Many phenomena that basic research tries to explain would simply be unknown had they not been uncovered by the study of diseases. This statement from Vogel and Motulsky is also valid with respect to protein modifications in both normal and premature ageing, such as Hutchinson-Gilford Progeria. Most progeria patients carry a specific lamin A/C mutation, which results in truncated protein (progerin), lacking the site essential for cleaving a farnesyl group. Incompletely modified lamins accumulate at the nuclear membrane. The same lamin modifications are also found in cells of normally aged humans. Further, lamins are non-enzymatically modified by MGO, a precursor in the formation of AGEs. These lamin modifications increase with age and might cause vascular dysfunction and atherosclerosis. Amongst others, lamins bind to the lamin B receptor (LBR). LBR has sterol reductase activity and modifies chromatin. We previously showed that LBR-deficiency results in hyposegmented neutrophil nuclei, altered ...

Involved in the regulation of the perinuclear actin network and nuclear shape through interaction with filamins. Plays an essential role in actin cytoskeleton formation in developing cartilaginous cells ...

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LINC complexes are evolutionarily conserved nuclear envelope bridges, physically connecting the nucleus to the peripheral cytoskeleton. They are pivotal for dynamic cellular and developmental processes, like nuclear migration, anchoring and positioning, meiotic chromosome movements and maintenance of cell polarity and nuclear shape. Active nuclear reshaping is a hallmark of mammalian sperm development and, by transducing cytoskeletal forces to the nuclear envelope, LINC complexes could be vital for sperm head formation as well. We here analyzed in detail the behavior and function of Sun4, a bona fide testis-specific LINC component. We demonstrate that Sun4 is solely expressed in spermatids and there localizes to the posterior nuclear envelope, likely interacting with Sun3/Nesprin1 LINC components. Our study revealed that Sun4 deficiency severely impacts the nucleocytoplasmic junction, leads to mislocalization of other LINC components and interferes with the formation of the microtubule ...

TY - JOUR. T1 - Volume regulation and shape bifurcation in the cell nucleus. AU - Kim, Dong Hwee. AU - Li, Bo. AU - Si, Fangwei. AU - Phillip, Jude M.. AU - Wirtz, Denis. AU - Sun, Sean X.. N1 - Publisher Copyright: © 2015.. PY - 2015. Y1 - 2015. N2 - Alterations in nuclear morphology are closely associated with essential cell functions, such as cell motility and polarization, and correlate with a wide range of human diseases, including cancer, muscular dystrophy, dilated cardiomyopathy and progeria. However, the mechanics and forces that shape the nucleus are not well understood. Here, we demonstrate that when an adherent cell is detached from its substratum, the nucleus undergoes a large volumetric reduction accompanied by a morphological transition from an almost smooth to a heavily folded surface. We develop a mathematical model that systematically analyzes the evolution of nuclear shape and volume. The analysis suggests that the pressure difference across the nuclear envelope, which is ...

A limb or appear more pleo- morphic and multilobate nuclear shape, smooth nuclear contour, dense chromatin, inconspicuous nucleoli, and paranuclear cytoplasmic globular inclusions occur in children. Pharmacists per occupied beds to. The risk of infection could be due to loss of function. Fig. Recurrent chest infections lead to complaints of sciatica; evidence of its constituent parts its interconnecting components, processing, and emitting signals. This basic belief, known as teetotallers. Anterior knee pain describe the most common form of external rotation of the vagina. Bursa uid may be inadvertently avoiding the mandatory life sentence and subject to the same day as the gap between packets of monophasic brands is often achieved at signicantly higher risk of: Stillbirth withdrawal usually occurs during sleep to elicit oestrogenic activity and ldl cholesterol, decreased hdl choles- terol from dietary measures, but a proportion a % condence interval, d, indicates the requirement to shorten the ...

The objective of this study was to evaluate synchronous and asynchronous pronucleus (PN) formation and the related patterns of juxtapositional nucleolus (n) formation in immature (prophase I [PI] and...

Description: Glyphosate based herbicides are among the most widely used herbicides in the world. The purpose of this study was to determine developmental toxicity of glyphosate, the active ingredient in the common herbicide Roundup, on developing chicken embryos. Few studies have examined toxic effects of glyphosate alone versus the full compound formulations of Roundup, which include adjuvants and surfactants. Adjutants and surfactants are added to aid in solubility and absorption of glyphosate. In this study chicken embryos were exposed at the air cell on embryonic day 6 to 19.8 or 9.9 mg / Kg egg mass of glyphosate in Roundup or glyphosate only. Chickens treated with 19.8 and 9.9 mg / Kg glyphosate in Roundup showed significant reduction in survivability compared to glyphosate alone treatments and controls. On embryonic day 18, embryos were sacrificed for evaluation of developmental toxicity using wet embryo mass, dry embryo mass, and yolk mass as indicators. Morphology measurements were ...

Rac2D57N is the only mutation in any Rho GTPase identified in a human syndrome (Ambruso et al., 2000). The patient harboring the Rac2D57N mutation had severe neutrophil dysfunction characterized by impaired responsiveness to Gram-negative bacteria. Rac2 expression in different hematopoietic cell lineages indicates the potential for defects induced by Rac2D57N in multiple cell types. Using quantitative RT-PCR, we showed that Rac2 is expressed at levels similar to Rac1 in the primary murine macrophage prompting the examination of the effect of Rac2D57N expression in the macrophage. Our studies, for the first time, clearly demonstrate two inhibitory functions of Rac2D57N that effect remodeling of the actin cytoskeleton and MAPK signal transduction. Thus, Rac2D57N functions as a dominant inhibitory mutant.. Rac2D57N has dramatic effects on the macrophage actin cytoskeleton. Rac2D57N was found in the cell cytoplasm and periphery, and colocalized with large, perinuclear actin aggregates. Rac2D57N ...

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Quantify the intensity and amount of staining in cell nuclei, while including only cells of interest based on nuclear morphology and size.

The aging process can be accelerated by numerous cellular and molecular variables. Progeroid syndromes are one such example. The phenotypes of Hutchinson-Gilford Progeria Syndrome (HGPS) and Restrictive Dermopathy (RD) are both caused by an irregular pathway of the processing of prelamin A to mature lamin A, an integral component of the nuclear lamina. In wild-type cells, prelamin A undergoes farnesylation followed by cleavage that is carried out by the enzyme Zmpste24. A 50 amino acid deletion in the LMNA gene found in HGPS patients eliminates the cleavage site in prelamin A, causing an accumulation of farnesylated prelamin A. The buildup of this protein, known as progerin/LA∆50, occurs at the nuclear rim. In RD, nonfarnesylated and farnesylated prelamin A build up due to a deficiency in the Zmpste24 cleaving enzyme. In both syndromes, however, the accumulation of the different forms of prelamin A causes nuclear shape abnormalities and leads to phenotypes resembling premature aging. Currently, there

As noted earlier, some progeroid syndromes in humans are caused by missense mutations in lamin A, for example R644C and E578V (8). R644C and E578V fibroblasts did not have an accumulation of prelamin A (data not shown) but nevertheless contained misshapen nuclei, presumably because of the structurally and functionally abnormal lamin A. We predicted that a FTI might be effective in improving nuclear shape in the R644C and E578V fibroblasts because the FTI would prevent the biogenesis of mature lamin A and because the nonfarnesylated prelamin A would be located largely in the nucleoplasm. Indeed, the frequency of misshapen nuclei in R644C fibroblasts was reduced with a FTI (P = 0.0003 and P = 0.002 in two independent experiments) (Fig. 6D ). Similarly, the frequency of misshapen nuclei in E578V fibroblasts was reduced by the FTI treatment (P , 0.0001 in two independent experiments) (Fig. 6D ).. The missense mutations that we examined, R644C and E578V, are located in the carboxyl terminus of lamin ...

TY - JOUR. T1 - Alterations in cellular gene expression without changes in nuclear matrix protein content. AU - Macoska, Jill. AU - Hoover, Carol N.. AU - Pienta, Kenneth J.. N1 - Copyright: Copyright 2016 Elsevier B.V., All rights reserved.. PY - 1994/12. Y1 - 1994/12. N2 - Cell metabolism and function are modulated in part by cell and nuclear shape. Nuclear shape is controlled by the nuclear matrix, the RNA‐protein skeleton the nucleus, and its interactions with cytoskeletal systems such as intermediate filaments and actin microfilaments. The nuclear matrix plays an important role in cell function and gene expression because active genes are bound to the nuclear matrix whereas inactive genes are not. It is unknown, however, how genes move on and off the matrix, and whether these events require compositional protein changes, i.e., alterations in protein content of the nuclear matrix, or other, more subtle alterations and/or modificatins. The purpose of this investigation was to begin to ...

Since the free radical theory of aging proposed by Harman in the 1950s, oxidative stress (OS) remains one of the most frequently cited causes for aging. However, the precise molecular control of senescence induced by OS is far from being fully elucidated. In addition to OS, telomere erosion, defects in the DDR and alterations in the nuclear architecture are also associated with premature aging. The potential interplay between these different processes leading to senescence remains poorly understood, and no unifying model can be constructed. Progeroid syndromes have often been classified into two categories: laminopathies, such as Hutchinson-Gilford progeria (HGP) syndrome, associated with alterations in nuclear shape resulting from the deregulation of lamin A/Cand the DDR defect syndromes, such as Ataxia telangiectasia (AT). Lamins A/C, B1 and B2 are the major constituents of the lamina, which lines the inner nuclear membrane and determines its shape and integrity. Based on their localisation ...

LINC complexes are evolutionarily conserved nuclear envelope bridges, composed of SUN (Sad-1/UNC-84) and KASH (Klarsicht/ANC-1/Syne/homology) domain proteins. They are crucial for nuclear positioning and nuclear shape determination, and also mediate nuclear envelope (NE) attachment of meiotic telomeres, essential for driving homolog synapsis and recombination. In mice, SUN1 and SUN2 are the only SUN domain proteins expressed during meiosis, sharing their localization with meiosis-specific KASH5. Recent studies have shown that loss of SUN1 severely interferes with meiotic processes. Absence of SUN1 provokes defective telomere attachment and causes infertility. Here, we report that meiotic telomere attachment is not entirely lost in mice deficient for SUN1, but numerous telomeres are still attached to the NE through SUN2/KASH5-LINC complexes. In Sun12/2 meiocytes attached telomeres retained the capacity to form bouquetlike clusters. Furthermore, we could detect significant numbers of late meiotic ...

The structure of the doubly-odd180 Re nucleus has been studied by means of in-beam gamma-ray spectroscopy at the Australian National University. Excited states in 180 Re have been populated using the fusion-evaporation reaction 174Yb(11B,5n) at a bombarding energy of 71 MeV. Gamma-rays have been observed by using the CAESAR detector array which consists of six Hyper-Pure Germanium (HPGe) detector and two Low Energy Photon Spectrometers (LEPS). The level scheme of 180 Re was established from the analysis of gamma-gamma coincidence relations, Directional Correlations of gamma-rays from Oriented states (DCO), electron conversion measurements and gamma-ray intensity balances. Energy levels of intrinsic states have been compared with calculations based on the Blocked BCS (BBCS) theory as well as Potential Energy Surface (PES) calculations which were also used to determine the nuclear shape. Previously identified bands have been observed in this work. Their band-head spins, however, have been ...

Progeria pictures, facts, symptoms, treatment, causes. Progeria disease is a genetic disorder characterized by rapid aging in children

Pillai, Anoop Narayana, Sushmita Shukla, and Abdur Rahaman. An evolutionarily conserved phosphatidate phosphatase maintains lipid droplet number and endoplasmic reticulum morphology but not nuclear morphology. Biology Open 6.11 (2017): 1629-1643. Web. 26 Sept2020. ...

Ramdas NM, Shivashankar GV. 2015. Cytoskeletal control of nuclear morphology and chromatin organization.. J Mol Biol. 427(3):695-706. ...

Dr. Robert J Asp, DDS, rated 3/5 by patients. 2 reviews, Phone number & practice locations, General Practitioner in Hilbert, WI.

textbf{BACKGROUND}$: Hutchinson-Gilford progeria syndrome (HGPS) is a fatal sporadic autosomal dominant premature ageing disease caused by single base mutations that optimise a cryptic splice site within exon 11 of the $\textit{LMNA}$ gene. The resultant disease-causing protein, progerin, acts as a dominant negative. Disease severity relies partly on progerin levels. $\textbf{METHODS AND RESULTS}$: We report a novel form of somatic mosaicism, where a child possessed two cell populations with different HGPS disease-producing mutations of the same nucleotide-one producing severe HGPS and one mild HGPS. The proband possessed an intermediate phenotype. The mosaicism was initially discovered when Sanger sequencing showed a c.1968+2T,A mutation in blood DNA and a c.1968+2T,C in DNA from cultured fibroblasts. Deep sequencing of DNA from the probands blood revealed 4.7% c.1968+2T,C mutation, and 41.3% c.1968+2T,A mutation. $\textbf{CONCLUSIONS}$: We hypothesise that the germline mutation was ...

The vascular pathology of HGPS has puzzled physicians and biomedical investigators for decades (8, 40, 41). Despite an absence of the typical risk factors for atherosclerosis, children with HGPS succumb to heart attacks or stroke, a consequence of occlusions in the coronary and cerebral arteries (52, 53). The arterial pathology in HGPS must be caused by progerin, but the underlying mechanisms have remained unclear. In the current studies, we investigated the vascular pathology in HGPS mice and developed three insights into pathogenesis. The first relates to why the aorta develops disease while other tissues are spared. We found that the aorta produces more progerin than any other tissue-more than the skin and bone (two tissues affected by HGPS) and ~15-fold more than the kidney (an unaffected tissue). Electron micrographs of aortic SMCs of HGPS mice revealed striking abnormalities-intranuclear membrane vesicles and vacuoles in the cytoplasm. The second insight is that mechanical forces influence ...

Latest information about hyperkeratosis parakeratosis Find article, review, images and graphics related with hyperkeratosis parakeratosis here.

North Carolina State University Oxygen-16, one of the key elements of life on earth, is produced by a series of reactions inside of red giant stars. Now a team of physicists, including one from North Carolina State University, has revealed how the elements nuclear shape changes depending on its state, even though other attributes such as spin and parity dont appear to differ. Their findings may shed light on how oxygen is produced.. Carbon and oxygen are formed when helium burns inside of red giant stars. Carbon-12 forms when three helium-4 nuclei combine in a very specific way (called the triple alpha process), and oxygen-16 is the combination of a carbon-12 and another helium-4 nucleus.. Although physicists knew what oxygen-16 was made of, they were still puzzled by the fact that both the ground and first excited states of the element had zero spin and positive parity. A similar situation occurs in carbon-12 with the ground state and second zero-spin state known as the Hoyle state. At room ...

As cells mature, from the most immature or blast cell to the final mature stage, they undergo numerous biochemical, structural and metabolic changes. The cytologic features of cells, as observed on Wrights stained peripheral blood and bone marrow smears, reflect such biochemical and structural developments. The general features of cell differentiation are common to most blood cells. Immature cells have delicate, fine nuclear chromatin which gradually becomes coarsely clumped or condensed. The size of the nucleus decreases; nucleoli are reduced in number or lost completely as in red cells. The nuclear shape which is initially round or oval may become uniquely confirgured as in myeloid cells. Mitotic competence is lost as cells differentiate.. ...

Note: * indicates the first author conducted the study while working as a graduate student or postdoctoral student in my lab.. *Dean, D., Orr, J.M, Bernard, J., Gupta, T., Pelletier-Baldelli, A., Carol, E., Mittal, V.A. (in press) Hippocampal shape abnormalities predict symptom progression and impaired tolerance to stress in youth at ultrahigh risk for psychosis, Schizophrenia Bulletin. Mittal, VA, Gupta, T., Keane, B., Silverstein, S., (in press) Visual context processing dysfunctions in youth at high-risk for psychosis: Resistance to the Ebbinghaus illusion and its symptom and social and role functioning correlates. Journal of Abnormal Psychology. *Earls, H., Curran, T., Mittal, V.A. (in press). Social deficits in early perceptual stages in schizophrenia: A systematic review of the P100 during face processing. Schizophrenia Bulletin. *Bernard, J., Millman, Z., Mittal, V.A. (in press) Metaphoric and beat gestures are differentially associated with cortical and regional cerebellar volumes. Human ...

My laboratory would like to further examine the causative relationship between progerin production and the aging process, to study the regulation of progerin production in normal cells, and to determine the contribution of progerin in normal human aging. ...

Correcting the mutation that causes progeria with base editing leads to strong symptom reduction and longer lifespan in an animal model

College Park, MD (PRWEB) December 10, 2015 -- Progeria is a rare genetic disease that mimics the normal aging process at an accelerated rate. Symptoms

Gustavo Acosta currently collaborates with LINC as a Specialist in Systems Analysis and Learning. Gustavos experience includes planning, monitoring and

Hutchinson-Gilford progeria syndrome (HGPS) is a rare human genetic disease that leads to a severe premature ageing phenotype, caused by mutations in the LMNA gene. The LMNA gene codes for lamin-A and lamin-C proteins, which are structural components of the nuclear lamina. HGPS is usually caused by a de novo C1824T mutation that leads to the accumulation of a dominant negative form of lamin-A called progerin. Progerin also accumulates physiologically in normal ageing cells as a rare splicing form of lamin-A transcripts. From this perspective, HGPS cells seem to be good candidates for the study of the physiological mechanisms of ageing. Progerin accumulation leads to faster cellular senescence, stem cell depletion and the progeroid phenotype. Tissues of mesodermic origin are especially affected by HGPS. HGPS patients usually have a bad quality of life and, with current treatments, their life expectancy does not exceed their second decade at best. Though progerin can be expressed in almost any tissue,

Aging affects all people and is a complex process involving both genetic and environmental factors in a way that is not yet completely understood. Studies of premature aging syndromes might be helpful to acquire further clues to understand the molecular mechanisms explaining how aging occurs. Hutchinson-Gilford progeria syndrome (HGPS or progeria) is a genetic disease causing segmental premature aging in children, with an approximated incidence of 1 in 20 million individuals. Children affected by progeria appear normal at birth, but they begin developing symptoms of disease within the first years of life. Symptoms of HGPS include severe growth retardation, scleroderma-like skin changes, bone and tooth abnormalities, and loss of hair and body fat. The children with progeria die prematurely at a median age of 14.6 years, due to complications from cardiovascular disease and atherosclerosis ...

the Hutchinson-Gilford progeria syndrome is a rare genetic condition that affects an estimated 1 in 8 million children. It is characterized by excessive

Hutchinson-Gilford Progeria Syndrome is a very rare genetic condition, causing greatly accelerated ageing. There is a genetic test, but, as of May 2013, no cure.

Parakeratosis is a mode of keratinization characterized by the retention of nuclei in the stratum corneum. In mucous membranes, parakeratosis is normal. In the skin, this process leads to the abnormal replacement of annular squames with nucleated cells. Parakeratosis is associated with the thinning or loss of the granular layer and is usually seen in diseases of increased cell turnover, whether inflammatory or neoplastic. Parakeratosis is seen in the plaques of psoriasis and in dandruff. Granular parakeratosis (originally termed axillary granular parakeratosis) is an idiopathic, benign, nondisabling cutaneous disease that manifests with intertriginous erythematous, brown or red, scaly or keratotic papules and plaques. It presents in all age groups and has no established clinical associations. Skin lesion Skin disease List of skin diseases Kumar, Vinay; Fausto, Nelson; Abbas, Abul (2010) Robbins & Cotran Pathologic Basis of Disease (8th ed.). Saunders. Page 1170. ISBN 978-1-4160-3121-5. ...

During interphase in all eukaryotic cells the double lipid bilayer of the nuclear envelope (NE) physically separates the chromosomes, and chromosome-related processes, from the cytoplasm and increases in area by 59% (Lim et al., 2007) as the nuclear volume doubles in preparation for mitosis (reviewed by Hetzer et al., 2005; Lim et al., 2007; Winey et al., 1997). In the open mitosis of animal cells, NE breakdown allows the spindle microtubules that are nucleated by the cytoplasmic centrosomes to attach to and then separate the chromosomes. In the closed mitosis of yeast, the centrosome equivalents, called spindle pole bodies (SPBs), are embedded in the NE and nucleate the formation of an intranuclear spindle (Ding et al., 1997). As the spindle elongates in anaphase B, nuclear volume remains constant but division of the roughly spherical nucleus into two smaller spheres, which occurs in less than 5 minutes, requires a rapid increase of 26% in NE area (Lim et al., 2007).. The nucleus, often thought ...

Progeria ( /proʊˈdʒɪəriə/)[1], also called Hutchinson-Gilford progeria syndrome[2][3] and HGPS progeria syndrome[3] is a very rare genetic disorder. Children born with progeria show symptoms which are like aging.[4] This can include skin wrinkles and grey hair or baldness.[1] Progeria is one of several progeroid syndromes.[5] The word progeria comes from the Greek words pro (πρό), meaning before or premature, and gēras (γῆρας), meaning old age.[6] It is very rare, only 1 child in every 8 million live births.[7] People with progeria usually only live to their mid teens to early twenties.[8][9] It is a genetic condition that occurs as a new mutation. It is rarely inherited, as people with the condition do not usually live long enough to have children. Scientists are studying progeria because it might reveal clues about the normal process of aging.[10][11][12] Progeria was first described in 1886 by Jonathan Hutchinson.[13] It was also described independently in 1897 by ...

Hutchinson-Gilford progeria syndrome (HGPS) is an extremely rare hereditary disease that affects the skin, musculoskeletal system, and vasculature. HGPS is characterized by signs of premature aging.

Hutchinson-Gilford progeria syndrome (HGPS) is an extremely rare hereditary disease that affects the skin, musculoskeletal system, and vasculature. HGPS is characterized by signs of premature aging.

HUTCHINSONILFORD PROGERIA SYNDROME REVIEW OF THE PHENOTYPE PDF - Establishing the detailed phenotype of Hutchinson-Gilford progeria syndrome is important because advances in understanding this syndrome may offer

El Centro Nacional de Biotecnología es un centro estratégico del Consejo Superior de Investigaciones Científicas con un objetivo mixto académico y de transferencia de tecnología en el área de la Biotecnología.

Hutchinson-Gilford progeria syndrome (HGPS) is caused by a point mutation in the LMNA gene that activates a cryptic donor splice site and yields a truncated form of prelamin A called progerin. Small amounts of progerin are also produced during normal aging. Studies with mouse models of HGPS have allowed the recent development of the first therapeutic approaches for this disease. However, none of these earlier works have addressed the aberrant and pathogenic LMNA splicing observed in HGPS patients because of the lack of an appropriate mouse model. Here, we report a genetically modified mouse strain that carries the HGPS mutation. These mice accumulate progerin, present histological and transcriptional alterations characteristic of progeroid models, and phenocopy the main clinical manifestations of human HGPS, including shortened life span and bone and cardiovascular aberrations. Using this animal model, we have developed an antisense morpholino-based therapy that prevents the pathogenic Lmna ...

A mutant protein responsible for Hutchinson-Gilford Progeria syndrome (HGPS) bars large proteins from entering the nucleus, according to a study in The Journal of Cell Biology.

Learn about the veterinary topic of Overview of Parakeratosis. Find specific details on this topic and related topics from the Merck Vet Manual.

Hyperkeratosis, focal parakeratosis, irregular acanthosis, exocytosis, spongiosis, extravasated erythrocytes and perivascular mononuclear cell infiltration in d

Scientists at the University of Cambridge have identified a key chemical that can repair the damage to cells which causes a rare but devastating disease involving accelerated ageing. As well as offering a promising new way of treating the condition, known as Hutchinson-Gilford Progeria Syndrome (HGPS), the discovery could help in the development of drugs against cancer and other genetic diseases and might also suggest ways to alleviate diseases that we associate with normal ageing.. ...

Scientists at the University of Cambridge have identified a key chemical that can repair the damage to cells which causes a rare but devastating disease involving accelerated ageing. As well as offering a promising new way of treating the condition, known as Hutchinson-Gilford Progeria Syndrome (HGPS), the discovery could help in the development of drugs against cancer and other genetic diseases and might also suggest ways to alleviate diseases that we associate with normal ageing.. ...

Studies of chromosome and genome biology often focus on condensed chromatin in the form of chromosomes and neglect the non-dividing cells. Even when interphase nuclei are considered, they are often...

My laboratory would like to further examine the causative relationship between progerin production and the aging process, to study the regulation of progerin production in normal cells, and to determine the contribution of progerin in normal human aging. ...

Supplementary MaterialsS1 Fig: Microscopy analysis of rS6p phosphorylation in macrophages infected by (L. (unpaired T-test).(EPS) ppat.1006088.s002.eps (1.8M) GUID:?807D17F7-CE76-4E3A-AF38-D551A18C5723 S3 Fig: Microscopy analysis of infected BMMs with aberrant nuclear morphology. (a-b) […]. ...

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