Relevant bibliographies by topics / FVB

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Academic literature on the topic 'FVB'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 January 2023

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Journal articles on the topic "FVB"

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Li, Tong-Tong, Susana Larrucea, Shiloe Souza, Suzanne M. Leal, José A. López, Edward M. Rubin, Bernhard Nieswandt, and Paul F. Bray. "Genetic variation responsible for mouse strain differences in integrin α2 expression is associated with altered platelet responses to collagen." Blood 103, no. 9 (May 1, 2004): 3396–402. http://dx.doi.org/10.1182/blood-2003-10-3721.

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Abstract As mouse models have become commonplace for studying hemostasis and thrombosis, we considered whether the mouse system had utility for assessing genetic alterations in platelet receptors. Platelets from 5 mouse strains (C57BL/6 [C57], FVB/N [FVB], BALB/c, C3H/He, and 129Sv) showed only minor differences in the expression of integrin αIIb, integrin β3, glycoprotein (GP) Ibα, or GPVI across strains. However, FVB platelets expressed approximately 50% the level of integrin α2 as platelets from other strains (P < .0001). We bred FVB mice with C57 and assessed α2 expression in FVB/C57xFVB/C57 (F2) offspring. Linkage analysis demonstrated the gene responsible for α2 levels is tightly linked to the D13mit260 marker (log odds [lod] score 6.7) near the α2 gene. FVB platelets showed reduced aggregation and a longer lag phase to collagen. FVB and C57 platelets aggregated similarly to collagen-related peptide, but FVB platelets showed a reduction in rhodocytin-induced Syk and PLCγ2 tyrosine phosphorylation. Thus, FVB platelets express half the level of α2 as other mouse strains, a trait linked to the α2 gene and seemingly responsible for reduced platelet aggregation to collagen. These strain differences serve as a useful model for the 2-fold difference in human platelet α2β1 expression and demonstrate that α2β1 participates in signaling during platelet activation. (Blood. 2004;103:3396-3402)
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Kim, Na-Won, Sun-Min Seo, Eun-Seon Yoo, Ah-Reum Kang, Ji-Hun Lee, Jae-Hoon Lee, Byeong-Cheol Kang, Han-Woong Lee, and Yang-Kyu Choi. "Short-term carcinogenicity study of N-methyl-N-nitrosourea in FVB-Trp53 heterozygous mice." PLOS ONE 18, no. 1 (January 6, 2023): e0280214. http://dx.doi.org/10.1371/journal.pone.0280214.

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Carcinogenicity tests predict the tumorigenic potential of various substances in the human body by studying tumor induction in experimental animals. There is a need for studies that explore the use of FVB/N-Trp53em2Hwl/Korl (FVB-Trp53+/-) mice, created by TALEN-mediated gene targeting in Korea, in carcinogenicity tests. This study was performed to determine whether FVB-Trp53+/- mice are a suitable model for short-term carcinogenicity studies. To compare the carcinogenicity at different concentrations, 25, 50, and 75 mg/kg of N-methyl-N-nitrosourea (MNU), a known carcinogen, were administered intraperitoneally to FVB-Trp53+/- and wild-type male mice. After 26 weeks, the survival rate was significantly reduced in FVB-Trp53+/- mice compared to the wild-type mice in the 50 and 75 mg/kg groups. The incidence of thymic malignant lymphoma (TML) in the 50 and 75 mg/kg groups was 54.2 and 59.1% in FVB-Trp53+/- male mice, respectively. TML metastasized to the lungs, spleen, lymph nodes, liver, kidney, and heart in FVB-Trp53+/- male mice. Furthermore, the incidence of primary lung tumors, such as adenomas and adenocarcinomas, was 65.4, 62.5, and 45.4% in the FVB-Trp53+/- mice of the 25, 50, and 75 mg/kg groups, respectively. The main tumor types in FVB-Trp53+/- mice were TML and primary lung tumors, regardless of the dose of MNU administered. These results suggest that systemic tumors may result from malfunctions in the p53 gene and pathway, which is an important factor in the pathogenesis of human cancers. Therefore, FVB-Trp53 heterozygous mice are suitable for short-term carcinogenicity tests using positive carcinogens, and that the best result using MNU, a positive carcinogen, might have a single dose of 50 mg/kg.
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Sclafani, Anthony, Steven Zukerman, and Karen Ackroff. "Fructose- and glucose-conditioned preferences in FVB mice: strain differences in post-oral sugar appetition." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 12 (December 15, 2014): R1448—R1457. http://dx.doi.org/10.1152/ajpregu.00312.2014.

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Recent studies indicate that, unlike glucose, fructose has little or no post-oral preference conditioning actions in C57BL/6J (B6) mice. The present study determined whether this is also the case for FVB mice, which overconsume fructose relative to B6 mice. In experiment 1, FVB mice strongly preferred a noncaloric 0.1% sucralose + 0.1% saccharin (S+S) solution to 8% fructose in a 2-day choice test but switched their preference to fructose after separate experience with the two sweeteners. Other FVB mice displayed a stronger preference for 8% glucose over S+S. In a second experiment, ad libitum-fed FVB mice trained 24 h/day acquired a significant preference for a flavor (CS+) paired with intragastric (IG) self-infusions of 16% fructose over a different flavor (CS−) paired with IG water infusions. IG fructose infusions also conditioned flavor preferences in food-restricted FVB mice trained 1 h/day. IG infusions of 16% glucose conditioned stronger preferences in FVB mice trained 24- or 1 h/day. Thus, fructose has post-oral flavor conditioning effects in FVB mice, but these effects are less pronounced than those produced by glucose. Further studies of the differential post-oral conditioning effects of fructose and glucose in B6 and FVB mice should enhance our understanding of the physiological processes involved in sugar reward.
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Hakim, Luthfi, Ragil Widyorini, Widyanto Dwi Nugroho, and Tibertius Agus Prayitno. "Performance of Citric Acid-Bonded Oriented Board from Modified Fibrovascular Bundle of Salacca (Salacca zalacca (Gaertn.) Voss) Frond." Polymers 13, no. 23 (November 24, 2021): 4090. http://dx.doi.org/10.3390/polym13234090.

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The fibrovascular bundle (FVB) in palm plants consists of fiber and vascular tissue. Geometrically, it is a long fiber that can be used as an oriented board raw material. This research aimed to examine the performance of citric acid-bonded orientation boards from modified FVB salacca frond under NaOH + Na2SO3 treatment and the bonding mechanism between the modified FVB frond and citric acid. The results showed that changes in the chemical composition of FVB have a positive effect on the contact angle and increase the cellulose crystallinity index. Furthermore, the mechanical properties of the oriented board showed that 1% NaOH + 0.2% Na2SO3 with 60 min immersion has a higher value compared to other treatments. The best dimension stability was on a board with the modified FVB of 1% NaOH + 0.2% Na2SO3 with 30 and 60 min immersion. The bonding mechanism evaluated by FTIR spectra also showed that there is a reaction between the hydroxyl group in the modified FVB and the carboxyl group in citric acid. This showed that the modified combination treatment of NaOH+Na2SO3 succeeded in increasing the mechanical properties and dimensional stability of the orientation board from the FVB salacca frond.
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Hakim, L., R. Widyorini, W. D. Nugroho, T. A. Prayitno, and Y. S. Lubis. "Contact angle of modified fibrovascular bundle of salacca (Salacca sumatrana Becc.) frond by NaOH+Na2SO3 combination." IOP Conference Series: Earth and Environmental Science 912, no. 1 (November 1, 2021): 012012. http://dx.doi.org/10.1088/1755-1315/912/1/012012.

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Abstract The fibrovascular bundle (FVB) of the salacca frond is one of the potential raw materials in the development of bio-composite technology. The purpose of this study was to investigate the wettability of FVB using the contact angle method after the alkali modification treatment. The method of this research was to use FVB frond of Salacca sumatrana Becc. which was treated with alkaline modification of the combination of NaOH+Na2SO3 at various concentrations. The results showed that the combination of NaOH 1M+Na2SO3 0.4 M had the smallest contact angle, which means that the FVB has a good wettability value compared to the control treatment. Based on the results, it can be concluded that the modification of NaOH+Na2SO3 can increase the wettability of FVB.
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Jung, Jin Hyuk, and Mary R. Loeken. "Diabetic Embryopathy Susceptibility in Mice Is Associated with Differential Dependence on Glucosamine and Modulation of High Glucose-Induced Oxidative Stress." Antioxidants 10, no. 8 (July 21, 2021): 1156. http://dx.doi.org/10.3390/antiox10081156.

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The high KM glucose transporter, GLUT2 (SLC2A2), is expressed by embryos and causes high rates of glucose transport during maternal hyperglycemic episodes in diabetic pregnancies and causes congenital malformations (diabetic embryopathy). GLUT2 is also a low KM transporter of the amino sugar, glucosamine (GlcN), which enters the hexosamine biosynthetic pathway (HBP) and provides substrate for glycosylation reactions. Exogenous GlcN also increases activity of the pentose phosphate pathway (PPP), which increases production of NADPH reducing equivalents. GLUT2-transported GlcN is inhibited by high glucose concentrations. Not all mouse strains are susceptible to diabetic embryopathy. The aim of this study was to test the hypothesis that susceptibility to diabetic embryopathy is related to differential dependence on exogenous GlcN for glycosylation or stimulation of the PPP. We tested this using murine embryonic stem cell (ESC) lines that were derived from embryopathy-susceptible FVB/NJ (FVB), and embryopathy-resistant C57Bl/6J (B6), embryos in the presence of low or high glucose, and in the presence or absence of GlcN. There were no significant differences in Glut2 expression, or of glucose or GlcN transport, between FVB and B6 ESC. GlcN effects on growth and incorporation into glycoproteins indicated that FVB ESC are more dependent on exogenous GlcN than are B6 ESC. GlcN stimulated PPP activity in FVB but not in B6 ESC. High glucose induced oxidative stress in FVB ESC but not in B6 ESC. These results indicate that FVB embryos are more dependent on exogenous GlcN for glycosylation, but also for stimulation of the PPP and NADPH production, than are B6 embryos, thereby rendering FVB embryos more susceptible to high glucose to induce oxidative stress.
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Ayme-Dietrich, Estelle, Sylvia Da Silva, Ghina Alame Bouabout, Alizée Arnoux, Jérôme Guyonnet, Guillaume Becker, and Laurent Monassier. "Characterization of the spontaneous degenerative mitral valve disease in FVB mice." PLOS ONE 16, no. 9 (September 2, 2021): e0257022. http://dx.doi.org/10.1371/journal.pone.0257022.

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Background The development of new non-surgical treatments dedicated to mitral valve degeneration is limited by the absence of relevant spontaneous and rapidly progressing animal experimental models. Animals We characterized the spontaneous mitral valve degeneration in two inbred FVB mouse strains compared to C57BL/6J and investigated a contribution of the serotonergic system. Methods Males and females FVB/NJ and FVB/NRj were compared to the putative C57BL/6J control at 12, 16, 20 and 24 weeks of age. Body weight, systolic blood pressure, heart rate, urinary 5-hydroxyindoleacetic acid (5-HIAA), whole blood and plasma serotonin, tail bleeding time, blood cell count, plasma TGF-β1 and plasma natriuretic peptide concentrations were measured. Myocardium and mitral valves were characterized by histology. mRNA mitral expression of 5-HT2A and 5-HT2B receptors was measured in the anterior leaflet. Cardiac anatomy and function were assessed by echocardiography. Results Compared to C57BL/6J, FVB mice strains did not significantly differ regarding body weight increase, arterial blood pressure and heart rate. A progressive augmentation of plasma pro-ANP was observed in FVB mice. Nevertheless, no cardiac hypertrophy or left-ventricular fibrosis were observed. Accordingly, plasma TGF-β1 was not different among the three strains. Conversely, FVB mice demonstrated a high prevalence of fibromyxoid highly cellularized and enriched in glycosaminoglycans lesions, inducing major mitral leaflets thickening without increase in length. The increased thickness was correlated with urinary 5-HIAA and blood platelet count. Whole blood serotonin concentration was similar in the two strains but, in FVB, a reduction of plasma serotonin was observed together with an increase of the bleeding time. Finally, echocardiography identified left atrial and left ventricular remodeling associated with thickening of both mitral leaflets and mitral insufficient in 30% of FVB mice but no systolic protrusion of mitral leaflets towards the atrium. Conclusion The FVB mouse strain is highly prone to spontaneous mitral myxomatous degeneration. A contribution of the peripheral serotonergic system is suggested.
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Criswell, David S., Frank W. Booth, Franco DeMayo, Robert J. Schwartz, Scott E. Gordon, and Marta L. Fiorotto. "Overexpression of IGF-I in skeletal muscle of transgenic mice does not prevent unloading-induced atrophy." American Journal of Physiology-Endocrinology and Metabolism 275, no. 3 (September 1, 1998): E373—E379. http://dx.doi.org/10.1152/ajpendo.1998.275.3.e373.

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This study examined the association between local insulin-like growth factor I (IGF-I) overexpression and atrophy in skeletal muscle. We hypothesized that endogenous skeletal muscle IGF-I mRNA expression would decrease with hindlimb unloading (HU) in mice, and that transgenic mice overexpressing human IGF-I (hIGF-I) specifically in skeletal muscle would exhibit less atrophy after HU. Male transgenic mice and nontransgenic mice from the parent strain (FVB) were divided into four groups ( n = 10/group): 1) transgenic, weight-bearing (IGF-I/WB); 2) transgenic, hindlimb unloaded (IGF-I/HU); 3) nontransgenic, weight-bearing (FVB/WB); and 4) nontransgenic, hindlimb unloaded (FVB/HU). HU groups were hindlimb unloaded for 14 days. Body mass was reduced ( P < 0.05) after HU in both IGF-I (−9%) and FVB mice (−13%). Contrary to our hypothesis, we found that the relative abundance of mRNA for the endogenous rodent IGF-I (rIGF-I) was unaltered by HU in the gastrocnemius (GAST) muscle of wild-type FVB mice. High-level expression of hIGF-I peptide and mRNA was confirmed in the GAST and tibialis anterior (TA) muscles of the transgenic mice. Nevertheless, masses of the GAST and TA muscles were reduced ( P < 0.05) in both FVB/HU and IGF-I/HU groups compared with FVB/WB and IGF-I/WB groups, respectively, and the percent atrophy in mass of these muscles did not differ between FVB and IGF-I mice. Therefore, skeletal muscle atrophy may not be associated with a reduction of endogenous rIGF-I mRNA level in 14-day HU mice. We conclude that high local expression of hIGF-I mRNA and peptide in skeletal muscle alone cannot attenuate unloading-induced atrophy of fast-twitch muscle in mice.
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Borenshtein, Diana, Prashant R. Nambiar, Elizabeth B. Groff, James G. Fox, and David B. Schauer. "Development of Fatal Colitis in FVB Mice Infected with Citrobacter rodentium." Infection and Immunity 75, no. 7 (April 30, 2007): 3271–81. http://dx.doi.org/10.1128/iai.01810-06.

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ABSTRACT Citrobacter rodentium is the causative agent of transmissible murine colonic hyperplasia. The disease is characterized by severe but temporary epithelial hyperplasia with limited inflammation in the descending colon of adult mice on a variety of genetic backgrounds. The natural history of infection with this murine pathogen has been characterized in outbred Swiss Webster (SW) mice but not in the cognate inbred FVB strain. In contrast to subclinical infection in SW mice, 12-week-old FVB mice developed overt disease with significant weight loss and mortality beginning by 9 days postinoculation (dpi). By 21 dpi, more than 75% of infected FVB mice died or had to be euthanized, whereas no mortality developed in SW mice. Mortality in FVB mice was fully prevented by fluid therapy. Fecal shedding of bacteria was similar in both groups through 9 dpi; however, a slight but significant delay in bacterial clearance was observed in FVB mice by 12 to 18 dpi. SW mice developed hyperplasia with minimal inflammation in the descending colon. FVB mice developed epithelial cell hyperproliferation, severe inflammation with erosions and ulcers, and epithelial atypia by 6 dpi in the descending colon. In the majority of surviving FVB mice, colonic lesions, including epithelial atypia, were reversible, although a small percentage (5 to 7%) exhibited chronic colitis through 7 months postinoculation. The existence of susceptible and resistant lines of mice with similar genetic backgrounds will facilitate the identification of host factors responsible for the outcome of infection and may lead to the development of novel strategies for preventing and treating infectious colitis.
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Hou, Xue-Fei, Ya-Bo Zhao, Yue-Xiong Yang, Chen Ma, Meng Li, Xin Li, Guo-Rui Ma, Li-Su Zhu, Lin Xu, and Qi-Xin Zhou. "High Morphine Use Disorder Susceptibility Is Predicted by Impaired Learning Ability in Mice." Brain Sciences 12, no. 12 (December 1, 2022): 1650. http://dx.doi.org/10.3390/brainsci12121650.

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An obvious reason for substance uses disorders (SUDs) is drug craving and seeking behavior induced by conditioned context, which is an abnormal solid context memory. The relationship between susceptibility to SUD and learning ability remains unclear in humans and animal models. In this study, we found that susceptibility to morphine use disorder (MUD) was negatively correlated with learning ability in conditioned place preference (CPP) in C57 mice. By using behavioral tests, we identified the FVB mouse as learning impaired. In addition, we discovered that learning-relevant proteins, such as the glutamate receptor subunits GluA1, NR1, and NR2A, were decreased in FVB mice. Finally, we assessed the context learning ability of FVB mice using the CPP test and priming. We found that FVB mice had lower learning performance with respect to normal memory but higher performance of morphine-reinstatement memory. Compared to C57 mice, FVB mice are highly sensitive to MUDs. Our results suggest that SUD susceptibility is predicted by impaired learning ability in mice; therefore, learning ability can play a simple and practical role in identifying high-risk SUD groups.
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Dissertations / Theses on the topic "FVB"

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Kress, Dagmar Corine. "Etablierung und Charakterisierung eines Wachstumshormon-transgenen Mausmodells auf Inzuchtbasis (FVB/N)." Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-56582.

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Benson, Brenda. "Downhill Treadmill Running Does Not Induce Muscle Damage in FVB Mice." BYU ScholarsArchive, 2014. https://scholarsarchive.byu.edu/etd/4259.

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Downhill treadmill running is a commonly used method to cause exercise-induced muscle damage, especially in rodents. Previous studies have evaluated which muscles in rats are more prone to damage. However research using downhill run mice (DHR) has shown some inconsistencies in which muscle is best analyzed for damage. Purpose: The purpose of this study was to quantify the damage in various muscles in a mouse after a single bout of DHR. Methods: Male FVB mice (5 months) were injected with Evans Blue dye (EBD) and then either used as control (CON) or run downhill (-16°) at 20 meters per minute (m/min) for 30 minutes. Twenty-four hours after exercise, the gastrocnemius, soleus, plantaris, tibialis anterior (TA), quadriceps, and triceps brachii muscles were harvested (n = 6 per group per muscle). Cross-sectional slices were obtained, fixed, and mounted to analyze EBD infiltration, dystrophin (Dys), and centralized nuclei. The samples were then imaged using a fluorescent microscope. The entire sample was captured using 20x magnification, and the total number of cells, EBD+, Dys-, and centralized nuclei, were counted. A blood sample was collected to measure plasma creatine kinase (CK) activity. Results: Total number of cells was not different between groups (p > 0.05). No significant difference in any of the markers of muscle damage was found in any muscle between CON and DHR (p > 0.05). Conclusion: These data suggest that DHR does not induce muscle damage in adult (5 months) male FVB mice.
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Werthat, Florian. "Postnatale Entwicklung einer Subpopulation GABAerger Interneurone im sensomotorischen Cortex der transgenen Mauslinie FVB-Tg(GadGFP)45704Swn/J." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-143154.

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Santos, Sergio Henrique Sousa. "Avaliação dos distúrbios metabólicos produzidos pela deleção genética do receptor de angiotensina - (1-7), mas, em camundongos FVB/N." Universidade Federal de Minas Gerais, 2007. http://hdl.handle.net/1843/MCSC-78BU5F.

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The metabolic syndrome, also known as insulin resistance syndrome, is characterized by the variable coexistence of obesity, insulin resistance, dislipidemy and hypertension. The angiotensin-(1-7) presents an important contaregulatory role inside Renin Angiotensin System, opposing some times to angiotensina II effects. It has been shown that G protein-coupled receptor, Mas, mediates many actions of angiotensin-(1-7). We have recently observed that Mas-knockout male mice (Mas-/-) in the pure, FVB/N genetic background, presents elevated blood pressure levels and endothelial dysfunction, alterations present in the metabolic syndrome. The aim of this study was to ascertain whether genetic deletion of Mas also changes lipidic and glycemic profile and the mechanisms of these alterations. Ten weeks old Mas-/- and WT mice were used. Curves of plasma glycemia versus time were built after intraperitoneal application of insulin (0.75U/Kg BW) or glucose (2g/Kg BW). After sacrifice, the tissues were weighted and reserved for western blotting and Real-Time PCR. The lipidic profile and the plasma levels of leptin and adiponectin were analyzed using ELISA kits and TGF-â, angiotensinogen and TNF-á mRNA expression was analyzed by Real Time PCR. Despite of having normal body weight (24.7 ± 0.35 vs 24.8± 0.24 g in WT), young Mas-/- mice presented a marked increase in the fat tissue mass (epididimal= 1.704 ± 0.1516 vs 1.150 ± 0.1259 % of BW in WT and retroperitoneal= 0.6747 ± 0.08576 vs 0.3781 ± 0.04575 % of BW in WT). In addition, these animals presented a state of insulin resistance and glucose intolerance as well as an increase in the fasting glycemia levels (86.6 ± 6.43 vs 56.40 ± 4.98 mg/dl in WT). Furthermore, a significant increase in total cholesterol (92.2 ± 3.65 vs 74.6± 5.67 mg/dl in WT) and triglycerides (70.6 ± 13.3 vs 41.4± 4.07 mg/dl in WT) levels were observed. Part of these alterations can be explained by the increase in the leptin plasma levels (1.3 ± 0.25 vs 0.73 ± 0.17 ng/ml in WT) and the decreased Glut4 receptor protein in Mas-/- adipose tissue. The mRNA expression of TGF-â and angiotensinogen was increased in Mas-/- adipose tissue, while the expression of TNF-á, the food intake and adiponectin plasma levels, were not altered. These results show that Mas deficiency in FVB/N mice leads to dramatic changes in glicemic and lipidic metabolism, inducing a metabolic syndrome- like state.
A síndrome metabólica, também conhecida como síndrome de resistência à insulina, é caracterizada pela coexistência variável de obesidade, hiperinsulinemia, dislipidemia e hipertensão. A angiotensina-(1-7) apresenta um importante papel contraregulatório dentro do Sistema Renina Angiotensina, se opondo, na maioria das vezes, aos efeitos da angiotensina II. Tem sido demonstrado que o receptor acoplado a proteína G, Mas, medeia várias ações da angiotensina-(1-7). Observamos recentemente que camundongos machos knockout para o receptor Mas (Mas-/-) com background genético FVB/N, apresenta pressão sanguínea elevada e disfunção endotelial, alterações presentes no quadro de síndrome metabólica. O objetivo desse estudo foi verificar se a deleção genética do receptor Mas altera o perfil lipídico e glicêmico desses animais e os mecanismos envolvidos nesse processo. Camundongos WT e knockout machos com aproximadamente dez semanas de vida foram utilizados. Curvas de glicemia pelo tempo foram construídas após aplicação intraperitoneal de insulina (0.75U/Kg) ou glicose (2g/Kg). Após o sacrifício os tecidos foram pesados e reservados para western blotting e Real-Time PCR. O perfil lipídico e os níveis plasmáticos de leptina e adiponectina foram avaliados utilizando kits de ELISA e a expressão do mRNA do TGF-â, angiotensinogênio e do TNF-á foram analisados pela técnica de Real-Time PCR. Apesar de apresentar peso corporal igual ao do controle (24.7 ± 0.35 vs 24.8± 0.24 g no WT), os camundongos Mas-/- jovens apresentaram marcante aumento no peso do tecido adiposo (epididimal= 1.704 ± 0.1516 vs 1.150 ± 0.1259 % do PC no WT e retroperitoneal= 0.6747 ± 0.08576 vs 0.3781 ± 0.04575 % do PC no WT). Além disso, esses animais apresentam resistência a insulina e maior intolerância a glicose, bem como um aumento na glicemia de jejum (86.6 ± 6.43 vs 56.40 ± 4.98 mg/dl no WT). Também foram encontrados aumentos significativos nos níveis plasmáticos de colesterol total (92.2 ± 3.65 vs 74.6± 5.67 mg/dl no WT) e triglicérides (70.6 ± 13.3 vs 41.4± 4.07 mg/dl no WT). Parte dessas alterações podem ser explicadas pelo aumento nos níveis séricos de leptina (1.3 ± 0.25 vs 0.73 ± 0.17 ng/ml no WT) e pela diminuição na expressão protéica do receptor Glut-4 no tecido adiposo epididimal dos Mas-/-. A expressão do RNA mensageiro do TGF-â e do angiotensinogênio estão aumentados no tecido adiposo, enquanto a expressão do TNF-á, o consumo de comida e os níveis plasmáticos de adiponectina, não estão alterados. Juntos, esses dados indicam um importante papel do receptor Mas na função cardiovascular e metabólica em camundongos FVB/N e sugerem um quadro de síndrome metabólica nos camundongos knockout Mas.
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Healy, Laura N. "Effect of background strain on the hematologic toxicity ofinhaled benzene in FVB/N-Tg.AC and C57BL/6- Trp 53 +/- knockout mice." NCSU, 2000. http://www.lib.ncsu.edu/theses/available/etd-20000110-094819.

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Benzene is an industrial solvent and a ubiquitous environmental pollutant that induces hematopoietic damage; although, the mechanism by which this damage occurs is uncertain. The hematologic effects of benzene vary widely among different mouse strains, and intermittent exposure of mice to benzene is more highly toxic and carcinogenic than low, constant exposure. The goal of the research described in this dissertation was to investigate the sensitivity of two genetically engineered mouse models of carcinogenesis, Tg.AC and p53 +/- mice, and parental strains FVB/N and C57BL/6 respectively, to hematologic toxicicity resulting from inhaled benzene. Tg.AC mice contain an activated v-Ha-ras oncogene, and the p53 +/- mouse is haplosufficient for the p53 gene. Hypotheses of this work included that benzene ishematotoxic, and that greater genotoxic damage caused by benzene would be evident in the p53 +/- mouse. Another hypothesis was that benzene would induce Tg.AC transgene expression in the spleen. The research was divided into three specific aims. First, genotoxicity resulting from exposure to benzene was determined by micronucleus formation in blood. These studies showed a time-dependent, but not a concentration-dependent increase in micronuclei following benzene exposure. The p53 +/- mice were not more sensitive to benzene-induced micronuclei than the parental strain (p53 +/+). For the second specific aim, benzene hematotoxicity was assessed and spleen analyses were conducted. Benzene induced a significant cytopenia and reduced spleen weight in all of the strains examined. The C57BL/6 mice were less sensitive to benzene hematotoxicity than the FVB/N strain for all of the hematologic parameters examined. For the third specific aim, expression of theTg.AC transgene mRNA was assessed by reverse transcriptase-polymerase chain reaction of splenic tissue. Evidence of the Tg.AC transgene expression was absent in these tissues. Overall, the findings showed a marked strain-related difference between FVB/N and C57BL/6 mice in the hematotoxicity of benzene. In most parameters investigated, the Tg.AC or p53+/- genetic alterations were not useful adjuncts for investigating the hematotoxic mechanisms of benzene. Investigation of the genetic differences between these two mouse strains may lead to further understanding of the biological determinants of benzene hematotoxicity.

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Li, Liang. "Innervation, distribution and morphology of calcitonin gene related peptide and substanceP immunoreactive axons in the whole-mount atria of FVB mice." Master's thesis, University of Central Florida, 2010. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/4598.

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Degeneration of nociceptive afferent axons and terminals in the heart is associated with painless sudden cardiac death. However, innervation, distribution and morphological structures of sympathetic cardiac nociceptive afferent axons and terminals have not yet been fully characterized. The aim of the present study is to characterize the density, arrangement, and structural features of differentiated sympathetic afferent axons and terminals in whole-mount FVB mouse atria. FVB mice (3-6 months old) were perfused and the tissues were fixed. The right and left atria were processed with immunohistochemistry. Calcitonin gene-related peptide (CGRP) and substance P (SP) are two neuropeptides which have been widely used to label sympathetic nociceptive afferent axons in many tissues. CGRP (rabbit anti-CGRP) and SP (Goat anti-SP) primary antibodies were applied, followed by Alexa Fluor 594 and 660 conjugated secondary antibodies. Whole-mount preparations of right and left atria were examined using a laser scanning confocal microscope. We found that 1) CGRP immunoreactive (IR) axon bundles innervated the right and left atria including the auricle and entrance area of the superior vena cava, the inferior vena cava, left precaval vein and pulmonary veins. Large axon bundles entered the area from the major veins and bifurcated into smaller axon bundles and single axon fibers to form terminal end-nets and free endings in the epicardium at each region with a similar pattern. In the atrial muscle layer, varicose CGRP-IR axons had close contacts with muscle fibers. In addition, CGRP-IR axons terminated in the intrinsic cardiac ganglia (ICGs) with varicosities surrounding individual ganglionic principle neurons (PNs). In the aortic arch, the CGRP-IR fibers exhibited similar terminal structures to those seen in the atria. 2) SP-IR axons also projected to the right and left atria and aorta.; Similar to CGRP-IR axons, these SP-IR axons also formed end-nets and free endings in these areas. In cardiac ganglia, SP-IR axons formed varicose endings around many individual PNs. However, a salient difference was found: There appeared to be fewer SP-IR axons and terminals than CGRP-IR axons and terminals in the atria. 3) None of the cardiac PNs in ICG were CGRP-IR or SP-IR. 4) Many SP-IR axon terminals around PNs within ICGs and atrial muscles were found to have colocalized expression of CGRP-IR. Collectively, our data for the first time documented the distribution patterns and morphology of sympathetic afferent axons and terminals in each region of the atria in the mouse model. This will provide a foundation for future analysis of the pathological changes of sympathetic afferent nerves in the atria in different disease models (e.g., diabetes, sleep apnea, and aging). This study was supported by NIH R01 HL-79636.
ID: 030423285; System requirements: World Wide Web browser and PDF reader.; Mode of access: World Wide Web.; Thesis (M.S.)--University of Central Florida, 2010.; Includes bibliographical references (p. 42-48).
M.S.
Masters
Department of Molecular Biology and Microbiology
Medicine
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Nitezki, Tina [Verfasser], and Burkhard [Akademischer Betreuer] Kleuser. "Charakterisierung von Stereotypien bei der FVB/NJ-Maus hinsichtlich metabolischer und immunologischer Aspekte auf die Stoffwechselleistung / Tina Nitezki ; Betreuer: Burkhard Kleuser." Potsdam : Universität Potsdam, 2017. http://d-nb.info/1218402806/34.

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Werthat, Florian [Verfasser], and Benedikt [Akademischer Betreuer] Grothe. "Postnatale Entwicklung einer Subpopulation GABAerger Interneurone im sensomotorischen Cortex der transgenen Mauslinie FVB-Tg(GadGFP)45704Swn/J / Florian Werthat. Betreuer: Benedikt Grothe." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2012. http://d-nb.info/1022524097/34.

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Silva, Fernanda Gaisler da. "Impacto da obesidade no trofismo cardíaco em camundongos C57BL/6 e FVB/NJ: participação da resposta inflamatória e dos receptores Toll-like." reponame:Repositório Institucional da UFABC, 2017.

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Orientadora: Profa. Dra. Marcela Sorelli Carneiro Ramos
Tese (doutorado) - Universidade Federal do ABC, Programa de Pós-Graduação em Biossistemas, 2017.
As doencas cardiovasculares correspondem ao maior risco de morte subita em todo o mundo, a populacao mundial tem se tornado cada vez mais sedentaria e junto as doencas cardiovasculares outros problemas de saude publica aumentam como a obesidade e diabetes mellitus. Os gastos com a saude publica aumentam muito devido a maior incidencia de doencas associadas ao sedentarismo, obesidade, tabagismo, estresse, hipertensao arterial entre outros. Especificamente a obesidade e considerada uma epidemia mundial, que esta associada aos habitos alimentares e sedentarismo, e esta amplamente relacionada ao fator de risco cardiovascular como hipertensao arterial, resistencia insulinica, dislipidemia e diabetes mellitus, que favorecem o processo aterosclerotico e a ocorrencia de eventos cardiovasculares. Ha uma maior prevalencia de hipertensao arterial em individuos obesos e presenca de hipertrofia cardiaca, que e a maior condicao de morbimortalidade cardiovascular. Trata-se de uma doenca cronica relacionada a eventos pro-inflamatorios com acao de diversas citocinas e quimiocinas alem de hormonios envolvidos na resposta imunologica inata. Os receptores Toll-Like fazem parte da Resposta Imunologica Inata e estao presentes em diversos tecidos, incluindo o coracao. Quando ativados desencadeiam uma resposta intracelular, ativando fatores transcricionais, como NF-kB, que leva a transcricao genica de citocinas inflamatorias: IL-6, TNF-¿¿, INF-gama, IL-1. Algumas doencas cardiovasculares sao antecedidas por inflamacoes sistemicas ou locais, demonstrando que as citocinas sao responsaveis por modular o trofismo cardiaco. Diante do exposto, uma analise mais completa envolvendo obesidade e processos inflamatorios com o risco cardiovascular se faz necessaria para a compreensao de moleculas e vias de sinalizacao, reguladas nessa patologia. O presente estudo tem como objetivo avaliar a contribuicao dos fatores inflamatorios na hipertrofia cardiaca induzida por modelo experimental de obesidade. Para tanto, foram utilizados camundongos C57Bl/6 e camundongos FVB/NJ submetidos ao tratamento com dieta rica em gordura contendo 23% proteina, 35,5% carboidrato e 35,9% gordura e foram comparados aos grupos chow (controle) submetidos a dieta composta por 19% de proteina, 56% de carboidrato, 3,5% de gordura por 68 dias de tratamento. Os animais C57Bl/6 apresentaram maior ganho de peso em relacao aos FVB/NJ ao final dos 68 dias de dieta High Fat. O aumento de colesterol serico, insulina, glicemia, epiWAT (epididymal white adipose tissue) foi maior nos animais C57Bl/6. As duas linhagens apresentaram Heart Weight/Body Lenght e Heart Weight/Tibia Lenght maior em relacao ao grupo Chow, ou seja, grupo controle. Atraves da tecnica de Q-PCR os niveis de mRNA dos marcadores moleculares de hipertrofia cardiaca foram avaliados, e o marcador alfa-actina mostrou-se aumentado na linhagem C57Bl/6 enquanto o marcador ANF (atrial natriuretic factor) mostrou-se aumentado na linhagem FVB/NJ, quando comparados aos seus respectivos grupos chow. Os genes TLR2, TLR4, TNF-¿¿, IL-6, MyD88 e NF-kB tambem foram avaliados. A expressao genica de TLR2, MyD88 e NF-kB mostrou-se diminuida nos animais FVB/NJ submetidos a dieta rica em gordura quando comparados aos animais controle. Na linhagem C57Bl/6, observou-se aumento na expressao genica de TNF-¿¿ e NF-kB. A inducao da obesidade promoveu maior ganho de peso na linhagem C57Bl/6 acompanhado de maior adiposidade abdominal e no tecido epididimal, essa linhagem apresentou maior sensibilidade a insulina e maiores niveis de colesterol na dieta High Fat em relacao a linhagem FVB/JN. Houve remodelamento cardiaco em ambas linhagens e a expressao genica de citocinas inflamatorias foi mais evidente na linhagem C57Bl/6, tambem apresentando maior expressao genica de NF-kB. A linhagem FVB/NJ apresentou diminuicao na expressao de MyD88 e NF-kB na dieta High Fat. Com base nos resultados obtidos verificamos que os camundongos C57Bl/6 mostraram-se mais suscetiveis a dieta enquanto a linhagem FVB/JN mostrou-se mais resistente.
Cardiovascular diseases correspond to an increased risk of worldwide sudden death, the world population has become increasingly sedentary and with cardiovascular diseases other public health problems increase such as obesity and diabetes mellitus. Expenditures on public health increase greatly due to a higher incidence of diseases associated with sedentarism, obesity, smoking, stress, hypertension among others. Obesity specifically is considered a worldwide epidemic, which is associated with eating habits and sedentary lifestyle, and is largely related to cardiovascular risk such as hypertension, insulin resistance, dyslipidemia and diabetes mellitus, which favor the atherosclerotic process and occurrence of cardiovascular events. There is a higher prevalence of hypertension in obese and presence of cardiac hypertrophy, which is a higher cardiovascular morbidity and mortality condition. It is a chronic disease related to pro-inflammatory events with the action of various cytokines and chemokines in addition to hormones involved in the innate immune response. Toll-like receptors are part of the innate immune response and are present in several tissues including the heart. When activated trigger an intracellular response, activating transcriptional factors such as NF-kB, which leads to the genetic transcription of inflammatory cytokines: IL-6, TNF- á, IFN-gamma, IL-1. Some cardiovascular diseases are antecedents of systemic or local inflammations, demonstrating that cytokines are responsible for modulating cardiac trophism. In summary, a more complete analysis involving obesity and inflammatory processes with cardiovascular risk to understand molecules and signaling pathways regulated in this pathology are needed. The present study aims to evaluate the contribution of inflammatory factors in cardiac hypertrophy induced by the experimental model of obesity. For this, C57Bl/6 mice and FVB/NJ mice submitted to a high fat diet containing 23% protein, 35.5% carbohydrate and 35.9% fat were compared to the Chow (control) groups submitted to a chow diet containing 19% protein, 56% carbohydrate, 3.5% fat for 68 days of treatment. The C57Bl/6 animals presented greater weight gain in relation to FVB/NJ at the end of 68 days of high fat diet. Serum cholesterol, insulin, glycemia, epiWAT (epididymal white adipose tissue) increased in C57B1/6 animals. Both strains presented Heart Weight/Body Lenght and Heart Weight/Tibia Lenght higher than the Chow group. mRNA levels of cardiac hypertrophy molecular markers were evaluated through Q-PCR technique, and the alpha-actin marker was shown to be increased in the C57B1/6 lineage while the ANF (atrial natriuretic factor) marker was shown to be increased in the FVB/NJ lineage, when compared to their respective chow groups. TLR2, TLR4, TNF-á, IL-6, MyD88 and NF-kB genes were also evaluated. Gene expression of TLR2, MyD88 and NF-kB were decreased in FVB / NJ animals submitted to a high fat diet when compared to control animals. There was an increase in the gene expression of TNF-á and NF-kB in C57Bl/6 lineage. The induction of obesity promoted greater weight gain in the C57Bl/6 mice followed by a greater abdominal and epididymal adiposity, this lineage presented higher insulin sensitivity and higher cholesterol levels in the High Fat diet when compared to the FVB/JN lineage. There was cardiac remodeling in both lineages and inflammatory cytokines gene expression were more evident in the C57Bl/6 mice, also presenting a greater gene expression of NF-kB. The FVB/NJ mice showed decreased expression of MyD88 and NF-kB on the High Fat diet. Based on the results, we found that the C57Bl/6 mice were more susceptible to the High Fat diet than the FVB/JN strain.
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Healy, Laura Nan. "Effect of background strain on the hematologic toxicity of inhaled benzene in FVB/N-Tg. AC and C57BL/6- Trp 53 +/- knockout mice." Raleigh, NC : North Carolina State University, 1999. http://www.lib.ncsu.edu/etd/public/etd-16489100100190/etd.pdf.

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Books on the topic "FVB"

1

(Firm), C. G. Boerner. Gedruckte Kunst vom Meister FVB bis Edvard Munch. Düsseldorf: C.G. Boerner, 1986.

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Fab. St. Asaph: Cluny Press, 2009.

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Sever, Aleksandr. FSB. Moskva: I︠A︡uza, 2010.

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(Federation), Russia. FSB Rossii. Moskva: Izdatelʹ E. Rodionova, 1997.

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30th Feb. [Singapore]: Chow Chee Yong, 2008.

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Albom, Mitch. Fab five. New York: Warner Books, 1994.

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ill, Swanson Maggie, and Wetzel Rick ill, eds. The fib. Waterbury, CT: Letter People Co., 2002.

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Bean, Anita. Fab abs. New York: McGraw-Hill, 2006.

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Wang, Zhiming M., ed. FIB Nanostructures. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-02874-3.

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Morel, Laure, and Serge Le Roux. Fab Labs. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781119318392.

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Book chapters on the topic "FVB"

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Sato, Yoji, Albrecht G. Schmidt, Helen Kiriazis, Brian D. Hoit, and Evangelia G. Kranias. "Compensated hypertrophy of cardiac ventricles in aged transgenic FVB/N mice overexpressing calsequestrin." In Cardiac Cell Biology, 19–25. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4757-4712-6_3.

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Hoffmann, Matthew J., Patrick J. Sinko, Robert J. Meeker, and Robert Snyder. "Pharmacokinetics of Benzene Following an Oral or Intradermal Dose in FVB and Tg.AC Mice." In Advances in Experimental Medicine and Biology, 455–58. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-0667-6_68.

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Rothenberger, Natalie J., and Laura P. Stabile. "Induction of Lung Tumors and Mutational Analysis in FVB/N Mice Treated with the Tobacco Carcinogen 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanone." In Molecular Toxicology Protocols, 149–60. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0223-2_7.

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Memmert, Daniel, and Dominik Raabe. "FCB versus FCB." In Data Analytics in Football, 105–22. Abingdon, Oxon ; New York, NY : Routledge, 2018.: Routledge, 2018. http://dx.doi.org/10.4324/9781351210164-12.

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Rawlings, Ron H., Andrew Shaw, Howard R. Champion, Lena M. Napolitano, Ben Singer, Andrew Rhodes, Maurizio Cecconi, et al. "FOB." In Encyclopedia of Intensive Care Medicine, 947. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_3119.

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Lichters, Roland, Roland Stamm, and Donal Gallagher. "FVA." In Modern Derivatives Pricing and Credit Exposure Analysis, 283–305. London: Palgrave Macmillan UK, 2015. http://dx.doi.org/10.1057/9781137494849_20.

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Desnick, Robert J., Orlando Guntinas-Lichius, George W. Padberg, Gustav Schonfeld, Xiaobo Lin, Maurizio Averna, Pin Yue, et al. "FDB." In Encyclopedia of Molecular Mechanisms of Disease, 647. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8512.

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Keller, Cesar A. "Diagnostic and Interventional Bronchoscopy in the Intensive Care Unit." In Mayo Clinic Critical and Neurocritical Care Board Review, edited by Eelco F. M. Wijdicks, James Y. Findlay, William D. Freeman, and Ayan Sen, 855–62. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190862923.003.0118.

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Shigeto Ikeda in Japan developed fiberoptic bronchoscopy (FOB), beginning a revolution in the diagnosis and treatment of diverse pulmonary conditions. FOB evolved with additional diagnostic and interventional tools. FOB has become an essential bedside tool for diagnosis and management in critically ill patients. FOB is safe, even in patients with respiratory failure and, if done cautiously, in patients with increased intracranial pressure.
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Vincent, Carol. "Promoting British values in schools." In Tea and the Queen?, 69–94. Policy Press, 2019. http://dx.doi.org/10.1332/policypress/9781447351955.003.0005.

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Chapter 4 starts with a general overview of the teacher-respondents’ reactions to the FBV. It then moves on to describe and analyse the four main school responses to the promotion of FBV identified in the research. These are Representing Britain, Repackaging FBV, Relocating FBV and Engagement with FBV (the latter is discussed in Chapter 5). The first response, Representing Britain, describes the use of symbols and stereotypes traditionally associated with Britain as a mechanism through which to promote FBV. Repackaging describes a ‘business-as-usual’ response where schools absorb the promotion of FBV into their existing practices. Relocating describes the rise in ‘inward-looking’ values/character education. I argue that this emphasis on personal development is preferred over more ‘outward-looking’ citizenship education. Throughout, I identify the characteristics of the ‘good’ citizen inherent in the different responses, focusing both on the desired characteristics of both the ‘good’ school citizen and the future adult citizen.
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Pasillas, Marcela Ramírez, and Hans Lundberg. "Corporate Social Venturing." In Research Anthology on Strategies for Maintaining Successful Family Firms, 47–66. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-6684-3550-2.ch003.

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This chapter has three purposes: first, to briefly outline corporate venturing as a sub-field in corporate entrepreneurship that recently has gained prominence in research on family-owned businesses (FOB); second, to highlight the missing social dimension in research on FOB that focuses on corporate venturing, conceptualize this added social dimension as corporate social venturing (CSV), and to empirically illustrate CSV with well-known Mexican FOB engaged in CSV; and third, to propose an agenda for researching CSV done by FOB.
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Conference papers on the topic "FVB"

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Wang, Li-Xin, Michael Berk, and Gregory E. Plautz. "Abstract 2478: A mAb within vivotherapeutic activity against spontaneous breast tumors in FVB-neuN mice recognizes SLP-2." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2478.

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Azevedo, Tiago, Tiago Ferreira, Maria João Pires, Maria João Neuparth, Lillian Barros, Isabel C. F. R. Ferreira, Eduardo Rosa, and Paula A. Oliveira. "Hematological and biochemical profile of FVB/n mice supplemented with an anthocyanin-rich elderberry (&lt;em&gt;Sambucus nigra&lt;/em&gt; L.) extract." In 7th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2021. http://dx.doi.org/10.3390/ecmc2021-11562.

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BARCHA LONGO, MARJORIE, and Valeria Cagnon Quitete. "ANÁLISE DA MORFOLOGIA E DE MMP-9, AR E IGFR-1 FRENTE À AÇÃO DA SENESCÊNCIA E DO EXCESSO DE PESO SOBRE O LOBO ANTERIOR DA PRÓSTATA DE CAMUNDONGOS (FVB) TRATADOS COM EXTRATO DE JABUTICABA." In XXIV Congresso de Iniciação Científica da UNICAMP - 2016. Campinas - SP, Brazil: Galoa, 2016. http://dx.doi.org/10.19146/pibic-2016-51414.

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Song, Hoseok, Dong Hae Kang, Jaeseok Park, Jeongun Choi, and Seongjun Cho. "Efficient Identification of Wafer Edge’s Defect with Volume Diagnosis Analysis and Plasma-FIB Planar Deprocessing." In ISTFA 2020. ASM International, 2020. http://dx.doi.org/10.31399/asm.cp.istfa2020p0067.

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Abstract In the failure analysis (FA) of modern semiconductor logic device manufactured in foundry fab, efficient identification of wafer edge’s defect was studied by using volume diagnosis analysis and plasma-focused ion beam (FIB) planar deprocessing. As the chip from wafer edge has multiple defective locations, there is the limitation of the conventional FA work to identify them. Here, we used volume diagnosis analysis to identify the multiple defective locations within chip and plasma-FIB planar deprocessing to delayer those locations and find out defects. The actual FA work verified that new workflow successfully identified the different defects from different layers from the chip of wafer edge and efficiently accelerated the quantity of FA results, importantly leading to more representative status of inline defect.
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Herschbein, Steven B., Hyoung H. Kang, Harvey E. Berman, Carmelo F. Scrudato, Aaron D. Shore, and Bing Dai. "Semi-Automated Full Wafer In-Line SRAM Failure Analysis by Dual Beam Focused Ion Beam (FIB)." In ISTFA 2010. ASM International, 2010. http://dx.doi.org/10.31399/asm.cp.istfa2010p0113.

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Abstract The presence of a full wafer dual-beam FIB on the process floor gave rise to an environment in which formerly segregated off-line lab and FAB tasks could be linked. One such idea involved a methodology for semi-automated defect targeting based on the spatial predictions of static random access memory (SRAM) electrical testing. The embedded memory blocks on some processors are fully configured and probe pad testable as early as the forth metal level. Using a unique navigation technique that combines electrically sorted SRAM bit map data with CAD coordinate information and stage driven X-Y stepping, the FIB tool was used to locate, section and image prior level defects. We believe that with the inclusion of suitable fiducial markers in the chip design and advanced pattern recognition to aid navigation and guide depth milling, a fully automated process for electrical yield detractor diagnosis could be introduced.
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Tavares, Rodrigo C., Marcos Carvalho, Marcos A. M. Vieira, Luiz F. M. Vieira, and Bhaskar Krishnamachari. "FWB." In MSWIM '18: 21st ACM Int'l Conference on Modelling, Analysis and Simulation of Wireless and Mobile Systems. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3242102.3242112.

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Apostolaki, Maria, Laurent Vanbever, and Manya Ghobadi. "FAB." In BS '19: 2019 Workshop on Buffer Sizing. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3375235.3375237.

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Saito, Yasushi, Svend Frølund, Alistair Veitch, Arif Merchant, and Susan Spence. "FAB." In the 11th international conference. New York, New York, USA: ACM Press, 2004. http://dx.doi.org/10.1145/1024393.1024400.

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Gohil, Varun, Shreyas Singh, and Manu Awasthi. "FAB." In ICPE '19: Tenth ACM/SPEC International Conference on Performance Engineering. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3302541.3313102.

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Li, Yuanjing (Jane), Steven Scott, and Howard Lee Marks. "Advanced Physical Analysis Methodology for Yield and Reliability of 28-nm, Bulk-Si, Flip-Chip ICs Using SEM and Backside Deprocessing." In ISTFA 2012. ASM International, 2012. http://dx.doi.org/10.31399/asm.cp.istfa2012p0197.

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Abstract This paper presents a backside chip-level physical analysis methodology using backside de-processing techniques in combination with optimized Scanning Electron Microscopic (SEM) imaging technique and Focused Ion Beam (FIB) cross sectioning to locate and analyze defects and faults in failing IC devices. The case studies illustrate the applications of the method for 28nm flip chip bulk Si CMOS devices and demonstrate how it is used in providing insight into the fab process and design for process and yield improvements. The methods are expected to play an even more important role during 20-nm process development and yield-ramping.
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Reports on the topic "FVB"

1

DeSteese, John G. FVB Energy Inc. Technical Assistance Project. Office of Scientific and Technical Information (OSTI), May 2011. http://dx.doi.org/10.2172/1015273.

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Girrens, Steven P. LANL Overview Feb 2016. Office of Scientific and Technical Information (OSTI), March 2016. http://dx.doi.org/10.2172/1240805.

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Mondragon, Krystal L. AMPP Newsletter - Feb 2020. Office of Scientific and Technical Information (OSTI), February 2020. http://dx.doi.org/10.2172/1601615.

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Arrowsmith, Marie Danielle. LDRD @ SNL Feb 2016. Office of Scientific and Technical Information (OSTI), March 2016. http://dx.doi.org/10.2172/1561027.

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Mondragon, Krystal. AMPP Newsletter - Feb 2021. Office of Scientific and Technical Information (OSTI), March 2021. http://dx.doi.org/10.2172/1771087.

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Shul, Randy J., Michael J. Rye, Greg Salazar, and Steve Ball. FEI FIB/SEM Failure Analysis. Office of Scientific and Technical Information (OSTI), January 2019. http://dx.doi.org/10.2172/1492079.

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Ahrens L., A. Dunbar, J. W. Glenn, and M. Tanaka. Testing the New FEB Bumps. Office of Scientific and Technical Information (OSTI), May 1995. http://dx.doi.org/10.2172/1132412.

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Garvock, James. DOI Test Feb 15, 2010. Washington, DC: The MAA Mathematical Sciences Digital Library, February 2010. http://dx.doi.org/10.4169/loci003289.

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Gillor, Osnat, Stefan Wuertz, Karen Shapiro, Nirit Bernstein, Woutrina Miller, Patricia Conrad, and Moshe Herzberg. Science-Based Monitoring for Produce Safety: Comparing Indicators and Pathogens in Water, Soil, and Crops. United States Department of Agriculture, May 2013. http://dx.doi.org/10.32747/2013.7613884.bard.

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Using treated wastewater (TWW) for crop irrigation represents an important opportunity for ensuring adequate food production in light of growing freshwater scarcity worldwide. However, the environmentally sustainable approach of using TWW for irrigation can lead to contamination of produce with fecal pathogens that may remain in treated water. The overall goal of this research was to evaluate the correlation between the presence of fecal indicator bacteria (FIB) and that of a suite of human pathogens in TWW, the irrigated soil, and crops. Field experiments were conducted to compare secondary and tertiary TWW with dechlorinated tap water for irrigation of tomatoes, a typical commercial crop, in Israel, a semi-arid country. Human pathogens including bacteria (Salmonella), protozoa (Cryptosporidiumand Giardia), and viruses (Adenovirus [AV Types A, B, C & 40/41] and Enterovirus [EV71 subtypes]) were monitored in two field trials using a combination of microscopic, cultivation-based, and molecular (qPCR) techniques. Results from the field trials indicate that microbial contamination on the surface of tomatoes did not appear to be associated with the source of irrigated waters; FIB contamination was not statistically different on tomatoes irrigated with TWW as compared to tomatoes irrigated with potable water. In fact, Indicator bacteria testing did not predict the presence of pathogens in any of the matrices tested. High concentrations of FIB were detected in water and on tomato surfaces from all irrigation treatment schemes, while pathogen contamination on tomato surfaces (Cryptosporidiumand Salmonella) was only detected on crops irrigated with TWW. These results suggest that regular monitoring for pathogens should take place to accurately detect presence of harmful microorganisms that could threaten consumer safety. A notable result from our study is that the large numbers of FIB in the water did not appear to lead to FIB accumulation in the soil. With the exception of two samples, E. coli that was present at 10³ to 10⁴ cells/100 mL in the water, was not detected in the soil. Other bacterial targets associated with the enteric environment (e. g., Proteusspp.) as well as protozoal pathogens were detected in the TWW, but not in the soil. These findings suggest that significant microbial transfer to the soil from TWW did not occur in this study. The pattern of FIB contamination on the surfaces of tomatoes was the same for all treatment types, and showed a temporal effect with more contamination detected as the duration of the field trial increased. An important observation revealed that water quality dramatically deteriorated between the time of its release from the wastewater treatment plant and the time it was utilized for irrigation, highlighting the importance of performing water quality testing throughout the growing season at the cultivation site.
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10

Anderson, David W. EE-3A Logging Report for Feb. 28th., 1994. Office of Scientific and Technical Information (OSTI), March 1994. http://dx.doi.org/10.2172/1248153.

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