• Title/Summary/Keyword: Central Nervous System Disease

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Research Progress of CXCR4-Targeting Radioligands for Oncologic Imaging

  • Yanzhi Wang;Feng Gao
    • Korean Journal of Radiology
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    • v.24 no.9
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    • pp.871-889
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    • 2023
  • C-X-C motif chemokine receptor 4 (CXCR4) plays a key role in various physiological functions, such as immune processes and disease development, and can influence angiogenesis, proliferation, and distant metastasis in tumors. Recently, several radioligands, including peptides, small molecules, and nanoclusters, have been developed to target CXCR4 for diagnostic purposes, thereby providing new diagnostic strategies based on CXCR4. Herein, we focus on the recent research progress of CXCR4-targeting radioligands for tumor diagnosis. We discuss their application in the diagnosis of hematological tumors, such as lymphomas, multiple myelomas, chronic lymphocytic leukemias, and myeloproliferative tumors, as well as nonhematological tumors, including tumors of the esophagus, breast, and central nervous system. Additionally, we explored the theranostic applications of CXCR4-targeting radioligands in tumors. Targeting CXCR4 using nuclear medicine shows promise as a method for tumor diagnosis, and further research is warranted to enhance its clinical applicability.

Heatstroke occurred in an American Pit Bull Terrier in Korea (국내 아메리칸 핏불테리어에서 발생한 열사병 증례 보고)

  • Lee, Seunghee;Jung, Ji-Youl;Jeong, Jae-Hoon;Lee, Hyunkyoung;Park, Jung-Won;Lee, Kyoung-Ki;Kim, Jong-Hwan;So, ByungJae;Yoon, Soon-Seek
    • Korean Journal of Veterinary Service
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    • v.41 no.3
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    • pp.211-216
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    • 2018
  • Heat stroke in a dog is a life-threatening syndrome characterized by a high body temperature over $41^{\circ}C$, by the central nervous system dysfunction, and by multiple organ dysfunction. A 11-month-old male American Pit Bull Terrier was presented to clarify the cause of death to diagnostic laboratory. This dog showed clinical signs such as high body temperature ($42^{\circ}C$), severe tachypnea, hematochezia, epistaxis and hemoptysis after transportation at hot summer time. At necropsy, there were hemorrhages in skin, serosa of stomach and small intestine, and also dark red fluid in lumen of intestine. Histopathologic examination revealed extensive hemorrhages in stomach, muscle, skin, and tongue. In microbiology, pathologic bacteria such as Pasteurella, Boedetella, Salmonella, Clostridium, and circulating virus in Korea such as CDV, CIV, CAV, CHV, CCV, CPIV were negative except CPV. There were many gross and microscopic lesions suggesting hest stroke while pathologic agents and related lesions were not detected. Therefore we diagnosed this case as heatstroke.

REPORT OF BECHET'S DISEASE (베체트병환자의 치험례)

  • Kim, Il-Kyu;Yun, Seung-Hwan;Oh, Sung-Seop;Kim, Hyung-Don;Choi, Jin-Ho;Oh, Nam-Sik;Kim, Eui-Seong
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.26 no.2
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    • pp.219-223
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    • 2000
  • Behcet's disease is a chronic, multisystemic disorder which is more frequently seen in the Mediterranean basin, Middle East, and Far East. The mean age at the first onset is third decades. In large series of patients, men predominate over women. Infectious agents, immune mechanisms, and genetic factors are implicated in the etiopathogenesis of the disease. Eyes, skin, joints, the oral cavity, blood vessels, and central nervous system are usually involved, although less frequently the heart, lung, kidney may be affected. The prognosis of the disease has been improved because of early diagnosis and suitable treatment. Local remedies and systemic administration of colchicine, corticosteoids, immunosuppressives, and other agents have been applied. Pathergy, or skin hypersensitivity to needle puncture has been reported as a diagnostic test for Behcet's disease. We have managed a Behcet's disease patient with pathergy test & corticosteroids therapy. We have obtained good result and report this case with review of literatures.

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Evaluation of JC and Cytomegalo Viruses in Glioblastoma Tissue

  • Afshar, Reza Malekpour;Mollaei, Hamid Reza;Zandi, Bahare;Iranpour, Maryam
    • Asian Pacific Journal of Cancer Prevention
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    • v.17 no.11
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    • pp.4907-4911
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    • 2016
  • Glioblastoma multiforme (GBM) is the most aggressive of the gliomas, a collection of tumors arising from glia in the central nervous system. Possible associations between the human cytomegalovirus (HCMV) and the JC virus with GBM are now attracting interest. Our present aim was to investigate the prevalence of the two viruses in Iranian patients from Kerman's cities in the south of Iran. In addition, the expression rates of pp65, large T antigen and p53 proteins were assessed and their relation with GBM evaluated using reverse transcription real time PCR (rReal Time PCR). A total of 199 patients with GBM cancer were enrolled, with $mean{\pm}SD$ ages of $50.0{\pm}19.5$ and $50.7{\pm}19.6$ years for males and females, respectively. The P53 rate was dramatically low suggesting an aetiological role,. Large T antigen expression was found in JC positive samples, while the PP65 antigen was observed in patients positive for CMV and JC. HCMV products and JC virus with oncogenic potential may induce the development of various tumors including glioblastomas. The JC virus produces an early gene product, T-antigen, which has the ability to associate with and functionally inactivate well-studied tumor suppressor proteins including p53 and pRB.

A Conclusive Review on Amyloid Beta Peptide Induced Cerebrovascular Degeneration and the Mechanism in Mitochondria

  • Merlin, Jayalal L.P.
    • Journal of Integrative Natural Science
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    • v.6 no.3
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    • pp.125-137
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    • 2013
  • Promising evidence suggests that amyloid beta peptide ($A{\beta}$), a key mediator in age-dependent neuronal and cerebrovascular degeneration, activates death signalling processes leading to neuronal as well as non-neuronal cell death in the central nervous system. A major cellular event in $A{\beta}$-induced apoptosis of non-neuronal cells, including cerebral endothelial cells, astrocytes and oligodendrocytes, is mitochondrial dysfunction. The apoptosis signalling cascade upstream of mitochondria entails $A{\beta}$ activation of neutral sphingomyelinase, resulting in the release of ceramide from membrane sphingomyelin. Ceramide then activates protein phosphatase 2A (PP2A), a member in the ceramide-activated protein phosphatase (CAPP) family. PP2A dephosphorylation of Akt and FKHRL1 plays a pivotal role in $A{\beta}$-induced Bad translocation to mitochondria and transactivation of Bim. Bad and Bim are pro-apoptotic proteins that cause mitochondrial dysfunction characterized by excessive ROS formation, mitochondrial DNA (mtDNA) damage, and release of mitochondrial apoptotic proteins including cytochrome c, apoptosis inducing factor (AIF), endonuclease G and Smac. The cellular events activated by $A{\beta}$ to induce death of non-neuronal cells are complex. Understanding these apoptosis signalling processes will aid in the development of more effective strategies to slow down age-dependent cerebrovascular degeneration caused by progressive cerebrovascular $A{\beta}$ deposition.

Effect of Neurotrophic Factors on Neuronal Stem Cell Death

  • KimKwon, Yun-Hee
    • BMB Reports
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    • v.35 no.1
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    • pp.87-93
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    • 2002
  • Neural cell survival is an essential concern in the aging brain and many diseases of the central nervous system. Neural transplantation of the stem cells are already applied to clinical trials for many degenerative neurological diseases, including Huntington's disease, Parkinson's disease, and strokes. A critical problem of the neural transplantation is how to reduce their apoptosis and improve cell survival. Neurotrophic factors generally contribute as extrinsic cues to promote cell survival of specific neurons in the developing mammalian brains, but the survival factor for neural stem cell is poorly defined. To understand the mechanism controlling stem cell death and improve cell survival of the transplanted stem cells, we investigated the effect of plausible neurotrophic factors on stem cell survival. The neural stem cell, HiB5, when treated with PDGF prior to transplantation, survived better than cells without PDGF. The resulting survival rate was two fold for four weeks and up to three fold for twelve weeks. When transplanted into dorsal hippocampus, they migrated along hippocampal alveus and integrated into pyramidal cell layers and dentate granule cell layers in an inside out sequence, which is perhaps the endogenous pathway that is similar to that in embryonic neurogenesis. Promotion of the long term-survival and differentiation of the transplanted neural precursors by PDGF may facilitate regeneration in the aging adult brain and probably in the injury sites of the brain.

Neuroinflammation and Psychiatric Illness (신경염증과 정신질환)

  • Song, Hoo Rim;Lee, Hwa-Young;Shim, Se-Hoon;Kwon, Young-Joon
    • Korean Journal of Biological Psychiatry
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    • v.23 no.1
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    • pp.12-17
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    • 2016
  • Neuroinflammation is one of important allostatic loads contributory to the various psychiatric illness. It is mediated mainly by glial cells, which produce both proinflammatory and antiinflammatory cytokines, and the balance of them determines the inflammatory process in the central nervous system. S100 calcium-binding protein B, which is used as an inflammatory marker is also released by glial cells. In the molecular level, oxidative stress contributes to the neuroinflammation. Their disturbances have been revealed in the psychiatric illness and related with the dysregulation of the glutamatergic and monoaminergic systems. There is a possibility to use them as disease markers. The approach for inflammation using antiinflammatory drugs and antioxidants could be connected to the development of disease-modifying treatments. Also, a searching examination about specific subtypes who are vulnerable to inflammation in the patients is required to confirm their efficacy clearly.

The Importance of Nutritional Assessment and Dietary Counseling in Infants and Young Children with Common Illnesses (소아의 흔한 질병 상황에서 식이, 영양의 중요성)

  • Jeong, Su-Jin
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • v.14 no.1
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    • pp.33-44
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    • 2011
  • The influence of nutrition during early life on physical growth as well as mental development has been thoroughly discussed in the literature. The physical dimensions of the body are greatly influenced by nutrition, particularly during the period of rapid growth in early childhood. Nutritional status affects every pediatric patient's response toillness. Good nutrition is important for achieving normal growth and development. It is indicated that permanent impairment of the central nervous system may result from dietary restriction of imbalance during certain periods of life. If children under 3 years of age show a good nutritional status, it may be assumed that they are well nourished. Several common diseases of children such as iron deficiency, chronic constipation and atopic dermatitis are known food related diseases. Patients with chronic illness and those at risk of malnutrition should have detailed nutritional assessments done. Components of a complete nutritional assessment include a medical history, nutritional history including dietary intake, physical examination, anthropometrics (weight, length or stature, head circumference, midarm circumference, and triceps skinfold thickness), pubertal staging, skeletal maturity staging, and biochemical tests of nutritional status. The use of age, gender, and disease-specific growth charts is essential in assessing nutritional status and monitoring nutrition interventions. Nutrition assessment and dietary counseling is helpful for the cure of disease, and moreover, the prevention of illness.

Potential Effects of Microglial Activation Induced by Ginsenoside Rg3 in Rat Primary Culture: Enhancement of Type A Macrophage Scavenger Receptor Expression

  • Joo, Seong-Soo;Lee, Do-Ik
    • Archives of Pharmacal Research
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    • v.28 no.10
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    • pp.1164-1169
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    • 2005
  • Brain microglia are phagocytic cells that are the major inflammatory response cells of the central nervous system and widely held to play important pathophysiologic roles in Alzheimer's disease (AD) in both potentially neurotoxic responses and potentially beneficial phagocytic responses. In the study, we examined whether ginsonoside Rg3, a by-product of red ginseng, enhances the microglial phagocytosis of $A{\beta}$. We found that Rg3 promoted $A{\beta}$ uptake, internalization, and digestion. Increased maximal $A{\beta}$ uptake was observed at 4 and 8 h after Rg3 pretreatment (25 ${\mu}g/mL$), and the internalized $A{\beta}$ was almost completely digested from cells within 36 h when pretreated with Rg3 comparing with single non-Rg3-treated groups. The expression of MSRA (type A MSR) was also up-regulated by Rg3 treatment in a dose- and time-dependent manner which was coincidently identified in western blots for MSRA proteins in cytosol. These results indicate that microglial phagocytosis of $A{\beta}$ may be enhanced by Rg3 and the effect of Rg3 on promoting clearance of $A{\beta}$ may be related to the MSRA-associated action of Rg3. Thus, stimulation of the MSRA might contribute to the therapeutic potentials of Rg3 in microglial phagocytosis and digestion in the treatment of AD.

Neuroprotective Effects of the Extract of Zingiberis Rhizoma (건강 추출물의 뇌세포 보호 작용)

  • Jeong, Gil-Saeng;Li, Bin;Lee, Dong-Sung;Choi, Hyun-Gyu;Kim, Youn-Chul
    • Korean Journal of Pharmacognosy
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    • v.41 no.3
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    • pp.190-195
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    • 2010
  • Glutamate-induced oxidative injury contributes to neuronal degeneration in many central nervous system (CNS) diseases, such as Parkinson's disease, Alzheimer's disease, epilepsy and ischemia. Inducible heme oxygenase (HO)-1 acts against oxidants that are thought to play a role in the pathogenesis of these diseases. NNMBS098, a composition comprising the water insoluble of the 70% EtOH extract of Zingiberis Rhizoma, showed the potent neuroprotective effects on glutamateinduced neurotoxicity by induced the expression of heme oxygenase (HO)-1 and increased HO activity in the mouse hippocampal HT22 cells. Furthermore, NNMBS098 caused the nuclear accumulation of nuclear factor E2-related factor 2 (Nrf2) in mouse hippocampal HT22 cells. In addition, we found that treatment with c-Jun N-terminal kinase (JNK) inhibitor (SP600125) reduced NNMBS098-induced HO-1 expression and NNMBS098 also increased JNK phosphorylation. Therefore, these results suggest that NNMBS098 increases cellular resistance to glutamate-induced oxidative injury in mouse hippocampal HT22 cells, presumably through JNK pathway-Nrf2-dependent HO-1 expression.