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Biomedical subjects

S Aiba

Publications and source records attributed to S Aiba.

At least 19 recordsLinked to original sources
PubMed2000

Kinetics of product inhibition in alcohol fermentation. Reprinted from Biotechnology and Bioengineering, Vol. X, Issue 6, Pages 845-864 (1968).

The inhibitory effect of ethanol concentration p in a medium on the specific rates of growth mu and ethanol production nu of a specific strain of baker's yeast was studied in a chemostat, where except for ethanol as the product, only the concentration of glucose S was controlled to limit the metabolic activity of the yeast. This was designed to supplement the previous findings from the batch experiment, in which ethanol was added artificially and no substrate components were limiting the metabolism of the same yeast, that mu = mu(0)e(-k(1)p) and nu = nu(0)e(-k(1)p), where k(1) and k(2) are empirical constants and subscript the 0 denotes respective values at p = 0. The effects of p on the values of mu and nu were confirmed by the Line-weaver-Burk plot to belong to noncompetitive inhibition. The formulas here for mu and nu as affected by p, if extrapolated to the case of no limiting substrates, were in good agreement in respective forms with those derived previously from the batch experiment, though the values of corresponding coefficients in these formulas were different. The differential equations for mu and nu as functions of both p and S and, in addition for the rate of glucose consumption as correlated by the yield factors either with the cell growth rate or the rate of ethanol production, were solved properly with a digital computer. A kinetic pattern calculated so far was discussed with reference to the data obtained in the batch experiment and those relevant to actual "sake" brewing.

Culture Media↗
PubMed1999

Preparation of chitooligosaccharides from chitosan by a complex enzyme.

Chitosan of 24% degree of acetylation was depolymerized by a mixture of cellulase, alpha amylase, and proteinase to give the title oligosaccharides. The removal of products by membrane separation permitted yield maximization of products having degree of polymerization in the 3-10 range.

Chitin↗
PubMed1999

Intracerebroventricular injection of arginine-vasopressin V1 receptor antagonist attenuates the surge of luteinizing hormone and prolactin secretion in proestrous rats.

In the present study, we examined the effect of arginine-vasopressin (AVP) V1 receptor antagonist ([Deamino-Pen1, Tyr(Me)2, Arg8]-vasopressin) injection (1 microg/2 microl saline) into the third ventricle in the proestrous rat on serum concentrations of luteinizing hormone (LH) and prolactin (PRL) which were determined between 1100 and 2100 h at 1-h intervals. Control rats were injected with 2 microl saline. The injection of AVP receptor antagonist at 1300 h resulted in significant decreases in both LH and PRL secretion compared to saline-injected rats. The present study provides evidence supporting our hypothesis that endogenous AVP plays a role in the induction of the surge of LH and PRL secretion as a stimulatory factor.

Animals↗
PubMed1999

Effects of mean and swing pressures on piston-type high-frequency oscillatory ventilation in rabbits with and without acute lung injury.

To determine whether low mean airway pressure (MAP) and/or stroke volume (SV) settings cause lung injury during piston-type high-frequency oscillatory ventilation (HFOV), we investigated the influence of various combinations of MAP and SV on the amplitude of the pressure swing at four different sites in the normal lung of rabbits. We also examined the effects of these factors on progression of lung injury in lavaged surfactant-deficient lungs. We measured changes in the mean pressure (MP) and swing pressure (SP) during HFOV at MAPs ranging between 5-30 cm H2O in combination with SVs ranging from 5-30 mL in 13 rabbits at four different sites: 1) the proximal airway, 2) the distal end of the endotracheal tube, 3) the bronchi, and 4) the pleural space. Lung lavage was performed in 8 rabbits and differences in MP and SP between normal and surfactant-deficient rabbits were investigated. In the remaining 5 rabbits, lungs were lavaged and subjected to two trials of sustained inflation to 30 cm H2O for 15 s to reverse atelectasis, and the resulting SP was measured. In normal lungs, SP increased at the bronchial and pleural sites as MAP was increased. Alterations in SV did not affect MP in normal or lavaged lungs. In the lavages, surfactant-deficient lungs at MAPs < or = 15 cm H2O, there were significant increases in SP at the distal end of the endotracheal tube and the bronchial sites. SP decreased to the prelavaged level following sustained inflation to 30 cm H2O for 15 s. We conclude that low MAP settings are insufficient to open alveoli in the low-compliance lung and allow for development of atelectasis rather than air trapping. SP was markedly increased in the presence of atelectasis, possibly leading to excessive expansion of the airway. In the clinical setting, such overexpansion of the distal airways may contribute to lung injury. Our findings suggest that physicians should use caution in reducing MAP during piston-type HFOV until lung compliance has normalized, especially in infants with respiratory distress syndrome.

Air Pressure↗
PubMed1999

The effects of dexamethasone, cyclosporine, and vitamin D(3) on the activation of dendritic cells stimulated by haptens.

By their potent antigen-presenting function, dendritic cells (DCs) play a crucial role in the initiation of T cell-mediated immunity, including allergic contact hypersensitivity. To acquire such potent antigen-presenting ability, DCs in tissue must be activated, with increased expression of costimulatory molecules. Recent progress in DC biology has demonstrated that DCs can be activated via a variety of substances, e.g. various cytokines, CD40 ligand, bacterial products, and haptens, to increase their antigen-presenting ability, probably by different mechanisms. Therefore, in this study, to elucidate the mechanisms underlying the efficacy of the immunosuppressive drugs dexamethasone (DEX), cyclosporine A (CY), and vitamin D(3) (Vit D3) in the modulation of allergic contact hypersensitivity reactions, we examined the effects of these drugs on CD86 and HLA-DR antigen expression and TNFalpha secretion by monocyte-derived DCs stimulated with two representative haptens, NiCl(2) and DNCB, in vitro. The augmented expression of CD86 induced by NiCl(2) and DNCB was significantly suppressed by DEX at concentrations in the range 10(-8) to 10(-5) M, which include concentrations less than its therapeutically effective concentration of 10(-7) M. Vit D3 also significantly suppressed NiCl(2)- and DNCB-induced augmented expression of CD86, at concentrations in the ranges 10(-9) to 10(-7) M and 10(-10) to 10(-7) M, respectively. In contrast, significant suppressive effects of CY on the NiCl(2)- or DNCB-induced augmented expression of CD86 were seen only at concentrations in the range 10(-6) to 10(-5) M, which are more than ten times higher than its effective concentration for T cell suppression. The augmented expression of HLA-DR antigen, which was only induced by stimulation with NiCl(2), was resistant to treatment with these three drugs. Only DEX suppressed HLA-DR antigen expression at 10(-5) M. TNFalpha secretion by stimulated DCs was suppressed by DEX and Vit D3, although their effects were not statistically significant. Thus DEX and Vit D3 could modulate allergic contact dermatitis by their clearly demonstrated suppressive effects on the activation of DCs by haptens.

Antigens, CD↗
PubMed1999

Dendritic cells play a crucial role in innate immunity to simple chemicals.

Recently, it has been demonstrated that immunity to infectious agents is composed of innate immunity and acquired immunity, and that dendritic cells (DC) and macrophages, both of which are the participants in the innate immunity, play a crucial role in acquired immune responses, via their expression of several costimulatory molecules and production of cytokines. It is clear that the immune system responds not only to infectious organisms but also to simple chemicals. Allergic contact hypersensitivity reaction is a good example of the immune response to simple chemicals. In contrast to the immunity to microorganisms, however, the role of the innate immune system in responses to simple chemicals still remains unclear. This paper demonstrates that the activation and apoptosis of DC are directly induced by certain simple chemicals, and we suggest that DC, as cells involved in the innate immune system, play a crucial role in the immunity to simple chemicals.

Antigens, CD↗
PubMed1999

Simple chemicals can induce maturation and apoptosis of dendritic cells.

As is well known in the case of Langerhans cells, dendritic cells (DCs) play a crucial role in the initiation of immunity to simple chemicals such as noted in the contact hypersensitivity. Because DCs are scattered in non-lymphoid organs as immature cells, they must be activated to initiate primary antigen-specific immune reactions. Therefore, we hypothesized that some simple chemicals must affect the function of DCs. In this paper, we first demonstrated that human monocyte-derived DCs responded to such simple chemicals as 2, 4-dinitrochlorobenzene (DNCB), 2,4,6-trinitrochlorobenzene (TNCB), 2, 4-dinitrofluorobenzene (DNFB), NiCl2, MnCl2, CoCl2, SnCl2, and CdSO4 by augmenting their expression of CD86 or human leucocyte antigen-DR (HLA-DR), down-regulating c-Fms expression or increasing their production of tumour necrosis factor-alpha (TNF-alpha). In addition, the DCs stimulated with the chemicals demonstrated increased allogeneic T-cell stimulatory function. Next, we found that, among these chemicals, only NiCl2 and CoCl2 induced apoptosis in them. Finally, we examined the effects of these chemicals on CD86 expression by three different macrophage subsets and DCs induced from the cultures of human peripheral blood monocytes in the presence of macrophage colony-stimulating factor (M-CSF), M-CSF + interleukin-4 (IL-4), granulocyte-macrophage colony-stimulating factor (GM-CSF), and GM-CSF + IL-4, respectively. Among them, only DCs dramatically augmented their expression of CD86. These observations have revealed unique characteristics of DCs, which convert chemical stimuli to augmentation of their antigen presenting function, although their responses to different chemicals were not necessarily uniform in the phenotypic changes, cytokine production or in the induction of apoptosis.

Antigens, CD↗
PubMed1998

A combination chemoendocrine therapy of mitoxantrone, doxifluridine, and medroxyprogesterone acetate for anthracycline-resistant advanced breast cancer.

Between January 1993 and October 1995, 34 patients with anthracycline-resistant advanced breast cancer were treated with a combination chemoendocrine therapy of mitoxantrone (MIT), doxifluridine (5'-DFUR) and medroxyprogesterone acetate (MPA). Of 34 patients, 28 were evaluable for efficacy of this combination therapy, and 30 including 2 for whom data were incomplete were assessed for adverse drug reactions. Adriamycin (ADM) was used for pretreatment in 12 patients, 4'-epi-ADM in 6, and THP-ADM in 12. In the eligible patients, 8.0 mg/m2 MIT was administered intravenously every 4 weeks, and 600 mg MPA and 600 mg 5'-DFUR were given orally every day. The median follow-up period was 25 weeks (range 2-90 weeks). The median cumulative dose of mitoxantrone was 66 mg (range 12-121 mg). Of the 28 patients, 11 (39.3%) responded to this combination therapy. As for response in relation to predominant site of lesion, 1 of 5 soft tissue lesions (20%) and 8 of 12 bone metastases (66.7%) showed a partial response, and one complete response and one partial response (25.0%) were seen in eight lung lesions. None of three pleural lesions responded to this therapy. The median duration of response was 31 +/- weeks (range 12-82 weeks). Adverse drug reactions were controllable or tolerable. Combined chemoendocrine therapy with a low dose of MIT is a well-tolerated and moderately effective regimen for the treatment of anthracycline-resistant advanced breast cancer.

Adult↗
PubMed1998

The importance of CD54 and CD86 costimulation in T cells stimulated with Candida albicans and Dermatophagoides farinae antigens in patients with atopic dermatitis.

A number of studies have demonstrated an increased frequency of allergen-specific T cells producing increased amounts of interleukin-4 (IL-4) and IL-5, but little interferon-y in both the peripheral blood and skin lesions of patients with atopic dermatitis (AD). In this study, to further clarify the characteristics of T cells obtained from AD patients, we examined the dependency of the antigen-specific proliferation of peripheral blood mononuclear cells (PBMC) from AD patients on costimulatory molecules. The antigens used were Candida albicans and Dermatophagoides farinae, for which AD patients show increased levels of IgE antibodies. PBMC from control healthy donors stimulated with these antigens incorporated [3H]-thymidine much more than PBMC from AD patients. The addition of anti-CD54, -CD40, -CD80 and -CD86 monoclonal antibodies to the cultures showed that the PBMC required only CD54 and CD86 for stimulation with C. albicans, but required CD54, CD80 and CD86 for stimulation with D. farinae. Among these monoclonal antibodies, the anti-CD54 antibody suppressed the proliferative responses of most PBMC, most effectively followed by the anti-CD86 antibody. However, there were no significant differences in the requirement for costimulatory molecules of PBMC proliferation stimulated with C. albicans or D. farinae between AD patients and healthy donors. Since many studies have suggested that T-helper type 1 and T-helper type 2 immune responses are different in their dependency on CD80 or CD86 costimulation, our present results suggest that the allergen-specific T cells of AD patients are not completely shifted to a T-helper type 2 subset.

Adolescent↗
PubMed1998

Dendritic cell activation induced by various stimuli, e.g. exposure to microorganisms, their products, cytokines, and simple chemicals as well as adhesion to extracellular matrix.

Before the establishment of procedures to cultured dendritic cells (DCs) from peripheral blood or bone marrow progenitor cells using a combination of several cytokines, Langerhans cells (LCs) of the epidermis have been used as the best characterized dendritic cell population. The studies using LCs freshly isolated from the skin or DCs from the blood or spleen and cultured DCs from progenitors have elucidated that although DCs are a unique cell population characterized by their potent antigen presenting function, especially by their induction of primary antigen-specific T cell responses, they are immature and less potent in antigen presenting function immediately after isolated from the skin or from other non-lymphoid tissues. Therefore, DCs must be stimulated to augment their antigen presenting function and to initiate a naive T cell response. Recently, it becomes clear that a variety of signals, such as microorganisms, cytokines, adhesion to extracellular matrix, and simple chemicals like haptens, can induce this activation process in DCs, which is also called as DC maturation. In this paper, we discuss what kinds of stimuli effectively activate DCs.

Animals↗
PubMed1998

Peripheral blood lymphocytes from psoriatic patients are hyporesponsive to beta-streptococcal superantigens.

The strong association of acute guttate psoriasis and streptococcal throat infection, together with the preferential use of T cells expressing a particular T-cell receptor, has suggested a role for bacterial superantigens in the pathogenesis of psoriasis. We examined the proliferative responses of peripheral blood lymphocytes (PBLs), obtained from patients with psoriasis and from healthy controls, to streptococcal superantigens, cytoplasmic membrane-associated protein (CAP) and secretion-type CAP (SCAP), isolated from group A, beta-haemolytic streptococci. PBLs from patients with psoriasis showed significantly less response to SCAP and CAP than those from healthy controls. Because there was no difference between psoriatic patients and controls in the proliferative response of PBLs to staphylococcal enterotoxin A or E (SEA, SEE) or the mitogen phytohaemagglutinin (PHA), these findings strongly suggest that the reduced reactivity to the streptococcal superantigens seems to reflect anergy of a population of PBLs to the superantigens. As the CAP used in the present study stimulates V beta 8 T cells selectively, we further examined the proliferation of V beta 8 T cells after such stimulation using flow cytometry. V beta 8 T cells obtained from three of four psoriatic patients failed to proliferate in the presence of CAP, whereas they proliferated vigorously in the presence of SEE, which activates V beta 8 T cells, confirming the specific hyporesponsiveness of PBLs from psoriatic patients to streptococcal superantigens. We then determined the effects of serum factors on the suppressed response of PBLs to the streptococcal superantigens with SCAP or CAP. It was partially restored when PBLs were cultured with sera obtained from healthy subjects, although the responses were still significantly lower than those of the healthy controls. In contrast, psoriatic sera markedly suppressed the proliferative response of PBLs from healthy controls to CAP or SCAP, but showed no suppression of the proliferative response of PBLs to SEA. Because these findings suggest the presence of specific inhibitory factors in psoriatic sera, we examined whether the inhibitory effect was caused by antisuperantigen antibody. However, no significant increase was detected in antibody titre to CAP in psoriatic sera, as has been noted in sera from patients with poststreptococcal glomerulonephritis. The present results show for the first time the hyporesponsiveness of PBLs to streptococcal superantigens and the presence of serum inhibitors that specifically inhibit T-cell response to the superantigens in psoriatic patients. These findings suggest a pathological role for streptococcal infections in the pathogenesis of psoriasis.

Adolescent↗
PubMed1998

Phyllodes tumor showing intracystic growth: a case report.

A phyllodes tumor often grows rapidly and occasionally contains microcysts; however, the tumor rarely shows a morphologically intracystic pattern. We experienced a rare case of a phyllodes tumor with a solid mass growing into the cyst. A 62-year-old female noticed a tumor in her right breast in January 1995. The tumor grew rapidly and she visited our out-patient clinic in February 1995. On physical examination, a 10 x 8 cm, well defined and movable mass with a smooth surface was palpated in the upper outer quadrant of the right breast. Mammography showed a large tumor shadow in the upper outer quadrant of the right breast without any microcalcification. Ultrasonography revealed a large cystic shadow with a low echoic lesion and solid component with heterogeneous internal echo in the cyst. Under general anesthesia, the tumor was widely excised. The resected specimen was 11.5 x 11 x 11 cm in size and the tumor was not invasive to surrounding tissues. Old bloody fluid was contained within the cyst. The gross appearance showed papillary process protrusions into a central cystic cavity. Histological examination revealed a borderline case of phyllodes tumor. Two years after the operation, she is doing well without any recurrence.

Breast Neoplasms↗
PubMed1998

Phorbol 12-myristate 13-acetate can transform monocyte-derived dendritic cells to different cell types similar to those found in dermatofibroma. A possible in vitro model of the histogenesis of dermatofibroma.

Dermatofibroma is composed largely of interlacing fascicles of slender spindle cells set within a loose collagenous stroma and of scattered foamy histiocytes and multinucleated giant cells. There is clear evidence indicating that factor XIIIa+ dermal dendritic cells (DDCs) are the cells constituting dermatofibromas. However, it is still unknown what stimulation is responsible for transforming DDCs into different cell types, producing different subtypes of dermatofibromas. Recently, it has become possible to obtain dendritic cells (DCs), that are identical with DDCs in their phenotypic and functional characteristics, from the culture of CD14+ peripheral blood monocytes to which IL-4 and GM-CSF were added. Using these monocyte-derived DCs, we examined the ability of various cytokines, such as IL-1beta , IL-3, IL-5, IL-6, IL-7, IL-8, IL-10, TNFalpha, TGFbeta, M-CSF, IFNalpha, and IFNgamma, and phorbol 12-myristate 13-acetate (PMA), to induce different cell types observed in DFs. Among them, only PMA could induce a variety of cell types such as histiocytic cells, fibroblastic spindle-shaped cells, and even multinucleated giant cells of Touton or foreign body type. Phenotypically, all the induced cell types expressed CD1a, CD80, CD86, HLA-DR, and CD68 in a magnitude similar to that of non-treated monocyte-derived DCs. The expression of factor XIIIa was strongest in histiocytic cells, moderate in fibroblastic cells, and weakest or negative in giant cells. These data suggest that dermatofibromas are a kind of neoplastic disease which is induced only by the effect of some tumor promoter on DDCs.

Carcinogens↗
PubMed1998

Solitary subcutaneous mucinosis surrounded by bizarre-shaped, factor XIIIa-positive cells with intranuclear vacuoles.

We describe a subcutaneous mucinosis developing in the right cheek of a 38-year-old man. Histologic examination revealed bipolar fibroblast-like cells embedded in a well demarcated mucinous stroma in the subcutis without a manifest reticulin network. In addition, bizarre, sometimes multinucleate, cells with intranuclear vacuoles were found at the periphery of the mucinous stroma. Immunohistologically, both the bipolar fibroblastic cells and bizarre-shaped cells were positive for vimentin, but were negative for smooth muscle A-actin, desmin, CD34, S100, trypsin, or chymotrypsin. However, the latter reacted to anti-factor XIIIa antibody, suggesting that they are derived from dermal dendritic cells. We think that this solitary subcutaneous mucinosis is a unique variant of cutaneous focal mucinosis, because neither a reticulin network nor reactivity to anti-smooth muscle A-actin antibody were demonstrable.

Adult↗
PubMed1998

An increased ratio of interleukin-1 receptor antagonist to interleukin-1alpha in inflammatory skin diseases.

IL-1 receptor antagonist (IL-1ra) is a cytokine that competitively binds the IL-1 receptor to antagonize IL-1 activity without any agonist function. Previous experiments indicated that the ratio of IL-1ra to IL-1alpha in the normal stratum corneum (SC) was much higher in the sun-exposed face than in the sun-protected area, upper arms. It was also reported by another laboratory that IL-1ra is increased in the lesional skin of psoriatic patients. This study was designed to measure the contents of IL-1alpha and IL-1ra in non-lesional and pathological SC obtained from inflammatory skin diseases including psoriasis and non-psoriatic dermatoses such as atopic dermatitis. The SC materials were obtained with a non-invasive tape-stripping method. Their soluble fractions were prepared and assayed for IL-1alpha and IL-1ra by enzyme-linked immunosorbent assays. As a result we confirmed the previous findings that the ratio of IL-1ra to IL-1alpha in the normal SC was much higher in the face than in the sun-protected sites, the trunk as well as extremities. Next, we found that IL-1alpha contents were significantly reduced in the SC samples obtained from inflammatory skin regardless of whether their IL-1ra contents increased or unchanged. Moreover, we noted that an increased ratio of IL-1ra to IL-1alpha in the SC was not specific to psoriasis, but was also found in other inflammatory skin diseases including atopic dermatitis. This ratio was found to become lower after successful treatment of these skin lesions with topical glucocorticoids. We conclude from these observations that the increased ratio of IL-1ra to IL-1alpha in the SC is a non-specific phenomenon that can occur in any inflammatory skin diseases regardless of the inflammatory pattern, probably reflecting a skin regulation process against various kinds of inflammation.

Dermatitis↗
PubMed1998

Maturation of dendritic cells induced by cytokines and haptens.

Recently, elucidation has progressed on a crucial role played by dendritic cells (DCs) in the induction of primary antigen-specific immune reactions. Although mature DCs exhibit potent antigen presenting function, DCs are scattered in nonlymphoid organs throughout the body as immature cells that have only minimum antigen presenting function. When they are stimulated to maturate, they increase their expression of class II major histocompatibility (MHC) antigen and several co-stimulatory molecules, resulting in the augmentation of antigen presenting function. Furthermore, these maturated DCs move to the T-dependent areas of secondary lymphoid organs to sensitize naive T cells for these antigens. Therefore, it is important to understand the mechanism to induce the maturation of DCs. Recent progress in the study of DC biology depicts various factors, such as cytokines, bacterial products and haptens, which are responsible for DC maturation. In this paper, the mechanism of DC maturation induced by cytokines and chemicals is described.

Animals↗
PubMed1997

Dendritic cells differently respond to haptens and irritants by their production of cytokines and expression of co-stimulatory molecules.

After application of haptens to the skin, Langerhans cells (LC), i.e. immature dendritic cells (DC) in the skin, move to secondary lymphoid organs to sensitize naive T cells. During this process, LC become mature DC with augmented expression of various co-stimulatory molecules and MHC class II antigens. In this scenario, however, critical questions remain as to what kind of chemicals can induce this maturation process through what kind of mechanisms. To clarify these questions, we used monocyte-derived CD1a+ DC instead of LC since LC maturated spontaneously in vitro culture. After we confirmed that monocyte-derived DC showed at least phenotypic characteristics and a response to TNF-alpha similar to LC, we added various chemicals, i.e., dinitrochlorobenzene (DNCB), trinitrochlorobenzene (TNCB), NiCl2, ZnCl2, sodium dodecyl sulfate (SDS), or benzalkonium chloride (BC), to a culture of purified monocyte-derived CD1a+ DC. Of these chemicals, only NiCl2 and DNCB significantly increased the surface expression of CD54, CD86, HLA-DR antigen, and interleukin (IL)-1 beta production, while SDS, BC, or ZnCl2 could not augment them, except for weak augmentation of CD86 expression by SDS. The increase in the expression of CD86 induced by NiCl2 or DNCB was most remarkable, being observed in DC from almost all the subjects we examined. TNCB could also induce responses similar to those induced with DNCB, but the number of subjects whose DC responded to it was far less than that of subjects whose DC responded to NiCl2 or DNCB. In spite of the augmented CD86 expression on DC treated with DNCB or NiCl2, these chemicals induced different responses of DC in their expression of CD54 and HLA-DR and the production of IL-6 and tumor necrosis factor (TNF)-alpha. In addition, the up-regulation of CD86 expression on DC treated with DNCB was significantly suppressed by either anti-IL-1 beta or anti-TNF-alpha antibody, while that by NiCl2 was relatively insensitive to these antibody treatments. Finally, the protein kinase C inhibitor, H7, but not staurosporine, could suppress the augmentation of CD86 expression on DC induced either by NiCl2 or by DNCB. These data suggest that DC respond to some haptens by changing their expression of several co-stimulatory molecules and their production of cytokines with a resultant change in antigen-presenting function. They also suggest that these chemicals stimulate DC by different mechanisms. By these responses, DC may modulate the final immune response to chemicals.

Antibodies↗