Biomedical subjects

Yu-Jen Chen

Publications and source records attributed to Yu-Jen Chen.

At least 19 recordsLinked to original sources

PubMed2007

Genomic and cDNA cloning, characterization of Delonix regia trypsin inhibitor (DrTI) gene, and expression of DrTI in Escherichia coli.

Degenerate primers were designed based on all possible sequences of the N-terminal and C-terminal regions of Delonix regia trypsin inhibitor (DrTI). Five hundred sixty-one bp of polymerase chain reaction (PCR) product was amplified using the above degenerate primers and genomic DNA and cDNA of Delonix regia as a template. The amplified PCR products were cloned and sequenced. DNA sequence analysis of cDNA and genomic clones of DrTI have the same nucleotide sequence in the coding region, and manifested a genomic clone without intervening sequences in the coding region. The amino acid sequence deduced from the DrTI genomic and cDNA clones agreed with that identified via amino acid sequencing analysis, except that two amino acid residues, Ser and Lys, existed between residues Lys141 and Ser142. DrTI open reading frame was then amplified and cloned in-frame with GST in pGEX4T-1 and overexpressed in Escherichia coli to yield a glutathione S-transferase (GST)-fusion protein with a calculated molecular mass of about 45 kDa. The recombinant DrTI (reDrTI) was derived by treating the GST-DrTI fusion protein with thrombin. Both the reDrTI and GST-DrTI fusion protein exhibited a strong identical inhibitory effect on trypsin activity.

Amino Acid Sequence↗

PubMed2006

The influence of estimated creatinine clearance on plasma homocysteine in hypertensive patients with normal serum creatinine.

OBJECTIVES: To examine the relation of estimated creatinine clearance (eCrCl) and plasma total homocysteine (tHcy) in hypertensive patients with a normal serum creatinine level. DESIGN AND METHODS: A total of 137 hypertensive patients (mean age 66.6 years, 69 men) with serum creatinine level </=1.5 mg/dL gave 10-h fasting blood samples for measurement of tHcy, serum folic acid, and serum vitamin B(12). RESULTS: 95 patients fell into a chronic renal insufficiency (CRI) group (eCrCl< or =60 mL/min/1.73 m(2)) and 42 into a normal renal function (NRF) group (eCrCl>60 mL/min/1.73 m(2)). The CRI group was older (p<0.001), had higher tHcy (p<0.001), higher serum urea nitrogen (p<0.001), higher serum creatinine (p<0.001), lower eCrCl (p<0.001), and lower diastolic blood pressure (p=0.001). In univariate analysis, eCrCl had the strongest correlation with tHcy (r=-0.453, p<0.001). Significant correlations, ranging in decreasing order from r=-0.418, p<0.001 to r=-0.170, p=0.047, were also noted between tHcy and twelve other variables. In multivariate analysis, only eCrCl (p<0.001), usage of fibrate (p<0.001), serum level of vitamin B(12) (p=0.002), serum level of folic acid (p=0.009), and smoking (p=0.027) were independent predictors of tHcy. CONCLUSION: eCrCl is a strong independent predictor of tHcy in hypertensive patients with normal serum creatinine.

Aged↗

PubMed2006

Autotomic behavior of the propeptide in propeptide-mediated folding of prosubtilisin E.

The 77 residue propeptide at the N-terminal end of subtilisin E plays an essential role in subtilisin folding as a tailor-made intramolecular chaperone. Upon completion of folding, the propeptide is autoprocessed and removed by subtilisin digestion. This propeptide-mediated protein folding has been used as a paradigm for the study of protein folding. Here, we show by three independent methods, that the propeptide domain and the subtilisin domain show distinctive intrinsic stability that is obligatory for efficient autoprocessing of the propeptide domain. Two tryptophan residues, Trp106 and Trp113, on the surface of subtilisin located on one of the two helices that form the interface between the propeptide and the subtilisin domains play a key role in maintaining the distinctive instability of the propeptide domain, after completion of folding. When either of the Trp residues was substituted with Tyr, the characteristic biphasic heat denaturation profile of two domains unfolding was not observed, resulting in a single transition of denaturation. The results provide evidence that the propeptide not only plays an essential role in subtilisin folding, but upon completion of folding it behaves as an independent domain. Once the propeptide-mediated folding is completed, the propeptide domain is readily eliminated without interference from the subtilisin domain. This "autotomic" behavior of the propeptide may be a prevailing principle in propeptide-mediated protein folding.

Circular Dichroism↗

PubMed2006

Bioconversion of shellfish chitin wastes for the production of Bacillus subtilis W-118 chitinase.

Bacillus subtilis W-118, a strain that produces antifungal materials, excreted a chitinase when cultured in a medium containing shrimp- and crab-shell powder as the major carbon source. This chitinase, purified by sequential chromatography, had a molecular mass of 20,600 Da and a pI of 6. The optimum pH, optimum temperature, and pH stability of the chitinase were pH 6, 37 degrees C, and pH 5-7, respectively. The unique characteristics of the purified chitinase include low molecular mass and acidic pI. In the investigation of the inhibitory activity, it was found that the growth of Fusarium oxysporum was 100% inhibited after incubation for 1 day with sterilized W-118 chitinase solution (5.6 units/mL). The chitinase hydrolyzates of chitin with low degrees of polymerization (DP 1-6) were analyzed by HPLC. Longer reaction times led to the generation of chitin oligosaccharides with lower DP. The chitin oligosaccharides were examined for their inhibitory effects on F. oxysporum and human leukemia cell lines.

Animals↗

PubMed2006

Association of mutant TP53 with alternative lengthening of telomeres and favorable prognosis in glioma.

The molecular basis for alternative lengthening of telomeres (ALT), a prognostic marker for glioma patients, remains unknown. We examined TP53 status in relation to telomere maintenance mechanism (TMM) in 108 patients with glioblastoma multiforme and two patients with anaplastic astrocytoma from New Zealand and United Kingdom. Tumor samples were analyzed with respect to telomerase activity, telomere length, and ALT-associated promyelocytic leukemia nuclear bodies to determine their TMM. TP53 mutation was analyzed by direct sequencing of coding exons 2 to 11. We found an association between TP53 mutation and ALT mechanism and between wild-type TP53 and telomerase and absence of a known TMM (P < 0.0001). We suggest that TP53 deficiency plays a permissive role in the activation of ALT.

Adolescent↗

PubMed2006

Acute glucose overload potentiates nitric oxide production in lipopolysaccharide-stimulated macrophages: the role of purinergic receptor activation.

The positive effects of high glucose on the cellular productivity of nitric oxide (NO), and the mechanisms of the enhancement, were investigated. Macrophages were shifted from normal-glucose medium (5.5 mM) to high-glucose medium (25 mM) and immediately treated with lipopolysaccharide (LPS). Inducible nitric oxide synthase (iNOS) expression was expressed significantly more quickly, and NO production also increased. High-glucose conditions reduced cell viability at 48 h. Pretreatment with oxidized adenosine triphosphate (o-ATP), the selective purinergic receptor antagonist, strongly reduced LPS-induced iNOS expression, NO production and cell death in cells exposed to high levels of glucose. Apyrase, an ATP-hydrolyzing enzyme, also reduced the effects of high-glucose content. High-glucose content promoted the LPS-induced release of endogenous ATP from RAW 264.7 cells, as measured by luciferin-luciferase assay. In summary, the results revealed that purinergic receptor is important in responding to LPS challenge, increasing LPS-induced NO production and cell death under high-glucose conditions, and promoting the release of ATP from macrophages in high-glucose medium.

Adenosine Triphosphate↗

PubMed2006

Rice (Oryza sativa L.) inhibits growth and induces differentiation of human leukemic U937 cells through activation of peripheral blood mononuclear cells.

Rice (Oryza sativa L.) is a staple food worldwide for centuries. In this study, the growth-inhibiting and immunopotentiating effects of commonly used rice were examined. The growth of human leukemic U937 cells was significantly inhibited by the peripheral blood mononuclear cell-conditioned medium (MNC-CM) derived from water extracts of Japonica rice milled Taiwan 9 (MT9) and brown Taiwan 9 (BT9). Furthermore, these MNC-CMs induced differentiation of U937 cells into mature monocytes/macrophages expressing superoxide-producing and phagocytic activity. The amounts of tumor necrosis factor-alpha and interferon-gamma in MNC-CMs prepared with MT9 and BT9 were greater than normal MNC-CM. However, growth of U937 cells was not inhibited by normal MNC-CM or rice extracts alone. The possible active components of MT9 and BT9, other than PHA-like glycoproteins and heat-sensitive proteins and lipopolysaccharides, remain to be determined. Our results demonstrate that MT9 and BT9 can inhibit growth and induce differentiation of leukemic U937 cells through activation of human peripheral blood MNC in vitro. These two types of rice as energy-providing food could be biological response modifiers for augmenting anti-leukemia immunity.

Adjuvants, Immunologic↗

PubMed2006

Role of peripatellar retinaculum in transmission of forces within the extensor mechanism.

BACKGROUND: The role of the peripatellar retinaculum as a frontal plane stabilizer of the patellofemoral joint has been well established. However, as a result of its unique orientation, the retinaculum also may influence the distribution of forces within the extensor mechanism. The objective of this study was to determine the extent to which the peripatellar retinaculum affects the magnitude of forces experienced by the patellar tendon. METHODS: Ten cadaver knees were used in this investigation. Each was mounted on a custom test apparatus that was fixed to an Instron frame. The extensor mechanism was loaded by applying forces through the individual heads of the quadriceps femoris. Patellar tendon tension was measured at 0 degrees , 20 degrees , 40 degrees , and 60 degrees of knee flexion with use of a buckle transducer under two conditions: (1) with the peripatellar retinaculum intact, and (2) with the peripatellar retinaculum removed. Patellar tendon tension was compared between the two conditions across the knee flexion angles. RESULTS: At each knee flexion angle, the patellar tendon tension was greater with the retinaculum removed than it was with the retinaculum intact. However, the difference was significant only at 0 degrees and 60 degrees , at which positions the force transmitted to the patellar tendon was increased by 16.6% and 9.6%, respectively. CONCLUSIONS: The observed increases in patellar tendon tension after removal of the peripatellar retinaculum is an indication of the load-sharing function of that structure as a part of the extensor mechanism. CLINICAL RELEVANCE: Our results suggest that compromise of the peripatellar retinaculum may alter patellar tendon and/or patellofemoral joint forces.

Biomechanical Phenomena↗

PubMed2005

Modulation of monocyte-derived dendritic cell differentiation is associated with ischemic acute renal failure.

BACKGROUND: Dendritic cells (DCs) play a central role in both stimulating and suppressing immune responses and are impacted by surgical injury, exercise, and other physiological stressors. This study aims to determine whether renal ischemia/reperfusion (I/R) injury alters the differentiation, maturation, and activation of DCs from peripheral blood monocytes (PBMo). MATERIALS AND METHODS: Sprague-Dawley (SD) rats were subjected to I/R injury or sham-operated. Creatinine clearance (CCr) was monitored daily during the 14 days of reperfusion that followed the ischemic insult. At 2 and 14 days of reperfusion, the following properties of PBMo derived-DCs were assessed: the amount of generated DCs, surface markers [CD11c, CD80, CD86, and MHC-II (IA)], and functional status including magnitude of mixed lymphocyte reaction (MLR), production of IL-12 p70 by DCs, and production of IFN-gamma and IL-4 by DC-stimulated T cells. RESULTS: CCr was greatly reduced in the injured rats 0 to 4 days after ischemia. Two days after I/R injury to kidney, the numbers of DCs differentiated from PBMo, IL-12 production by DCs, expression of MHC-II (IA), and IFN-gamma production by DC-stimulated T cells were significantly increased in the I/R injured group (compared to the sham-operated group). After 14 days of reperfusion, there was no between-group differences in the numbers of DCs derived from PBMo, MLR, expression of CD80, CD86, and MHC-II (IA), and production of IL-12, IFN-gamma, and IL-4. CONCLUSIONS: The increases seen at 2 days of reperfusion may reflect a preparatory step in the renal I/R injury pathway. The relationship between up-regulation of DC differentiation and ischemic acute renal failure (ARF) remains to be elucidated.

Acute Kidney Injury↗

PubMed2005

The influence of patellofemoral joint contact geometry on the modeling of three dimensional patellofemoral joint forces.

The purpose of this study was to determine the influence of patellofemoral joint contact geometry on the modeling of three-dimensional patellofemoral joint forces. To achieve this goal, patellofemoral joint reaction forces (PFJRFs) that were measured from an in-vitro cadaveric set-up were compared to PFJRFs estimated from a computer model that did not consider patellofemoral joint contact geometry. Ten cadaver knees were used in this study. Each was mounted on a custom jig that was fixed to an Instron frame. Quadriceps muscle loads were accomplished using a pulley system and weights. The force in the patellar ligament was obtained using a buckle transducer. To quantify the magnitude and direction of the PFJRF, a six-axis load cell was incorporated into the femoral fixation system so that a rigid body assumption could be made. PFJRF data were obtained at 0 degrees , 20 degrees , 40 degrees and 60 degrees of knee flexion. Following in vitro testing, SIMM modeling software was used to develop computational models based on the three-dimensional coordinates (Microscribe digitizer) of individual muscle and patellar ligament force vectors obtained from the cadaver knees. The overall magnitude of the PFJRF estimated from the computer generated models closely matched the direct measurements from the in vitro set-up (Pearson's correlation coefficient, R(2)=0.91, p<0.001). Although the computational model accurately estimated the posteriorly directed forces acting on the joint, some discrepancies were noted in the forces acting in the superior and lateral directions. These differences however, were relatively small when expressed as a total of the overall PFJRF magnitude.

Biomechanical Phenomena↗

PubMed2005

Caffeic acid phenethyl ester preferentially sensitizes CT26 colorectal adenocarcinoma to ionizing radiation without affecting bone marrow radioresponse.

PURPOSE: Caffeic acid phenethyl ester (CAPE), a component of propolis, was reported capable of depleting glutathione (GSH). We subsequently examined the radiosensitizing effect of CAPE and its toxicity. METHODS AND MATERIALS: The effects of CAPE on GSH level, GSH metabolism enzyme activities, NF-kappaB activity, and radiosensitivity in mouse CT26 colorectal adenocarcinoma cells were determined. BALB/c mouse with CT26 cells implantation was used as a syngeneic in vivo model for evaluation of treatment and toxicity end points. RESULTS: CAPE entered CT26 cells rapidly and depleted intracellular GSH in CT26 cells, but not in bone marrow cells. Pretreatment with nontoxic doses of CAPE significantly enhanced cell killing by ionizing radiation (IR) with sensitizer enhancement ratios up to 2.2. Pretreatment of CT26 cells with N-acetyl-L-cysteine reversed the GSH depletion activity and partially blocked the radiosensitizing effect of CAPE. CAPE treatment in CT26 cells increased glutathione peroxidase, decreased glutathione reductase, and did not affect glutathione S-transferase or gamma-glutamyl transpeptidase activity. Radiation activated NF-kappaB was reversed by CAPE pretreatment. In vivo study revealed that pretreatment with CAPE before IR resulted in greater inhibition of tumor growth and prolongation of survival in comparison with IR alone. Pretreatment with CAPE neither affected body weights nor produced hepatic, renal, or hematopoietic toxicity. CONCLUSIONS: CAPE sensitizes CT26 colorectal adenocarcinoma to IR, which may be via depleting GSH and inhibiting NF-kappaB activity, without toxicity to bone marrow, liver, and kidney.

Adenocarcinoma↗

PubMed2005

Renal ischemia/reperfusion injury inhibits differentiation of dendritic cells derived from bone marrow monocytes in rats.

Dendritic cells (DCs) are impacted by surgical injury, exercise, and other physiological stressors. This study aims to determine whether renal I/R injury affects 1) the differentiation of myeloid DCs from bone marrow monocytes (BMMos) and the maturation and activation state of these DCs and 2) DC infiltration of kidney. Sprague-Dawley rats were subjected to I/R injury or sham-operated. Creatinine clearance was monitored daily during the 14 d of reperfusion that followed the ischemic insult. At 2 and 14 d of reperfusion, the following were assessed 1) properties of BMMo-derived DCs (i.e., the amount of generated DCs, differentiation state markers [CD11c, CD80, CD86, and Ia], and functional state [MLR and amount of IL-12 produced]), and 2) the presence of DCs in the kidney. Numbers of BMMo-derived DCs were significantly decreased in the I/R injured group (compared with the sham-operated group) at 2 d but not 14 d. A comparison of the their functionality found mixed lymphocyte response [MLR] and IL-12 production were similar in the two groups at both time points. Also, immunohistochemistry showed infiltrating DCs in the outer medulla of the I/R injured kidney at 2 d but not 14 d of reperfusion. Thus, I/R stress reduces the number of DCs differentiated from BMMos but not the functional activity of these DCs. This decrease may reflect a stress-induced downshift in the capacity of BMMos to differentiate into DCs and a parallel upshift in the capacity of DCs to infiltrate the kidney.

Animals↗

PubMed2005

Platonin modulates differentiation and maturation of human monocyte-derived dendritic cells.

Platonin is a photosensitizer with NF-kappaB inhibitory activity that activates macrophages and suppresses lymphocyte response. In this study, we tested the effect of platonin on differentiation and maturation of human myeloid dendritic cells (DC) from CD14+ monocytes. Triggering of DC differentiation by GM-CSF and IL-4 resulted in typical immature DCs that were further stimulated to maturation by combination of cytokines. When platonin (2 to 50 ng/mL) was added to the culture, the resulting DCs had thicker and blunter protruding projections, lower CD83 expression, greater CD80 expression, and less stimulatory activity on allogeneic naive CD4+CD45RA+ T cells in terms of their proliferation and interferon-gamma production. This suggests that platonin redirects DC differentiation toward an intermediate stage of maturation, whereby the DCs have uniquely enhanced expression of CD80 which may confer some degree of immune tolerance.

Cell Count↗

PubMed2005

Esophagectomy for locally advanced esophageal cancer, followed by chemoradiotherapy and adjuvant chemotherapy.

AIM: To compare the efficacy and toxicity of a three-step combination therapy with post-operative radiation alone for locally advanced esophageal cancer. METHODS: Patients with T3-4 and N0-1 esophageal carcinoma from a number of institutions were non-randomly, prospectively enrolled in the study. All patients underwent single-stage curative en bloc esophagectomy. The patients were then assigned into one of two treatment groups based on treatment consisting of either post-operative concurrent chemoradiotherapy (CCRT) with weekly cisplatin 30 mg/m2 followed by systemic adjuvant chemotherapy (four monthly cycles of cisplatin 20 mg/m2 and 5-fluorouracil 1 000 mg/m2 for five consecutive days), or, post-operative radiation alone. The radiotherapy dose was 55-60 Gy for all patients. Primary end-point of this study was to assess the per-protocol patients' improvement of overall survival benefit. Secondary end-point was designed to evaluate both the per-protocol and intent-to-treat patients' outcome of survival. RESULTS: A total of 60 patients (n = 30 per group) were enrolled in this study. The two groups were generally comparable for demographic characteristics and hematological and non-hematological toxicities. The CCRT with weekly cisplatin was well tolerated, with significantly better overall survival (30.9 mo vs 20.7 mo; 95% CI, 27.5-36.4 vs 15.2-26.1) and 3-year survival (70.0% vs 33.7%; P = 0.003). Low histological grade of tumor (P<0.001) was associated with favorable survival in these locally advanced patients. CONCLUSION: For locally advanced esophageal cancer, the combination of esophagectomy, post-operative CCRT with weekly cisplatin and systemic adjuvant chemotherapy is well tolerated and effective. A large-scale, prospective randomized trial of this regimen is in progress.

Aged↗

PubMed2005

Etoposide sensitizes CT26 colorectal adenocarcinoma to radiation therapy in BALB/c mice.

AIM: To investigate the combined effect of etoposide and radiation on CT26 colorectal adenocarcinoma implanted into BALB/c mice. METHODS: We evaluated the radiosensitizing effect of etoposide on CT26 colorectal adenocarcinoma in a syngeneic animal model. BALB/c mice were subcutaneously implanted with CT26 cells and divided into four groups: control (intra-peritoneal salineX2) group, etoposide (5 mg/kg intra-peritoneallyX2) group, radiation therapy (RT 5 GyX2 fractions) group, and combination therapy with etoposide (5 mg/kg intra-peritoneally 1 h before radiation) group. RESULTS: Tumor growth was significantly inhibited by RT and combination therapy. The effect of combination therapy was better than that of RT. No significant changes were noted in body weight, plasma alanine aminotransferase, or creatinine in any group. The leukocyte count significantly but transiently decreased in the RT and combination therapy groups, but not in the etoposide and control groups. There was no skin change or hair loss in the RT and combination therapy groups. CONCLUSION: Etoposide can sensitize CT26 colorectal adenocarcinoma in BALB/c mice to RT without significant toxicity.

Adenocarcinoma↗

PubMed2005

Involvement of protein kinase C in the inhibition of lipopolysaccharide-induced nitric oxide production by thapsigargin in RAW 264.7 macrophages.

This study explored the effects of inhibition of endoplasmic reticulum (ER) Ca(2+)-ATPase on lipopolysaccharide (LPS)-induced protein kinase C (PKC) activation, nuclear factor-kappaB (NF-kappaB) translocation, inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) production in RAW 264.7 macrophages. Thapsigargin (TG) irreversibly inhibits ER Ca(2+)-ATPase and LPS-induced NO production is reduced even after washout. TG also attenuated LPS-stimulated iNOS expression by using immunoblot analysis. However, another distinct fully reversible ER Ca(2+)-ATPase inhibitor, 2,5-di-tert-butylhydroquinone (DBHQ), ionophore A23187 and ionomycin could exert a similar effect to TG in increasing intracellular calcium concentration; however, these agents could not mimic TG in reducing iNOS expression and NO production. LPS increased PKC-alpha and -beta activation, and TG pretreatment attenuated LPS-stimulated PKC activation. Not did pretreatment with DBHQ, A23187 and ionomycin reduce LPS-stimulated PKC activation. Furthermore, NF-kappaB-specific DNA-protein-binding activity in the nuclear extracts was enhanced by treatment with LPS, and TG pretreatment attenuated LPS-stimulated NF-kappaB activation. None of DBHQ, A23187 and ionomycin pretreatment reduced LPS-stimulated NF-kappaB activation. These data suggest that persistent inhibition of ER Ca(2+)-ATPase by TG would influence calcium release from ER Ca2+ pools that was stimulated by the LPS activated signal processes, and might be the main mechanism for attenuating PKC and NF-kappaB activation that induces iNOS expression and NO production.

Animals↗

PubMed2005

Colchicine sensitizes human hepatocellular carcinoma cells to damages caused by radiation.

AIM: We studied the effect of colchicine combined with radiation on the survival of human hepatocellular carcinoma (HCC) HA22T/VGH cells. METHODS: Twenty-four hours after treatment with 0-8 ng/mL colchicine, HA22T/VGH cells were irradiated at various doses (0, 1, 2, 4, and 8 Gy). Colony assay was performed to assess the surviving cell fraction. Survival curves were fitted by using a linear-quadratic model to estimate the sensitizer enhancement ratio (SER). Flow cytometry was used for cell cycle analysis. RESULTS: Colchicine at lower concentrations (1 and 2 ng/mL) had obvious synergy with radiation to inhibit HCC cell growth, whereas higher concentrations (4 and 8 ng/mL) had only additive effect to radiation. Pretreatment with 1 and 2 ng/mL colchicine for 24-h enhanced cell killing by radiation with SERs of 1.21 and 1.53, respectively. G(2)/M arrest was only observed with higher colchicine doses (8 and 16 ng/mL) after 24-h treatment; this effect was neither seen with lower doses (1, 2, and 4 ng/mL) nor with any dose after only 1 h of treatment. CONCLUSION: Our results suggest that colchicine has potential as an adjunct to radiotherapy for HCC treatment. Lower doses of colchicine possess radiosensitizing effects via some mechanism other than G(2)/M arrest. Further study is necessary to elucidate the mechanism.

Carcinoma, Hepatocellular↗

PubMed2005

Change of plasma transforming growth factor-beta1 levels in nasopharyngeal carcinoma patients treated with concurrent chemo-radiotherapy.

OBJECTIVE: Our aim was to study the correlation between plasma transforming growth factor (TGF)-beta1 level and radiation-induced mucositis and dermatitis in nasopharyngeal carcinoma (NPC) patients. METHODS: Blood samples obtained from patients treated with concurrent chemo-radiotherapy (CCRT) were divided into two groups according to the pre-treatment plasma TGF-beta1 level (> or =7.5 ng/ml as group 1 and < 7.5 ng/ml as group 2). Enzyme-linked immunosorbent assay (ELISA) was used for the measurement of the TGF-beta1 level. Radiation toxicity was evaluated according to Radiation Treatment Oncology Group criteria. Data were analyzed by the generalized estimation equation method. RESULTS: TGF-beta1 levels of group 1 patients were decreased significantly (P = 0.002) at the end of the treatment. The rate of decrease was 0.12 ng/ml per fraction (P = 0.02). The average TGF-beta1 level in patients who suffered acute radiation morbidity (grade > or =2) was significantly higher (P = 0.0057) than that of those who suffered less (grade < 2). CONCLUSION: A lower pre-treatment plasma TGF-beta1 level and the grade of radiation toxicity both appeared to contribute to the elevated plasma TGF-beta1 after CCRT.

Antineoplastic Agents↗