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Elevated ABHD16A triggered by ACh was associated with poor prognosis in patients with gastric cancer. A, Representative IHC images of ABHD16A expression in human normal gastric tissues and gastric cancer tissues from the TMA with magnifications of 40×, 100×, and 200×. Scale bar for 200×, 100 μm. B–D, Relationship of ABHD16A IHC score to clinical stage ( B ), pT stage ( C ), and lymph node metastasis ( n = 80; D ). E, Cumulative survival curves of patients with gastric cancer with high or low ABHD16A expression based on the TMA. F, IHC images and score of ABHD16A in S100 + or S100 − gastric cancer tissues. Scale bar, 100 μm. G, Procedure for coculture <t>of</t> <t>DRG</t> neurons and gastric cancer cells. H, Western blotting was used to analyze ABHD16A levels in MFC cells cocultured with DRG neurons or DRG neuron–derived CM. GAPDH served as the loading control. I, Expression of HIF1A and ABHD16A in neurotransmitter [HA, dopamine (DA), 5-HT, norepinephrine (NE), ACh]-treated MFC cells and ACh-treated MGC-803 cells. J, ACh concentration was detected in DRG CM by <t>ELISA.</t> K, Tumor volume of orthotopic gastric cancer tumors with or without vagotomy. L, Representative mIF staining images of FOXP3, CD163, CD11b, CD8, PD-L1, and Pan-CK in gastric cancer tissues with high or low expression of ABHD16A. Scale bar, 100 μm. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
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Elevated ABHD16A triggered by ACh was associated with poor prognosis in patients with gastric cancer. A, Representative IHC images of ABHD16A expression in human normal gastric tissues and gastric cancer tissues from the TMA with magnifications of 40×, 100×, and 200×. Scale bar for 200×, 100 μm. B–D, Relationship of ABHD16A IHC score to clinical stage ( B ), pT stage ( C ), and lymph node metastasis ( n = 80; D ). E, Cumulative survival curves of patients with gastric cancer with high or low ABHD16A expression based on the TMA. F, IHC images and score of ABHD16A in S100 + or S100 − gastric cancer tissues. Scale bar, 100 μm. G, Procedure for coculture <t>of</t> <t>DRG</t> neurons and gastric cancer cells. H, Western blotting was used to analyze ABHD16A levels in MFC cells cocultured with DRG neurons or DRG neuron–derived CM. GAPDH served as the loading control. I, Expression of HIF1A and ABHD16A in neurotransmitter [HA, dopamine (DA), 5-HT, norepinephrine (NE), ACh]-treated MFC cells and ACh-treated MGC-803 cells. J, ACh concentration was detected in DRG CM by <t>ELISA.</t> K, Tumor volume of orthotopic gastric cancer tumors with or without vagotomy. L, Representative mIF staining images of FOXP3, CD163, CD11b, CD8, PD-L1, and Pan-CK in gastric cancer tissues with high or low expression of ABHD16A. Scale bar, 100 μm. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
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Elevated ABHD16A triggered by ACh was associated with poor prognosis in patients with gastric cancer. A, Representative IHC images of ABHD16A expression in human normal gastric tissues and gastric cancer tissues from the TMA with magnifications of 40×, 100×, and 200×. Scale bar for 200×, 100 μm. B–D, Relationship of ABHD16A IHC score to clinical stage ( B ), pT stage ( C ), and lymph node metastasis ( n = 80; D ). E, Cumulative survival curves of patients with gastric cancer with high or low ABHD16A expression based on the TMA. F, IHC images and score of ABHD16A in S100 + or S100 − gastric cancer tissues. Scale bar, 100 μm. G, Procedure for coculture <t>of</t> <t>DRG</t> neurons and gastric cancer cells. H, Western blotting was used to analyze ABHD16A levels in MFC cells cocultured with DRG neurons or DRG neuron–derived CM. GAPDH served as the loading control. I, Expression of HIF1A and ABHD16A in neurotransmitter [HA, dopamine (DA), 5-HT, norepinephrine (NE), ACh]-treated MFC cells and ACh-treated MGC-803 cells. J, ACh concentration was detected in DRG CM by <t>ELISA.</t> K, Tumor volume of orthotopic gastric cancer tumors with or without vagotomy. L, Representative mIF staining images of FOXP3, CD163, CD11b, CD8, PD-L1, and Pan-CK in gastric cancer tissues with high or low expression of ABHD16A. Scale bar, 100 μm. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
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Elevated ABHD16A triggered by ACh was associated with poor prognosis in patients with gastric cancer. A, Representative IHC images of ABHD16A expression in human normal gastric tissues and gastric cancer tissues from the TMA with magnifications of 40×, 100×, and 200×. Scale bar for 200×, 100 μm. B–D, Relationship of ABHD16A IHC score to clinical stage ( B ), pT stage ( C ), and lymph node metastasis ( n = 80; D ). E, Cumulative survival curves of patients with gastric cancer with high or low ABHD16A expression based on the TMA. F, IHC images and score of ABHD16A in S100 + or S100 − gastric cancer tissues. Scale bar, 100 μm. G, Procedure for coculture <t>of</t> <t>DRG</t> neurons and gastric cancer cells. H, Western blotting was used to analyze ABHD16A levels in MFC cells cocultured with DRG neurons or DRG neuron–derived CM. GAPDH served as the loading control. I, Expression of HIF1A and ABHD16A in neurotransmitter [HA, dopamine (DA), 5-HT, norepinephrine (NE), ACh]-treated MFC cells and ACh-treated MGC-803 cells. J, ACh concentration was detected in DRG CM by <t>ELISA.</t> K, Tumor volume of orthotopic gastric cancer tumors with or without vagotomy. L, Representative mIF staining images of FOXP3, CD163, CD11b, CD8, PD-L1, and Pan-CK in gastric cancer tissues with high or low expression of ABHD16A. Scale bar, 100 μm. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
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Elevated ABHD16A triggered by ACh was associated with poor prognosis in patients with gastric cancer. A, Representative IHC images of ABHD16A expression in human normal gastric tissues and gastric cancer tissues from the TMA with magnifications of 40×, 100×, and 200×. Scale bar for 200×, 100 μm. B–D, Relationship of ABHD16A IHC score to clinical stage ( B ), pT stage ( C ), and lymph node metastasis ( n = 80; D ). E, Cumulative survival curves of patients with gastric cancer with high or low ABHD16A expression based on the TMA. F, IHC images and score of ABHD16A in S100 + or S100 − gastric cancer tissues. Scale bar, 100 μm. G, Procedure for coculture <t>of</t> <t>DRG</t> neurons and gastric cancer cells. H, Western blotting was used to analyze ABHD16A levels in MFC cells cocultured with DRG neurons or DRG neuron–derived CM. GAPDH served as the loading control. I, Expression of HIF1A and ABHD16A in neurotransmitter [HA, dopamine (DA), 5-HT, norepinephrine (NE), ACh]-treated MFC cells and ACh-treated MGC-803 cells. J, ACh concentration was detected in DRG CM by <t>ELISA.</t> K, Tumor volume of orthotopic gastric cancer tumors with or without vagotomy. L, Representative mIF staining images of FOXP3, CD163, CD11b, CD8, PD-L1, and Pan-CK in gastric cancer tissues with high or low expression of ABHD16A. Scale bar, 100 μm. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
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Adenosine mitigated the neuromuscular blockade caused by B. multicinctus venom. a) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in chick biventer cervicis (BC) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; b) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous <t>acetylcholine</t> (ACh; 1 mM), carbachol (CCh; 20 µM) and potassium chloride (KCl; 40 mM) in BC preparations; c) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in mouse phrenic nerve-diaphragm (PND) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; d) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous ACh (1 mM), CCh (20 μM), and KCl (40 mM) in PND preparations. The points in a/c and the columns in b/d represent the mean ± standard error of mean (n = 3 for each group); * P < 0.05, significantly different from the venom-only group. ADO refers to adenosine .
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Adenosine mitigated the neuromuscular blockade caused by B. multicinctus venom. a) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in chick biventer cervicis (BC) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; b) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous <t>acetylcholine</t> (ACh; 1 mM), carbachol (CCh; 20 µM) and potassium chloride (KCl; 40 mM) in BC preparations; c) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in mouse phrenic nerve-diaphragm (PND) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; d) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous ACh (1 mM), CCh (20 μM), and KCl (40 mM) in PND preparations. The points in a/c and the columns in b/d represent the mean ± standard error of mean (n = 3 for each group); * P < 0.05, significantly different from the venom-only group. ADO refers to adenosine .
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Adenosine mitigated the neuromuscular blockade caused by B. multicinctus venom. a) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in chick biventer cervicis (BC) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; b) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous <t>acetylcholine</t> (ACh; 1 mM), carbachol (CCh; 20 µM) and potassium chloride (KCl; 40 mM) in BC preparations; c) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in mouse phrenic nerve-diaphragm (PND) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; d) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous ACh (1 mM), CCh (20 μM), and KCl (40 mM) in PND preparations. The points in a/c and the columns in b/d represent the mean ± standard error of mean (n = 3 for each group); * P < 0.05, significantly different from the venom-only group. ADO refers to adenosine .
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Image Search Results


Elevated ABHD16A triggered by ACh was associated with poor prognosis in patients with gastric cancer. A, Representative IHC images of ABHD16A expression in human normal gastric tissues and gastric cancer tissues from the TMA with magnifications of 40×, 100×, and 200×. Scale bar for 200×, 100 μm. B–D, Relationship of ABHD16A IHC score to clinical stage ( B ), pT stage ( C ), and lymph node metastasis ( n = 80; D ). E, Cumulative survival curves of patients with gastric cancer with high or low ABHD16A expression based on the TMA. F, IHC images and score of ABHD16A in S100 + or S100 − gastric cancer tissues. Scale bar, 100 μm. G, Procedure for coculture of DRG neurons and gastric cancer cells. H, Western blotting was used to analyze ABHD16A levels in MFC cells cocultured with DRG neurons or DRG neuron–derived CM. GAPDH served as the loading control. I, Expression of HIF1A and ABHD16A in neurotransmitter [HA, dopamine (DA), 5-HT, norepinephrine (NE), ACh]-treated MFC cells and ACh-treated MGC-803 cells. J, ACh concentration was detected in DRG CM by ELISA. K, Tumor volume of orthotopic gastric cancer tumors with or without vagotomy. L, Representative mIF staining images of FOXP3, CD163, CD11b, CD8, PD-L1, and Pan-CK in gastric cancer tissues with high or low expression of ABHD16A. Scale bar, 100 μm. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

Journal: Cancer Research

Article Title: Nerves Stimulate Cross-talk Between Gastric Cancer and Group 3 Innate Lymphoid Cells to Enhance Immunosuppression

doi: 10.1158/0008-5472.CAN-25-3092

Figure Lengend Snippet: Elevated ABHD16A triggered by ACh was associated with poor prognosis in patients with gastric cancer. A, Representative IHC images of ABHD16A expression in human normal gastric tissues and gastric cancer tissues from the TMA with magnifications of 40×, 100×, and 200×. Scale bar for 200×, 100 μm. B–D, Relationship of ABHD16A IHC score to clinical stage ( B ), pT stage ( C ), and lymph node metastasis ( n = 80; D ). E, Cumulative survival curves of patients with gastric cancer with high or low ABHD16A expression based on the TMA. F, IHC images and score of ABHD16A in S100 + or S100 − gastric cancer tissues. Scale bar, 100 μm. G, Procedure for coculture of DRG neurons and gastric cancer cells. H, Western blotting was used to analyze ABHD16A levels in MFC cells cocultured with DRG neurons or DRG neuron–derived CM. GAPDH served as the loading control. I, Expression of HIF1A and ABHD16A in neurotransmitter [HA, dopamine (DA), 5-HT, norepinephrine (NE), ACh]-treated MFC cells and ACh-treated MGC-803 cells. J, ACh concentration was detected in DRG CM by ELISA. K, Tumor volume of orthotopic gastric cancer tumors with or without vagotomy. L, Representative mIF staining images of FOXP3, CD163, CD11b, CD8, PD-L1, and Pan-CK in gastric cancer tissues with high or low expression of ABHD16A. Scale bar, 100 μm. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

Article Snippet: ACh in the dorsal root ganglion (DRG)–derived conditioned medium (CM) was detected using the ACh ELISA kit (Elabscience, E-EL-0081).

Techniques: Expressing, Western Blot, Derivative Assay, Control, Concentration Assay, Enzyme-linked Immunosorbent Assay, Staining

Adenosine mitigated the neuromuscular blockade caused by B. multicinctus venom. a) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in chick biventer cervicis (BC) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; b) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous acetylcholine (ACh; 1 mM), carbachol (CCh; 20 µM) and potassium chloride (KCl; 40 mM) in BC preparations; c) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in mouse phrenic nerve-diaphragm (PND) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; d) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous ACh (1 mM), CCh (20 μM), and KCl (40 mM) in PND preparations. The points in a/c and the columns in b/d represent the mean ± standard error of mean (n = 3 for each group); * P < 0.05, significantly different from the venom-only group. ADO refers to adenosine .

Journal: Journal of Advanced Research

Article Title: Preclinical evidence of adenosine for early intervention in Bungarus multicinctus envenomation

doi: 10.1016/j.jare.2025.06.012

Figure Lengend Snippet: Adenosine mitigated the neuromuscular blockade caused by B. multicinctus venom. a) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in chick biventer cervicis (BC) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; b) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous acetylcholine (ACh; 1 mM), carbachol (CCh; 20 µM) and potassium chloride (KCl; 40 mM) in BC preparations; c) The effect of B. multicinctus venom (3 µg/mL) on the inhibition of indirect twitches in mouse phrenic nerve-diaphragm (PND) preparations, and the role of adenosine (30 µg/mL) in alleviating neuromuscular blockade; d) Columns representing the effects of B. multicinctus venom (3 µg/mL) and adenosine (30 µg/mL) on responses to exogenous ACh (1 mM), CCh (20 μM), and KCl (40 mM) in PND preparations. The points in a/c and the columns in b/d represent the mean ± standard error of mean (n = 3 for each group); * P < 0.05, significantly different from the venom-only group. ADO refers to adenosine .

Article Snippet: Acetylcholine (ACh), d-tubocurarine chloride (dTC), KCl, and chlorogenic acid were acquired from Sigma-Aldrich Chemical Co. (St. Louis, MO, USA), and carbamylcholine (CCh) was purchased from MedChem Express Co., Ltd. (Monmouth Junction, NJ, USA).

Techniques: Inhibition

Adenosine mitigates Bungarus multicinctus venom-induced muscle and membrane damage, as well as neuromuscular blockade. (a) Serum levels of ALP, CK, LDH, ALT, and AST were quantified in PBS control (grey), venom only (yellow), and venom-plus-adenosine (blue) groups. (b) Diaphragm sections from PBS control, venom-only, and venom-plus-adenosine groups were incubated with FITC-conjugated α-bungarotoxin antibody and imaged. Green fluorescence indicates the distribution of nAChR channels at neuromuscular junctions. Scale bars: 50 µm. (c) Quantification of intracellular fluorescence intensity in Diaphragm sections from PBS control (grey), venom-only (yellow), and venom-plus-adenosine (blue) groups. All data in (a and c) represent mean ± SEM (n = 5 for each group). ****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05, ns: not significant (one-way ANOVA followed by Tukey’s post hoc test). Abbreviations: AST – Aspartate Aminotransferase, ALT – Alanine Aminotransferase, Cr – Creatinine, ALP – Alkaline Phosphatase, CK – Creatine Kinase, LDH – Lactate Dehydrogenase. nAChR-nicotinic acetylcholine receptor. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: Journal of Advanced Research

Article Title: Preclinical evidence of adenosine for early intervention in Bungarus multicinctus envenomation

doi: 10.1016/j.jare.2025.06.012

Figure Lengend Snippet: Adenosine mitigates Bungarus multicinctus venom-induced muscle and membrane damage, as well as neuromuscular blockade. (a) Serum levels of ALP, CK, LDH, ALT, and AST were quantified in PBS control (grey), venom only (yellow), and venom-plus-adenosine (blue) groups. (b) Diaphragm sections from PBS control, venom-only, and venom-plus-adenosine groups were incubated with FITC-conjugated α-bungarotoxin antibody and imaged. Green fluorescence indicates the distribution of nAChR channels at neuromuscular junctions. Scale bars: 50 µm. (c) Quantification of intracellular fluorescence intensity in Diaphragm sections from PBS control (grey), venom-only (yellow), and venom-plus-adenosine (blue) groups. All data in (a and c) represent mean ± SEM (n = 5 for each group). ****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05, ns: not significant (one-way ANOVA followed by Tukey’s post hoc test). Abbreviations: AST – Aspartate Aminotransferase, ALT – Alanine Aminotransferase, Cr – Creatinine, ALP – Alkaline Phosphatase, CK – Creatine Kinase, LDH – Lactate Dehydrogenase. nAChR-nicotinic acetylcholine receptor. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: Acetylcholine (ACh), d-tubocurarine chloride (dTC), KCl, and chlorogenic acid were acquired from Sigma-Aldrich Chemical Co. (St. Louis, MO, USA), and carbamylcholine (CCh) was purchased from MedChem Express Co., Ltd. (Monmouth Junction, NJ, USA).

Techniques: Membrane, Control, Incubation, Fluorescence