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M Ishida

Publications and source records attributed to M Ishida.

At least 343 records · Page 19Linked to original sources

Acceleration of cell necrosis following reperfusion after ischemia in the pig heart without collateral circulation.

A study of whether reperfusion accelerates cell death was performed in 35 pig hearts without collateral circulation. In 15 animals, the distal one-third of the left anterior descending coronary artery was occluded for 1 hour followed by 1-, 3-, or 7-hour reperfusion in 5 animals each. As controls, 5 hearts each were examined after 1, 2, 4 and 8 hours of occlusion of the artery without reperfusion. Heart rate and aortic pressure before and during occlusion and reperfusion did not change in any group. The subepicardial and subendocardial regional blood flow decreased to almost zero in all hearts after occlusion (85 +/- 1 to 2 +/- 2) but recovered during reperfusion (65 +/- 15 ml/100 g/min). Specimens were histologically examined by an enzyme method using nitrotetrazolium blue, an immunohistochemical method using myoglobin antibody, by staining with hematoxylin-eosin and Masson's trichrome. In the control hearts, clear demarcation of the infarct area was observed 4 hours after occlusion. However, in the reperfusion group, clear demarcation of the infarct was seen after 1-hour reperfusion, namely, 2 hours after the onset of infarct. Demarcation was seen not only in the tissue with contraction band necrosis, but also in the tissue with coagulation necrosis. Therefore, it is concluded that reperfusion accelerates cell death due to both contraction band necrosis and coagulation necrosis.

Animals↗

A conformationally restricted analogue of L-glutamate, the (2S,3R,4S) isomer of L-alpha-(carboxycyclopropyl)glycine, activates the NMDA-type receptor more markedly than NMDA in the isolated rat spinal cord.

Depolarizing actions of 4 conformationally restricted L-glutamate analogues, (2S,3S,4S) isomer (L-CCG-I), (2S,3R,4R) isomer (L-CCG-II), (2S,3S,4R) isomer (L-CCG-III) and (2S,3R,4S) isomer (L-CCG-IV) of L-alpha-(carboxycyclopropyl)-glycine (L-CCG), were investigated in the isolated rat spinal cord by extracellular recordings of potential changes of motoneurones from the ventral roots, in order to study the interaction between the conformation of glutamate and its receptor subtype. The order of the depolarizing activity was quisqualate greater than L-CCG-IV = kainate greater than NMDA greater than L-CCG-I greater than L-CCG-III greater than L-CCG-II. The depolarization caused by L-CCG-IV was effectively blocked by the NMDA antagonists and Mg2+ ions, while the L-CCG-I response was not affected by these blockers. These results suggest that the NMDA-type receptor is activated by a folded form of L-glutamate.

Action Potentials↗

Affinity of single- or double-stranded oligodeoxyribonucleotides containing a thymine photodimer for T4 endonuclease V.

A gene for T4 endonuclease V was constructed by joining chemically synthesized oligodeoxyribonucleotides and expressed efficiently in Escherichia coli under the control of the E. coli tryptophan promoter. Overproduced T4 endonuclease V, which can cleave thymine photodimers as well as the corresponding phosphodiester linkage of DNA, was used to investigate the precise mode of the reaction with single- or double-stranded synthetic DNA fragments containing a thymine photodimer. The substrates, three oligodeoxyribonucleotides, d(GCGGTTGGCG) (10-mer), d(CGAAGGTTGGAAGC) (14-mer), and d(CACGAAGGTTGGAAGCAC) (18-mer), were prepared by UV irradiation of the nascent oligonucleotides. These single-stranded oligonucleotides were cleaved by the enzyme with a concentration 100 times higher than that required for the corresponding duplexes. The Km values for the TT duplex (14- and 18-mer) were found to be on the order of 10(-8) M. Dissociation constants for the 14- and 18-mer duplexes were measured by a binding assay on a nitrocellulose filter and found to be 10(-9).

Amino Acid Sequence↗

Breast cancer imaging with mouse monoclonal antibodies.

The localization of 111In-labelled MA5 monoclonal antibody, reactive with a breast tumor associated antigen, was studied in 17 patients. MA5 was selected because 1) it reacts with greater than 95% of primary and metastatic lesions, 2) the recognized antigen is present on the cell surface in vivo and 3) MA5 gives excellent localization in human breast tumor xenografts. Each patient received 2 mg antibody labeled with 5 mCi 111In and in some cases, 3 mg or 18 mg unlabeled carrier antibody. No serious allergic reactions were noted. There was a large uptake in the liver, less significant uptake in the spleen and bone, and minimal accumulation in the bowel. Bone lesions, primary tumors, soft tissue recurrences and lung metastases larger than 3 cm diameter were imaged, while only 1 lesion smaller than 3 cm was detected. Non specific accumulation of tracer was noted at the site of a port-a-cath, in a hematoma, in fibrocystic lesions, and at sites of previous radiation treatment. Extensive fibrosis and poor vascularization characteristic of breast tumors may explain in part the limited sensitivity of the imaging.

Antibodies, Monoclonal↗

A prognostic evaluation of endoscopic intravariceal injection sclerotherapy for esophageal varices.

Eighty cases of endoscopic injection sclerotherapy for esophageal varices were retrospectively studied to evaluate their prognoses. These cases were evaluated in terms of post-therapeutic bleeding, survival rates and causes of death. Post-therapeutic bleeding occurred in 50% of the emergency cases (26 cases), 25% of the elective cases (16 cases) and 23.7% of the prophylactic cases (38 cases). The frequency of post-therapeutic bleeding was significantly lower in cases with variceal obliteration than in cases without obliteration. An evaluation of the survival rates by the Kaplan-Meier method revealed that poor prognostic factors in sclerotherapy cases were emergency cases, Child's C group, post-therapeutic cases with unsuccessfully obliterated varices, and cases with post-therapeutic bleeding. Concerning early death within 7 days after sclerotherapy, 4 emergency cases died from initial variceal bleeding despite sclerotherapy. Three of these 4 were hepatocellular carcinoma cases, and all 3 cases had tumor thrombi of the portal vein. We recommend prophylactic sclerotherapy from the standpoint of the prognosis after sclerotherapy. However, in the bleeding cases of hepatocellular carcinoma in Child's C group complicated by tumor thrombi of the portal vein, overly enthusiastic application of the therapy should be avoided.

Actuarial Analysis↗

Depression of decerebrate rigidity in the rat by antagonists of excitatory amino acids.

Effects of intravenous antagonists of excitatory amino acids on decerebrate rigidity in the rat were examined. Kynurenate, ketamine, (4S, 5R)-4-(2-methylpropyl)-3-[3-(perhydroazepin-1-yl)propyl]-5-phenyl- 1,3- oxazolidin-2-one hydrochloride (MLV-6976), (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclo-hepten-5,10-imine maleate (MK-801), 3-((/-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) and DL-2-amino-7-phosphonoheptanoic acid (APH) reduced the severity of decerebrate rigidity in a dose-dependent manner, although there was a large variability in the effective doses. The blood pressure, which was determined simultaneously, did not show a uniform change in the presence of these antagonists. The time course of the change of the blood pressure did not coincide with that of decerebrate rigidity. These results suggest a possibility that the glutamatergic system may function, at least in part, in the onset of the decerebrate rigidity.

Amino Acids↗

Response of large and small coronary arteries of pigs to intracoronary injection of acetylcholine: angiographic and histologic analysis.

With coronary arteriography we examined the effect of acetylcholine (ACh) on large and small coronary arteries. ACh (12.5 to 200 micrograms) was injected into the right coronary arteries of 10 pigs during left ventricular pacing. The percentage of narrowing of the epicardial major coronary artery was used as an indicator of the constriction of the large coronary arteries, and the time required for the contrast medium to reach the posterior descending coronary artery from the ostium of the right coronary artery (blood-flow delay) was used as an indicator of the constriction of the same coronary arteries. A small dose of ACh (12.5 to 100 micrograms) induced mild narrowing (14 to 41%) of the epicardial major coronary artery and a marked blood-flow delay of over 7.0 sec (control: less than or equal to 1.8 sec) in all 10 pigs. A large dose of ACh (100 to 200 micrograms) caused over 75% narrowing of the epicardial major coronary artery and a marked blood-flow delay in 4 of the 10 pigs. When the marked blood-flow delay appeared, the perfused right ventricular myocardium became macroscopically anemic (ischemic). The constriction of large and small coronary arteries was not prevented by diphenhydramine (H1 blocker: 100 mg i.v.), but was prevented by pretreatment with atropine (1.0 mg i.v.). The intracoronary injection of histamine (1.5 mg) in 5 pigs constricted the epicardial major coronary artery over 75% in 2 pigs, 50 to 75% in 1 pig, and 25 to 50% in 2 pigs, but there was no evidence of blood-flow delay. Neither methoxamine nor norepinephrine caused any significant coronary artery narrowing. The histology of the large and small coronary arteries was examined quantitatively with an image analyzer. The coronary artery showed no intimal thickening, and the endothelium was intact on light microscopic examination. The % area of the smooth muscle layer (media) to the calculated total vascular area, and the ratio of the calculated medial thickness to the calculated inner radius (h/Ri) were 64 +/- 7% (mean +/- SD) and 0.69 +/- 0.16, respectively, in the small coronary arteries less than 100 microns in external diameter, 47 +/- 9% and 0.39 +/- 0.12 in the small coronary arteries 100 to 2000 microns in external diameter, and 34 +/- 4% and 0.24 +/- 0.03 in the large right coronary arteries over 2000 microns in external diameter; the % area of the media and the h/Ri showed a negative correlation with the size of the coronary arteries.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗

Influence of propranolol on high energy phosphate and tissue acidosis in regional ischemic myocardium of pigs: assessment with arterial pressure and respiration gated in vivo 31-phosphorus magnetic resonance spectroscopy.

In an attempt to define the metabolic abnormalities of the ischemic myocardium, the changes in high energy phosphates, inorganic phosphate and intracellular pH were serially and quantitatively evaluated in ischemic porcine hearts having no collateral circulation, using arterial pressure and respiration gated in vivo 31P magnetic resonance spectroscopy. The protocol was also modified for propranolol pretreatment (0.6 mg/kg intravenously) to define its effect on the metabolism of ischemic myocardium. In the non-treated group, creatine phosphate was rapidly depleted by 10 minutes after ischemia; by 40 minutes, ATP and intracellular pH gradually decreased to 10 +/- 11% of control and to 5.90 +/- 0.26, respectively, and inorganic phosphate rose to 303 +/- 43% of control. In the propranolol treated group, the concentrations of creatine phosphate and ATP were higher, and those of inorganic phosphate and tissue pH were similar compared with controls during 40 minutes of ischemia. This suggests that the beneficial effect of propranolol on the ischemic myocardium is due to the preservation of ATP, an essential energy resource for numerous enzymatic reactions in viable myocardium.

Acid-Base Equilibrium↗

Potent NMDA-like actions and potentiation of glutamate responses by conformational variants of a glutamate analogue in the rat spinal cord.

1. Neuropharmacological actions of all possible-state isomers of alpha-(carboxycyclopropyl)glycine (CCG), conformationally restricted analogues of glutamate, were examined for electrophysiological effects in the isolated spinal cord of the newborn rat. 2. Eight CCG stereoisomers demonstrated a large variety of depolarizing activities. Among them, the (2R, 3S, 4S) isomers of CCG (D-CCG-II) showed the most potent depolarizing activity, followed by the (2S, 3R, 4S) isomer (L-CCG-IV). 3. The depolarization evoked by L-CCG-IV, D-CCG-II and other D-CCG isomers was effectively depressed by N-methyl-D-aspartate (NMDA) antagonists. D-CCG-II was about 5 times more potent than NMDA in causing a depolarization. 4. The (2S, 3S, 4S) isomer of CCG (L-CCG-I) was more potent than L-glutamate in causing a depolarization of spinal motoneurones. The depolarization was slightly depressed by NMDA antagonists, but residual amplitudes of responses to L-CCG-I in the presence of NMDA antagonists We almost insensitive to 6,7-dinitro-quinoxaline-2,3-dione (DNQX) or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), suggesting that L-CCG-I might be a novel potent agonist. 5. After application of the (2S, 3S, 4R) isomer of CCG (L-CCG-III), responses to L-glutamate, D- and L-aspartate were markedly enhanced. The enhancement lasted for a period of several hours without a further application of L-CCG-III. 6. L-CCG-III also caused a depolarization, but it seemed unlikely that the potentiation of the glutamate response was directly related to the depolarization evoked by L-CCG-III. 7. The potentiation might be due to inhibition of uptake processes, but L-CCG-III was superior to L-(-)-threo-3-hydroxyaspartate, a potent uptake inhibitor of L-glutamate and L-aspartate, in enhancing the response to L-glutamate in terms of amplitude and duration of responses. 8. CCG isomers should provide useful pharmacological tools for analysis of glutamate neurotransmitter systems.

Amino Acids, Dicarboxylic↗

Cineangiographic and pathological features of the infarct related vessel in successful and unsuccessful thrombolysis.

The postmortem histology and the results of cineangiography after selective intracoronary thrombolysis in vessels that were recanalized and in those that were not were compared in 21 patients who died within seven days (mean 2 days) of selective intracoronary thrombolysis. There was a persistent intraluminal thrombus in the infarct related coronary artery in five of six segments in which recanalisation was unsuccessful and in one of 15 segments in which recanalisation was successful. Rupture and haemorrhage of the atheromatous plaque were seen in most of the infarct related segments, both in those in which recanalisation was achieved and in those in which it was not. Irregular narrowing and filling defects on the coronary cineangiograms were associated with rupture and haemorrhage of the atheromatous plaque. These results suggest that failure of coronary thrombolysis to recanalize the infarct related artery does not indicate that the occlusion was not caused by thrombus.

Aged↗

Related glycoproteins from normal secretory and malignant breast cells. Purification and initial comparative characterizations.

Monoclonal antibody MA5 recognizes an epitope present on the surface and in the cytoplasm of human breast cancer cells and on the human milk fat globule membrane (MFGM). These immunoreactive determinants are found on tumor-associated glyco-proteins with apparent molecular weights of 280 and 300 kdaltons, whereas the cross-related milk fat globule membrane antigen appears larger (330 kdaltons). Comparative electrophoretic migration analyses following neuraminidase digestion, as well as differential binding to various lectins, established that these molecules are extensively sialylated, and that the tumor antigens were sialylated to a greater extent than normal antigen. Immunoaffinity purification of this class of differentiation antigens from tumor and MFGM demonstrated similar size distributions, lectin affinities and buoyant densities as their respective crude antigens.

Antibodies, Monoclonal↗

Ventricular expression of atrial natriuretic polypeptide and its relations with hemodynamics and histology in dilated human hearts. Immunohistochemical study of the endomyocardial biopsy specimens.

To investigate the mechanism of expression of atrial natriuretic polypeptide (ANP) in human ventricles, we conducted an immunohistochemical study of ANP in biventricular endomyocardial biopsy specimens obtained from a total of 49 patients with cardiac dilatation due to dilated cardiomyopathy (21 patients), postmyocarditis (18 patients), or volume overload (five patients) and subjects with no dilatation as controls (five patients). Four-micron thick sections were stained by an indirect immunoperoxidase method using monoclonal antibody to alpha-human ANP as the primary antibody. The frequency of ANP-present myocytes was calculated in each specimen and compared with clinical, echocardiographic, hemodynamic, angiographic, and histologic parameters. ANP-present myocytes were noted in all of the 21 patients with dilated cardiomyopathy, in 11 of the 18 patients with postmyocarditis, in four of the five patients with volume overload, and in zero of the five controls. The mean percentage of ANP-present myocytes was significantly greater in the left-side specimens (35 +/- 37%) than in the right-side ones (2 +/- 4%). The percentage of ANP-present myocytes in the left-side specimens significantly correlated with peak systolic or end-diastolic wall stress (r = 0.67 and 0.58), left ventricular end-systolic or end-diastolic volume index (r = 0.75 and 0.69), or left ventricular end-diastolic pressure (r = 0.42) and inversely correlated with ejection fraction (r = -0.73), systolic left ventricular wall thickness (r = -0.58), or cardiac index (r = -0.30). Expression of ANP was rarely seen in the cases with normal wall stresses, normal ejection fraction, normal volume, or normal myocyte size. However, it was seen frequently even in hearts with normal levels of left ventricular end-diastolic pressure and cardiac index (compensated hearts). The percent of ANP-present myocytes in both sides significantly correlated with size of myocytes (r = 0.48 at right and r = 0.57 at left side) or degree of fibrosis (r = 0.45 at right and r = 0.48 at left side). These results suggest that ANP expression is augmented in the dilated ventricles regardless of the causes of dilatation and that the augmentation is a compensatory mechanism as prevention against decompensation responding to reduced contractility, excess of wall stresses, or both, concomitantly occurring with cardiac dilatation and myocardial hypertrophy.

Adult↗

Infarct size and the protection of ischemic myocardium in pig, dog and human.

To define whether recanalization after occlusion can reduce the myocardial infarct size, we compared the infarct size in 25 pig hearts without collateral circulation, 35 dog hearts with collateral circulation and 11 human autopsied hearts with coronary thrombolysis at 2 to 6 hours after the onset of acute myocardial infarction. The data showed that % infarct size in the risk area increased according to the duration of occlusion. In the pig, % infarct size was 80 +/- 9% in the recanalization after 1 hour occlusion and 96 +/- 2% in the recanalization after 2 hour occlusion. There was no significant difference between these and the permanent occlusion group (95 +/- 3%). In the dog, % infarct size was 35 +/- 31% in the recanalization after 4 hour occlusion and 59 +/- 27% in the permanent occlusion group. In human autopsied hearts, the infarct size was the same between the recanalization group (82 +/- 6%) and the permanent occlusion group (80 +/- 11%). The % infarct size in the recanalization groups was less than or the same as that in the hearts with permanent occlusion in dog, pig and human. Thus, it is concluded that, to reduce conclusively the infarct size, recanalization should be done within 1 hour after the occlusion in the hearts without collateral circulation and within 4 hours in the hearts with collateral circulation. So called reperfusion injury which means the greater expansion of the % infarct size than that in the permanent occlusion is not present.

Animals↗

Immunohistochemical localization and semi-quantification of atrial natriuretic polypeptide (ANP) in formalin-fixed-paraffin-embedded normal human hearts--comparative study with radioimmunoassay.

The presence of atrial natriuretic polypeptide (ANP) was immunohistochemically demonstrated in the formalin-fixed and paraffin-embedded tissues of 25 autopsied normal human hearts using monoclonal antibody. The ANP amounts were immunohistochemically semiquantified and compared with amounts measured by radioimmunoassay (RIA). The 25 autopsied hearts were divided into 5 groups according to the interval of formalin fixation or the length of time between death and fixation. Formalin-fixation intervals were one week in group 1A and 1B; 1 year in group 2; 4 to 5 years in group 3 and 10 to 12 years in group 4. The hearts of group 1A, 2, 3 and 4 were fixed within 5 hours after death. Those of group 1B were fixed 14 to 18 hours at 4 degrees C. After fixation, the left and right atrial appendages (LAA and RAA), the left and right atrial free walls (LA and RA), the left and right ventricular free walls (LV and RV) and the ventricular septum (VS) were transmurally dissected from each heart. They were embedded in paraffin, cut into 4 microns sections and immunohistochemically stained by the avidin-biotin-peroxidase complex (ABC) method using monoclonal antibody against alpha-human ANP. Under a light microscope, they were evaluated semiquantitatively according to the incidence of ANP-positive cells and the intensity of immunostaining. For every heart in group 1A, the tissue concentrations of ANP in the different parts were also measured separately by RIA before fixation. ANP-positive myocytes were noted in the atria of all hearts of all groups, but no in any ventricular myocytes. Both their incidence and grade in the atria were similar among groups 1A, 1B and 2. However, they were less in group 3, and least in group 4 among all groups. For all groups, they decreased in the following order: LAA greater than RAA not equal to LA greater than RA; the inner 1/3 greater than the middle 1/3 greater than the outer 1/3 of the atrial walls. The order in LAA, RAA, LA and RA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Anti-TSH antibodies in Graves' disease and their failure to interact with TSH receptor antibodies.

The occasional occurrence in sera of patients with Graves' disease of negative values in the assay for TSH receptor antibodies led to the discovery of endogenous antibodies to TSH. We examined the sera of approximately 2500 patients with Graves' disease. Eight positive sera were found. The IgG in all 8 sera showed higher binding with both bTSH and porcine TSH (pTSH) than with human TSH (hTSH). This means that autoantibodies to TSH in sera from patients with Graves' disease are rare and often directed towards heterologous bovine and porcine TSH. When hTSH levels were determined in sera of hyperthyroid patients with positive antibodies to hTSH, discrepancies in serum hTSH levels were observed when using different assay methods, i.e. hTSH levels were higher with the double-antibody technique, and lower with immunoradiometric assays. Antibodies in these sera showed higher binding to pTSH-alpha subunit than to -beta subunit. The binding of the two pTSH subunits with antibodies could be displaced by intact bTSH. Neither stimulation in Graves' disease nor blocking in primary hypothyroidism of TSH receptor antibodies interfered with the binding of the anti-TSH antibodies to 125I-labelled pTSH, pTSH-alpha, and pTSH-beta. Consequently, using this type of autoantibodies to TSH we were unable to obtain evidence that the TSH receptor antibodies of patients with Graves' disease was an anti-idiotype antibody against anti-TSH antibodies.

Graves Disease↗

Enterohepatic circulation of 2,4-dinitrobenzaldehyde, a mutagenic metabolite of 2,4-dinitrotoluene, in male Wistar rat.

1. The major biliary metabolite of 2,4-dinitrotoluene (2,4-DNT) in male Wistar rat was 2,4-dinitrobenzyl alcohol glucuronide and the minor metabolites were 2,4-dinitrobenzyl alcohol, 2,4-dinitrobenzaldehyde, 2-acetylamino-4-nitrotoluene, 4-amino-2-nitro(2-amino-4-nitro)benzyl alcohol sulphate, 2,4-dinitrobenzoic acid, 2,4-diacetylaminobenzoic acid and 2-amino-4-nitrobenzoic acid. 2. 2,4-Dinitrobenzyl alcohol, 2,4-dinitrobenzaldehyde, 2,4-dinitrobenzyl alcohol glucuronide and 4-amino-2-nitro(2-amino-4-nitro)benzyl sulphate were excreted in the bile of male Wistar rat dosed with 2,4-dinitrobenzyl alcohol. 3. 2,4-Dinitrobenzaldehyde, 2,4-dinitrobenzyl alcohol, 2,4-dinitrobenzyl glucuronide, 4-amino-2-nitro(2-amino-4-nitro)benzyl alcohol sulphate and 2,4-diacetylaminobenzoic acid were excreted in the bile of male Wistar rat dosed with 2,4-dinitrobenzaldehyde. 4. These results indicate that the common biliary metabolites of 2,4-DNT, 2,4-dinitrobenzyl alcohol and 2,4-dinitrobenzaldehyde are 2,4-dinitrobenzyl alcohol and its glucuronide, and 2,4-dinitrobenzaldehyde, and suggest the enterohepatic circulation of 2,4-dinitrobenzaldehyde in the metabolism of 2,4-DNT.

Animals↗

[Mucormycosis in paranasal sinuses].

Paranasal sinus mucormycosis is a rare and often fatal condition that occasionally occurs in patients with debilitating disease. Five mucormycosis cases with paranasal sinus involvement are reported. Two also complicated diabetes mellitus. These diabetic patients rapidly developed meningitis after the onset of symptoms. One case was soon operated upon and necrotic masses with fungus were excised. Despite i.v. amphotericin B administration, two patients lost their consciousness in a few days, relapsed into coma and died. In these cases, the infection originated from the ethmoidal sinus and directly spread towards the orbit and brain. The remaining three cases with mucormycosis had operations after the initial diagnosis of sinusitis. All of the three patients are alive and well. The combination of an excisional operation and antifungal therapy resulted in favorable response. High resolution CT scanning is valuable both in planning treatment and monitoring the response to therapy.

Adult↗

Cross-reactivity between human and canine helper and suppressor T cell antigens using monoclonal antibodies RPA-T4 and HuLy-m8.

The murine monoclonal antibodies RPA-T4 and HuLy-m8, specific for a framework determinant of human helper/inducer and suppressor/cytotoxic T cell antigens, cross-reacted with canine cell membrane molecules recognizing a biomolecular complex (50,000 to 55,000 daltons) similar to that described in humans. We investigated the distribution of these helper and suppressor T cell-like antigens on canine peripheral blood lymphocytes. With complement-mediated lymphocytotoxicity, 34% and 35% of the canine lymphocytes expressed the helper T cell-like antigens and the suppressor-like T cell antigens, respectively. When the lymphocytes were treated with RPA-T4 and HuLy-m8, the respective helper and suppressor function was significantly inhibited.

Animals↗