Dunna, Nageswara Rao;Vure, Sugunakar;Sailaja, K.;Surekha, D.;Raghunadharao, D.;Rajappa, Senthil;Vishnupriya, S.
Asian Pacific Journal of Cancer Prevention
/
v.13
no.1
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pp.347-350
/
2012
TP53 is the mostly commonly mutated gene in many cancers and the P53 tumor suppressor protein is involved in multiple cellular processes, including transcription, DNA repair, genomic stability, senescence, cell cycle control and apoptosis. A common single nucleotide polymorphism located within the proline rich region of TP53 gene at codon 72 in exon 4 encodes either proline or arginine. TP53 Arg 72 is more active than TP53 Pro 72 in inducing apoptosis. The aim of this study was to understand the association of the 72 codon polymorphism with acute leukemia development and prognosis. A total of 288 acute leukemia cases comprising 147 acute lymphocytic leukemia (ALL) and 141 acute myeloid leukemia (AML), as well as 245 controls were recruited for analysis of the TP53 72 polymorphism using PCR-RFLP method. Significant association of homozygous arginine genotype with AML was observed (${\chi}^2$- 133.53; df-2, p < 0.001. When data were analyzed with respect to clinical variables, elevation in mean WBC, blast %, LDH levels and slight reduction in DFS in ALL cases with the arginine genotype was observed. In contrast, AML patients with Pro/Pro had elevated WBC, Blast%, LDH levels with slightly reduced DFS. Our study indicates that Arg/Arg genotype might confer increased risk to development of acute myeloid leukemia.
Journal of Physiology & Pathology in Korean Medicine
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v.17
no.1
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pp.157-164
/
2003
Cervi Parvum Cornu(CPC) is that the young horn of deer family and has been traditionally used as a medicine in Eastern. The purpose of present study was to investigate the effects of CPC on cell cycle progression and its molecular mechanism in human periodontal ligament cells (HPOLC). In cell proliferation assay, 1 ng/ml, 10 ng/ml, 100 ng/ml, 1 ㎍/ml and 10 ㎍/ml of CPC were used, all treatment groups increased the cell growth. Maximal cell proliferation was observed in cells exposed to 100 ng/ml of CPC at 4 day, and 10 ng/ml and 100 ng/ml of CPC at 6 days. S phase was increased and G1 phase was decreased in the group treated with 100 ng/ml of CPC in cell cycle analysis. The protein levels of cyclin D1 were not changed, but the levels of cyclin E, cdk 2, cdk 4 and cdk 6 were increased. The protein levels of p21, pRb were decreased as compared to that of control group, but the levels of p53 was not changed in the cells both treated with CPC Md untreated. These results suggested that CPC increases the cell proliferation and cell cycle progression in HPDLC, which is linked to an increased cellular levels of cyclin E, cdk 2, cdk 4 and cdk 6, and decreased the levels of p53, p21.
Journal of the Korea Organic Resources Recycling Association
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v.6
no.1
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pp.43-52
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1998
The objective of this study is to investigate the optimum conditions of extracting collagen without chrome ion from the leather waste. The effect of temperature, pH, and the concentration of alkaline solution on the collagen extraction has been studied. The result indicated that the incipient denatured temperature of collagen measured by viscosity was $25^{\circ}C$ and the complete denatured temperature was $31.5^{\circ}C$. The optimum solubilization condition for temperature was between $15^{\circ}C$ and $20^{\circ}C$, pH was 1.5, the concentration of alkaline solution was 3% of sodium hydroxide. The almost complete chrome ion separation was possible around the pH of 1.5. The separation efficiency of chrome ion from tannery waste was more than 99.5%. Extraction efficiency of crude protein from leather waste was about 89.5%. The hydroxyproline and collagen content in the extracted crude protein were 8.53% and 63.62%, respectively.
Purpose: An underlying factor for the failure of several clinical trials of anti-epidermal growth factor receptor (EGFR) therapies is the lack of an effective method to identify patients who overexpress EGFR protein. The quantitative dot blot method (QDB) was used to measure EGFR protein levels objectively, absolutely, and quantitatively. Its feasibility was evaluated for the prognosis of overall survival (OS) of patients with gastric cancer. Materials and Methods: Slices of 2×5 ㎛ from formalin-fixed paraffin-embedded gastric cancer specimens were used to extract total tissue lysates for QDB measurement. Absolutely quantitated EGFR protein levels were used for the Kaplan-Meier OS analysis. Results: EGFR protein levels ranged from 0 to 772.6 pmol/g (n=246) for all gastric cancer patients. A poor correlation was observed between quantitated EGFR levels and immunohistochemistry scores with ρ=0.024 and P=0.717 in Spearman's correlation analysis. EGFR was identified as an independent negative prognostic biomarker for gastric cancer patients only through absolute quantitation, with a hazard ratio of 1.92 (95% confidence interval, 1.05-3.53; P=0.034) in multivariate Cox regression OS analysis. A cutoff of 208 pmol/g was proposed to stratify patients with a 3-year survival probability of 44% for patients with EGFR levels above the cutoff versus 68% for those below the cutoff based on Kaplan-Meier OS analysis (log rank test, P=0.002). Conclusions: A QDB-based assay was developed for gastric cancer specimens to measure EGFR protein levels absolutely, quantitatively, and objectively. This assay should facilitate clinical trials aimed at evaluation of anti-EGFR therapies retrospectively and prospectively for gastric cancer.
An experiment was carried out to assess the effect of feeding concentrate mixtures varying in bypass protein levels with urea-treated or untreated grass on the performance of twelve Red Kandhari calves (14 months of age and 78.15 kg body weight) for a period of 75 days. Dry grass was treated with 4 percent urea solution and ensiled for 30 days. The CP ($N{\times}6.25$) content in urea treated grass increased from 3.96 to 8.89 percent. Two iso-caloric and iso-nitrogenous concentrate mixtures (CM-I and CM-II) varying in RDP to UDP ratio viz., 65:35 and 55.45 were prepared. The calves in control group ($T_1$) were fed concentrate mixture-I with ad libitum untreated dry grass and those in experimental group ($T_2$) were fed concentrate mixture-II with ad libitum urea treated dry grass. The dry matter consumption in group $T_2$ was significantly (p<0.01) higher as compared to group $T_1$. The total DMI in $T_1$ and $T_2$ was 146.92 and 166.95 kg respectively, whereas the DMI per day and per 100 kg body weight was 1.94 and 2.22 and 1.90 and 2.35 kg, respectively. The average total gain in body weight (kg) and average daily gain (g) of calves in $T_2$ was significantly (p<0.01) higher as compared to those in $T_1$ the values being 28.66, 18.33 and 382.16, 244.44, respectively. Feed efficiency in terms of kg DM per kg gain in body weight was significantly (p<0.01) lower in group $T_1$ than in $T_2$. The cost of feed per kg gain in body weight for $T_2$ and $T_1$ group was Rs. 21.14, 28.22, respectively. The digestibility coefficients of DM, CP, EE, CF, NFE, NDF and ADF were 59.60, 57.50, 53.00, 65.04, 45.82, 48.48, 52.48 and 55.73 for $T_1$ group. The coressponding values were 68.78, 67.80, 59.83, 71.41, 49.93, 53.37 and 57.81, respectively for $T_2$ group. The digestibility coefficients for all the proximate principles in $T_2$ were significantly (p<0.01) higher as compared to $T_1$. However, NDF and ADF digestibilities were not significantly different. Nutritive value determined in terms of DCP and TDN for The experimental ration was significantly (p<0.01) higher than control ration, the values being 7.32 and 47.34 and 9.39 and 52.40% respectively. The blood urea nitrogen levels at 0, 3 and 6 h interval after feeding were significantly (p<0.01) lower in calves fed experiment ration as compared to control. The overall results indicated that in Red Kandhari calves an optimum growth can be economically achieved by feeding 4 percent urea treated dry and mature grass as basal roughage supplemented with a concentrate mixture containing 20 percent CP, 70% TDN and 45% UDP/bypass protein.
Defatted soybean, larvae of brown mealworm (Tenebrio molitor), and powdered pupae of silkworm (Bombyx mori) were fermented in solid and liquid forms using Aspergillus oryzae and Bacillus subtilis. The protein degradation rate (NDR) through solid fermentation was the highest in the fermented soybean control sample (54.69±6.54%), followed by silkworm pupae (34.82±5.99%) and brown mealworm larvae (30.54±3.80%). When these edible insects were fermented in liquid form, solid extraction yield was 37.73-46.88%, and protein yield was 47.47-63.02%. NDR of fermented liquid form products increased to 58.90, 52.62, and 50.13% for soybean, brown mealworm larvae, and silkworm pupae, respectively. SDS-PAGE of the liquid fermented products confirmed that microbial fermentation decomposed higher-molecular-weight proteins into small polypeptides. In vitro digestibility of liquid forms of edible insects increased by 1.26 to 1.53 times after fermentation. The protein solubility, foaming ability, and foam stability of liquid-fermented edible insects all tended to increase through fermentation.
Korean Lentinus edodes SR-1 was cultured to multiply the mycelia in the complete broth medium (C/N=13.1) for mushroom, and protein-bound polysaccharides were extracted from the cultured broth containing mycelia (The whole cultured broth was used to increase the yields: 80% of protein-bound polysaccharides were existed at the cell wall of mycelia and 20% of those were secreted extracellularily in this culture). Protein-bound polysaccharides in the cultured broth containing mycelia were extracted by using three different methods: 1) Extraction with hot water, 2) Disintegration of cell wall by glass bead mill treatment before extraction with hot water, and 3) Cellulase treatment before extraction with hot water. The highest yield was obtained (930 mg polysaccharides/100 mL culture broth) when protein-bound polysaccharides were extracted with 2) method. The extracted crude protein-bound polysaccharides were purified using protease, DEAE-cellulose and Sephadex G-100. The growth inhibition activity for $P_{388}$, mouse leukemic cell, increased (53.7, 62.2, 93.7% and 97.4%) as the purification level increased. Protein-bound polysaccharides contained 46.1% of polysaccharides, 7.3% of protein, and trace amounts of minerals. Polysaccharides contained glucose, galactose, xylose and mannose. The content of proline and glycine were high, however, methionine and leucine were not found. The major minerals were Na, K, Zn, and Ca.
Jin, Hye Young;Kang, Kyoung In;Kim, Sun Young;Youn, You Sook;Kang, Joon Won;Jo, Deog Yeon;Kwon, Kye Chul;Park, Kyung Duk
Clinical and Experimental Pediatrics
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v.51
no.1
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pp.73-77
/
2008
Purpose : p16 gene, mapped to the 9p21 chromosomal region, has emerged as a candidate tumor suppressor gene in human neoplasm. It is an inhibitor of cyclin-dependent kinase and inhibits Rb phosphorylation. In a variety of tumors including childhood acute lymphoblastic leukemia (ALL), deletion and/or mutation of the p16 gene has been found. Despite their high frequency, the prognostic importance of p16 alterations is still controversial in ALL and has been reported to be either unfavorable or similar to that of other patients. We studied the correlation between loss of p16 protein confirmed by immunohistochemical staining and clinical outcomes of patients diagnosed as ALL. Methods : We performed an immunohistochemical staining for p16 protein in 74 cases of bone marrow biopsy slide initially diagnosed as ALL between January 1998 and December 2006. We reviewed the clinical manifestations, laboratory findings, treatment outcomes retrospectively. Results : Of 74 slides, 12 were negative for p16 protein. Seven were males and 5 were females with a median age at diagnosis was 5.8 (1.3-18.8) years. Initial WBC were 17,225 $(500-403,300)/{\mu}L$. By immunologic surface marker analysis, 7 patients were early pre-B CALLA (+) and 5 patients were T-cell ALL. Two patients of intermediate risk group had relapsed and died. Three patients had family history of breast cancer. Four patients died and overall survival rates were $53.5{\pm}18.7%$. Conclusion : Loss of p16 protein is supposed to be an independent risk factor of childhood ALL associated with poor outcomes. In clinical setting, the clinician must take into account p16 status, not only at the genomic but also at the protein level. Further clinical experience on thoroughly investigated cases will help a better understanding between p16 status and clinical outcomes.
This study was designed to investigate the effects of Ca and/or vitamin D supplementation for 53 weeks on bone metabolism in postmenopausal women. The subjects were healthy 18 women aged from 59 to 69 years old. They were divided into three groups : placebo, Ca(1000mg/day) supplementation and Ca(1000mg/day) with vitamin D(12.5$\mu\textrm{g}$/day) supplementation. During the experimental periods except for metabolic studies, the subjects ate their usual diets and the use of drugs as well as excessive exercise was prohibited. Metabolic studies were conducted in the 1st week and in the 53rd week of the experimental periods. The subjects ate experimental diets which consisted of 1787.3kcal, 69.6g of protein, 561.5mg of Ca and 1078.6mg of P daily during both of the metabolic study periods. The results were summarized as follows; 1) Bone density of the second lumbar spine and trochanter measured after treatment decreased significantly in control group as compared with pre-experimental level(p<0.05). On the contrary, bone density of femoral neck and Ward's triangle in Ca group and the second lumbar spine in Ca.Vit D group increased significantly after treatment. 2) Serum PTH and calcitonin levels did not show any significant differences among groups before and after treatment. But serum PTH level increased significantly in all groups after treatment(P<0.05). 3) Serum Ca and P levels did not show any significant differences among groups before and after treatment. But serum Ca level increased significantly in all groups after treatment (P<0.05) and serum P level decreased significantly in Ca.Vit D group after treatment(P<0.05). 4) Mean 24-hours fecal Ca excretion of Ca group was the highest in the 1st week of treatment(P<0.01), and that of control group was the lowest in the 53rd week of treatment(P<0.01). Fecal Ca excretion increased significantly in control and Ca.Vit D group in the 53rd week of treatment(P<0.05). Urinary Ca excretion did not show any significant differences among groups in the 1st and 53rd week of treatment, but that of Ca.Vit D group was the highest the 1st week of treatment(P<0.01). In the 53rd week of treatment Ca and Ca.Vit D group showed positive Ca balance, but control group showed negative Ca balance. The above results showed that it will be difficult to prevent degenerative bone loss without Ca and/or vitamin D supplementation in postmenopausal women eating Korean usual diets.
Aminoacyl tRNA synthetase complex interacting multifunctional protein 2 (AIMP2) is a scaffolding protein required for the assembly of multi-tRNA synthetase, and it can exert pro-apoptotic activity in response to DNA damage. In the presence of DNA damage, AIMP2 binds to mouse double minute 2 homolog (MDM2) to protect p53 from MDM2 attack. TGF-β signaling results in the nuclear translocation of AIMP2, whereby AIMP2 interacts with FUSE-binding protein, and, thus, suppresses c-myc. TNF receptor-associated factor 2 (TRAF2) is an important mediator between TNF-receptors 1 and 2 which are involved in the signaling of c-Jun N-terminal kinase (JNK), nuclear factor κB (NF-κB), and p38 mitogen-activated protein kinases (MAPKs). TRAF2 is required for the activations of JNK and NF-κB via TNF-α and the mediation of anti-apoptosis signaling. AIMP2 can also enhance pro-apoptosis in the TNF-α signaling. During this signaling, AIMP2 assists the association of E3 ubiquitin ligase, the cellular inhibitor of apoptosis protein 1 (c-IAP1) which is well known and responsible for the degradation of TRAF2. The formation of a complex among AIMP2, TRAF2, and c-IAP1 results in proteasome-mediated TRAF2 degradation. AIMP2 can induce apoptosis via downregulation of TRAF2 to interact directly in TNF-α signaling. This review provides new insight into the molecular mechanism responsible for AIMP2 and TRAF2 complex formation and treatments for TNFα-associated diseases.
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