Effects of Methyl Cellulose and Soybean Protein Isolate Coating on Amount of Oil and Chemical Hazards in Chinese Fried Dough Cake.

ABSTRACT: Fat-related diseases and chemical hazards produced during the frying process pose a major threat to human health. Coatings have been used as a practical method to reduce the amount of oil and chemical hazards associated with fried foods. Methyl cellulose (MC) and soy protein isolate were used as coating materials to pretreat Chinese fried dough cake (CFDC) before frying. The 1.5% MC concentration was the best choice for coating to simultaneously lower oil and chemical hazards in CFDC. The CFDC prepared using 1.5% MC had 11.3% oil, 73.70 µg/kg acrylamide, 0.15 mg KOH/100 kg acid, 8.54 mmol/kg peroxide, p-anisidine value of 6.36, 0.36 µg/g malondialdehyde, 0.13 µg/g 4-hydroxy-2-(E)-hexenal (HHE), 0.51 µg/g 4-hydroxy-2-(E)-nonenal (HNE), and 4,272 µg/kg glycidyl ester. In contrast, the uncoated CFDC had 19.2% oil, 117.55 µg/kg acrylamide, 0.25 mg KOH/100 kg acid, 14.40 mmol/kg peroxide, p-anisidine value of 9.76, 0.63 µg/g malondialdehyde, 0.23 µg/g HHE, 0.86 µg/g HNE, and 5,758 µg/kg glycidyl ester. MC and soy protein isolate enhanced the oil barrier of the coating film, which effectively reduced the heat transfer coefficients, oil transfer, oil oxidation, and chemical hazards in the CFDC. Our work on this edible coating contributes to methods for control of oil and chemical hazards in fried foods.

Human Kaposi's sarcoma cell-mediated tumorigenesis in human immunodeficiency type 1 tat-expressing transgenic mice.

BACKGROUND: The human immunodeficiency virus type 1 (HIV-1) transactivator (Tat) protein has been linked to the development and course of Kaposi's sarcoma (KS) associated with acquired immunodeficiency disease syndrome (AIDS-KS). Tat is an 86-101 amino-acid protein encoded by two exons. To evaluate the growth-promoting effects of Tat in AIDS-KS in vivo, we developed transgenic mice expressing the one-exon-encoded 72 amino-acid protein (Tat(72)) and the two-exon-encoded 86 amino-acid protein (Tat(86)). METHODS: Human KS SLK cells were injected subcutaneously into CD4(+) T-cell-depleted male mice, and the tumors that formed after 3-4 weeks were recovered and analyzed for the expression of Tat protein(s), different cytokine messenger RNAs (mRNAs), and matrix metalloproteinases (MMPs). All statistical tests were two-sided. RESULTS: The average tumor weight was maximum in Tat(86) mice ( approximately 600 mg) compared with Tat(72) ( approximately 200 mg) and nontransgenic ( approximately 100 mg) mice (P<.005). Histologic examination of tumors showed spindle-shaped SLK cells with prominent infiltrates of inflammatory cells. All of the tumors from Tat mice expressed abundant Tat mRNA, suggesting that the infiltrating mouse cells actively expressed Tat. A comparison of the growth-promoting cytokines in the tumors from Tat(86)-transgenic and nontransgenic mice showed that the expression of the following cytokines was substantially increased in the tumors of the Tat(86) mice: tumor necrosis factor-alpha, interleukin 6, interleukin 8, granulocyte-macrophage colony-stimulating factor, and basic fibroblast growth factor. Furthermore, these tumors showed abundant expression of a 105-kd MMP activity associated with infiltrates of host leukocytes in the lesions. CONCLUSION: Our in vivo data clearly suggest that extracellular Tat can contribute to the growth and tumorigenesis of human KS cells.

[Prolactin secretion in patients with endometriosis and its relationship to luteal phase defect and infertility].

UNLABELLED: Serum prolactin (PRL) levels and PRL response to TRH stimulation were studied in 49 patients with endometriosis (EM) during mid-luteal phase. Eight cases with other gyn-diseases and 14 normal fertile women served as controls. Their luteal function were also estimated by three serum progesterone(P) measurements during the luteal phase and endometrial dating in the late luteal phase. RESULTS: The incidence of hyperprolactinemia in EM group (32.7%), and in EM with primary infertility group (61.5%) was significantly higher than that in normal controls (7.1%) (P < 0.05). However, the PRL secretory capacity was not positively correlated to the severity of EM. There was no difference in serum P levels between EM and two control groups. But delayed endometrial maturation was shown in 6 EM infertile cases suggesting luteal phase defect, an incidence of 27.3% (6/22) in EM group or 42.9% (6/14) in EM infertile group. Five out of the six were hyperprolactinemic and had no other identified causes of infertility. These data implied that hyperprolactinemia may impair the luteal function causing infertility in EM patients.