• Maxillofacial Plastic and Reconstructive Surgery
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• 제27권6호
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• pp.528-534
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• 2005

Angiogenesis is important for the growth and metastasis of solid tumors. Some growth factors, inflammatory cytokines, and angiogenin are known to promote tumor angiogenesis. Among them, Vascular endothelial growth factor (VEGF) is the most intriguing factor in regard to tumor angiogenesis. Inhibition of VEGF activity by neutralizing antibodies or by the introduction of dominant negative VEGF receptors into endothelial cells of tumor-associated blood vessels resulted in the inhibition of tumor growth and in tumor regression, indicating that VEGF is a major initiator of tumor angiogenesis. VEGF promotes angiogenesis through their receptors, Flt-1 and Flk-1/KDR. on vascular endothelial cells. These two receptors were usually believed to be expressed specifically on vascular endothelial cell. Several reports have now shown that VEGF is not only significantly associated with microvessel density but also has prognostic value in both node-negative and node-positive oral squamous cell carcinoma. For many years several histologic features of the neoplasms are being considered when assessing the influence of malignancy grading on recurrence and prognosis. Among the characteristics investigated, degree of keratinization, nuclear pleomorphism, mode of invasion, microscopic depth of invasion, intravascular invasion, lymphocyte infiltration, and number of mitoses have been considered as important prognostic factors. So, this study was conducted to evaluate the correlation of vascular endothelial growth factor expression with malignancy in paraffin-embedded biopsy specimens from 11 patients with tongue cancers. Our results showed that high immunoreactivity specimens of VEGF expression were significantly lower keratinization degree and more pronounced nuclear pleomorphism than in low immunoreactivity specimens. Thus, VEGF expression could be used as a prognostic marker in tongue cancer.

• BMB Reports
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• 제45권9호
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• pp.489-495
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• 2012

Ischemia is a blockage of blood supply due to an embolism or a hemorrhage in a blood vessel. When an organ cannot receive oxygenated blood and can therefore no longer replenish its blood supply due to ischemia, stresses, such as the disruption of blood glucose homeostasis, hypoglycemia and hypoxia, activate the AMPK complex. LKB1 and $CaMKK{\beta}$ are essential activators of the AMPK signaling pathway. AMPK triggers proangiogenic effects through the eNOS protein in tissues with ischemic conditions, where cells are vulnerable to apoptosis, autophagy and necrosis. The AMPK complex acts to restore blood glucose levels and ATP levels back to homeostasis. This review will discuss AMPK, as well as its key activators (LKB1 and $CaMKK{\beta}$), as a central energy regulator and evaluate the upstream and downstream regulating pathways of AMPK. We will also discuss how we can control this important enzyme in ischemic conditions to prevent harmful effects in patients with vascular damage.

• The Korean Journal of Physiology and Pharmacology
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• 제26권5호
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• pp.389-396
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• 2022

The increased expression of receptors for advanced glycation end-product (RAGE) is known as a key player in the progression of vascular remodeling. However, the precise signal pathways regulating RAGE expression in vascular smooth muscle cells (VSMCs) in the injured vasculatures are unclear. Given the importance of mitogen-activated protein kinase (MAPK) signaling in cell proliferation, we investigated the importance of MAPK signaling in high-mobility group box 1 (HMGB1)-induced RAGE expression in VSMCs. In HMGB1 (100 ng/ml)-stimulated human VSMCs, the expression of RAGE mRNA and protein was increased in association with an increase in AGE-induced VSMC proliferation. The HMGB1-induced RAGE expression was attenuated in cells pretreated with inhibitors for ERK (PD98059, 10 μM) and p38 MAPK (SB203580, 10 μM) as well as in cells deficient in ERK and p38 MAPK using siRNAs, but not in cells deficient of JNK signaling. In cells stimulated with HMGB1, the phosphorylation of ERK, JNK, and p38 MAPK was increased. This increase in ERK and p38 MAPK phosphorylation was inhibited by p38 MAPK and ERK inhibitors, respectively, but not by JNK inhibitor. Moreover, AGE-induced VSMC proliferation in HMGB1-stimulated cells was attenuated in cells treated with ERK and p38 MAPK inhibitors. Taken together, our results indicate that ERK and p38 MAPK signaling are involved in RAGE expression in HMGB1-stimulated VSMCs. Thus, the ERK/p38 MAPK-RAGE signaling axis in VSMCs was suggested as a potential therapeutic target for vascular remodeling in the injured vasculatures.

• Journal of International Society for Simulation Surgery
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• 제1권1호
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• pp.41-44
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• 2014

The aim of this report is showing the case that we could give exact navigation of perigastric vessels for gastrectomy with 3D CTA. A 74-year-old male patient visited hospital with gastric cancer. Early gastric cancer, type IIb was found at stomach antrum great curvature side. Before surgery, he underwent 3D CT angiography. 3D volume rendering images and MIP images were made by post processing. He had replaced Lt. hepatic artery arising from Lt. gastric artery. Surgeon could get patient's specific vascular anatomy before surgery including surgically relevant anatomical distance and direction and could finish gastrectomy within 4 hours and just 53ml blood loss.

• 한국약용작물학회지
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• 제14권6호
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• pp.342-346
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• 2006

Anatomical characters of the Bupleurum latissimum Nakai, an endemic species of Korea, were investigated to confirm its phylogenetic relationships. Compare to other species with anatomical characters, B. latissimum is very similar with B, euphorbioides and B, longeradiatum in point of lacking of pith in the stem, shape of involucres, number of vascular bundles in radical leaf and cauline leaf, and lacking stomata in adaxial leaf surface. The other hand, protruded pollen aperture character appears in B. latissimum and B. euphorbioides. On the based of anatomical characters, therefore, B. latissimum has closest relationships with B. euphorbioides and B. longeradiatum. It also needs molecular study including Asian species in order to confirm phylogenetic position and speciation process apparently.

• Archives of Plastic Surgery
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• 제39권2호
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• pp.94-105
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• 2012

Simple or complex defects in the lower leg, and especially in its distal third, continue to be a challenging task for reconstructive surgeons. A variety of flaps were used in the attempt to achieve excellence in form and function. After a long evolution of the reconstructive methods, including random pattern flaps, axial pattern flaps, musculocutaneous flaps and fasciocutaneous flaps, the reappraisal of the works of Manchot and Salmon by Taylor and Palmer opened the era of perforator flaps. This era began in 1989, when Koshima and Soeda, and separately Kroll and Rosenfield described the first applications of such flaps. Perforator flaps, whether free or pedicled, gained a high popularity due to their main advantages: decreasing donor-site morbidity and improving aesthetic outcome. The use as local perforator flaps in lower leg was possible due to a better understanding of the cutaneous circulation, leg vascular anatomy, angiosome and perforasome concepts, as well as innovations in flaps design. This review will describe the evolution, anatomy, flap design, and technique of the main distally pedicled propeller perforator flaps used in the reconstruction of defects in the distal third of the lower leg and foot.

• Applied Microscopy
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• 제26권2호
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• pp.157-175
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• 1996

The development of flexor digital tendon of the hand was studied by electron microscopy in human fetuses ranging from 9 mm to 260 mm crown rump length. The primordium of tendons was first identified as discrete collection of mesenchymal cells at 25 mm fetus. Synovial sheath formation had commenced by 40 mm fetus and was complete by 70 mm fetus. Cell junction or adhesion sites at all ages were noted between the tendon cells. When dilatation of the synovial cavity occurred, two types of synovial cells were observed. A-type cells had numerous vesicles and large vacuoles. In contrast, B-type cells were characterized by abundant rough endoplasmic reticulum and well-developed Golgi complex. By $150mm{\sim}260mm$ fetuses, a mojority of the synovial cells were type B. The most remarkable difference between the synovial cells of full-term fetus and adult was the larger amount of collagen fibers in the latter. The vascular buds were first observed between the individual fibril bundles in the interfascicular space at 150 mm fetus. At 25 mm fetus, collagen fibrils were first noted within narrow cytoplasmic recesses which were continued with the extracellular space. Collagen fibrils were filled in almost entire extracellular space at 150 mm fetus. Besides collagen fibrils in the extracellular space small elastic fibers were also identified and followed in their development.

• Applied Microscopy
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• 제26권2호
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• pp.177-195
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• 1996

Fine structure of the processes of intramembranous ossification and endochondral ossification at the tip of the distal phalanx of human fetuses was studied by electron microscopy. In 50 mm fetus, intramembranous ossification of the tip of cartilaginous phalanx was first noted. The osteoblasts of the perichondral zone of tip of cartilaginous phalanx started to lay down a thick membranous bony lamella. Most of the hypertrophied chondrocytes in the marginal parts of tip of the distal phalanx remained viable after being embeded in mineralized cartilaginous septa. The tuberosity of the distal phalanx was formed by membranous bony trabeculae on the exterior of the subperiosteal cap at 80 mm fetus. At this stage endochondral ossification was first observed in distal extremity of the distal phalanx. The maority of hypertrophied chondrocytes in the center of distal extremity appeared to be disintegrating. Resorption of calcified matrix was undertaken by perivascular cells and chondroclasts. From the periosteum, zone of calcification, vascular sprouts expanded within a recently opened lacunae, and the invading osteoblasts laid down osteoid and bone. After 120 mm fetus, endochondral and subperiosteal ossification proceeded in only one direction, just proximally. These findings demonstrate that intramembranous ossification, calcification, and endochondral ossification start at tip of the distal phalanx instead of at the center of the shaft, as was the case in other long bones.

• Applied Microscopy
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• 제24권1호
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• pp.59-76
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• 1994

Fine structure of the distal femoral epiphysis of growing mouse was studied by electron microscopy. The first morphological evidence of developing secondary center of ossification in the distal femoral epiphysis was found at newborn mouse. Ossification center was in the form of multiple foci of calcification and its cells were represented by remnant of degenerated cells within large lacunae that were separated by mineralized cartilaginous septa. Endochondral ossification beneath the articular cartilage proceeded in a less orderly manner than metaphyseal endochondral ossification. Columns of hypertrophied chondrocytes were not distinctly parallel to intercellular mineralized septa in all direction. Hypertrophied chondrocytes in the inner zone of the epiphseal center of ossification showed disintegrated. Resorption of mineralized cartilaginous septa was undertaken by perivascular cells and multinucleated chondroclasts. Resorption of the calcified cartilage was restricted to the region of ruffled border of the chondroclast. Growth along the metaphyseal side of the epiphyseal center of ossification was different from that along the articular surface. As the secondary center expanded toward the metaphyseal side, many vascular buds penetrated unmineralized cartilaginous septa and invaded viable chondrocytes. Many hypertrophied chondrocytes bodering the metaphyseal side of bone center remained viable after they became embedded in mineralized cartilaginous septa. This result suggested that the hypertrophied.

• The Korean Journal of Physiology and Pharmacology
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• 제28권3호
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• pp.197-207
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• 2024

The potential of tivozanib as a treatment for oral squamous cell carcinoma (OSCC) was explored in this study. We investigated the effects of tivozanib on OSCC using the Ca9-22 and CAL27 cell lines. OSCC is a highly prevalent cancer type with a significant risk of lymphatic metastasis and recurrence, which necessitates the development of innovative treatment approaches. Tivozanib, a vascular endothelial growth factor receptor inhibitor, has shown efficacy in inhibiting neovascularization in various cancer types but has not been thoroughly studied in OSCC. Our comprehensive assessment revealed that tivozanib effectively inhibited OSCC cells. This was accompanied by the suppression of Bcl-2, a reduction in matrix metalloproteinase levels, and the induction of intrinsic pathway-mediated apoptosis. Furthermore, tivozanib contributed to epithelial-to-mesenchymal transition (EMT) inhibition by increasing E-cadherin levels while decreasing N-cadherin levels. These findings highlight the substantial anticancer potential of tivozanib in OSCC and thus its promise as a therapeutic option. Beyond reducing cell viability and inducing apoptosis, the capacity of tivozanib to inhibit EMT and modulate key proteins presents the possibility of a paradigm shift in OSCC treatment.