Search PubMed⌕ Search

Biomedical subjects

N Haga

Publications and source records attributed to N Haga.

At least 91 records · Page 5Linked to original sources

Effect of cinpropazide on ischemic myocardial acidosis in dogs.

In dogs anesthetized with pentobarbital, the left anterior descending coronary artery (LAD) was occluded by an occluder so that the LAD flow could be set to about half the original flow (partial occlusion). Partial occlusion of the LAD continued for 90 min, and myocardial pH decreased by 0.71 pH unit 30 min after the start of partial occlusion. Cinpropazide, a coronary vasodilator, was injected intravenously 30 min after partial occlusion. Cinpropazide at the dose of 1 mg/kg, which increased LAD flow insignificantly in the nonischemic normal heart, attenuated the myocardial pH that has been reduced by partial occlusion, with a slight reduction in diastolic blood pressure. Restoration of myocardial [H+] 60 min after the injection of cinpropazide was 75.3%, and that of saline solution was 29.5%, indicating that cinpropazide restored the myocardial [H+] by 45.8% during ischemia. The effect of cinpropazide to increase myocardial pH was not observed in the dog with nonischemic heart, however. It is concluded that cinpropazide attenuates myocardial acidosis during ischemia.

Acidosis↗

Ultrastructural localization of hCG in the placenta and in testicular germ cell tumors.

Human chorionic gonadotrophin(hCG)-producing cells in the human placenta and in testicular germ cell tumors have been investigated by ultrastructural immunohistochemistry using labeled Fab'fragments of anti-hCG-alpha and anti-hCG-beta. Most reaction products were demonstrated in the rough endoplasmic reticulum (rER) and perinuclear spaces of syncytiotrophoblastic giant cells ( STGC ) occurring in embryonal carcinomas and in syncytial cells observed in choriocarcinomas and in normal placenta. The rER of placental and choriocarcinomatous syncytial cells was highly developed and invariably showed a positive reaction. However, the rER of STGCs varied both with regard to its degree of development and its immunoreactivity with hCG. Localization of hCG in the Golgi apparatus and in cytoplasmic granules was indefinite. Mononuclear cells reacting positively with anti-hCG-alpha or -beta were also demonstrated. Cytotrophoblast-like cells which failed to react with anti-hCG-alpha or -beta were noted adjacent to sTGCs and the significance of these cells is discussed.

Choriocarcinoma↗

Characterization and purification of a soluble protein controlling Ca-channel activity in paramecium.

The analysis of the voltage-sensitive Ca++ channel of the unicellular eucaryote, Paramecium has been extended to a biochemical level based on recent observations that the transfer of cytoplasm from wild-type cells into mutants lacking Ca++-channel function ("pawn" in P. tetraurelia and "CNR" in P. caudatum) causes mutant cells to regain Ca++-channel function. We have microinjected various cytoplasmic fractions into mutant cells and measured the restored Ca++-channel function using a convenient behavioral assay. Following the "curing" activity, we characterized and purified the component from wild-type cytoplasm that can restore the function missing in cells carrying mutations in the cnrC gene. The curing factor is not an RNA, but a heat-labile, -SH-containing protein that appears to affect existing mutant channels on the ciliary membrane. We have purified this factor over 500-fold from the soluble cytoplasm using conventional techniques. The protein is of low apparent molecular weight (less than 30,000 daltons), acidic, soluble, and does not have the properties of calmodulin.

Animals↗

Is ischemia-induced pH decrease of dog myocardium respiratory or metabolic acidosis?

Ischemia causes myocardial acidosis and elevation of myocardial CO2 tension (PCO2). We performed the present study to examine whether accumulation of hydrogen ion is a cause or result of accumulation of CO2. The myocardial pH and PCO2 were measured simultaneously in the dog heart, and the concentration of HCO-3 [( HCO-3]) was calculated according to the Henderson-Hasselbalch equation. Ischemia was induced by either partial or complete occlusion of the left anterior descending coronary artery (LAD). After LAD occlusion, the myocardial pH decreased with a marked decrease in [HCO-3], indicating that metabolic acidosis occurred. We ascertained in experiments with blood sample in vitro that an addition of lactic acid into blood decreased both [HCO-3] and pH (metabolic acidosis), whereas an addition of CO2 gas into blood increased [HCO-3] and decreased pH (respiratory acidosis). These findings suggest that ischemic acidosis is not respiratory in nature, but metabolic. The myocardial pH decrease due to ischemia, however, cannot be explained by the tissue lactate accumulation alone, because the decrease of [HCO-3] is far greater than the increase of lactic acid during ischemia.

Acidosis↗

Characterization of cytoplasmic factors which complement Ca2+ channel mutations in Paramecium tetraurelia.

The analysis of Ca2+-channel function in the single-celled eukaryote Paramecium can be extended to a biochemical based on recent observations that transfer of cytoplasm from wild-type cells into mutants lacking Ca2+-channel function ("pawn" mutants) causes the mutant cells to regain Ca2-channel activity. Using a convenient behavioral assay for Ca2+-channel function, we have used microinjection of cytoplasmic fractions into mutant cells to enrich for and characterize those components from wild-type cytoplasm which can "cure" cells carrying mutations in the 3 different pawn genes affecting Ca2+-channel activity (pwA,pwB, and pwC). In each case, the curing factor appears to be a protein component of an intracellular membrane. They are distinguishable on the basis of thermal, pH and divalent ion sensitivities. In addition, the factor curing the pwC mutational defect has been purified more than 180-fold. Furthermore, the pwB curing activity appears to be amplified during sequential transfer between pwB cells.

Animals↗

Intra- and interspecific complementation of membrane-inexcitable mutants of Paramecium.

Membrane excitation was the basis for backward swimming of Paramecium facing stimulus. According to standard genetic tests, inexcitable mutants fell into three complementation groups for both Paramecium tetraurelia (pwA, pwB, and pwC) and Paramecium caudatum (cnrA, cnrB, and cnrC). Cytoplasm from a wild type transferred to a mutant through microinjection restored the excitability. Transfusions between genetically defined complementation groups of the same species effected curing, whereas transfusions between different mutants (alleles) of the same group or between sister cells of the same mutant clone did not. Cytoplasmic transfers of all combinations among the six groups of mutants of the two species showed that any cytoplasm, except those from the same group, was able to cure. Since the pawns and the caudatum nonreversals complement one another through transfusion, they appeared to belong to six different complementation groups. The extent of curing, the amount of transfer needed to cure, and the time course of curing were characteristic of the group that received the transfusion. Variations in these parameters further suggested that the six groups represented six different genes. Because the donor cytoplasms from either species were equally effective quantitatively in curing a given mutant, the curing factors were not species specific. These factors are discussed.

Animals↗

Microinjection of cytoplasm as a test of complementation in Paramecium.

Mutants in Paramecium tetraurelia, unable to generate action potentials, have been isolated as cells which show no backward swimming in response to ionic stimulation. These "pawn" mutants belong to at least three complementation groups designated pwA, pwB, and pwC. We have found that microinjection of cytoplasm from a wild-type donor into a pawn recipient of any of the three complementation groups restores the ability of the pawn to generate action potentials and hence swim backward. In addition, the cytoplasm from a pawn cannot restore a recipient of the same complementation group, but that from a pawn of a different group can. Electrophysiological analysis had demonstrated that the restoration of backward swimming is not due to a simple addition of ions but represents a profound change in the excitable membrane of the recipient pawn cells. Using known pawn mutants and those which had previously been unclassified, we have been able to establish a perfect concordance of genetic complementation and complementation by cytoplasmic transfer through microinjection. This method has been used to classify pawn mutants that are sterile or hard-to-mate and to examine the ability of cytoplasms from different species of ciliated protozoa to restore the ability to swim backward in the pawn mutants of P. tetraurelia. A cell homogenate has also been fractionated by centrifugation to further purify the active components. These results demonstrate that transfer of cytoplasm between cells by microinjection can be a valid and systematic method to classify mutants. This test is simpler to perform than the genetic complementation test and can be used under favorable conditions in mutants that are sterile and in cells of different species.

Action Potentials↗

A protein called immaturin controlling sexual immaturity in Paramecium.

As in many metazoans, clones of some species of Paramecium have, after conjugation, a period of immaturity during which the cells cannot mate. The duration of immaturity is measured by the number of cell generations, which remains fairly constant, although duration in time varies with rate of cell reproduction. Genic involvement is shown by mutants with reduced periods of immaturity. In three different groups of Paramecium species, the cytoplasm of immature cells apparently contains the same substance which represses mating activity when injected into sexually mature cells. The immaturity-inducing substance seems to be absent from sexually mature cells, as brei made not only from mature cells in the stationary phase (mating-reactive cells), but also from those in the log phase (mating-non-reactive cells), does not repress mating activity when injected into mature cells. Variations in the amount of the substance during immaturity suggest that it controls the duration of the period. We have isolated and partially characterized the substance-a single protein called immaturin. The activity of immaturin is dose dependent and associated with a heat-labile protein of molecular weight (MW) 10,000.

Animals↗

Restoration of membrane excitability in a behavioral mutant of Paramecium caudatum during conjugation and by microinjection of wild-type cytoplasm.

When cells of the behavioral mutant cnrC of Paramecium caudatum were mated with the wild type, phenotype change from CNR (no backward swinning) to wild type in the cnrC mate occurred immediately after the formation of tight pairs. No change of phenotype occurred when cells of cnrA or cnrB were mated with wild type. Phenotypic change from CNR to wild type in cells of cnrC was also induced by microinjection of wild-type cytoplasm. Microinjection of wild-type cytoplasm induced no change in cells of cnrA or cnrB. Phenotypic change in the cnrC mate during conjugation can be explained by cytoplasmic exchange during conjugation, though transfer of membrane sites for excitability through membrane fluidity cannot be ruled out.

Action Potentials↗

Pathologic dislocation of the hip in von Recklinghausen's disease: a report of two cases.

We report two cases of von Recklinghausen's disease in which hip dislocations occurred gradually without trauma. In one case, the right hip joint dislocated at the age of 8 years, and in another case, the left hip dislocated at 2 years and the right hip at 3 years. Each case was accompanied by bone changes around the affected hips, vertebral deformity, and spinal tumor. One case had hemihypertrophy of the involved lower extremity. Both structural changes around the hip joint and paralysis may have resulted in the hip dislocation.

Bone Neoplasms↗

Laparoscopic Nissen fundoplication using laparosonic coagulating shears: report of a case.

A 64-year-old man was admitted to Gunma University Hospital because of gastroesophageal reflux disease and hiatus hernia. Endoscopic examination showed a linear ulcer and mucosal redness in the lower esophagus. Gastrointestinal contrast study revealed a large esophageal hiatal sliding hernia. Laparoscopic Nissen fundoplication was then performed. Short gastric vessels were divided and lesser omentum was ablated with laparosonic coagulating shears, and the fundus of the stomach was used to construct the wrap around the esophagus. Three hundred and sixty degree fundoplication was undertaken using four sutures to secure the wrap. The patient is well and is currently free from reflux symptoms. Laparoscopic Nissen fundoplication is effective in the control of gastroesophageal reflux in the patient with hiatus hernia. This case report demonstrates that the use of laparosonic coagulating shears is effective for the division of the short gastric vessels.

Cautery↗