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Biomedical subjects

D Yin

Publications and source records attributed to D Yin.

At least 109 records · Page 6Linked to original sources
PubMed1996

Biochemical basis of lipofuscin, ceroid, and age pigment-like fluorophores.

Serious studies of the formation mechanisms of age-related pigments and their possible cellular influence have been hampered for a long time by discrepancies and controversies over the definition, fluorescence emission, origin, and composition of these pigments. This review discusses several critical controversies in this field and lay special emphasis on the cellular and biochemical reactions related to the formation mechanisms of lipofuscin, ceroid, advanced glycation end-products (AGEs), and age pigment like fluorophores (APFs). Various amino compounds and their reaction with secondary aldehydic products of oxygen free radical-induced oxidation, particularly lipid peroxidation, are important sources of the fluorophores of ceroid/lipofuscin, which progressively accumulate as a result of phagocytosis and autophagocytosis of modified biomaterials within secondary lysosomes of postmitotic and other cells. Lipofuscin is the classical age pigment of postmitotic cells, while ceroid accumulates due to pathologic and experimental processes. There are good reasons to consider both ceroid and lipofuscin as materials of the same principal origin. The age-related intracellular fluorophores of retinal pigment epithelium (RPE) seems to represent a special class of lipofuscin, which partly contains derivatives of retinoids and carotenoids. Saccharide-originated fluorophores, principally AGEs formed during glycation/Maillard reactions, may be mainly responsible for the extracellular fluorescence of long-lived proteins, such as collagen, elastin, and lens crystalline. Although lipofuscin, ceroid, AGEs, and APFs can be produced from different types of biological materials due to different side reactions of essential biology, the crosslinking of carbonyl-amino compounds is recognized as a common process during their formation.

Aging↗
PubMed1996

Porcine somatotrophin differentially down-regulates expression of the GLUT4 and fatty acid synthase genes in pig adipose tissue.

The present study was conducted to determine whether porcine somatotropin (pST) differentially regulates expression of the GLUT4 and fatty acid synthase (FAS) genes in pig adipose tissue. Three different experiments were conducted in which pigs were treated daily with different doses of pST for different time periods (7 or 14 d and from 60 to 90 kg of body wt). In these experiments, pST significantly and consistently decreased FAS mRNA levels (80%, 66% and 85%, respectively); however, GLUT4 mRNA was not affected by pST in two of the three experiments, and in the one showing an effect (Experiment 2), the decrease was less than observed for FAS (44%). Because of these results, we conducted subsequent experiments to see if the effects of pST on glucose metabolism in cultured pig adipose tissue (48 h) differed when glucose concentrations were changed from 1 to 5 mmol/L. These studies revealed that the antagonistic effect of pST on insulin action was more potent when glucose transport was saturated (5 mmol/L) than when glucose concentration limited glucose entry into the cell (1 mmol/L). In summary, these results suggest that the effects of pST on glucose transport in pig adipocytes are secondary to changes elicited by the hormone on intracellular glucose use for lipogenesis. When considered in the context of the decrease previously observed in glucose transport in pig adipocytes, the findings reported herein suggest that pST acts to decrease GLUT4 protein activity and/or distribution between the plasma membrane and the intracellular pool with little alteration in GLUT4 gene expression or total cell GLUT4 protein.

Actins↗
PubMed1996

Involvement of interleukin-1 beta-converting enzyme in apoptosis of bFGF-deprived murine aortic endothelial cells.

Apoptosis (programmed cell death) is an essential physiological process that is genetically regulated and contributes to the balance between cell growth, differentiation, and the maintenance of normal cells. Recent studies show that deprivation of growth factor induces apoptosis in endothelial cells. However, the molecular mechanisms regulating apoptosis remain unclear. In this study, we demonstrate that deprivation of basic fibroblast growth factor (bFGF) increased the expression of interleukin-1 beta-converting enzyme (ICE) protein, and subsequently induced apoptosis in murine aortic endothelial (MAE) cells. In contrast, the proteins of the tumor suppressor p53 and c-myc were undetected during apoptosis. This apoptosis was suppressed by the tetrapeptide ICE inhibitor, Ac-YVAD-CMK. Overexpression of murine ICE, in addition, induced apoptosis in MAE cells using gene transfer techniques. These results strongly suggest that ICE may mediate apoptosis in bFGF-deprived endothelial cells, and the suppression of ICE function could represent a novel approach for the protection of endothelial cells from damages.-Kondo, S., Kondo, Y., Yin, D., Barnett, G. H., Kaakaji, R., Peterson, J. W., Morimura, T., Kubo, H., Takeuchi, J., Barna, B. P. Involvement of interleukin-1 beta converting enzyme in apoptosis of bFGF-deprived murine aortic endothelial cells.

Animals↗
PubMed1996

Cost analysis and the practicing radiologist/manager: an introduction to managerial accounting.

Cost analysis is inherently one of the most tedious tasks falling on the shoulders of any manager. In today's world, whether in a service business such as radiology or medicine or in a product line such as car manufacturing, accurate cost analysis is critical to all aspects of management: marketing, competitive strategy, quality control, human resource management, accounting (financial), and operations management, to name but a few. This is a topic that we will explore with the intention of giving the radiologist/manager the understanding and the basic skills to use cost analysis efficiently, making sure that major financial decisions are being made with adequate cost information, and showing that cost accounting is really managerial accounting in that it pays little attention to the bottom line of financial statements but places much more emphasis on equipping managers with the information to determine budgets, prices, salaries, and incentives and influences capital budgeting decisions through an understanding of product profitability rather than firm profitability.

Accounting↗
PubMed1996

Strategy for repeat biopsy of patients with prostatic intraepithelial neoplasia detected by prostate needle biopsy.

PURPOSE: We evaluated the strategy for repeat biopsy of patients with prostatic intraepithelial neoplasia without concurrent carcinoma detected on prostate needle biopsy. MATERIALS AND METHODS: Of 1,275 consecutive patients undergoing prostate needle biopsy 61 were identified with prostatic intraepithelial neoplasia but without concurrent prostate carcinoma. Of the 61 patients 53 had undergone repeat biopsy. The medical records, transrectal ultrasound, and operative and pathological reports of these patients were reviewed. RESULTS: Repeat biopsy was done in 53 patients with prostatic intraepithelial neoplasia, yielding carcinoma in 15, prostatic intraepithelial neoplasia without carcinoma in 8 and benign tissue in 30. The yield of carcinoma from repeat biopsy of a prostatic intraepithelial neoplasia site was 8.3% (7 of 84 sites). A total of 18 sites of carcinoma was detected by repeat biopsy of a previous random biopsy site (8), a prostatic intraepithelial neoplasia site only (5), a transrectal ultrasound nodule (3), a palpable nodule and prostatic intraepithelial neoplasia site (1), and a transrectal ultrasound nodule and prostatic intraepithelial neoplasia site (1). Carcinoma was as frequently detected by repeat biopsy of a prostatic intraepithelial neoplasia site (6 patients) as by random repeat biopsy (6 patients). CONCLUSIONS: Repeat prostate needle biopsy of patients with prostatic intraepithelial neoplasia should include random repeat biopsy and repeat biopsy of transrectal ultrasound abnormalities as well as previous sites of prostatic intraepithelial neoplasia.

Adenocarcinoma↗
PubMed1996

[Effects of recombinant human tumor necrosis factor on the development of ascitic tumor and expression of c-erbB2 in the nude mouse models of ovarian cancer].

OBJECTIVE: To investigate the effects of recombinant human tumor necrosis factor (rhTNF) on the growth of ascitic tumor and expression of c-erbB2 in the nude mouse models of ovarian cancer. METHODS: By intraabdominal injection, rhTNF was delivered to the peritoneal cavity of nude mouse with ovarian cancer as well as control group, after 6 days treatment, tumor cell counting and expression of c-erbB2 were detected by indirect fluorescence flow cytometry. RESULTS: There is a significant difference in tumor cell counting between the study group and control group (P < 0.01). Expression of c-erbB2 in study group was lower than that in control group. CONCLUSION: rhTNF was demonstrated to have effects on both inhibition of ascitis tumor development and down regulation of c-erbB2 expression in nude mouse with ovarian cancer.

Animals↗
PubMed1995

Induction of tolerance to heart allografts in high responder rats by combining anti-CD4 with CTLA4Ig.

It has been difficult to induce donor-specific transplantation tolerance in high responder Lewis rats. Results presented below demonstrate that amounts of pretransplant anti-CD4 sufficient to allow allograft tolerance in low responder strains (5 mg/kg x 4 days) did not prevent the acute rejection of ACI heart allografts in high responder Lewis recipients. Higher doses of pretransplant anti-CD4 (10 mg/kg, 15 mg/kg, and 20 mg/kg) given alone could delay but not prevent allograft rejection. Pretransplant anti-CD4 combined with anti-CD8, thymectomy, and total lymphoid irradiation all failed to produce tolerance to ACI heart allografts. However, a regimen of anti-CD4 combined with CTLA4Ig allowed indefinite survival of ACI heart allografts (mean survival time, > 100 day). Second-donor matched heart grafts were permanently accepted, and third-party heart grafts were permanently accepted, and third-party heart allografts were rejected by the tolerant recipients. These results suggest a new combination therapeutic strategy for clinical transplantation.

Abatacept↗
PubMed1995

Test-tube simulated lipofuscinogenesis. Effect of oxidative stress on autophagocytotic degradation.

Cysteine-stimulated oxidation of a rat liver lysosomal-mitochondrial fraction (LMF) was studied. The process would simulate oxidative stress-related events during the degradation of autophagocytosed material within secondary lysosomes, which may contribute to the formation of lipofuscin or age pigment. Millimolar concentration of cysteine was needed to stimulate LMF lipid peroxidation, measured as thiobarbituric acid reactive substances (TBARS). The amount of endogenous LMF iron was 545 micrograms/l and was enough to initiate peroxidation, probably through the reduction of ferric to ferrous iron by cysteine with induction of Fenton chemistry. Peroxidation could be completely inhibited by the addition of the iron chelator desferal or the antioxidant BHT. A substantial amount of the formed TBARS was associated with trichloroacetic acid (TCA) precipitable proteins. Elevated protein carbonyls was observed 1-2 h after the increase of TBARS. The tryptophan-tyrosine related protein autofluorescence (280/335 nm) decreased sharply during the first few hours of incubation. In contrast, a lipofuscin-type autofluorescence (345/430 nm) appeared only after a few days, suggesting that the latter fluorophore is not an immediate product of protein oxidation. The sequential formation of TBARS, protein carbonyls and lipofuscin-type autofluorescence as well as their dependence on iron and reducing agent add further support to the concept that lipofuscin forms in secondary lysosomes as a result of iron-catalyzed oxidative reactions involving autophagocytosed materials.

Animals↗
PubMed1995

CD4-positive suppressor cells block allotransplant rejection.

Mechanisms of maintenance of transplantation tolerance induced in adult rats by depletive regimens of anti-CD4 before transplantation of vascularized heart allografts were studied. Despite the fact that there has been little evidence that tolerant lymphocytes could prevent allograft rejection after adoptive transfer, we demonstrated a suppressive role for lymphocytes from tolerant animals in vivo. These experiments analyzed the ability of lymphocytes from tolerant rats to protect passenger leukocyte-depleted Lewis heart grafts that had been "parked" in ACI rats (treated with pretransplant anti-CD4 and maintained for > 100 days) compared with their ability to protect transplantation of fresh Lewis heart grafts in naive ACI rats. Although parked Lewis heart grafts were rejected in unmanipulated ACI recipients, parked hearts (but not naive Lewis heart allografts), were permanently accepted by naive ACI rats when syngeneic tolerant spleen cells were adoptively transferred at the time of transplantation. Further, we demonstrated that the suppressor cells in the tolerant spleen cells were CD4+. These results suggest that CD4+ spleen cells from tolerant rats inhibit allograft recognition and may maintain allograft tolerance by blocking the indirect pathway of allorecognition.

Animals↗
PubMed1995

Tissue-specific effects of anti-CD4 therapy in induction of allograft unresponsiveness in high and low responder rats.

In these experiments, we studied the role of anti-CD4 (Ox38) monoclonal antibody in the prevention of heart and/or kidney allograft rejection in low (ACI) and high (Lewis) responder rats. In low responder ACI rats, donor-specific tolerance for heart and kidney allografts (individually or in combination) was achieved by pretransplant anti-CD4 therapy. In high responder Lewis rats, anti-CD4 therapy alone (or combined with anti-CD8 (Ox8), thymectomy or total lymphoid irradiation) did not prevent first-set rejection of heart allografts. This difference was correlated with a more profound and longer lasting CD4+ cell depletion in the low responder strain. Anti-CD4 treatment, however, produced tolerance of kidney transplants in high responder rats. Additionally, anti-CD4 treatment induced tolerance to heart (as well as kidney) allografts in Lewis recipients of combined kidney and heart allografts from ACI. The effects of anti-CD4 treatment thus depend upon the recipient responder status as well as the organs transplanted and the order of transplantation.

Animals↗
PubMed1995

Combination therapy with cisplatin and nifedipine induces apoptosis in cisplatin-sensitive and cisplatin-resistant human glioblastoma cells.

We attempted to determine whether calcium channel blockers (CCBs) enhance the anti-tumour activity of cis-diamminedichloroplatinum (cisplatin) against both cisplatin-sensitive human glioblastoma U87 MG cells and cisplatin-resistant U87-MG-CR cells, the latter of which we developed for resistance to cisplatin. Nifedipine, a dihydropyridine class CCB, significantly enhanced the anti-tumour effect of cisplatin on these two cell types in vitro and in vivo. Our findings also indicated that, in the absence of normal extracellular Ca2+ nifedipine was capable of enhancing the cytotoxicity of cisplatin. In addition, this anti-tumour activity was partially inhibited by actinomycin D and cycloheximide, suggesting that it is possibly dependent upon new RNA and protein synthesis. Interestingly, ultrastructural analysis, DNA fragmentation assay and cell cycle analysis demonstrated that synergism between cisplatin and nifedipine results in apoptosis (programmed cell death) at a relatively low concentration of cisplatin, which when tested alone did not induce apoptosis. Furthermore, we demonstrated that nuclei from these cells lack a Ca(2+)-dependent endonuclease that degrade chromatin in the linker region between nucleosomes. In conclusion, our studies suggest that the non-cytotoxic agent nifedipine is able to synergistically enhance the anti-tumour effects of cisplatin on U87-MG and U87-MG-CR cells lacking a Ca(2+)-dependent endonuclease and subsequently to induce apoptosis via interaction of nifedipine with an as yet uncharacterised functional site other than a calcium channel on target cells.

Animals↗
PubMed1995

Cost-effectiveness of MR angiography in cases of limb-threatening peripheral vascular disease.

PURPOSE: To evaluate the cost-effectiveness of magnetic resonance (MR) angiography in the preoperative planning of treatment in patients with limb-threatening peripheral vascular disease (PVD). MATERIALS AND METHODS: A decision model was developed to study the effects of MR angiography on the outcome and cost of treatment. The authors calculated the incremental cost per quality-adjusted life-years gained (ie, cost-effectiveness ratio) when conventional angiography was replaced or supplemented with MR angiography. Previously reported data regarding the accuracies of MR and conventional angiography were used in the analysis. RESULTS: The cost-effectiveness ratio of MR angiography ranged from negative (cost-reducing) values to $78,000. For the base case in which the sensitivity and specificity of MR angiography for the evaluation of inflow vessels were 92% and 88% and those of conventional angiography were 97% and 97%, respectively, the cost-effectiveness ratio was $25,895. CONCLUSION: MR angiography may be a cost-effective alternative to conventional angiography in patients with limb-threatening PVD if its accuracy for the inflow evaluation reaches certain thresholds. Further prospective investigation is warranted.

Angiography↗
PubMed1995

Studies on age pigments evolving into a new theory of biological aging.

A variety of age pigment-like fluorophores have been recognized, identified and investigated during the past three decades. They are mainly the end-products of various side-reactions of essential biological processes. Among these, the lipid peroxidation-related fluorophores formed via aldehyde-protein crosslinking are of general importance. Fluorescent advanced glycation end-products formed during glycation/Maillard reactions, are oxygen independent, carbohydrate-associated age pigment-like substances. Age pigments, particularly those identified in retinal pigment epithelium, represent another type of age pigment that originates from polyenic biomolecules, including retinoids and carotenoids. Various alpha beta-unsaturated aldehydes can also react with the amino groups of nucleotides to induce biological alteration. Although age pigments can be produced from different types of biological materials, the crosslinking of carbonyl and amino compounds is a common toxiferous process during biological life. In the context of various aging phenomena and degenerative diseases, this process may constitute an essential mechanism of aging--the carbonyl toxification process of biological aging.

Aging↗
PubMed1995

Tumor necrosis factor-alpha induces p53-dependent apoptosis in rat glioma cells.

In this study, we demonstrated that tumor necrosis factor (TNF)-alpha inhibited the viability of rat glioma (C6) cells and induced apoptosis but did not affect the viability of rat newborn brain, mainly astroglial cells. The antitumor activity of TNF-alpha against C6 cells was partially inhibited by actinomycin D and cycloheximide, suggesting that it is possibly dependent upon new ribonucleic acid and protein synthesis. The results of immunoblotting assay demonstrated that TNF-alpha decreased the expression of mutant p53 protein but induced the expression of wild-type p53 in C6 cells during apoptosis. We suggest that TNF-alpha may activate the function of wild-type p53 protein by the suppression of mutant p53, at least indirectly, and induce p53-dependent apoptosis in glioma cells.

Animals↗
PubMed1995

Hepatic enhancement during helical CT: a comparison of moderate rate uniphasic and biphasic contrast injection protocols.

OBJECTIVE: The purpose of this study was to compare the degree and timing of peak hepatic enhancement, optimal scanning intervals, and optimal delay times of moderate-rate uniphasic and biphasic contrast material injection protocols for hepatic helical CT. MATERIALS AND METHODS: One hundred fifty patients were randomized into three injection protocols, receiving 42.3 g iodine (150 ml iothalamate meglumine) delivered using 3 ml/sec uniphasic, 2 ml/sec uniphasic, or biphasic (3 ml/sec [50 ml], 1 ml/sec [100 ml]) technique. Statistically fitted aortic and hepatic enhancement curves were generated from dynamic incremental CT data for each patient. Protocols were compared by maximum hepatic enhancement, and contrast enhancement indices were modeled for a 38-sec helical acquisition. RESULTS: The 3 ml/sec and 2 ml/sec uniphasic protocols produced higher peak hepatic enhancement (64 +/- 15 H and 62 +/- 15 H [mean +/- 1 SD]) than the 3 ml/sec biphasic protocol (52 +/- 10 H; p < .001). Contrast enhancement indices for the 3 ml/sec uniphasic and 2 ml/sec uniphasic protocols (385 +/- 398 H/sec and 397 +/- 412 H/sec) were significantly greater than the index for the 3 ml/sec biphasic protocol (123 +/- 194 H/sec; p < .0001) at a 50-H threshold. Optimal scan delay times were 50 +/- 8, 75 +/- 7, and 119 +/- 8 sec, respectively, for the 3 ml/sec uniphasic, 2 ml/sec uniphasic, and 3 ml/sec biphasic techniques. CONCLUSION: The moderate-rate uniphasic injections studied provided greater hepatic enhancement throughout the helical acquisition without requiring the prohibitively long delay time necessitated by the moderate-rate biphasic injection. These findings differ from prior results that showed that a uniphasic injection may provide comparable levels of hepatic enhancement when compared with a high-flow-rate biphasic injection.

Adult↗