Biomedical subjects

M Tomita

Publications and source records attributed to M Tomita.

At least 19 recordsLinked to original sources

PubMed1997

Graft damage after a single lung transplantation for pulmonary hypertension in a rat model.

The hemodynamic effect and degree of damage in grafts of single lung transplants for pulmonary hypertension were studied in rats with monocrotaline-induced pulmonary hypertension. Inbred male Lewis rats (weight 200-230 g) were divided into two groups. Group 1 (control group, n = 16) underwent isogenic left lung transplantation, while group 2 (n = 15) received an intravenous administration of monocrotaline (80 mg/kg i.v.) and underwent isogenic left single lung transplantation 3 week later. Hemodynamic evaluations were performed prior to transplantation, at 1 h postoperatively, and on days 3 and 7 after transplantation. Mean pulmonary arterial pressure (mPAP) rapidly declined after transplantation in group 2, from 39.3 +/- 8.7 mmHg to 18.5 +/- 3.0 mmHg 1 h after transplantation, and remained stable on day 7 after transplantation. No significant difference in the mPAP between the two groups was observed after transplantation. The extravascular lung water volume (ELWV: dry/wet ratio) in the right lung of group 2 significantly increased on day 3 (0.86 +/- 0.02) (P < 0.01), and subsequently decreased to control levels on day 7 (0.83 +/- 0.02). There was no significant difference in the ELWV in the grafted lungs between the two groups (0.84 +/- 0.03 vs 0.86 +/- 0.04), but there was tendency toward an increase in ELWV in group 2 on days 3 and 7. These data thus demonstrated that a hemodynamic improvement was obtained by single lung transplantation; however the degree of graft damage was remarkable in the pulmonary hypertension group.

Animals↗

PubMed1997

Effect of aging and dietary restriction on hepatocyte proliferation and death in male F344 rats.

The proliferation and death of hepatocytes in rats fed ad libitum and rats on dietary restriction were evaluated in 3 to 24-month-old rats by employing immunocytochemistry for proliferating cell nuclear antigen (PCNA) and terminal dUTP nick end labeling (TUNEL). These techniques were also used to examine hepatic tissue infiltrated with leukemic cells in 24-month-old rats fed ad libitum. PCNA-strongly positive hepatocytes, PCNA-positive hepatocytes, and TUNEL-positive hepatocytes were reported previously to be equivalent to hepatocytes in the S phase, hepatocytes in the cell cycle, and dying hepatocytes, respectively. The proportion of PCNA-strongly positive hepatocytes and PCNA-positive hepatocytes declined with age. Dietary restriction diminished PCNA-strongly positive hepatocytes significantly but not PCNA-positive hepatocytes in young rats, but the proportion of PCNA-strongly positive hepatocytes was significantly higher following dietary restriction than that in rats fed ad libitum in advanced age. Growth stimulation by leukemic cell infiltration resulted in a recovery of the age-related decline of PCNA-strongly positive hepatocytes. Aging was associated with a progressive increase in the proportion of TUNEL-positive hepatocytes, with a smaller effect following dietary restriction than in rats fed ad libitum after 6 months of age. Our results indicate that age and dietary restriction induce proliferative inhibition. The inhibition depends on PCNA expression; this suggests that suppression of cell proliferation and cell death are enhanced in hepatocytes of senile rats.

Aging↗

PubMed1997

Serial histopathologic myocardial findings in a patient with ectopic atrial tachycardia-induced cardiomyopathy.

A 17-year-old woman was found to have ectopic atrial tachycardia by her physician. Echocardiography and cardiac catheterization revealed findings resembling dilated cardiomyopathy at the time of initial presentation. The tachycardia was controlled with atenolol only at a dose of 50 mg/day. However, at the age of 22, the presence of ectopic atrial tachycardia was once again confirmed. We successfully performed catheter ablation for persistent ectopic atrial tachycardia. Serial echocardiographic findings showed the left ventricular dimension and function appeared to return to normal 1 year postablation. However, despite pharmacologic control and catheter ablation therapy, histopathology revealed myocardial fibrosis presumably representing permanent damage of the heart secondary to tachycardia 1 year postablation.

Adolescent↗

PubMed1996

Intravascular substance P dilates cerebral parenchymal vessels through a specific tachykinin NK1 receptor in cats.

The role of substance P in the cerebral parenchymal circulation was examined in 19 anesthetized cats. The local cerebral blood volume in the temporoparietal cortex was measured by our photoelectric method. Cerebral blood volume reflects the cumulative dimensions of the parenchymal microvessels. Intravenous injection of 0.01, 0.1, and 1 mg/kg FK888 (N2-[(4R)-4-hydroxy-1-(1-methyl-1H-indol-3-yl) carbonyl-L-prolyl]-N-methyl-N-phenylmethyl-3-(2-naphthyl)-L-alaninamide) , a selective tachykinin NK1 receptor antagonist, had no significant effects (compared to the vehicle, ethanol) on cerebral blood volume and mean arterial blood pressure. Intracarotid injection of 1, 10, 100 pmol/kg, and 1 nmol/kg substance P increased cerebral blood volume (P < 0.01) in a dose-dependent manner (maximal increase of 6.5% at 5 min). Following injection of 1 nmol/kg substance P, cerebral blood volume was initially reduced, possibly due to the marked fall in mean arterial blood pressure (P < 0.01). The cerebral blood volume increase elicited by 1 nmol/kg substance P was strongly blocked (P < 0.05) by prior injection of 1 mg/kg FK888. However, the depressor effect of 1 nmol/kg substance P (-24 +/- 4 mm Hg at 30 s, P < 0.01) was partially inhibited (P < 0.01) by FK888. We conclude that endogenous substance P may not have a significant role in the maintenance of resting tone of cerebral parenchymal vessels. Intravascular substance P, however, dilates the small microvessels through a specific tachykinin NK1 receptor and could be involved in the development of pathologic processes such as migraine headache.

Animals↗

PubMed1996

Cloning and characterization of the cDNA encoding human biliverdin-IX alpha reductase.

Biliverdin reductase is classified into two isoforms in substrate specificity; biliverdin-IX alpha reductase and biliverdin-IX beta reductase with a molecular mass of 22 kDa and 34-42 kDa, respectively. We have cloned the cDNA encoding human biliverdin-IX alpha reductase from MOLT4 cDNA library. The cDNA of 1146 bp in nucleotide length contained an entire reading frame coding 296 amino acid residues. The NADH/NADPH binding consensus sequence was found in the amino-terminal region. Comparison between human and rat biliverdin-IX alpha reductases showed 82.8% identity in amino acid sequences and 80.3% identity in the coding nucleotides. The amino acid sequence of human biliverdin-IX alpha reductase showed no significant homology to that of human biliverdin-IX beta reductase. Northern blot analysis of poly(A) RNA from eight different human tissues revealed that the reductase mRNA was abundant in the brain, lung and pancreas but not in the liver. The distribution pattern of biliverdin-IX alpha message was different from that of heme oxygenase activity which is known to be high in the liver and to be low in the heart and lung.

Amino Acid Sequence↗

PubMed1996

Marked expression of plasma brain natriuretic peptide is a special feature of hypertrophic obstructive cardiomyopathy.

OBJECTIVES: We examined whether plasma brain natriuretic peptide levels are abnormally elevated in hypertrophic obstructive cardiomyopathy compared with other cardiac diseases. BACKGROUND: We previously reported that plasma brain and atrial natriuretic peptide levels were elevated in hypertrophic cardiomyopathy. METHODS: We compared plasma concentrations of brain and atrial natriuretic peptide and hemodynamic and echocardiographic data in 50 patients with hypertrophic obstructive cardiomyopathy (n = 15, mean [+/-SD] intraventricular pressure gradient 37 +/- 16 mm Hg), hypertrophic nonobstructive cardiomyopathy (n = 15), aortic stenosis (n = 10, mean pressure gradient 41 +/- 18 mm Hg) and hypertensive heart disease (n = 10, mean systolic/diastolic blood pressure 203 +/- 16/108 +/- 11 mm Hg, respectively) and 10 normal subjects. RESULTS: Plasma brain natriuretic peptide levels were higher in the hypertrophic obstructive cardiomyopathy group (397.1 +/- 167.8 pg/ml*) than in the hypertrophic nonobstructive cardiomyopathy (60.0 +/- 48.1 pg/ml*), hypertensive heart disease (53.9 +/- 31.4 pg/ml*), aortic stenosis (75.4 +/- 54.3 pg/ml*) and normal groups (9.8 +/- 6.4 pg/ml [*p < 0.05 vs. normal group, p < 0.05 vs. hypertrophic obstructive cardiomyopathy group]). Although plasma atrial natriuretic peptide levels were higher in the hypertrophic obstructive cardiomyopathy group than the other patient groups, the brain/atrial natriuretic peptide ratio in the hypertrophic obstructive cardiomyopathy group was higher (4.5 +/- 2.3) than those in the other three patient groups (1.1 to 1.4) and the normal group (0.7 +/- 0.5). Left ventricular end-diastolic pressure and left ventricular end-diastolic volume index were similar among the four patient groups. The interventricular septal thickness and the ratio of interventricular septal thickness to left ventricular posterior wall thickness were similar between the hypertrophic obstructive and nonobstructive cardiomyopathy groups. CONCLUSIONS: Abnormal elevations of plasma brain natriuretic peptide levels are difficult to explain on the basis of hemodynamic and echocardiographic data and are a special feature of hypertrophic obstructive cardiomyopathy.

Adult↗

PubMed1996

Susceptibility of hepatocytes to cell death induced by single administration of cycloheximide in young and old F344 rats. Effect of dietary restriction.

We evaluated the effect of a single dose of 1.0 mg/100 g body weight of cycloheximide (CHX) on the susceptibility of hepatocytes to cell death in young (6 months old) and old (24 months old) F344 rats fed ad libitum (AL) or on dietary restriction (DR), using terminal dUTP nick end labeling (TUNEL). The proportion of TUNEL-positive hepatocytes (TPH) at baseline (without administration of CHX) was significantly higher in advanced age. However, dietary intake did not influence the proportion of TPH at baseline irrespective of age Hepatocytes cell death, detected by TUNEL, was induced in the animal by a single intravenous injection of CHX. The proportion of TPH increased with time and reached a plateau 2.5 h after the administration of CHX in young AL and DR rats and old DR rats, but continued to significantly increase 4 hours after the administration of CHX in old AL rats. Our results indicate that the death of hepatocytes at baseline and susceptibility to cell death was enhanced by CHX in hepatocytes of senile rats. Our results also suggest that dietary restriction does not suppress the enhancement of cell death at baseline, but prevents age-associated increase in the susceptibility to cell death.

Aging↗

PubMed1996

Application of capillary gel electrophoresis to the diagnosis of the aldehyde dehydrogenase 2 genotype.

This study dealt with the application of capillary gel electrophoresis (CGE) to diagnosis of the aldehyde dehydrogenase 2 (ALDH-2) genotype. Electrophoresis was performed on a low cross-linked polyacrylamide gel ¿3% T [g acrylamide+g Bis (N,N'-methylenebisacrylamide)], 0.5% C (g Bis/% T)¿ in 100 mM Tris-borate buffer (pH 8.3) at -10 kV with on-column UV detection (260 nm). During the PCR reaction, DNA from the wild-type allele generated a MboII restriction site, which is an amplification created restriction site. This did not occur, however, with DNA fragments from the mutant allele. Therefore, determination of the heterozygous genotype, the coexistence of wild-type and mutant alleles, was easily possible. Analysis of the MboII restriction digests of the PCR products was completed in less than 20 min, showing two peaks corresponding to fragments of 125 (cleaved) and 135 (uncleaved) base pairs (bp), respectively. On the other hand, determination of the homozygous genotype, wild-type or mutant, was difficult in one electrophoresis run. The CGE of the MboII restriction digests gave a single peak and the identification, cleaved or uncleaved, was difficult under our experimental conditions. However, the addition of aliquots of the PCR reaction mixture to the restriction digests, followed by re-electrophoresis, allowed successful diagnosis, yielding two peaks (cleaved and uncleaved) for the wild-type and one peak (uncleaved) for the mutant allele. This study demonstrated that CGE offers a high-speed, high-resolution analytical tool for determining genetic types, as compared with the conventional slab gel methodologies.

Aldehyde Dehydrogenase↗

PubMed1996

cDNA cloning of rat pS2 peptide and expression of trefoil peptides in acetic acid-induced colitis.

By using a combination of the methods of reverse transcription-PCR and rapid amplification of cDNA ends, a cDNA for rat pS2 peptide (rpS2) was successfully cloned and sequenced from rat stomach. By RNA blot analysis, the gene was shown to be expressed abundantly in the stomach and only faintly in the duodenum, but not in other tissues including the distal small and large intestines. rpS2 expression was also examined in the rectum during the course of acetic acid-induced colitis; rpS2 mRNA was detected during the acute phase of colitis but not in normal controls or during the recovery phase. On the other hand, expression of rat intestinal trefoil factor (rITF) was down-regulated during the acute phase of colitis and then up-regulated during the recovery phase, whereas rat spasmolytic peptide was not detectable throughout the course of the induced colitis. These results indicate that the patterns and timing of the expression of these trefoil peptides are different from each other. rpS2 may play an important role in the proliferation of intestinal epithelial cells during the acute phase of mucosal ulceration, whereas rITF may be involved in differentiation of the cells, particularly to form goblet cells, during the recovery phase.

Acetic Acid↗

PubMed1996

A novel type of programmed neuronal death in the cervical spinal cord of the chick embryo.

We examined the massive early cell death that occurs in the ventral horn of the cervical spinal cord of the chick embryo between embryonic days 4 and 5 (E4 and E5). Studies with immunohistochemical, in situ hybridization, and retrograde-tracing methods revealed that many dying cells express Islet proteins and Lim-3 mRNA (motoneuron markers) and send their axons to the somatic region of the embryo before cell death. Together, these data strongly suggest that the dying cells are somatic motoneurons. Cervical motoneurons die by apoptosis and can be rescued by treatment with cycloheximide and actinomycin D. Counts by motoneuron numbers between E3.5 and E10 revealed that, in addition to cell death between E4 and E5, motoneuron death also occur between E6 and E10 in the cervical cord. Studies with [3H]thymidine autoradiography and morphological techniques revealed that in the early cell-death phase (E4-E5), genesis of motoneurons, axonal elongation, and innervation of muscles is still ongoing. However, studies with [3H]thymidine autoradiography also revealed that the cells dying between E4 and E5 become postmitotic before E3.5. Increased size of peripheral targets, treatment with neuromuscular blockade, and treatment with partially purified muscle or brain extracts and defined neurotropic agents, such as NGF, BDNF, neurotrophin-3, CNTF, bFGF, PDGF, S100-beta, activin, cholinergic differentiation factor/leukemia inhibitory factor, bone morphogenetic protein-2, IGF-I, interleukin-6, and TGF-beta 1, were all ineffective in rescuing motoneurons dying between E4 and E5. By contrast, motoneurons that undergo programmed cell death at later stages (E6-E10) in the cervical cord are target-dependent and respond to activity blockade and trophic factors. Experimental approaches revealed that early cell death also occurs in a notochord-induced ectopic supernumerary motoneuron column in the cervical cord. Transplantation of the cervical neural tube to other segmental regions failed to alter the early death of motoneurons, whereas transplantation of other segments to the cervical region failed to induce early motoneuron death. These results suggest that the mechanisms that regulate motoneuron death in the cervical spinal cord between E4 and E5 are independent of interactions with targets. Rather, this novel type of cell death seems to be determined by signals that either are cell-autonomous or are derived from other cells within the cervical neural tube.

Animals↗

PubMed1996

Application of capillary electrophoresis to the simultaneous screening and quantitation of benzodiazepines.

Capillary electrophoresis (CE) is an attractive approach for the analysis of drugs in body fluids. We made a simultaneous analysis of nitrazepam, diazepam, estazolam, bromazepam, triazolam and flurazepam using CE with on-column detection at 200 nm. We obtained the best electropherograms under a condition of 5 mM phosphate-borate (pH 8.5) containing 50 mM SDS and 15% methanol. We examined the effect of the sample solvent matrix on the electropherograms obtained, indicating that increasing the methanol content in the sample solvent or the injection volume above a certain threshold limit decreased the resolution. We then focused on application of the CE to the analysis of the drugs in spiked serum, being appropriate for an analysis within 25 min. Linearity, the detection limit, accuracy and reproducibility were established using this method. The calibration curve was linear up to 1 mg/l of serum concentration. The lower limit of detection was 5 pg per injection and 0.025 mg/l of the serum concentration for all the compounds except for flurazepam, for which they were 40 pg/injection and 0.2 mg/l. The detection limits obtained allowed toxicological and pharmacological determinations for nitrazepam, diazepam, estazolam and bromazepam, but not for triazolam and flurazepam. Only toxic blood levels for the latter two benzodiazepines could be quantified by this method. We concluded that the CE could at least be applicable to simultaneous screening for toxic levels of benzodiazepines. We suggest that this technique may offer criminal toxicologists a rapid, simple and adaptable approach for the estimation of many other drugs in body fluids.

Autoanalysis↗

PubMed1996

Cloning of the cDNAs for mast-cell chymases from the jejunum of Mongolian gerbils, Meriones unguiculatus, and their sequence similarities with chymases expressed in the connective-tissue mast cells of mice and rats.

By using the combination of reverse-transcription CR and rapid amplification of cDNA ends methods, two distinct cDNAs encoding mast-cell proteases (chymases; MCPs), designated as gMCP-1 and -2, were successfully cloned and sequenced from the jejunum of Mongolian gerbil, Meriones unguiculatus, infected with Nippostrongylus brasiliensis. On the basis of a comparison of the deduced amino acid sequences with those of known rodent mast-cell chymases, gMCP-1 was found to be highly similar to mouse mast-cell protease (mMCP)-4 and rat mast-cell protease (rMCP)-1, while gMCP-2 was similar to mMCP-5 and rMCP-3. Alghough mMCP-4 and -5 and rMCP-1 and -3 were restrictedly or mainly expressed in connective-tissue mast cells and serosal mast cells, the gMCP-1 and -2 genes were mainly transcribed in the jejunal mucosa and to a lesser extent in the skin and tongue. Moreover, kinetic study after infection revealed that the amounts of the gMCP-1 and -2 mRNAs in jejunum paralleled well the degree of intestinal mastocytosis. The expression of gMCP-1 and -2 in mucosal mast cells of gerbil jejunum was also confirmed by in situ hybridization. Since a tryptase, another type of MCP, was also expressed in mucosal mast cells of gerbils but not in those of mice and rats, the expression of MPCs in mucosal mast cells of gerbils is different from those of mice and rats. The Mongolian gerbil would be a useful model with which to investigate the physiopathological role of MCPs.

Amino Acid Sequence↗

PubMed1996

Postoperative chemotherapy for colorectal cancer by combining 5-fluorouracil infusion and 1-hexylcarbamoyl-5-fluorouracil administration after curative resection.

BACKGROUND: Colorectal cancer is one of the major malignant diseases and, recently, its incidence appears to be increasing. Surgical resectability is an important prognostic determinant; however, recurrent tumors are commonly noted, even after apparently curative surgery. Because such metastatic disease cannot be cured, better adjuvant therapies are urgently called for. METHODS: We studied the effect of postoperative chemotherapy using 5-fluorouracil (5-FU) infusions and 1-hexylcarbamoyl-5-fluorouracil (HCFU) oral administration for curatively resected Stage II to IV colorectal cancer. This study was prospectively randomized and controlled and 251 (93.3%) of 269 patients were determined to be candidates for statistical assessment. The inductive regimen for Group A included a total of 6 5-FU intravenous injections, 10 mg/kg, on postoperative days 0, 1, 2, 7, 8, and 9. For maintenance therapy, Group A also received oral HCFU, 300 mg daily for 52 weeks beginning 2 weeks after surgery. The regimen for Group B included only 5-FU injections of Group A. RESULTS: There were no differences in the prognostic factors or doses of 5-FU between Groups A and B. In addition, no difference was observed in the toxicity rate between the two groups. Group A, with 5-FU infusions plus oral HCFU administration, produced a reduction in the recurrence rate and a prolongation of the survival time for patients with rectal cancer. In a retrospective analysis, this protocol was also effective for patients with Stage III to IV, wall invasion-positive, and lymph node metastasis-positive colorectal cancers. CONCLUSIONS: This study suggests that the combination of 5-FU infusions and the continuous oral administration of HCFU is a reasonable therapeutic approach for patients with surgically resected colorectal cancer and a high risk of recurrence.

Adult↗

PubMed1996

Leukocytes, macrophages and secondary brain damage following cerebral ischemia.

The involvement of white blood cells in microvascular derangement as a cause of secondary brain damage following cerebral ischemia is reviewed. Relevant data from the literature are arranged in the chronological sequence of the microvascular derangement of the brain that occurs after cerebral arterial occlusion (as based on our own experimental observations). The inflammatory processes which appeared to be elicited by polymorphonuclear leukocytes (PMNL) in the ischemic region of the brain may begin with adhesion of PMNLs to endothelial cells, followed by blood-brain barrier disruption, transudation/exudation, edema, necrosis, and scar formation. Stimulated by cytokines released from damaged neurons and axons, two types of macrophages (ameboid and ramified) appear, increase in number in the ischemic lesion, and engulf the debris of dead neurons, degenerated axons. Further, macrophages may release cytokines which stimulate healing processes, such as astroglial proliferation and revascularization, and release neurotoxins which could gradually kill surviving neurons. Even under such circumstances, individual leukocytes/macrophages are well regulated by specific mediators/cytokines. An urgent task is thus to find ways of controlling these key mediators/cytokines to reduce the inflammatory process and the extent of neuronal death for attenuating the secondary brain damage, without altering their beneficial effects.

Acute-Phase Reaction↗

PubMed1996

Numerical aberrations of chromosomes 11 and 17 in colorectal adenocarcinomas.

Fluorescence in situ hybridization (FISH) is an easy and efficient means of measuring numerical chromosome aberrations in the interphase nuclei of solid tumors; however, the correlation between numerical chromosome aberrations and the clinical stage of solid tumors remains unknown. Thus, in the present study, we investigated the relationship between numerical chromosome aberrations and clinicopathologic features in colorectal adenocarcinomas. FISH was applied to surgically resected colorectal cancer samples from 45 patients to evaluate the numerical aberrations of chromosomes 11 and 17. The mean age of the patients was 65.1 years, and they comprised 13 women and 32 men. According to Dukes' classification, 5 patients were categorized as stage A, 21 as stage B, 10 as stage C, and 9 as stage D. Histologically, 18 of the samples were lymph node metastasis-positive. FISH revealed numerical aberrations of chromosome 11 in 27 out of the 45 patients (60%), and those with a lower chromosome 11 number had a significantly lower incidence of lymph node metastasis (P < 0.05). Chromosome 17 proved to have numerical abnormalities in 33 of the 45 patients (73%), and those with a higher chromosome 17 number had more DNA aneuploidy (P < 0.005). This is the first report to reveal the relationship between monosomy 11 and lymph node metastasis in colorectal adenocarcinomas.

Adenocarcinoma↗

PubMed1996

Bronchoscopic evaluation of bronchial healing after carinal reconstruction.

Bronchoscopic evaluation of the anastomoses created by carinal reconstruction was carried out over a period of 7 weeks in 6 patients who had undergone carinal and lobar resections for lung cancer, and 4 who had undergone carinal resection without pulmonary resection for carinal tumors. The techniques of reconstruction included end-to-end and end-to-side tracheobronchial anastomoses with omental, fat, or pleural wrapping. Bronchial healing at the anastomosis was evaluated using a bronchial healing score (BHS) based on the bronchoscopic findings. The degree of healing was scored on a 0 to 4 scale, with 0 indicating normal mucosa; 1, edema or reddening; 2, mucosal color changes; 3, ulceration; and 4, diffuse ulceration. One postoperative death occurred as a result of anastomotic leakage. The remaining nine patients were divided into three groups according to the bronchoscopic findings on postoperative day (POD) 7: group A (n = 3) had mild ischemia at the anastomosis, group B (n = 3) had moderate ischemia at the anastomosis, and group C (n = 3) had severe ischemia at the anastomosis. Bronchial healing of the anastomosis improved over a 7-week period in groups A and B, but was delayed in group C. These findings led to the conclusion that wound healing of the anastomosis following carinal reconstruction requires more than 7 weeks due to the consequent devascularization resulting from the extended bronchial resection and lymph node dissection.

Aged↗

PubMed1996

Effect of boiled barley-rice-feeding in hypercholesterolemic and normolipemic subjects.

Barley contains approximately 10% dietary fiber and is easily cooked with rice, the dominant cereal in Japan, to increase the intake of dietary fiber. This research involved three experiments to examine the influence of barley on blood lipids in human subjects. All subjects received a boiled barley-rice (50/50 w/w mix) supplement two times per day in place of rice for 2 or 4 weeks. In the normolipemic subjects, serum lipids were unaffected by the ingestion of barley for 4 weeks. In twenty hypercholesterolemic men aged 41 +/- 5 years, the ingestion of barley was associated with a significant fall in serum total cholesterol, LDL-cholesterol, phospholipids and LDL and VLDL-lipoproteins. In seven mildly hypercholesterolemic women aged 56 +/- 7 years, a significant improvement of serum lipid profiles was observed. The present study suggests the possibility that the ingestion of barley-rice could lower serum lipids in hypercholesterolemic subjects.

Adult↗

PubMed1996

Spinal tracts producing slow components of spinal cord potentials evoked by descending volleys in man.

Slow negative (N) and slow positive (P) waves are frequently produced in the posterior epidural space at the lumbosacral enlargement by epidural stimulation of the rostral part of human spinal cord. The production of these slow potentials are thought to be responsible for analgesia at the stimulated segment as well as below that level. In order to define the spinal tract which mediates these slow potentials, we stimulated directly or from the epidural space the dorsal, dorsolateral, lateral and ventral columns at the cervical or thoracic level, and epidurally recorded spinal cord potentials (des.SCPs) at the lumbosacral enlargement in 7 patients who underwent spine or spinal cord surgery. The des.SCPs recorded in the lumbosacral enlargement consisted of polyphasic spike potentials followed by slow N and P waves. At a near threshold level of stimulus intensity the slow N and P potentials were consistently elicited only by stimulation of the dorsal column. The slow waves were also produced by intense stimulation of other tracts, but remained significantly (P < 0.05 - P < 0.01) smaller than those evoked by dorsal column stimulation when compared at the same stimulus intensity. Moreover, the slow P wave could not be elicited even by intense stimulation (10 times the threshold strength for the initial spike potentials) of the ventral column. Thus, the results suggest that the slow N and P waves are mostly mediated by the antidromic impulses descending through the dorsal column.

Adult↗