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Biomedical subjects

D Yu

Publications and source records attributed to D Yu.

At least 181 records · Page 10Linked to original sources
PubMed1998

[The chemical constituents of Goniothalamus howii Merr].

Two new compounds were isolated from the chloroform soluble fraction of ethanolic extract of bark of Goniothalamus howii Merr. On the basis of their chemical properties and spectral data (MS, UV, IR, 1H and 13CNMR) they were identified as 6S (1R-hydroxy-2R-cinnamyloxyphenethyl) 5, 6-dihydro-5S-hydroxy-2-pyrone named Howiinol A and 6S-(1S, 2R-epoxyphenethyl-5S-cinnamyloxy) 5, 6-dihydro-2-pyrone named Howiinin A. Howiinol A showed significant antitumor activities toward human tumor cell in vitro and in vivo and less toxic.

Animals↗
PubMed1998

[Pharmacokinetic profile of naftopidil in rats].

Naftopidil(Naf), a novel antihypertensive drug, was determined by HPLC-UV method. The plasma concentration and pharmacokinetics of naftopidil have been investigated in rats after single oral doses of 10, 20 and 30 mg.kg-1. The drug was found to conform to a two-compartment model. Tp was in the range of 0.42 h to 0.90 h. T1/2 beta was 7.08 h after the 10 mg.kg-1 dose, 4.78 h after the 20 mg.kg-1 dose and 5.83 h after the 30 mg.kg-1 dose. The Cmax, AUC and CL/F appeared to be dose dependent at the doses not higher than 20 mg.kg-1. Naf was found in many tissues after a single oral dose of 20 mg.kg-1. The top level tissues were intestine, liver and lung at 15 minutes after administration, while the utero-ovarian tissue was the highest at 6 h. Naf can be extensively metabolized since the total excretion of the parent compound in urine and faeces was less than 1% of the dose. From 82% to 97% of Naf in plasma was shown to be bound to protein.

Animals↗
PubMed1998

[Characteristic of vibration spectra for hydration state of herring sperm DNA fibers].

By different temperature treatment, the herring sperm DNA fibers at various relative humidity have been analyzed using Raman scattering spectroscopic method for estimation of bound water content in fiber according to the typical peak intensity ratio between deoxyribosyl C-H stretching vibration (at 2964cm(-1)) and bound water O-H stretching vibration (at 3204cm(-1)). We found the bound water content of the fibers to be 9-14 water molecules per nucleotide pair (i.e. base pair) at variance with the calculated value of calf thymus DNA fiber by Tao's Raman test formula, but in similarity to the determined value by IR spectroscopy, X-ray diffraction, BET gravimetric analysis and differential scanning calorimetry analysis. Thus, herring sperm DNA fibers should have the same hydration state as both calf thymus DNA and salmon sperm DNA, that has been confirmed with the new formula: 2.5926 x I2964/I3204.

Animals↗
PubMed1998

Infrequent mutation of the p16/MTS1 gene and overexpression of cyclin-dependent kinase 4 in human primary soft-tissue sarcoma.

The pl6INK4a/MTS1 (p16) gene encodes a specific inhibitor of cyclin-dependent kinase (CDK)4 and CDK6. The p16 gene is frequently mutated or deleted in many types of cancer cell lines as well as in certain types of primary tumors. p16 knockout mice are viable but predisposed to sarcoma and B-cell lymphoma. To investigate the role of p16 in human soft-tissue sarcoma tumor progression, we examined the p16 gene by Southern blot analysis and PCR sequencing in 30 pairs of primary soft-tissue sarcomas and autologous normal tissue. Only one tumor sample showed possible rearrangement of the p16 gene. In contrast, Western blot analysis of the p16 protein in 20 pairs of samples showed decreased p16 expression in only 20% of the tumors but elevated p16 expression in 40% of the tumors when compared with the autologous normal controls. Overexpression of p16 was not concomitant with loss of the RB protein as is found in several other types of cancers, because more than one-half of the tumors with increased p16 expression also had high levels of RB protein. On the other hand, the p16 target protein CDK4 was overexpressed in at least 60% of the tumors. In the majority of cases, CDK4 overexpression accompanied elevated p16 and/or RB levels. Our results suggest that: (a) alteration of the p16 gene is infrequent in primary soft-tissue sarcoma; (b) Cdk4 may act as an oncogene in soft-tissue sarcoma; and (c) elevated p16 and RB levels might be the result of compensatory up-regulation of these proteins to counteract CDK4 overexpression in these tumors. Our results also suggest that it is more informative to examine aberrations in the "p16-CDK4/cyclin D-RB" pathway than to selectively examine individual components in this pathway when investigating genetic changes involved in human malignancy.

Animals↗
PubMed1998

Telomerase activity of sarcoma cell lines and fibroblasts is independent of p53 status.

Telomerase activity is necessary for the stabilization of telomeres, which function to overcome cellular senescence and are linked to unlimited cell proliferation. Activation of telomerase is characteristic of immortalized cell lines and most tumors. The p53 gene has been implicated as a crucial barrier to unlimited cell proliferation, and its absence has been shown to allow direct immortalization of cells by certain oncogenes. The p53 gene may have an additional function of signaling cell growth arrest in response to telomere shortening, which occurs with repeated cellular divisions and ultimately threatens chromosomal stability. This prompted us to consider whether the enzyme telomerase, responsible for adding new telomeres to chromosomal ends, may be affected by the p53 status of normal and malignant cells. We investigated whether a relationship between telomerase and p53 could be demonstrated in a human sarcoma cell line containing a missense p53 mutation and several stable transfectants that express the wild-type p53 gene or a temperature-sensitive mutant of p53. All cell lines had readily detectable telomerase activity regardless of p53 status. In addition, murine fibroblast cell strains established from tissues of p53+/+ and p53-/- (p53 knockout) mice expressed telomerase regardless of the p53 status of their tissue of origin. Levels of telomerase subunit mRNA (hEST2) were comparable among cell lines and tissues with different p53 status. These results imply that p53 status is not associated with telomerase activity per se and that activation of telomerase can occur either in cells completely devoid of p53 or in cells that have functional p53.

Animals↗
PubMed1998

Wild-type p53 and a p53 temperature-sensitive mutant suppress human soft tissue sarcoma by enhancing cell cycle control.

Soft-tissue sarcomas are a heterogeneous group of tumors that are putatively mesenchymal in origin. Therapeutic advances in this disease have been limited over the past several decades. Approximately one-half of all patients will ultimately succumb, usually to uncontrollable pulmonary metastases. Although little is known about the underlying molecular determinants driving soft-tissue sarcoma inception, proliferation, and metastasis, mutation of the p53 gene is the most frequently detected molecular alteration in this disease. Accordingly, we were interested in determining whether transduction of wild-type (wt) p53 into soft-tissue sarcomas bearing mutated p53 genes might alter the malignant phenotype. SKLMS-1 is a human-derived leiomyosarcoma cell line with a codon 245 p53 point mutation. Cationic liposome was used to transfect wt p53 or 143Ala temperature-sensitive mutant p53 into this cell line. SKLMS-1 stable transfectants expressing wt p53 had decreased cell proliferation in vitro, decreased in vitro colony formation in soft agar, and decreased tumorigenicity in severe combined immunodeficient mice in vivo. Flow cytometric analysis of cell cycle components demonstrated markedly increased G1 cell cycle arrest and decreased entry into S phase, which corresponded to the induction of p21cip1 protein in the transfectants. Using SKLMS-1 stable transfectants expressing the 143Ala p53 temperature-sensitive mutant, we demonstrated the kinetics of and the causal relationship between wt p53 expression, the wt p53-dependent induction of cell cycle inhibitor p21cip1, and inhibition of cell cycle progression in p53-transfected SKLMS-1 cells. The ability to restore wt p53 growth-regulatory functions in soft-tissue sarcoma may ultimately be useful as a future therapy in patients with soft-tissue sarcomas.

Animals↗
PubMed1997

Cross-reactivity of C219 anti-p170(mdr-1) antibody with p185(c-erbB2) in breast cancer cells: cautions on evaluating p170(mdr-1)

BACKGROUND: Increased expression of the multidrug resistance gene (MDR-1)-encoded P-glycoprotein (p170[mdr-1]) is a major cause of tumor cell multidrug resistance. p170(mdr-1) functions as a drug-efflux pump to reduce the cellular accumulation of specific drugs. MDA-MB-435 human breast cancer cells that have been transfected with oncogene c-erbB2 complementary DNA (435.eb cells) express high levels of the transmembrane glycoprotein p185(c-erbB2) and exhibit increased resistance to the chemotherapeutic agent paclitaxel via p170(mdr-1)-independent mechanisms. We have recently discovered that the widely used monoclonal antibody C219, which is specific for p170(mdr-1), may cross-react with p185(c-erbB2) in 435.eb cells. In this study, we have investigated the nature of this cross-reactivity. METHODS: Immunoprecipitation experiments involving the use of breast cancer cells that express different levels of p185(c-erbB2) were performed, and C219 was used for western blot analysis of immunoprecipitated proteins. Immunohistochemical analyses were performed on acetone-fixed slides of human breast cancer cells. Peptide sequence comparisons and enzyme-linked immunosorbent assays were performed to determine the molecular basis of C219 cross-reactivity with p185(c-erbB2). RESULTS: The cross-reactivity of C219 with p185(c-erbB2) was demonstrated by both western blot and immunohistochemical analyses. Peptide sequence comparisons revealed that C219 recognizes an epitope in p170(mdr-1) (C219 epitope) that shares sequence homology with p185(c-erbB2). Enzyme-linked immunosorbent assays demonstrated that C219 recognizes synthetic peptides derived from both the C219 epitope in p170(mdr-1) and the C219 epitope-homologous region in p185(c-erbB2). CONCLUSIONS: The anti-p170(mdr-1) monoclonal antibody C219 cross-reacts with p185(c-erbB2) through a peptide sequence in p185(c-erbB2) that is homologous to the C219 epitope in p170(mdr-1).

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1997

Sensing homology at the strand-swapping step in lambda excisive recombination.

lambda Site-specific recombination requires a short stretch of sequence homology that might be sensed during strand swapping, during ligation and/or during isomerization of the obligate Holliday junction intermediate. Here, we use half-att site suicide substrates to study single and double top-strand-transfers, isolated from the subsequent steps of the reaction. The double-strand-transfer is analogous to a top-strand exchange and consists of one normal top-strand and one "contrary" bottom-strand to top-strand ligation between the half-att site substrate and its full-site partner. The resulting covalent three-way DNA junctions are poor substrates for resolution in the forward or reverse direction. We show that both the rate and the efficiency of Y-junction formation are homology dependent. Pairing of three nucleotides (either in the forward or in the contrary alignment) provides maximal stability to strand swapping. Complementary base-pairing next to one top-strand site (with or without ligation) stimulates strand-transfer at the other mismatched site. The data suggest that homology can be sensed at the strand-swapping step before ligation. However, homology also stimulates ligation and stabilizes the products, as is evident from the different rates of closed Y-junction formation in the presence or absence of homology. Furthermore, under recombination conditions, single top-strand-transfers are subject to reversal even in the presence of sequence homology; stability depends on a double-strand-transfer, i.e. dissociation of covalent Int.

Bacterial Proteins↗
PubMed1997

Chemosensitization of HER-2/neu-overexpressing human breast cancer cells to paclitaxel (Taxol) by adenovirus type 5 E1A.

Breast cancer cells that overexpress HER-2/neu are more resistant to chemotherapeutic agents such as paclitaxel (Taxol) and docetaxel (Taxotere) than those that do not overexpress HER-2/neu. In previous work, we showed that the adenovirus type 5 E1A can repress HER-2/neu expression at the transcriptional level. Here we first demonstrated that paclitaxel sensitivity correlates with HER-2/neu expression level in a panel of mouse fibroblasts expressing different levels of HER-2/ neu, and that downregulation of HER-2/neu expression by E1A sensitizes the cells to paclitaxel. To further test whether E1A can sensitize HER-2/neu-overexpressing human breast cancer cells to paclitaxel through E1A-mediated HER-2/neu repression, an adenoviral vector was used to transfer the E1A gene into two human breast cancer cell lines, MDA-MB-453 and MDA-MB-361, that overexpress HER-2/neu. After E1A delivery, we observed that HER-2/neu expression level was reduced, and cells were treated with paclitaxel. Cell proliferation assays showed a synergistic growth inhibition effect of E1A and paclitaxel. The synergistic effect was also confirmed by soft agar colony-formation assay. Breast cancer cell lines that express low levels of HER-2/neu, MDA-MB-435 and MDA-MB-231 cells showed no synergistic growth inhibition effect when treated on the same protocols. Thus, we concluded that the adenovirus type 5 E1A gene can sensitize paclitaxel-resistant HER-2/neu-overexpressing breast cancer cells to the drug by repressing HER-2/neu expression. This in turn may have important implications for the development of a novel therapy that combines chemotherapy and gene therapy.

Adenovirus E1A Proteins↗
PubMed1997

Influence of luminal hepatocyte growth factor on small intestine mucosa in vivo.

In 1984, a growth factor was identified that stimulated hepatocyte DNA synthesis. This growth factor, referred to as hepatocyte growth factor (HGF), has been shown to enhance growth of intestinal epithelial cells in vitro. Recently, we reported that HGF can increase absorption and intestinal mass when given systemically in an in vivo model. This study was designed to examine if luminally administrated HGF can stimulate intestinal epithelial cell mass and function. Twenty-five young adult Sprague-Dawley rats had catheters inserted into the small intestine and connected to subcutaneously placed osmotic minipumps. The rats were divided into five groups (n = 5 for each group) based on the contents in the osmotic pump: group 1 received normal saline (control); groups 2, 3, 4, and 5 received HGF in increasing doses of 30, 75, 150, and 300 microg/kg/day, respectively. Following a 14-day infusion, [14C]galactose and [14C]glycine absorption was measured in 10-cm segments of mid-small intestine using an in vivo closed-recirculation technique. Mucosal DNA content and protein content of the same small bowel segment were determined for each group. HGF significantly increased galactose absorption at doses of 75 (P < 0.01) and 150 (P < 0.05) microg/kg/day and glycine absorption at doses of 30 (P < 0.05) and 75 (P < 0.01) microg/kg/day. HGF significantly increased DNA content (P < 0.01) at each dose and protein content when given at 30 (P < 0.01) and 75 (P < 0.01) microg/kg/ day. These data demonstrate that luminal administration of HGF can increase intestinal epithelial cell mass and function in vivo. HGF may be clinically useful in patients with inadequate intestinal function.

Animals↗
PubMed1997

Mapping of adenovirus 5 E1A domains responsible for suppression of neu-mediated transformation via transcriptional repression of neu.

Overexpression of neu (also known as c-erbB-2 or HER-2) commonly occurs in human cancer and is also known to enchance tumor metastasis and chemoresistance. Our earlier reports showed that the adenovirus 5 E1A can suppresss the neu-mediated transformation by repression of neu. Thus, E1A has the potential to be used as a therapeutic agent against the neu-overexpressing human cancers. However, a serious concern to this approach is that E1A is also capable of immortalizing primary culture cells and can co-operate with ras or E1B oncogenes to transform them. The E1A CR2 domain (amino acid residues 120 to 140) necessary for binding to RB is believed to be required for this oncogenic function. Here, we report that deletion of CR2 region did not affect E1A's capability to repress neu. Interestingly, deletion of the amino acid residues 4 to 25 or 40 to 80 completely disrupted E1A-mediated neu repression. By deleting the amino acid residues from 81 to 185, we have successfully generated a mini-E1A mutant that was sufficient to inhibit neu promoter activity and suppress neu-mediated transformation. The mini-E1A mutant does not contain the CR2 domain that is crucial for RB binding and immortalization, and hence, may serve as a more selective tumor suppressor, and a safer therapeutic agent. It may also be a useful tool to further investigate the molecular mechanism(s) of neu overexpression and E1A-mediated transcriptional repression in cancer cells.

3T3 Cells↗
PubMed1997

Overexpression of the c-erbB-2 gene enhanced intrinsic metastasis potential in human breast cancer cells without increasing their transformation abilities.

Overexpression of the c-erbB-2 gene-encoded p185 has been reported in approximately 30% of human breast cancers and has been correlated with lymph node metastasis and poor prognosis in breast cancer patients. To investigate whether overexpression of p185 can enhance the metastatic potential of human breast cancer cells, we have introduced the human c-erbB-2 gene into the very low p185-expressing MDA-MB-435 human breast cancer cells and established 435.eB transfectants that express higher levels of p185. In this study, we compared the metastatic phenotypes of the parental MDA-MB-435 cells and the 435.eB transfectants. In vivo experimental metastasis assays in which we injected MDA-MB-435 parental cells or 435.eB transfectants into the tail veins of ICR-SCID mice demonstrated that mice injected with p185-overexpressing 435.eB transfectants formed significantly more metastatic tumors than the mice injected with parental and control cells. The changes in experimental metastatic potential in vivo were accompanied by increased invasiveness in vitro. In addition, the secretion of basement membrane-degradative enzymes, which is an important step in the invasion and metastasis process, was also increased in the p185-overexpressing 435.eB transfectants. These results indicated that p185 overexpression can enhance the metastatic potential of MDA-MB-435 human breast cancer cells. To investigate whether enhanced metastatic potential in the p185-overexpressing 435.eB transfectants was the result of increased cancer cell growth and transformation potential, we compared the growth rate, anchorage-independent growth ability, and tumorigenicity of the 435.eB transfectants with that of the parental cells. The transfectants and the parental cells all had similar growth rates and anchorage-independent growth abilities and demonstrated similar tumorigenic potential. These findings suggest that c-erbB-2 is a metastasis-promoting gene for breast cancers that is distinct from other tumor-promoting genes in that the c-erbB-2 gene can enhance the intrinsic metastatic potentials of MDA-MB-435 cells without increasing their transformation abilities.

Animals↗
PubMed1997

Domain-directed polymerase chain reaction capable of distinguishing bacterial from host DNA at the single-cell level: characterization of a systematic method to investigate putative bacterial infection in idiopathic disease.

The use of a broad-range PCR to target conserved sequences in the bacterial ribosome has long been recognized as an approach to investigating idiopathic human diseases for the presence of bacteria. An important example is rheumatoid arthritis where the hypothesis of a bacterial etiology remains viable despite failure of previous methods to identify a causative organism. Practical implementation of this strategy, however, was impeded by requirements unique to the study of these diseases. Hence, an adequately characterized method for achieving this has not appeared. We now describe such a method based on the use of a broadly reactive pair of deoxyinosine-containing primers. Detailed characterization addressing these requirements provided evidence that DNA from at least 96% of potential prokaryotic pathogens would be detected. The sensitivity was shown to approximate that of a single organism per reaction. Importantly, this sensitivity was shown to be maintained among multiple targets and to be unimpaired by a large excess of human DNA. Similar results were obtained with extracts of inflamed human synovial fluid to which as little as 0.01 pg of bacterial DNA or, alternately, a single organism per reaction was added. This method was also shown correctly to detect the causative bacteria in clinically infected synovial fluids, further documenting its applicability to such specimens. Finally, it was converted to an in situ method by which bacterial sequences were histochemically localized to Michaelis-Guttman bodies in tissue sections from a patient with malakoplakia, a poorly understood infectious disease. The broad reactivity and high sensitivity achieved by this approach translate into a high likelihood of detecting an unknown bacterium if present in a clinical specimen. Conversely, if properly controlled, the failure of this method to detect such organisms can provide evidence supporting rejection of the bacterial etiology hypothesis, an important aspect unique to this approach. For those bacterial sequences that are detected, the ability to localize them in situ would help define their histologic context and hence facilitate their pathogenetic interpretation. The present method should therefore be appropriate for use in systematically studying rheumatoid arthritis as well as a number of other important idiopathic disorders where a bacterial etiology is suspect.

Bacterial Infections↗
PubMed1997

Soluble oligonucleosomal complexes in synovial fluid from inflamed joints.

OBJECTIVE: To determine whether soluble oligonucleosomal DNA, typical of that released during apoptotic cell death, is present in synovial fluids from inflamed joints and, if so, whether it is present in sufficient concentrations to have pathophysiologic significance. METHODS: Fifty synovial fluid specimens from 46 patients were studied, 41 from joints with a variety of inflammatory disorders and 9 from osteoarthritic joints. DNA from freshly collected synovial fluid was isolated and quantitated by microfluorometry, and the oligonucleosomal fraction was measured by radiolabeling, gel electrophoresis, and autoradiography. Specific immunoprecipitation with monoclonal antihistone antibody, after DNA radiolabeling in whole synovial fluid, was used to detect histone binding. RESULTS: DNA with a typical oligonucleosomal ladder was observed in most specimens. The mean +/- SD oligonucleosomal DNA concentration was 14.1 +/- 18.5 microg/ml in synovial fluids from inflamed joints, considerably higher than that in osteoarthritic synovial fluids. Additionally, the DNA was shown to be complexed with histone, as would be expected. Control experiments were performed to show that the oligonucleosomal DNA was present in soluble form and did not arise due to in vitro artifact. The DNA concentrations were found to correlate significantly with the concentrations of synovial fluid leukocytes, most of which were neutrophils. CONCLUSION: Synovial fluids from inflamed joints contain oligonucleosomal DNA typical of that released during apoptotic cell death. The probable source is fluid-phase neutrophils undergoing apoptotic cell death, although this was not directly demonstrated. The concentrations are sufficient to have biologic activity similar to that shown in vitro, including lymphoproliferation and stimulation of interleukin-6 secretion. A mechanism by which oligonucleosomal DNA may contribute to perpetuation of rheumatoid synovitis is proposed. If it is generalizable to other sites of inflammation, as seems probable, similar oligonucleosomal DNA release accompanying inflammation may play a pathogenetic role in other disorders, including systemic lupus erythematosus.

DNA↗
PubMed1997

Hepatocyte growth factor enhances intestinal mucosal cell function and mass in vivo.

Hepatocyte growth factor (HGF), originally known to stimulate hepatocyte DNA synthesis, recently has been shown to enhance growth of intestinal epithelial cells in vitro. However, there have been no studies on the effect of HGF on the function of intestinal epithelial cells in vivo. This study was designed to examine the effect of systemically administrated HGF on intestinal epithelial cell mass and function. Twenty young adult male Sprague-Dawley rats underwent placement of jugular venous catheters connected to subcutaneously placed osmotic minipumps. The rats were divided into four groups based on the contents in the osmotic pump: Group 1 (control, n = 5), normal saline; Group 2 (n = 5), HGF 75 microg/kg/d; Group 3 (n = 5), HGF 150 microg/kg/d; and Group 4 (n = 5), HGF 300 microg/kg/d. After a 14 day infusion, [C14] galactose and [C14] glycine absorption were measured in a 10-cm segment of mid small intestine using an in vivo closed-recirculation technique. Mucosal DNA content and protein content of the same small bowel segment were determined for each group. With all three doses, HGF significantly increased DNA content (P < .01) and protein content (P < .05). HGF also significantly increased galactose absorption (P < .01) with all three doses. Glycine absorption was increased with a dose of 75 (P < .05) and 150 microg/kg/d (P < .01), but not at a dose of 300 microg/kg/d. These data demonstrate that HGF can increase intestinal epithelial cell mass and function in vivo. HGF may be clinically useful in patients with short bowel syndrome.

Animals↗
PubMed1997

Growth factor enhancement of intestinal function: dramatic response but lack of synergism.

BACKGROUND/PURPOSE: The authors have shown that gastrin and epidermal growth factor (EGF) exert a trophic effect on intestinal epithelial cells. Because these peptides may have different mechanisms by which they stimulate these cells, this study was designed to determine the effect of gastrin and EGF on the intestinal epithelial cell and to evaluate their potential synergistic effect. METHODS: Twenty young adult male Sprague-Dawley rats underwent placement of jugular venous catheters that were connected to subcutaneously placed osmotic minipumps. The rats were divided into four groups based on the content of the osmotic pump: Group 1, saline (control, n = 5); Group 2, EGF at 150 microg/kg/d (n = 5); Group 3, gastrin at 13.5 nmol/kg/d (n = 5); and Group 4, EGF at 150 microg/kg/d plus gastrin at 13.5 nmol/kg/d (n = 5). After a 14-day intravenous infusion, [C14] galactose and [C14] glycine absorption (pmol/cm2 intestine), mucosal DNA content (microg/mg mucosa), and protein content (microg/mg mucosa) were measured in the small intestine of each rat. RESULTS: The galactose absorption, glycine absorption, DNA content, and protein content were significantly increased by EGF (69%, 28%, 64%, and 55%, respectively) and gastrin (72%, 60%, 93%, and 48%, respectively) when compared with control. Combining EGF and gastrin also significantly increased these parameters (61%, 44%, 96%, and 70%, respectively) when compared with control. However, these data demonstrate no further enhancement than the effect of each peptide alone. CONCLUSION: EGF and gastrin individually may be useful for patients who have inadequate intestinal function, but when combined did not exert a synergistic benefit.

Analysis of Variance↗