[Immunochemical fecal occult blood test].
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Feces↗
Biomedical subjects
M Okamoto
Publications and source records attributed to M Okamoto.
[Cauda equina syndrome due to recurrent malignant lymphoma of the spinal cord. A case report].
A 50-year-old man noticed a mass in the right cervical region and presented to our hospital. He underwent biopsy of a cervical lymph node, which revealed non-Hodgkin's lymphoma (diffuse large B cell, lymphoblastic type) histologically. He was treated with chemotherapy (CHOP) and radiation, and achieved complete remission. Two months later, he was admitted because of distal pain and extensive numbness of the lower limb as well as weakness of the left leg. Lumbar MRI showed an area of abnormal intensity in the cauda equina. Cytological examination of cerebrospinal fluid showed class V (lymphoma cells), so he was diagnosed as having recurrent malignant lymphoma of the spinal cord. He was treated with intrathecal chemotherapy and irradiation. After the treatment the mass in the cauda equina disappeared and the neurological symptoms in his legs resolved. It is rare for malignant lymphoma to recur in the spinal cord, particularly the cauda equina. It is well known that cauda equina syndrome can be caused by vertebral lesions and primary spinal cord tumors, but it is also necessary to keep malignant lymphoma of the cauda equina in mind.
Aged↗
Structure/function relationship of CYP11B1 associated with Dahl's salt-resistant rats--expression of rat CYP11B1 and CYP11B2 in Escherichia coli.
Dahl's salt-resistant normotensive rats (DR rats) have been previously reported to express cytochrome P-450 (CYP11B1) containing five missense mutations [Matsukawa, N., Nonaka, Y., Higaki, J., Nagano, M., Mikami H., Ogihara, T. & Okamoto, M. (1993) J. Biol. Chem. 268, 9117-9121]. To investigate structure-function relationships of CYP11B, wild-type rat CYP11B1 and CYP11B2 and DR-CYP11B1 (mutant CYP11B1 in Dahl's salt-resistant rats) have been successfully expressed in Escherichia coli. Steroid 11beta-hydroxylase (11beta-OHase) activity observed with DR-CYP11B1 was similar to that of wild-type CYP11B1, while 18-hydroxylase (18-OHase) activity of DR-CYP11B1 was lower than that of wild-type CYP11B1. Mutant CYP11B1s containing a single or a double amino acid substitution associated with DR-CYP11B1 have been also expressed in E. coli to investigate effects of the substitutions on enzymatic activity. Each of the single mutant enzymes showed lower 18-OHase activity than wild-type CYP11B1, but not as low as DR-CYP11B1. A double mutant CYP11B1 with V381L and I384L showed 18-OHase activity at a similar low level to that of DR-CYP11B1. The 19-hydroxylation (19-OHase) activity of DR-CYP11B1 was about one-third of that of the wild-type enzyme and this low activity appeared due to the V443M mutation. These results suggest that three of five amino acid substitutions present in DR-CYP11B1 account for the decreased 18-OHase and 19-OHase activities. A decrease in these enzyme activities may be responsible for the normotension of the DR rats when fed a high-salt diet.
Amino Acid Sequence↗
[New clinical tests that physicians should know for diagnosis of digestive system diseases].
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Antibodies, Bacterial↗
Potent inhibition of HIV type 1 replication by an antiinflammatory alkaloid, cepharanthine, in chronically infected monocytic cells.
Cepharanthine is a biscoclaurine alkaloid isolated from Stephania cepharantha Hayata and has been shown to have antiinflammatory, antiallergic, and immunomodulatory activities in vivo. As several inflammatory cytokines and oxidative stresses are involved in the pathogenesis of HIV-1 infection, we investigated the inhibitory effects of cepharanthine on tumor necrosis factor alpha (TNF-alpha)- and phorbol 12-myristate 13-acetate (PMA)-induced HIV-1 replication in chronically infected cell lines. Two chronically HIV-1-infected cell lines, U1 (monocytic) and ACH-2 (T lymphocytic), were stimulated with TNF-alpha or PMA and cultured in the presence of various concentrations of the compound. HIV-1 replication was determined by p24 antigen level. The inhibitory effects of cepharanthine on HIV-1 long terminal repeat (LTR)-driven gene expression and nuclear factor kappaB (NF-kappaB) activation were also examined. Cepharanthine dose dependently inhibited HIV-1 replication in TNF-alpha- and PMA-stimulated U1 cells but not in ACH-2 cells. Its 50% effective and cytotoxic concentrations were 0.016 and 2.2 microg/ml in PMA-stimulated U1 cells, respectively. Cepharanthine was found to suppress HIV-1 LTR-driven gene expression through the inhibition of NF-kappaB activation. These results indicate that cepharanthine is a highly potent inhibitor of HIV-1 replication in a chronically infected monocytic cell line. Since biscoclaurine alkaloids, containing cepharanthine as a major component, are widely used for the treatment of patients with various inflammatory diseases in Japan, cepharanthine should be further pursued for its chemotherapeutic potential in HIV-1-infected patients.
Alkaloids↗
A tripartite protein complex with the potential to couple synaptic vesicle exocytosis to cell adhesion in brain.
We identify a complex of three proteins in brain that has the potential to couple synaptic vesicle exocytosis to neuronal cell adhesion. The three proteins are: (1) CASK, a protein related to MAGUKs (membrane-associated guanylate kinases); (2) Mint1, a putative vesicular trafficking protein; and (3) Veli1, -2, and -3, vertebrate homologs of C. elegans LIN-7. CASK, Mint1, and Velis form a tight, salt-resistant complex that can be readily isolated. CASK, Mint1, and Velis contain PDZ domains in addition to other modules. However, no PDZ domains are involved in complex formation, leaving them free to recruit cell adhesion molecules, receptors, and channels to the complex. We propose that the tripartite complex acts as a nucleation site for the assembly of proteins involved in synaptic vesicle exocytosis and synaptic junctions.
Adaptor Proteins, Signal Transducing↗
Prodigiosins uncouple lysosomal vacuolar-type ATPase through promotion of H+/Cl- symport.
We reported previously [Kataoka, Muroi, Ohkuma, Waritani, Magae, Takatsuki, Kondo, Yamasaki and Nagai (1995) FEBS Lett. 359, 53-59] that prodigiosin 25-C (one of the red pigments of the prodigiosin group produced by micro-organisms like Streptomyces and Serratia) uncoupled vacuolar H+-ATPase, inhibited vacuolar acidification and affected glycoprotein processing. In the present study we show that prodigiosin, metacycloprodigiosin and prodigiosin 25-C, all raise intralysosomal pH through inhibition of lysosomal acidification driven by vacuolar-type (V-)ATPase without inhibiting ATP hydrolysis in a dose-dependent manner with IC50 values of 30-120 pmol/mg of protein. The inhibition against lysosomal acidification was quick and reversible, showing kinetics of simple non-competitive (for ATP) inhibition. However, the prodigiosins neither raised the internal pH of isolated lysosomes nor showed ionophoric activity against H+ or K+ at concentrations where they strongly inhibited lysosomal acidification. They required Cl- for their acidification inhibitory activity even when driven in the presence of K+ and valinomycin, suggesting that their target is not anion (chloride) channel(s). In fact, the prodigiosins inhibited acidification of proteoliposomes devoid of anion channels that were reconstituted from lysosomal vacuolar-type (V-)ATPase and Escherichia coli phospholipids. However, they did not inhibit the formation of an inside-positive membrane potential driven by lysosomal V-ATPase. Instead, they caused quick reversal of acidified pH driven by lysosomal V-ATPase and, in acidic buffer, produced quick acidification of lysosomal pH, both only in the presence of Cl-. In addition, they induced swelling of liposomes and erythrocytes in iso-osmotic ammonium salt of chloride but not of gluconate, suggesting the promotion of Cl- entry by prodigiosins. These results suggest that prodigiosins facilitate the symport of H+ with Cl- (or exchange of OH- with Cl-) through lysosomal membranes, resulting in uncoupling of vacuolar H+-ATPase.
Adenosine Triphosphate↗
Elongational Flow Birefringence of Reactor-Made Linear Low-Density Polyethylene.
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Journal Article↗
Interleukin-6 and epidermal growth factor promote anchorage-independent growth of immortalized human prostatic epithelial cells treated with N-methyl-N-nitrosourea.
BACKGROUND: Epidermal growth factor (EGF) and interleukin (IL)-6 are implicated in the growth of benign and malignant prostatic epithelial cells. We investigated the role of EGF and IL-6 during the process of prostate carcinogenesis. METHODS: Using growth in soft agar as an index of transformation, we examined the effect of EGF and IL-6 on the enhancement of N-methyl-N-nitrosourea (MNU)-initiated transformation of immortalized, nontumorigenic prostatic epithelial cell lines (PWR-1E and RWPE-1) developed in our laboratory. The effect of EGF and IL-6 on the growth of MNU-induced transformants isolated from soft agar was assessed both in monolayer culture and in a soft agar. RESULTS: After a 1 hr exposure to N-methyl-N-nitrosourea (50 microg/ml), cells (5 x 10(4)) were grown in soft agar in the presence of EGF (5 ng/ml) or IL-6 (10 or 100 ng/ml). Addition of EGF or IL-6 significantly increased colony formation in soft agar of both immortalized prostatic epithelial cell lines initiated with MNU (P < 0.001-0.05). Only a very small number of colonies was observed with the parental cell lines PWR-1E and RWPE-1 not exposed to MNU, and their numbers increased by the addition of EGF or IL-6. All of the transformants, derived by exposure to MNU and isolated from soft agar, exhibited a higher cell growth potential in monolayer cultures than did their parental cell lines. Furthermore, as compared to the parental cell lines, growth response of MNU-transformants to 5alpha-dihydrotestosterone (5alpha-DHT), EGF, or IL-6 in monolayer culture was better in 5 of 8, 6 of 8, and 7 of 8 cell lines, respectively. All of the MNU-transformants exhibited a far higher colony-forming efficiency in soft agar than did the parental cell lines. However, the degree of responsiveness to EGF or IL-6 in soft agar varied among the MNU-transformants. CONCLUSIONS: The results of the present study suggest that IL-6 and EGF may enhance prostate carcinogenesis in vitro by preferentially stimulating the growth of transformed cells.
Cell Adhesion↗
The binding and utilization of hemoglobin by Prevotella intermedia.
Prevotella intermedia, a putative periodontopathic microorganism, requires iron for growth. Hemoglobin can be a major source of iron for bacterial growth in vivo since it is present in the crevicular fluid collected from periodontitis sites. Experiments studying the growth of P. intermedia in iron-depleted Todd-Hewitt broth supplemented with human hemoglobin showed that the bacteria were able to utilize human hemoglobin as a source of iron. The uptake of iron from hemoglobin by P. intermedia appears to be initiated by the binding of hemoglobin to the bacteria as shown by direct binding studies using 125I-labeled human hemoglobin. Scatchard analysis of saturation binding data revealed that 125I-labeled human hemoglobin had a dissociation constant (Kd) of 2.53 x 10(-8) M for the receptor on P. intermedia. Binding of labeled hemoglobin to P. intermedia was competitively inhibited by unlabeled human hemoglobin showing that the binding was specific. The ability of bovine hemoglobin, but not hemin or non-hemoglobin heme-containing compounds, to inhibit binding competitively suggested that the globin moiety of the hemoglobin molecule is recognized by the hemoglobin binding receptors.
Animals↗
Hepatocyte growth factor prevents renal fibrosis and dysfunction in a mouse model of chronic renal disease.
Chronic renal disease (CRD) is generally thought to be incurable, except through renal transplantation, and the number of patients with CRD is on the increase. Glomerulosclerosis and tubulointerstitial fibrosis represent the morphological equivalent of end-stage CRD. In this study, we demonstrated the preventive effect of hepatocyte growth factor (HGF) on the progression of renal dysfunction and fibrosis, using a spontaneous mouse model for CRD (ICGN strain). The mice progressively developed glomerular sclerotic injury, tubular atrophy, and renal dysfunction until they were 17 wk of age. When recombinant HGF was injected into these mice during a 4-wk-period (from weeks 14-17 after birth), DNA synthesis of tubular epithelial cells was found to be 4.4-fold higher than in mice without HGF injection, thereby suggesting tubular parenchymal expansion promoted by HGF. Notably, HGF suppressed the expression of transforming growth factor-beta and of platelet-derived growth factor as well as myofibroblast formation in the affected kidney. Consequently, the onset of tubulointerstitial fibrosis was almost completely inhibited by HGF, while HGF attenuated the progression of glomerulosclerosis, both leading to preventing manifestation of renal dysfunction. From our results, supplement therapy with HGF may be taken into consideration as a novel option for prevention and treatment of CRD.
Animals↗
Immunosuppressive effects of FTY720 alone or in combination with cyclosporine and/or sirolimus.
BACKGROUND: We examined the ability of FTY720, a novel immunosuppressant that prolongs the survival of allografts in experimental animal models, to potentiate the immunosuppressive effects of cyclosporine (CsA) and/or sirolimus (SRL) in vitro and in vivo. METHODS: FTY720 alone (10-5000 ng/ml) or in combination with other drugs was added to human peripheral blood lymphocytes (PBLs) undergoing stimulation in vitro with phytohemagglutinin (PHA) or OKT3 monoclonal antibody. The combination index (CI) values were calculated to evaluate the nature of the interactions between FTY720 and CsA and/or SRL: CI values <1 reflect synergistic, CI=1, additive, and CI>1, antagonistic interactions. In addition, Wistar Furth (RT1u) rat recipients of Buffalo (RT1b) heart allografts were treated with FTY720 alone or in combination with other agents. FTY720 alone was also tested to block small bowel or liver allograft rejection in rats. RESULTS: FTY720 alone produced only modest inhibition of the proliferation of human PBL stimulated with PHA or OKT3 monoclonal antibody. In combination with CsA or SRL, however, FTY720 produced synergistic effects, namely, CI values of 0.58 and 0.36, respectively. A 14-day course of FTY720 (0.05-8.0 mg/kg/day) by oral gavage prolonged heart allograft survival in dose-dependent fashion. Although a 14-day oral course of CsA (1.0 mg/kg/day) alone was ineffective (mean survival time=7.0+/-0.7 vs. 6.4+/-0.6 days in treated vs. untreated hosts), treatment with a combination of 1.0 mg/kg/day CsA and 0.1 mg/kg/day FTY720 extended allograft survival to 62.4+/-15.6 days (P<0.001; CI=0.15). Similarly, a 14-day oral course of 0.08 mg(kg/day SRL alone was ineffective (6.8+/-0.6 days; NS), but the combination of SRL with 0.5 mg/kg/day FTY720 extended the mean survival time to 34.4+/-8.8 days (CI=0.28). The CsA/SRL (0.5/0.08 mg/kg/day) combination acted synergistically with FTY720 (0.1 mg/kg/day) to prolong heart survivals to >60 days (CI=0.18). CONCLUSIONS: FTY720 potentiates the immunosuppressive effects of CsA and/or SRL both in vitro (by inhibiting of T-cell proliferative response) and in vivo (by inhibiting allograft rejection).
Animals↗
Muscarinic facilitation of GABA release in substantia gelatinosa of the rat spinal dorsal horn.
1. Blind patch clamp recordings were made from substantia gelatinosa (SG) neurones in the adult rat spinal cord slice to study the mechanisms of cholinergic modulation of GABAergic inhibition. 2. In the majority of SG neurones tested, carbachol (10 microM) increased the frequency (677 % of control) of spontaneous GABAergic inhibitory postsynaptic currents (IPSCs). A portion of these events appeared to result from the generation of spikes by GABAergic interneurones, since large amplitude IPSCs were eliminated by tetrodotoxin (1 microM). 3. The effect of carbachol on spontaneous IPSCs was mimicked by neostigmine, suggesting that GABAergic interneurones are under tonic regulation by cholinergic systems. 4. The frequency of GABAergic miniature IPSCs in the presence of tetrodotoxin (1 microM) was also increased by carbachol without affecting amplitude distribution, indicating that acetylcholine facilitates quantal release of GABA through presynaptic mechanisms. 5. Neither the M1 receptor agonist McN-A-343 (10-300 microM) nor the M2 receptor agonist, arecaidine (10-100 microM), mimicked the effects of carbachol. All effects of carbachol and neostigmine were antagonized by atropine (1 muM), while pirenzepine (100 nM), methoctramine (1 microM) and hexahydrosiladifenidol hydrochloride, p-fluoro-analog (100 nM) had no effect. 6. Focal stimulation of deep dorsal horn, but not dorsolateral funiculus, evoked a similar increase in IPSC frequency to that evoked by carbachol and neostigmine. The stimulation-induced facilitation of GABAergic transmission lasted for 2-3 min post stimulation, and the effect was antagonized by atropine (100 nM). 7. Our observations suggest that GABAergic interneurones possess muscarinic receptors on both axon terminals and somatodendritic sites, that the activation of these receptors increases the excitability of inhibitory interneurones and enhances GABA release in SG and that the GABAergic inhibitory system is further controlled by cholinergic neurones located in the deep dorsal horn. Those effects may be responsible for the antinociceptive action produced by the intrathecal administration of muscarinic agonists and acetylcholinesterase inhibitors.
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
Biochemical and pharmacological characterization of FR134043, a novel elastase inhibitor.
FR134043, disodium(Z,1S,15S,8S,24S,27R,29S,34S,37R)-29-ben zyl-21-ethylidene-27-hydroxy-15-isobutyrylamino-34-isopropyl-31,37 -dimethyl-10,16,19,22,30,32,35,38-octaoxo-36-oxa-9,11,17,20,23,28, 31,33-octaazatetracyclo[16.13.6.1(24),(28).0(3),(8)]octatricont a-3,5,7-trien-5,6-diyl disulfate, is a water-soluble inhibitor of human neutrophil elastase with a molecular mass of 1166.15 Da. FR134043 demonstrated a characteristic competitive inhibition of human neutrophil elastase with a Ki of 8 nM. In studies using synthetic substrates, FR134043 inhibited both neutrophil elastase activity and porcine pancreatic elastase activity with IC50 values of 35 nM and 49 nM respectively. FR134043 also inhibited hydrolysis of bovine neck ligament elastin by human neutrophil elastase with an IC50 value of 210 nM. In in vivo experiments, FR134043 protected animals against human neutrophil elastase (50 microg/animal)-induced lung hemorrhage in hamsters with an ED50 value of 3.1 microg/animal for intratracheal administration and 5.0 mg/kg for intravenous administration. Subcutaneous treatment with FR134043 significantly suppressed human neutrophil elastase (20 microg/paw)-induced paw edema in mice with an ED50 value of 3.3 mg/kg when evaluated 4 h after elastase injection. The potency of FR134043 given intratracheally to protect against porcine pancreatic elastase (100 microg/animal)-induced emphysema in hamsters was relatively low (Quasi-static lung compliance; ED50 = 1590 microg/animal) compared to that in acute animal models. FR134043 (10 mg/kg per h i.v. infusion) significantly improved lipopolysaccharide (0.25 mg/kg per h i.v. infusion)-induced thrombocytopenia and some coagulation parameters in rats. These results suggest that systemic administration of FR134043 would be advantageous over intratracheal administration of FR134043 for the treatment of adult respiratory distress syndrome, septic shock and pulmonary emphysema and other pathophysiologic conditions in which elastases are thought to be involved.
Animals↗
Ergonovine-induced alterations in coronary flow velocity preceding onset of occlusive spasm in patients without significant coronary artery stenoses.
This study examined serial changes in coronary flow velocity to elucidate the dynamic change of coronary circulation during coronary spasm. Twenty patients with variant angina and 27 control patients were studied. Coronary flow velocity was monitored using a Doppler guidewire following intracoronary ergonovine administration. In the control group, diastolic flow velocity either did not change or increased slightly in response to ergonovine. However, in patients with variant angina, 2 patterns of flow velocity alterations were observed. In the first pattern, flow initially increased and then suddenly decreased (16 of 20 patients). In the second pattern, flow gradually decreased (3 of 20 patients). In the remaining patient, the coronary flow alteration could not be detected because of branch spasm. When abnormally high flow velocity was defined as a 100% increase in flow after ergonovine administration within 1 minute, and abnormally low flow velocity was defined as a 50% decrease in flow to diagnose variant angina, sensitivities of 35%, 75%, and 85% were noted if flow was measured 1.0, 2.0, and 3.0 minutes after ergonovine administration, respectively. These abnormal flow velocities were observed before ischemic ST changes appeared. In conclusion, in patients with variant angina, characteristic serial changes in coronary flow velocity occur before occlusive spasm. Variant angina may be diagnosed earlier by monitoring flow velocity rather than by monitoring for ischemic electrocardiographic changes.
Aged↗
Purification and characterization of a catalytic domain of rat intestinal phospholipase B/lipase associated with brush border membranes.
A brush border membrane-associated phospholipase B/lipase was solubilized from the distal two-thirds of rat small intestine by autolysis during storage at -35 degrees C over 1 month, and then the enzyme was purified to homogeneity and characterized enzymatically and structurally. The purified enzyme exhibited broad substrate specificity including esterase, phospholipase A2, lysophospholipase, and lipase activities. SDS-gel electrophoretic and reverse-phase high performance liquid chromatographic analyses demonstrated that a single enzyme catalyzes these activities. It preferred hydrolysis at the sn-2 position of diacylphospholipid and diacylglycerol without strict stereoselectivity, whereas it apparently exhibited no positional specificity toward triacylglycerol. Diisopropyl fluorophosphate, an irreversible inhibitor of serine esterases and lipases inhibited purified enzyme. When the position of enzyme on SDS-gel electrophoresis under the non-reducing conditions was determined by assaying the activity eluted from sliced gels, brush border membrane-associated enzyme corresponded to a approximately 150-kDa protein; autolysis gave a 35-kDa product, in agreement with the results of immunoblot analysis. The purified 35-kDa enzyme consisted of a 14-kDa peptide and a glycosylated 21-kDa peptide. Their NH2-terminal amino acid sequences were determined and found in the second repeat of 161-kDa phospholipase B/lipase with 4-fold tandem repeats of approximately 38 kDa each, which we cloned and sequenced in the accompanying paper (Takemori, H., Zolotaryov, F., Ting, L., Urbain, T., Komatsubara, T., Hatano, O., Okamoto, M., and Tojo, H. (1988) J. Biol. Chem. 273, 2222-2231). These results indicate that the purified enzyme is the catalytic domain derived from the second repeat of brush border membrane-associated phospholipase B/lipase.
Amino Acid Sequence↗
Identification of functional domains of rat intestinal phospholipase B/lipase. Its cDNA cloning, expression, and tissue distribution.
A cDNA encoding a rat intestinal Ca(2+)-independent phospholipase B/lipase (PLB/LIP) was cloned from an ileac mucosa cDNA library using a probe amplified by polymerase chain reaction based on the purified enzyme's sequence. PLB/LIP consists of an NH2-terminal signal peptide, four tandem repeats of about 350 amino acids each, and a hydrophobic domain near the COOH terminus. The enzyme purified previously was found to be derived from the second repeat part. To examine the function of each domain, the full-length PLB/LIP, individual repeats, and a protein lacking the COOH-terminal hydrophobic stretch were expressed in COS-7 cells. The results showed that the second repeat, but not the other repeats, had all the activities (phospholipase A2, lysophospholipase, and lipase) found in the purified natural and expressed full-length enzymes, suggesting repeat 2 is a catalytic domain. The full-length enzyme was mainly present in membrane fractions and efficiently solubilized by treatment with 1% Triton X-100, but not with phosphatidylinositol-specific phospholipase C. Deletion of the COOH-terminal hydrophobic stretch caused the secretion of > 90% of synthesized PLB/LIP into culture media. These results suggest the hydrophobic domain is not replaced by a glycosylphosphatidylinositol anchor but serves as a membrane anchor directly. A message of the full-length PLB/LIP was abundantly expressed in the ileum and also, in a smaller, but significant amount, in the esophagus and testis. Immunohistochemistry showed that PLB/LIP is localized in brush border membranes of the absorptive cells, Paneth cells, and acrosomes of spermatid, suggesting its roles related and unrelated to intestinal digestion.
Amino Acid Sequence↗
Concanavalin A-immobilized polystyrene nanospheres capture HIV-1 virions and gp120: potential approach towards prevention of viral transmission.
To establish an effective tool for the prevention of HIV-1 transmission, lectin-immobilized polystyrene nanospheres were synthesized and examined for their HIV-1 capture activity. When concanavalin A (Con A) was immobilized on the surface of polystyrene nanospheres (400 nm in diameter) with poly(methacrylic acid) branches and incubated with HIV-1 suspension at room temperature for 60 min, the nanospheres (Con A-NSs) achieved a >3.3 log and a 2.2 log reduction of viral infectivity in HIV-1 (IIIB strain) suspension at a concentration of 2 and 0.5 mg/ml, respectively. Meanwhile, Con A-free nanospheres, which were not immobilized with Con A, achieved only a 0.29 log reduction at 0.5 mg/ ml. Con A-NSs (2 mg/ml) could also reduce the gp120 level of III(B) and HE strains to <7.1% and 5.5% of each control, respectively. The combination of Con A-NS treatment followed by filtration with a microporous membrane efficiently removed virion-free gp120 as well as infectious viral particles from HIV-1 suspension. Electron microscopic examination demonstrated that HIV-1 virions were trapped on the surface of Con A-NSs. Thus, Con A-NSs can capture HIV-1 virions and gp120 with high affinity, and may have potential as an effective tool for the prevention of HIV-1 transmission.
Concanavalin A↗