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Tumor growth inhibition of tumor xenografts in nude NMRI mice treated with LNA PO ODNs. ( A ) NMRI nu/nu mice were injected s.c. in the flank with 10 6 15PC3 cells from culture in 300 µl Matrigel. After 1 week of tumor growth the mice received an osmotic <t>minipump</t> (Alzet model 1002) which was implanted dorsally. The osmotic minipumps were filled with LNA PO ODNs against POLR2A : Cur616 (full match), Cur222 (single mismatch), Cur942 (four mismatch) or saline control at dosages of 0.5, 1 and 2.5 mg/kg/day. The tumor growth was monitored after implantation of the osmotic pump. The results are expressed as mean tumor volume ± SEM ( n = 5 per group). ( B ) Amount of radioactivity expressed as specific uptake (percentage of injected dose divided by tissue weight) ± SEM recovered in 15PC3 tumor xenografts 30 min post-injection. ( C ) Photographs of representative tumors of a mouse treated with saline (top) and a mouse treated with a full matching LNA PO ODN against POLR2A at 1 mg/kg/day dose (bottom).
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Images

1) Product Images from "In vivo tumor growth inhibition and biodistribution studies of locked nucleic acid (LNA) antisense oligonucleotides"

Article Title: In vivo tumor growth inhibition and biodistribution studies of locked nucleic acid (LNA) antisense oligonucleotides

Journal: Nucleic Acids Research

doi:

Tumor growth inhibition of tumor xenografts in nude NMRI mice treated with LNA PO ODNs. ( A ) NMRI nu/nu mice were injected s.c. in the flank with 10 6 15PC3 cells from culture in 300 µl Matrigel. After 1 week of tumor growth the mice received an osmotic minipump (Alzet model 1002) which was implanted dorsally. The osmotic minipumps were filled with LNA PO ODNs against POLR2A : Cur616 (full match), Cur222 (single mismatch), Cur942 (four mismatch) or saline control at dosages of 0.5, 1 and 2.5 mg/kg/day. The tumor growth was monitored after implantation of the osmotic pump. The results are expressed as mean tumor volume ± SEM ( n = 5 per group). ( B ) Amount of radioactivity expressed as specific uptake (percentage of injected dose divided by tissue weight) ± SEM recovered in 15PC3 tumor xenografts 30 min post-injection. ( C ) Photographs of representative tumors of a mouse treated with saline (top) and a mouse treated with a full matching LNA PO ODN against POLR2A at 1 mg/kg/day dose (bottom).
Figure Legend Snippet: Tumor growth inhibition of tumor xenografts in nude NMRI mice treated with LNA PO ODNs. ( A ) NMRI nu/nu mice were injected s.c. in the flank with 10 6 15PC3 cells from culture in 300 µl Matrigel. After 1 week of tumor growth the mice received an osmotic minipump (Alzet model 1002) which was implanted dorsally. The osmotic minipumps were filled with LNA PO ODNs against POLR2A : Cur616 (full match), Cur222 (single mismatch), Cur942 (four mismatch) or saline control at dosages of 0.5, 1 and 2.5 mg/kg/day. The tumor growth was monitored after implantation of the osmotic pump. The results are expressed as mean tumor volume ± SEM ( n = 5 per group). ( B ) Amount of radioactivity expressed as specific uptake (percentage of injected dose divided by tissue weight) ± SEM recovered in 15PC3 tumor xenografts 30 min post-injection. ( C ) Photographs of representative tumors of a mouse treated with saline (top) and a mouse treated with a full matching LNA PO ODN against POLR2A at 1 mg/kg/day dose (bottom).

Techniques Used: Inhibition, Mouse Assay, Injection, Radioactivity

2) Product Images from "Peripheral inflammation increases seizure susceptibility via the induction of neuroinflammation and oxidative stress in the hippocampus"

Article Title: Peripheral inflammation increases seizure susceptibility via the induction of neuroinflammation and oxidative stress in the hippocampus

Journal: Journal of Biomedical Science

doi: 10.1186/s12929-015-0157-8

The COX-2-dependent upregulations of antioxidant proteins in the hippocampus after intraperitoneal LPS infusion. Representative gels (insert) and densitometric analysis of results from Western blot showing changes in expression of cupper/zinc superoxide dismutase (Cu/ZnSOD) ( a ), manganese SOD (MnSOD) ( b ), catalase ( c ), or glutathione peroxide (GPx) ( d ) in hippocampus, measured on day 7 after intraperitoneal infusion via an osmotic minipump of saline or LPS (2.5 mg/kg/day) for 7 days alone or with additional intracerebroventricular infusion of NS398 (5 μg/μl/h, dissolved in 1 % DMSO), tempol (2.5 μg/μl/h, dissolved in saline) or the corresponding vehicle. Values are mean ± SEM, n = 8–10 rats per group. *P
Figure Legend Snippet: The COX-2-dependent upregulations of antioxidant proteins in the hippocampus after intraperitoneal LPS infusion. Representative gels (insert) and densitometric analysis of results from Western blot showing changes in expression of cupper/zinc superoxide dismutase (Cu/ZnSOD) ( a ), manganese SOD (MnSOD) ( b ), catalase ( c ), or glutathione peroxide (GPx) ( d ) in hippocampus, measured on day 7 after intraperitoneal infusion via an osmotic minipump of saline or LPS (2.5 mg/kg/day) for 7 days alone or with additional intracerebroventricular infusion of NS398 (5 μg/μl/h, dissolved in 1 % DMSO), tempol (2.5 μg/μl/h, dissolved in saline) or the corresponding vehicle. Values are mean ± SEM, n = 8–10 rats per group. *P

Techniques Used: Western Blot, Expressing

Intraperitoneal LPS infusion induces a COX-2-dependent microglial activation in the hippocampus. Gels (inset) and densitometric analysis of results from Western blot showing changes in the expression of Iba-1 ( a ) or representative photomicrographs ( b - d ) showing immunoreactivity to Iba-1 in hippocampal area (CA1, CA3, and dentate gyrus, DG), measured on day 7 after intraperitoneal infusion via an osmotic minipump of saline or LPS (2.5 mg/kg/day) for 7 days alone or with additional intracerebroventricular infusion of NS398 (5 μg/μl/h, dissolved in 1 % DMSO), tempol (2.5 μg/μl/h, dissolved in saline) or the corresponding vehicle. Also shown are photomicrographs of a typical activated microglia in a higher magnification (insets in b - d ). Values are mean ± SEM, n = 8–10 rats per group. *P
Figure Legend Snippet: Intraperitoneal LPS infusion induces a COX-2-dependent microglial activation in the hippocampus. Gels (inset) and densitometric analysis of results from Western blot showing changes in the expression of Iba-1 ( a ) or representative photomicrographs ( b - d ) showing immunoreactivity to Iba-1 in hippocampal area (CA1, CA3, and dentate gyrus, DG), measured on day 7 after intraperitoneal infusion via an osmotic minipump of saline or LPS (2.5 mg/kg/day) for 7 days alone or with additional intracerebroventricular infusion of NS398 (5 μg/μl/h, dissolved in 1 % DMSO), tempol (2.5 μg/μl/h, dissolved in saline) or the corresponding vehicle. Also shown are photomicrographs of a typical activated microglia in a higher magnification (insets in b - d ). Values are mean ± SEM, n = 8–10 rats per group. *P

Techniques Used: Activation Assay, Western Blot, Expressing

COX-2-dependent and redox-sensitive increase in seizure susceptibility after intraperitoneal LPS infusion. Time-course changes in kainic acid-induced seizure stage (a), total seizure activity (stages) ( b ) and seizure onset time to stage 3 ( c ) measured on day 7 after intraperitoneal infusion via an osmotic minipump of saline or LPS (2.5 mg/kg/day) for 7 days alone or with additional intracerebroventricular infusion of NS398 (5 μg/μl/h, dissolved in 1 % DMSO), tempol (2.5 μg/μl/h, dissolved in saline) or the corresponding vehicle. Values are mean ± SEM, n = 8-10 rats per group. *P
Figure Legend Snippet: COX-2-dependent and redox-sensitive increase in seizure susceptibility after intraperitoneal LPS infusion. Time-course changes in kainic acid-induced seizure stage (a), total seizure activity (stages) ( b ) and seizure onset time to stage 3 ( c ) measured on day 7 after intraperitoneal infusion via an osmotic minipump of saline or LPS (2.5 mg/kg/day) for 7 days alone or with additional intracerebroventricular infusion of NS398 (5 μg/μl/h, dissolved in 1 % DMSO), tempol (2.5 μg/μl/h, dissolved in saline) or the corresponding vehicle. Values are mean ± SEM, n = 8-10 rats per group. *P

Techniques Used: Activity Assay

Intraperitoneal LPS infusion induces peripheral inflammation which is not affected by intracerebroventricular infusion of NS398 or tempol. Plasma levels of interleukin-1β (IL-1β, a ), IL-6 ( b ), and tumor necrosis factor-α (TNF-α, c ) measured on day 7 after intraperitoneal infusion via an osmotic minipump of saline or LPS (2.5 mg/kg/day) for 7 days alone or with additional intracerebroventricular infusion of NS398 (5 μg/μl/h, dissolved in 1 % DMSO), tempol (2.5 μg/μl/h, dissolved in saline), or the corresponding vehicle. Values are mean ± SEM, n = 10–12 rats per group. * P
Figure Legend Snippet: Intraperitoneal LPS infusion induces peripheral inflammation which is not affected by intracerebroventricular infusion of NS398 or tempol. Plasma levels of interleukin-1β (IL-1β, a ), IL-6 ( b ), and tumor necrosis factor-α (TNF-α, c ) measured on day 7 after intraperitoneal infusion via an osmotic minipump of saline or LPS (2.5 mg/kg/day) for 7 days alone or with additional intracerebroventricular infusion of NS398 (5 μg/μl/h, dissolved in 1 % DMSO), tempol (2.5 μg/μl/h, dissolved in saline), or the corresponding vehicle. Values are mean ± SEM, n = 10–12 rats per group. * P

Techniques Used:

Intraperitoneal LPS infusion induces a COX-2-dependent neuroinflammation in the hippocampus. Tissue levels of IL-1β ( a ), IL-6 ( b ) and TNF-α ( c ) in hippocampus measured on 7 day after intraperitoneal infusion via an osmotic minipump of saline or LPS (2.5 mg/kg/day) for 7 days alone or with additional intracerebroventricular infusion of NS398 (5 μg/μl/h, dissolved in 1 % DMSO), tempol (2.5 μg/μl/h, dissolved in saline), or the corresponding vehicle. Values are mean ± SEM, n = 10–12 rats per group. *P
Figure Legend Snippet: Intraperitoneal LPS infusion induces a COX-2-dependent neuroinflammation in the hippocampus. Tissue levels of IL-1β ( a ), IL-6 ( b ) and TNF-α ( c ) in hippocampus measured on 7 day after intraperitoneal infusion via an osmotic minipump of saline or LPS (2.5 mg/kg/day) for 7 days alone or with additional intracerebroventricular infusion of NS398 (5 μg/μl/h, dissolved in 1 % DMSO), tempol (2.5 μg/μl/h, dissolved in saline), or the corresponding vehicle. Values are mean ± SEM, n = 10–12 rats per group. *P

Techniques Used:

The COX-2-dependent upregulations of the NADPH oxidase subunits in the hippocampus after intraperitoneal LPS infusion. Representative gels (insert) and densitometric analysis of results from Western blot showing changes in expression of gp91 phox ( a ), p47 phox ( b ) and p67 phox ( c ) in the hippocampus, measured on day 7 after intraperitoneal infusion via an osmotic minipump of saline or LPS (2.5 mg/kg/day) for 7 days alone or with additional intracerebroventricular infusion of NS398 (5 μg/μl/h, dissolved in 1 % DMSO), tempol (2.5 μg/μl/h, dissolved in saline) or the corresponding vehicle. Values are mean ± SEM, n = 8–10 rats per group. *P
Figure Legend Snippet: The COX-2-dependent upregulations of the NADPH oxidase subunits in the hippocampus after intraperitoneal LPS infusion. Representative gels (insert) and densitometric analysis of results from Western blot showing changes in expression of gp91 phox ( a ), p47 phox ( b ) and p67 phox ( c ) in the hippocampus, measured on day 7 after intraperitoneal infusion via an osmotic minipump of saline or LPS (2.5 mg/kg/day) for 7 days alone or with additional intracerebroventricular infusion of NS398 (5 μg/μl/h, dissolved in 1 % DMSO), tempol (2.5 μg/μl/h, dissolved in saline) or the corresponding vehicle. Values are mean ± SEM, n = 8–10 rats per group. *P

Techniques Used: Western Blot, Expressing

Intraperitoneal LPS infusion induces a COX-2-dependent and redox-sensitive increase in tissue superoxide levels in the hippocampus. Tissue level of superoxide anion, measured by electron paramagnetic resonance (EPR) spectroscopy, in the hippocampus on day 7 after intraperitoneal infusion via an osmotic minipump of saline or LPS (2.5 mg/kg/day) for 7 days alone with additional intracerebroventricular infusion NS398 (5 μg/μl/h, dissolved in 1% DMSO), tempol (2.5 μg/μl/h, dissolved in saline) or the corresponding vehicle. The concentration of superoxide in arbitrary unit was derived from computer simulation of the EPR spectra by normalized line shapes. Values are mean ± SEM, n = 8–10 rats per group. *P
Figure Legend Snippet: Intraperitoneal LPS infusion induces a COX-2-dependent and redox-sensitive increase in tissue superoxide levels in the hippocampus. Tissue level of superoxide anion, measured by electron paramagnetic resonance (EPR) spectroscopy, in the hippocampus on day 7 after intraperitoneal infusion via an osmotic minipump of saline or LPS (2.5 mg/kg/day) for 7 days alone with additional intracerebroventricular infusion NS398 (5 μg/μl/h, dissolved in 1% DMSO), tempol (2.5 μg/μl/h, dissolved in saline) or the corresponding vehicle. The concentration of superoxide in arbitrary unit was derived from computer simulation of the EPR spectra by normalized line shapes. Values are mean ± SEM, n = 8–10 rats per group. *P

Techniques Used: Electron Paramagnetic Resonance, Spectroscopy, Concentration Assay, Derivative Assay

3) Product Images from "Development of nonfibrotic left ventricular hypertrophy in an ANG II‐induced chronic ovine hypertension model. Development of nonfibrotic left ventricular hypertrophy in an ANG II‐induced chronic ovine hypertension model"

Article Title: Development of nonfibrotic left ventricular hypertrophy in an ANG II‐induced chronic ovine hypertension model. Development of nonfibrotic left ventricular hypertrophy in an ANG II‐induced chronic ovine hypertension model

Journal: Physiological Reports

doi: 10.14814/phy2.12897

Development of mean arterial blood pressure ( MAP ) during follow‐up. MAP increases in animals after implantation of ANG II ‐containing osmotic minipumps ( n = 9), whereas no changes were detected in vehicle control ( n = 7). Data are expressed as mean ± SD .
Figure Legend Snippet: Development of mean arterial blood pressure ( MAP ) during follow‐up. MAP increases in animals after implantation of ANG II ‐containing osmotic minipumps ( n = 9), whereas no changes were detected in vehicle control ( n = 7). Data are expressed as mean ± SD .

Techniques Used:

Study protocol. Mean arterial blood pressure ( MAP ) was measured weekly throughout the experiment, starting 2 weeks before the implantation of osmotic minipumps (baseline). Cardiovascular magnetic resonance was performed in the same procedure as pump implantation and after 7 weeks of treatment (follow‐up). Two animals were implanted with cardiac rhythm monitoring devices. After 8 weeks, all animals were electrophysiologically characterized using epicardial multielectrode mapping.
Figure Legend Snippet: Study protocol. Mean arterial blood pressure ( MAP ) was measured weekly throughout the experiment, starting 2 weeks before the implantation of osmotic minipumps (baseline). Cardiovascular magnetic resonance was performed in the same procedure as pump implantation and after 7 weeks of treatment (follow‐up). Two animals were implanted with cardiac rhythm monitoring devices. After 8 weeks, all animals were electrophysiologically characterized using epicardial multielectrode mapping.

Techniques Used:

4) Product Images from "Pyridostigmine Restores Cardiac Autonomic Balance after Small Myocardial Infarction in Mice"

Article Title: Pyridostigmine Restores Cardiac Autonomic Balance after Small Myocardial Infarction in Mice

Journal: PLoS ONE

doi: 10.1371/journal.pone.0104476

Mean arterial pressure and heart rate obtained before, one week (1 wk) and four weeks (4 wk) after myocardial infarction (MI) in mice treated with saline [n = 8] or pyridostigmine (PYR) [n = 7]. Values are presented as mean ± SEM. *p
Figure Legend Snippet: Mean arterial pressure and heart rate obtained before, one week (1 wk) and four weeks (4 wk) after myocardial infarction (MI) in mice treated with saline [n = 8] or pyridostigmine (PYR) [n = 7]. Values are presented as mean ± SEM. *p

Techniques Used: Mouse Assay

Tachycardic response caused by methyl atropine (Vagal Tone) [left and right upper panel], bradycardic response caused by propranolol (Sympathetic Tone) [left and right middle panel] and intrinsic heart rate (IHR) [left and right lower panel] before, one week (1 wk) and four weeks (4 wk) after MI with or without pyridostigmine (PYR) treatment. Values are presented as mean ± SEM. *p
Figure Legend Snippet: Tachycardic response caused by methyl atropine (Vagal Tone) [left and right upper panel], bradycardic response caused by propranolol (Sympathetic Tone) [left and right middle panel] and intrinsic heart rate (IHR) [left and right lower panel] before, one week (1 wk) and four weeks (4 wk) after MI with or without pyridostigmine (PYR) treatment. Values are presented as mean ± SEM. *p

Techniques Used:

Cross sections of representative hearts, stained with picrosirius red, from control and mice with myocardial infarction (MI), treated, or not, with pyridostigmine (PYR). Bar = 1 mm.
Figure Legend Snippet: Cross sections of representative hearts, stained with picrosirius red, from control and mice with myocardial infarction (MI), treated, or not, with pyridostigmine (PYR). Bar = 1 mm.

Techniques Used: Staining, Mouse Assay

Photomicrographs and bar graphs of the minor diameter of myocytes and collagen density from the left ventricle of control and myocardial infarcted mice (MI) with or without pyridostigmine (PYR) treatment. Values are presented as the mean ± SEM. Bar = 60 µm.
Figure Legend Snippet: Photomicrographs and bar graphs of the minor diameter of myocytes and collagen density from the left ventricle of control and myocardial infarcted mice (MI) with or without pyridostigmine (PYR) treatment. Values are presented as the mean ± SEM. Bar = 60 µm.

Techniques Used: Mouse Assay

5) Product Images from "Cyclodextrin has conflicting actions on autophagy flux in vivo in brains of normal and Alzheimer model mice"

Article Title: Cyclodextrin has conflicting actions on autophagy flux in vivo in brains of normal and Alzheimer model mice

Journal: Human Molecular Genetics

doi: 10.1093/hmg/ddx001

CYCLO ICV infusion increases the number of autophagosomes. TgCRND8 (CRND8) and WT mice (8∼9-mo-old) were treated (ICV infusion) with CYCLO or Saline for two weeks. ( A–D ) Brain sections were processed for EM analysis and images taken from the pyramidal cell layer of the CA1 sector are shown. Arrows = autophagosomes, defined as double-membrane-bound vacuoles with low electron density and relatively “intact” contents (e.g. recognizable organelles or membrane). Empty arrows = autolysosomes, characterized by single-limiting membrane with higher electron density and amorphous heterogeneous contents. White stars = lysosomes, defined as small round/oval vacuoles with single-limiting membrane, homogenous content and being devoid of undigested material. # signs = multi-vacuolated autophagosomes, which exhibit recognizable double-membrane in some areas (arrowheads) and consist of multiple small vacuoles. ( C2 ) An example for clusters of these multi-vacuolated autophagosomes—3 such profiles can be identified from bottom-left to top-right. Inset: immune-EM with anti-CTSD antibody showing the appearance of gold particles within the multi-vacuolated autophagosomes similar to those marked with # in (C2). ( E ) EM images (19,000X) were taken from the CA1 pyramidal cell layer. The numbers of autophagosomes in the neuronal perikarya were counted for quantitative analysis (n = 2-3 mouse brains per genotype per condition; 1-2 tissue blocks per brain; average 40 images per tissue block). Significant differences were analyzed by one way ANOVA followed by post hoc Bonferroni’s multiple comparisons test. ** P
Figure Legend Snippet: CYCLO ICV infusion increases the number of autophagosomes. TgCRND8 (CRND8) and WT mice (8∼9-mo-old) were treated (ICV infusion) with CYCLO or Saline for two weeks. ( A–D ) Brain sections were processed for EM analysis and images taken from the pyramidal cell layer of the CA1 sector are shown. Arrows = autophagosomes, defined as double-membrane-bound vacuoles with low electron density and relatively “intact” contents (e.g. recognizable organelles or membrane). Empty arrows = autolysosomes, characterized by single-limiting membrane with higher electron density and amorphous heterogeneous contents. White stars = lysosomes, defined as small round/oval vacuoles with single-limiting membrane, homogenous content and being devoid of undigested material. # signs = multi-vacuolated autophagosomes, which exhibit recognizable double-membrane in some areas (arrowheads) and consist of multiple small vacuoles. ( C2 ) An example for clusters of these multi-vacuolated autophagosomes—3 such profiles can be identified from bottom-left to top-right. Inset: immune-EM with anti-CTSD antibody showing the appearance of gold particles within the multi-vacuolated autophagosomes similar to those marked with # in (C2). ( E ) EM images (19,000X) were taken from the CA1 pyramidal cell layer. The numbers of autophagosomes in the neuronal perikarya were counted for quantitative analysis (n = 2-3 mouse brains per genotype per condition; 1-2 tissue blocks per brain; average 40 images per tissue block). Significant differences were analyzed by one way ANOVA followed by post hoc Bonferroni’s multiple comparisons test. ** P

Techniques Used: Mouse Assay, Blocking Assay

CYCLO ICV infusion induces SQSTM1 accumulation in autophagosomes. TgCRND8 (CRND8) and WT mice (8∼9-mo-old) were treated (ICV infusion) with CYCLO or Saline for two weeks. ( A1 ) Brain sections were immunostained with an anti-SQSTM1 antibody and confocal microscopy images from the hippocampal CA1 sector are shown. (A1 Insets) High magnification single optical plane images depict the detail of SQSTM1-positive clumps such as the hollow appearance (arrow). ( A2 ) SQSTM1 clumps were quantified and expressed as relative area of immunoreactivity normalized to that of WT-saline condition. Values are the mean ± SEM for each group ( n = 4 mice per treatment). Significant differences between the two treatment groups of each genotype were analyzed by two-tailed Student’s t -test. * P
Figure Legend Snippet: CYCLO ICV infusion induces SQSTM1 accumulation in autophagosomes. TgCRND8 (CRND8) and WT mice (8∼9-mo-old) were treated (ICV infusion) with CYCLO or Saline for two weeks. ( A1 ) Brain sections were immunostained with an anti-SQSTM1 antibody and confocal microscopy images from the hippocampal CA1 sector are shown. (A1 Insets) High magnification single optical plane images depict the detail of SQSTM1-positive clumps such as the hollow appearance (arrow). ( A2 ) SQSTM1 clumps were quantified and expressed as relative area of immunoreactivity normalized to that of WT-saline condition. Values are the mean ± SEM for each group ( n = 4 mice per treatment). Significant differences between the two treatment groups of each genotype were analyzed by two-tailed Student’s t -test. * P

Techniques Used: Mouse Assay, Confocal Microscopy, Two Tailed Test

CYCLO ICV infusion enhances brain protein levels and activity of cathepsins and protein levels of NPC1 and ABAC1. TgCRND8 (CRND8) and WT mice (8∼9-mo-old) were treated (ICV infusion) with CYCLO or Saline for two weeks. ( A , B ) Equal amounts of proteins from brain homogenates were subjected to SDS-PAGE and processed for WB with antibodies directed against CTSB, CTSD, NPC1 or ABCA1 and representative blots are shown ( A1 , B1, D1, E1 ). Quantification of blots is shown on the right next to the corresponding blot ( A2 , B2, D1, E1 ). ( C ) Results of enzymatic activity assays for CTSB and CTSL ( C1 ) or CTSD ( C2 ) activities in brain homogenates. ( C3 ) The CTSD activity shown in ( C2 ) was recalculated against the β-actin normalized CTSD values obtained from the immunoblots probed with anti-CTSD and anti-β-actin (B1) to yield the CTSD-specific activity for which the combined values from the three mature forms (i.e. 42-, 32- and 14-kDa) were used for the calculation. Values for WB densities or enzymatic activities are the mean ± SEM for each group ( n = 4-5 mice per genotype per treatment). Significant differences between the two treatment groups of each genotype were analyzed by two-tailed Student’s t -test. * P
Figure Legend Snippet: CYCLO ICV infusion enhances brain protein levels and activity of cathepsins and protein levels of NPC1 and ABAC1. TgCRND8 (CRND8) and WT mice (8∼9-mo-old) were treated (ICV infusion) with CYCLO or Saline for two weeks. ( A , B ) Equal amounts of proteins from brain homogenates were subjected to SDS-PAGE and processed for WB with antibodies directed against CTSB, CTSD, NPC1 or ABCA1 and representative blots are shown ( A1 , B1, D1, E1 ). Quantification of blots is shown on the right next to the corresponding blot ( A2 , B2, D1, E1 ). ( C ) Results of enzymatic activity assays for CTSB and CTSL ( C1 ) or CTSD ( C2 ) activities in brain homogenates. ( C3 ) The CTSD activity shown in ( C2 ) was recalculated against the β-actin normalized CTSD values obtained from the immunoblots probed with anti-CTSD and anti-β-actin (B1) to yield the CTSD-specific activity for which the combined values from the three mature forms (i.e. 42-, 32- and 14-kDa) were used for the calculation. Values for WB densities or enzymatic activities are the mean ± SEM for each group ( n = 4-5 mice per genotype per treatment). Significant differences between the two treatment groups of each genotype were analyzed by two-tailed Student’s t -test. * P

Techniques Used: Activity Assay, Mouse Assay, SDS Page, Western Blot, Two Tailed Test

CYCLO ICV infusion does not have effects on brain protein levels of autophagy induction markers. TgCRND8 (CRND8) and WT mice (8∼9-mo-old) were treated (ICV infusion) with CYCLO or Saline for two weeks. Equal amounts of proteins from brain homogenates were subjected to SDS-PAGE and processed for WB with antibodies directed against total MTOR, p-MTOR, total RPS6KB1, p-RPS6KB1, α-spectrin, ATG5 or BECN1, and representative blots are shown. Quantification of blots is shown below the corresponding blot(s). Values are the mean ± SEM for each group ( n = 4-5 mice per genotype per treatment). Significant differences between the two treatment groups of each genotype were analyzed by two-tailed Student’s t -test. The β-actin or GAPDH blots serve as loading controls.
Figure Legend Snippet: CYCLO ICV infusion does not have effects on brain protein levels of autophagy induction markers. TgCRND8 (CRND8) and WT mice (8∼9-mo-old) were treated (ICV infusion) with CYCLO or Saline for two weeks. Equal amounts of proteins from brain homogenates were subjected to SDS-PAGE and processed for WB with antibodies directed against total MTOR, p-MTOR, total RPS6KB1, p-RPS6KB1, α-spectrin, ATG5 or BECN1, and representative blots are shown. Quantification of blots is shown below the corresponding blot(s). Values are the mean ± SEM for each group ( n = 4-5 mice per genotype per treatment). Significant differences between the two treatment groups of each genotype were analyzed by two-tailed Student’s t -test. The β-actin or GAPDH blots serve as loading controls.

Techniques Used: Mouse Assay, SDS Page, Western Blot, Two Tailed Test

CYCLO ICV infusion elevates brain protein levels of LC3-II, SQSTM1 and ubiquitinated proteins. TgCRND8 (CRND8) and WT mice (8∼9-mo-old) were treated (ICV infusion) with CYCLO or Saline for two weeks. Equal amounts of proteins from brain homogenates were subjected to SDS-PAGE and processed for WB with antibodies directed against LC3, SQSTM1, or ubiquitin, and representative blots are shown. Quantification of blots is shown below the corresponding blot(s). Values are the mean ± SEM for each group ( n = 4-5 mice per genotype per treatment). Significant differences between the two treatment groups of each genotype were analyzed by two-tailed Student’s t -test. * P
Figure Legend Snippet: CYCLO ICV infusion elevates brain protein levels of LC3-II, SQSTM1 and ubiquitinated proteins. TgCRND8 (CRND8) and WT mice (8∼9-mo-old) were treated (ICV infusion) with CYCLO or Saline for two weeks. Equal amounts of proteins from brain homogenates were subjected to SDS-PAGE and processed for WB with antibodies directed against LC3, SQSTM1, or ubiquitin, and representative blots are shown. Quantification of blots is shown below the corresponding blot(s). Values are the mean ± SEM for each group ( n = 4-5 mice per genotype per treatment). Significant differences between the two treatment groups of each genotype were analyzed by two-tailed Student’s t -test. * P

Techniques Used: Mouse Assay, SDS Page, Western Blot, Two Tailed Test

6) Product Images from "Recruitment of the Sonic hedgehog signalling cascade in electroconvulsive seizure-mediated regulation of adult rat hippocampal neurogenesis"

Article Title: Recruitment of the Sonic hedgehog signalling cascade in electroconvulsive seizure-mediated regulation of adult rat hippocampal neurogenesis

Journal:

doi:

Cyclopamine prevents the electroconvulsive seizure-mediated increase in the proliferation of dentate granule cell progenitors. Rats received i.c.v. administration of either vehicle or cyclopamine through osmotic minipumps prior to the administration of
Figure Legend Snippet: Cyclopamine prevents the electroconvulsive seizure-mediated increase in the proliferation of dentate granule cell progenitors. Rats received i.c.v. administration of either vehicle or cyclopamine through osmotic minipumps prior to the administration of

Techniques Used:

7) Product Images from "Dopamine Promotes Motor Cortex Plasticity and Motor Skill Learning via PLC Activation"

Article Title: Dopamine Promotes Motor Cortex Plasticity and Motor Skill Learning via PLC Activation

Journal: PLoS ONE

doi: 10.1371/journal.pone.0124986

PLC inhibitor impairs motor skill acquisition and the potential for M1 synaptic plasticity. (a) Motor skill acquisition was assessed in rats that received continuous intracortical injection (grey bar) of PLC inhibitor U-73122 (blue), PKA inhibitor H-89 (green) and inactive PLC inhibitor U-73343 (black) into the M1 forelimb area via osmotic minipumps. The success rate and the latency, a measure of motivation, were impaired in the presence of PLC but not PKA inhibitor. Error bars indicate SEM. (b) Temporary application of PLC and PKA inhibitors directly to M1 on training day 2 3 (time of steepest learning) reveal the same effect as with continuous application. Arrows indicate local injection days. The inset illustrates the rate of learning from day 1–2, day 3–4, and day 4–5 indicating a lack of improvement from day 2–3. (c) Maximum synaptic strength (LTP saturation) by repeated induction of LTP (multiple arrows) in layer II/III horizontal connections in brain slices. Peak amplitudes were assessed in the M1 forelimb area in ACSF (dark blue) and in the presence of PLC inhibitor U-73122 (light blue). Each FP trace (insets) represents an average of 10 individual responses at times indicated by numbers. (d) Maximum LTP in the presence of PKA inhibitor is not significantly different from control LTP. Arrows indicate multipe LTP attempts. (e) Summary histogram of LTP. Grey: Control; green: PKA inhibition; blue: PLC inhibition.
Figure Legend Snippet: PLC inhibitor impairs motor skill acquisition and the potential for M1 synaptic plasticity. (a) Motor skill acquisition was assessed in rats that received continuous intracortical injection (grey bar) of PLC inhibitor U-73122 (blue), PKA inhibitor H-89 (green) and inactive PLC inhibitor U-73343 (black) into the M1 forelimb area via osmotic minipumps. The success rate and the latency, a measure of motivation, were impaired in the presence of PLC but not PKA inhibitor. Error bars indicate SEM. (b) Temporary application of PLC and PKA inhibitors directly to M1 on training day 2 3 (time of steepest learning) reveal the same effect as with continuous application. Arrows indicate local injection days. The inset illustrates the rate of learning from day 1–2, day 3–4, and day 4–5 indicating a lack of improvement from day 2–3. (c) Maximum synaptic strength (LTP saturation) by repeated induction of LTP (multiple arrows) in layer II/III horizontal connections in brain slices. Peak amplitudes were assessed in the M1 forelimb area in ACSF (dark blue) and in the presence of PLC inhibitor U-73122 (light blue). Each FP trace (insets) represents an average of 10 individual responses at times indicated by numbers. (d) Maximum LTP in the presence of PKA inhibitor is not significantly different from control LTP. Arrows indicate multipe LTP attempts. (e) Summary histogram of LTP. Grey: Control; green: PKA inhibition; blue: PLC inhibition.

Techniques Used: Planar Chromatography, Injection, Inhibition

8) Product Images from "Neuroinflammation and oxidative stress in rostral ventrolateral medulla contribute to neurogenic hypertension induced by systemic inflammation"

Article Title: Neuroinflammation and oxidative stress in rostral ventrolateral medulla contribute to neurogenic hypertension induced by systemic inflammation

Journal: Journal of Neuroinflammation

doi: 10.1186/1742-2094-9-212

Infusion of LPS into the peritoneal cavity elevates blood pressure and plasma level of pro-inflammatory cytokines. Time-course changes in mean SAP (MSAP) (A) , HR (B) , or plasma level of CRP (C) , TNF-α (D) , and IL-1β (E) , measured on days 7 or 14 after intraperitoneal infusion of saline or LPS (1.2 mg/kg/day) via an osmotic minipump for 14 days, alone or with additional intracisternal infusion of NS398 (1.5 nmol/μL/h). Values are mean ± SEM ( n =8 to 10 animals in each experimental group). * P
Figure Legend Snippet: Infusion of LPS into the peritoneal cavity elevates blood pressure and plasma level of pro-inflammatory cytokines. Time-course changes in mean SAP (MSAP) (A) , HR (B) , or plasma level of CRP (C) , TNF-α (D) , and IL-1β (E) , measured on days 7 or 14 after intraperitoneal infusion of saline or LPS (1.2 mg/kg/day) via an osmotic minipump for 14 days, alone or with additional intracisternal infusion of NS398 (1.5 nmol/μL/h). Values are mean ± SEM ( n =8 to 10 animals in each experimental group). * P

Techniques Used:

9) Product Images from "The 14th Ile residue is essential for Leptin function in regulating energy homeostasis in rat"

Article Title: The 14th Ile residue is essential for Leptin function in regulating energy homeostasis in rat

Journal: Scientific Reports

doi: 10.1038/srep28508

I14 in mature LEP is essential for LEP-LEPR interaction and the downstream STAT3 pathway. ( A ) Sanger-sequencing of the RT-PCR products showed that the Lep mRNA of Lep ∆ I14/ ∆ I14 rat had a deletion of 3 nucleotides ATC encoding an Ile residue. ( B ) Western blot showed that the mature LEP ∆I14 protein is stably expressed in the WAT of Lep ∆ I14/ ∆ I14 rats. Shown is one of three independent experiments. ( C ) ELISA showed that serum LEP ∆I14 in male Lep ∆ I14/ ∆ I14 rats (n = 5) is significantly increased compared to that of serum LEP WT in the male WT controls (n = 5). ( D ) Computer assimilation of LEP-LEPR interaction using available information from their human homologs: LEP (PDB number: 1AX8) and LEPR (PDB number: 3V6O). ( E ) STAT3 reporter assay. 293FT cells were treated with WT and mutant recombinant rat LEP proteins at different concentrations after transient transfection of pcDNA-Lepr, pRL-TK and pGL6-Stat3. Relative luciferase activity was determined by firefly luciferase light units normalized by that of renilla luciferase.
Figure Legend Snippet: I14 in mature LEP is essential for LEP-LEPR interaction and the downstream STAT3 pathway. ( A ) Sanger-sequencing of the RT-PCR products showed that the Lep mRNA of Lep ∆ I14/ ∆ I14 rat had a deletion of 3 nucleotides ATC encoding an Ile residue. ( B ) Western blot showed that the mature LEP ∆I14 protein is stably expressed in the WAT of Lep ∆ I14/ ∆ I14 rats. Shown is one of three independent experiments. ( C ) ELISA showed that serum LEP ∆I14 in male Lep ∆ I14/ ∆ I14 rats (n = 5) is significantly increased compared to that of serum LEP WT in the male WT controls (n = 5). ( D ) Computer assimilation of LEP-LEPR interaction using available information from their human homologs: LEP (PDB number: 1AX8) and LEPR (PDB number: 3V6O). ( E ) STAT3 reporter assay. 293FT cells were treated with WT and mutant recombinant rat LEP proteins at different concentrations after transient transfection of pcDNA-Lepr, pRL-TK and pGL6-Stat3. Relative luciferase activity was determined by firefly luciferase light units normalized by that of renilla luciferase.

Techniques Used: Sequencing, Reverse Transcription Polymerase Chain Reaction, Western Blot, Stable Transfection, Enzyme-linked Immunosorbent Assay, Reporter Assay, Mutagenesis, Recombinant, Transfection, Luciferase, Activity Assay

10) Product Images from "Differential effect of angiotensin II and blood pressure on hippocampal inflammation in mice"

Article Title: Differential effect of angiotensin II and blood pressure on hippocampal inflammation in mice

Journal: Journal of Neuroinflammation

doi: 10.1186/s12974-018-1090-z

Effect of hydralazine on hippocampal gliosis induced by Ang II. Relative fluorescence intensity units (RFU) of Iba-1 ( a ) and GFAP ( b ) in the hippocampus after 1 week systemic perfusion of Ang II 1000 ng/kg/min or 0.9% saline (CTL). Hydralazine (150 mg/L) was administered in the drinking water starting 3 days before minipump implantation. Animals in the vehicle group received regular drinking water. In each experiment, a treated-to-control ratio was calculated (* p
Figure Legend Snippet: Effect of hydralazine on hippocampal gliosis induced by Ang II. Relative fluorescence intensity units (RFU) of Iba-1 ( a ) and GFAP ( b ) in the hippocampus after 1 week systemic perfusion of Ang II 1000 ng/kg/min or 0.9% saline (CTL). Hydralazine (150 mg/L) was administered in the drinking water starting 3 days before minipump implantation. Animals in the vehicle group received regular drinking water. In each experiment, a treated-to-control ratio was calculated (* p

Techniques Used: Fluorescence, CTL Assay

11) Product Images from "Dopamine Promotes Motor Cortex Plasticity and Motor Skill Learning via PLC Activation"

Article Title: Dopamine Promotes Motor Cortex Plasticity and Motor Skill Learning via PLC Activation

Journal: PLoS ONE

doi: 10.1371/journal.pone.0124986

PLC inhibitor impairs motor skill acquisition and the potential for M1 synaptic plasticity. (a) Motor skill acquisition was assessed in rats that received continuous intracortical injection (grey bar) of PLC inhibitor U-73122 (blue), PKA inhibitor H-89 (green) and inactive PLC inhibitor U-73343 (black) into the M1 forelimb area via osmotic minipumps. The success rate and the latency, a measure of motivation, were impaired in the presence of PLC but not PKA inhibitor. Error bars indicate SEM. (b) Temporary application of PLC and PKA inhibitors directly to M1 on training day 2 3 (time of steepest learning) reveal the same effect as with continuous application. Arrows indicate local injection days. The inset illustrates the rate of learning from day 1–2, day 3–4, and day 4–5 indicating a lack of improvement from day 2–3. (c) Maximum synaptic strength (LTP saturation) by repeated induction of LTP (multiple arrows) in layer II/III horizontal connections in brain slices. Peak amplitudes were assessed in the M1 forelimb area in ACSF (dark blue) and in the presence of PLC inhibitor U-73122 (light blue). Each FP trace (insets) represents an average of 10 individual responses at times indicated by numbers. (d) Maximum LTP in the presence of PKA inhibitor is not significantly different from control LTP. Arrows indicate multipe LTP attempts. (e) Summary histogram of LTP. Grey: Control; green: PKA inhibition; blue: PLC inhibition.
Figure Legend Snippet: PLC inhibitor impairs motor skill acquisition and the potential for M1 synaptic plasticity. (a) Motor skill acquisition was assessed in rats that received continuous intracortical injection (grey bar) of PLC inhibitor U-73122 (blue), PKA inhibitor H-89 (green) and inactive PLC inhibitor U-73343 (black) into the M1 forelimb area via osmotic minipumps. The success rate and the latency, a measure of motivation, were impaired in the presence of PLC but not PKA inhibitor. Error bars indicate SEM. (b) Temporary application of PLC and PKA inhibitors directly to M1 on training day 2 3 (time of steepest learning) reveal the same effect as with continuous application. Arrows indicate local injection days. The inset illustrates the rate of learning from day 1–2, day 3–4, and day 4–5 indicating a lack of improvement from day 2–3. (c) Maximum synaptic strength (LTP saturation) by repeated induction of LTP (multiple arrows) in layer II/III horizontal connections in brain slices. Peak amplitudes were assessed in the M1 forelimb area in ACSF (dark blue) and in the presence of PLC inhibitor U-73122 (light blue). Each FP trace (insets) represents an average of 10 individual responses at times indicated by numbers. (d) Maximum LTP in the presence of PKA inhibitor is not significantly different from control LTP. Arrows indicate multipe LTP attempts. (e) Summary histogram of LTP. Grey: Control; green: PKA inhibition; blue: PLC inhibition.

Techniques Used: Planar Chromatography, Injection, Inhibition

12) Product Images from "Reactive Neurogenesis and Down-Regulation of the Potassium-Chloride Cotransporter KCC2 in the Cochlear Nuclei after Cochlear Deafferentation"

Article Title: Reactive Neurogenesis and Down-Regulation of the Potassium-Chloride Cotransporter KCC2 in the Cochlear Nuclei after Cochlear Deafferentation

Journal: Frontiers in Pharmacology

doi: 10.3389/fphar.2016.00281

Ki67 immunostaining was used to confirm BrdU cell proliferation. (A) Photomicrographs showing Ki67 immunostainings in the deafferented AVCN and PVCN of control cats and cats infused with NaCl or Muscimol immediately after UCN and at sacrifice (D3). Scale bar: 100 μm. (B) Quantitative evaluation. Histograms comparing the mean values (±SEM) of Ki67-immunopositive cells in the deafferented CN 3 days after UCN in control cats or cats submitted to NaCl or Muscimol infusion using ANOVA followed by the Scheffé test ( p
Figure Legend Snippet: Ki67 immunostaining was used to confirm BrdU cell proliferation. (A) Photomicrographs showing Ki67 immunostainings in the deafferented AVCN and PVCN of control cats and cats infused with NaCl or Muscimol immediately after UCN and at sacrifice (D3). Scale bar: 100 μm. (B) Quantitative evaluation. Histograms comparing the mean values (±SEM) of Ki67-immunopositive cells in the deafferented CN 3 days after UCN in control cats or cats submitted to NaCl or Muscimol infusion using ANOVA followed by the Scheffé test ( p

Techniques Used: Immunostaining

Newborn cells generated 3 days after UCN survived up to 1 month depending on the treatment administrated. (A) Illustrations of BrdU immunoreactivity in both the deafferented AVCN and PVCN at different time points (post-lesion D3 or D30) in UCN animals treated with NaCl-, AraC-, or Muscimol-intra-cerebroventricular infusion. Note that in AraC treated animals, no BrdU+ cells were observed at D3 (data not shown) or D30. Scale bar: 100 μm and n = 4 animals per group. (B) Histograms showing the effects of drug infusion (NaCl, AraC, or Muscimol) on the number of BrdU-immunopositive cells observed in the deafferented cochlear nuclei. Only values recorded on the lesioned side are illustrated. Different letters indicate significant differences between all other groups of animals. Analyzes were assessed by ANOVA followed by the Scheffé test for all VN and groups ( p
Figure Legend Snippet: Newborn cells generated 3 days after UCN survived up to 1 month depending on the treatment administrated. (A) Illustrations of BrdU immunoreactivity in both the deafferented AVCN and PVCN at different time points (post-lesion D3 or D30) in UCN animals treated with NaCl-, AraC-, or Muscimol-intra-cerebroventricular infusion. Note that in AraC treated animals, no BrdU+ cells were observed at D3 (data not shown) or D30. Scale bar: 100 μm and n = 4 animals per group. (B) Histograms showing the effects of drug infusion (NaCl, AraC, or Muscimol) on the number of BrdU-immunopositive cells observed in the deafferented cochlear nuclei. Only values recorded on the lesioned side are illustrated. Different letters indicate significant differences between all other groups of animals. Analyzes were assessed by ANOVA followed by the Scheffé test for all VN and groups ( p

Techniques Used: Generated

Study designs. The first protocol (#1) was elaborated using BrdU and Ki67 as cell proliferation markers to study the time-dependent effect of a UCN on reactive cell proliferation in cochlear nuclei. Protocol number 2 (#2) was designed using a continuous infusion of NaCl, AraC, or Muscimol in the fourth ventricle to examine alterations in newborn cell survival (BrdU marker), astrogenesis (GFAP marker), GABA cells (GAD67 marker), neuronal cells (NeuN marker), and microglial cells (IBA1 marker) in the cochlear nuclei. BrdU, 5-bromo-2′deoxyuridine; i.p., intraperitoneal injection; GAD67, glutamic acid decarboxylase; GFAP, glial fibrillary acidic protein; CN, cochlear nuclei; n = 4 animals per group.
Figure Legend Snippet: Study designs. The first protocol (#1) was elaborated using BrdU and Ki67 as cell proliferation markers to study the time-dependent effect of a UCN on reactive cell proliferation in cochlear nuclei. Protocol number 2 (#2) was designed using a continuous infusion of NaCl, AraC, or Muscimol in the fourth ventricle to examine alterations in newborn cell survival (BrdU marker), astrogenesis (GFAP marker), GABA cells (GAD67 marker), neuronal cells (NeuN marker), and microglial cells (IBA1 marker) in the cochlear nuclei. BrdU, 5-bromo-2′deoxyuridine; i.p., intraperitoneal injection; GAD67, glutamic acid decarboxylase; GFAP, glial fibrillary acidic protein; CN, cochlear nuclei; n = 4 animals per group.

Techniques Used: Marker, Injection

13) Product Images from "Recruitment of the Sonic hedgehog signalling cascade in electroconvulsive seizure-mediated regulation of adult rat hippocampal neurogenesis"

Article Title: Recruitment of the Sonic hedgehog signalling cascade in electroconvulsive seizure-mediated regulation of adult rat hippocampal neurogenesis

Journal:

doi:

Cyclopamine prevents the electroconvulsive seizure-mediated increase in the proliferation of dentate granule cell progenitors. Rats received i.c.v. administration of either vehicle or cyclopamine through osmotic minipumps prior to the administration of
Figure Legend Snippet: Cyclopamine prevents the electroconvulsive seizure-mediated increase in the proliferation of dentate granule cell progenitors. Rats received i.c.v. administration of either vehicle or cyclopamine through osmotic minipumps prior to the administration of

Techniques Used:

14) Product Images from "Role of type 2A phosphatase regulatory subunit B56α in regulating cardiac responses to β-adrenergic stimulation in vivo"

Article Title: Role of type 2A phosphatase regulatory subunit B56α in regulating cardiac responses to β-adrenergic stimulation in vivo

Journal: Cardiovascular Research

doi: 10.1093/cvr/cvy230

Histological, gravimetric and molecular analysis of cardiac responses to sustained β-adrenergic stimulation. ( A ) Cross-sections of the LV stained with haematoxylin and eosin to allow quantification of myocyte cross-sectional area. Representative images (magnification ×400) and quantitative data from male WT and HOM mice following subcutaneous infusion of ISO (30 mg/kg/day) or vehicle for 14 days. Scale bar: 20 μm. Lines show mean ± SE ( > 50 myocytes were measured from 5 to 8 hearts per group); * P
Figure Legend Snippet: Histological, gravimetric and molecular analysis of cardiac responses to sustained β-adrenergic stimulation. ( A ) Cross-sections of the LV stained with haematoxylin and eosin to allow quantification of myocyte cross-sectional area. Representative images (magnification ×400) and quantitative data from male WT and HOM mice following subcutaneous infusion of ISO (30 mg/kg/day) or vehicle for 14 days. Scale bar: 20 μm. Lines show mean ± SE ( > 50 myocytes were measured from 5 to 8 hearts per group); * P

Techniques Used: Staining, Mouse Assay

Echocardiographic analysis of cardiac responses to sustained β-adrenergic stimulation. Echocardiographic assessment of ( A ) LV anterior wall thickness (LVAW), ( B ) LV posterior wall thickness (LVPW), ( C ) LV internal dimension (LVID) at end-diastole (d) and end-systole (s), ( D ) LV fractional shortening (LVFS), ( E ) LV ejection fraction (LVEF), and ( F ) heart rate in male WT and HOM mice following subcutaneous infusion of ISO (30 mg/kg/day) or vehicle for 14 days. Lines show mean ± SE ( n = 6–8 per group); * P
Figure Legend Snippet: Echocardiographic analysis of cardiac responses to sustained β-adrenergic stimulation. Echocardiographic assessment of ( A ) LV anterior wall thickness (LVAW), ( B ) LV posterior wall thickness (LVPW), ( C ) LV internal dimension (LVID) at end-diastole (d) and end-systole (s), ( D ) LV fractional shortening (LVFS), ( E ) LV ejection fraction (LVEF), and ( F ) heart rate in male WT and HOM mice following subcutaneous infusion of ISO (30 mg/kg/day) or vehicle for 14 days. Lines show mean ± SE ( n = 6–8 per group); * P

Techniques Used: Mouse Assay

15) Product Images from "Inhibition of Prolyl Oligopeptidase Restores Spontaneous Motor Behavior in the α-Synuclein Virus Vector–Based Parkinson's Disease Mouse Model by Decreasing α-Synuclein Oligomeric Species in Mouse Brain"

Article Title: Inhibition of Prolyl Oligopeptidase Restores Spontaneous Motor Behavior in the α-Synuclein Virus Vector–Based Parkinson's Disease Mouse Model by Decreasing α-Synuclein Oligomeric Species in Mouse Brain

Journal: The Journal of Neuroscience

doi: 10.1523/JNEUROSCI.2309-16.2016

The effect of KYP-2047 on mouse brain PREP activity. A–C , KYP-2047 intraventricular administration significantly reduced PREP activity in mouse striatum and cortex 1 week after osmotic minipump implantation ( A , B ), and PREP inhibition was observed after 4 week intraperitoneal KYP-2047 administration in mouse cortex ( C ) compared to vehicle administration. Intraventricular VEH, n = 3; intraventricular KYP-2047, n = 5; intraperitoneal VEH, n = 23; intraperitoneal KYP-2047, n = 21). Error bars represent means ± SEM. * p
Figure Legend Snippet: The effect of KYP-2047 on mouse brain PREP activity. A–C , KYP-2047 intraventricular administration significantly reduced PREP activity in mouse striatum and cortex 1 week after osmotic minipump implantation ( A , B ), and PREP inhibition was observed after 4 week intraperitoneal KYP-2047 administration in mouse cortex ( C ) compared to vehicle administration. Intraventricular VEH, n = 3; intraventricular KYP-2047, n = 5; intraperitoneal VEH, n = 23; intraperitoneal KYP-2047, n = 21). Error bars represent means ± SEM. * p

Techniques Used: Activity Assay, Inhibition

16) Product Images from "Oxycodone, fentanyl, and morphine amplify established neuropathic pain in male rats"

Article Title: Oxycodone, fentanyl, and morphine amplify established neuropathic pain in male rats

Journal: Pain

doi: 10.1097/j.pain.0000000000001652

Exacerbation of CCI allodynia by oxycodone and fentanyl when dosing begins 10 days after injury. Chronic constriction injury was performed with one 6–0 chromic gut suture. Fentanyl (0.01 mg/kg/h), oxycodone (2 mg/kg twice per day), or equivolume saline was administered for 5 days, beginning at day 10 after surgery. (A) Von Frey testing was conducted before and after CCI surgery, and after completion of opioid administration. (B) Area-under-curve analysis of von Frey threshold of all timepoints after opioid treatment. *Oxycodone vs all saline, #fentanyl vs all saline. BL, baseline, * P
Figure Legend Snippet: Exacerbation of CCI allodynia by oxycodone and fentanyl when dosing begins 10 days after injury. Chronic constriction injury was performed with one 6–0 chromic gut suture. Fentanyl (0.01 mg/kg/h), oxycodone (2 mg/kg twice per day), or equivolume saline was administered for 5 days, beginning at day 10 after surgery. (A) Von Frey testing was conducted before and after CCI surgery, and after completion of opioid administration. (B) Area-under-curve analysis of von Frey threshold of all timepoints after opioid treatment. *Oxycodone vs all saline, #fentanyl vs all saline. BL, baseline, * P

Techniques Used:

Exacerbation of CCI allodynia by morphine, oxycodone, or fentanyl when dosing begins 1 month after injury. Chronic constriction injury was performed with one chromic gut 6–0 suture. Morphine (5 mg/kg twice per day), fentanyl (0.01 mg/kg/h), oxycodone (2 mg/kg twice per day), or equivolume saline was administered for 5 days, beginning at day 28 after surgery. (A) Von Frey testing was conducted before and after CCI surgery, and after completion of opioid administration. (B) Area-under-curve analysis of von Frey threshold of all timepoints after opioid treatment. *Oxycodone vs all saline, #fentanyl vs all saline #, $morphine vs all saline, BL: baseline, * P
Figure Legend Snippet: Exacerbation of CCI allodynia by morphine, oxycodone, or fentanyl when dosing begins 1 month after injury. Chronic constriction injury was performed with one chromic gut 6–0 suture. Morphine (5 mg/kg twice per day), fentanyl (0.01 mg/kg/h), oxycodone (2 mg/kg twice per day), or equivolume saline was administered for 5 days, beginning at day 28 after surgery. (A) Von Frey testing was conducted before and after CCI surgery, and after completion of opioid administration. (B) Area-under-curve analysis of von Frey threshold of all timepoints after opioid treatment. *Oxycodone vs all saline, #fentanyl vs all saline #, $morphine vs all saline, BL: baseline, * P

Techniques Used:

No exacerbation of CCI allodynia by morphine, oxycodone, or fentanyl when dosing begins 1 hour after injury. Chronic constriction injury was performed with one chromic gut 6–0 suture. Morphine (5 mg/kg twice per day), (fentanyl (0.01 mg/kg/h), oxycodone (2 mg/kg twice per day), or equivolume saline was administered for 5 days, beginning at one-hour after surgery. (A) Von Frey testing was conducted before and after CCI surgery, and after completion of opioid administration. (B) Area-under-curve analysis of von Frey threshold of all timepoints after opioid treatment. BL, baseline. n = 6/group. CCI, chronic constriction injury.
Figure Legend Snippet: No exacerbation of CCI allodynia by morphine, oxycodone, or fentanyl when dosing begins 1 hour after injury. Chronic constriction injury was performed with one chromic gut 6–0 suture. Morphine (5 mg/kg twice per day), (fentanyl (0.01 mg/kg/h), oxycodone (2 mg/kg twice per day), or equivolume saline was administered for 5 days, beginning at one-hour after surgery. (A) Von Frey testing was conducted before and after CCI surgery, and after completion of opioid administration. (B) Area-under-curve analysis of von Frey threshold of all timepoints after opioid treatment. BL, baseline. n = 6/group. CCI, chronic constriction injury.

Techniques Used:

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