Chronic low level lead exposure precociously induces rat glial development in vitro and in vivo

Recent studies confirmed that some Hepatozoon-like blood parasites (Apicomplexa) of birds are closely related to the amphibian parasite Lankesterella minima. Little is known about the biology of these pathogens in birds, including their distribution, life cycles, specificity, vectors, and molecular characterization. Using blood samples of 641 birds from 16 species, we (i) determined the prevalence and molecular diversity of Lankesterella parasites in naturally infected birds; (ii) investigated the development of Lankesterella kabeeni in laboratory-reared mosquitoes, Culex pipiens forma molestus and Aedes aegypti; and (iii) tested experimentally the susceptibility of domestic canaries, Serinus canaria, to this parasite. This study combined molecular and morphological diagnostic methods and determined 11% prevalence of Lankesterella parasites in Acrocephalidae birds; 16 Lankesterella lineages with a certain degree of host specificity and two new species (Lankesterella vacuolata n. sp. and Lankesterella macrovacuolata n. sp.) were found and characterized. Lankesterella kabeeni (formerly Hepatozoon kabeeni) was re-described. Serinus canaria were resistant after various experimental exposures. Lankesterella sporozoites rapidly escaped from host cells in vitro. Sporozoites persisted for a long time in infected mosquitoes (up to 42 days post exposure). Our study demonstrated a high diversity of Lankesterella parasites in birds, and showed that several avian Hepatozoon-like parasites, in fact, belong to Lankesterella genus.

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Low-Level Light in Combination with Metabolic Modulators for Effective Therapy of Injured Brain

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.2015.87 ◽

2015 ◽

Vol 35 (9) ◽

pp. 1435-1444 ◽

Cited By ~ 33

Author(s):

Tingting Dong ◽

Qi Zhang ◽

Michael R Hamblin ◽

Mei X Wu

Keyword(s):

Learning And Memory ◽

Memory Function ◽

Light Illumination ◽

Low Level ◽

Metabolic Substrates ◽

Secondary Damage ◽

Injured Brain ◽

Combinational Treatment

Vascular damage occurs frequently at the injured brain causing hypoxia and is associated with poor outcomes in the clinics. We found high levels of glycolysis, reduced adenosine triphosphate generation, and increased formation of reactive oxygen species and apoptosis in neurons under hypoxia. Strikingly, these adverse events were reversed significantly by noninvasive exposure of injured brain to low-level light (LLL). Low-level light illumination sustained the mitochondrial membrane potential, constrained cytochrome c leakage in hypoxic cells, and protected them from apoptosis, underscoring a unique property of LLL. The effect of LLL was further bolstered by combination with metabolic substrates such as pyruvate or lactate both in vivo and in vitro. The combinational treatment retained memory and learning activities of injured mice to a normal level, whereas other treatment displayed partial or severe deficiency in these cognitive functions. In accordance with well-protected learning and memory function, the hippocampal region primarily responsible for learning and memory was completely protected by combination treatment, in marked contrast to the severe loss of hippocampal tissue because of secondary damage in control mice. These data clearly suggest that energy metabolic modulators can additively or synergistically enhance the therapeutic effect of LLL in energy-producing insufficient tissue–like injured brain.

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Development of embryonic rat eyes in organ culture

Development ◽

10.1242/dev.19.3.407 ◽

1968 ◽

Vol 19 (3) ◽

pp. 407-414

Author(s):

R. Christy Armstrong ◽

Joel J. Elias

Keyword(s):

Organ Culture ◽

Culture Medium ◽

Folic Acid Deficiency ◽

Experimental Conditions ◽

Acid Deficiency ◽

Series Of Experiments ◽

Development In Vitro ◽

Ocular System

Abnormalities of the ocular system which appear in organ culture in Waymouth's medium with freshly added glutamine (Armstrong & Elias, 1968) resemble those caused by transitory pteryolglutamic acid (PGA or folic acid) deficiency in vivo (Armstrong & Monie, 1966). The configurations of such malformations as lens herniations, retinal diverticula, and rosette-like formations of the retina are remarkably similar in both cases. The experiments reported in this paper were undertaken in an effort to understand the mechanisms involved in the production of similar abnormalities by two very different experimental conditions: the addition of glutamine in vitro and the transitory deficiency of PGA in vivo. One series of experiments involved the effects of manipulation of the PGA and glutamine content of the culture medium on eye development in vitro. Parallel studies on PGA-deficiency in vivo were undertaken in conjunction with organ-culture experiments in order to compare the effects on abnormal eye morphogenesis.

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Drug NP031112 development: In vitro and in vivo studies predict no phototoxicity

Toxicology Letters ◽

10.1016/j.toxlet.2008.06.332 ◽

2008 ◽

Vol 180 ◽

pp. S152

Author(s):

Nicolas Fabre ◽

Isolde Anglade ◽

Genevieve Arcelin ◽

Conxita de Castellarnau ◽

Petra Giannini ◽

...

Keyword(s):

In Vivo Studies ◽

Development In Vitro

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Recombinant human megakaryocyte growth and development factor stimulates thrombocytopoiesis in normal nonhuman primates

Blood ◽

10.1182/blood.v86.1.54.bloodjournal86154 ◽

1995 ◽

Vol 86 (1) ◽

pp. 54-59 ◽

Cited By ~ 145

Author(s):

AM Farese ◽

P Hunt ◽

T Boone ◽

TJ MacVittie

Keyword(s):

Bone Marrow ◽

Peripheral Blood ◽

Growth And Development ◽

Nonhuman Primates ◽

Normal Male ◽

Platelet Counts ◽

Development Factor ◽

Development In Vitro

Megakaryocyte growth and development factor (MGDF) is a novel cytokine that binds to the c-mpl receptor and stimulates megakaryocyte development in vitro and in vivo. This report describes the ability of recombinant human (r-Hu) MGDF to affect megakaryocytopoiesis in normal nonhuman primates. r-HuMGDF was administered subcutaneously to normal, male rhesus monkeys once per day for 10 consecutive days at dosages of 2.5, 25, or 250 micrograms/kg of body weight. Bone marrow and peripheral blood were assayed for clonogenic activity and peripheral blood counts were monitored. Circulating platelet counts increased significantly (P < .05) for all doses within 6 days of r-HuMGDF administration and reached maximal levels between day 12 and day 14 postcytokine administration. The 2.5, 25.0, and 250.0 micrograms/kg/d doses elicited peak mean platelet counts that were 592%, 670%, and 449% of baseline, respectively. Bone marrow-derived clonogenic data showed significant increases in the concentration of megakaryocyte (MEG)- colony-forming unit (CFU) and granulocyte-erythroid-macrophage- megakaryocyte (GEMM)-CFU, whereas that of granulocyte-macrophage (GM)- CFU and burst-forming unit-erythroid (BFU-e) remained unchanged during the administration of r-HuMGDF. These data show that r-HuMGDF is a potent stimulator of thrombocytopoiesis in the normal nonhuman primate.

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A Novel Homozygous Deletion within the FRY Gene Associated with Nonsyndromic Developmental Delay

Cytogenetic and Genome Research ◽

10.1159/000502598 ◽

2019 ◽

Vol 159 (1) ◽

pp. 19-25 ◽

Cited By ~ 1

Author(s):

Prabakaran Paulraj ◽

Michelle Bosworth ◽

Maria Longhurst ◽

Callie Hornbuckle ◽

Garrett Gotway ◽

...

Keyword(s):

Developmental Delay ◽

Autosomal Recessive ◽

Pediatric Population ◽

Homozygous Deletion ◽

Homozygous Mutation ◽

Biallelic Mutation ◽

Snp Microarray ◽

Low Level

The role of autosomal recessive (AR) variants in clinically heterogeneous conditions such as intellectual disability and developmental delay (ID/DD) has been difficult to uncover. Implication of causative pathogenic AR variants often requires investigation within large and consanguineous families, and/or identifying rare biallelic variants in affected individuals. Furthermore, detection of homozygous gene-level copy number variants during first-line genomic microarray testing in the pediatric population is a rare finding. We describe a 6.7-year-old male patient with ID/DD and a novel homozygous deletion involving the FRY gene identified by genomic SNP microarray. This deletion was observed within a large region of homozygosity on the long arm of chromosome 13 and in a background of increased low-level (2.6%) autosomal homozygosity, consistent with a reported common ancestry in the family. FRY encodes a protein that regulates cell cytoskeletal dynamics, functions in chromosomal alignment in mitosis in vitro, and has been shown to function in the nervous system in vivo. Homozygous mutation of FRY has been previously reported in 2 consanguineous families from studies of autosomal recessive ID in Middle Eastern and Northern African populations. This report provides additional supportive evidence that deleterious biallelic mutation of FRY is associated with ID/DD and illustrates the utility of genomic SNP microarray detection of low-level homozygosity.

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Development of dual fluorescent stage specific reporter strain of Toxoplasma gondii to follow tachyzoite and bradyzoite development in vitro and in vivo

Microbes and Infection ◽

10.1016/j.micinf.2015.09.016 ◽

2016 ◽

Vol 18 (1) ◽

pp. 39-47 ◽

Cited By ~ 6

Author(s):

T.C. Paredes-Santos ◽

T. Tomita ◽

M. Yan Fen ◽

W. de Souza ◽

M. Attias ◽

...

Keyword(s):

Toxoplasma Gondii ◽

Reporter Strain ◽

Development In Vitro

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Development, in-vitro and in-vivo characterization of gelatin nanoparticles for delivery of an anti-inflammatory drug

Journal of Drug Delivery Science and Technology ◽

10.1016/j.jddst.2016.09.007 ◽

2016 ◽

Vol 36 ◽

pp. 55-61 ◽

Cited By ~ 10

Author(s):

Alok Mahor ◽

Sunil Kumar Prajapati ◽

Amita Verma ◽

Rishikesh Gupta ◽

Thakur Raghu Raj Singh ◽

...

Keyword(s):

Gelatin Nanoparticles ◽

Inflammatory Drug ◽

Anti Inflammatory ◽

Development In Vitro ◽

In Vivo Characterization

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Injury effects of ginkgolide B on maturation of mouse oocytes, fertilization, and fetal development in vitro and in vivo

Toxicology Letters ◽

10.1016/j.toxlet.2009.03.004 ◽

2009 ◽

Vol 188 (1) ◽

pp. 63-69 ◽

Cited By ~ 16

Author(s):

Nion-Heng Shiao ◽

Wen-Hsiung Chan

Keyword(s):

Fetal Development ◽

Ginkgolide B ◽

Mouse Oocytes ◽

Development In Vitro

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Low-Level Aflatoxin B1 Promotes Influenza Infection and Modulates a Switch in Macrophage Polarization from M1 to M2

Cellular Physiology and Biochemistry ◽

10.1159/000493294 ◽

2018 ◽

Vol 49 (3) ◽

pp. 1151-1167 ◽

Cited By ~ 9

Author(s):

Yuhang Sun ◽

Zixuan Liu ◽

Dandan Liu ◽

Jin Chen ◽

Fang Gan ◽

...

Keyword(s):

Electron Microscopy ◽

Scanning Electron Microscopy ◽

Influenza Virus ◽

Matrix Protein ◽

Macrophage Polarization ◽

Low Level ◽

Siv Infection ◽

Scanning Electron

Background/Aims: Swine influenza virus (SIV) is a major pathogen of both animals and humans. Afatoxin B1 (AFB1) is one of the most common mycotoxins in feed and food. However, the central contribution of AFB1 to SIV infection remains unclear. Methods: Here, TCID50 assays, fluorescence-based quantitative real-time PCR, western blotting, immunofluorescence staining, histopathological examination, flow cytometry and scanning electron microscopy were performed to investigate the involvement and underlying mechanism of AFB1 in SIV infection in vivo and in vitro using mouse models and porcine alveolar macrophage (PAM) models, respectively. Results: The in vivo study showed that low levels of AFB1 promoted SIV infection and increased its severity, as demonstrated by the increased mRNA expression of viral matrix protein (M); by the increased protein expression of nucleoprotein (NP), matrix protein 1 and ion channel protein; and by animal weight loss, lung index and lung histologic damage. In addition, the increased occurrence of SIV infection accompanied by increases in the level of IL-10 in sera and lungs, in the spleen index and in the number of CD206-positive mouse alveolar macrophages but decreases in the level of TNF-α in sera and lungs, in the thymus index and in the number of CD80-positive mouse alveolar macrophages was observed in SIV-infected mice after low-level AFB1 exposure. The in vitro study showed that low concentrations of AFB1 promoted SIV infection, as demonstrated by the increases in viral titers and viral M mRNA and NP expression levels in SIV-infected PAMs as well as by the number of cells positive for NP protein expression. Furthermore, AFB1 promoted the polarization of SIV-infected PAMs to the M1 phenotype at 8 hpi and to the M2 phenotype at 24 hpi, as measured by the increases in IL-10 expression and in the number of CD206-positive PAMs as well as by the morphological changes observed by scanning electron microscopy. The administration of the immune stimulant lipopolysaccharide (LPS) reversed the switch in PAM polarization from M2 to M1 and thereby counteracted the promotion of influenza virus infection induced by AFB1. Conclusion: Our results are the first to confirm that low-level exposure to AFB1 promotes SIV infection and modulates a switch in macrophage polarization from M1 to M2. The work reported here provides important data that point to a role for AFB1 in SIV infection, and it opens a new field of study.

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