somatostatin Search Results


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  • 86
    Millipore tyr1 somatostatin
    Tyr1 Somatostatin, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    95
    Abcam somatostatin
    A – C : Immunohistochemistry for insulin (green), glucagon, <t>somatostatin,</t> and pancreatic polypeptide (red) of normal ( A ) and diabetic ( B and C ) islets. Images were prepared from nPOD cases 6153 ( A [healthy]), 6052 ( B [T1D]), and 6064 ( C [T1D]). Scale bar: 25 μm. D – G : Quantitative analysis of the islet cell composition and HA-positive areas in human pancreas. D : Relative proportion of the classic pancreatic hormone-producing cells. Blue bars, normal tissues; red bars, diabetic tissues. Data are mean ± SD of measurements obtained from tissues of 17 healthy and 19 T1D donors. * P
    Somatostatin, supplied by Abcam, used in various techniques. Bioz Stars score: 95/100, based on 159 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Tocris somatostatin 14
    HFD results in changes in SST secretion. A. <t>Somatostatin</t> (Sst) secretion from islets isolated from control (CTL) and high-fat diet (HFD) fed mice (n = 16 replicates from 5 HFD and 5 CTL mice). t -test; ∗ P
    Somatostatin 14, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Tocris somatostatin 28
    ODT8-SST and <t>somatostatin-28</t> injected intracerebroventricularly prevent the surgery-induced delay of gastric emptying. ODT8-SST (A, 1 μg/rat in 10 μl ddH 2 O), somatostatin-28 (B, 1 μg/rat in 10 μl ddH 2 O containing 0.1% BSA)
    Somatostatin 28, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Millipore somatostatin
    G42 mice identify GABAergic non-SST INs at P9. a , Immunohistochemical labeling of GFP in the somatosensory cortex (SSC) of G42 (GAD1-eGFP) mice at P9. Coimmunolabeling of GFP in G42 mice with markers on inhibitory INs. a1–a5 , GFP (left). a1 , GABA. a2 , <t>Somatostatin.</t> a3 , PV. a4 , GAD67. a5 , Calretinin (middle), colabel (right) in layer V of the SSC. b , Table showing abundant colabeling of GFP + cells with GABA immunolabeling at P9. Sections from 4 mice were used to quantify colocalization. c , Average evoked APs from whole-cell recordings from GFP + cells in G42 mice (red), L5Ps (black), and Td-tomato + neurons in SST-Cre X Ai9 mice (blue). d , dV/dt analysis of APs shown in c . e , AP half-width. f , AP threshold. g , Afterhyperpolarization amplitude. h , Fraction of cells showing spontaneous AP firing in GFP + cells in G42 mice (red), L5P neurons (black), and Td-Tomato + neurons in SST-Cre X Ai9 mice (blue). * p
    Somatostatin, supplied by Millipore, used in various techniques. Bioz Stars score: 93/100, based on 794 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Millipore somatostatin 28
    G42 mice identify GABAergic non-SST INs at P9. a , Immunohistochemical labeling of GFP in the somatosensory cortex (SSC) of G42 (GAD1-eGFP) mice at P9. Coimmunolabeling of GFP in G42 mice with markers on inhibitory INs. a1–a5 , GFP (left). a1 , GABA. a2 , <t>Somatostatin.</t> a3 , PV. a4 , GAD67. a5 , Calretinin (middle), colabel (right) in layer V of the SSC. b , Table showing abundant colabeling of GFP + cells with GABA immunolabeling at P9. Sections from 4 mice were used to quantify colocalization. c , Average evoked APs from whole-cell recordings from GFP + cells in G42 mice (red), L5Ps (black), and Td-tomato + neurons in SST-Cre X Ai9 mice (blue). d , dV/dt analysis of APs shown in c . e , AP half-width. f , AP threshold. g , Afterhyperpolarization amplitude. h , Fraction of cells showing spontaneous AP firing in GFP + cells in G42 mice (red), L5P neurons (black), and Td-Tomato + neurons in SST-Cre X Ai9 mice (blue). * p
    Somatostatin 28, supplied by Millipore, used in various techniques. Bioz Stars score: 92/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Abcam anti somatostatin
    Immunohistochemistry of canine pancreas by region. Tissue sections of the three major regions of the pancreas were stained with antibodies for insulin (top row), <t>somatostatin</t> (center row), and glucagon (bottom row) to identify the three major islet cell types (beta, delta, and alpha cells, respectively). Insulin positive cells were primarily located in the body (center column) and tail (right column), with the highest concentration and largest sized clusters in the tail. Insulin positive cells in the head of the pancreas (left column) were far less prevalent and occurred primarily in very small clusters or single cells. Similar patterns were observed for somatostatin, while glucagon positive cells were present in extremely low numbers in the head and body and often appeared as isolated single cells. Glucagon images are displayed at higher magnification to better illustrate single cells. Scale bars = 200 μm
    Anti Somatostatin, supplied by Abcam, used in various techniques. Bioz Stars score: 94/100, based on 45 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    A – C : Immunohistochemistry for insulin (green), glucagon, somatostatin, and pancreatic polypeptide (red) of normal ( A ) and diabetic ( B and C ) islets. Images were prepared from nPOD cases 6153 ( A [healthy]), 6052 ( B [T1D]), and 6064 ( C [T1D]). Scale bar: 25 μm. D – G : Quantitative analysis of the islet cell composition and HA-positive areas in human pancreas. D : Relative proportion of the classic pancreatic hormone-producing cells. Blue bars, normal tissues; red bars, diabetic tissues. Data are mean ± SD of measurements obtained from tissues of 17 healthy and 19 T1D donors. * P

    Journal: Diabetes

    Article Title: Hyaluronan and Hyaluronan-Binding Proteins Accumulate in Both Human Type 1 Diabetic Islets and Lymphoid Tissues and Associate With Inflammatory Cells in Insulitis

    doi: 10.2337/db13-1658

    Figure Lengend Snippet: A – C : Immunohistochemistry for insulin (green), glucagon, somatostatin, and pancreatic polypeptide (red) of normal ( A ) and diabetic ( B and C ) islets. Images were prepared from nPOD cases 6153 ( A [healthy]), 6052 ( B [T1D]), and 6064 ( C [T1D]). Scale bar: 25 μm. D – G : Quantitative analysis of the islet cell composition and HA-positive areas in human pancreas. D : Relative proportion of the classic pancreatic hormone-producing cells. Blue bars, normal tissues; red bars, diabetic tissues. Data are mean ± SD of measurements obtained from tissues of 17 healthy and 19 T1D donors. * P

    Article Snippet: Antibodies to glucagon, somatostatin, pancreatic polypeptide (Abcam), TSG-6, and IαI ( , ) were used at a dilution of 1:1,000.

    Techniques: Immunohistochemistry

    Expression of C3 and C5 complement proteins by mouse and human pancreas. A – D Co-localisation of C3 ( A , B ) and C5 ( C , D ) complement proteins (green) with the islet hormones insulin ( a – c ), glucagon ( d – f ) and somatostatin ( g – i ) (red) in mouse ( A , C ) and human ( B , D ) islets. Nuclei have been counterstained with DAPI (blue). C3 and C5 were also expressed by exocrine cells in both mouse and human pancreas. E , G C3 co-localises in mouse and human islets with insulin, glucagon and somatostatin, indicating expression of C3 in β-, α- and δ-cells. F , H C5 co-localises in mouse and human islets primarily with insulin, indicating predominant expression of C5 in β-cells

    Journal: Cellular and Molecular Life Sciences

    Article Title: C3aR and C5aR1 act as key regulators of human and mouse β-cell function

    doi: 10.1007/s00018-017-2655-1

    Figure Lengend Snippet: Expression of C3 and C5 complement proteins by mouse and human pancreas. A – D Co-localisation of C3 ( A , B ) and C5 ( C , D ) complement proteins (green) with the islet hormones insulin ( a – c ), glucagon ( d – f ) and somatostatin ( g – i ) (red) in mouse ( A , C ) and human ( B , D ) islets. Nuclei have been counterstained with DAPI (blue). C3 and C5 were also expressed by exocrine cells in both mouse and human pancreas. E , G C3 co-localises in mouse and human islets with insulin, glucagon and somatostatin, indicating expression of C3 in β-, α- and δ-cells. F , H C5 co-localises in mouse and human islets primarily with insulin, indicating predominant expression of C5 in β-cells

    Article Snippet: The glucagon antibody was from Sigma-Aldrich (Dorset, UK), insulin antibody from DAKO UK Ltd. (Ely, UK) and somatostatin antibody from Abcam plc (Cambridge, UK).

    Techniques: Expressing

    The regulation of TPM on gastrointestinal hormones which were interrupted by atropine-treatment in rats. The serum levels of gastrointestinal hormones, which including gastrin (GAS) (A), motilin (MTL) (B), somatostatin (SS) (C) and p substance (PS) (D), were measured in control (Ctrl), atropine-treated (Atropine) and TPM-pretreated/atropine-treated (TPM + atropine) rats via ELISA method. Data are shown as mean ± SD (n = 8). *: P

    Journal: International Journal of Clinical and Experimental Medicine

    Article Title: The protective effects of total phenols in magnolia officinalix rehd. et wils on gastrointestinal tract dysmotility is mainly based on its influence on interstitial cells of cajal

    doi:

    Figure Lengend Snippet: The regulation of TPM on gastrointestinal hormones which were interrupted by atropine-treatment in rats. The serum levels of gastrointestinal hormones, which including gastrin (GAS) (A), motilin (MTL) (B), somatostatin (SS) (C) and p substance (PS) (D), were measured in control (Ctrl), atropine-treated (Atropine) and TPM-pretreated/atropine-treated (TPM + atropine) rats via ELISA method. Data are shown as mean ± SD (n = 8). *: P

    Article Snippet: Gastrin (GAS), motilin (MTL), somatostatin (SS) and p substance (PS) levels in serum were measured by using enzyme-linked immunosorbent assay (ELISA) kits (Abcam, USA).

    Techniques: Enzyme-linked Immunosorbent Assay

    The co-localization of ErbB4 with GABAergic cells (GABA, GAD67, Parvalbumin (PV) and Somatostatin (SOM)) at 28 days. The representative images in the sham group are listed in the left four columns (A,C,E,G) and the images in the 2VO group are listed in the right (B,D,F,H) . Horizontal bar = 50 μm. Note that ErbB4 is expressed in GABA, GAD67 and PV-positive cells, but not in SOM-positive cells.

    Journal: Frontiers in Aging Neuroscience

    Article Title: The Expression of Hippocampal NRG1/ErbB4 Correlates With Neuronal Apoptosis, but Not With Glial Activation During Chronic Cerebral Hypoperfusion

    doi: 10.3389/fnagi.2018.00149

    Figure Lengend Snippet: The co-localization of ErbB4 with GABAergic cells (GABA, GAD67, Parvalbumin (PV) and Somatostatin (SOM)) at 28 days. The representative images in the sham group are listed in the left four columns (A,C,E,G) and the images in the 2VO group are listed in the right (B,D,F,H) . Horizontal bar = 50 μm. Note that ErbB4 is expressed in GABA, GAD67 and PV-positive cells, but not in SOM-positive cells.

    Article Snippet: The sections were incubated overnight with rabbit-anti ErbB4 (1:100, Santa Cruz Biotechnology, Santa Cruz, CA, USA) or mouse anti-ErbB4 (1:50, Abcam, CA, USA), and mouse antibodies of neuronal nuclei (NeuN; 1:200), GFAP (1:200), GABA (1:50), GAD67 (1:100), PV(1:50), Somatostatin (SOM) (1:50; Abcam, CA, USA), or rabbit anti-Iba1 (1:100, Abcam, CA, USA), and then detected with secondary antibodies (goat anti-rabbit Alexa Fluor 488-conjugated and goat anti-mouse Alexa Fluor 594-conjugated) (Invitrogen, Carlsbad, CA, USA) (room temperature for 3 h followed by 0.0001% DAPI (Beyotime, China) staining) to see the distribution and location of ErbB4 receptors.

    Techniques:

    Immunohistochemical staining of neuronostatin and somatostatin in different tissues. A , pancreas; B , stomach; C , small intestine. Tissues were obtained from adult male mice and fixed before staining with neuronostatin or somatostatin antibodies. Panels

    Journal:

    Article Title: Neuronostatin Encoded by the Somatostatin Gene Regulates Neuronal, Cardiovascular, and Metabolic Functions *Neuronostatin Encoded by the Somatostatin Gene Regulates Neuronal, Cardiovascular, and Metabolic Functions * S⃞

    doi: 10.1074/jbc.M804784200

    Figure Lengend Snippet: Immunohistochemical staining of neuronostatin and somatostatin in different tissues. A , pancreas; B , stomach; C , small intestine. Tissues were obtained from adult male mice and fixed before staining with neuronostatin or somatostatin antibodies. Panels

    Article Snippet: After soaking in xylene and series of ethanol concentrations, sections were treated with 0.01 m sodium citrate at 95 °C for 15 min followed by 0.1% trypsin at 37 °C for 15 min before immunostaining using affinity-purified, rabbit polyclonal antibodies against rat neuronostatin-13 (1: 200, Phoenix Pharmaceutical Inc.), human somatostatin (1: 500 dilution, Abcam, Cambridge, MA) or preimmune IgG.

    Techniques: Immunohistochemistry, Staining, Mouse Assay

    Changes in islet morphology and β-cell proliferation in the offspring. A : representative immunofluorescent images of islets from male offspring at different ages coimmunostained for insulin (red), glucagon (blue), and somatostatin (green). Top

    Journal: American Journal of Physiology - Endocrinology and Metabolism

    Article Title: Maternal insulin resistance and transient hyperglycemia impact the metabolic and endocrine phenotypes of offspring

    doi: 10.1152/ajpendo.00210.2014

    Figure Lengend Snippet: Changes in islet morphology and β-cell proliferation in the offspring. A : representative immunofluorescent images of islets from male offspring at different ages coimmunostained for insulin (red), glucagon (blue), and somatostatin (green). Top

    Article Snippet: The sections were washed, blocked with 5% donkey serum for 1 h, and incubated overnight at 4°C with the primary antibodies guinea pig anti-insulin (1:200; Abcam), mouse anti-glucagon (1:50; Sigma-Aldrich), rabbit anti-somatostatin (1:50; Abcam), or mouse anti-Ki-67 (1:50; BD Bioscience).

    Techniques:

    Changes in the number of islet clusters and α-cell area in the offspring. A : representative immunofluorescent images of newly formed islets from 10-day-old male offspring coimmunostained for insulin (Ins; red), glucagon (Glu; blue), and somatostatin

    Journal: American Journal of Physiology - Endocrinology and Metabolism

    Article Title: Maternal insulin resistance and transient hyperglycemia impact the metabolic and endocrine phenotypes of offspring

    doi: 10.1152/ajpendo.00210.2014

    Figure Lengend Snippet: Changes in the number of islet clusters and α-cell area in the offspring. A : representative immunofluorescent images of newly formed islets from 10-day-old male offspring coimmunostained for insulin (Ins; red), glucagon (Glu; blue), and somatostatin

    Article Snippet: The sections were washed, blocked with 5% donkey serum for 1 h, and incubated overnight at 4°C with the primary antibodies guinea pig anti-insulin (1:200; Abcam), mouse anti-glucagon (1:50; Sigma-Aldrich), rabbit anti-somatostatin (1:50; Abcam), or mouse anti-Ki-67 (1:50; BD Bioscience).

    Techniques:

    The expression pattern of eIF5A Hyp in T2D and control pancreatic tissue. In controls (matched for age, gender and BMI) and T2D pancreas, we evaluated the co-expression of eIF5A Hyp with all islet hormones and found no overlap with insulin (A,B), glucagon (C,D), ghrelin (E,F) or somatostatin (G,H).

    Journal: PLoS ONE

    Article Title: Hypusinated eIF5A is expressed in the pancreas and spleen of individuals with type 1 and type 2 diabetes

    doi: 10.1371/journal.pone.0230627

    Figure Lengend Snippet: The expression pattern of eIF5A Hyp in T2D and control pancreatic tissue. In controls (matched for age, gender and BMI) and T2D pancreas, we evaluated the co-expression of eIF5A Hyp with all islet hormones and found no overlap with insulin (A,B), glucagon (C,D), ghrelin (E,F) or somatostatin (G,H).

    Article Snippet: Primary antibodies used included guinea pig anti-insulin (DAKO; 1:500), mouse anti-glucagon (Abcam; 1:500), rat anti-somatostatin (abcam; 1:200), goat anti-pancreatic polypeptide (abcam; 1:200), goat anti-ghrelin (Santa Cruz; 1:500), mouse anti-Pax5 (DAKO; 1:200), mouse anti-CD8 (Thermo Fisher; 1:500), mouse anti-CD4 (Leica; 1:500), rabbit anti-eIF5AHyp ([ , ]; 1:1000).

    Techniques: Expressing

    HFD results in changes in SST secretion. A. Somatostatin (Sst) secretion from islets isolated from control (CTL) and high-fat diet (HFD) fed mice (n = 16 replicates from 5 HFD and 5 CTL mice). t -test; ∗ P

    Journal: Molecular Metabolism

    Article Title: Reduced somatostatin signalling leads to hypersecretion of glucagon in mice fed a high-fat diet

    doi: 10.1016/j.molmet.2020.101021

    Figure Lengend Snippet: HFD results in changes in SST secretion. A. Somatostatin (Sst) secretion from islets isolated from control (CTL) and high-fat diet (HFD) fed mice (n = 16 replicates from 5 HFD and 5 CTL mice). t -test; ∗ P

    Article Snippet: The pancreas was perfused with KRB containing varying concentrations of glucose and somatostatin-14 (Tocris, Cat. No 1157) as indicated in the figures, at a speed of 1.34 μL/min/mg pancreas weight using an Ismatec REGLO Digital MS2/12 peristaltic pump.

    Techniques: Isolation, Mouse Assay

    ODT8-SST and somatostatin-28 injected intracerebroventricularly prevent the surgery-induced delay of gastric emptying. ODT8-SST (A, 1 μg/rat in 10 μl ddH 2 O), somatostatin-28 (B, 1 μg/rat in 10 μl ddH 2 O containing 0.1% BSA)

    Journal: Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society

    Article Title: Central administration of pansomatostatin agonist ODT8-SST prevents abdominal surgery-induced inhibition of circulating ghrelin, food intake and gastric emptying in rats

    doi: 10.1111/j.1365-2982.2011.01721.x

    Figure Lengend Snippet: ODT8-SST and somatostatin-28 injected intracerebroventricularly prevent the surgery-induced delay of gastric emptying. ODT8-SST (A, 1 μg/rat in 10 μl ddH 2 O), somatostatin-28 (B, 1 μg/rat in 10 μl ddH 2 O containing 0.1% BSA)

    Article Snippet: ODT8-SST (des-AA1,2,4,5,12,13 -(DTrp8 )-SRIF, MW 1078.5, compound #1 in ), the sst1 agonist, S-406-062 (des-AA1,4–6,10,12,13 -[DTyr2 ,D-Agl(NMe,2naphtoyl)8 ,IAmp9 ]-SRIF-Thr-NH2 , MW 1238.5, compound #25 in ), sst2 agonist, S-346-011 (des-AA1,4–6,11–13 -[DPhe2 ,Aph7 (Cbm),DTrp8 ]-Cbm-SRIF-Thr-NH2 , MW 1132.5, compound #2 in ), sst4 agonist, S-315-297 (des-AA1,2,4,5,12,13 -[Aph7 ]-Cbm-SRIF, MW 1137.4, compound #15 in ) and somatostatin-28 (MW 3148.6) were synthesized by the solid phase approach and purity was characterized by high pressure liquid chromatography, capillary zone electrophoresis and mass spectrometry as we have previously described., – The sst5 agonist, BIM-23052 (D-Phe-Phe-Phe-D-Trp-Lys-Thr-Phe-Thr-NH2 , MW 1122.3) was obtained from Tocris bioscience (Ellisville, MO).

    Techniques: Injection

    Permeabilizing potency of neuropeptides against E.coli ML-35p, determined by β-galactosidase assay with ONPG as its substrate. Bacteria at 10 6 CFU/ml were incubated at 37°C for 90 min in the presence of the indicated micromolar concentrations of neuropeptides: neuropeptide Y (NPY), fragment of neuropeptide Y (NPYf = NPY 18–36 ), calcitonin gene related peptide (CGRP), substance P (SP), and somatostatin (SOM). In negative controls, bacteria incubated in neuropeptide-free NAPB containing 1/100 of TSB showed no net hydrolysis of ONPG. Polymyxin B (PMB) at 1 μg/ml was included as a positive control. The representative curves of at least three independent experiments are presented.

    Journal: BMC Immunology

    Article Title: Innate immune properties of selected human neuropeptides against Moraxella catarrhalis and nontypeable Haemophilus influenzae

    doi: 10.1186/1471-2172-13-24

    Figure Lengend Snippet: Permeabilizing potency of neuropeptides against E.coli ML-35p, determined by β-galactosidase assay with ONPG as its substrate. Bacteria at 10 6 CFU/ml were incubated at 37°C for 90 min in the presence of the indicated micromolar concentrations of neuropeptides: neuropeptide Y (NPY), fragment of neuropeptide Y (NPYf = NPY 18–36 ), calcitonin gene related peptide (CGRP), substance P (SP), and somatostatin (SOM). In negative controls, bacteria incubated in neuropeptide-free NAPB containing 1/100 of TSB showed no net hydrolysis of ONPG. Polymyxin B (PMB) at 1 μg/ml was included as a positive control. The representative curves of at least three independent experiments are presented.

    Article Snippet: Neuropeptides, reagents, and media Calcitonin gene related peptide (α-CGRP), neuropeptide Y (NPY), substance P (SP), and somatostatin (SOM) were purchased from TOCRIS bioscences (Ellisville, MO, USA), NPY amino acid fragment NPY18-36 (NPYf) was bought from Sigma Chemicals (St Louis, MO, USA).

    Techniques: Incubation, Positive Control

    Grpr-Cre neurons expressing GCaMP6 are activated by somatostatin through disinhibition. Example traces from representative samples are shown. ( a ) Grpr-Cre neurons expressing GCaMP6 in an intact spinal cord. Numbers 1 and 2 indicate two neurons showing somatostatin-induced activity. ( b ) Fluorescence change traces from the intact spinal cord neurons indicated in a . ( c ) Proportion of Grpr-Cre neurons in the non-spontaneously active population expressing GCaMP6 in intact spinal cord that showed somatostatin-induced activity. ( d ) 300 µM coronal slice with Grpr-Cre neurons expressing GCaMP6. Numbers 1–4 indicate four different neurons showing somatostatin-induced activity. ( e ) Fluorescence change traces from the neurons indicated by 1–4 in ( d–f ) Proportion of Grpr-Cre neurons in the non-spontaneously active population expressing GCaMP6 in coronal slices that showed somatostatin-induced activity. ( g ) Mean values for fluorescence change ( ΔF/F %) in GCaMP6 intensity for the intact cord and coronal slices, imaged at control conditions and when somatostatin was bath applied. Scale bar corresponds to 40 µm. The data is presented as mean ± standard error.

    Journal: Scientific Reports

    Article Title: Spinal gastrin releasing peptide receptor expressing interneurons are controlled by local phasic and tonic inhibition

    doi: 10.1038/s41598-019-52642-3

    Figure Lengend Snippet: Grpr-Cre neurons expressing GCaMP6 are activated by somatostatin through disinhibition. Example traces from representative samples are shown. ( a ) Grpr-Cre neurons expressing GCaMP6 in an intact spinal cord. Numbers 1 and 2 indicate two neurons showing somatostatin-induced activity. ( b ) Fluorescence change traces from the intact spinal cord neurons indicated in a . ( c ) Proportion of Grpr-Cre neurons in the non-spontaneously active population expressing GCaMP6 in intact spinal cord that showed somatostatin-induced activity. ( d ) 300 µM coronal slice with Grpr-Cre neurons expressing GCaMP6. Numbers 1–4 indicate four different neurons showing somatostatin-induced activity. ( e ) Fluorescence change traces from the neurons indicated by 1–4 in ( d–f ) Proportion of Grpr-Cre neurons in the non-spontaneously active population expressing GCaMP6 in coronal slices that showed somatostatin-induced activity. ( g ) Mean values for fluorescence change ( ΔF/F %) in GCaMP6 intensity for the intact cord and coronal slices, imaged at control conditions and when somatostatin was bath applied. Scale bar corresponds to 40 µm. The data is presented as mean ± standard error.

    Article Snippet: Spontaneous calcium imaging activities from superficial dorsal horn Grpr-Cre AAV9-CAG-DIO-GCaMP6-infected neurons, and from superficial Grpr-Cre AAV9-CAG-DIO-GCaMP6-infected neurons in the presence of bath applied somatostatin (1 µM, Tocris), were recorded through a blue LED excitation light and signals were acquired in a frame rate of 2 Hz.

    Techniques: Expressing, Activity Assay, Fluorescence

    Expression of Somatostatin and its receptors in HT29 and SW480 colon cancer cell lines and patient matched normal and tumor tissue samples. a Cells were grown to 70–80% confluency, RNA was isolated and RT-PCR was performed. The HT29 cells express SST, SSTR1, SSTR2, and SSTR4. The SW480 cells express faint SSTR1, SSTR2, SSTR3, and SSTR4. This analysis was repeated three times and the gel images are representative of one data set for each cell line. b RT-PCR was performed to look at mRNA levels of SST and SSTR1-5 in these 5 patient samples. In all the normal samples, SST and SSTR1 were expressed. However, in the matching tumor samples, SST expression was gone and SSTR1 was present in 4 out of 5samples. N1 and T1 = matched normal and tumor tissue of patient #1. c Sorted ALDH+ and ALDH- cells from SW480 and HT29 cell lines were analyzed for mRNA expression of somatostatin and its receptors. RT-PCR analysis was performed on ALDH- and ALDH+ cells. These results indicate that the ALDH+ cells do not co-express somatostatin or its receptors in either cell line

    Journal: BMC Cancer

    Article Title: Somatostatin signaling via SSTR1 contributes to the quiescence of colon cancer stem cells

    doi: 10.1186/s12885-016-2969-7

    Figure Lengend Snippet: Expression of Somatostatin and its receptors in HT29 and SW480 colon cancer cell lines and patient matched normal and tumor tissue samples. a Cells were grown to 70–80% confluency, RNA was isolated and RT-PCR was performed. The HT29 cells express SST, SSTR1, SSTR2, and SSTR4. The SW480 cells express faint SSTR1, SSTR2, SSTR3, and SSTR4. This analysis was repeated three times and the gel images are representative of one data set for each cell line. b RT-PCR was performed to look at mRNA levels of SST and SSTR1-5 in these 5 patient samples. In all the normal samples, SST and SSTR1 were expressed. However, in the matching tumor samples, SST expression was gone and SSTR1 was present in 4 out of 5samples. N1 and T1 = matched normal and tumor tissue of patient #1. c Sorted ALDH+ and ALDH- cells from SW480 and HT29 cell lines were analyzed for mRNA expression of somatostatin and its receptors. RT-PCR analysis was performed on ALDH- and ALDH+ cells. These results indicate that the ALDH+ cells do not co-express somatostatin or its receptors in either cell line

    Article Snippet: Somatostatin treatment HT29 and SW480 cells were treated with somatostatin (500nM) (Tocris).

    Techniques: Expressing, Isolation, Reverse Transcription Polymerase Chain Reaction

    Somatostatin treatment on HT29 and SW480 cells does not change the ALDH+ population size or self-renewal abilities but inhibition of somatostatin decreases the ALDH+ population size. HT29 and SW480 cells were serum starved and then treated with 500 nM somatostatin or cyclosomatostatin for 48 h. Cells were trypsinized and analyzed for changes in ALDH positive cells, cell numbers, and cell viability. Somatostatin treatment did not significantly change the percentage of ALDH positive cells in either cell line for the number of ALDH positive cells ( a ), cell number ( b ), or cell viability ( c ), as compared to the control untreated cells. Cyclosomatostatin decreased the percentage of ALDH positive cells in both cells lines and only the cell number in HT29 cells, as compared to the controls. Data points represent the mean average values of treated cells over the controls ( N = 3) * p ≤ 0.05. HT29 and SW480 cells were plated in ultra low attachment 6-well plates for colonosphere assay comparing untreated cells to somatostatin and cyclosomatostatin treatments, After 10 days, the number of spheres per well were counted and average numbers per well were calculated. Data points represent the mean average values of treated cells over the controls ( d ). SST = Somatostatin and CycloSST = Cyclosomatostatin

    Journal: BMC Cancer

    Article Title: Somatostatin signaling via SSTR1 contributes to the quiescence of colon cancer stem cells

    doi: 10.1186/s12885-016-2969-7

    Figure Lengend Snippet: Somatostatin treatment on HT29 and SW480 cells does not change the ALDH+ population size or self-renewal abilities but inhibition of somatostatin decreases the ALDH+ population size. HT29 and SW480 cells were serum starved and then treated with 500 nM somatostatin or cyclosomatostatin for 48 h. Cells were trypsinized and analyzed for changes in ALDH positive cells, cell numbers, and cell viability. Somatostatin treatment did not significantly change the percentage of ALDH positive cells in either cell line for the number of ALDH positive cells ( a ), cell number ( b ), or cell viability ( c ), as compared to the control untreated cells. Cyclosomatostatin decreased the percentage of ALDH positive cells in both cells lines and only the cell number in HT29 cells, as compared to the controls. Data points represent the mean average values of treated cells over the controls ( N = 3) * p ≤ 0.05. HT29 and SW480 cells were plated in ultra low attachment 6-well plates for colonosphere assay comparing untreated cells to somatostatin and cyclosomatostatin treatments, After 10 days, the number of spheres per well were counted and average numbers per well were calculated. Data points represent the mean average values of treated cells over the controls ( d ). SST = Somatostatin and CycloSST = Cyclosomatostatin

    Article Snippet: Somatostatin treatment HT29 and SW480 cells were treated with somatostatin (500nM) (Tocris).

    Techniques: Inhibition

    SSTR1 cell signaling limits sphere formation and cell proliferation of ALDH positive cells. ALDH positive cells were cultured in low attachment dishes for colonosphere assay under various conditions with or without exogenous SST for HT29 ( a and c ) and SW480 ( b and d ) cells. These experiments were all done in duplicate, * p ≤ 0.05. SST = Somatostatin and CycloSST = Cyclosomatostatin

    Journal: BMC Cancer

    Article Title: Somatostatin signaling via SSTR1 contributes to the quiescence of colon cancer stem cells

    doi: 10.1186/s12885-016-2969-7

    Figure Lengend Snippet: SSTR1 cell signaling limits sphere formation and cell proliferation of ALDH positive cells. ALDH positive cells were cultured in low attachment dishes for colonosphere assay under various conditions with or without exogenous SST for HT29 ( a and c ) and SW480 ( b and d ) cells. These experiments were all done in duplicate, * p ≤ 0.05. SST = Somatostatin and CycloSST = Cyclosomatostatin

    Article Snippet: Somatostatin treatment HT29 and SW480 cells were treated with somatostatin (500nM) (Tocris).

    Techniques: Cell Culture

    G42 mice identify GABAergic non-SST INs at P9. a , Immunohistochemical labeling of GFP in the somatosensory cortex (SSC) of G42 (GAD1-eGFP) mice at P9. Coimmunolabeling of GFP in G42 mice with markers on inhibitory INs. a1–a5 , GFP (left). a1 , GABA. a2 , Somatostatin. a3 , PV. a4 , GAD67. a5 , Calretinin (middle), colabel (right) in layer V of the SSC. b , Table showing abundant colabeling of GFP + cells with GABA immunolabeling at P9. Sections from 4 mice were used to quantify colocalization. c , Average evoked APs from whole-cell recordings from GFP + cells in G42 mice (red), L5Ps (black), and Td-tomato + neurons in SST-Cre X Ai9 mice (blue). d , dV/dt analysis of APs shown in c . e , AP half-width. f , AP threshold. g , Afterhyperpolarization amplitude. h , Fraction of cells showing spontaneous AP firing in GFP + cells in G42 mice (red), L5P neurons (black), and Td-Tomato + neurons in SST-Cre X Ai9 mice (blue). * p

    Journal: The Journal of Neuroscience

    Article Title: Tonic Activation of GluN2C/GluN2D-Containing NMDA Receptors by Ambient Glutamate Facilitates Cortical Interneuron Maturation

    doi: 10.1523/JNEUROSCI.1392-18.2019

    Figure Lengend Snippet: G42 mice identify GABAergic non-SST INs at P9. a , Immunohistochemical labeling of GFP in the somatosensory cortex (SSC) of G42 (GAD1-eGFP) mice at P9. Coimmunolabeling of GFP in G42 mice with markers on inhibitory INs. a1–a5 , GFP (left). a1 , GABA. a2 , Somatostatin. a3 , PV. a4 , GAD67. a5 , Calretinin (middle), colabel (right) in layer V of the SSC. b , Table showing abundant colabeling of GFP + cells with GABA immunolabeling at P9. Sections from 4 mice were used to quantify colocalization. c , Average evoked APs from whole-cell recordings from GFP + cells in G42 mice (red), L5Ps (black), and Td-tomato + neurons in SST-Cre X Ai9 mice (blue). d , dV/dt analysis of APs shown in c . e , AP half-width. f , AP threshold. g , Afterhyperpolarization amplitude. h , Fraction of cells showing spontaneous AP firing in GFP + cells in G42 mice (red), L5P neurons (black), and Td-Tomato + neurons in SST-Cre X Ai9 mice (blue). * p

    Article Snippet: The 40 μm brain slices were stained, as described above, with primary antibodies against GFP (1:1000, chicken, Abcam) and one of the following markers: GABA (1:5000, rabbit, Sigma-Aldrich), parvalbumin (PV, 1:2000, mouse, Swant), glutamate decarboxylase 67 (GAD67, 1:10,000, mouse, Millipore), somatostatin (SST, 1:100, rat, Millipore), and calretinin (CalR, 1:5000, mouse, Swant).

    Techniques: Mouse Assay, Immunohistochemistry, Labeling, Immunolabeling

    β-cells escaping Mnx1 deletion in Mnx1 Δbeta repopulate the islets. (A,B) Lineage-tracing analysis using the ROSA26R EYFP reporter shows that the majority of Mnx1 Δbeta β-cells at 2 months of age are escaper β-cells, as they are EYFP − compared with RIP2-Cre;ROSA26R EYFP . (C,D) Immunolabeling with Mnx1, insulin and somatostatin show that the majority of the Mnx1 Δbeta insulin + β-cells are devoid of Mnx1 at P5. (E,F) Most of the Mnx1 Δbeta insulin + β-cells are Mnx1 + . (G-N) The escaper β-cells in Mnx1 Δbeta islets are Glut2 + (G,H), Pdx1 + (I,J), Nkx6.1 + (K,L) and MafA + (M,N). (O,P) Intraperitoneal glucose tolerance tests indicate that Mnx1 Δbeta mice are glucose intolerant at 4 months (O), but glucose clearance improved by 6 months of age (P). Scale bars: 50 µm. Data are shown as mean±s.e.m. * P

    Journal: Development (Cambridge, England)

    Article Title: Inactivating the permanent neonatal diabetes gene Mnx1 switches insulin-producing β-cells to a δ-like fate and reveals a facultative proliferative capacity in aged β-cells

    doi: 10.1242/dev.126011

    Figure Lengend Snippet: β-cells escaping Mnx1 deletion in Mnx1 Δbeta repopulate the islets. (A,B) Lineage-tracing analysis using the ROSA26R EYFP reporter shows that the majority of Mnx1 Δbeta β-cells at 2 months of age are escaper β-cells, as they are EYFP − compared with RIP2-Cre;ROSA26R EYFP . (C,D) Immunolabeling with Mnx1, insulin and somatostatin show that the majority of the Mnx1 Δbeta insulin + β-cells are devoid of Mnx1 at P5. (E,F) Most of the Mnx1 Δbeta insulin + β-cells are Mnx1 + . (G-N) The escaper β-cells in Mnx1 Δbeta islets are Glut2 + (G,H), Pdx1 + (I,J), Nkx6.1 + (K,L) and MafA + (M,N). (O,P) Intraperitoneal glucose tolerance tests indicate that Mnx1 Δbeta mice are glucose intolerant at 4 months (O), but glucose clearance improved by 6 months of age (P). Scale bars: 50 µm. Data are shown as mean±s.e.m. * P

    Article Snippet: Insulin and somatostatin concentration in the culture medium, and insulin and somatostatin content in islet extracts, were determined by radioimmunoassay (insulin, RI-13K, Millipore; somatostatin, RK-060-14, Phoenix Pharmaceuticals).

    Techniques: Immunolabeling, Mouse Assay

    Dramatic increase in δ-cell numbers and significant decrease in β-cell numbers in Mnx1 Δendo . (A) Schematic of conditional Mnx1 deletion in endocrine progenitors with Ngn3- Cre. (B) Random blood-glucose measurement showed that Mnx1 Δendo mutant pups were hyperglycemic at P2 ( n =10). (C,D) Immunolabeling with insulin, glucagon and somatostatin showed a dramatic increase in δ-cell number, concomitant with a decrease β-cell number at P2. (E) Significant decrease in β:δ cell ratio in Mnx1 Δendo mutants at P2 ( n =4). (F,G) Quantification of endocrine cell types fraction (F) and area (G) at E18.5, indicating significant increase in δ-cells at the expense of β-cells in Mnx1 Δendo pancreas ( n =4). Scale bars: 50 µm. Data shown as mean±s.e.m. * P

    Journal: Development (Cambridge, England)

    Article Title: Inactivating the permanent neonatal diabetes gene Mnx1 switches insulin-producing β-cells to a δ-like fate and reveals a facultative proliferative capacity in aged β-cells

    doi: 10.1242/dev.126011

    Figure Lengend Snippet: Dramatic increase in δ-cell numbers and significant decrease in β-cell numbers in Mnx1 Δendo . (A) Schematic of conditional Mnx1 deletion in endocrine progenitors with Ngn3- Cre. (B) Random blood-glucose measurement showed that Mnx1 Δendo mutant pups were hyperglycemic at P2 ( n =10). (C,D) Immunolabeling with insulin, glucagon and somatostatin showed a dramatic increase in δ-cell number, concomitant with a decrease β-cell number at P2. (E) Significant decrease in β:δ cell ratio in Mnx1 Δendo mutants at P2 ( n =4). (F,G) Quantification of endocrine cell types fraction (F) and area (G) at E18.5, indicating significant increase in δ-cells at the expense of β-cells in Mnx1 Δendo pancreas ( n =4). Scale bars: 50 µm. Data shown as mean±s.e.m. * P

    Article Snippet: Insulin and somatostatin concentration in the culture medium, and insulin and somatostatin content in islet extracts, were determined by radioimmunoassay (insulin, RI-13K, Millipore; somatostatin, RK-060-14, Phoenix Pharmaceuticals).

    Techniques: Mutagenesis, Immunolabeling

    β-to-δ cell transdifferentiation in Mnx1 Δbeta mutants. (A) Schematic showing β-cell-specific Mnx1 deletion using RIP2- Cre transgenics. (B,C) Immunolabeling with insulin, somatostatin and glucagon showed an increase in δ- and α-cells, as well as larger islet size in the Mnx1 Δbeta islets. (D) Quantitative analysis of β-, δ- and α-cell fraction indicate an increased in δ- and α-cell populations concomitant with decreased in percentage of β-cells ( n =3). (E,F) Lineage-tracing analysis using ROSA26R EYFP reporter show co-expression of EYFP and somatostatin, indicating that a subset of δ-cells in the Mnx1 Δbeta mutant are derived from β-cells. (G,H) β-to-δ transdifferentiation, as indicated by EYFP + somatostatin + insulin + cells (arrows), can be detected as early as P5. (I,J) Measurement of islet somatostatin secretion (I) and total somatostatin content (J) in vitro indicate that mutant δ-cells hypersecrete somatostatin and actively synthesize more somatostatin compared with control islets ( n =3). Somatostatin secretion was normalized to islet number. Scale bars: 50 µm. Data are shown as mean±s.e.m. ** P

    Journal: Development (Cambridge, England)

    Article Title: Inactivating the permanent neonatal diabetes gene Mnx1 switches insulin-producing β-cells to a δ-like fate and reveals a facultative proliferative capacity in aged β-cells

    doi: 10.1242/dev.126011

    Figure Lengend Snippet: β-to-δ cell transdifferentiation in Mnx1 Δbeta mutants. (A) Schematic showing β-cell-specific Mnx1 deletion using RIP2- Cre transgenics. (B,C) Immunolabeling with insulin, somatostatin and glucagon showed an increase in δ- and α-cells, as well as larger islet size in the Mnx1 Δbeta islets. (D) Quantitative analysis of β-, δ- and α-cell fraction indicate an increased in δ- and α-cell populations concomitant with decreased in percentage of β-cells ( n =3). (E,F) Lineage-tracing analysis using ROSA26R EYFP reporter show co-expression of EYFP and somatostatin, indicating that a subset of δ-cells in the Mnx1 Δbeta mutant are derived from β-cells. (G,H) β-to-δ transdifferentiation, as indicated by EYFP + somatostatin + insulin + cells (arrows), can be detected as early as P5. (I,J) Measurement of islet somatostatin secretion (I) and total somatostatin content (J) in vitro indicate that mutant δ-cells hypersecrete somatostatin and actively synthesize more somatostatin compared with control islets ( n =3). Somatostatin secretion was normalized to islet number. Scale bars: 50 µm. Data are shown as mean±s.e.m. ** P

    Article Snippet: Insulin and somatostatin concentration in the culture medium, and insulin and somatostatin content in islet extracts, were determined by radioimmunoassay (insulin, RI-13K, Millipore; somatostatin, RK-060-14, Phoenix Pharmaceuticals).

    Techniques: Immunolabeling, Expressing, Mutagenesis, Derivative Assay, In Vitro

    Sustained proliferation of escaper β-cells leads to islet hyperplasia in Mnx1 Δbeta aged mice, and alleviates hyperglycemia following STZ treatment. (A-D) Quantification of total area of hormone + (A), insulin + (B), somatostatin + (C) and glucagon + (D) area demonstrate a twofold increase in total endocrine, insulin + and glucagon + area, in addition to the approximately fourfold increase in somatostatin + area. (E,F) Immunolabeling with insulin shows the presence of hyperplastic islet in Mnx1 Δbeta pancreata. (G) Measurement of resting blood glucose over 6-month period upon streptozotocin (STZ) treatment showed the return of blood glucose to normal levels 2 months post-STZ treatment compared with Mnx1 fl/fl mice. (H) Summary of processes occurring in Mnx1 Δbeta mutant. (I) Model showing novel Mnx1 function in promoting β-cell fate and suppressing δ-cell fate in the Pax6 + endocrine precursors. Mnx1 is continuously required to maintain β-cell fate in the developing β-cells. When Mnx1 − β-cells transdifferentiate into δ-cells, a subset of Mnx1 + β-cells start to repopulate islets by proliferation, leading to islet hyperplasia in aged mice. Scale bars: 100 µm. Data are shown as mean±s.e.m. * P

    Journal: Development (Cambridge, England)

    Article Title: Inactivating the permanent neonatal diabetes gene Mnx1 switches insulin-producing β-cells to a δ-like fate and reveals a facultative proliferative capacity in aged β-cells

    doi: 10.1242/dev.126011

    Figure Lengend Snippet: Sustained proliferation of escaper β-cells leads to islet hyperplasia in Mnx1 Δbeta aged mice, and alleviates hyperglycemia following STZ treatment. (A-D) Quantification of total area of hormone + (A), insulin + (B), somatostatin + (C) and glucagon + (D) area demonstrate a twofold increase in total endocrine, insulin + and glucagon + area, in addition to the approximately fourfold increase in somatostatin + area. (E,F) Immunolabeling with insulin shows the presence of hyperplastic islet in Mnx1 Δbeta pancreata. (G) Measurement of resting blood glucose over 6-month period upon streptozotocin (STZ) treatment showed the return of blood glucose to normal levels 2 months post-STZ treatment compared with Mnx1 fl/fl mice. (H) Summary of processes occurring in Mnx1 Δbeta mutant. (I) Model showing novel Mnx1 function in promoting β-cell fate and suppressing δ-cell fate in the Pax6 + endocrine precursors. Mnx1 is continuously required to maintain β-cell fate in the developing β-cells. When Mnx1 − β-cells transdifferentiate into δ-cells, a subset of Mnx1 + β-cells start to repopulate islets by proliferation, leading to islet hyperplasia in aged mice. Scale bars: 100 µm. Data are shown as mean±s.e.m. * P

    Article Snippet: Insulin and somatostatin concentration in the culture medium, and insulin and somatostatin content in islet extracts, were determined by radioimmunoassay (insulin, RI-13K, Millipore; somatostatin, RK-060-14, Phoenix Pharmaceuticals).

    Techniques: Mouse Assay, Immunolabeling, Mutagenesis

    Embryonic endocrine lineage-allocation defect, followed by postnatal β-to-δ transdifferentiation as two major routes to increased δ-cell numbers. (A,B) Representative sections from E16.5 pancreata with immunodetection of Hhex, insulin and somatostatin illustrate the increase in Hhex + somatostatin − δ-cell precursors in Mnx1 Δendo mutants. (C,D) Quantitative analysis of E16.5 Mnx1 fl/fl and Mnx1 Δendo pancreata indicate a dramatic increase in total number Hhex + somatostatin − δ-cell precursors (C) and total Hhex + somatostatin + δ-cell numbers (D) in Mnx1 Δendo mutant. (E,F) Immunofluorescence analysis of Hhex, insulin and somatostatin on P2 pancreas demonstrates the presence of Hhex + insulin + somatostatin + cells (white arrows) in Mnx1 Δendo pancreas tissue, an indirect indicator of β-to-δ transdifferentiation. (G) Model showing early stage endocrine lineage-allocation defects and late-stage β-to-δ transdifferentiation when Mnx1 is inactivated in endocrine progenitors. (H-J) Quantification indicates that total endocrine area was reduced in Mnx1 Δendo mutant (H), but total Pax6 + endocrine precursors were increased in Mnx1 Δendo mutant at E18.5 (I), indicating failure of a subset of Pax6 + precursors to differentiate towards hormone-producing endocrine cells in the absence of Mnx1 (J). Scale bars: 50 µm. Data are shown as mean±s.e.m. ** P

    Journal: Development (Cambridge, England)

    Article Title: Inactivating the permanent neonatal diabetes gene Mnx1 switches insulin-producing β-cells to a δ-like fate and reveals a facultative proliferative capacity in aged β-cells

    doi: 10.1242/dev.126011

    Figure Lengend Snippet: Embryonic endocrine lineage-allocation defect, followed by postnatal β-to-δ transdifferentiation as two major routes to increased δ-cell numbers. (A,B) Representative sections from E16.5 pancreata with immunodetection of Hhex, insulin and somatostatin illustrate the increase in Hhex + somatostatin − δ-cell precursors in Mnx1 Δendo mutants. (C,D) Quantitative analysis of E16.5 Mnx1 fl/fl and Mnx1 Δendo pancreata indicate a dramatic increase in total number Hhex + somatostatin − δ-cell precursors (C) and total Hhex + somatostatin + δ-cell numbers (D) in Mnx1 Δendo mutant. (E,F) Immunofluorescence analysis of Hhex, insulin and somatostatin on P2 pancreas demonstrates the presence of Hhex + insulin + somatostatin + cells (white arrows) in Mnx1 Δendo pancreas tissue, an indirect indicator of β-to-δ transdifferentiation. (G) Model showing early stage endocrine lineage-allocation defects and late-stage β-to-δ transdifferentiation when Mnx1 is inactivated in endocrine progenitors. (H-J) Quantification indicates that total endocrine area was reduced in Mnx1 Δendo mutant (H), but total Pax6 + endocrine precursors were increased in Mnx1 Δendo mutant at E18.5 (I), indicating failure of a subset of Pax6 + precursors to differentiate towards hormone-producing endocrine cells in the absence of Mnx1 (J). Scale bars: 50 µm. Data are shown as mean±s.e.m. ** P

    Article Snippet: Insulin and somatostatin concentration in the culture medium, and insulin and somatostatin content in islet extracts, were determined by radioimmunoassay (insulin, RI-13K, Millipore; somatostatin, RK-060-14, Phoenix Pharmaceuticals).

    Techniques: Immunodetection, Mutagenesis, Immunofluorescence

    Non-peptide somatostatin receptor subtype-specific agonists

    Journal: British Journal of Pharmacology

    Article Title: Anti-secretory properties of non-peptide somatostatin receptor agonists in isolated rat colon: luminal activity and possible interaction with p-glycoprotein

    doi: 10.1038/sj.bjp.0704614

    Figure Lengend Snippet: Non-peptide somatostatin receptor subtype-specific agonists

    Article Snippet: Native somatostatin (SST-14) and forskolin were purchased from Sigma-Aldrich Chemical Co. Ltd. (Poole, Dorset, U.K.).

    Techniques:

    Immunohistochemistry of canine pancreas by region. Tissue sections of the three major regions of the pancreas were stained with antibodies for insulin (top row), somatostatin (center row), and glucagon (bottom row) to identify the three major islet cell types (beta, delta, and alpha cells, respectively). Insulin positive cells were primarily located in the body (center column) and tail (right column), with the highest concentration and largest sized clusters in the tail. Insulin positive cells in the head of the pancreas (left column) were far less prevalent and occurred primarily in very small clusters or single cells. Similar patterns were observed for somatostatin, while glucagon positive cells were present in extremely low numbers in the head and body and often appeared as isolated single cells. Glucagon images are displayed at higher magnification to better illustrate single cells. Scale bars = 200 μm

    Journal: BMC Veterinary Research

    Article Title: Improved yield of canine islet isolation from deceased donors

    doi: 10.1186/s12917-017-1177-2

    Figure Lengend Snippet: Immunohistochemistry of canine pancreas by region. Tissue sections of the three major regions of the pancreas were stained with antibodies for insulin (top row), somatostatin (center row), and glucagon (bottom row) to identify the three major islet cell types (beta, delta, and alpha cells, respectively). Insulin positive cells were primarily located in the body (center column) and tail (right column), with the highest concentration and largest sized clusters in the tail. Insulin positive cells in the head of the pancreas (left column) were far less prevalent and occurred primarily in very small clusters or single cells. Similar patterns were observed for somatostatin, while glucagon positive cells were present in extremely low numbers in the head and body and often appeared as isolated single cells. Glucagon images are displayed at higher magnification to better illustrate single cells. Scale bars = 200 μm

    Article Snippet: The following primary antibodies were used to stain the pancreas: anti-insulin (1:400, Abcam, Cambridge, MA, #ab7842), anti-glucagon (1:400, Abcam, #ab10988), anti-somatostatin (1:400, Abcam, #ab53165).

    Techniques: Immunohistochemistry, Staining, Concentration Assay, Isolation

    Immunofluorescence of canine pancreas by region. Pancreatic sections were triple-stained with fluorescent antibodies for insulin (green), glucagon (red), and somatostatin (blue) to identify variations in the clustering patterns of pancreatic cell types within different regions of the pancreas. Interestingly, glucagon-positive cells were rarely observed in the head of the pancreas, and were not associated with insulin- and somatostatin-positive cells. Insulin- and somatostatin-positive cells were observed within single clusters in the head region, which were typically comprised of only a few cells. In contrast, the tail and body region contained structures consisting of large numbers of cells that predominantly contained all three endocrine cell types, with the highest concentration and largest clusters of cells located in the tail region. Scale bars = 100 μm

    Journal: BMC Veterinary Research

    Article Title: Improved yield of canine islet isolation from deceased donors

    doi: 10.1186/s12917-017-1177-2

    Figure Lengend Snippet: Immunofluorescence of canine pancreas by region. Pancreatic sections were triple-stained with fluorescent antibodies for insulin (green), glucagon (red), and somatostatin (blue) to identify variations in the clustering patterns of pancreatic cell types within different regions of the pancreas. Interestingly, glucagon-positive cells were rarely observed in the head of the pancreas, and were not associated with insulin- and somatostatin-positive cells. Insulin- and somatostatin-positive cells were observed within single clusters in the head region, which were typically comprised of only a few cells. In contrast, the tail and body region contained structures consisting of large numbers of cells that predominantly contained all three endocrine cell types, with the highest concentration and largest clusters of cells located in the tail region. Scale bars = 100 μm

    Article Snippet: The following primary antibodies were used to stain the pancreas: anti-insulin (1:400, Abcam, Cambridge, MA, #ab7842), anti-glucagon (1:400, Abcam, #ab10988), anti-somatostatin (1:400, Abcam, #ab53165).

    Techniques: Immunofluorescence, Staining, Concentration Assay