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Biomedical subjects

Y Yamaguchi

Publications and source records attributed to Y Yamaguchi.

At least 451 records · Page 25Linked to original sources
PubMed1997

Contrasting effects of TGF-beta 1 and TNF-alpha on the development of dendritic cells from progenitors in mouse bone marrow.

Dendritic cells (DC) are a distinct population of leukocytes and specialized antigen-presenting cells for T cell responses. Prior work has shown that GM-CSF can induce the development of large numbers of DC from proliferating progenitors in mouse bone marrow. We have monitored the effects of potentially enhancing and suppressive cytokines in these cultures. In this system, many immature DC develop from proliferating precursors during the first six days of culture, and between days 6-8 maturation of typical nonadherent and nonreplicating DC takes place. The maturation is accompanied by a large increase in the expression of major histocompatibilities complex class II (MHC II) and B7-2/CD86, and in mixed leukocyte reaction stimulating activity. Tumor necrosis factor-alpha (TNF-alpha), previously shown to be required for development of human DC, was found to enhance the maturation of mouse DC in the last two days of culture. Transforming growth factor-beta 1 (TGF-beta 1), on the other hand, almost totally blocked DC maturation, but it had to be given in the first six days of culture when the DC were actively proliferating. TGF-beta 1 did not block the production of immature, MHC II-positive but B7-2/CD86-negative DC. Maturation would take place between days 6-8 as long as the cultures were depleted of Fc-receptor-bearing cells, or if TNF-alpha were added. In both instances, maturation was not blocked even when TGF-beta 1 remained in the culture. We conclude that the development of DC, in response to GM-CSF, can be modified by other cytokines. TGF-beta 1 is suppressive but only indirectly via Fc-receptor-bearing suppressive cells, presumably suppressive macrophages, while TNF-alpha enhances the final maturation of DC.

Animals↗
PubMed1997

Inhibition of 8-hydroxyguanine repair in testes after administration of cadmium chloride to GSH-depleted rats.

The main goal of this study is to investigate the mechanism of cadmium (Cd)-induced carcinogenesis by reactive oxygen species. Rats were divided into four groups and were treated with (i) saline (control), (ii) cadmium chloride (CdCl2), (iii) l-buthionine-[S, R]-sulfoximine (BSO, an inhibitor of GSH biosynthesis), and (iv) CdCl2 and BSO, respectively. They were euthanized at 0, 24, 48, and 72 hr after these treatments, and the lungs and testes were analyzed. After treatment with both CdCl2 and BSO, the testicular 8-OH-Gua level increased (48 hr), its repair activity decreased (48 and 72 hr), the GSH content was markedly suppressed (48 and 72 hr), the superoxide dismutase activities slightly (48 and 72 hr) decreased, and the lipid peroxidation level increased (24 and 72 hr) in the testes as compared to the control levels. These results suggest that under GSH-depleted conditions, CdCl2 inhibits 8-OH-Gua repair activity in the rat testis and 8-OH-Gua accumulates in the DNA, which may pertain to testicular carcinogenesis.

Animals↗
PubMed1997

Evolutionary motif and its biological and structural significance.

We developed a method for multiple alignment of protein sequences. The main feature of this method is that it takes the evolutionary relationships of the proteins in question into account repeatedly for execution, until the relationships and alignment results are in agreement. We then applied this method to the data of the international DNA sequence databases, which are the most comprehensive and updated DNA databases in the world, in order to estimate the "evolutionary motif" by extensive use of a supercomputer. Though a few problems needed to be solved, we could estimate the length of the motifs in the range of 20 to 200 amino acids, with about 60 the most frequent length. We then discussed their biological and structural significance. We believe that we are now in a position to analyze DNA and protein not only in vivo and in vitro but also in silico.

Amino Acid Sequence↗
PubMed1997

Establishment of internal-image anti-idiotype monoclonal antibodies to a human antibody to lung cancer.

Internal-image anti-idiotype antibodies are expected to enhance anticancer effector mechanisms in vivo. The objective of this study was to establish hybridomas producing anti-idiotype monoclonal antibodies against a human monoclonal antibody (hmAb) 4G12 that reacts strongly with lung squamous cell carcinomas. BALB/c female mice 6 weeks old were immunized with 4G12. Splenocytes were hybridized with P3U1 cells and hybrid cells secreting anti-4G12 hmAb were cloned. Two clones reacted with 4G12 hmAb but not with 3H12 IgM hmAb, human IgM, human serum or fetal calf serum. These two Ab2 antibodies (IgG1 kappa) 2B12 and 2H1 demonstrated 91.5% and 90.3% inhibition in their reactivity with radiolabelled 4G12 on PC10 cells, indicating that 2B12 and 2H1 antibodies were of the Ab2 beta type. In criss-cross inhibition assays, the binding of 2B12 or 2H1 to 4G12 was not inhibited by 2H1 or 2B12. Thus 2B12 and 2H1 were thought to recognize the different epitopes on the antigen-binding sites. Antisera against 2B12 and 2H1 demonstrated specific reactivity to PC10 cells. The two Ab2 beta antibodies, 2B12 and 2H1, express internal images of lung squamous cell carcinoma recognized by the 4G12 antibody and may be useful for cancer immunotherapy.

Animals↗
PubMed1997

Cerulein-induced in vitro activation of trypsinogen in rat pancreatic acini is mediated by cathepsin B.

BACKGROUND & AIMS: One of the central, unresolved issues in the pathogenesis of acute pancreatitis is the uncertainty regarding the mechanisms responsible for the premature intrapancreatic activation of digestive enzyme zymogens. The aim of the current study was to develop and characterize an in vitro system that might mimic the events leading to trypsinogen activation within the pancreas during pancreatitis. METHODS: Activation of trypsinogen in response to stimulation with cerulein was quantitated in isolated rat pancreatic acini. RESULTS: Activation of trypsinogen was detected within 10 minutes of exposing isolated rat pancreatic acini, in Ca2+-containing buffer, to a supramaximally stimulating concentration of cerulein in vitro. Complete inhibition of pancreatic cathepsin B activity with E-64d, a specific, potent and irreversible cathepsin B inhibitor, prevents cerulein-induced in vitro trypsinogen activation. CONCLUSIONS: In vitro activation of trypsinogen can be detected when pancreatic acini are exposed to a supramaximally stimulating dose of cerulein. The results using this in vitro system support the hypothesis that the appearance of active trypsin within the pancreas during the early stages of cerulein-induced pancreatitis reflects activation of trypsinogen by the lysosomal hydrolase cathepsin B.

Amylases↗
PubMed1997

Effect of burn injury on glucose and nitrogen metabolism in the liver: preliminary studies in a perfused liver system.

BACKGROUND: The direct impact of burn injury on liver metabolism was studied in a rat liver perfusion system to remove the influence of systemic factors that modulate liver metabolism. METHODS: Seven animals received a burn injury covering 20% of the total body surface area, and seven were sham burned. The in situ liver perfusion studies were carried out in these animals after 3 days of isonitrogenous-isocaloric enteral feeding. In each study oxygen consumption and the rates of uptake and release of glucose, urea, and various amino acids were measured. RESULTS: Burn injury significantly increased urea production (18.5 +/- 0.4 versus 12.2 +/- 0.6 micromol/gm liver/hr and oxygen consumption (3.23 +/- 0.17 versus 1.21 +/- 0.03 micromol/gm liver/min) in the liver but did not alter the rate of gluconeogenesis. The change in amino acid concentrations in the perfusion medium implies an increased net protein breakdown. CONCLUSIONS: Our study indicates that (1) burn injury induces a hypermetabolic state in the liver, (2) the observed enhancement of gluconeogenesis in vivo after burn in probably regulated by factors outside the liver, and (3) the liver itself plays an active role in up-regulating urea production in burn injury. Identifying intrahepatic factors that up-regulate urea production may provide an "intrahepatic approach" to ameliorate the severe nitrogen loss after burn injury.

Amino Acids↗
PubMed1997

Mesangial phenotypic changes associated with cellular lesions in primary focal segmental glomerulosclerosis.

Injury to glomerular visceral epithelial cells has been proposed as the initial step in glomerular scar formation in primary focal segmental glomerulosclerosis (FSGS); however, the subsequent process that ultimately results in glomerular scar formation remains uncertain. This study examined whether phenotypically altered mesangial cells determine the early progression of primary FSGS. Cellular lesion characterized by proliferative epithelial cell reaction with occasional endocapillary hypercellularity has been considered to be an early morphologic feature in the development of glomerular scar in primary FSGS. We compared the immunohistologic findings of 10 patients with primary FSGS showing cellular lesion, 15 patients with primary FSGS showing only segmental scar, and 10 patients with minimal-change nephrotic syndrome. Histologically normal kidney tissue samples obtained from three patients with renal trauma were used as normal controls. Alpha-smooth muscle actin expression detected by a mouse anti-human monoclonal antibody as well as de novo type III collagen expression determined by a goat polyclonal antibody were prominent in the glomerular tufts with cellular lesions in FSGS patients. A significant increase in the number of glomerular CD68+ (a mouse anti-human monoclonal antibody) macrophages was also observed in association with the cellular lesion. Repeat renal biopsies in six of the 10 FSGS patients with a cellular lesion showed disappearance of the cellular lesion, reduced glomerular alpha-smooth muscle actin expression, decreased number of glomerular CD68+ macrophage, and progression of glomerular scar formation. These results indicate that mesangial cells undergo phenotypic changes to myofibroblasts in association with the cellular lesion in primary FSGS. Thus, the phenotypically altered mesangial cells acquiring features of a myofibroblast may have an important role in the early process of glomerular scar formation in certain types of primary FSGS.

Actins↗
PubMed1997

A new substance (Yoshixol) with an interesting antibiotic mechanism from wood oil of Japanese traditional tree (Kiso-Hinoki), Chamaecyparis obtusa.

1. A neutral wood oil was extracted from Chamaecyparis obtusa (Kiso-Hinoki), which has been trusted nationally and preserved historically in the central part of Japan (Kiso, Nagano). 2. Hinokitiol, or thujaplicin (C10H12O2), which has been believed to exist in Cupressaceae, was not found in this neutral wood oil. Some differences between the extracting processes of the natural products are discussed. 3. A new chemical substance (Yoshixol, 4,4-dimethyl-6-methylene-2-cyclohexen-1-one) was simulated by several criteria (details in the text) as a major candidate of the neutral wood oil from Chamaecyparis obtusa. Thus, Yoshixol was newly synthesized. 4. The antibiotic effects of hinokitiol, the neutral wood oil and Yoshixol on methicillin-resistant Staphylococcus aureus (MRSA) were examined bacteriologically and morphologically. 5. All of the aforementioned three test materials showed complete antibiotic effects on MRSA by the bacteriological examination. However, the morphological findings showed entirely different aspects of cell death. 6. Hinokitiol caused an aggregative, degenerative and/or necrotic aspect, but the neutral wood oil and Yoshixol produced characteristic aspects: separation of contacted cells, blebbing, bugging-like eruption, formation of granules and an extensive reduction of individual cell size of MRSA. 7. Yoshixol was able to enhance those antibiotic effects on MRSA distinctly more than the neutral wood oil. 8. Yoshixol also showed a strong antibiotic effect on Escherichia coli, Mycobacterium chelonei, Pseudomonas aureginosa and Candida albicans. Morphological observations of those bacilli after Yoshixol revealed characteristic aspects of separation of contacted cells, bugging-like swelling, granulation, ballooning and reduction of cell size. 9. A possible mechanism of Yoshixol is discussed in regard to a molecular orbital theory on the basis of its electron orbits and to a thermodynamic interaction with the prokaryotic cell membrane. On the basis of the molecular properties of Yoshixol, future biological interests and possible biological effects of Yoshixol are suggested.

Anti-Bacterial Agents↗
PubMed1997

Apoptosis-like (possible quantum thermodynamic) cell death induced by Yoshixol and wood oil of Chamaecyparis obtusa (Kiso-Hinoki) on HeLa cell.

1. We report on the cytotoxic effects of neutral wood oil extracted from Chamaecyparis obtusa (Kiso-Hinoki) and of the newly synthetized substance Yoshixol (4,4-dimethyl-6-methylene-2-cyclohexen-1-one) on cultured HeLa cells. 2. The neutral wood oil produced cell death, led to the formation of granules, which were connected with fibrous networks, and reduced cell size. 3. Yoshixol caused a separation of cells, granulation, formation of high-density materials (probably apoptotic body), and reduction of cell size. 4. DNA fragmentation on the electrophoresis was observed with Yoshixol. A low-molecular-weight smear band appeared in the supernatant after treatment with the neutral wood oil. Neither treatment showed higher lactate dehydrogenase (LDH) activity in the culture medium than seen with ethanol as a control. 5. These findings suggest that both the neutral wood oil and Yoshixol have a similar cytotoxic mechanism, reducing cell size and producing a granulation (fragmentation) of eukaryotic cells. 6. Yoshixol may be a potent antitumor agent that induces apoptotic-like cell death. This possible mechanism is discussed.

Apoptosis↗
PubMed1997

Oxygen-induced embryopathy and the significance of glutathione-dependent antioxidant system in the rat embryo during early organogenesis.

We investigated the effect of glutathione (GSH)-dependent antioxidant system against hydrogen peroxide (H2O2) formation in oxygen-induced embryopathy. Exposure of rat embryos to a high concentration of oxygen (20%) during early neurulation (day 9 to 10) significantly increased the incidence of neural tube defects compared with control embryos (10% vs 0%, p < 0.01) exposed to a low O2 concentration (5%). The concentration of GSH in 20% O2-exposed embryos was significantly reduced compared with that in control embryos (10.68 +/- 0.72 vs 12.34 +/- 0.65 nmol/mg protein, p < 0.001). The activity of gamma-glutamylcysteine synthetase (gamma-GCS), the rate-limiting GSH synthesizing enzyme increased in 20% O2-exposed embryos (24.83 +/- 0.71 vs 21.00 +/- 0.94 microunits/mg protein). Increased activity of gamma-GCS was associated with increased expression of gamma-GCS mRNA. Substantial increases were also observed in the activities of glutathione peroxidase (GPX) and glutathione S-transferase (GST) in 20% O2-exposed embryos. The formation of intracellular H2O2, measured by flow cytometer using 2',7'-dichlorofluorescein diacetate (DCFH-DA), increased in isolated embryonic cells of 20% O2-exposed embryos. The addition of buthionine sulfoxamine (BSO), a specific inhibitor of gamma-GCS, to culture media exposed to 20% O2 produced a marked decrease in the concentration of GSH in association with a further increase in the incidence of embryonic malformations (24.4% vs. 10%, P < 0.01). The addition of 2.0 mM GSH ester to culture media exposed to 20% O2 prevented the development of embryonic malformations through the restoration of normal GSH contents and reduction of H2O2. Our results demonstrated that oxygen-induced embryonic malformations were induced by increased production of H2O2 in the presence of an immature free radical scavenger system. We suggest that impaired responsiveness of the GSH dependent antioxidant system against oxidative stress plays a crucial role in oxygen-induced embryopathy.

Animals↗
PubMed1997

Donor-specific cytotoxic lymphocyte activity from bronchoalveolar lavage during acute canine lung allograft rejection.

OBJECTIVE: We investigated the relationship between acute lung rejection and donor-specific cytotoxic activity (DSCA) in recipient's lymphocytes obtained from bronchoalveolar lavage (BAL). METHODS: A total of 26 mongrel dogs underwent left lung allotransplantation. Dogs received either no immunosuppressive treatment (group I), cyclosporine (group II), or cyclosporine and methylprednisolone for evidence of acute rejection (group III). DSCA was measured by a 51Cr release assay, using lymphocytes from BAL samples as effector cells and 51Cr-labeled donor skin fibroblasts as target cells. The pathologic findings of the transplanted lungs were classified according to the working formulation for classification and grading of pulmonary rejection. In addition, the degree of cellular infiltration in the perivascular, peribronchial, interstitial, and intraalveolar areas was determined based on an infiltration score. RESULTS: DSCA in BAL samples was elevated during mild, moderate and severe acute rejection. The accuracy of the diagnosis of mild or moderate rejection was 92.3% at effector:target (E:T) ratios of 100:1 and 50:1. The DSCA in the BAL fluid and the total infiltration score were correlated closely with correlation coefficients of 0.859 and 0.828 at E:T ratios of 100:1 in group I and group II dogs, respectively. Lung aeration improved and DSCA decreased with methylprednisolone therapy in three of four dogs with grade 2 rejection. CONCLUSION: There is a direct relationship between the DSCA in BAL fluid and the degree of tissue damage caused by acute rejection. The DSCA can be detected by a 51Cr release assay which may hold promise for future clinical applications.

Animals↗
PubMed1997

Enhanced expression of cytokine-induced neutrophil chemoattractant (CINC) by bronchoalveolar macrophages in cerulein-induced pancreatitis rats.

The role of bronchoalveolar macrophages (BAMs) in the aggravation of cerulein-induced pancreatitis was studied by measuring expression of cytokine-induced neutrophil chemoattractant (CINC) in vitro. Pancreatitis was induced by four intramuscular injections of cerulein (50 microg/kg at 1-hr intervals). Pancreatitis rats were injected intraperitoneally with 30 mg/kg lipopolysaccharide (LPS) 6 hr following the first cerulein injection as a septic challenge. Rats were divided into four groups: group I, nonpancreatitis without LPS; group II, pancreatitis without LPS; group III, nonpancreatitis with LPS; and group IV, pancreatitis with LPS. Hyperactivity of BAMs in response to LPS was assessed as a function of in vitro CINC production. CINC concentrations of the serum and bronchoalveolar lavage fluid in group IV were significantly higher than those in groups I, II, and III. BAMs in group II harvested 6 hr following the first cerulein injection had significantly greater CINC production than those in group I. Northern blot analysis revealed abundant CINC mRNA transcripts in BAMs from groups III and IV. Additionally, myeloperoxidase activity in the lung of group IV rats 8 and 12 hr following the first cerulein injection was significantly higher than that in group I, II, and III rats. Significant differences in static lung compliance in group IV were found compared with groups I, II, and III. These results indicate that BAMs from rats with cerulein-induced pancreatitis were primed and had enhanced release of CINC following LPS exposure. Enhanced expression of CINC may modulate the pathogenesis of pancreatitis-associated lung injury complicated with sepsis.

Acute Disease↗
PubMed1997

Recombinant human hepatocyte growth factor facilitates biliary transport after hepatocyte transplantation in Eisai hyperbilirubinemic rats.

Hepatocyte transplantation may offer an attractive treatment for inborn errors of liver metabolism. However, factor(s) are required as stimuli to induce proliferation of the limited number of hepatocytes transplanted. The Eisai hyperbilirubinemic rat (EHBR) is a Sprague-Dawley (SD) mutant rat with conjugated hyperbilirubinemia. EHBRs have impaired canalicular excretory transport of organic anions, bile acid glucuronide, and sulfate. Recombinant human hepatocyte growth factor (rhHGF) (100 microg/kg) was injected intravenously at 2-hr intervals for 10 hr, immediately and 35 days following the intraportal injection of 1 x 10(7) wild-type SD rat hepatocytes. Serum bilirubin concentrations decreased significantly within 35 days and were maintained at significantly reduced levels for 120 days following transplantation. Biliary excretion was demonstrated by the biliary transport of indocyanine green and sulfobromophthalein sodium into the bile. These results indicate that hepatic transport of bile acid conjugates in EHBRs can be restored by hepatocyte transplantation combined with repeated administration of exogenous rhHGF, in conjunction with functioning of the recipient's excretory biliary system.

Animals↗
PubMed1997

Autoregulation of Pax6 transcriptional activation by two distinct DNA-binding subdomains of the paired domain.

BACKGROUND: Pax6 is a transcription factor that plays a central role in eye development. Pax6 contains a DNA-binding domain called paired domain, which consists of a highly conserved N-terminal subdomain and a variable C-terminal subdomain. Recent findings have suggested that both subdomains possess distinct DNA-binding activities. RESULTS: To understand the mechanism of DNA-binding and transcriptional activation by Pax6 via these subdomains, we employed Pax6 paired domain mutants previously isolated from patients with ocular disorders. Analysis of these mutants by gel shift assay revealed that the N-terminal and C-terminal subdomains can independently bind to their respective cognate sites, P6CON and 5aCON. Results from a luciferase assay, however, showed that the two functional subdomains negatively regulate their transactivation potentials each other. Wild-type Pax6 and its hyperactive variants show different patterns of DNA contact. CONCLUSION: These results support a new model for the regulation of Pax6 transactivation: When one DNA-binding subdomain binds to its cognate site, the other subdomain also interacts with the flanking sequences nonspecifically, and this interaction constrains its structure to give a reduced level of transactivation.

Animals↗
PubMed1997

Neutrophil elastase inhibitor reduces neutrophil chemoattractant production after ischemia-reperfusion in rat liver.

BACKGROUND & AIMS: Neutrophils are important in the development of tissue injury induced by ischemia-reperfusion. The ability of an inhibitor of neutrophil elastase (ONO-5046) to protect against ischemia-reperfusion injury in rat liver was investigated by measuring serum concentrations of cytokine-induced neutrophil chemoattractant. METHODS: Liver ischemia was induced in rats by occluding the portal vein for 30 minutes, and ONO-5046 or anticoagulants were injected intravenously 5 minutes before vascular clamping. RESULTS: Serum concentration of cytokine-induced neutrophil chemoattractant increased after reperfusion, reached a maximum at 6 hours, and then gradually decreased. However, pretreatment of animals with heparin (50 U/kg), antithrombin III (250 U/kg), or ONO-5046 (10 mg/kg) resulted in significantly smaller increases in the serum concentration of cytokine-induced neutrophil chemoattractant after reperfusion. Pretreatment with both ONO-5046 and heparin, or both ONO-5046 and antithrombin III, produced additive effects. Pretreatment of rats with both ONO-5046 and heparin or both ONO-5046 and antithrombin III also inhibited the increase in cytokine-induced neutrophil chemoattractant mRNA in liver. These combined treatments significantly reduced the increases in both the number of neutrophils accumulated in the liver and the hepatic activity of myeloperoxidase. CONCLUSIONS: Cytokine-induced neutrophil chemoattractant production after ischemia-reperfusion in the liver is mediated by neutrophil elastase and activation of coagulation within the hepatic microcirculation.

Animals↗
PubMed1997

Enhanced expression of cytokine-induced neutrophil chemoattractant in rat hepatic allografts during acute rejection.

The kinetics of messenger RNA (mRNA) and protein levels of cytokine-induced neutrophil chemoattractant (CINC) in rat hepatic allografts during acute rejection were investigated. Infiltrating cells were identified by double immunostaining with anti-CINC and anti-macrophage monoclonal antibodies, ED1 and ED2. The serum CINC concentration in untreated hepatic allograft recipients increased significantly at a constant rate over time after transplantation. No significant increases in serum CINC concentrations were observed in hepatic isografts or allografts treated with the immunosuppressant FK506. The number of neutrophils in untreated hepatic allografts increased significantly at a constant rate. Conversely, neutrophil accumulation in isografts or allografts treated with FK506 was much less than in untreated hepaticallografts. Immunostaining revealed that in the portal areas, mononuclear cells infiltrating untreated allograft liver were mainly positive for CINC and that CINC+ cells represented a subpopulation (approximately 25%) of the ED1+ cells. On the other hand, in the sinusoidal areas CINC+ cells were scattered and mainly positive for ED2. Levels of CINC mRNA in liver tissues taken from untreated hepatic allografts increased after transplantation, peaked on day 5, and decreased thereafter. Hepatic allografts treated with FK506 or isografts showed much lower levels of CINC mRNA than untreated allografts. Allogeneic mixed lymphocyte reactions induced CINC production. The cellular source of CINC was mononuclear cells. CINC production in mixed lymphocyte reactions was inhibited in the presence of anti-tumor necrosis factor alpha (TNF-alpha) antibody. These results suggest that enhanced expression of CINC mRNA and prominent accumulation of neutrophils in the liver grafts are characteristic features of the immune response during acute rejection.

Animals↗
PubMed1997

Mastication-related neurons in the orofacial first somatosensory cortex of awake cats.

In the orofacial area of the first somatosensory cortex (SI), we recorded single unit activity from 699 neurons in 11 awake cats. Fifty-two percent (362/699) were mastication-related neurons (MRNs) showing activity related to some aspects of masticatory movements. MRNs were divided into three types by their activity patterns: (1) the rhythmical type, showing rhythmical bursts in pace with the masticatory rhythm; (2) the sustained type, showing a sustained firing during the period of taking food and (3) the transient (biting) type, showing intense discharges in coincidence with biting hard food. MRNs had mechanoreceptive fields in the perioral, tongue, periodontal and mandibular regions. The activities of perioral rhythmical-MRNs, mandibular transient-MRNs, tongue rhythmical-MRNs and periodontal transient-MRNs were correlated with food texture, while perioral rhythmical-MRNs, perioral sustained-MRNs and tongue sustained-MRMs were not. Both facial and intraoral MRNs were scattered throughout the facial and intraoral projection areas in SI. These findings provide evidence that the orofacial SI monitors masticatory movements for food ingestion.

Afferent Pathways↗