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Biomedical subjects

M T Huang

Publications and source records attributed to M T Huang.

At least 91 records · Page 5Linked to original sources
PubMed1993

Gene targeting technology for creating transgenic models of lymphopoiesis.

Naturally occurring immunodeficient mouse strains express a variety of genetic defects in myeloid and/or lymphoid cell development. These strains have served as valuable animal models for studying immune cell differentiation and mechanisms of transplant rejection. Some of the most commonly used strains carry mutations at the nude, scid, beige, and/or xid loci. Gene targeting technology can now be used to directly modify endogenous alleles via homologous recombination with exogenous DNA. By performing DNA targeting in embryonic stem (ES) cells, germline transmission of these modifications can be obtained by breeding chimeras generated from cloned ES cells. This approach can be used to target the inactivation, modification, or replacement of specific genes and has been used to examine the role of several alleles in hematopoiesis. This review describes the use of this technology to generate mutations that influence the development and function of T and B lymphocytes.

Animals↗
PubMed1992

Inhibitory effect of green tea on the growth of established skin papillomas in mice.

In 10 separate experiments, mice with established chemically induced or UV light-induced skin papillomas were treated continuously with green tea in the drinking water or with i.p. injections of a green tea polyphenol fraction or (-)-epigallocatechin gallate three times a week for 4-10 weeks. Partial tumor regression or > 90% inhibition of tumor growth, as measured by changes in tumor volume per mouse, was observed in 5 experiments, and marked inhibition of tumor growth (46-89%) was observed in 5 additional experiments. Treatment of the mice with green tea or green tea constituents had an inhibitory effect on body weight increases in several but not all of the studies. Examination of the data from all ten experiments revealed that complete tumor regression occurred in 14 of 346 papilloma-bearing mice (4%) that were treated with green tea in the drinking water or with i.p. injections of green tea constituents, whereas none of the 220 papilloma-bearing control mice treated with only vehicle exhibited complete tumor regression. These observations indicate that oral administration of green tea, i.p. administration of a green tea polyphenol fraction, or i.p. administration of (-)-epigallocatechin gallate inhibited the growth and/or caused the regression of established experimentally induced skin papillomas.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1992

Splanchnic uptake of haloperidol and release of reduced haloperidol in vivo in the guinea pig.

Splanchnic uptake of haloperidol (HAL) and release of reduced haloperidol (RHAL) were studied in vivo in guinea pigs. Anesthetized animals with implanted cannulae in the aorta, the hepatic vein and the inferior vena cava were infused intravenously with HAL at a rate of 9.6 micrograms/min/animal for 90 min. Plasma HAL and RHAL in samples taken from the arterial and hepatic venous cannulae were measured by HPLC with an electrochemical detector. Contamination of the hepatic venous samples by blood from the inferior vena cava was ruled out by the validation method of tritiated water washout [Huang MT, J Appl Physiol 71: 359-364, 1991]. HAL concentrations plateaued at 70-80 ng/mL in the aorta and 5-7 ng/mL in the hepatic vein during the final 30 min of infusion. Splanchnic extraction of HAL was 91%. Hepatic blood flow was estimated to be 1.95 +/- 0.40 (SD) mL/min/g. If assuming that splanchnic uptake of HAL took place in the liver, a rate of uptake of HAL in the liver of 79.2 +/- 18.6 (SD) ng/min/g could be calculated by the Fick principle. The uptake in the whole liver accounted for 14% of the rate of HAL infusion into the animal. Plasma RHAL in the aorta, 6.4 +/- 6.6 (SD) ng/mL at 60 min and 9.4 +/- 4.6 (SD) ng/mL at the end of HAL infusion, was about 10-12-fold less than aortic HAL. The concentrations of RHAL in the hepatic vein were not significantly different from those in the aorta, indicating that splanchnic tissues including the liver are not responsible for plasma RHAL secretion. The highly efficient uptake of HAL as well as the ketone reductases found previously in vitro in liver microsomes of guinea pigs were probably involved only in biliary excretion of HAL.

Animals↗
PubMed1992

Effect of dietary curcumin and ascorbyl palmitate on azoxymethanol-induced colonic epithelial cell proliferation and focal areas of dysplasia.

Curcumin, a major yellow pigment of turmeric obtained from powdered rhizomes of the plant Curcuma longa Linn., is commonly used as a coloring agent in foods, drugs and cosmetics. Ascorbyl palmitate is a lipid soluble derivative of ascorbic acid. Both curcumin and ascorbyl palmitate have antioxidant activity and are potent inhibitors of 12-O-tetradecanoyl-phorbol-13-acetate-induced tumor promotion in mouse skin. The effects of dietary curcumin and ascorbyl palmitate on azoxymethanol (AOM)-induced hyperproliferation of colonic epithelial cells and the incidence of focal areas of dysplasia (FADs) were evaluated in female CF-1 mice fed an AIN 76A diet. Subcutaneous injections of AOM (10 mg/kg body wt. once weekly for 6 weeks) caused hyperplasia and the formation of FADs in the colon. Administration of 2% curcumin in the diet inhibited AOM-induced formation of FADs while administration of 2% ascorbyl palmitate in the diet did not demonstrate inhibition. This result suggests that dietary curcumin may inhibit AOM-induced colonic neoplasia in mice.

Animals↗
PubMed1992

Inhibition of N-nitrosodiethylamine- and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced tumorigenesis in A/J mice by green tea and black tea.

The effect of p.o. administration of tea on nitrosamine-induced carcinogenesis was investigated. Female A/J mice were given N-nitrosodiethylamine (NDEA) (10 mg/kg) p.o. once a week for 8 weeks and were killed 16 weeks after the last dose. More than 90% of the mice had forestomach and lung tumors. The animals had an average of 8.3 forestomach and 2.5 lung tumors/mouse. With 0.63 or 1.25% green tea infusion (12.5 g green tea leaves brewed with 1 liter of boiling water) as the sole source of drinking water for the entire experimental period, the pulmonary tumor incidence was decreased by 18 or 44%, and the tumor multiplicity was reduced by 36 or 60%, respectively. The treatments also decreased the forestomach tumor incidence by 18 or 26% and tumor multiplicity by 59 or 63%, respectively. Administration of 0.63 or 1.25% green tea infusion, either during the NDEA treatment period only or starting 1 week after the completion of NDEA treatment, also decreased the pulmonary tumor incidence and multiplicity and the forestomach tumor multiplicity. The inhibitory effects of green tea infusion were also observed in a similar experiment using a higher dosage of NDEA (20 mg/kg). Treatment of female A/J mice with a single dose (103 mg/kg) of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) resulted in the formation of pulmonary adenomas in almost all of the animals with an average of 9.3 tumors/mouse after 16 weeks. When 0.6% decaffeinated green tea or black tea extract was given during the NNK-treatment period, tumor multiplicity was reduced by 67 or 65%, respectively. When the tea extract was given after the NNK-treatment period until the end of the experiment, 0.6% green tea extract decreased the tumor incidence and multiplicity by 30 and 85%, respectively. In this protocol, 0.6% black tea extract reduced tumor multiplicity by about 63% but did not significantly affect the tumor incidence. The results clearly demonstrated an inhibitory action of green tea and black tea on nitrosamine-induced tumorigenesis.

Animals↗
PubMed1992

Inhibitory effect of green tea in the drinking water on tumorigenesis by ultraviolet light and 12-O-tetradecanoylphorbol-13-acetate in the skin of SKH-1 mice.

Green tea was prepared by extracting 12.5 g of green tea leaves twice with 500 ml of boiling water, and the extracts were combined. This 1.25% green tea extract (1.25 g of tea leaves/100 ml of water) contained 4.69 mg of green tea extract solids per ml and was similar in composition to some green tea beverages consumed by humans. A 2.5% green tea extract (2.5 g of tea leaves/100 ml of water) was prepared similarly. Treatment of female SKH-1 mice with 180 mJ/cm2 of ultraviolet B light (UVB) once daily for 7 days resulted in red sunburn lesions of the skin. The intensity of red color and area of these lesions were inhibited in a dose-dependent fashion by the administration of 1.25 or 2.5% green tea extract as the sole source of drinking water before and during UVB treatment. Treatment of female SKH-1 mice with 180 mJ/cm2 of UVB once daily for 10 days followed 1 wk later by twice weekly application of 12-O-tetradecanoylphorbol-13-acetate for 25 wk resulted in the development of skin tumors. The formation of skin tumors was inhibited by administration of 1.25% green tea extract as the sole source of drinking water prior to and during the 10 days of UVB treatment and for 1 wk after UVB treatment. In additional experiments, female SKH-1 mice were treated with 200 nmol of 7,12-dimethylbenz(a)anthracene followed 3 wk later by irradiation with 180, 60, or 30 mJ/cm2 of UVB twice weekly for 30 wk. UVB-induced formation of skin tumors and increased spleen size were inhibited by administration of 1.25% green tea extract as the sole source of drinking water prior to and during the 30 wk of UVB treatment. In these experiments, treatment of the animals with the green tea extract not only decreased the number of skin tumors but also decreased substantially the size of the tumors. In additional studies, SKH-1 mice were initiated by topical application of 200 nmol of 7,12-dimethylbenz(a)anthracene followed by twice weekly application of 12-O-tetradecanoylphorbol-13-acetate for 25 wk. Administration of 1.25% green tea extract as the sole source of drinking water during promotion with 12-O-tetradecanoylphorbol-13-acetate reduced the number and incidence of skin tumors.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1992

Inhibitory effect of green tea on tumorigenesis by chemicals and ultraviolet light.

Topical application of a green tea polyphenol fraction inhibited 12-O-tetradecanoyl-phorbol-13-acetate-induced tumor promotion in CD-1 mice previously initiated with 7,12-dimethylbenz[a]anthracene (DMBA). Oral administration of a green tea infusion as the sole source of liquid sustenance to SKH-1 mice inhibited ultraviolet B light (UVB)-induced sunburn lesions, UVB-induced initiation of skin tumors, UVB-induced formation of skin tumors in mice previously initiated with DMBA, and nitrosodiethylamine-induced forestomach and lung tumors in A/J mice. In addition to inhibiting UVB-induced formation of skin tumors in DMBA-initiated mice, oral administration of green tea markedly decreased tumor size.

Animals↗
PubMed1992

Inhibitory effects of curcumin on tumor initiation by benzo[a]pyrene and 7,12-dimethylbenz[a]anthracene.

The effects of topical administration of curcumin on the formation of benzo[a]pyrene (B[a]P)-DNA adducts and the tumorigenic activities of B[a]P and 7,12-dimethylbenz[a]anthracene (DMBA) in epidermis were evaluated in female CD-1 mice. Topical application of 3 or 10 mumol curcumin 5 min prior to the application of 20 nmol [3H]B[a]P inhibited the formation of [3H]B[a]P-DNA adducts in epidermis by 39 or 61% respectively. In a two-stage skin tumorigenesis model, topical application of 20 nmol B[a]P to the backs of mice once weekly for 10 weeks followed a week later by promotion with 15 nmol 12-O-tetradecanoylphorbol-13-acetate (TPA) twice weekly for 21 weeks resulted in the formation of 7.1 skin tumors per mouse, and 100% of the mice had tumors. In a parallel group of mice, in which the animals were treated with 3 or 10 mumol curcumin 5 min prior to each application of B[a]P, the number of tumors per mouse was decreased by 58 or 62% respectively. The percentage of tumor-bearing mice was decreased by 18-25%. In an additional study, topical application of 3 or 10 mumol curcumin 5 min prior to each application of 2 nmol DMBA once weekly for 10 weeks followed a week later by promotion with 15 nmol TPA twice weekly for 15 weeks decreased the number of tumors per mouse by 37 or 41% respectively.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1992

Inhibitory effect of topical application of a green tea polyphenol fraction on tumor initiation and promotion in mouse skin.

A green tea polyphenol fraction was evaluated for its ability to inhibit tumor initiation by polycyclic aromatic hydrocarbons and tumor promotion by a phorbol ester in the skin of CD-1 mice. Topical application of the green tea polyphenol fraction inhibited benzo[a]pyrene- and 7,12-dimethylbenz[a]-anthracene-induced tumor initiation as well as 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced tumor promotion. Topical application of the green tea polyphenol fraction also inhibited TPA-induced inflammation, ornithine decarboxylase activity, hyperplasia and hydrogen peroxide formation. Studies with individual polyphenolic compounds in green tea indicated that topical application of (-)-epigallocatechin gallate, (-)-epigallocatechin and (-)-epicatechin gallate inhibited TPA-induced inflammation in mouse epidermis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1992

[Experimental study on tea in inhibiting mutational specificity of 6 antineoplastic drugs].

According to the principles of SOS response, the authors tested the mutational specificity of tea and its inhibitory effects to the mutational specificity of 6 antineoplastic drugs by using the method of mutational and anti-mutational synchronous test. The results revealed that the tea had no mutational toxicity but anti-mutation effect. It also had the inhibitory effect on mutational toxicity of 6 antineoplastic drugs, including Mitomycin C, Bleomycin, Fluorouracil, Cisdiaminodichoroplatinum, Arabinosylcytosin and Mustargen. These results have provided referential basis for further study on anti-cancer effect and clinical use of tea.

Antimutagenic Agents↗
PubMed1992

[A study of vitamin inhibition on the mutagenicity of the antineoplastic drugs].

The inhibitory effects on the mutational specificity of antineoplastic drugs of 14 kinds of vitamin were tested with the method of mutational and anti-mutational synchoronous test, add S9 and no S9. Vit C, Vit B6, and nicotinic acid had distinct inhibitory effects on the mutational specificity of 6 antineoplastic drugs, namely, mitomycin C, bleomycin, fluorouracil, cis-Diaminodichloroplatinum, arabinosylcytosine and mustargen Vit K3 showed inhibitory effect to mitomycin C, fluorouracil, cis-diaminodichloroplatinum, and arabinosylcytosine but Vit AD, Vit B1, Vit B2, Vit Bco, Vit D3, Vit E, Rutin, Vit K1, Vit K4 and folic acid did not. The fact that Vit C, Vit B6, nicotinic acid and Vit K3 showed anti-mutational effects is of some significance with reference to clinical therapeutics and prevention of tumours.

Antimutagenic Agents↗
PubMed1992

Serum interleukin-2 and soluble interleukin-2 receptor in renal transplant recipients.

Interleukin-2 (IL-2) and soluble interleukin-2 receptor (sIL-2R), released during T-lymphocyte activation, were measured in serial samples of serum from 32 patients with renal allografts and other uremic patients. Patients undergoing chronic hemodialysis had elevated sIL-2R levels (1,801.93 +/- 753.23 U/mL) which dropped after stable renal transplantation (822 +/- 438 u/mL). However, these values were higher than those of a normal control group (397.3 +/- 84.5 u/mL, p < 0.01). Marked elevation of sIL-2R (1,503.78 +/- 640 u/mL) was noted in patients with acute rejection episodes compared to those in a stable allograft condition (p < 0.02) and those with cyclosporine nephrotoxicity (793.2 +/- 245.2 u/mL, p < 0.01), but returned to a stable level after successful anti-rejection treatment (745.91 +/- 345.8 u/mL, p < 0.01). Acute tubular necrosis and infection also showed a comparable rise in the sIL-2R level. The increase in sIL-2R with rejection was found one to four days earlier than the clinical diagnosis of acute rejection. There was a marked rise in the serum IL-2 level of uremic and post-transplant patients when compared to normal subjects (34.76 +/- 32.16 u/mL and 9.3 +/- 12.7 u/mL vs 4.38 +/- 3.38 u/mL, p < 0.001), but no significant differences were found between the IL-2 level of patients with acute rejection and cyclosporine nephrotoxicity or acute tubular necrosis (3.74 +/- 4.51 u/mL, 1.57 +/- 1.25 u/mL and 6.73 +/- 6.3 u/mL, p > 0.05). The diagnostic value of sIL-2R assay was more meaningful than that of IL-2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Monitoring of serum neopterin in renal transplant recipients.

Postoperative management of kidney allograft recipients requires a reliable and rapid diagnostic method so that proper therapy can be initiated. In this study, we tried to correlate serum neopterin levels with different conditions after transplantation. Serial serum neopterin levels were assessed after operation. Serum neopterin levels of uremic patients were significantly higher than those of healthy persons (239.9 +/- 177.7 nmole/L, n = 33 vs 6.14 +/- 2.78 nmole/L, n = 10, p < 0.001). In recipients with a stable post-transplant course, the serum neopterin level was low. On the contrary, acute rejection episodes were associated with a high level of serum neopterin which declined after successful treatment, although the difference was not significant (96.2 +/- 57.7 nmole/L vs 56 +/- 38.1 nmole/L, p > 0.05). The serum neopterin level was also high in post-transplant acute tubular necrosis (ATN, 256.6 nmole/L), which gradually declined parallel to the resolution of ATN. The neopterin level was low in patients with cyclosporine nephrotoxicity (17.8 +/- 7.6 nmole/L). In summary, the serum neopterin levels were persistently high in uremic and post-transplant ATN patients. Acute rejection episodes were correlated with an increased level of neopterin. It appears that daily measurement of the serum neopterin level may be useful for biochemical detection of immunologic complications in allograft recipients.

Adult↗
PubMed1992

[A SOS induction test screening study for vegetables inhibiting mutagenicity caused by antineoplastic drugs].

Using mutational and anti-mutational synchronous in SOS inductest (+/- S9), We found that 7 out of 11 kinds of commonly eaten vegetables had the ability to inhibit mutagenicity caused by chemical drugs such as Mitomycin C, Bleomycinia, Fluorouracil, Cis-Diaminodichloroplatinum, Arabinosylcytosin and mustargen, They were garlic, green Chinese onion, onion, garlic bulb, tomato, cucumber and water radish. The other 4 lacking this ability were rape, chinese toon, ginger and asparagus lettuce stalk. We believe that our results can be helpful in the preparation. of cancer patients' diet, who are receiving chemotherapy and in the prevention of cancer.

Antimutagenic Agents↗
PubMed1991

Inhibitory effects of curcumin on in vitro lipoxygenase and cyclooxygenase activities in mouse epidermis.

Topical application of curcumin, the yellow pigment in turmeric and curry, strongly inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ornithine decarboxylase activity, DNA synthesis, and tumor promotion in mouse skin (Huang et al., Cancer Res., 48: 5941-5946, 1988). Chlorogenic acid, caffeic acid, and ferulic acid (structurally related dietary compounds) were considerably less active. In the present study, topical application of curcumin markedly inhibited TPA- and arachidonic acid-induced epidermal inflammation (ear edema) in mice, but chlorogenic acid, caffeic acid, and ferulic acid were only weakly active or inactive. The in vitro addition of 3, 10, 30, or 100 microM curcumin to cytosol from homogenates of mouse epidermis inhibited the metabolism of arachidonic acid to 5-hydroxyeicosatetraenoic acid (5-HETE) by 40, 60, 66, or 83%, respectively, and the metabolism of arachidonic acid to 8-HETE was inhibited by 40, 51, 77, or 85%, respectively [IC50 (concentration needed for 50% inhibition) = 5-10 microM]. Chlorogenic acid, caffeic acid, or ferulic acid (100 microM) inhibited the metabolism of arachidonic acid to 5-HETE by 36, 10, or 16%, respectively, and these hydroxylated cinnamic acid derivatives inhibited the metabolism of arachidonic acid to 8-HETE by 37, 20, or 10%, respectively (IC50 greater than 100 microM). The metabolism of arachidonic acid to prostaglandin E2, prostaglandin F2 alpha, and prostaglandin D2 by epidermal microsomes was inhibited approximately 50% by the in vitro addition of 5-10 microM curcumin. Chlorogenic acid, caffeic acid, and ferulic acid (100 microM) were inactive. In vitro rat brain protein kinase C activity was not affected by 50-200 microM curcumin, chlorogenic acid, caffeic acid, or ferulic acid. The inhibitory effects of curcumin, chlorogenic acid, caffeic acid, and ferulic acid on TPA-induced tumor promotion in mouse epidermis parallel their inhibitory effects on TPA-induced epidermal inflammation and epidermal lipoxygenase and cyclooxygenase activities.

Animals↗