• Journal of Ecology and Environment
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• v.33 no.3
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• pp.245-251
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• 2010

We evaluated the interaction between Cd and Zn in the bioaccumulation of seven clones of Salix caprea, which were exposed both to Cd and Zn alone and to a combination of Cd and Zn. Cadmium (Cd) and Zn concentration in the four treatments were administered in the following order: root > leaf > stem, and obvious differences were noted among the treatments and clones. The leaf Cd concentration of clone BH2 and stem Cd concentration of clone BH5 in the combined Cd and Zn treatment group was increased by 62% and 110%, respectively, relative of that of the Cd alone treatment group. On the other hand, the leaf and stem Zn concentration of clone BH8 in the combined Cd and Zn treatment group was reduced by 66% and 61%, respectively, relative to that of the Zn alone treatment group. Translocation of Cd and Zn from the root was higher in the leaf than in the stem, and the combined Cd and Zn treatment stimulated the translocation of Cd from the root to the leaf and stem, whereas it suppressed the translocation of Zn from the root to the leaf and stem. Therefore, the interaction effects were considered strongly synergistic with Cd in the presence of Zn, but proved antagonistic to Zn in the presence of Cd in the combined Cd and Zn treatment group. The phytoremediation potentials of the seven clones, which were estimated from standard indices of Cd and Zn concentration in Cd and Zn alone and the combined Cd and Zn treatment groups, were highest in clone BH3, and lowest in clone BH5. Therefore, we recognize S. caprea as an appropriate material for phytoremediation, and this is particularly the case with clone BH3. However, further research will be required to evaluate the effects of Cd and Zn on the physiological changes as well as tolerance mechanisms against metal toxicity in S. caprea clones.

• Clinical and Experimental Reproductive Medicine
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• v.21 no.1
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• pp.131-135
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• 1994

A 27-year-old pregnant woman who had one son with mental and growh retardation and dysmorphic features, was referred for genetic counselling. Cytogenetic investigations revealed 4/22 translocation in the mother(46, XX, t(4;22)(p14;P11)), partial trisomy 4p in son(46, XY, -22, +der(22), t(4;22)(p14;p11)mat). The father had normal karyotype. Amniocentesis and chorionic villi sampling were performed in 3 successive pregnancies. The karyotypes of fetus in 3rd, 4th pregnancies by amniocentesis were 46, XX, t(4;22)(p14;p11) and 46, XX, t(4;22) (p14;p11), and the karyotype of fetus in 5th pregnancy by chorionic villi sampling was found to be 46, XX, -22, +der(22) t(4;22)(p14;p11)mat. We report 3 succesive prenatally diagnosed familial partial trisomy 4p and 4/22 translocation of maternal origin with review of literature.

• Clinical and Experimental Pediatrics
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• v.59 no.2
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• pp.91-95
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• 2016

We report the case of a 22-month-old boy with a new mosaic partial unbalanced translocation of 1q and 18q. The patient was referred to our Pediatric Department for developmental delay. He showed mild facial dysmorphism, physical growth retardation, a hearing disability, and had a history of patent ductus arteriosus. White matter abnormality on brain magnetic resonance images was also noted. His initial routine chromosomal analysis revealed a normal 46,XY karyotype. In a microarray-based comparative genomic hybridization (aCGH) analysis, subtle copy number changes in 1q32.1-q44 (copy gain) and 18q21.33-18q23 (copy loss) suggested an unbalanced translocation of t(1;18). Repeated chromosomal analysis revealed a low-level mosaic translocation karyotype of 46,XY,der(18)t(1;18) (q32.1;q21.3)[12]/46,XY[152]. Because his parents had normal karyotypes, his translocation was considered to be de novo. The abnormalities observed in aCGH were confirmed by metaphase fluorescent in situ hybridization. We report this patient as a new karyotype presenting developmental delay, facial dysmorphism, cerebral dysmyelination, and other abnormalities.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.9
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• pp.3793-3797
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• 2015

Background: Chronic myeloid leukemia (CML) is a myeloproliferative disorder of pluripotent stem cells, caused by reciprocal translocation between the long arms of chromosomes 9 and 22, t(9;22)(q34;q11), known as the Philadelphia chromosome. Materials and Methods: A total of 51 CML patients were recruited in this study. Complete blood counts of all CML patients were performed to find out their total leukocytes, hemoglobin and platelets. FISH was performed for the detection of BCR-ABL fusion and cryptogenic tests using bone marrow samples were performed for the conformation of Ph (9;22)(q34;q11) and variant translocation mechanisms. Results: In cytogenetic analysis we observed that out of 51 CML patients 40 (88.9%) were Ph positive and 4 (8.88%) had Ph negative chromosomes. Mean values of WBC 134.5 $10^3/{\mu}l$, hemoglobin 10.44 mg/dl, and platelets 288.6 $10^3/{\mu}l$ were observed in this study. Conclusions: In this study, Ph positive translocation between chromosome (9:22)(q34;q11) were observed in 40 (88.9%) CML patients.

• Proceedings of the Korean Society of Crop Science Conference
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• 2017.06a
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• pp.174-174
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• 2017

To cope with phosphate (Pi) deficient stress, plants modulate various physiological and developmental processes, such as gene expression, Pi uptake and translocation, and root architecture changes. Here, we report the identification and characterization of novel activation-tagged mutant involved in Pi starvation signaling in Arabidopsis. The hpd (${\underline{h}ypersensitive}$ to ${\underline{P}i}$ $ {\underline{d}eficiency}$) mutant exhibits enhanced phosphate uptake and altered root architectural change under Pi starvation compared to wild type. Expression analysis of auxin-responsive DR5::GUS reporter gene in hpd mutant indicated that auxin translocation in roots under Pi starvation are suppressed in hpd mutant plants. Impaired auxin translocation in roots of hpd mutant was attributable to abnormal root architecture changes in Pi starvation conditions. Our results indicated that abnormal auxin translocation in hpd mutant might be due to mis-regulation of auxin efflux carrier proteins, PIN-FORMED (PIN) 1, and 2 under Pi starvation conditions. Not only expression levels but also expression domains of PIN proteins were altered in hpd mutant in response to Pi starvation. Molecular genetic analysis of hpd mutant revealed that the mutant phenotype is caused by the lesion in ENHANCED SILENCING PHENOTYPE4 (ESP4) gene whose function is proposed in mRNA 3'-end processing. The results suggest that mRNA processing plays crucial roles in Pi homeostasis as well as developmental reprograming in response to Pi deprivation in Arabidopsis.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.7
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• pp.3377-3380
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• 2016

The proportion of lung cancer patients under 50 years old is small at approximately 5-10%, but as with patients older than 50, the number is on the rise. Although lung cancer treatment strategies have undergone extensive transformation in recent years based on the presence or absence of oncogenic driver mutations, there are few reports regarding these mutations in the young or the relationship between clinical setting and prognosis. Therefore, we conducted a study of clinical features in 36 patients under the age of 50 who were diagnosed with primary lung cancer from October 2008 to November 2015. The 22 patients in stages I through III A underwent operations, and all 17 whose lung cancer were detected through screening were candidates for surgery. Gene analysis was conducted for 26 (72.2%); 10 (38.5%) were positive for EGFR gene mutations, and ALK gene translocation was present in 4 (15.4%). In stage IV patients, the median progression free survival (PFS) in the ALK translocation positive and negative patients was 518 days and 130 days, respectively, and the median overall survival (OS) was not reached and 280 days, respectively. A trend toward extended PFS (p=0.203) and OS (p=0.056) was observed in patients positive for ALK translocation. We must strive for early detection by increasing screening rates and evaluate oncogenic driver mutations important for prognosis of lung cancer in the young.

• BMB Reports
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• v.41 no.10
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• pp.745-750
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• 2008

Selenium, an essential trace element possessing anti-carcinogenic properties, can induce apoptosis in cancer cells. We have previously shown that sodium selenite can induce apoptosis by activating the mitochondrial apoptosis pathway in NB4 cells. However, the detailed mechanism remains unclear. Presently, we demonstrate that p53 contributes to apoptosis by directing signaling at the mitochondria. Immunofluorescent and Western blot procedures revealed selenite-induced p53 translocation to mitochondria. Inhibition of p53 blocked accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential, suggesting that mitochondrial p53 acts as an upstream signal of ROS and activates the mitochondrial apoptosis pathway. Selenite also disrupted cellular calcium ion homeostasis in a ROS-dependent manner and increased mitochondrial calcium ion concentration. p38 kinase mediated phosphorylation and mitochondrial translocation of p53. Taken together, these results indicate that p53 involves selenite-induced NB4 cell apoptosis by translocation to mitochondria and activation mitochondrial apoptosis pathway in a transcription-independent manner.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.6
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• pp.487-496
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• 2000

Insulin stimulates glucose transport in muscle and fat cells by promoting the translocation of glucose transporter (GLUT4) to the cell surface. Phosphatidylinositide 3-kinase (PI3-kinase) has been implicated in this process. However, the involvement of protein kinase B (PKB)/Akt and $PKC-{\zeta}$, those are known as the downstream target of PI3-kinase in regulation of GLUT4 translocation, is not known yet. An interesting possibility is that these protein kinases phosphorylate GLUT4 directly in this process. In the present study, $PKB-{\alpha}$ and $PKC-{\zeta}$ were added exogenously to GLUT4-containing vesicles purified from low density microsome (LDM) of the rat adipocytes by immunoadsorption and immunoprecipitation for direct phosphorylation of GLUT4. Interestingly GLUT4 was phosphorylated by $PKC-{\zeta}$ and its phosphorylation was increased in insulin stimulated state but GLUT4 was not phosphorylated by $PKB-{\alpha}.$ However, the GST-fusion proteins, GLUT4 C-terminal cytoplasmic domain (GLUT4C) and the entire major GLUT4 cytoplasmic domain corresponding to N-terminus, central loop and C-terminus in tandem (GLUT4NLC) were phosphorylated by both $PKB-{\alpha}$ and $PKC-{\zeta}.$ The immunoblots of $PKC-{\zeta}$ and $PKB-{\alpha}$ antibodies with GLUT4-containing vesicles preparation showed that $PKC-{\zeta}$ was co-localized with the vesicles but not $PKB-{\alpha}.$ From the above results, it is clear that $PKC-{\zeta}$ interacts with GLUT4-containing vesicles and it phosphorylates GLUT4 protein directly but $PKB-{\alpha}$ does not interact with GLUT4, suggesting that insulin-elicited signals that pass through PI3-kinase subsequently diverge into two independent pathways, an Akt pathway and a $PKC-{\zeta}$ pathway, and that later pathway contributes, at least in part, insulin stimulation of GLUT4 translocation in adipocytes via a direct GLUT4 phosphorylation.

• Journal of Veterinary Clinics
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• v.29 no.1
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• pp.112-117
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• 2012

This report evaluated the convenience and accessibility of a penile translocation surgery in the lateral recumbency of a calf using a tilt-up mobile compared with that of dorsal recumbency on the ground of a barn. One nine-month-old F-1 (Korean native sire x Holstein dam) calf was sedated with xylazine (0.03 mg/kg, IV) and restrained in the right lateral recumbency position on a tilt-up restraint mobile (90 cm high), whereas the other nine-month-old Korean native calf was administered xylazine (0.3 mg/kg, IV) and restrained in dorsal recumbency position on the ground of a barn, with assistance by one person. For the two calves, lidocaine was administered subcutaneously from the preputial orifice to the S-shaped penis. The preputial orifice was incised, and the preputial sheath and penis were separated bluntly, then laterally translocated to the site toward the left flank at a $40^{\circ}$ angle. Anti-inflammatory drug (ketoprofen) and antibiotics (penicillin) were administered following the surgery. The duration of surgery was 30 min shorter in the calf that received the surgery in lateral recumbency using the tilt-up mobile with operator's standing posture (60 min) than the one that underwent surgery in dorsal recumbency on the ground with operator's bending posture (90 min). One week after the surgery, the operation area, including the translocated preputial orifice, was healed without complications in both cases. The results detailed in this report demonstrate that penile translocation surgery in the lateral recumbency position using a tilt-up mobile might be used conveniently in calves due to the convenience of restraint, reduced surgery time, and reduced physical inconvenience for the surgeon.

• Molecules and Cells
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• v.22 no.1
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• pp.97-103
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• 2006

Phosphoinositides are critical regulators of ion channel and transporter activity. There are multiple isomers of biologically active phosphoinositides in the plasma membrane and the different lipid species are non-randomly distributed. However, the mechanism by which cells impose selectivity and directionality on lipid movements and so generate a non-random lipid distribution remains unclear. In the present study we investigated which structural elements of phosphoinositides are responsible for their subcellular location and movement. We incubated phosphatidylinositol (PI), phosphatidylinositol 4-monophosphate (PI(4)P) and phosphatidylinositol 4,5-bisphosphate ($PI(4,5)P_2$) with short or long acyl chains in CHO and HEK cells. We show that phosphate number and acyl chain length determine cellular location and translocation movement. In CHO cells, $PI(4,5)P_2$ with a long acyl chain was released into the cytosol easily because of a low partition coefficient whereas long chain PI was released more slowly because of a high partition coefficient. In HEK cells, the cellular location and translocation movement of PI were similar to those of PI in CHO cells, whereas those of $PI(4,5)P_2$ were different; some mechanism restricted the translocation movement of $PI(4,5)P_2$, and this is in good agreement with the extremely low lateral diffusion of $PI(4,5)P_2$. In contrast to the dependence on the number of phosphates of the phospholipid head group of long acyl chain analogs, short acyl chain phospholipids easily undergo translocation movement regardless of cell type and number of phosphates in the lipid headgroup.