Presence of brain natriuretic peptide in urine.
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
M Kawakami
Publications and source records attributed to M Kawakami.
[A case of antiphospholipid syndrome associated with left subclavian artery thrombosis and left external iliac vein thrombosis].
Arterial thrombosis is one of the major symptoms of antiphospholipid syndrome (APS). However, thrombosis in a primary branch of the aorta has rarely been reported in APS. We report here a case of APS complicated by thromboses in both the left subclavian artery and the left external iliac vein. A 32-year-old woman was admitted in May, 1990 complaining of no pulse in the left superficial arteries (e.g., left radial artery) for the past 5 years and acute swelling of the left lower extremity. A left ascending phlebography showed an occlusion of the external iliac vein and arteriography revealed obstruction in the left subclavian artery. Collateral circulations were developed at the site of each thrombus. Clotting and immunological studies revealed a prolonged APTT, a high titer of anticardiolipin antibody and lupus anticoagulant positive. We ruled out various diseases and clinical risk factors predisposing to both arterial and venous thromboses. Accordingly, we concluded that both thromboses were based on APS. Following treatment with anticoagulants, aspirin and corticosteroid, the swelling of her left thigh was diminished and the antibody titer was decreased within 3 months.
Adult↗
[Clinical analysis of 6 cases of pericardial cysts].
We present a clinical analysis of 6 cases of pericardial cysts. There were two males and four females. Only one case of them had complaint of persistent cough. Four of 6 were observed in right costo-phrenic angle, and 2 were in left costo-phrenic angle. Surgical excision was performed in 6 cases, and all patients recovered good health. We suggest that in cases of pericardial cysts, surgical treatment should be performed, even if patients would not have remarkable complaint.
Adult↗
Bilateral adrenocortical adenomas causing Cushing's syndrome. Report of two cases with enzyme histochemical and ultrastructural studies and a review of the literature.
Patient 1 (a 50-year-old woman) with bilateral adrenocortical adenomas causing Cushing's syndrome underwent right-sided adrenalectomy. After an interval of 4 years 5 months, she underwent left-sided tumorectomy. Patient 2 (a 46-year-old woman) underwent bilateral tumorectomy after a frozen-section diagnosis. Each adrenal contained a single macronodule that consisted of compact cells, clear cells, and oxyphilic cells, which had characteristic enzyme histochemical and ultrastructural features. In addition, the adrenals had a so-called pigmented nodule and extracapsular small focus of compact and clear cell proliferation in case 2. The nonnodular part of the cortex was atrophic in both cases. Fourteen patients (mean +/- SD age, 42.5 +/- 5.55 years) with bilateral adrenocortical adenomas associated with Cushing's syndrome have been described in the literature. Thirteen (93%) of the patients were female. Three patients had unilateral or bilateral multiple adenomas. While the earlier described patients underwent bilateral total adrenalectomy, those in recent reports had part of the adrenal resected unilaterally or bilaterally (ie, tumorectomy). The above features are useful in differentiating bilateral adrenocortical adenoma from other types of bilateral adrenocortical lesions.
Adenoma↗
Brain natriuretic peptides in human plasma, spinal cord and cerebrospinal fluid.
In cases of heart failure, the plasma level of immunoreactive human brain natriuretic peptide (IR-hBNP) measured by radioimmunoassay increased 6- to 46-fold over normal level (4.1 +/- 1.0 pg/ml), depending upon the severity. These levels did not significantly correlate to the levels of IR-human atrial natriuretic peptide in individuals. A 4-kDa IR-hBNP, corresponding to authentic hBNP (1-32), was predominant in normal plasma. In cases of cardiac disease, larger molecules which were assumed to be precursors of the 4-kDa form were accumulated in plasma. IR-hBNP was detected in spinal cords (7-24 pg/mg protein) and cerebrospinal fluid (8-19 pg/ml) of patients with noncardiac diseases. The major molecular form corresponded to the hBNP (1-32).
Adult↗
12-Deoxyphorbol 13-isobutyrate contracts isolated rat thoracic arteries.
The vasocontractile effect of 12-deoxyphorbol 13-isobutyrate (DPB), an activator of protein kinase C (PKC), was studied to clarify the mechanism of the vascontractile response elicited by activation of PKC. DPB induced both a sustained increase in intracellular Ca2+ levels and contraction in isolated rat thoracic artery. For a given increase in intracellular Ca2+ levels. DPB induced a greater contraction than high K+ or ionomycin. In Ca(2+)-free media, DPB induced concentration-dependent contraction with a slow rate of rise without causing detectable changes in intracellular Ca2+ levels. The DPB-induced contractions in Ca(2+)-free media were less inhibited by the inhibitors of calmodulin or myosin light chain kinase than ionomycin-induced contractions in normal media were. These results indicate that activation of PKC might increase the Ca2+ sensitivity of contractile elements due to mechanisms not associated with the Ca(2+)-calmodulin pathway.
Animals↗
Prevention by nicardipine of dog basilar artery spasm caused by oxyhemoglobin in vivo and in vitro.
Intravenous infusions of nicardipine in a dose insufficient to lower blood pressure prevented the generation of the basilar artery spasm provoked by oxyhemoglobin (oxyHb) injected intracisternally in anesthetized dogs. The plasma concentration of nicardipine was comparable to that sufficient to suppress the oxyHb-induced contraction in isolated dog basilar arteries. Nicardipine appears to be similarly effective in antagonizing the vasoconstrictor action of oxyHb in vivo and in vitro.
Animals↗
Major component of Ra-reactive factor, a complement-activating bactericidal protein, in mouse serum.
A complement-activating bactericidal protein, Ra-reactive factor was isolated from mouse serum by an affinity method. The m.w. of the isolated RaRF estimated by glycerol density gradient sedimentation (around 300,000) was the same as that of the active material in mouse serum. As evidenced by gel filtration, the intact RaRF was decomposed into high (higher than 200,000) and low (50,000 to 200,000) m.w. components by treatment with 10% acetonitrile. SDS- and acid/urea-PAGE demonstrated that the high m.w. component was completely dissociated into equimolar quantities of two kinds of 28 kDa polypeptides, P28a and P28b, under reducing conditions, indicating that the association of these polypeptides was stabilized by disulfide bonds. The ability to bind specifically to the Ra determinant was retained in the high m.w. component, although the complement-activating potency was lost. The amino acid compositions of P28a and P28b polypeptides were compared with those of related serum proteins. The P28a and P28b polypeptides were found to have the highest homology to rat mannan-binding protein and mouse and human C1q subcomponent of complement.
Amino Acids↗
Effect of dietary fish oil on plasma thromboxane B2 and 6-keto-prostaglandin F1 alpha levels in septic rats.
Increased mortality from sepsis is associated with high levels of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (PGF1 alpha). Linoleic acid, an n-6 essential fatty acid, is the usual precursor of TXB2 and PGF1 alpha, while fish oil is rich in n-3 essential fatty acid, the precursor of less active moieties. Rats were fed chow, an essential fatty acid-deficient diet, or an essential fatty acid-deficient diet supplemented with linoleic acid or fish oil for 2 weeks. The animals then underwent a sham operation or cecal ligation and puncture to induce sepsis. Six hours later, blood was obtained for analysis. The chow and linoleic acid diets produced significant (twofold to fivefold) increases in levels of both TXB2 and PGF1 alpha after sepsis. The essential fatty acid-deficient diet and fish oil diet protected against increases in levels of TXB2 or PGF1 alpha during sepsis. Dietary restriction of linoleic acid or fish oil supplementation may play an important role in altering the inflammatory mediator response to sepsis.
6-Ketoprostaglandin F1 alpha↗
Relationship between cochlear blood flow and perilymphatic oxygen tension.
To clarify the characteristics of the blood circulation in the cochlea, we correlated cochlear blood flow and perilymphatic oxygen tension at various blood pressures. Cochlear blood flow was measured in guinea pigs by laser Doppler flowmetry, and perilymphatic oxygen tension by polarography. Blood pressure changes were induced by angiotensin II injection, trimetaphan camsylate injection and blood withdrawal. Cochlear blood flow generally paralleled systemic blood pressure, indicating a close correlation. In contrast, perilymphatic oxygen tension was slower to increase and decrease. However, when systemic blood pressure was lowered more gradually, perilymphatic oxygen tension did not show the same lag. These findings indicate that perilymphatic oxygen tension parallels systemic blood pressure when changes induced are slower and in a physiological range.
Angiotensin II↗
Autoregulation of cochlear blood flow. A comparison of cerebral blood flow with muscular blood flow.
The cochlear blood flow of healthy adult guinea pigs was measured with a laser Doppler flowmeter and flow dynamics were analyzed on the basis of autoregulation. Angiotensin II infusion was used to raise blood pressure, while phlebotomy was done to lower blood pressure. The characteristics of autoregulation of cerebral blood flow and muscular blood flow were also investigated. Cochlear blood flow was considered to have some autoregulation but was less than brain blood flow, which showed significant regulation. Muscular blood flow seemed to have no similar regulatory mechanism.
Angiotensin II↗
Activation of MAP kinase and enhanced phosphorylation of the 350-kDa protein by mitogenic stimuli in quiescent Balb/c 3T3 cells.
In quiescent Balb/c 3T3 cells, competence factors such as platelet-derived growth factor and 12-O-tetradecanoylphorbol-13-acetate (TPA) activated MAP kinase, whereas progression factors such as insulin did not. Insulin was, however, capable of activating MAP kinase in cells pretreated with TPA. Moreover, TPA plus insulin activated MAP kinase more strongly and for a longer time period than did TPA alone. Treatment of Balb/c 3T3 cells with competence factors stimulated phosphorylation of the 350-kDa protein which was immunoprecipitated with antibodies against brain high-molecular-weight microtubule-associated protein MAP1, whereas insulin treatment did not stimulate the phosphorylation. Insulin could induce, however, further increase in the phosphorylation of the 350-kDa protein, when added simultaneously with TPA or added to the TPA-treated cells. The enhanced phosphorylation of the 350-kDa protein thus correlated with the MAP kinase activation. As insulin acts synergistically with TPA to induce initiation of DNA synthesis in the quiescent Balb/c 3T3 cells, it seems that activation of MAP kinase and enhanced phosphorylation of the 350-kDa protein are accompanied by the initiation of DNA synthesis.
Animals↗
Immune suppression after acute ethanol ingestion and thermal injury.
Acute alcohol ingestion is commonly associated with burn injury. Both alcohol ingestion and burn injury produce immune suppression, but the combination of these factors on immune function has not been investigated. To study this combined effect, immune function was measured in rats with a 30% burn injury following a single ingestion of 2.4 g/kg of ethanol (EtOH) and compared to that of animals with burn injury only, animals with EtOH only, and animals with neither alcohol nor burn injury. Four days after ethanol and/or burn, animals receiving both ethanol and burn injury had significant suppression of in vivo chemotaxis and lymphocyte responsiveness to lipopolysaccharide (LPS) compared to animals receiving either burn injury alone or EtOH alone (P less than 0.05). There was no difference in responsiveness to concanavalin A (Con A). Serum corticosterone was significantly elevated by burn injury but not EtOH ingestion. EtOH treatment prior to injury caused a further increase in corticosterone level that was significantly associated with a decrease in immune function. These results indicate that a single EtOH exposure prior to burn injury produces greater immune suppression than does burn injury alone. This further decrease in immune function may contribute to increased susceptibility to infection and increased mortality in burn patients with acute EtOH ingestion.
Alcohol Drinking↗
Interleukin 5 up-regulates high-affinity interleukin 2 receptor expression by human resting peripheral T cells: a comparison with the effect of interleukin 4 on B cells.
The separate regulation mechanisms of cytokines on two classes of interleukin 2 receptors (IL-2R) on human peripheral T and B cells were analyzed by a flow cytometer using a double stain with IL-2R alpha (55 kilodalton Tac) and IL-2R beta (75 kilodalton mik beta 1, mik beta 3). Although the expression of IL-2R alpha by T cells was slightly enhanced by IL-2 and IL-4, expression of the beta chain was diminished by both cytokines. IL-5 by itself did not alter the expression of either IL-2R alpha or beta, but preculturing with IL-2 for 24 h followed by IL-5 for another 24 h induced an increase in IL-2R alpha expression and in simultaneous alpha/beta chain expression. Increased numbers of high-affinity IL-2R were confirmed by 125I binding assays. On B cells, IL-4 increased alpha, beta, and simultaneous alpha/beta chain expression, but IL-4-treated B cells did not show an increased number of high-affinity IL-2R.
B-Lymphocytes↗
Comparison of the effects of hydrostatic compressive force on glycosaminoglycan synthesis and proliferation in rabbit chondrocytes from mandibular condylar cartilage, nasal septum, and spheno-occipital synchondrosis in vitro.
We have developed a simple in vitro model whereby precise quantities of compressive force can be applied to cultured chondrocytes from craniofacial cartilage: mandibular condylar cartilage (MCC), nasal septal cartilage (NSC), and spheno-occipital synchondrosis (SOS). Using this model, we found that hydrostatic compressive force stimulated glycosaminoglycan (GAG) synthesis, a cartilage phenotype, in MCC and SOS chondrocytes and DNA synthesis in MCC, NSC, and SOS chondrocytes. These stimulations were dependent on force magnitude and duration, reaching maximal GAG synthesis at 27 hours and maximal DNA synthesis at 20 hours after application of force. The maximal increase of GAG synthesis induced by compressive force was about 60% at 100 gm/cm2 for 5 minutes in nonstimulated MCC chondrocytes and 40% at 50 gm/cm2 for 1 minute in nonstimulated SOS chondrocytes. The maximal increase in DNA synthesis, produced by a compressive force of 50 gm/cm2 for 1 minute, was 50% in NSC chondrocytes, 50% in SOS chondrocytes, and 30% in MCC chondrocytes. There was no stimulation of GAG synthesis in NSC chondrocytes. These observations suggest that extrinsic force regulates craniofacial growth by controlling the differentiation and proliferation of chondrocytes in the craniofacial skeleton and that the difference in their responses to compressive force may reflect differences in the characteristics of these cells and their physiologic function in vivo.
Animals↗
Role of endogenous endothelin in the development of hypertension in rats.
To further elucidate the pathophysiologic role of endogenous endothelin (ET), we have studied the chronic effect of anti-ET gamma-globulin on the development of hypertension in spontaneously hypertensive rats (SHR) and stroke prone SHR (SHR-SP) for three weeks. In neither SHR nor SHR-SP did repetitive bolus injection of anti-ET gamma-globulin suppress the rise in blood pressure. The present data suggest that endogenous ET is not likely to play a key role in the development of hypertension, although ET may induce a local vasoconstriction at the injured vascular wall.
Animals↗
Endothelin-1- and endothelin-3-like immunoreactivity in human cerebrospinal fluid.
Using highly specific and sensitive radioimmunoassays (RIAs) for endothelin-1 (ET-1) and endothelin-3 (ET-3), we have determined the concentrations of ET-1- and ET-3-like immunoreactivities (LI) in human cerebrospinal fluid (CSF). The concentration of ET-3-LI (82.5 +/- 4.8 pg/ml) was about 1.5-fold greater than that of ET-1-LI (34.3 +/- 1.3 pg/ml). There was no significant correlation between ET-1-LI and ET-3-LI concentrations in human CSF (r = 0.44). Reverse-phase high-performance liquid chromatography (HPLC) revealed a single major component of ET-1-LI and ET-3-LI coeluting with authentic ET-1 and ET-3, respectively. It is suggested that ET-1 and ET-3 play a neuropeptide-like role in the central nervous system.
Chromatography, High Pressure Liquid↗
Suppression of the cerebral vasospastic actions of oxyhemoglobin by ascorbic acid.
Oxyhemoglobin (Oxy-Hb) produced a concentration-dependent contraction of monkey, dog, and bovine cerebral artery strips. Treatment of Oxy-Hb with ascorbic acid suppressed the ability of Oxy-Hb to contract the arteries, especially in the monkey arteries. The ability of intracisternally applied Oxy-Hb to constrict the basilar artery in anesthetized dogs was diminished when Oxy-Hb was treated previously with ascorbic acid (AsA-Hb). The contraction caused by Oxy-Hb was suppressed by treatment with indomethacin and aspirin in isolated bovine cerebral arteries. Endothelium-dependent relaxations elicited by substance P and relaxations induced by stimulation of the vasodilator nerves with nicotine were suppressed by treatment with Oxy-Hb and AsA-Hb; however, the inhibitory effect of AsA-Hb was markedly less. Oxy-Hb attenuated nitroglycerin-induced relaxations in a dose-dependent fashion, whereas AsA-Hb in concentrations up to 1.6 x 10(-5) M did not significantly influence the relaxations. It is concluded that incubation of Oxy-Hb with ascorbic acid alters markedly the biological activity of Oxy-Hb; the vasoconstrictor activity is suppressed, and the ability to diminish vasodilator actions is minimized. These findings provide a rationale for the use of ascorbic acid in cisternal irrigation to prevent the development of cerebral vasospasm after a subarachnoid hemorrhage.
Animals↗