When she ran out of options, Laurie turned to the internet, where she found a video of robotic fibroid removal by Dr. Cystic fibrosis heterozygote resistance to cholera toxin in the cystic fibrosis mouse model. It is from the time point they learn about the center to the time when they are fibroid pain symptoms 2017 by the centers providers. Vegetables, fruits, nuts, seed and whole grains are some examples of how to treat fibroids naturally.
Cystic fibrosis, a genetic disease associated with frequent lung infections and a shortened life span, is caused by a defect in the CFTR gene, which encodes a membrane transporter. Although it is not clear exactly how defective CFTR links to the symptoms, the mutant protein is known to increase the pH in intracellular organelles. On the basis of results obtained from patients cells and from mice carrying mutated Cftr (which produces a cystic fibrosis-like disease), Teichgräber et al. suggest that this rise in pH increases susceptibility to lung infection by altering levels of ceramide, a membrane constituent that can also trigger cell death. The higher pH inhibits the enzyme that breaks down ceramide, and the resulting excess of ceramide increases vulnerability to lung infection. Blocking the biosynthesis of ceramide via acid sphingomyelinase normalizes ceramide levels and, most tellingly, renders the Cftr-deficient mice resistant to lung infections. This block can be achieved with ...
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To gain insight into aberrant cytokine regulation in cystic fibrosis (CF), we compared the phenotypic manifestations of allergen challenge in gut-corrected CFTR-deficient mice with background-matched C57Bl6 (B6) mice. Aspergillus fumigatus (Af) antigen was used to mimic allergic bronchopulmonary aspergillosis, a peculiar hyper-IgE syndrome with a high prevalence in CF patients. CFTR-/-, C57BL/6 and FVB/NJ mice were sensitized with Af antigen by serial intraperitoneal injections. Control mice were mock sensitized with PBS. Challenges were performed by inhalation of Af antigen aerosol. After Af antigen challenge, histologic analysis showed goblet cell hyperplasia and lymphocytic infiltration in both strains. However, total serum IgE levels were markedly elevated in CF mice. Sensitized CF mice showed a five-fold greater IgE response to sensitization as compared with B6- and FVB-sensitized controls. Additional littermate controls to fully normalize for B6-FVB admixture in the strain background confirmed the
GFP-tagged CFTR transgene is functional in the G551D cystic fibrosis mouse colon.: Trafficking of the cystic fibrosis transmembrane conductance regulator (CFTR)
Cystic fibrosis (CF) is a common life-shortening, autosomal recessive disease caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel (1). CFTR is expressed in epithelia of multiple organs and its loss causes airway, pancreatic, intestinal, liver, and vas deferens disease. The ΔF508 mutation (also called F508del) is the most common CF-causing mutation, accounting for ~70% of CF alleles; most patients carry at least one ΔF508 allele.. Numerous studies have expressed human CFTR-ΔF508 in vitro and found that its biosynthetic processing is disrupted. The mutant protein is retained in the endoplasmic reticulum (ER) and rapidly degraded (2-4), and as a result, CFTR-ΔF508 fails to reach the apical membrane. However, CFTR-ΔF508 can be induced to traffic to the cell surface by reducing the incubation temperature or adding chemicals that facilitate folding. Once at the membrane, CFTR-ΔF508 retains channel function, although its lifetime ...
In the pathogenesis of renal fibrosis, oxidative stress (OS) enhances the production of reactive oxygen species (ROS) leading to sustained cell growth, inflammation, excessive tissue remodelling and accumulation, which results in the development and acceleration of renal damage. In our previous work (128) we established protein DJ-1 (PARK7) as an important ROS scavenger and key player in renal cell response to OS. In the present study we investigated the impact of profibrogenic agonists on DJ-1 and shed light on the role of this protein in renal fibrosis. Treatment of renal fibroblasts and epithelial cells with the profibrogenic agonist ANG II or PDGF resulted in a significant up-regulation of DJ-1 expression parallel to an increase in the expression of fibrosis markers. Monitoring of DJ-1 expression in kidney extract and tissue sections from renal fibrosis mice model (Col4a3-deficient) revealed a disease grad dependent regulation of the protein. Overexpression of DJ-1 prompted cell resistance ...
Shop a large selection of products and learn more about CFTR Mouse anti-Human, Alexa Fluor 750, Clone: CFTR/1341, Novus Biologicals CFTR Antibody; Alexa Fluor™ 750; 0.1
Antibiotic therapy in the cystic fibrosis (CF) mouse model has been shown to result in reduced bacterial load of the intestine and significant body mass gain. The effect was suggested to be linked to the improvement of intestinal digestion and absorption. Therefore, we aimed to assess the influence of routinely applied antibiotic therapy in CF patients on fat assimilation. Twenty-four CF patients aged 6 to 30 years entered the study. Inclusion criteria comprised confirmed exocrine pancreatic insufficiency and bronchopulmonary exacerbation demanding antibiotic therapy. Exclusion criteria comprised: antibiotic therapy six weeks prior to the test, liver cirrhosis, diabetes mellitus, oxygen dependency, the use of systemic corticosteroids. In all enrolled CF subjects, 13C-labelled mixed triglyceride breath test (13C MTG-BT) was performed to assess lipid digestion and absorption, before and after antibiotic therapy. Sixteen subjects were treated intravenously with ceftazidime and amikacin, eight ...
Day 159 has 30 protein-coding genes (browser view) including CFTR (cystic fibrosis transmembrane conductance regulator.). Like Day 64: (3p22.1-3p21.2): CCR5 Δ32, an HIV resistance mutation, the ΔF508 cystic fibrosis mutation in CFTR is at surprisingly high frequency (1 in 30 Europeans), which has led to speculation that it has been a target of recent evolution - it may provide protection against cholera in people with one copy, despite causing cystic fibrosis when inheriting two copies.. Click here to see all 8386630 letters of Day 159 with the CFTR ΔF508 mutation flashing.. ...
A Prospective Study to Evaluate Biological and Clinical Effects of Significantly Corrected CFTR Function (the PROMISE Study) (PROMISE-OB-18 ...
Knowledge of cystic fibrosis transmembrane conductance regulator (CFTR) protein structure will contribute toward the understanding of CFTR function and CF biology, the mechanisms of action for CF drugs, and provide additional insight toward new drug discovery through structure-based drug design.
Cystic fibrosis (CF) remains the most common fatal hereditary lung disease. The discovery of the cystic fibrosis transmembrane conductance regulator (CFTR) gene 25 years ago set the stage for: 1) unravelling the molecular and cellular basis of CF lung disease; 2) the generation of animal models to study in vivo pathogenesis; and 3) the development of mutation-specific therapies that are now becoming available for a subgroup of patients with CF. This article highlights major advances in our understanding of how CFTR dysfunction causes chronic mucus obstruction, neutrophilic inflammation and bacterial infection in CF airways. Furthermore, we focus on recent breakthroughs and remaining challenges of novel therapies targeting the basic CF defect, and discuss the next steps to be taken to make disease-modifying therapies available to a larger group of patients with CF, including those carrying the most common mutation ΔF508-CFTR. Finally, we will summarise emerging evidence indicating that acquired CFTR
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Structural information is required to define the molecular basis for chloride conduction through CFTR (cystic fibrosis transmembrane conductance regulator). Towards this goal, we expressed MSD2, the second of the two MSDs (membrane-spanning domains) of CFTR, encompassing residues 857-1158 in Sf9 cells using the baculovirus system. In Sf9 plasma membranes, MSD2 migrates as expected for a dimer in non-dissociative PAGE, and confers the appearance of an anion permeation pathway suggesting that dimeric MSD2 mediates anion flux. To assess directly the function and quaternary structure of MSD2, we purified it from Sf9 cells by virtue of its polyhistidine tag and nickel affinity. Reconstitution of MSD2 into liposomes conferred a 4,4′-di-isothiocyanostilbene-2,2′-disulphonate-inhibitable, chloride-selective electrodiffusion pathway. Further, this activity is probably mediated directly by MSD2 as reaction of its single cysteine residue (Cys866) with the thiol modifying reagent, ...
Deletion of phenylalanine 508 (delta Phe-508) in the cystic fibrosis transmembrane conductance regulator (CFTR) protein causes approximately 70% of all cases of cystic fibrosis. This residue lies in a region of the protein that we have synthesized chemically and shown to bind adenine nucleotides (Th …
Provided herein are bioactive agents comprising a compound that inhibits the ion transport activity of a cystic fibrosis transmembrane conductance regulator (CFTR) and that is linked to a macromolecule that interacts with a cell that expresses CFTR. The bioactive agents described herein are useful for treating diseases, disorders, and sequelae of diseases, disorders, and conditions that are associated with aberrantly increased CFTR activity, for example, secretory diarrhea.
Severe deficiency of cystic fibrosis transmembrane conductance regulator messenger RNA carrying nonsense mutations R553X and W1316X in respiratory epithelial cells of patients with cystic fibrosis Academic Article ...
T75 plated Cells $750.00 shipped at room temperature. Cat#66009-10-T75. 120 Population doublings or up to 12 passages.. This product would require pre-coated flasks with Mouse Nasal Epithelial Stem Cells Extra-cellular Matrix Cat# E66009-10 and Nasal Epithelial Stem Cells Media Cat# M66009-10. Source: Mouse Nasal Epithelial Tissue. Positive Markers: ICAM-1, MUC 8, CK-8, Nestin, ESA,Ki67. For non-academic use please inquire for pricing.. Cells are only guaranteed with purchase of Celprogen Media and Celprogen Extra Cellular Matrix for appropriate cell culture, for 30 days from the date of shipment.. ...
Cystic fibrosis is characterized by an impaired cyclic adenosine 3,5-monophosphate (cAMP) activated Cl- conductance in parallel with an enhanced amiloride sensitive Na+ conductance (ENaC) of the respiratory epithelium. Very recently, acute downregulation of ENaC by the cystic fibrosis transmembrane …
Трансмембранный регулятор муковисцидоза (англ. CFTR - Cystic Fibrosis Transmembrane conductance Regulator) - белок, участвующий в транспорте ионов хлора через мембрану клетки, а также название гена, кодирующего этот белок. Ген CFTR находится на длинном плече 7-й хромосомы. Мутации в гене CFTR приводят к возникновению заболевания муковисцидоз, а также могут быть причиной мужского бесплодия. Наиболее часто встречается мутация ΔF508 (более 50 % из всех выявляемых мутаций гена), при которой происходит делеция остатка фенилаланина-508 из полипептидной цепочки, что приводит к нарушению ...
臺大位居世界頂尖大學之列,為永久珍藏及向國際展現本校豐碩的研究成果及學術能量,圖書館整合機構典藏(NTUR)與學術庫(AH)不同功能平台,成為臺大學術典藏NTU scholars。期能整合研究能量、促進交流合作、保存學術產出、推廣研究成果。. To permanently archive and promote researcher profiles and scholarly works, Library integrates the services of "NTU Repository" with "Academic Hub" to form NTU Scholars.. ...
1CKY: Cystic fibrosis transmembrane conductance regulator: solution structures of peptides based on the Phe508 region, the most common site of disease-causing DeltaF508 mutation.
BACKGROUND The role of the macrophages in cystic fibrosis (CF) lung disease has been poorly studied. We hypothesized that alternatively activated M2 macrophages are abnormal in CF lung disease. METHODS Blood samples were collected from adults (n=13) children (n=27) with CF on admission for acute pulmonary exacerbation and when clinically stable. Monocytes were differentiated into macrophages and polarized into classical (M1) and alternatively-activated (M2) phenotypes, function determined ex-vivo and compared with healthy controls. RESULTS In the absence of functional cystic fibrosis trans-membrane conductance regulator (CFTR), either naturally in patients with CF or induced with CFTR inhibitors, monocyte-derived macrophages do not respond to IL-13/IL-4, fail to polarize into M2s associated with a post-transcriptional failure to produce and express IL-13Rα1 on the macrophage surface Polarization to the M1 phenotype was unaffected. CONCLUSIONS CFTR-dependent imbalance of macrophage phenotypes and
Zkratka CFTR označuje speciální buněčný membránový receptor (cystic fibrosis transmembrane conductance regulator), který je určen genem stejného názvu, a který je zodpovědný za transport molekul chloru mezi buňkou a okolím. Mutace v CFTR genu mohou způsobit vznik cystické fibrózy ...
CFTR با عنوانِ کاملِ «تنظیم‌کنندهٔ هدایت تراغشایی فیبروز سیستیک» (انگلیسی: Cystic fibrosis transmembrane conductance regulator) یک پروتئین تراپوسته‌ای و همچنین مجرای کلریدی در مهره‌داران است که که توسط ژن «CFTR» کُد می‌شود.[۲][۳] این ژن، نوعی مجرای یونیِ پروتئینی متعلق به ردهٔ «حامل‌های ABC» را کد می‌کند که کارش هدایت کلرید[۴] و تیوسیانات[۵] از خلالِ غشاءِ سلول‌های بافت پوششی است. جهش در این ژن سبب می‌شود که مجرای یونیِ کلریدی دچار ناکارآمدی شده و جریان مایع در سلول‌های بافت پوششی ریه، لوزالمعده و سایر ارگان‌ها مختل شود و بیماری فیبروز سیستیک بروز می‌کند که در آن، بلغم و ...
Membrane, Mutations, Cystic Fibrosis, Fibrosis, Mutation, ATP, Endoplasmic Reticulum, Reticulum, Chloride Channel, Disease, Cystic Fibrosis Transmembrane Conductance Regulator, Cells, Retention, Atpase, Cftr Protein, Epithelial Cells, Phosphorylation, Proteins, Role, Cell
囊狀纖維化(CF)是一種遺傳性的基因突變疾病,屬於體染色體隱性遺傳,在白種人較為常見,帶因比例約為3%,發病率約為1/3300,而其中亞裔僅佔1/32000。近年來,隨著國人與外籍人士通婚比例增加,可能提高此遺傳疾病之發生率,但目前仍然屬於國內十分罕見的疾病之一。. 囊狀纖維化的基因突變位在第七對染色體長臂 7q31.2 區域的鹼基對上,進而導致人體中特定蛋白功能的缺陷,這些蛋白被稱為「囊狀纖維化跨膜傳導調節節因子」(CFTR, cystic fibrosis transmembrane conductance ...
SWISS-MODEL Template Library (SMTL) entry for 1r0x. Cystic fibrosis transmembrane conductance regulator (CFTR) nucleotide-binding domain one (NBD1) with ATP
CFTR modulators for treatment of Cystic Fibrosis - 42 compounds. The largest collection of small molecules that rescue the cell surface expression (CFTR correctors) and function (CFTR potentiators) of CF mutants.. If you do not see a compound you are looking for please try search by structure or send inquiry for custom synthesis service.. ...
Testing that is specifically for use in diagnosing Cystic Fibrosis. The main test at this time is the Sweat Test although a Nasal Potential Difference test (NPD) is also used. The third diagnostic test is genetic which can be found under its own subcategory.
Abstract Background Cystic fibrosis (CF) is caused by mutations in the CFTR gene that impair the function of CFTR, a cAMP-regulated anion channel. In the small intestine loss of CFTR function creates a dehydrated, acidic ...
TY - JOUR. T1 - Cystic fibrosis transmembrane conductance regulator. T2 - The NBF1 + R (nucleotide-binding fold 1 and regulatory domain) segment acting alone catalyses a Co2+/Mn2+/Mg2+-ATPase activity markedly inhibited by both Cd2+ and the transition-state analogue orthovanadate. AU - Annereau, Jean Philippe. AU - Ko, Young Hee. AU - Pedersen, Peter L.. PY - 2003/4/15. Y1 - 2003/4/15. N2 - Cystic fibrosis (CF) is caused by mutations in the gene encoding CFTR (cystic fibrosis transmembrane conductance regulator), a regulated anion channel and member of the ATP-binding-cassette transporter (ABC transporter) superfamily. Of CFTRs five domains, the first nucleotide-binding fold (NBF1) has been of greatest interest both because it is the major hotspot for mutations that cause CF, and because it is connected to a unique regulatory domain (R). However, attempts have failed to obtain a catalytically active NBF1 + R protein in the absence of a fusion partner. Here, we report that such a protein can ...
The level of the mature native 170 kDa form of CFTR (cystic fibrosis transmembrane conductance regulator) at the plasma membrane is under the control of a selective proteolysis catalysed by calpain. The product of this limited digestion, consisting of discrete fragments still associated by strong interactions, is removed from the plasma membrane and internalized in vesicles and subject to an additional degradation. This process can be monitored by visualizing the accumulation of a 100 kDa fragment in a proliferating human leukaemic T-cell line and in human circulating lymphocytes. In reconstructed systems, and in intact cells, the conversion of native CFTR into the 100 kDa fragment linearly correlated with calpain activation and was prevented by addition of synthetic calpain inhibitors. A reduction in Ca2+ influx, by blocking the NMDA (N-methyl-D-aspartate) receptor Ca2+ channel, inhibited the conversion of the native 170 kDa fragment into the 100 kDa fragment, whereas an endosome acidification ...
Function and Expression of Cystic Fibrosis Transmembrane Conductance Regulator after Small Intestinal Transplantation in Mice. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Background: Nasal potential difference (NPD) test has long been used to assist in the diagnosis of Cystic Fibrosis (CF) and more recently as an outcome measure in clinical trials of new CF therapies. This test has also been adapted to the mouse nose. Objectives: We aimed at evaluating variability of the NPD measurements in CF patients displaying two severe CFTR mutations and in sex-matched healthy controls. NPD recorded from F508del-CF and normal wild-type mice were also compared. Methods and results: In each setting, tests were performed by a single qualified operator. In the clinical setting, the latest standardized operation protocol of the CF foundation was followed. A total of 80 tracings were obtained from 10 patients (23.2 y; range 14 to 32) and 10 healthy subjects (34 y; range 24 to 53), each tested twice, in both nostrils. Two CF and two controls were excluded from the statistical data analysis due to the presence of a single non interpretable NPD tracing (4/80, 5%). To achieve equal sample
Sigma-Aldrich offers abstracts and full-text articles by [Chatchai Muanprasat, Lalida Sirianant, Sunhapas Soodvilai, Ratchanaporn Chokchaisiri, Apichart Suksamrarn, Varanuj Chatsudthipong].
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
In gene-targeted mouse models for cystic fibrosis (CF), the disease is mainly manifested by mucus obstruction in the intestine. To explore the mucus composition, mucins insoluble and soluble in 6 M guanidinium chloride were purified by three rounds of isopycnic ultracentrifugation from the small and large intestines of CF mice (Cftr(m1UNC)/Cftr(m1UNC)) and compared with wild-type mice. The amino acid composition was typical of that for mucins and showed increased amounts of the insoluble (2.5-fold increase) and soluble (7-fold increase) mucins in the small intestine of the CF mice compared with wild-type mice. Mucins from the large intestine of both wild-type and CF mice showed a high but constant level of fucosylation. In contrast, the insoluble and soluble mucins of the small intestine in CF mice revealed a large increase in fucose, whereas those of wild-type mice contained only small amounts of fucose. This increased fucosylation was analysed by releasing the O-linked oligosaccharides ...
Small-molecule therapies that restore defects in cystic fibrosis transmembrane conductance regulator (CFTR) gating (potentiators) or trafficking (correctors) are being developed for cystic fibrosis (CF) in a mutation-specific fashion. Options for pharmacological correction of CFTR-p.Phe508del (F508del) are being extensively studied but correction of other trafficking mutants that may also benefit from ... read more corrector treatment remains largely unknown.We studied correction of the folding mutants CFTR-p.Phe508del, -p.Ala455Glu (A455E) and -p.Asn1303Lys (N1303K) by VX-809 and 18 other correctors (C1-C18) using a functional CFTR assay in human intestinal CF organoids.Function of both CFTR-p.Phe508del and -p.Ala455Glu was enhanced by a variety of correctors but no residual or corrector-induced activity was associated with CFTR-p.Asn1303Lys. Importantly, VX-809-induced correction was most dominant for CFTR-p.Phe508del, while correction of CFTR-p.Ala455Glu was highest by a subgroup of compounds ...
TY - JOUR. T1 - Light and alcohol evoked electro-oculograms in cystic fibrosis. AU - Constable, Paul. AU - Lawrenson, John. AU - Arden, Geoffrey. PY - 2006. Y1 - 2006. N2 - Cystic fibrosis (CF) is caused by a defect in the cystic fibrosis transmembrane conductance regulator (CFTR) which is a chloride channel. CFTR is expressed in the retinal pigment epithelium (RPE) where it is believed to be important in generating the fast oscillations (FOs) and potentially contributing to the light-electrooculogram (EOG). The role of CFTR in the alcohol-EOG is unknown. We recruited six individuals with CF (three homozygotes for δ508 and three heterozygous for δ508) and recorded the light- and alcohol-EOGs as well as the FOs and compared them to a control group. The results showed that in the CF group the amplitude of the alcohol- and light-EOGs were normal. However, the time to peak of the light- and alcohol-rises were significantly faster than in the control group. We conclude that CFTR is not primarily ...
Pathogenesis and treatment of cystic fibrosis; cystic fibrosis transmembrane conductance regulator (CFTR) function; infection, inflammation, and airway cell processes (e.g., ion transport, signaling) in disease; airway mucous and inhaled particle secretion; gene-editing; new research models ...
The CFTR Antibodies Distribution Program works to streamline access to reagents specific for the detection of cystic fibrosis transmembrane conductance regulator (CFTR) expression.
Cystic fibrosis (CF) is an autosomal recessive disease that greatly diminishes life span owing to impaired function of the lungs and intestinal epithelia. Although the F508 homozygous mutation in the anion channel protein cystic fibrosis transmembrane conductance regulator (CFTR) is commonly found in CF patients, the mechanisms by which this mutation causes disease are unclear. To investigate this issue in vivo, Ostedgaard et al. generated pigs homozygous for CFTR-F508. Unlike previously established mouse models of CF, CFTR-F508 pigs develop airway and intestinal disease that closely resembles human CF pathology. In vivo studies agreed with previous results carried out in cell culture systems, and showed that the F508 mutation causes CFTR misfolding and degradation, and the failure of the protein to localise at the apical surface of epithelial cells. CFTR-F508 pigs provide a relevant model to further investigate mechanisms of CF pathogenesis and for testing therapies that aim to increase CFTR ...
Its been known since the 1940s that CF was a genetic disease, but it wasnt until 1989 that the gene itself was identified as the cystic fibrosis transmembrane conductance regulator (CFTR). In healthy people with normal copies of this gene, the CFTR protein forms small pores on the surfaces of cells that open and close, allowing ions to flow in and out, thereby regulating the balance of salts and water. Different mutations to this gene cause different types of protein malfunctions: Some proteins crumple up and cant be transported to the cell surface. Others wont open and close properly. Some are left only half-built, and others get broken down too quickly. The result is CF.. Like most genes in the genome, we all inherit one copy of CFTR from mom, and the other from dad. People who inherit one mutated copy and one normal copy are called carriers. They are healthy (more or less - see the sidebar "The New Story About CF Carriers"), because their bodies get by on only half the normal amount of ...
Vertex Pharmaceuticals Inc. (Nasdaq: VRTX) announced positive data from a Phase 2 trial [1] of a second drug candidate, in addition to Kalydeco, aimed at treating cystic fibrosis. The company said it plans to start pivotal, or Phase 3, trials on VX-809 next year.. VX-809 was tested in combination with Kalydeco, or ivacaftor, a drug for which Vertex received approval earlier this year in both the U.S. [2] and in Europe for treatment of the most common mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, F508del. ...
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Cystic Fibrosis (CF) is the many common life-shortening hereditary disease among Caucasians, caused by mutations in the gene encoding the Cystic Fibrosis Transmembrane conductance Regulator (CFTR).... Read More ...
No rebound inflammation after INO-1001 is discontinued. Rats were treated with INO-1001 (or vehicle) beginning 1 day after TBI in one of two regimens: i) for 12