechol) methoxychlor metabolite (tris-OH-M) inhibited 6 beta-hydroxylation in PB-microsomes competitively and noncompetitively, respectively; however, these methoxychlor metabolites did not exhibit a time-dependent inhibition. Methoxychlor inhibited competitively the formation of 7 alpha-hydroxytestosterone (7 alpha-OH-T) and 16 alpha-hydroxytestosterone (16 alpha-OH-T) but exhibited little or no time-dependent inhibition of generation of these metabolites, indicating that P450s 2A1, 2B1/B2, and 2C11 were inhibited but not inactivated. Methoxychlor inhibited in a time-dependent fashion the 2-hydroxylation of E2 in PB-microsomes. However, bis-OH-M exhibited solely reversible inhibition of the 2-hydroxylation, supporting our conclusion that the inactivation of P450s does not involve participation of the demethylated metabolites. Both competitive inhibition and time-dependent inactivation of human liver P450 3A (6 beta-hydroxylase) by methoxychlor, was observed. As with rat liver microsomes, the human 6 beta-hydroxylase was inhibited by bis-OH-M and tris-OH-M competitively and noncompetitively, respectively. Testosterone and estradiol strongly inhibited the irreversible binding of methoxychlor to microsomal proteins. This might explain the "clean" competitive inhibition by methoxychlor of the 6 beta-OH-T formation when the compounds were coincubated.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1993

Slit lamp laser Doppler interferometer.

A slit lamp laser interferometer is described for clinical in vivo eye length measurements. The basic components are a laser Doppler interferometer, a slit lamp attachment, and a commercial slit lamp. First measurements of the axial length of the eye yielded a standard deviation of 0.04 mm and less.

Eye↗

PubMed1993

Serological response to Ureaplasma urealyticum in the neonate.

A serovar-specific antibody response to Ureaplasma urealyticum was observed in stillborns, neonates, and mothers by means of the modified metabolic inhibition test. Elevated levels of ureaplasma antibody were found in cases of stillbirth and neonatal respiratory disease. There was a higher risk of mortality among neonates with respiratory disease who had elevated levels of ureaplasma antibody. IgG and IgM serovar-specific antibody responses to U. urealyticum serovars were confirmed by the immunoperoxidase and immunofluorescence assays. In contrast to ELISA-based assays that use soluble membrane proteins as antigen, these three assays use whole intact cells. These observations suggest that the serovar-specific antibody response may be associated with the ureaplasma extramembranous carbohydrate (lypoglycan) coat, which comes off during centrifugation. With the immunoperoxidase assay, a heel-prick blood sample (20 microL) can be screened for 16 IgM or IgG + IgM + IgA (combined) responses in 4 hours. The predictive value of IgM antibody for U. urealyticum infection and other mycoplasma infections and for the risk of stillbirth and development of chronic lung disease should now be assessed.

Antibodies, Bacterial↗

PubMed1993

[Mutation and expression of Rb gene in human esophageal cancer].

The mutation and expression of Rb gene in human esophageal cancer (EC) were investigated by PCR-direct sequencing and Northern blot hybridization. In PCR amplification analysis, in one of 20 (5%) cases of EC was found to have Rb gene deletion in exon 17 and 21; in one of 6 cases of the adjacent non-tumours tissue was found to have deletion in exon 21. Esophageal carcinoma of human fetus induced by NMBzA had Rb gene deletion in exon 17 and 21 too. In PCR-direct sequencing analysis, four of 10 (40%) EC were found to contain Rb gene mutations in exon 17 and 21. In northern blot analysis, seven of 12 (58.3%) EC exhibited abnormal Rb gene expression, including inactivation in 6 abbreviated expression in one. The results suggest that Rb tumor suppressor gene might play an important role in carcinogenesis of EC. The mechanisms of Rb gene mutation, deletion or abnormal expression related to carcinogenic nitrosamine in the environment need further study.

Adult↗

PubMed1993

[The effects of angiotensin II and other vasoactive agents on the blood flow in Yoshida ascites hepatoma].

The effects of angiotensin II and other six vasoactive agents on tissue blood flow of Yoshida rat ascites hepatoma AH109A and normal liver were measured by the hydrogen clearance method. The mean blood flow in the tumor peripheral part under normotensin was 11.9 +/- 8.2 ml/min/100 g tissue and was not influenced by tumor size. Tumor blood flow was more significantly increased in infusion angiotensin II than 0.5 mg/ml methoxamine; however, normal liver blood flow of tumor-bearing rats was unchanged in contrast to an increase seen in the tumor. A Pronounced reduction of tumor blood flow was found after administration of epinephrine, norepinephrine and ethylphenylephrine. In addition, metaraminol, phenylephrine as well as 1.0 and 2.5 mg/ml methoxamine were not found to significantly change the blood flow of the tumor.

Angiotensin II↗

PubMed1990

[Retinoblastoma gene in human esophageal cancer].

Retinoblastoma gene (Rb) is a tumor suppressor gene. In 21 esophageal cancer and 43 pericancerous non-tumor samples obtained from patients who had undergone surgery for esophageal cancer in Linxian County, a high incidence area of esophageal cancer, Rb gene was studied. DNAs were extracted from the above esophageal tissues, then were separately digested with Hind III, EcoRI, BamHI, PstI, MspI, HpaII and subjected to Southern analysis. The Southern blots were sequentially probed with two fragments of Rb cDAN clone: 0.9 kb and 3.8 kb. Of 43 adjacent non-tumor tissues examined, 15 were found to have structural anomaly (34.9%). Seven of 21 esophageal cancers also showed structural anomaly (33.3%). In order to study the cause of Rb gene deletion, esophageal carcinoma of human fetal origin induced by N-methyl-N-benzylnitrosamine (NMBzA) in nude mice were similarly examined and found to be deleted of Rb gene. Thus, deletional inactivation of Rb gene may play an important role in the pathogenesis of esophageal cancer in this high-risk area. N-nitrosamine may play a causative role in deletion of Rb gene. The above data for the first time demonstrate structural anomaly of Rb gene in esophageal cancer and confirm that chemical carcinogens, such as N-nitrosamines, can delete the antioncogene.

Blotting, Southern↗