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K Okada

Publications and source records attributed to K Okada.

At least 217 records · Page 12Linked to original sources
PubMed2000

Intracellular Na+ directly modulates Na+,K+-ATPase gene expression in normal rat kidney epithelial cells.

BACKGROUND: In a wide variety of cell systems, increases in cell Na+ ([Na+]i) lead to an induction of N+,K+-ATPase mRNA expression. On the other hand, the increase in [Na+]i can also induce a rise in cell Ca2+ ([Ca2+]i) through a secondary inhibition of Na+/Ca2+ exchange and a decrease in cell pH (pHi) through a secondary inhibition of Na+/H+ exchange. It is not known whether [Na+]i, [Ca2+]i, and/or pHi directly modulate N+,K+-ATPase mRNA expression. METHODS: We used normal rat kidney epithelial cells (NRK) to examine the effects of ouabain on N+,K+-ATPase alpha1- and beta1-mRNA accumulation by Northern blot analysis and the relationship between the mRNA accumulation and [Na+]i, [Ca2+]i, or pHi. [Na+]i, [Ca2+]i, and pHi were measured using a Na+-sensitive fluorescent dye (SBFI), a Ca2+-sensitive fluorescent dye (Fura-2), and a pH-sensitive fluorescent dye (BCECF), respectively. RESULTS: Ouabain (1 mmol/L) significantly increased [Na+]i. Upon addition of ouabain, alpha1-mRNA levels increased to 2. 3 times the control level at three hours, with maximum 3.3-fold elevations at 12 hours. beta1-mRNA levels also increased to 2.4 times the control level at 3 hours, with a maximum 3.3-fold increase at 12 hours. The ouabain-mediated alpha1- and beta1-mRNA induction was inhibited by both the RNA transcription inhibitor (actinomycin D) and the protein synthesis inhibitor (cycloheximide). Ouabain at three hours caused an increase in [Ca2+]i. Similar increases in [Ca2+]i, which were elicited by the Ca2+ ionophore (ionomycin) in the presence of extracellular Ca2+, had no effect on alpha1- or beta1-mRNA levels. In Ca2+-free medium treated with EGTA, ouabain at three hours caused a significant increase in [Na+]i without any changes in [Ca2+]i, and also increased alpha1- and beta1-mRNA levels. Ouabain at three hours caused a significant decrease in pHi. Similar decreases in pHi, which were elicited by the specific inhibitor of Na+/H+ exchange (ethylisopropylamiloride), caused no effect on alpha1- or beta1-mRNA levels. Exposure of NRK to the Na+ ionophore (monensin) in the absence of extracellular Ca2+ increased [Na+]i and alpha1- and beta1-mRNA levels. The increases in alpha1- and beta1-mRNA levels upon addition of ouabain were associated with significant increases in alpha1- and beta1-subunit proteins. CONCLUSIONS: In NRK, ouabain causes an increase in [Na+]i, which directly modulates Na+,K+-ATPase alpha1- and beta1-mRNA accumulation.

Animals↗
PubMed2000

Glucocorticoid modulates Na+/H+ exchange activity in vascular smooth muscle cells by nongenomic and genomic mechanisms.

BACKGROUND: In vascular smooth muscle cells (VSMCs), Na+/H+ exchange (NHE) plays an important role in intracellular pH (pHi) regulation. The genomic effect of glucocorticoid (GC) on NHE activity has been suggested in VSMCs. However, the nongenomic and genomic effects of GC on NHE activity and the underlying intracellular signaling mechanisms have not yet been demonstrated in VSMCs. Also, it is not known whether there are specific surface-binding sites of GC to the plasma membrane of VSMCs. METHODS: The effects of short (3 h)- and long (24 h)-term exposure to corticosterone (CORTI) on NHE activity were studied in cultured rat aortic VSMCs by using pHi measurement with the pH-sensitive fluorescent dye 2'7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. The NHE activity was calculated from the initial rate of Na+-dependent pHi recovery after the acid load. RESULTS: Short-term exposure of VSMCs to CORTI (10-6 mol/L) increased NHE activity, whereas long-term exposure to CORTI decreased it. The inhibitors of gene transcription (actinomycin D) and of protein synthesis (cycloheximide) did not affect the short-term effect of CORTI on NHE activity, but inhibited the long-term effect of CORTI on NHE activity. The cytosolic GC receptor (GR) antagonist (RU38486) inhibited both the short- and long-term effects of CORTI on NHE activity, but the cytosolic mineralocorticoid receptor antagonist (spironolactone) did not influence either the short- or long-term CORTI effects. Two protein kinase C (PKC) inhibitors (staurosporine A and calphostin C) and PKC down-regulation [24-h pre-exposure to phorbol 12-myristate 13-acetate (PMA)] inhibited both short- and long-term CORTI effects. Exposure to PMA for three hours mimicked the short-term CORTI effect. The short-term CORTI effect was inhibited by the disruptor of microtubule (colchicine), but not by the disruptor of filamentous-actin (cytochalasin B). The long-term exposure to CORTI decreased NHE (NHE-1) mRNA levels to 0.65 times the control level, whereas the short-term exposure to CORTI caused no effect. Scatchard analysis of [3H]CORTI surface binding to VSMCs showed a single class of CORTI binding sites with a Bmax of 876.2 fmol per mg of cell protein and a Kd of 12.2 nmol/L. RU38486 also inhibited [3H]CORTI surface binding to VSMCs. CONCLUSIONS: In VSMCs, NHE activity is stimulated by short-term exposure to CORTI, but is inhibited by long-term exposure to CORTI. The short-term stimulatory effect of CORTI on NHE activity is independent of gene transcription and protein synthesis, is mediated through the CORTI surface receptor, and occurs through a microtubule-dependent process. The long-term inhibitory effect of CORTI on NHE activity requires gene transcription and protein synthesis and occurs only through the cytosolic GR. The short- and long-term effects of CORTI on NHE activity occur via PKC activation. Therefore, CORTI differentially modulates NHE activity in VSMCs by nongenomic and genomic mechanisms.

Animals↗
PubMed2000

Low-grade intraosseous osteosarcoma in northern Japan: advantage of AgNOR and MIB-1 staining in differential diagnosis.

Low-grade intraosseous osteosarcoma is an uncommon form of bone cancer. It is occasionally difficult to recognize as a malignant tumor and is commonly misdiagnosed as a benign fibrous lesion. We retrospectively studied the records of 8 patients with low-grade intraosseous osteosarcoma in the files of the Tohoku Musculoskeletal Tumor Society in Japan. All tumors arose in the lower limb. The most common symptom was pain, with a duration exceeding 2 years in 4 patients. Radiologic findings, including those at magnetic resonance imaging (MRI), suggested malignancy in 5 lesions, whereas 3 were diagnosed as benign. Two patients initially presented with pathological fracture. The initial pathological diagnosis was malignant in 5 patients and benign in 3. All eight tumors were grade 1 in Broders' classification. The tumor showed a permeative pattern in all eight cases, but this pattern could not be confirmed in the multiple tiny fragments obtained as biopsy specimens in 3 cases. The number of silver-staining nucleolar organizer regions (AgNOR) per nucleus and MIB-1-positive rate were significantly higher in low-grade intraosseous osteosarcoma than in fibrous dysplasia, offering an advantage in differential diagnosis. Three patients (38%) developed high-grade sarcoma at the site of local recurrence after multiple intralesional excisions, and one of them died of the disease. The other 5 patients had a good clinical course after surgery with a wide margin. These findings indicate that preoperative diagnosis with radiologic investigation, including magnetic resonance (MR) imaging and histologic examination of biopsy specimens is essential in preparation for surgery with a wide margin, assuring a good clinical course, and the results of AgNOR and immunohistochemical MIB-1 staining might be helpful in differentiating low-grade intraosseous osteosarcoma from fibrous dysplasia.

Adolescent↗
PubMed2000

Effect of the 21-aminosteroid on nuclear factor-kappa B activation of Kupffer cells in endotoxin shock.

BACKGROUND: The 21-aminosteroid (U-74389G) is a nonglucocorticoid steroid that was synthesized to inhibit lipid peroxidation without the glucocorticoid activity. We recently demonstrated that the 21-aminosteroid administered to endotoxin shock mice reduces liver injury and improves the survival rate of mice through inhibition of nuclear factor-kappa B activation in the liver. The study was undertaken to determine whether the 21-aminosteroid could suppress pro-inflammatory gene up-regulation through inhibition of nuclear factor-kappa B activation in Kupffer cells. METHODS: Kupffer cells were isolated from rats by collagenase perfusion followed by pronase digestion. After a lipopolysaccharide addition, each assay was performed for tumor necrosis factor-alpha, interleukin-6, tumor necrosis factor-alpha messenger RNA, nuclear factor-kappa B, and I kappa B proteins. RESULTS: After the lipopolysaccharide addition, Kupffer cells released both tumor necrosis factor-alpha and interleukin-6. The 21-aminosteroid treatment suppressed the release of tumor necrosis factor-alpha in a dose-dependent manner. The 21-aminosteroid also inhibited the increase of tumor necrosis factor-alpha messenger RNA expression and nuclear factor-kappa B activation in Kupffer cells 1 hour and 30 minutes, respectively, after lipopolysaccharide addition. Furthermore, the 21-aminosteroid treatment suppressed the degradation of I kappa B proteins in lipopolysaccharide-stimulated Kupffer cells. CONCLUSIONS: These results suggest that the 21-aminosteroid inhibits release of the tumor necrosis factor-alpha and interleukin-6 from lipopolysaccharide-stimulated Kupffer cells by inhibiting nuclear factor-kappa B activation. This is accomplished by inhibiting I kappa B degradation in endotoxin shock and this may prove useful for the treatment of endotoxin shock.

Animals↗
PubMed2000

Aortic arch branches are no longer a blind zone for transesophageal echocardiography: a new eye for aortic surgeons.

OBJECTIVES: Branch arteries of the aortic arch have been a blind zone for transesophageal echocardiography. Information regarding blood flow, which is important in both planned and emergency operations on the aorta, has therefore been limited. We have established a technique for visualizing these arteries in nearly all cases. METHODS: In 25 consecutive patients requiring either planned or emergency operations on the aorta, the branch arteries were visualized whenever cerebral malperfusion was suspected. Lateral flexion of the probe tip was used when the trachea interfered with visualization of the arteries. RESULTS: The left subclavian, left and right common carotid, right subclavian, innominate, and left and right vertebral arteries were visualized in 96% (24/25), 92% (23/25), 96% (24/25), 100% (25/25), 84% (21/25), 92% (22/24), and 88% (21/24), respectively. The origin of the innominate artery was visualized in 36% (9/25). In some cases, dissection extended into branch arteries during surgery or during conservative therapy. When the subclavian artery was clamped, retrograde flow was detected in the vertebral artery (steal flow). The cannula for selective cerebral perfusion occasionally was entered into the right common carotid or subclavian artery and obstructed the other branch with a balloon. CONCLUSIONS: The branch arteries of the aortic arch, including the vertebral artery, are no longer a blind zone for transesophageal echocardiography. The information obtained with our new transesophageal echocardiography technique is helpful for diagnosis, monitoring, and decision making during aortic surgery and in critical care medicine. Visualizing these vessels is worth the effort.

Adult↗
PubMed2000

Echocardiography-assisted surgery in transaortic endovascular stent grafting: role of transesophageal echocardiography.

OBJECTIVE: Transesophageal echocardiography was applied to visualizing endovascular procedures during transaortic stent grafting for aneurysm and dissection at the distal arch, and the use of transesophageal echocardiography was evaluated. METHODS: The 16 consecutive patients (13 with aneurysms and 3 with dissections) were examined. Transesophageal echocardiography was used for (1) determining graft size, (2) guiding placement of the catheter in the descending aorta at an appropriate position without intimal damage, (3) guiding graft tailoring with a balloon catheter, and (4) examining the results after the procedures. RESULTS: Visualization was disturbed in one patient who had undergone a previous operation. The graft size was appropriate, except in one patient as a result of underestimation. Transesophageal echocardiography was helpful for navigating the graft placement and tailoring without intimal damage. We tried to keep a distance from the diaphragm of 9 cm and an attachment portion of 4 cm. In one patient the graft was placed too distally (7 cm from the diaphragm) to cover the thick atheromatous plaque with the graft. The patient had paraplegia. Transesophageal echocardiographic assessment of endoleak and thromboexclusion was identical to that of postoperative computed tomography or angiography, with a sensitivity of 100% (1/1) and a specificity of 100% (13/13). Leakage at the proximal suture and graft kinking were found in 3 patients. Successful thromboexclusion by transesophageal echocardiographic assessment (13 patients) was predictive of subsequent regression of aneurysm and dissection in the midterm follow-up period: there was complete and partial regression in 5 and 8 patients, respectively. CONCLUSION: Transesophageal echocardiography enables echocardiography-assisted operations with secure step-by-step endoluminal procedures and immediate intraoperative assessment, which is predictive of the postoperative results.

Adult↗
PubMed2000

Response of rabbit ciliary process cyclic nucleotides to specific phosphodiesterase inhibitors.

PURPOSE: To determine which cyclic nucleotide phosphodiesterase family activities can be identified in rabbit ciliary processes. METHODS: Freshly excised rabbit ciliary processes were incubated in vitro with family selective phosphodiesterase inhibitors in the absence or presence of activators of soluble or membrane bound guanylate cyclase. The resulting increases of cyclic AMP and cyclic GMP were measured by RIA. RESULTS: Rabbit ciliary process cyclic AMP levels were increased by the phosphodiesterase 1 and 4 selective inhibitors, 8-methoxymethyl-IBMX and rolipram, respectively. Cyclic GMP levels were increased by 8-methoxymethyl-IBMX; whereas the phosphodiesterase 5 and 6 selective inhibitor, zaprinast, increased cyclic GMP little. Nitric oxide donors increased cyclic AMP in addition to cyclic GMP, and inhibition of soluble guanylate cyclase eliminated the increase of cyclic AMP. The effects of sodium nitroprusside and the phosphodiesterase 3 selective inhibitor, cilostamide, on cyclic AMP were not additive suggesting that the sodium nitroprusside mediated increase of cyclic GMP, like cilostamide, inhibited phosphodiesterase 3. CONCLUSIONS: Cyclic AMP in rabbit ciliary processes is hydrolyzed primarily by phosphodiesterases 1 and 4, and, when cyclic GMP levels are low, by phosphodiesterase 3; cyclic GMP is hydrolyzed primarily by phosphodiesterase 1.

Animals↗
PubMed2000

Early results of LH-RH agonist treatment with or without chlormadinone acetate for hormone therapy of naive localized or locally advanced prostate cancer: a prospective and randomized study. The Prostate Cancer Study Group.

BACKGROUND: The majority of patients with localized and some cases of locally advanced prostate cancer undergo radical prostatectomy. However, radical prostatectomy cannot always be selected for those patients. In this situation, primary hormone therapy is an alternative treatment option. We have designed a prospective randomized study of the effects of primary hormone therapy for such patients. METHODS: A total of 151 patients with T1b, T1c, T2a, T2b or T3a prostate cancer who were not scheduled for radical prostatectomy were enrolled into this study. Patients were randomly allocated into two groups; Group I received luteinizing hormone-releasing hormone (LH-RH) agonist monotherapy (leuprorelin acetate depot, 3.75 mg monthly) and Group II received LH-RH agonist in combination with chlormadinone acetate (100 mg/day). Effects on serum prostate-specific antigen level, progression-free survival and survival were observed for 2 years. RESULTS: The reasons why radical prostatectomy was not scheduled were poor risk for surgery (38%), patient's wish (32%) and physician's recommendation (30%). After 12 weeks of treatment, 49% of the patients in both groups showed a complete response (CR). Of the patients showing a partial response (PR) after 12 weeks of treatment, 25% in Group I and 52% in Group II improved to CR 1 year later (p<0.05). Group II showed a longer progression-free survival (p <0.05). Progression-free survival rates were 62% (Group I) and 91% (Group II) in T2b patients and 43% (Group I) and 73% (Group II) in T3 patients. Only one patient in each group died from prostate cancer. CONCLUSIONS: Early primary hormone therapy is a reasonable treatment option for localized or locally advanced prostate cancer patients if radical prostatectomy was not scheduled. Chlormadinone acetate showed an additive effect with LH-RH agonist, at least in 2 years' observation.

Aged↗
PubMed2000

The effect of argatroban on injured endothelial cells by thrombin.

When endothelial cells are exposed to thrombin, they become perturbed and acquire thrombogenic properties. Argatroban is an arginine derivative, synthetic small molecule that binds to the active site of thrombin and inhibits its catalytic activity. Therefore, the effects of argatroban on endothelial cells, which had been injured by thrombin, were investigated. The established endothelial cell line, TKM-33, which had been cloned from human umbilical vein endothelial cells, was used. Endothelial cells produce plasminogen activator (PA) to prevent thrombosis and maintain the blood flow. When the endothelial cells were injured by thrombin, secretion of plasminogen activator inhibitor-1 (PAI-1) increased and then the PA activity proportionally decreased. The treatment of endothelial cells with argatroban after thrombin injury did not restore their reduced PA activity. However, the treatment of endothelial cells with argatroban prior to thrombin injury resulted in inhibiting the induction of PAI-1 secretion. Thus, pretreatment of endothelial cells with argatroban suppresses the inhibition of their PA activity by thrombin. Since the effect of thrombolytic agent may be modified by the fibrinolytic factors produced by the endothelial cells, the activity of staphylokinase (SAK) was measured in the presence of endothelial cells that had been injured by thrombin. SAK is a newly developed thrombolytic agent. SAK activity in the presence of injured endothelial cells by thrombin was lower than that in the presence of endothelial cells without thrombin injury. However, treatment of endothelial cells with argatroban prior to thrombin injury revealed higher SAK activity than that after thrombin injury. These findings indicate that argatroban pretreatment prevents thrombin injury of endothelial cells, which may then maintain their physiological function.

Arginine↗
PubMed2000

Analysis of plasminogen activation by the plasmin-staphylokinase complex in plasma of alpha2-antiplasmin-deficient mice.

Staphylokinase (SAK) expresses plasminogen activator (PA) activity by forming a complex with plasmin; this PA activity is inhibited by alpha2-antiplasmin (alpha2-AP) in plasma. However, SAK's activity is protected against inhibition by alpha2-AP in the presence of fibrin because the plasmin-SAK complex binds to fibrin. In the present study, the interaction between SAK and murine plasminogen was investigated in the plasma of alpha2-AP-deficient (alpha2-AP-/-) mice or plasminogen-deficient (Plg-/-) mice. Although the human plasmin-SAK complex was formed in equimolar mixtures of plasmin and SAK, the murine plasmin-SAK complex was not formed. Human plasminogen was activated by the human plasmin-SAK complex, although equimolar mixtures of murine plasmin and SAK did not activate murine plasminogen. These findings suggest that SAK does not react with murine plasmin. However, the murine plasminogen was activated by the human plasmin-SAK complex, although this activation was approximately 100-fold weaker than human plasminogen. Human and wild-type mouse plasminogens were not activated by the human plasmin-SAK complex in their plasma. In alpha2-AP-/- mouse plasma, murine plasminogen was activated by the human plasmin-SAK complex. Human or murine plasminogen, which had been added to Plg-/- mouse plasma, was not activated by the human plasmin-SAK complex. However, plasma clot lysis by the human plasmin-SAK complex was observed in both human and murine plasma. These findings indicate that: (1) murine plasmin does not react with SAK, (2) human plasmin-SAK complex activates murine plasminogen, (3) this activation is inhibited by murine alpha2-AP, but (4) this activation is not inhibited by murine alpha2-AP in the presence of fibrin.

Animals↗
PubMed2000

Characterization of the endothelin receptor subtypes in human prostate.

Endothelin (ET) receptor subtypes in human prostate with benign prostatic hyperplasia were investigated by binding and functional studies. In the displacement experiment, LU224332 [endothelin-A/-B (ET(A)/ET(B)) nonselective antagonist] competed for [125I]ET-1 binding with a monophasic curve. On the other hand, LU135252 (ET(A)-selective antagonist) and sarafotoxin S6c (S6c, ET(B)-selective agonist) competed for [125I]ET-1 binding with shallow and biphasic curves. The analysis of the displacement curves for LU135252 and S6c showed that both ET(A) and ET(B) subtypes coexist but that ET(A) is the dominantly expressed receptor. In human prostate strips, 10 microM of both LU135252 and LU224332 strongly inhibited the contractile response to ET-1 with equal potency. However, 10 microM of BQ788 (ET(B)-selective antagonist) did not show a clear inhibition. S6c also produced a contractile response, which was potently inhibited by LU224332 or BQ788, and slightly suppressed by LU135252. These results suggest that in human prostate both ET(A) and ET(B) subtypes are functional receptors mediating contraction, but that ET-1-mediated contractions are predominantly mediated by activation of dominant receptor subtype, ET(A).

Aged↗
PubMed2000

Five geranylgeranyl diphosphate synthases expressed in different organs are localized into three subcellular compartments in Arabidopsis.

Geranylgeranyl diphosphate (GGPP) is the precursor for the biosynthesis of gibberellins, carotenoids, chlorophylls, isoprenoid quinones, and geranylgeranylated proteins in plants. There is a small gene family for GGPP synthases encoding five isozymes and one related protein in Arabidopsis, and all homologs have a putative localization signal to translocate into specific subcellular compartments. Using a synthetic green fluorescent protein (sGFP), we studied the subcellular localization of these GGPP synthases. When these fusion proteins were expressed by the cauliflower mosaic virus 35S promoter in Arabidopsis, GGPS1-sGFP and GGPS3-sGFP proteins were translocated into the chloroplast, GGPS2-sGFP and GGPS4-sGFP proteins were localized in the endoplasmic reticulum, and the GGPS6-sGFP protein was localized in the mitochondria. Both GGPS1 and GGPS3 proteins synthesized in vitro were taken up into isolated intact pea chloroplasts and processed to the mature form. RNA-blot and promoter-beta-glucuronidase (GUS) analysis showed that these GGPP synthases genes are organ-specifically expressed in Arabidopsis. GGR and GGPS1 were ubiquitously expressed, while GGPS2, GGPS3, and GGPS4 were expressed specifically in the flower, root, and flower, respectively. These results suggest that each GGPP synthase gene is expressed in different tissues during plant development and GGPP is synthesized by the organelles themselves rather than being transported into the organelles. Therefore, we predict there will be specific pathways of GGPP production in each organelle.

Alkyl and Aryl Transferases↗
PubMed2000

RPT2. A signal transducer of the phototropic response in Arabidopsis.

The blue light receptor NPH1 (for nonphototropic hypocotyl) has been considered to be the only UV-A/blue light receptor that induces a phototropic response by the hypocotyl and root of Arabidopsis. By analysis of root phototropism (rpt) mutants, we show, however, the involvement of another blue light receptor as well as the existence of two separate signaling pathways working downstream of these receptors in the phototropic response. A newly isolated gene, RPT2, controls one of these pathways. The RPT2 gene is light inducible; encodes a novel protein with putative phosphorylation sites, a nuclear localization signal, a BTB/POZ domain, and a coiled-coil domain; and belongs to a large gene family that includes the recently isolated NPH3 gene. From genetic, physiological, and biochemical evidence, we propose a genetic model of the signaling pathways that induce the phototropic response in Arabidopsis.

Amino Acid Sequence↗
PubMed2000

Crystallization and preliminary crystallographic analysis of the Rho-binding domain of bovine Rho-kinase.

Rho-kinase binds to a small GTPase Rho in a GTP-dependent manner and regulates many cytoskeletal events in the cell. The minimum region of bovine Rho-kinase sufficient for Rho-binding was expressed as a fusion protein with glutathione S-transferase. After removal of the glutathione S-transferase, thin plate crystals were obtained. The selenomethionine-substituted protein was introduced and crystallized, as was the native protein. The crystals of the Rho-binding domain of Rho-kinase belong to the space group C2, with unit-cell parameters a = 148.0 (2), b = 26.1 (1), c = 39.6 (1) A, beta = 90.3 (1) degrees. The crystals diffract to a resolution beyond 1.5 A.

Animals↗
PubMed2000

The neuroimmunomodulatory peptide alpha-MSH.

Alpha-melanocyte-stimulating hormone (alpha-MSH), a neuroimmunomodulatory peptide of ancient origin, is known to be involved in the control of host responses. In inflammatory cells, in the periphery and within the central nervous system, alpha-MSH modulates the production and action of proinflammatory cytokines. This broad influence occurs via endogenous alpha-MSH (melanocortin) receptors. The key to this anti-inflammatory influence is inhibition of NF-kappa B. Indeed alpha-MSH inhibits activation of this nuclear factor through preservation of I kappa B alpha, which binds to NF-kappa B and prevents its migration to the nucleus. Cells transfected with alpha-MSH plasmid vector are resistant to challenge with bacterial lipopolysaccharide. The peptide also act on central melanocortin receptors to modulate inflammation in the periphery. In brief, alpha-MSH and certain of its fragments such as alpha-MSH [11-13] KPV modulate inflammation via three general actions: direct actions on peripheral host cells; actions on inflammatory cells within the brain to modulate local reactions; and descending neural anti-inflammatory pathways that control inflammation in peripheral tissues.

Animals↗
PubMed2000

[Antibody levels for diphtheria, tetanus and pertussis in young adult females immunized with whole cell pertussis-diphtheria-tetanus toxoid vaccine in infancy].

Antibody levels for diphtheria, tetanus and pertussis in 84 young adult females were measured. They had been immunized with whole cell pertussis-diphtheria-tetanus toxoid (DTwP) vaccine as a routine immunization in their infancy. Their history of DTwP vaccination were confirmed in their Maternal and Child Health Handbook, which includes their immunization record. Among the 84 cases, 4 cases (4.7%) had been immunized with the first dose of DTwP, 5 cases (6.0%) with the second dose, 23 cases (27.4%) with the third dose and 52 cases (61.9%) with the fourth dose. Of the 84 cases, 89.3% had received DTwP vaccine more than the third dose. In the 15-19 years after the last DTwP vaccination, the antibody positive rate for diphtheria and tetanus (> or = 0.01 IU/ml) were 86.9% and 94.0%, respectively. On the other hand, antibody positive rate for anti-pertussis toxin (anti-PT) and anti-filamentous hemaggulutinin (anti-FHA) (> or = 10 EU/ml) were 35.7% and 55.9%, respectively. The positive rate for pertussis compared with those for diphtheria and tetanus were lower. These findings suggested that DTwP vaccination in infancy does not provide sufficient immunity for young adults against pertussis, but DTwP vaccination provides adequate immunity against diphtheria and tetanus.

Adult↗