A Candida antigen detection system for fungus infection in renal transplant patients.
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Biomedical subjects
Publications and source records attributed to M Kawaguchi.
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To assess the thrombopoietic activity of erythropoietin (Epo) in vivo in mice, we consecutively administered recombinant human Epo (rEpo) i.p. to intact and splenectomized mice for varying time intervals. Recombinant human Epo increased platelet counts in a dose-dependent fashion in a short-term trial for 5 days. An 18% +/- 12% increase in platelet counts was observed in intact mice injected with a total of 50 U rEpo over 5 days, whereas an increase of 31% +/- 15% was found in splenectomized mice treated in the same manner. The factor also elicited a significant increase in bone marrow megakaryocytic size of the same magnitude in both groups. The numbers of megakaryocytes and megakaryocytic progenitors in bone marrow were not altered by the treatment. In addition, rEpo induced a dose-related increment in spleen weight. Ultrastructural analysis of spleens in mice injected with rEpo for 5 days revealed no significant increase in sectional platelet counts and in the numbers of vacuolar and platelet-phagocytoid cells when compared with control mice treated with heated rEpo. These findings suggest that Epo has an effect on thrombocytopoiesis, functioning as a late stimulator in short-term administration, they also suggest that its ability is partially masked by splenic pooling by enlarged spleens, giving rise to the discrepancy in platelet counts between and splenectomized mice. However, the induced increases in both parameters, platelet counts and megakaryocytic size, declined after 5 days. Platelet counts returned to normal levels in intact mice 15 days after initiation of the injection, whereas no significant difference in megakaryocytic size was noticed on day 10 compared with controls. The same results came out in splenectomized mice. Anti-human rEpo antibody was not detected in the sera of treated mice in a series of experiments. The splenic weight remained at plateau levels for up to 30 days. Thus, the substantial effects of rEpo on megakaryocytopoiesis and platelet production are transient, neither due to the appearance of the antibody to human rEpo nor the concealment by splenic pooling. The mechanisms of the transient action of Epo on thrombocytopoiesis remain to be further studied.
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We noninvasively evaluated the effects of nicardipine on cerebral vascular responses to hypocapnia and blood flow velocity in the middle cerebral artery of 10 patients aged 17-60 (mean +/- SD 46.1 +/- 11.8) years. During fentanyl/diazepam/nitrous oxide anesthesia, mean blood flow velocity in the middle cerebral artery was measured and cerebral vascular reactivity to hypocapnia induced by hyperventilation was assessed before and during the administration of nicardipine. Mean blood flow velocity was measured using transcranial Doppler ultrasonography, and the cerebral vascular reactivity was expressed as the percentage change in mean blood flow velocity per unit change in end-tidal PCO2. During the administration of 5.1 +/- 1.3 micrograms/kg/min nicardipine, which caused a 26% reduction in mean arterial blood pressure, mean blood flow velocity increased significantly from 57.2 +/- 19.2 to 64.2 +/- 21.6 cm/sec (p less than 0.01, paired t test), whereas cerebral vascular reactivity showed no significant change (4.0 +/- 1.2% and 4.9 +/- 2.5%, respectively). In conclusion, during fentanyl/diazepam/nitrous oxide anesthesia in patients, cerebral vascular reactivity to hypocapnia was maintained and nicardipine-induced hypotension resulted in increased middle cerebral artery blood flow velocity with maintenance of carbon dioxide reactivity to hypocapnia.
The effects of local anesthetics (procaine and lidocaine) on the gamma-aminobutyric acid (GABA) and L-glutamic acid (Glu) levels in rat spinal cord were studied during the convulsive process. The present study also investigated the influence of central GABA manipulations on the local anesthetic-induced convulsions. An increase in spinal GABA levels was observed at the preconvulsive and convulsive states after administration of procaine (170 mg/kg, i.p.) or lidocaine (120 mg/kg, i.p.), which induced clonic convulsions; in the depressive state, GABA levels returned to normal; in all states, Glu levels were unchanged. Semicarbazide (25-100 mg/kg, i.p.), a glutamic acid decarboxylase inhibitor, produced a decrease in spinal GABA content and strongly enhanced both local anesthetic-induced convulsions as shown by a shortening of the latency and an increase in the mortality. Aminooxyacetic acid (AOAA; 10-40 mg-kg, i.p.), a GABA transaminase inhibitor, dose-dependently increased spinal GABA content and markedly suppressed procaine-induced convulsions. However, lidocaine-induced convulsions were enhanced by AOAA. These results suggest that the spinal GABA neuron may respond to the convulsions induced by local anesthetics. Furthermore, there is a clear relationship between spinal GABA content and procaine-induced, but not lidocaine-induced, convulsions.
We studied the effect of maternal hypoglycemia on skeletal growth in the offspring of nondiabetic and diabetic rats. Female Wistar rats were injected with streptozocin (30 mg/kg i.v.) 2-3 wk before mating, and diabetes was confirmed by an intraperitoneal glucose tolerance test. On postconception day 9.5 or 10.5, both control and diabetic dams received saline or Actrapid human insulin (400 mU/rat i.p.). Hypoglycemia (approximately 2.8 mM) was induced for 120 min in the insulin-treated mothers. Pregnancy was terminated on gestational day 20. Fetal bones and cartilage were double-stained with alizarin red S and alcian blue 8GS. Insulin-induced hypoglycemia caused delayed ossification in the fetuses of the control dams. The number of malformations, e.g., costal fusion waves, increased greatly. These effects were more striking in the fetuses of dams that had received insulin on day 10.5 rather than on day 9.5 of embryo development. This type of insulin-induced hypoglycemia further delayed ossification of the fetal bones in diabetic dams. The influence of maternal hypoglycemia on skeletal malformations and/or variations was greater in the fetuses of diabetic dams than in the fetuses of control dams. These data suggest that maternal hypoglycemia in early pregnancy has a striking effect on skeletal growth and malformations in fetuses. In addition, mild glucose intolerance in dams may amplify these hypoglycemic effects.
A 22-year old female with Takayasu disease, who underwent bilateral aorto-carotid bypass surgery developed hyperperfusion syndrome postoperatively. Following the operation, convulsion and headache developed and mean velocity in the middle cerebral artery, measured by transcranial doppler, elevated. Mean velocity gradually decreased on the 10th postoperatively day and became a plateau at 200% of preoperative value. Pulsatility index as a index of cerebral vascular resistance was low just after the operation, became normal the following day and gradually increased 10 days after the operation. These changes seem to be recovery of cerebral autoregulation. On the 20th postoperative day, computed tomography scan was examined and multiple low density areas were found in the basal ganglia regions, but these changes disappeared 2 months after the operation. These reversible changes of CT scan might show ischemic changes or cerebral edema induced by cerebral vasospasm.
Transcranial Doppler (TCD) and fiberoptic oximetry for continuous measurement of jugular venous oxygen saturation (SjO2) were used as perioperative monitoring of cerebral circulation in a patient with Takayasu disease who received bilateral aorto-carotid bypass. Following revascularization of the left carotid artery, mean velocity in the middle cerebral artery (MV) increased (lt 300%, rt 200% of control values) and SjO2 also increased. Following revascularization of right carotid artery, MV increased (lt 500%, rt 400% of control values) but SjO2 was unchanged. After bilateral revascularization, high velocity continued for about 10 days, and convulsion with headache occurred. Therefore hyperperfusion syndrome was suspected. By perioperative monitoring of MV and SjO2, it might be possible to evaluate intracranial hemodynamics, necessity of shunt operation as well as bilateral bypass, and postoperative hyperperfusion syndrome.
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Blood and urine samples were analyzed for ethanol, acetaldehyde, acetate and acetone during experimental hangover in 6 healthy male volunteers (A, B, C, D, E, F). They drank freely for some 4 hr. In flushers (A, F) at 9 hr after ingestion (ethanol: 92 g, 1.2 g/kg and 1.3 g/kg), acetaldehyde levels were low in the blood, but high in the urine (37 microM, 45 microM). Heavy drinkers, non-flushers of B (ethanol: 176 g, 2.5 g/kg), C (157 g, 2.4 g/kg) and E (182 g, 2.9 g/kg) had a slightly high [lactate]/[pyruvate] ratio and 3-hydroxybutyrate in the blood at 11 hr after alcohol ingestion. Blood ethanol levels were dose dependent and blood acetaldehyde in B and C had a slightly high 6.3 microM and 8.0 microM 9 hr later, respectively. B, C and E had a high urine acetone concentration (100 microM over) in hangover. In C, in particular, urine acetate and acetone levels were unusually high. The ratio in blood (urine) among alcohol metabolites at 9 hr after drinking was approximately ethanol 1000 (1000): acetaldehyde 0.2-1.0 (0.1-5.9): acetate 36-163 (22-1554): acetone 1-11 (3-47).
We described a transient low or non-selective proteinuria after forced lordosis as a characteristic of orthostatic proteinuria and the heteroporous theory and sieving function theory which might explain the mechanism of orthostatic proteinuria. The angiogenic action of the renin-angiotensin system played an important part in these theories. Angiotensin II was recognized as the key regulator of renal sodium excretion, because it reduced the urinary Na/K ratio. Since the purpose of this study is to investigate the influence of the renin-angiotensin system on the mechanism of orthostatic proteinuria, proteins and electrolytes in the urine were examined before and after lordosis in 9 healthy children (Group A) and in 6 children with orthostatic proteinuria (Group B). The urinary ratio of protein/creatinine (P/cre) in Group B was already significantly higher than that in Group A before lordosis and significantly increased after lordosis, while P/cre in group A did not increase after lordosis. The urinary Na/K ratio (Na/K) in Group B was already significantly lower than that in Group A before lordosis, and after forced lordosis, Na/K in Group A decrease with no difference between both groups observed. It is suggested that a significant increase on P/cre after lordosis was obtained only in Group A, whereas in both groups the renal vein may be compressed by forced lordosis and as a result angiotensin II may be stimulated. There might be a difference of the responsibility to angiotensin II in glomerular mesangium contraction between both groups.
Four patients with acute myocardial infarction (MI) complicating double rupture; interventricular septum and ventricular free wall ruptures, were studied. All patients had histories of hypertension, and pre-infarction angina pectoris of short duration less than 8 days without previous MI. The sites of infarction were anteroseptal in 2 patients and inferoposterior in the other 2. Only one case was complicated with mild pump failure (Killip class II). Blood pressure was adequately controlled after the onset of MI in all patients. Interventricular septal rupture occurred between 2 and 10 days after the onset of MI. Free wall rupture occurred between 2 and 22 days after MI. Types of free wall ruptures were oozing in 2 patients and blow-out in the other 2. Surgical repair was performed in 2 patients with the oozing type rupture, who however died soon after surgery. The autopsy findings were as follows: 3 patients had left ventricular free wall ruptures and one had right ventricular free wall rupture. One of the patients with left ventricular free wall rupture showed a secondary rupture of a pseudo-ventricular aneurysm. Postmortem coronary angiograms revealed 3 patients with single-vessel disease and one patient with double-vessel disease, indicating that coronary arterial lesions and complicated heart failure were not severe in these 4 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
A 63-year-old female, who had been suffering from idiopathic interstitial pneumonia (IIP) since two years and four months previously, was admitted with general fatigue, body weight loss, bloody sputum and progression of dyspnea. Chest roentgenogram on admission showed diffuse coarse ring shadows in the right middle and lower lung fields and in the left middle lung filed. Chest CT clearly showed honeycombing in bilateral dorso-basal segments of the lung. Serum CA19-9 level was elevated, and continued to increase during her clinical course. Sputum cytology was positive. Autopsy showed papillary adenocarcinoma of the lung (alveolar cell type). Immunohistochemical study of lung tissue showed positive CA19-9 staining on the surface of adenocarcinoma cells.
To know whether the pathogenesis of impending myocardial infarction(IMI) could be predicted by the direction of ST segment shifts during an ischemic chest pain, we studied 62 patients with IMI and undergoing emergent coronary angiography(CAG). They were selected from a consecutive number of 474 patients with unstable angina. IMI was defined when patients had more than 2 episodes of chest pain at rest under intensive pharmacological interventions after their CCU admission, and at least one of those was not relieved by nitroglycerin given intravenously. They were divided into 2 groups according to ST segment shifts during chest pain; 35 patients with ST elevation (G-1) and 27 patients with ST depression (G-2). The time of CAG was individually determined in each patient according to the severity of illness. Those with acute MI within 3 months before the study and 24 hours following the chest pain just before CAG were excluded from the study. New onset angina accounted for 49% in G-1 and 4% in G-2(p less than 0.01). Average history length of IMI, frequency of symptoms after CCU admission, and interval from the last symptom to CAG were similar in each groups. Single vessel disease was more predominant in G-1 than in G-2 (54% vs 11% p less than 0.01). Intracoronary thrombus(IT) in an ischemia related artery(IRA) was found in 97% of G-1 and 22% of G-2(p less than 0.001), while complex lesions(CL) proposed by Ambrose as another genesis of IMI were in 26% of G-1 and 74% of G-2(p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
We report a case of pernicious anemia in which the possession of platelet peroxidase (PPO)-like activity was proved in its erythroblasts. PPO-positive cells were found in a distinct minor population of hemoglobinized (as a mean of differentiated) erythroid cells in the bone marrow before treatment, but these cells disappeared following therapy with vitamin B12. The present report is considered to be the first case to identify PPO-like activity in mature erythroblasts from the nonmalignant clone. The existence of PPO in erythroid lineage in cases with pernicious anemia is discussed.
Adult rat hepatocytes formed floating multicellular spheroids in primary culture in an uncoated plastic dish with a positively charged surface. Cells in the spheroids formed in such a simple way were similar to those formed in dishes coated with proteoglycan fraction isolated from rat liver reticulin fibers; in both cases, cells maintained high ability to produce albumin and poor ability to proliferate in response to epidermal growth factor. Coating dishes with albumin was also helpful in spheroid formation; coating with 2-hydroxymethyl methacrylate resulted in formation of incomplete spheroids. Elimination of serum factors was essential for the formation of spheroids; when cells were washed with serum-containing medium before seeding or if the medium was replaced with a serum-containing medium, spheroid formation was completely inhibited. Collagens, fibronectin, and laminin, all of which promote the adhesion and spreading of hepatocytes on substrates, inhibited spheroid formation. Furthermore, collagens disintegrated spheroids, and cells in the monolayer initiated proliferation. Thus, two distinct, mutually exclusive features of primary culture of adult hepatocytes apparently exist; monolayer culture with proliferative activity in an adherent environment and spheroid culture with poor proliferative activity and high albumin-producing ability in a nonadherent environment.
23 patients with myelodysplastic syndromes (MDS) and 8 normal controls were analyzed for dysmegakaryopoiesis (DMP) in the bone marrow by alkaline phosphatase anti-alkaline phosphatase (APAAP) technique and by conventional May-Giemsa staining. In the immunocytochemical study, monoclonal antibody (MoAb) against glycoprotein (GP) IIb/IIIa was utilized to demonstrate megakaryocytic cells. 91% (21/23) of MDS cases were detected as having DMP by APAAP method, while only 52% (12/23) were detectable by Giemsa stain. There were difficulties in recognizing small micromegakaryocytes (micro MKs), designated as type 1 atypical MKs, by Giemsa staining. Furthermore, megakaryoblasts (MKBs) were detectable only by APAAP technique. In 8 normal controls, no type 1 and type 3 atypical MKs (round shaped multinuclear MKs) were observed either by Giemsa staining or by the APAAP method, suggesting that they are a distinctive feature of MDS. These results indicate the necessity of immunocytochemical technique for accurate recognition of DMP in MDS.
Campylobacter jejuni enterotoxin was partially purified from culture supernatant. The purified fraction after gel filtration indicated three bands at 68, 54, and 43 kilodaltons on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). This fraction enhanced the adenylate cyclase activity of HeLa cell membranes by 1.5-fold over that of the control. The study with anti-cholera toxin immunoglobulin G (IgG) and ganglioside affinity column chromatographies revealed that the eluent from the anti-cholera toxin IgG column chromatography exhibited a single band (68 kDa) on SDS-PAGE and native PAGE, whereas the eluent from ganglioside column chromatography exhibited two bands (68 and 54 kDa) on SDS-PAGE. These suggest that the 68-kDa polypeptide should have an immunological relationship with cholera toxin, and the 68- and 54-kDa polypeptides might be responsible for the recognition of ganglioside.