Search PubMed⌕ Search

Biomedical subjects

M Endoh

Publications and source records attributed to M Endoh.

At least 163 records · Page 9Linked to original sources
PubMed1996

Intraglomerular C3 synthesis in human kidney detected by in situ hybridization.

Complements 3 and 4 are known to be synthesized in diseased renal tissue and the mRNA of these complements has been demonstrated, using polymerase chain reaction, in renal biopsies from nephritic patients. However, the types of cells producing the complements in intact renal tissue have not been defined. To identify the renal cellular components involved in complement synthesis, we analyzed the expression of C3 mRNA in renal tissues from patients with immune-complex glomerulonephritis by a high-resolution in situ hybridization using digoxigenin-labeled oligonucleotide. Renal tissues from 15 patients with immunoglobulin (Ig) A nephropathy (IgAN), five with lupus nephritis (LN), and five with minimal change nephrotic syndrome (MCNS) were examined. Uninvolved portions of surgically removed kidney with tumors served as normal controls. C3 mRNA was detected in mesangial cells, glomerular epithelial cells, and Bowman's capsule in IgAN and LN. In the interstitium, some tubules and some infiltrating mononuclear cells were positively stained for C3 mRNA. C3 mRNA was not detected in MCNS and control tissues. Our results confirm that the glomerular resident cells can synthesize C3 in immune-mediated glomerulonephritis and suggest that locally synthesized complement may be involved in tissue injury in glomerulonephritis.

Biopsy↗
PubMed1996

A serologic Mycobacteria leprae gelatin particle agglutination (MLPA) in the diagnosis of leprosy: comparison with conventional enzyme-linked immunoassay and bacterial index.

A gelatin particle agglutination test (MLPA) for the detection of anti-phenolic glycolipid-1 (PGL-1) antibodies was compared with the slit skin smear method in the diagnosis of leprosy. MLPA and BI tests showed a good agreement rate of 88.1% and MLPA and ELISA tests showed an excellent agreement rate 96.2%. This MLPA test is simple and reliable, it will be very convenient for the medical practitioners, it would be of great benefit for leprosy patient as well because this test would look like a routine blood examination compared with slit skin smear method which is widely known diagnostic tool for leprosy.

Agglutination Tests↗
PubMed1996

The positive inotropic effect and the hydrolysis of phosphoinositide induced by endothelin-3 in rabbit ventricular myocardium: inhibition by a selective antagonist of ET(A) receptors, FR139317.

Endothelin-3 (ET-3), an isopeptide of ET, had a concentration-dependent positive inotropic effect (PIE) on rabbit papillary muscle. The maximal inotropic response to ET-3 was 65% of the maximal response to isoproterenol. ET-1 elicited a PIE below 10(-9) M, namely, over a concentration range at which ET-3 did not elicit a PIE. The selective ET(A) antagonist FR139317 effectively antagonized the PIE of ET-3. FR139317 abolished the PIE induced by ET-1 (<10(-9)M) but did not inhibit the PIE induced by high concentrations of ET-1. FR139317 also antagonized the PIE of sarafotoxin S6c. ET-3 caused a time- and concentration-dependent increase in [3H]inositol phosphates (inositol monophosphate, inositol bisphosphate and inositol trisphosphate). FR139317 at 10(-5) M decreased the ET-3-induced increase in inositol phosphates by about 60%, whereas it attenuated the increase in [3H]IP1 induced by ET-1 (3 x 10(-8)M) by only 20%. Thus, in the presence of FR139317, the PIEs of ET-3 and ET-1 were partially dissociated from the PI hydrolysis that was induced by these isopeptides. FR139317 inhibited the specific binding of [125I]ET-1 and of [125I]ET-3, and it was apparent that FR139317 had a high-affinity and a low-affinity site for competing for specific binding with each ligand. These findings indicate that different subtypes of the ET receptor are involved in the induction of the PIEs of ET-3 and ET-1. The PIE of ET-3 may be mediated predominantly by ET(A1) receptors that are susceptible to FR139317 and BQ-123 and partially by ET(B) receptor that are inhibited by RES-701-1. Both ET(A1) and ET(A2) receptors may be responsible for the PIE of ET-1, depending on the concentration in rabbit ventricular myocardium.

Animals↗
PubMed1996

Monocyte superoxide generation and its IgA-receptor in IgA nephropathy.

Recent studies indicated that polymorphonuclear leukocytes (PMNL) were primed to produce superoxide (O2-) in various types of glomerulonephritis with a particular importance in IgA nephropathy (IgAN). In this study, we have examined O2- production and receptor expression for the Fc portion of IgA (Fc alpha R) in monocytes to evaluate their incorporation in IgAN, since infiltration of these cells in the glomeruli are more commonly observed than that of PMNL. Similar to PMNL, monocytes obtained from IgA nephropathy (IgAN) seemed to be primed both non-specifically and specifically, as increased O2- generation was observed to N-formyl methionyl leucyl phenylalanine (FMLP) and phorbol myristate acetate (PMA), as well as IgA aggregates stimulants, respectively. Monocytes O2- generation to IgA aggregates was comparatively higher in amount than in PMNL, and showed a correlation with the severity of proteinuria in IgAN patients. Flow cytometric assessment showed an increased expression of Fc alpha R on circulating monocytes in IgAN patients which showed a linear correlation with the amount of IgA-induced O2- generation. Comparing with the previous literature on PMNL, inflammation-related substances such as cytokines/immune complexes, particularly IgA immune complexes which present in the circulation of IgAN, can prime the phagocytic cells in the circulation for a burst of O2- generation to a second stimulus. The increased expression of Fc alpha R appears to be associated with the increase in priming and the degree of priming can be reflected in the severity of proteinuria/hematuria, although it can not be defined as a cause or consequence of this disease.

Adult↗
PubMed1996

[Effect of intra-operative fluid on renal function during hypotensive anesthesia with trimethaphan].

During induced hypotensive anesthesia in 26 cases with trimethaphan, either Ringer's lactate solution (LR group) or 2/3 lactate-saline solution (2/3 LS group) was infused at the same rate. Urine volume, creatinine clearance (Ccr), FENa, urinary gamma-GTP index and urinary Na/K ratio were determined before hypotension, during hypotension and after the operation. During hypotension, FENa and urine Na/K ratio decreased in both groups. In 2/3 LS group, these remained low after the operation compared with the values before hypotension and in LR group. These results suggest that LR solution might depress an endocrine response which is induced by hypotensive anesthesia. As urine volume and Ccr were unchanged by hypotension, and infusion of colloid solution (Hespander) could not increase these figures, circulating blood volume might not be decreased during hypotensive anesthesia. Since urinary gamma-GTP index increased slightly during hypotension or after the operation, there might have been a slight epithelial cell damage of tubules with hypotensive anesthesia.

Adult↗
PubMed1996

[Epidural administration of buprenorphine after combined spinal epidural anesthesia].

We compared the efficacy of epidurally administered buprenorphine (0.2 mg) after combined spinal-epidural anesthesia (CSE group) and that after general anesthesia combined with epidural anesthesia (EPI + GEN group). Postoperatively epidural buprenorphine was administered for initial pain relief significantly later in CSE group than in EPI + GEN group. The duration of pain relief with epidural buprenorphine was similar in both groups (about 11 hours). The time period until postoperative first walk and the number of pain relief medication were also similar in both groups. We had the impression that the onset of pain relief was faster in CSE group, probably because there might be flux of buprenorphine through a dural hole just after epidural administration.

Analgesia, Epidural↗
PubMed1995

Neurotransmitter synthesis by SN6 cell lines, a family of hybrid cell lines of embryonic septal origin.

Previously, we reported the presence of multiple neurotransmitters in subclones of SN6, a septal cholinergic hybrid cell line. To obtain information concerning the functionality of these transmitters, we measured transmitter contents, activities of transmitter-producing enzymes, and the effect of serum-free culture medium in two different batches (SN6.1.6 and SN6.10.2.2) and two subclones of the SN6 cell line (SN6.2a and SN6.1b). Except for SN6.1b, SN6 cell lines and subclones had basically the same neurotransmitter characteristics. Among the transmitters, only acetylcholine seemed to be functional. Monoamine oxidase was missing and activity of aromatic amino acid decarboxylase was diminished in SN6 cell lines. Even in serum-containing medium, SN6.1b had a more mature morphology than the other cell lines, and it contained choline acetyltransferase and acetylcholine but not tyrosine hydroxylase or catecholamines. Similar characteristics were acquired by the mother cell line in response to serum-free conditions. Thus, SN6.1b is the most mature of these central cholinergic neuronal cell lines, at least with regard to neurotransmitter profiles.

Animals↗
PubMed1995

Enhancement of 5-hydroxytryptamine-stimulated phosphoinositide hydrolysis in the rat cerebral cortex by repeated immobilization stress.

The present study was undertaken to investigate the influence of repeated immobilization stress on phosphoinositide hydrolysis induced by 5-hydroxytryptamine (5-HT) and noradrenaline in the rat cerebral cortex. Three groups of rats subjected to stress intervention were immobilized for 2 h per day for 3, 7, and 14 days. The stress intervention of any duration did not alter noradrenaline-stimulated phosphoinositide hydrolysis. The 3- and 7-day repeated immobilization enhanced 5-HT-stimulated phosphoinositide hydrolysis, whereas the characteristics of 5-HT2 receptor binding did not change. Chronic treatment with imipramine partially, but significantly, suppressed the increase in 5-HT-stimulated phosphoinositide hydrolysis, induced by the 3-day repeated immobilization. These findings imply that modulation of 5-HT-stimulated phosphoinositide hydrolysis occurs in stressful situations and that the therapeutic effects of tricyclic antidepressant drugs might be related to the modulation of phosphoinositide hydrolysis mediated by 5-HT receptors.

Animals↗
PubMed1995

Angiotensin II activation of a chloride current in rabbit cardiac myocytes.

1. The effects of angiotensin II (Ang II) on membrane currents were investigated in single ventricular myocytes from the rabbit heart by the whole-cell voltage-clamp method. 2. In the presence of an inhibitor of Ca2+ currents (nifedipine at 3 microM or CdCl2 at 0.3 mM) and a beta-adrenoceptor blocker (bupranolol at 1 microM), 1 microM Ang II significantly increased the membrane conductance. 3. After elimination of K+ from external and internal solutions and its replacement by Cs+, Ang II at 0.1 microM increased an outwardly rectifying current that reached a maximum after about 40 min. The effect was concentration dependent (10(-9)-10(-6) M) and was inhibited by saralasin, an antagonist of Ang II receptors. 4. The reversal potential of the Ang II-induced current in the absence of K+ was compatible with the Cl- equilibrium potential at various external concentrations of Cl-. 5. A Cl- channel blocker, 4,4'-dinitrostilbene-2,2'-disulphonic acid (DNDS, at 5 mM), reversibly decreased the Ang II-induced current. 6. The Ang II-induced current developed when the internal solution contained Ca2+ (pCa 7.2 or 7.0) but not when it contained 10 mM EGTA without Ca2+. 7. Besides developing a Cl- current, Ang II at 1 microM increased the inwardly rectifying K+ current (IK1) and this effect reached maximum within 3 min. 8. The effect of Ang II on the action potential was biphasic: the duration of the action potential was initially reduced and then it was increased. 9. These results suggest that Ang II induces a Cl- current that appears likely to modulate the action potential in rabbit ventricular myocytes.

Action Potentials↗
PubMed1995

Acetylcholine and adenosine activate the G protein-gated muscarinic K+ channel in ferret ventricular myocytes.

The properties of the K+ channel activated by acetylcholine (ACh) and adenosine (Ado) were examined in single ferret ventricular myocytes using patch-clamp techniques. In the whole-cell configuration, ACh and Ado induced an inwardly rectifying K+ current and shortened the action potential duration. The effect of ACh was blocked by atropine, while the Ado effect was interrupted by 8-cyclopentyl,1,2-dipropyl xanthine, a specific Ado A1 receptor antagonist. In cell-attached recordings, ACh and Ado added to the pipette solution activated a single population of inwardly rectifying K+ channels, distinct from the iK1 channel. The channel had a slope conductance of approximately 40 pS in symmetrical 150 mM K+ solutions and a mean open time of 0.8 ms. Excision of the patch into the inside-out patch configuration in guanosine triphosphate (GTP)-free solution abolished the channel activity. The channel was reversibly reactivated by adding GTP to the intracellular side of the patch. GTP gamma S activated the channel irreversibly. When the inside-out patch was treated with the A protomer of pertussis toxin (PTX), intracellular GTP no longer activated the K+ channel. The results show that ferret ventricular myocytes possess a K+ channel activated by both muscarinic and Ado A1 receptors. Its electrophysiological properties and the gating by a PTX-sensitive G protein in a membrane-delimited fashion are identical with those of the muscarinic K+ channels in nodal and atrial tissues of other species. In conclusion, the G protein-gated muscarinic K+ channel is expressed in ferret ventricular myocardium and may underlie the direct negative inotropism of ACh and Ado in this tissue.

Acetylcholine↗
PubMed1995

The effects of various drugs on the myocardial inotropic response.

1. The signal transduction process mediated by cyclic AMP that leads to the characteristic positive inotropic effect (PIE) in association with a positive lusitropic effect (acceleration of rate of twitch relaxation) has been well established. Relationships between accumulation of cyclic AMP, changes in intracellular Ca2+ transients and the PIE differ, however, depending on the mechanism of particular drugs that affect different steps in the metabolism of cyclic AMP. Selective partial agonists of beta 1-adrenoceptors and inhibitors of phosphodiesterase (PDE) III cause the accumulation of less cyclic AMP for a given PIE than does isoproterenol. In addition, in aequorin-microinjected canine ventricular muscle, selective inhibitors of PDE III, OPC 18790 and Org 9731, produced smaller decreases in the responsiveness of myofilaments to Ca2+ ions than isoproterenol, while a partial agonist of beta 1-adrenoceptors, denopamine, elicits a decrease in Ca2+ responsiveness of the same extent as does isoproterenol. 2. Activation of myocardial alpha 1-adrenoceptors, as well as stimulation of receptors for endothelin and angiotensin II, which accelerates hydrolysis of phosphoinositide (PI) to result in production of inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG) are associated with very similar inotropic regulation: (1) the dependence on the species of animals of induction of the PIE; (2) an excellent correlation between the extent of acceleration of hydrolysis of PI and the PIE; (3) isometric contraction curves associated with a negative lusitropic effect; (4) the PIE associated with increases in myofibrillar responsiveness to Ca2+ ions; and (5) the selective inhibition of the PIE by an activator of protein kinase C (PKC), phorbol 12,13-dibutyrate (PDBu), with little effect on the PIE of isoproterenol and Bay k 8644. 3. A novel class of cardiotonic agents, namely, Ca2+ sensitizers such as EMD 53998 and Org 30029, act on the Ca(2+)-binding site of troponin C, increasing the affinity of these sites for Ca2+ ions, or at the actin-myosin interface to facilitate the cycling of cross-bridges. These agents produce a PIE with little change or decrease in Ca2+ transients and may bring about a significant breakthrough in the development of drugs for reversal of myocardial failure in the treatment of congestive heart failure.

Adenosine↗
PubMed1995

Effects of a novel cardiotonic agent, Org 9731, on force and aequorin light transients in intact ventricular myocardium of the dog: involvement of a cyclic AMP-mediated mechanism and myofibrillar responsiveness to Ca2+ ions.

The action of a novel cardiotonic agent, Org 9731 (4-fluoro-N-hydroxy-5, 6-dimethoxy-benzo[b]thiophene-2-carboximidamide methanesulphonate), on intracellular aequorin light transients and isometric contractions was investigated in ventricular trabeculae isolated from dogs. The positive inotropic effect of Org 9731 at 3 microM and higher (up to 0.1 mM) was associated with an increase in the amplitude of the intracellular Ca2+ transient, but the effect of the compound at 0.3 and 1 mM was accompanied by a decrease of the transient. The maximum inotropic response to Org 9731 was approximately 70% of the maximum response to isoproterenol, while the maximum increase in the amplitude of Ca2+ transients produced by Org 9731 was about 30% of the maximum increase induced by isoproterenol. The duration of isometric contractions was prolonged by Org 9731 at 0.3 and 1 mM, with accompanying prolongation of the duration of light transients. The concentration-response curve for the positive inotropic effect of Org 9731 was markedly shifted by carbachol (3 microM), being moved to the right and downward, and the maximum response to Org 9731 was about 10% of that to isoproterenol in the presence of carbachol. Carbachol abolished the increase in the light transient and the accumulation of adenosine 3',5'-cyclic monophosphate (cyclic AMP) induced by Org 9731. These results indicate that Org 9731 increases cardiac contractility, mainly through the accumulation of cyclic AMP up to a concentration of 0.1 mM and also by increasing the responsiveness of myofibrils to Ca2+ ions at 0.3 mM and higher in association with the attenuation of Ca2+ transients. The structure-activity relationship implies that the introduction of a fluorine atom at position 4 of the benzothiophene ring of Org 30,029 attenuated its Ca(2+)-sensitizing action but markedly increased the activity of mechanisms dependent on cyclic AMP.

Aequorin↗
PubMed1995

The G-protein G(o) in mammalian cardiac muscle: localization and coupling to A1 adenosine receptors.

To investigate the functional relevance of the G-protein G(o) to adenosine-induced effects in the heart, we studied the localization of G(o) and its interaction with A1 adenosine receptors. Concentrations of G(o) in various mammalian hearts differed markedly between the atrial and the ventricular muscle, as well as among species. In most species examined, the concentration of G(o) was much higher in the atrium than in the ventricle. The highest levels of G(o) in atria and ventricles were found in the ferret heart. An immunohistochemical study of the ferret heart with G(o) alpha-specific antibodies showed that G(o) was localized throughout the membranes of cardiac myocytes, including the intercalated disks. In addition, G(o) was densely distributed in the nerve fibers and Purkinje fibers. Analyses of G(o) alpha subtypes showed that bovine atrium mainly contained G(o)A alpha, while bovine ventricle contained only G(o)B alpha. By contrast, ferret ventricle contained both subtypes of G(o) alpha. To study the coupling of G(o) to A1 adenosine receptors, receptors in ventricular membranes of ferrets, which had been pretreated with pertussis toxin, or purified receptors were reconstituted with purified G(o)A and G(o)B. The reconstitution experiments indicated that both subtypes of G(o) coupled with A1 adenosine receptors. These results suggest that the effect of adenosine is mediated by both G(o)A and G(o)B in membranes of ferret cardiac myocytes.

Animals↗
PubMed1995

Species-related differences in inotropic effects of angiotensin II in mammalian ventricular muscle: receptors, subtypes and phosphoinositide hydrolysis.

1. Experiments were carried out to clarify the mechanisms responsible for variations in the positive inotropic effect (PIE) of angiotensin II (AII) on ventricular muscles from various mammals. We examined the density of AII receptors, the relative proportions of receptor subtypes and the acceleration of the hydrolysis of phosphoinositide that was induced by AII, as well as the PIE of AII in ventricular muscles from the rabbit, dog, rat and ferret. 2. In the rabbit, AII (1 microM) in the presence of bupranolol (0.3 microM) and prazosin (0.1 microM) elicited a concentration-dependent PIE, which was antagonized by a selective AT1 subtype antagonist, losartan, but not by an AT2 antagonist, PD123319. AII did not have any inotropic effects in ventricular muscles from the dog, rat and ferret. 3. Specific high-affinity binding of [125I]-AII, with a similar Kd value in each case (1-2 nM), was observed with membrane fractions derived from ventricular muscle of all four species tested. 4. In the rabbit, losartan and PD123319 each displaced approximately 50% of [125I]-AII specific binding having high affinity for the receptors, and indicating that AT1 and AT2 subtypes were present in equal numbers. In the other species the AT1 subtype of receptors was predominant. 5. In all four species AII caused a concentration-dependent acceleration of the hydrolysis of phosphoinositide in ventricular slices that had been prelabelled with myo-[3H]-inositol. 6. The results indicate that the signal-transduction process distal to acceleration of the hydrolysis of phosphoinositide may be responsible for the wide range of species variations in the inotropic action of AII on mammalian ventricular myocardium.

Angiotensin I↗
PubMed1995

Calcium compartments in vascular smooth muscle cells as detected by aequorin signal.

1. To examine whether cytosolic Ca2+ in smooth muscle cells distributes evenly, cytosolic Ca2+ levels were measured with two different Ca2+ indicators in the ferret isolated portal vein; a fluorescent indicator, fura-PE3, that shows the average Ca2+ level, and a photoprotein, aequorin, that preferentially shows a high Ca2+ compartment. 2. A noradrenaline (10 microM)-induced sustained contraction was associated with a sustained increase in the fura-PE3 signal, or a transient increase followed by small sustained increase in the aequorin signal. A high K(+)-induced contraction was associated with a sustained increase in both the fura-PE3 and aequorin signals. 3. A second application of noradrenaline or high K+ induced reproducible contractions and fura-PE3 signals. In contrast, the aequorin signal resulting from a second application of noradrenaline or high K+ was much smaller than the first signal. 4. Following a 13 h but not a 3 h resting period, the aequorin signal stimulated by noradrenaline or high K+ recovered, without any change in the contractile response. 5. In Ca(2+)-free solution, high K+ was ineffective, whereas noradrenaline induced only a small aequorin signal and contraction compared to those obtained in the presence of external Ca2+. After the addition of Ca2+, the first application of noradrenaline induced a large aequorin signal and a large contraction, although a second application induced a much smaller aequorin signal accompanied by a large contraction. 6. These results suggest that high K+ and noradrenaline increase Ca2+ in at least two cytosolic compartments; a compartment that is coupled to the contractile mechanism ('contractile' Ca2+ compartment; major portion of cytoplasm containing contractile elements) and a compartment that is not coupled to contractile mechanisms ('non-contractile' Ca2+ compartment; small sub-membrane area that does not contain contractile elements). On stimulation, the Ca2+ level in the 'contractile' compartment may increase to a level high enough to stimulate myosin light chain kinase but not so high as to consume aequorin rapidly. In contrast, the Ca2+ level in the 'non-contractile' compartment may increase so greatly that aequorin in this compartment is rapidly consumed. These two compartments may be separated by a diffusion barrier and, during a resting period, aequorin may slowly diffuse from the 'contractile' compartment to the 'non-contractile' compartment and thus restore the full aequorin signal. An increase in Ca2+ in the 'non-contractile' compartment seems to be dependent mainly on Ca2+ influx and partly on Ca2+ release.

Aequorin↗
PubMed1995

In situ hybridization of interleukin 6 in diabetic nephropathy.

Increased mesangial expansion is one of the most characteristic histological changes in diabetic nephropathy (DN). Although the pathogenesis of DN remains unclear, recent studies associate interleukin (IL) 6 with mesangial proliferative glomerulonephritis. To elucidate the expression and localization of IL-6 mRNA in renal tissues of patients with DN, a high-resolution in situ hybridization using digoxigenin-labeled oligonucleotide was performed. Patients were divided into three groups based on light microscopy findings: mild (group 1), moderate (group 2), and severe (group 3) mesangial expansion. The relationship between the expression of IL-6 mRNA and the degree of glomerular mesangial expansion in DN was examined. Individual cells positive for IL-6 mRNA were observed in glomeruli. These cells were mesangial cells, glomerular epithelial cells, and Bowman's capsule. The signal intensity was strongest in tissues from group 2 but was weak in those from groups 1 and 3. Most cells in the area of mesangial proliferation were strongly stained for IL-6 mRNA, and few positive cells were found in the Kimmelstiel-Wilson nodular lesion. In the interstitium, some tubules, particularly atrophic tubules, and some infiltrating cells were positively stained for IL-6 mRNA. The interstitial expression of IL-6 mRNA correlated significantly with the degree of interstitial injury and was remarkable in tissues from groups 2 and 3. We conclude that IL-6 mRNA is expressed by glomerular resident cells and interstitial cells in the renal tissue of patients with DN and that its expression may be associated with mesangial proliferation and may be involved in the tissue injury of DN.

Adolescent↗
PubMed1995

Possible predictive markers of immunotherapy in esophageal cancer: retrospective analysis of a randomized study. The Cooperative Study Group for Esophageal Cancer in Japan.

The aim of this report is to evaluate retrospectively the data from a prospective randomized study of 158 esophageal cancer patients who actually completed therapy with protein-bound polysaccharide P (PSK) and the 5-year survivals with and without raised alpha 1-antichymotrypsin and sialic acid levels to determine the value of these parameters in predicting effectiveness of immunotherapy. There was a significant difference in survival between the patients with and without PSK therapy. The survival of the radiochemotherapy plus PSK group treated for > 3 months was significantly better than that of the radiochemotherapy group. Among the patients with abnormal levels of alpha 1-antichymotrypsin and sialic acid, those who received PSK may have a significantly better survival than those without PSK. These results indicate that the preoperative serum levels of alpha 1-antichymotrypsin and sialic acid may possibly predict the effectiveness of immunotherapy using PSK.

Adult↗