• 제목/요약/키워드: Unknown protein

검색결과 630건 처리시간 0.03초

급성저혈압에 의한 내측전정신경핵 신경세포의 흥분성 변화를 분석하기 위한 테트로드 기법의 적용 (Application of Tetrode Technology for Analysis of Changes in Neural Excitability of Medial Vestibular Nucleus by Acute Arterial Hypotension)

  • 김영;구호;박병림;문세진;양승범;김민선
    • Research in Vestibular Science
    • /
    • 제17권4호
    • /
    • pp.142-151
    • /
    • 2018
  • Objectives: Excitability o medial vestibular nucleus (MVN) in the brainstem can be affected by changes in the arterial blood pressure. Several animal studies have demonstrated that acute hypotension results in the alteration of multiunit activities and expression of cFos protein in the MVN. In the field of extracellular electrophysiological recording, tetrode technology and spike sorting algorithms can easily identify single unit activity from multiunit activities in the brain. However, detailed properties of electrophysiological changes in single unit of the MVN during acute hypotension have been unknown. Methods: Therefore, we applied tetrode techniques and electrophysiological characterization methods to know the effect of acute hypotension on single unit activities of the MVN of rats. Results: Two or 3 types of unit could be classified according to the morphology of spikes and firing properties of neurons. Acute hypotension elicited 4 types of changes in spontaneous firing of single unit in the MVN. Most of these neurons showed excitatory responses for about within 1 minute after the induction of acute hypotension and then returned to the baseline activity 10 minutes after the injection of sodium nitroprusside. There was also gradual increase in spontaneous firing in some units. In contrast small proportion of units showed rapid reduction of firing rate just after acute hypotension. Conclusions: Therefore, application of tetrode technology and spike sorting algorithms is another method for the monitoring of electrical activity of vestibular nuclear during acute hypotension.

Cloning and expression of lin-28 homolog B gene in the onset of puberty in Duolang sheep

  • Xing, Feng;Zhang, Chaoyang;Kong, Zhengquan
    • Asian-Australasian Journal of Animal Sciences
    • /
    • 제32권1호
    • /
    • pp.23-30
    • /
    • 2019
  • Objective: Recent studies have demonstrated that lin-28 homolog B (LIN28B)/miRNA let-7 (let-7) plays a role in the regulation of pubertal onset in mammals. However, the role of LIN28B/let-7 in the onset of ovine puberty remains unknown. We cloned the Duolang sheep Lin28B cDNA sequence, detected the expression change of LIN28B, let-7a and let-7g in hypothalamus, pituitary and ovary tissues at three different pubertal stages. Methods: The reverse transcriptase polymerase chain reaction (RT-PCR) was used to clone the cDNA sequence of LIN28B gene from Duolang sheep and the bioinformatics methods were applied to analyze the amino acid sequence of LIN28B protein. The mRNA expression levels of the LIN28B gene at different pubertal stages were examined by real time RT-PCR. Results: LIN28B cDNA of Duolang sheep was cloned, and two transcripts were obtained. The amino acid sequence of transcript 1 shares 99.60%, 98.78%, and 94.80% identity with those of goat, wild yak and pig, respectively. Strong LIN28B mRNA expression was detected in the hypothalamus, pituitary, ovary, oviduct and uterus, while moderate expression was found in the liver, kidney, spleen and heart, weak expression was observed in the heart. No expression was found in the lungs. Quantitative real-time PCR (QPCR) and western-blot analysis revealed that the LIN28B was highly expressed in the hypothalamus and ovary at prepuberty stages, and this expression significantly decreased from the prepuberty to puberty stages (p<0.05). Markedly increased levels of mRNA expression were detected in the pituitary from prepuberty to puberty (p<0.05) and then significantly decreased from puberty to post-puberty (p<0.05). The expression levels of let-7a and let-7g showed no significant changes among different pubertal stages (p>0.05). Conclusion: These results provided a foundation for determining the functions of LIN28B/let-7 and their role in the onset of sheep puberty.

저염화 라면의 소비자 선호 분석을 활용한 기술사업화 전략 (Technological Commercialization Strategy based on Consumer Preference Analysis of Low-sodium Instant noodle Ramen)

  • 오상호;임춘성
    • 한국식생활문화학회지
    • /
    • 제33권6호
    • /
    • pp.523-530
    • /
    • 2018
  • The purpose of this study was to develop a technology commercialization strategy by analyzing the consumer preference for low-sodium instant noodle ramen, which has a sodium content of 1,730 mg or less. For the commercialization of such low-sodium ramen, this study examined how much consumers would pay through an analysis of consumer preference by conjoint analysis. This study surveyed 1,004 men and women in their 20 s and 50 s between the ages of 20 and 50 years in Korea using an online survey. If the price of conventional instant noodle ramen is KRW 4,000 (approximately USD 3.57) per 5 packs for one pack of 5 servings in a supermarket, this study surveyed how much more they respondents would pay if the sodium was reduced by 10.0, 20.0, and 30.0%. The study found that if sodium was reduced by 10.0, 20.0, and 30.0%, the respondents would pay as much as KRW 4,180, KRW 4,307, and KRW 4,515, respectively. The attributes of low-sodium instant noodle ramen were examined according to the degree of sodium reduction, vegetable protein ingredients, brand, where to buy and price with each level. The Marginal Willingness To Pay (MWTP) was analyzed as follows. If the sodium content of ramen soup is reduced by 1.0%, the amount that can be paid would be KRW 105.78. Respondents could pay KRW 1,673 more for famous brand ramen than an unknown brand ramen. The study results indicated that when a new product is developed and released, it can be expected to increase sales of the new product by understanding the foreseeable value that consumers could pay for and realize the technological commercialization of the technology.

A study of the effectiveness of using the serum procalcitonin level as a predictive test for bacteremia in acute pyelonephritis

  • Lee, Ga Hee;Lee, Yoo Jin;Kim, Yang Wook;Park, Sihyung;Park, Jinhan;Park, Kang Min;Jin, Kyubok;Park, Bong Soo
    • 고신대학교 의과대학 학술지
    • /
    • 제33권3호
    • /
    • pp.337-346
    • /
    • 2018
  • Objectives: Serum procalcitonin (PCT) is a specific biomarker that rises after bacterial infection, and levels of PCT are known to correlate with the severity and mortality of patients with pneumonia and sepsis. However, the usefulness of PCT levels in acute pyelonephritis is unknown. This study aimed to evaluate the effectiveness of using the PCT level as a predictive test for bacteremia in acute pyelonephritis. Methods: Between January 2012 and June 2013, 140 patients diagnosed with acute pyelonephritis were admitted to Haeundae Paik Hospital. Serum PCT, C-reactive protein (CRP), and white blood cell (WBC) levels at pre- and post- treatment were measured. Blood and urine cultures were obtained from all patients. The levels of PCT, CRP, and WBCs were each compared between the blood culture-positive and blood culture-negative groups to assess their effectiveness in predicting bacteremia. Results: Pre-treatment PCT level was 0.77 ng/mL (95% CI: 0.42-1.60 ng/mL) in the blood culture-negative group and 4.89 ng/mL (95% CI: 2.88-9.04 ng/mL) in the blood culture-positive group, and the increase between the two groups was statistically significant. The area under the receiver operating characteristic curve of PCT level for prediction of bacteremia was 0.728. A cut-off value of 1.23 ng/mL indicated a sensitivity of 79.0 % and specificity of 60.0 % for PCT level. Conclusions: Serum PCT level is a useful predictive test for bacteremia in acute pyelonephritis. Through the early detection of bacteremia, serum PCT level can help estimate the prognosis and predict complications such as sepsis.

Heat Shock Factor 1 Predicts Poor Prognosis of Gastric Cancer

  • Kim, Seok-Jun;Lee, Seok-Cheol;Kang, Hyun-Gu;Gim, Jungsoo;Lee, Kyung-Hwa;Lee, Seung-Hyun;Chun, Kyung-Hee
    • Yonsei Medical Journal
    • /
    • 제59권9호
    • /
    • pp.1041-1048
    • /
    • 2018
  • Purpose: Heat shock factor 1 (HSF1) is a key regulator of the heat shock response and plays an important role in various cancers. However, the role of HSF1 in gastric cancer is still unknown. The present study evaluated the function of HSF1 and related mechanisms in gastric cancer. Materials and Methods: The expression levels of HSF1 in normal and gastric cancer tissues were compared using cDNA microarray data from the NCBI Gene Expression Omnibus (GEO) dataset. The proliferation of gastric cancer cells was analyzed using the WST assay. Transwell migration and invasion assays were used to evaluate the migration and invasion abilities of gastric cancer cells. Protein levels of HSF1 were analyzed using immunohistochemical staining of tissue microarrays from patients with gastric cancer. Results: HSF1 expression was significantly higher in gastric cancer tissue than in normal tissue. Knockdown of HSF1 reduced the proliferation, migration, and invasion of gastric cancer cells, while HSF1 overexpression promoted proliferation, migration, and invasion of gastric cancer cells. Furthermore, HSF1 promoted the proliferation of gastric cancer cells in vivo. In Kaplan-Meier analysis, high levels of HSF1 were associated with poor prognosis for patients with gastric cancer (p=0.028). Conclusion: HSF1 may be closely associated with the proliferation and motility of gastric cancer cells and poor prognosis of patients with gastric cancer. Accordingly, HSF1 could serve as a prognostic marker for gastric cancer.

Chicken serum uric acid level is regulated by glucose transporter 9

  • Ding, Xuedong;Peng, Chenglu;Li, Siting;Li, Manman;Li, Xinlu;Wang, Zhi;Li, Yu;Wang, Xichun;Li, Jinchun;Wu, Jinjie
    • Animal Bioscience
    • /
    • 제34권4호
    • /
    • pp.670-679
    • /
    • 2021
  • Objective: Glucose transporter 9 (GLUT9) is a uric acid transporter that is associated with uric absorption in mice and humans; but it is unknown whether GLUT9 involves in chicken uric acid regulation. This experiment aimed to investigate the chicken GLUT9 expression and serum uric acid (SUA) level. Methods: Sixty chickens were divided into 4 groups (n = 15): a control group (NC); a sulfonamide-treated group (SD) supplemented with sulfamonomethoxine sodium via drinking water (8 mg/L); a fishmeal group (FM) supplemented with 16% fishmeal in diet; and a uric acid-injection group (IU), where uric acid (250 mg/kg) was intraperitoneally injected once a day. The serum was collected weekly to detect the SUA level. Liver, kidney, jejunum, and ileum tissues were collected to detect the GLUT9 mRNA and protein expression. Results: The results showed in the SD and IU groups, the SUA level increased and GLUT9 expression increased in the liver, but decreased in the kidney, jejunum, and ileum. In the FM group, the SUA level decreased slightly and GLUT9 expression increased in the kidney, but decreased in the liver, jejunum, and ileum. Correlation analysis revealed that liver GLUT9 expression correlated positively, and renal GLUT9 expression correlated negatively with the SUA level. Conclusion: These results demonstrate that there may be a feedback regulation of GLUT9 in the chicken liver and kidney to maintain the SUA balance; however, the underlying mechanism needs to be investigated in future studies.

Mechanistic insight into the progressive retinal atrophy disease in dogs via pathway-based genome-wide association analysis

  • Sheet, Sunirmal;Krishnamoorthy, Srikanth;Park, Woncheoul;Lim, Dajeong;Park, Jong-Eun;Ko, Minjeong;Choi, Bong-Hwan
    • Journal of Animal Science and Technology
    • /
    • 제62권6호
    • /
    • pp.765-776
    • /
    • 2020
  • The retinal degenerative disease, progressive retinal atrophy (PRA) is a major reason of vision impairment in canine population. Canine PRA signifies an inherently dissimilar category of retinal dystrophies which has solid resemblances to human retinis pigmentosa. Even though much is known about the biology of PRA, the knowledge about the intricate connection among genetic loci, genes and pathways associated to this disease in dogs are still remain unknown. Therefore, we have performed a genome wide association study (GWAS) to identify susceptibility single nucleotide polymorphisms (SNPs) of PRA. The GWAS was performed using a case-control based association analysis method on PRA dataset of 129 dogs and 135,553 markers. Further, the gene-set and pathway analysis were conducted in this study. A total of 1,114 markers associations with PRA trait at p < 0.01 were extracted and mapped to 640 unique genes, and then selected significant (p < 0.05) enriched 35 gene ontology (GO) terms and 5 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways contain these genes. In particular, apoptosis process, homophilic cell adhesion, calcium ion binding, and endoplasmic reticulum GO terms as well as pathways related to focal adhesion, cyclic guanosine monophosphate)-protein kinase G signaling, and axon guidance were more likely associated to the PRA disease in dogs. These data could provide new insight for further research on identification of potential genes and causative pathways for PRA in dogs.

CircCOL1A2 Sponges MiR-1286 to Promote Cell Invasion and Migration of Gastric Cancer by Elevating Expression of USP10 to Downregulate RFC2 Ubiquitination Level

  • Li, Hang;Chai, Lixin;Ding, Zujun;He, Huabo
    • Journal of Microbiology and Biotechnology
    • /
    • 제32권7호
    • /
    • pp.938-948
    • /
    • 2022
  • Gastric cancers (GC) are generally malignant tumors, occurring with high incidence and threatening public health around the world. Circular RNAs (circRNAs) play crucial roles in modulating various cancers, including GC. However, the functions of circRNAs and their regulatory mechanism in colorectal cancer (CRC) remain largely unknown. This study focuses on both the role of circCOL1A2 in CRC progression as well as its downstream molecular mechanism. Quantitative polymerase chain reaction (qPCR) and western blot were adopted for gene expression analysis. Functional experiments were performed to study the biological functions. Fluorescence in situ hybridization (FISH) and subcellular fraction assays were employed to detect the subcellular distribution. Luciferase reporter, RNA-binding protein immunoprecipitation (RIP), co-immunoprecipitation (Co-IP), RNA pull-down, and immunofluorescence (IF) and immunoprecipitation (IP) assays were used to explore the underlying mechanisms. Our results found circCOL1A2 to be not only upregulated in GC cells, but that it also propels the migration and invasion of GC cells. CircCOL1A2 functions as a competing endogenous RNA (ceRNA) by sequestering microRNA-1286 (miR-1286) to modulate ubiquitin-specific peptidase 10 (USP10), which in turn spurs the migration and invasion of GC cells by regulating RFC2. In sum, CircCOL1A2 sponges miR-1286 to promote cell invasion and migration of GC by elevating the expression of USP10 to downregulate the level of RFC2 ubiquitination. Our study offers a potential novel target for the early diagnosis and treatment of GC.

SCFFBS1 Regulates Root Quiescent Center Cell Division via Protein Degradation of APC/CCCS52A2

  • Geem, Kyoung Rok;Kim, Hyemin;Ryu, Hojin
    • Molecules and Cells
    • /
    • 제45권10호
    • /
    • pp.695-701
    • /
    • 2022
  • Homeostatic regulation of meristematic stem cells accomplished by maintaining a balance between stem cell self-renewal and differentiation is critical for proper plant growth and development. The quiescent center (QC) regulates root apical meristem homeostasis by maintaining stem cell fate during plant root development. Cell cycle checkpoints, such as anaphase promoting complex/cyclosome/cell cycle switch 52 A2 (APC/CCCS52A2), strictly control the low proliferation rate of QC cells. Although APC/CCCS52A2 plays a critical role in maintaining QC cell division, the molecular mechanism that regulates its activity remains largely unknown. Here, we identified SCFFBS1, a ubiquitin E3 ligase, as a key regulator of QC cell division through the direct proteolysis of CCS52A2. FBS1 activity is positively associated with QC cell division and CCS52A2 proteolysis. FBS1 overexpression or ccs52a2-1 knockout consistently resulted in abnormal root development, characterized by root growth inhibition and low mitotic activity in the meristematic zone. Loss-of-function mutation of FBS1, on the other hand, resulted in low QC cell division, extremely low WOX5 expression, and rapid root growth. The 26S proteasome-mediated degradation of CCS52A2 was facilitated by its direct interaction with FBS1. The FBS1 genetically interacted with APC/CCCS52A2-ERF115-PSKR1 signaling module for QC division. Thus, our findings establish SCFFBS1-mediated CCS52A2 proteolysis as the molecular mechanism for controlling QC cell division in plants.

Inhibition of VRK1 suppresses proliferation and migration of vascular smooth muscle cells and intima hyperplasia after injury via mTORC1/β-catenin axis

  • Sun, Xiongshan;Zhao, Weiwei;Wang, Qiang;Zhao, Jiaqi;Yang, Dachun;Yang, Yongjian
    • BMB Reports
    • /
    • 제55권5호
    • /
    • pp.244-249
    • /
    • 2022
  • Characterized by abnormal proliferation and migration of vascular smooth muscle cells (VSMCs), neointima hyperplasia is a hallmark of vascular restenosis after percutaneous vascular interventions. Vaccinia-related kinase 1 (VRK1) is a stress adaption-associated ser/thr protein kinase that can induce the proliferation of various types of cells. However, the role of VRK1 in the proliferation and migration of VSMCs and neointima hyperplasia after vascular injury remains unknown. We observed increased expression of VRK1 in VSMCs subjected to platelet-derived growth factor (PDGF)-BB by western blotting. Silencing VRK1 by shVrk1 reduced the number of Ki-67-positive VSMCs and attenuated the migration of VSMCs. Mechanistically, we found that relative expression levels of β-catenin and effectors of mTOR complex 1 (mTORC1) such as phospho (p)-mammalian target of rapamycin (mTOR), p-S6, and p-4EBP1 were decreased after silencing VRK1. Restoration of β-catenin expression by SKL2001 and re-activation of mTORC1 by Tuberous sclerosis 1 siRNA (siTsc1) both abolished shVrk1-mediated inhibitory effect on VSMC proliferation and migration. siTsc1 also rescued the reduced expression of β-catenin caused by VRK1 inhibition. Furthermore, mTORC1 re-activation failed to recover the attenuated proliferation and migration of VSMC resulting from shVrk1 after silencing β-catenin. We also found that the vascular expression of VRK1 was increased after injury. VRK1 inactivation in vivo inhibited vascular injury-induced neointima hyperplasia in a β-catenin-dependent manner. These results demonstrate that inhibition of VRK1 can suppress the proliferation and migration of VSMC and neointima hyperplasia after vascular injury via mTORC1/β-catenin pathway.