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Biomedical subjects

A Tanaka

Publications and source records attributed to A Tanaka.

At least 163 records · Page 9Linked to original sources
PubMed2001

Stimulation of arterial smooth muscle cell proliferation by remnant lipoprotein particles isolated by immuno-affinity chromatography with anti-apo A-I and anti-apo B-100.

Postprandial lipidemia, characterized by high plasma triglyceride-rich lipoprotein remnants, is associated with atherosclerosis. It has also been known that proliferation of vascular smooth muscle cells is crucial for the development of atherosclerosis. In this study, we investigated the direct effect of remnant lipoprotein particles, which consist of chylomicron remnants and very low density lipoprotein remnants, on vascular smooth muscle cell proliferation. Blood was collected from six patients with postprandial lipidemia two hours after their usual meal. Remnant lipoprotein particles were isolated from plasma by immuno-affinity chromatography containing two monoclonal antibodies, anti-apo A-I (H-12) and anti-apo B-100 (JI-H). Remnant lipoprotein particles, as well as betaVLDL, significantly stimulated the proliferation of porcine coronary artery smooth muscle cells in a concentration-dependent manner, whereas very low density lipoprotein (d < 1.006) was virtually ineffective. These observations are consistent with recent reports that triglyceride-rich lipoprotein remnants, which are rich in apo E as well, are atherogenic.

Animals↗
PubMed2001

Triglyceride-rich lipoprotein cholesterol exceeds low-density lipoprotein cholesterol in hypertriglyceridemia patients.

The atherogenicity of triglyceride-rich lipoprotein has been revealed. This study was performed to explore the clinical importance of triglyceride-rich lipoprotein by measuring its cholesterol content and comparing it with other lipoprotein fractions. Blood samples were obtained from 103 patients whose fasting plasma triglyceride concentration exceeded 300 mg/dl. The cholesterol monitor using the technique of high-performance liquid chromatography was used for the measurement of their plasma cholesterol concentrations and the determination of cholesterol distribution among lipoprotein fractions. This monitor showed 4 peaks: large-triglyceride-rich lipoprotein, small-triglyceride-rich lipoprotein, low-density lipoprotein, and high-density lipoprotein. Total cholesterol increased with increasing triglyceride. The increment of total cholesterol was nearly equal to that of small-triglyceride-rich lipoprotein cholesterol. Small-triglyceride-rich lipoprotein cholesterol exceeded low-density lipoprotein cholesterol where plasma triglyceride concentration was over 500 mg/dl. In conclusion, triglyceride-rich lipoprotein may be clinically important for hypertriglyceridemic patients as a source of cholesteryl ester in arteriosclerotic plaques, and increased triglyceride-rich lipoprotein cholesterol may be used as a basis for hypertriglyceridemia atherogenicity. Our study suggests that hypertriglyceridemia should be treated to prevent arteriosclerotic disease.

Apolipoproteins E↗
PubMed2001

Clinical spectrum of epileptic spasms associated with cortical malformation.

The spectrum of clinico-electrical characteristics of epileptic spasms associated with cortical malformation was studied in detail. The subjects were 15 patients suffering from spasms and cortical malformation demonstrated by MRI. The types of cortical malformation causing spasms were various, including hemimegalencephaly, diffuse pachygyria, focal cortical dysplasia, and polymicrogyria. Ohtahara syndrome was diagnosed in 3 patients, and West syndrome in 8. Symptomatic localization-related epilepsy preceded West syndrome in 4 patients, and a transition from Ohtahara syndrome to West syndrome was observed in one. West syndrome was followed by symptomatic generalized epilepsy including Lennox-Gastaut syndrome in 4 patients. Nine patients showed a condition which was labeled "epilepsy with partial seizures and spasms" (EPS) and characterized by the coexistence of partial seizures and spasms, and multifocal epileptic discharges on EEG. Spasms occurred only as EPS in 5 patients. EPS appeared following Ohtahara syndrome or West syndrome in 4 patients, and showed a transition to symptomatic localization-related epilepsy in 4. However, EPS did not evolve into generalized epilepsy, and persisted until the time of last follow-up in 5 patients. Therefore, the clinico-electrical pictures of patients with spasms and cortical malformation were diverse and not always limited within those of typical generalized epilepsy.

Cerebral Cortex↗
PubMed2001

Effects of minor surgery and endotracheal intubation on postoperative breathing patterns in patients anaesthetized with isoflurane or sevoflurane.

We studied the effects of minor surgery and endotracheal intubation on postoperative breathing patterns. We measured breathing patterns and laryngeal resistance during the periods immediately before intubation (preoperative) and immediately after extubation following minor surgery (postoperative) in eight patients anaesthetized with sevoflurane and eight patients anaesthetized with isoflurane, breathing spontaneously through a laryngeal mask airway at a constant end-tidal anaesthetic concentration (1.0 MAC). In both sevoflurane-anaesthetized and isoflurane-anaesthetized patients, expiratory time was reduced and inspiratory and expiratory laryngeal resistance increased after surgery. In sevoflurane-anaesthetized patients, occlusion pressure (P0.1) increased without changes in inspiratory time (T(I)). Occlusion pressure did not change and T(I) was greater in isoflurane-anaesthetized patients after surgery. Minor surgery may have a small but significant influence on breathing and increased laryngeal resistance following endotracheal intubation may modulate these changes. The difference in breathing pattern between sevoflurane and isoflurane may be a result of different responses of the central nervous system to different anaesthetics in the presence of increased laryngeal resistance.

Adult↗
PubMed2001

Rearrangements of the DNA in carbon ion-induced mutants of Arabidopsis thaliana.

To elucidate the nature of structural alterations in plants, three carbon ion-induced mutations in Arabidopsis thaliana, gl1-3, tt4(C1), and ttg1-21, were analyzed. The gl1-3 mutation was found to be generated by an inversion of a fragment that contained GL1 and Atpk7 loci on chromosome 3. The size of the inverted fragment was a few hundred kilobase pairs. The inversion was found to accompany an insertion of a 107-bp fragment derived from chromosome 2. The tt4(C1) mutation was also found to be due to an inversion. The size of the intervening region between the breakpoints was also estimated to be a few hundred kilobase pairs. In the case of ttg1-21, it was found that a break occurred at the TTG1 locus on chromosome 5, and reciprocal translocation took place between it and chromosome 3. From the sequences flanking the breakpoints, the DNA strand breaks induced by carbon ions were found to be rejoined using, if present, only short homologous sequences. Small deletions were also observed around the breakpoints. These results suggest that the nonhomologous end-joining (NHEJ) pathway operates after plant cells are exposed to ion particles.

Arabidopsis↗
PubMed2001

Two-generation reproductive toxicity study of tributyltin chloride in male rats.

A 2-generation reproductive toxicity study of tributyltin chloride (TBTCl) was conducted in male rats using dietary concentrations of 5, 25, and 125 ppm TBTCl to evaluate its effect on sexual development and the reproductive system. F1 males were killed on postnatal day 119 and F2 males were killed on postnatal day 91. TBTCl affected the male reproductive system of rats. The weights of the testis and epididymis were decreased and homogenization-resistant spermatid and sperm count were reduced mainly in the 125 ppm TBTCl group. Histopathologic changes were also observed in the testis of this group and included vacuolization of the seminiferous epithelium, spermatid retention, and delayed spermiation. However, the changes were minimal in nature. The weight of the ventral prostate was decreased to 84% of the control value in the 125 ppm group in the F1 generation and decreased to 84 and 69% of the control value in the 25 ppm and 125 ppm TBTCl groups, respectively, in the F2 generation. The serum 17beta-estradiol concentration was also decreased to 55% of the control value in the 125 ppm group in the F1 generation and decreased to 78 and 57% of the control value in the 25 ppm and 125 ppm TBTCl groups, respectively, in the F2 generation. However, the serum concentrations of luteinizing hormone (LH) and testosterone were not decreased in these groups. These changes corresponded with those caused by aromatase inhibition and therefore TBTCl might be a weak aromatase inhibitor in male rats.

Animals↗
PubMed2001

Detection of E-cadherin expression after nerve repair in a rat sciatic nerve model.

The authors investigated E-cadherin expression during nerve regeneration after nerve suture using the rat sciatic nerve model. Five rats were used during each postoperative period. E-cadherin expression was detected by Western blot analysis and immunofluorescent staining with an anti-E-cadherin monoclonal antibody. The level of E-cadherin expression was calculated as the amount relative to that found in normal control nerve. The level of E-cadherin expression was decreased at first, and then gradually increased. The maximum level of E-cadherin was 1.92 +/- 0.07 fold in the sutured nerve. The level of E-cadherin expression in the sutured nerve was significantly greater (p < 0.0001) than that of the normal control nerve from postoperative day 3 to 21, and that of sutured nerve returned to the control level by postoperative day 28. The immunofluorescent staining results indicated that E-cadherin expression was almost negative or decreased immediately after the operation, but the degree of expression increased gradually in Schwann's cells. The degree of E-cadherin expression was significantly greater than that of normal control nerves from postoperative day 7 to 14, and returned to the control level by postoperative day 21. These results demonstrate that E-cadherin expression increases during nerve regeneration, and the expression was observed mainly in Schwann's cells. The degree of E-cadherin expression may affect the rate of nerve regeneration.

Animals↗
PubMed2001

The differential expression of N-cadherin in vascularized and nonvascularized nerve grafts: a study in a rat sciatic nerve model.

The authors investigated N-cadherin expression in vascularized and nonvascularized nerve grafts using a rat sciatic nerve model. The vascularized and nonvascularized nerve grafts were elevated, and then both nerves were sutured to the original site. At various periods after the operation, the entire graft was removed. N-cadherin expression was detected via Western blot analysis and histochemical staining using anti-N-cadherin antibody. In both grafts, the level of N-cadherin expression increased after the operation, but during postoperative weeks 6, 9, and 12, the level in the vascularized graft was significantly (p = 0.00023, 0.0018, and 0.0010, respectively) higher than that in the nonvascularized graft. At postoperative week 14, the level of both grafts returned to the control level. Histochemical findings showed that N-cadherin was expressed around the regenerated axons in both grafts, and the degree of regeneration was greater in the vascularized graft than in the nonvascularized graft. These results demonstrate that the expression of N-cadherin increases during the process of axonal regeneration in both grafts, and that the degree of the expression is augmented by vascularization of the nerve graft.

Animals↗
PubMed2001

Molecular response to ischemia-reperfusion of rat skin: study of expression of p53, p21WAF-1, and Bax proteins, and apoptosis.

The authors investigated the expression of p53, p21WAF-1, and Bax proteins, and apoptosis to elucidate the cellular response to ischemia-reperfusion of the skin. The rat left lower limb was dissected at the inguinal region retaining the bone and femoral vessels, and the vessels were clamped to produce an ischemic condition. After 6 hours the clamps were removed, and the plantar skin was resected at various times up to 72 hours after reperfusion. Five skin specimens were obtained at each time point from 5 rats. When a rat died during the study, additional rats were used until five specimens could be obtained from 5 rats at each time point. The expression of the three proteins was detected by Western blot analysis. The apoptotic cells were detected using the terminal deoxytransferase-mediated dUDP nick-end labeling assay. After reperfusion, the levels of p53 and p21WAF-1 were significantly higher in the ischemia-reperfusion rats compared with the sham-operated rats. However, the levels of Bax protein did not show a noticeable increase at any period. The apoptotic cells in both the epidermis and dermis were not evident compared with the sham skin, which were similar to those in the nontreated, normal skin. These results demonstrate that p53 and p21WAF-1 proteins accumulate after 6 hours of ischemia of the skin during reperfusion. Moreover, it is speculated that accumulation of these proteins plays an important role in the survival of the skin by inducing growth arrest of the cells, but not apoptosis.

Animals↗
PubMed2001

Experience with surgical treatment of hidradenitis suppurativa.

The authors report their experience with 23 sites of hidradenitis suppurativa, including cases with musculocutaneous flap repair, and discuss the surgical methods applied. Twenty-three sites in 19 patients with chronic inflammatory skin lesions were reviewed. The lesions were divided into two groups: The limited group was comprised of mild lesions, which appear isolated and have limited abscesses without sinus tract formations. The severe group was compromised of severe lesions, which included diffuse, multiple abscesses with severe sinus tract formation and fibrosis. Nine sites were limited and 14 sites were severe. After resecting the lesion, the defect was covered with a split-thickness skin graft (four sites were limited, nine sites severe), a musculocutaneous flap (five sites severe), primary closure (four sites limited), and a local skin flap (one site limited). In six sites in 6 severe-group patients, local recurrence occurred. The local recurrence rate differed significantly between the limited and the severe groups. The reason for this may be because the lesions in the limited group could be resected completely, whereas the lesions in the severe group were diffuse and total resection was sometimes difficult for various reasons. The method of surgical repair did not affect the local recurrence rate. In recurrent cases, four sites treated with skin grafting required further surgical treatment, and two sites treated with musculocutaneous flaps were controlled with oral antibiotics. In conclusion, sufficient resection of the lesion is the most important issue in treating follicular occlusion triad disease. In lesions that can be resected completely, the surgical procedure to cover the lesions should be selected to suit the size and site of the defect. However, in cases that cannot be resected completely, a musculocutaneous flap is recommended instead of a skin graft for enhanced postoperative management of the recurring wound, and its contribution to aesthetic and functional improvement.

Adult↗
PubMed2001

The occurrence of various collagen diseases in one family: a sister with ISSc, PBC, APS, and SS and a brother with systemic lupus erythematosus.

We encountered siblings who had collagen diseases and related symptoms. Case 1 was a 53-year-old woman who had limited cutaneous systemic sclerosis (ISSc) associated with primary biliary cirrhosis (PBC), antiphospholipid antibody syndrome (APS), and subclinical Sjögren's syndrome (SS). Case 2 was a 48-year-old man, her younger brother, with systemic lupus erythematosus (SLE) that developed at 32 years of age. Investigation of their family revealed that their mother had Raynaud's phenomenon, arthritis, and subclinical Sjögren's syndrome, and that another younger brother of Cases 1 and 2 had Raynaud's phenomenon and general fatigue. HLA analysis revealed that the sister and brother had some identical HLA antigens in common, including A2, A33 (19), B67, B44 (12), Cw7, DR2, DR6, DR52, and DQ1. The sister, brother and their mother had common HLA antigens including A2, B67, Cw7, DR2, and DQ1. Although Cases 1 and 2 shared the same HLA system, they presented different phenotypes of collagen disease.

Antiphospholipid Syndrome↗
PubMed2001

Frameshift mutations at mononucleotide repeats in RAD50 recombinational DNA repair gene in colorectal cancers with microsatellite instability.

To identify additional genes targeted for microsatellite instability (MSI), we search for human genes which contain mononucleotide repeats in their coding region, selected 7 genes (RAD50, DNA-PKcs, FLASH, Apaf-1, XPG, CtIP, and MLSN1), and analyzed frameshift mutations in them. Here we report that 60% (3 out of 5) of human colorectal cancer cell lines exhibiting a high frequency of MSI (MSI-H) and 46% (6 out of 13) of MSI-H primary colorectal tumors had mutations in the (A)9 repeat of RAD50 recombinational repair gene. In contrast, no frameshift mutations were found in any of the 5 MSI-negative colorectal cancer cell lines, 8 colorectal tumors exhibiting a low frequency of MSI (MSI-L), or 28 MSI-negative colorectal tumors. No mutations were found in the mononucleotide repeats of 6 other genes, even in MSI-H cancers. These results suggest that RAD50 frameshift mutations may play a role in the tumorigenesis of MSI-H colorectal cancers.

Colorectal Neoplasms↗
PubMed2001

Genetic and familial considerations of primary biliary cirrhosis.

The genetic basis of human autoimmune diseases is receiving increasing attention. Primary biliary cirrhosis (PBC) is a model autoimmune disease reflective of other organ-specific autoimmune pathology. PBC is an enigmatic autoimmune disease that predominantly affects women and leads to destruction of intrahepatic bile ducts. The serological hallmark of this disease is characterized by antimitochondrial antibodies that specifically react with the E2 components of 2-oxodehydrogenase enzymes, including PDC-E2. There are no clear major histocompatibility complex associations with the development of PBC, despite the observation that first-degree relations of index patients with PBC have a 4-6% prevalence of development of PBC. This risk factor is comparable or higher than any other human autoimmune disease and suggests that a genome-wide approach towards dissection of genetic associations would lead to valuable new insights. In this review, we place these concepts in perspective and highlight in particular the genetic associations in PBC and the importance of studying siblings with PBC who are concordant for disease.

Adult↗
PubMed2001

Metabolism of triglyceride-rich lipoproteins and their role in atherosclerosis.

Recent large-scale clinical trials indicate that hypertriglyceridemia is a risk factor in coronary artery disease; however, the mechanism has not yet been completely clarified. We are currently studying the metabolism of triglyceride-rich lipoproteins and their role in atherosclerosis. Remnants, one of atherogenic lipoproteins, showed a marked increase and remained high even 8 hours after fat loading, especially in patients with coronary artery disease or diabetes mellitus. This shows that the postprandial state persists almost the whole day in these patients. Accordingly, it may be important to assess post-prandial remnant concentrations when evaluating risk factors for atherosclerosis. We identified apo B100 expression in the epithelial cells of the small intestine by immunoblotting with anti-apo B100 monoclonal antibody and dot-blotting of PCR-amplified cDNA. This indicates that not only apo B48, but also apo B100 is expressed in human small intestinal epithelium. The expression of apo B100 suggests that dietary VLDL may be synthesized in human small intestinal epithelium and converted into LDL, which may play an important role in atherosclerosis. A new receptor, apo B48, which binds and internalizes triglyceride-rich lipoproteins via a domain in apo B48, was identified in human monocyte-macrophages. The receptor differs from the scavenger receptor family and LDL receptor family because it does not bind acetyl LDL and it does bind VLDL devoid of apo E. Immunohistochemical studies indicate colocalization of anti-apo B48 receptor antibody in human atherosclerotic lesion foam cells, suggesting that apo B48 receptor may contribute to foam cell formation and atherosclerosis.

Arteriosclerosis↗
PubMed2001

Potential role of recombinant annexin II in diabetic vascular injury.

Hyperinsulinemia and hyperglycemia have been associated with vascular injury such as atherosclerosis in diabetes mellitus. Recently, annexin II, a member of annexin family proteins, has been found to work as co-receptor on endothelial cells for plasminogen and tissue plasminogen activator, facilitating plasmin generation on the surface of vascular endothelium. In this review, we overviewed the effect of glucose and insulin on plasmin generation in endothelial cells and its potential modulation by recombinant annexin II (rAN II) based on our data.

Annexin A2↗
PubMed2001

Increased cholesteryl ester transfer protein and changes in lipid metabolism from initiating insulin therapy.

Insulin therapy is often necessary for glycemic control, and its effect on plasma lipids is an important issue with respect to arteriosclerosis. Previous reports suggested that increased cholesteryl ester transfer protein (CETP) appeared in diabetic patients with hyperinsulinemia or given a lot of insulin is atherogenic. We investigated whether insulin always increases CETP and whether increased CETP by insulin is always atherogenic. In 40 patients the amount and activity of CETP were assessed before and 2 weeks after initiation of insulin therapy. After starting insulin, plasma concentrations of total cholesterol, triglycerides, LDL-cholesterol, and remnant lipoprotein cholesterol decreased. No change occurred in HDL-cholesterol. Starting insulin therapy increased the amount and activity of CEIP. No significant correlation was observed between changes in CETP and in lipids including HDL-cholesterol or apolipoprotein concentrations. This is the first prospective study to show increased CETP activity after initiation of insulin therapy. After initiating insulin, CETP increases without accompanying atherogenic changes in lipid metabolism. Based on the changes observed, CETP in itself does not have atherogenicity and the increase, but no excess, of CETP by appropriate insulin therapy cannot be atherogenic.

Apolipoproteins↗