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Biomedical subjects

T Koike

Publications and source records attributed to T Koike.

At least 217 records · Page 12Linked to original sources
PubMed1999

Helicobacter pylori infection inhibits reflux esophagitis by inducing atrophic gastritis.

OBJECTIVE: Although it is widely accepted that Helicobacter pylori (H. pylori) infection is an important cause of atrophic gastritis, few studies have examined the relationship between H. pylori-induced atrophic gastritis and the occurrence of reflux esophagitis. The present study was aimed to examine the relationship between H. pylori infection, atrophic gastritis, and reflux esophagitis in Japan. METHODS: A total of 175 patients with reflux esophagitis were compared with sex- and age-matched 175 control subjects. Diagnosis of H. pylori infection was made by gastric mucosal biopsy, rapid urease test, and serum IgG antibodies. Severity of atrophic gastritis was assessed by histology and serum pepsinogen I/II ratio. RESULTS: H. pylori infection was found in 59 (33.7%) patients with reflux esophagitis, whereas it was found in 126 (72.0%) control subjects. The grade of atrophic gastritis was significantly lower in the former than in the latter. Among the H. pylori-positive patients, atrophic gastritis was milder in the patients with reflux esophagitis than in the patients without it. CONCLUSIONS: These findings suggest that most cases of reflux esophagitis in Japan occur in the absence of H. pylori infection and atrophic gastritis, and it may also tend to occur in patients with milder gastritis even in the presence of H. pylori infection. Therefore, H. pylori infection may be an inhibitory factor of reflux esophagitis through inducing atrophic gastritis and concomitant hypoacidity.

Adult↗
PubMed1999

Involvement of SHP-1, a phosphotyrosine phosphatase, during myeloid cell differentiation in acute promyelocytic leukemia cell lines.

We investigated the modulation of the expression and phosphatase activity of SHP-1 during granulocytic differentiation of human myeloid leukemia cell line, HL60 and t(15;17) positive APL cell line, HT93, in response to all-trans retinoic acid (ATRA) or dimethylsulfoxide (DMSO). ATRA induced differentiation in both cell lines which was associated with marked growth inhibition and S-phase reduction. On the other hand, DMSO induced it only in HL60 without obvious growth inhibition and S-phase reduction. The expression and phosphatase activity of SHP-1 were upregulated only when the 2 cell lines were differentiated to granulocytes. Furthermore, the changes were not dependent on the inducers or the growth inhibition. These findings suggest that SHP-1 is involved in common myeloid differentiation, and that upregulation of SHP-1 is not always related to myeloid cell growth.

Cell Cycle↗
PubMed1999

Reflex sympathetic dystrophy in a patient with the antiphospholipid syndrome.

We describe a 50-year-old woman who developed severe pain of the left lower limb after an episode of thrombophlebitis. Bone scintigraphy and thermography showed results indicative of reflex sympathetic dystrophy. Laboratory analysis revealed the presence of the lupus anticoagulant. The patient was diagnosed as antiphospholipid syndrome complicated with reflex sympathetic dystrophy of the left lower limb. To our knowledge, this is the first report of a patient with reflex sympathetic dystrophy with underlying antiphospholipid syndrome.

Antiphospholipid Syndrome↗
PubMed1999

A pilot study of a response oriented chemotherapeutic regimen combined with autologous peripheral blood progenitor cell transplantation in aggressive non-Hodgkin's lymphoma.

Fourteen consecutive patients with poor-risk aggressive NHL who at presentation had any one of four risk factors underwent response oriented induction chemotherapy and successive high-dose chemotherapy followed by autologous PBPC transplantation. After treatment with three cycles of conventional CHOP with G-CSF support (CHOP-G), the response was evaluated. For patients who achieved a complete remission (CR), an additional three cycles of CHOP-G were administered, while for partial response patients, another induction regimen including some non-cross-resistant agents was given; three cycles of VIPDexa-G (etoposide, ifosfamide, cisplatinum and dexamethasone) +/- two cycles of ENAP-G (mitoxantrone, etoposide, cytosine arabinoside and prednisone), were given. The scheduled induction chemotherapy, was followed by treatment with a high-dose cytoreductive regimen followed by autologous PBPC transplantation. After three cycles of CHOP-G, four patients (29%) achieved a CR, and 10 (71%) achieved a partial response (PR). When all scheduled induction therapy was completed, 10 patients (71%) had a CR. All 14 patients received high-dose therapy and obtained a complete hematologic recovery, except for one with a bone marrow relapse two months after transplantation. Evaluation of response after high-dose therapy showed 12 CRs (86%) which included three additional CRs, one PR, and one toxicity-related death. With a median follow-up of 12 months (range, 4 to 40), 12 are alive, with 11 in continuous first CR, and one relapse. The 2-year overall survival (OS) rate and event-free survival (EFS) rate are 77% and 79%, respectively, while the disease-free survival (DFS) rate is 92%. In conclusion, this pilot study suggests that response oriented induction chemotherapy and successive high-dose chemotherapy followed by autologous PBPC transplantation is commendable and can be associated with a high rate of remission and DFS for poor risk subjects with aggressive NHL.

Adolescent↗
PubMed1999

[Increased acid secretion after Helicobacter pylori eradication is the important risk factor of acute duodenitis and reflux esophagitis].

The aims of this study were to investigate whether the changes in gastric acid secretion after H. pylori eradication might influence the development of acute duodenitis (AD) and reflux esophagitis (RE). Stimulated acid output was assessed by EGT (mEq/10 min), which is the new endoscopic method of gastric secretory testing described previously. Changes in the EGT values before and after eradication were divided into 4 groups; decreased group, no change group, increased group, markedly increased group. Results estimated by EGT demonstrated that AD and RE development after eradication significantly correlated with the increase of acid secretion. In conclusion, the increase of acid secretion was thought to be one of the most important risk factors of both AD and RE developed after H. pylori eradication.

Acute Disease↗
PubMed1999

Platelet activation induced by combined effects of anticardiolipin and lupus anticoagulant IgG antibodies in patients with systemic lupus erythematosus--possible association with thrombotic and thrombocytopenic complications.

Antiphospholipid antibodies (aPL) are well known to be associated with arterial and venous thrombosis. In a series of 180 patients with systemic lupus erythematosus (SLE), the prevalence of arterial thrombosis was obviously higher in the patients who had both anticardiolipin antibodies (aCL) and lupus anticoagulant (LA) (17/35, 48.6%, p<0.05) (Table 1) than in the other patients bearing aCL or LA alone or neither of them (2/145, 1.4%). Since a substantial fraction of the former group of patients with arterial thrombosis also had thrombocytopenia (12/17, 70.6%), there was a possibility that aCL and LA might have enhanced platelet activation and aggregation. To test this possibility, we studied the in vitro effects of aCL and LA on the enhancement of platelet activation by flow cytometric analysis using anti-CD62P and anti-CD41 monoclonal antibodies directed against platelet activation-dependent granule-external membrane (PADGEM) protein and platelet glycoprotein IIb (GPIIb), respectively. Platelet activation defined by the surface expression of CD62P was not induced by aCL+ x LA+ plasma only, but was significantly augmented by aCL+ x LA+ plasma in combination with adenosine diphosphate (ADP) at a low concentration that had only a modest effect on platelet activation. In contrast, aCL+ x LA-, aCL- x LA+ and aCL- x LA- plasma samples were incapable of enhancing platelet activation in the presence or absence of ADP stimulation. In addition to plasma samples, the purified IgG from aCL+ x LA+ plasma (aCL+ x LA+-IgG) also yielded apparent enhancement of platelet activation induced by ADP. Furthermore, platelet activation was generated by the mixture of aCL+ x LA--IgG and aCL- x LA+-IgG fractions prepared from individual patients, but not by each fraction alone. These results suggest that aCL and LA may cooperate to promote platelet activation, and may be involved, at least partially, in the pathogenesis of arterial thrombosis and thrombocytopenia in patients with SLE.

Adolescent↗
PubMed1999

Radiologic and histopathologic evaluation of canine artery occlusion after collagen-coated platinum microcoil delivery.

BACKGROUND AND PURPOSE: Platinum coil embolization is one of the significant advances in interventional neuroradiologic techniques that has been introduced this decade. Our purpose was to evaluate the angiographic and histologic effects of collagen-coated platinum microcoil delivery in the canine artery. METHODS: We embolized the bilateral internal maxillary arteries of 18 dogs; one uncoated and one collagen-primed coil was used in each dog. We evaluated all coils by angiography, macroscopy, and scanning electron microscopy within 30 minutes of embolization. We then studied a proportional number of coated and collagen-primed coils at either 1 or 3 days, or 1, 2, 3, 4, 8, 12, or 16 weeks postoperatively. RESULTS: Six (33%) of 18 arteries embolized with uncoated coils were occluded 30 minutes after delivery, whereas 11 (61%) of 18 arteries treated with collagen-primed coils were occluded within 30 minutes of embolization. Late occlusion (3 weeks after embolization) occurred in 2 (25%) of 8 arteries embolized with untreated coils, and 6 (75%) of 8 arteries embolized with collagen-primed coils. We calculated differences in late occlusion rates by the chi2 (chi-square) test, and found these differences were significant (P=.04). Histologic findings of arteries embolized with unprimed coils revealed endothelial cell growth was limited to the organized thrombi 4 weeks after coil delivery. In contrast, endothelial cells grew directly on the collagen-primed coils 3 days postoperatively, and coils were completely covered by endothelial cells within 2 weeks. We found an organized thrombus in the inner space of coils in angiographically occluded arteries, a finding that was not evident in angiographically patent arteries. CONCLUSION: Collagen-coated platinum coils can produce rapid and stable occlusion of embolized vessels.

Angiography↗
PubMed1999

Detection of noncarboxymethyllysine and carboxymethyllysine advanced glycation end products (AGE) in serum of diabetic patients.

BACKGROUND: The advanced stage of the Maillard reaction, which leads to the formation of advanced glycation end products (AGE), plays an important role in the pathogenesis of angiopathy in diabetic patients and in the aging process. N(epsilon)-(carboxymethyl)lysine (CML) is thought to be an important epitope for many of currently available AGE antibodies. However, recent findings have indicated that a major source of CML may be by pathways other than glycation. A distinction between CML and non-CML AGE may increase our understanding of AGE formation in vivo. In the present study, we prepared antibodies directed against CML and non-CML AGE. MATERIALS AND METHODS: AGE-rabbit serum albumin prepared by 4, 8, and 12 weeks of incubation with glucose was used to immunize rabbits, and a high-titer AGE-specific antiserum was obtained without affinity for the carrier protein. To separate CML and non-CML AGE antibodies, the anti-AGE antiserum was subjected to affinity chromatography on a column coupled with AGE-BSA and CML-BSA. Two different antibodies were obtained, one reacting specifically with CML and the other reacting with non-CML AGE. Circulating levels of CML and non-CML AGE were measured in 66 type 2 diabetic patients without uremia by means of the competitive ELISA. Size distribution and clearance by hemodialysis detected by non-CML AGE and CML were assessed in serum from diabetic patients on hemodialysis. RESULTS: The serum non-CML AGE level in type 2 diabetic patients was significantly correlated with the mean fasting blood glucose level over the previous 2 months (r = 0.498, p < 0.0001) or the previous 1 month (r = 0.446, p = 0. 0002) and with HbA(1c) (r = 0.375, p = 0.0019), but the CML AGE level was not correlated with these clinical parameters. The CML and non-CML AGE were detected as four peaks with apparent molecular weights of 200, 65, 1.15, and 0.85 kD. The hemodialysis treatment did not affect the high-molecular-weight protein fractions. Although the low-molecular-weight peptide fractions (absorbance at 280 nm and fluorescence) were decreased by hemodialysis, there was no difference before and after dialysis in the non-CML AGE- and CML-peptide fractions (1.15 and 0.85 kD fractions). CONCLUSIONS: We propose that both CML and non-CML AGE are present in the blood and that non-CML AGE rather than CML AGE should be more closely evaluated when investigating the pathophysiology of AGE-related diseases.

Animals↗
PubMed1999

Embolization of cerebral arteriovenous malformations achieved with polyvinyl alcohol particles: angiographic reappearance and complications.

BACKGROUND AND PURPOSE: The appropriate choice of embolic materials with respect to the permanency of obliterated nidi after embolization and complications related to the procedure is essential for safe and effective embolization of cerebral arteriovenous malformations (AVMs). Our purpose was to ascertain the recanalization and complication rates after AVM treatment with polyvinyl alcohol (PVA) particles. METHODS: Between 1988 and 1994, 36 AVMs were embolized with PVA particles at our institution. Follow-up angiographic findings and occurrence of complications during the embolization procedures were analyzed retrospectively. RESULTS: Complete obliteration of the nidus immediately after embolization was achieved in five patients, and 80% to 99% obliteration was attained in 12 patients. Fifty-one follow-up angiographic examinations were performed 1 week to 60 months (mean, 7 months) after embolization in 31 patients. An increase in nidal size was seen on 15 follow-up angiograms (29%) and a decrease was seen in seven (14%). In 28 of the 51 angiograms obtained more than 1 month after follow up (mean, 13 months), 12 (43%) showed AVM enlargement. In four (80%) of five cases of complete obliteration, nidi reappeared on follow-up angiograms. Hemorrhagic complications occurred in three cases and ischemic ones in seven. One patient (3%) died and five (14%) suffered persistent neurologic deficits. CONCLUSION: Embolization with PVA particles can produce significant volume reduction in AVM nidal size, but recanalization is a distinct possibility.

Adolescent↗
PubMed1999

[The value of intracellular CD41 antigen detection to the diagnosis of acute megakaryoblastic leukemia].

An 11-month-old boy was transferred to our hospital because of fever and bleeding tendency on March 13, 1998. Laboratory studies showed a white blood cell count of 43,360/microliter with 75% blasts, a hemoglobin concentration of 8.4 g/dl, and a platelet count of 23 x 10(3)/microliter. Surface marker analysis with a flow cytometer revealed that only 21% and 11% of the blasts, respectively, were positive for CD41 and CD42b. Treatment with a permeabilizing agent apparently increased the reactivity of the blasts with anti-CD41 monoclonal antibody (MoAb), which can recognize IIb independently of IIIa. However no significant differences were observed in reactivity with anti-CD41 MoAb (which recognizes the IIb/IIIa complex) anti-CD61 MoAb and anti-CD42b MoAb before or after fixation. Blasts positive for platelet peroxidase were observed by electron microscopy, thus confirming the diagnosis of acute megakaryoblastic leukemia. We concluded that the detection of intracellular antigens is useful for the quick diagnosis of acute megakaryoblastic leukemia characterized by low surface expression of megakaryocytic lineage antigens.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1999

Dendritic cells stimulate the expansion of PML-RAR alpha specific cytotoxic T-lymphocytes: its applicability for antileukemia immunotherapy.

Dendritic cells (DC), the most potent "professional" antigen-presenting cells, hold promise for improving the immunotherapy of cancer. In this study, we investigated the ability of normal donor DC pulsed ex vivo with 12 mer PML-RAR alpha (A) peptide (SGAGEAAIETQS) to generate peptide specific autologous cytotoxic T-lymphocytes. The peptide pulsed DC-primed peripheral blood lymphocytes (PBL) displayed significantly higher cytotoxic activity compared with that of peptide non-pulsed DC-primed PBL against peptide-pulsed autologous macrophages (P<0.001). Both CD8+ and CD4+ T lymphocytes were involved in the effector cell populations. The PML-RAR alpha peptide-pulsed DC-primed T-cells were significantly superior in their production of GM-CSF and TNF-alpha, compared with peptide non-pulsed DC-primed T-cells. These intriguing preclinical studies, suggest that PML-RAR alpha pulsed-DC could be a promising immunotherapeutic modality for patients with acute promyelocytic leukemia.

CD4-Positive T-Lymphocytes↗
PubMed1998

Oral tolerance to low dose beta 2-glycoprotein I: immunomodulation of experimental antiphospholipid syndrome.

Oral tolerance was induced in BALB/c mice by feeding low dose beta2-glycoprotein I (beta2GPI). The beta2GPI-fed mice did not develop serologic and clinical markers of experimental antiphospholipid syndrome (APS) upon immunization with the autoantigen. The treated group was characterized by low titers of serum anti-beta2GPI and anticardiolipin Abs in the serum, lack of fetal resorptions, low incidence of thrombocytopenia, and normal aPTT (activated partial thromboplastin time) values. Beta2GPI given orally before priming with beta2GPI resulted in complete prevention of experimental APS development; beta2GPI given at an early stage of the disease reduced clinical manifestations. However, administration of beta2GPI 70 days postimmunization had a less significant effect on disease expression. Tolerized mice exhibited a diminished T lymphocyte proliferation response to beta2GPI in comparison with beta2GPI-immunized mice fed with OVA. When nontolerant beta2GPI-primed T lymphocytes were mixed with T lymphocytes derived from tolerized mice, a significant inhibition of proliferation upon exposure to beta2GPI was observed. The induction of suppression was beta2GPI specific and driven, as well as TGF-beta mediated. The beta2GPI-specific response of T lymphocytes from the beta2GPI-fed mice was reversed by anti-TGF-beta Abs. The tolerance was adoptively transferred by CD8+ T cells from the tolerized mice into naive mice. Those CD8+ cells were MHC class I restricted, found to secrete TGF-beta, and had no cytolytic activity. Oral administration of beta2GPI suppressed priming of CTLs in the recipient mice. In sum, beta2GPI-induced oral tolerance has an immunomodulatory effect in experimental APS, demonstrating the importance of beta2GPI in the pathogenesis of the disease.

Administration, Oral↗
PubMed1998

Analysis of postoperative liver function of donors in living-related liver transplantation: comparison of the type of donor hepatectomy.

BACKGROUND: There is a potentially significant risk to the donor in living-related liver transplantation. METHODS: We analyzed surgical risk and stress to 35 donors in living-related liver transplantation with special reference to the types of donor hepatectomy. Donor surgery was performed in one of three ways: (1) lateral segmentectomy without ligation of the middle hepatic vein (MHV) in the remnant liver (group 1, n=21); (2) lateral segmentectomy with ligation of MHV in the remnant liver (group 2, n=6); and (3) left lobectomy with MHV (group 3, n=8). RESULTS: No critical complications were observed in any group. The postoperative enzyme levels in group 2 were significantly higher than those in groups 1 and 3 (P<0.01). Although blood loss was covered by autologous blood transfusion in the first six cases, no banked blood was transfused in any of the cases. Surgical duration was significantly longer and blood loss was significantly greater in group 3 than in group 1 (P<0.05). Follow-up computed tomography showed atrophic changes in segment IV in groups 1 and 2. No remarkable changes were seen in segments V or VIII in any of the three groups. CONCLUSION: Regardless of the donor hepatectomy procedure, serious complications did nor occur after surgery. Although it should be noted that the type of donor hepatectomy affects postoperative donor liver function, left lateral segmentectomy with ligation of MHV in the remnant liver is a useful method for obtaining liver grafts from living-related donors who have unusual anatomic variations of the hepatic veins.

Adult↗
PubMed1998

The attenuated effect of ATP-sensitive K+ channel opener pinacidil on renal haemodynamics in spontaneously hypertensive rats.

In hypertension, impairment of hyperpolarization by K+ efflux through ATP-sensitive K+ (K(ATP)) channels may contribute to the elevated renal vascular resistance. To elucidate such a role for K(ATP) channels in the renal vasculature, we used micropuncture techniques to examine the effect of K(ATP) channel opener, pinacidil (0.15 mg/h per kg body wt i.v.), on renal and glomerular haemodynamics in spontaneously hypertensive rats (SHR) and in normotensive controls (Wistar Kyoto, WKY). Since pinacidil reduced blood pressure significantly in both groups, the abdominal aorta was clamped before pinacidil administration to yield a renal perfusion pressure equivalent to that during pinacidil infusion. Pinacidil significantly decreased renal vascular resistance in both groups, but the relative change from baseline value was greater in WKY than in SHR. These effects of pinacidil were abolished by pretreatment with glibenclamide (3 mg/kg body wt i.v.). Proximal tubular stop-flow pressure (Psf), an index of glomerular capillary pressure, was significantly elevated by pinacidil infusion in WKY, a response abolished by pretreatment with glibenclamide, but not in SHR. The tubuloglomerular feedback response of Psf was not affected by pinacidil in either group. These data suggest that the activity of K(ATP) channels in SHR may be attenuated in the renal microvasculature. This may contribute to the elevated vascular tone in the renal preglomerular vasculature in SHR.

Animals↗
PubMed1998

Upregulation of a new microglial gene, mrf-1, in response to programmed neuronal cell death and degeneration.

Cerebellar granule neurons isolated from postnatal day 7 (P7) rats and grown in normal K+ medium begin to degenerate at approximately 4 d in vitro (DIV) and die. To search for genes upregulated in the process of neuronal cell death, differential hybridization was performed with subtracted cDNA probes and a cDNA library from 5 DIV. One of the genes isolated was microglial response factor-1 (mrf-1), which encoded a sequence of 177 amino acids with a single EF-hand calcium-binding motif. By Northern blots, the transcript was upregulated in cerebellar culture at 4 DIV, peaked at 6 DIV, and decreased at 7 DIV. Upregulation was also found when the apoptosis of granule cells was induced by replacing high K+ medium with normal K+ medium. However, when non-neuronal cells were thoroughly eliminated with aphidicolin, an antimitotic agent, the upregulation at 4-7 DIV did not occur. By immunocytochemistry, MRF-1 was detected at 5 DIV in OX-42-positive cells (microglia), and it exhibited an increase in response to granule cell death. MRF-1 levels in microglia purified from cerebral cortex also upregulated in the presence of 5 DIV granule cells. In the developing cerebellum in vivo, levels of mrf-1 mRNA transiently increased in the early postnatal stages, reaching a peak at P7 when cerebellar neurons and astrocytes undergo extensive apoptosis. In adult brain sections, MRF-1 was detected in the perikarya and processes of ramified/resting microglia, and peripheral motor nerve dissection prominently increased the expression in activated microglia surrounding injured central motoneurons. Therefore, mrf-1 appears to be one of the microglial genes that respond to neuronal cell death and degeneration.

Amino Acid Sequence↗