Biomedical subjects
Publications and source records attributed to T Fukushima.
A case with a midline dermoid cyst of the frontal bone away from the anterior fontanel is reported. Although a few such cases have been reported, detailed descriptions are not given. Possible intracranial extension of these lesions is discussed with review of the pertinent literature.
The fatty acid concentration of each lipid fraction of plerocercoids of Spirometra erinacei and the host snake serum was investigated. The major fatty acids of phospholipid of the plerocercoids were C18:1, C18:0 and C16:0, and those of the host snake serum were C16:0, C18:1 and C18:0, in order of amount in both cases. The changes of the fatty acid composition of phospholipid of the plerocercoids when they were incubated in physiological saline at 18 degrees C and at 37 degrees C for 24 h were investigated in both cases. Polyunsaturated fatty acids increased at 18 degrees C, and saturated fatty acids increased at 37 degrees C. Michaelis constants (Km) of beta-hydroxyacyl-CoA dehydrogenase (HAD), NADH: ubiquinone oxidoreductase (complex I) (NADH: ferricyanide reaction) and complex I (NADH: ubiquinone reaction) for NADH were 20.6, 50 and 13.3 microM, respectively. The ATP production in mitochondria of the plerocercoids was accelerated by adding ADP and inhibited by adding such electron transport system inhibitors as rotenone, antimycin A and sodium cyanide. These results suggested that the fatty acids in the plerocercoids played an important role in regulating the fluidity of membrane by changing the composition in membrane lipid corresponding with the change of temperature circumstance. The NADH reduced by HAD might be accepted by the complex I in the electron transport system, and thus the parasites were capable of ATP production in a classical pathway of the oxidative phosphorylation system.
The clinical, genetic, and neuroradiologic characteristics of dentatorubral-pallidoluysian atrophy (DRPLA) are delineated in six patients from three generations of a Japanese family. The clinical characteristics of the disease varied, the age at onset depending on patients with juvenile-onset were characterized by myoclonus, epilepsy, and mental retardation whereas cerebellar ataxia, choreoathetosis, and dementia were typical of adult- and senile-onset patients. All affected individuals showed one expanded allele with the repeat number of CAG at the DRPLA locus, ranging from 58 to 82, and a normal allele, ranging from 10 to 21. The most severely affected patient, a case of maternal transmission and with the largest allele, became bedridden in a vegetative state by age 12. On the CT and MRI, varying degrees of brain atrophy were present in all patients. T2-weighted MRI in patients with senile-onset showed symmetric high-signal lesions in the cerebral white matter, globus pallidus, thalamus, midbrain, and pons. However, MRI in younger patients revealed no such lesions and CT failed to demonstrate lesions in the globus pallidus and brain stem. Thus, intrafamilial heterogeneity of DRPLA was also evident on MRI. High-signal lesions involving both, subcortical white matter and thalamus may be characteristics of senile-onset patients and may correlate with their dementia.
To determine whether cytoplasmic motility relates to phagocytic activity of alveolar macrophages (AM), we measured the remanent field strength (RFS) from the AM containing Fe3O4 particles (5 x 10(6) cells) and the number of phagocytized fluorescent latex spheres in the AM without having Fe3O4 particles (10(6) cells) harvested by broncho-alveolar lavage from dog lungs in vitro. Cytoplasmic motility was estimated from the relaxation rate (lambda o; min-1) calculated from the decay curve of RFS and the number of phagocytized latex spheres was counted using fluorescent microscopy after the addition of latex spheres (5 x 10(7)). The tumor necrosis factor increased both lambda o and the number of phagocytized latex spheres, and cytochalasin D and colchicine decreased them in a concentration-dependent fashion. Increases and decreases in lambda o induced by drugs paralleled the number of phagocytized latex spheres. These results suggest that cytoplasmic motility reflects phagocytic activity of AM and both cytoplasmic movement and phagocytosis may be regulated by a similar mechanism in the cytoskeletal system.
Recent advances in the field of molecular biology have revolutionized our understanding of the functioning of living organisms and facilitated the development of robust tools for both diagnosis and treatment of diseases. With particular reference to the field of critical care medicine, development of molecular biology techniques have aided in the following: (1) rapid and highly specific detection of pathogenic infectious agents (eg, Mycobacterium tuberculosis, Pneumocystis carinii, cytomegalovirus, Legionella); (2) development of assays for measurement of circulating cytokines such as tumor necrosis factor (TNF) and interleukin (IL)-1 that has helped our understanding of the pathogenesis of the sepsis syndrome; (3) administration of antibodies or soluble receptors to attempt to prevent untoward effects of cytokines such as TNF or IL-1; and (4) the administration of recombinant deoxyribonucleic acid (DNA) or proteins to patients in an attempt to alter the course of a disease such as antioxidant enzymes (superoxide dismutase). The rapidity of progress in this field has been staggering, which necessitates frequent updating of our knowledge for clinicians to put these molecular tools to their best use. This brief review attempts to explain the basic principles of commonly used techniques in molecular biology including recombinant DNA, polymerase chain reaction, DNA libraries, gene therapy, and protein biochemistry in a manner that is understandable to those without an in-depth knowledge of the field.
Mutations in the p53 gene were analysed in 50 cases with breast cancer by PCR-SSCP and direct DNA sequencing. Mutations were found in 10 of 50 cases (20%) including a case with Tis, and loss of the normal allele was found in five of these cases. Eight of the 10 mutations occurred within highly conserved domains, but no mutational hot spots were found. GC to AT transitions were the most frequent mutations (six of 10 cases), while mutations at CpG dinucleotides were found in three cases (30%). AT to TA transversions were the second most frequent mutation (20%). The level of expression of p53 protein was assessed by Western blot analysis in 62 cases. Overexpression of p53 protein was detected in 21 of 62 cases (34%) including a case with Tis. There was a strong correlation between missense mutations in the p53 gene and overexpression of p53 protein. Overexpression of p53 protein was closely associated with increasing tumour size and ER-negative status among the various factors investigated, suggesting that p53 overexpression may reflect the lack of differentiation in breast cancer.
In order for neutrophils to function effectively in host defense, they have evolved specific attributes including the ability to migrate to the site of inflammation and release an array of toxic products including proteolytic enzymes, reactive oxygen species, and cationic proteins. While these compounds are intended for killing invading pathogens, if released inappropriately, they may also contribute to tissue damage. Such inflammatory tissue injury may be important in the pathogenesis of a variety of clinical disorders including arthritis, ischemia-reperfusion tissue injury, the systemic inflammatory response syndrome (SIRS), and the acute respiratory distress syndrome (ARDS). Despite the importance of neutrophil function in host defense and dysfunction in disease states, much remains unknown about the intracellular signaling pathways regulating neutrophil activity. This review will focus on the signaling molecules regulating leukocyte 'effector' functions including receptors, GTP-binding proteins, phospholipases, polyphosphoinositide metabolism, and protein kinases and phosphatases.
Leukocytes possess many properties critical to their effective functioning in inflammation, including the ability to migrate to the site of inflammation and release an impressive armamentarium of toxic products such as proteolytic enzymes, reactive oxygen species, and cationic proteins, capable of killing invading pathogens. This review focuses on the transmembrane signaling events whereby factors present in an inflammatory milieu activate these leukocyte effector functions. In the past several years, many of the components of these pathways have been elucidated at the molecular level, but large gaps remain in our understanding. The discussion follows the path beginning from the exofacial side of the plasma membrane toward the cell interior: from membrane receptors, GTP-binding proteins and adapter proteins to intermediary pathways including phospholipases and protein kinases. A detailed understanding of these regulatory mechanisms will have important therapeutic implications for amelioration of inflammatory tissue injury.
A 21-year-old man who had an increased number of eosinophils with morphological abnormalities, bone marrow fibrosis and multiple organ dysfunction failed to respond to methylprednisolone and hydroxyurea. He was diagnosed with hypereosinophilic syndrome (HES) probably due to myeloproliferative disorder, and underwent allogeneic bone marrow transplantation (allo-BMT) from an HLA-identical sibling. The engraftment was confirmed on day 21 after BMT, but the patient developed acute graft-versus-host disease (GVHD) with grade I veno-occlusive disease, and transient increase of eosinophils of the donor type followed by chronic GVHD of the extensive type. These complications were eventually controlled with cyclosporin A. The patient survived free of disease for more than a year after BMT. Allo-BMT seems to be a possible treatment of HES/MPD.
In a patient with Creutzfeldt-Jakob disease (Heidenhain type), which was characterized by the initial onset of visual symptoms and proved by autopsy, there was an antagonizing correlation between spontaneously-induced periodic synchronous discharges and photically induced giant evoked responses. In addition, the two electroencephalogram features appeared and disappeared in parallel with each other during the clinical course of the illness.
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Ingested ferrimagnetic (Fe3O4) particles were used to estimate noninvasively the motion of organelles in alveolar macrophages (AM) in intact rats during viral respiratory infection by parainfluenza type 1 (Sendai) virus. Four days after instillation of Fe3O4 particles (3 mg/kg) into the lung, remnant field strength (RFS) was measured at the body surface immediately after magnetization of Fe3O4 particles by an externally applied magnetic field. RFS decreases with time, due to particle rotation (relaxation) which is related to cytoplasmic motility of AM. Viral infection increased the relaxation rate (lambda o per min), and increases in lambda o reached a maximum 3 days after nasal inoculation (day 3). Viral infection (day 3)-induced increases in lambda o were dose dependently inhibited by either the L-arginine analogue N-nitro-L-arginine or by methylene blue, an inhibitor of guanylate cyclase activity. Bronchoalveolar lavage fluid obtained from infected rats contained significantly higher levels of nitrite than that from control rats (P < 0.01). In in vitro experiments, AM from infected rats showed significantly higher lambda o, nitrite production, and intracellular guanosine 3',5'-cyclic monophosphate levels than those from control rats (P < 0.01). Sodium nitroprusside, known to release nitric oxide concentration dependently, increased lambda o of AM from noninfected rats in vitro. These results suggest that nitric oxide plays an important role in AM cytoplasmic motility during viral respiratory infection.
D-Ala and D-Ser were detected in the sera of both normal subjects and patients with renal dysfunction, and their concentrations were higher in the patients than in the normal subjects. A positive correlation between the concentration of D-Ala or D-Ser and that of creatinine (r = 0.733, p < 0.001 or r = 0.634, p < 0.001) or blood urea nitrogen (BUN) (r = 0.449, p < 0.05 or r = 0.629, p < 0.001) was observed in sera from 20 patients with renal dysfunction. The fraction (%D) of D-Ala in the total Ala in serum ([D/(D+L)] x 100) correlated well with the concentration of creatinine (r = 0.811, p < 0.001), suggesting that it is a candidate as a marker for renal proximal tubular dysfunction. The correlations of %D of Ser with creatinine and BUN levels were 0.796 (p < 0.001) and 0.919 (p < 0.001), respectively, indicating that %D of Ser may reflect protein turnover or catabolism in certain tissues as well as renal proximal tubular dysfunction.
The enzyme xanthine oxidase (XOD) has an affinity for heparin and can bind to cultured porcine aortic endothelial cells. We have reported that the exposure of human XOD (h-XOD) to the lysine-specific reagent trinitrobenzenesulfonic acid or the arginine-specific reagent phenylglyoxal caused it to lose its affinity for heparin-Sepharose. The heparin-binding sites in h-XOD are further studied in the present article. From a chymotryptic digest of cyanogen bromide fragmented h-XOD, two peptides with an affinity for heparin-HPLC, A-1 and A-2, were isolated. Amino acid sequence analysis showed that both peptides had lysine and/or arginine residues. The A-1 region may direct its charged side chains toward the solvent while burying its hydrophobic side chains against the hydrophobic inside, because the A-1 peptide forms a highly amphipathic structure. Peptide A-2 contains triple lysine residues and constitutes a hydrophilic region.
The morphology of the cardiac veins that drain into the coronary sinus was studied in 31 human hearts, with special reference to the coronary artery dominant pattern (Barnes' classification). The results were as follows: 1. Great cardiac vein (GCV) The average GCV index of Barnes type I (BI) did not differ significantly from that of Barnes type II (BII). 2. Left marginal vein (LMV) (1) The LMVs were divided into two types, according to the angle made by the LMV and the truncal vein: rect (18 cases, 58%) and acute (11 cases, 38%) angular influx type. (2) The average LMV angle of BI (n = 9, mean +/- SD 77.0 +/- 23.2) was greater than that of BII (n = 19, mean +/- SD 48.1 +/- 34.3) and the difference was statistically significant (p < 0.05). (3) The average LMV index of BI did not differ significantly from that of BII. 3. Left posterior ventricular vein (LPVV) (1) The average LPVV influx angle of BI did not differ significantly from that of BII. (2) The average LPVV index of BI did not differ significantly from that of BII. 4. Middle cardiac vein (MCV) The average MCV index of BI did not differ significantly from that of BII. 5. Small cardiac vein (SCV) The average SCV index of BI did not differ significantly from that of BII. 6. Anterior cardiac veins (ACVs) The number of ACVs correlated with the SCV index, and the correlation was statistically significant (n = 31, r = -0.416, p < 0.02). 7. Coronary sinus (CS) The average CS index of BI did not differ significantly from that of BII. The right ventricular wall may not be perfused effectively during open heart surgery when retrograde coronary sinus perfusion (RCSP) is used. The present study demonstrated that this method can produce poor right ventricular perfusion in cases when the ACVs developed well.
A 63-year-old female presented with recurrent glioblastoma at the site of a right parietal glioblastoma which was diagnosed 1 year before. She was treated at that time by total removal of the tumor, irradiation, and chemotherapy. Four months after the initial treatment, serial thallium-201 single photon emission computed tomography (201Tl SPECT) showed increased uptake at the edge of the original tumor site. The index, the ratio of 201Tl uptake in the lesion to the normal brain, was 2.9 which suggested a recurrent tumor. Magnetic resonance images with gadolinium over the next 7 months demonstrated an enhanced mass lesion at the site of primary tumor resection and a new enhanced mass in the right temporal lobe. The lesion in the right parietal lobe had a 201Tl uptake index of 2.5, while the lesion in the right temporal lobe had an index of 1.5. Re-craniotomy and total resection of the tumors in the right parietal and temporal lobes were performed. The histological diagnosis of both tumors was glioblastoma. The proposed use of 201Tl SPECT for the differential diagnosis of recurrent glioma and radiation necrosis should be carefully considered because the 201Tl uptake index can vary in tumor with the same malignancy grade.
A 68-year-old male patient with renovascular hypertension (RVHT) and nephrotic syndrome (NS) is described. He was admitted to our hospital for detailed investigation of severe hypertension and massive proteinuria. After admission, a diagnosis of RVHT with a right non-functional kidney and NS was made. Nephrectomy and contralateral renal biopsy were performed for refractory hypertension and detailed investigation of the NS, respectively. The renal biopsy showed focal segmental glomerulosclerosis (FGS) in the left kidney, whereas the nephrectomised kidney exhibited only ischemic change. After the operation, his blood pressure became stable without anti-hypertensive agents, but proteinuria remained in the nephrotic range. Six months later, proteinuria had disappeared and his renal function was stable. These findings suggest that NS and FGS might have resulted from an activated renin-angiotensin-axis and that the prolonged NS was due to severe glomerular injury. Although there have been many reports describing the relationship between RVHT and FGS in an experimental environment, this relationship is very rare in clinical cases. Therefore we present this case to increase understanding of the cause of FGS.
In sarcomagenesis in rats infected neonatally with feline sarcoma virus (ST-FeSV), v-fes product (P85) was previously shown by us to be a predictive and preventive determinant. In order to explore the part played by P85 in tumor suppression, DNA was extracted from precancerous granulomas and from slow or rapid growing sarcomas induced by neonatal injection of the virus. The v-fes signal from extracted DNA was analyzed by PCR-SSCP. The prototype v-fes gene signal was detected in most lesions and found to be generally amplified in rapid growing sarcomas and in some granulomas. Several v-fes homologs showing varying mobilities in gel were seen in most sarcomas and some granulomas with or without the prototype v-fes signal. In slow growing sarcomas and granulomas induced in hosts that were immunized with ST-FeSV induced syngeneic sarcoma and proved to carry IgG antibody to P85, the prototype v-fes gene was found to be down-regulated and v-fes homologs were found to be reduced in number or eliminated. These results suggest that the development of v-fes mutations is associated with the growth potential of cells carrying the v-fes gene, and that host immunity to v-onc product influences the development of virogene rearrangements and results in slow and suppressed growth of tumors caused by neonatal infection with retrovirus.