Treatment of orthostatic intolerance with inflatable abdominal band.
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Adolescent↗
Biomedical subjects
H Yamaguchi
Publications and source records attributed to H Yamaguchi.
Molecular pathogenesis of type I congenital plasminogen deficiency: expression of recombinant human mutant plasminogens in mammalian cells.
We previously reported the genetic abnormality in a Japanese family with type I congenital plasminogen deficiency caused by a Ser572 to Pro572 mutation. To characterize the molecular pathogenesis of the disease in this family, we expressed recombinant human wild-type and mutant (rS572P) plasminogens in COS-1 cells. Activation-resistant wild-type and mutant plasminogen stable transfectants in CHO-K1 cells also were established. Transient transfection and metabolic labeling experiments followed by immunoprecipitation analysis showed that the mutant plasminogen was secreted from COS-1 cells in reduced amounts, compared with the wild type. Endo H digestion of the wild-type and mutant plasminogen showed no shift in their migrations on sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis, indicating that both contain complex type oligosaccharide structures and could therefore be secreted. Furthermore, the secretion of activation-resistant mutant plasminogen was significantly reduced. Pulse-chase experiments and Northern blot analysis showed that the impaired secretion of the mutant plasminogen was the consequence of the accumulation of the mutant protein inside the cells but not of reduced plasminogen mRNA. Immunocytochemical staining of stable transfectants also revealed that CHO-K1 cells expressing the activation-resistant mutant plasminogen stained mainly in the perinuclear area, suggesting delayed processing of the mutant protein in the intracellular transport pathway. We conclude that the impaired secretion of mutant plasminogen, due to intracellular accumulation, is the molecular pathogenesis of type I congenital plasminogen deficiency caused by a Ser572 to Pro572 mutation.
Animals↗
Stomach-partitioning gastrojejunostomy for unresectable gastric carcinoma.
OBJECTIVES: To analyze the results of a new type of bypass procedure, stomach-partitioning gastrojejunostomy (SPGJ), for unresectable gastric carcinoma and to compare these results with those of conventional gastrojejunostomy (GJ). DESIGN: Retrospective review. SETTING: A university hospital in Japan. PATIENTS: Eight patients underwent SPGJ in 1 group, and 13 underwent conventional GJ in the other group. Staging was determined using preoperative diagnostic imagings and intraoperative findings. MAIN OUTCOME MEASURES: Assessment of food intake and mean survival rates. RESULTS: There were no significant differences between the 2 groups regarding male-female ratio, mean age, and histological type of carcinoma. All patients had stage IV cancers according to the classification of the Union Internationale Contre le Cancer. The rates of taking a regular meal at 2 weeks after an operation were 88% in the SPGJ group and 31% in the GJ group (P < .05). The mean 1-year survival rates for SPGJ and GJ groups were 42.9% and 7.7%, respectively (P < .05). The mean survival times were 13.4 months in the SPGJ group and 5.8 months in the GJ group (P < .05). CONCLUSIONS: Stomach-partitioning gastrojejunostomy achieved an improved quality of life and a better prognosis for patients, and it is the preferred bypass procedure for unresectable gastric carcinoma.
Aged↗
Thoracic esophageal carcinoma above the carina: a more formidable adversary?
BACKGROUND: Prognosis with esophageal carcinoma above the carina is generally thought to be the worst without any conclusive demonstration. METHODS: Clinicopathologic features of 101 patients with thoracic esophageal carcinoma above the carina (AC group) were compared with those of 665 patients with a tumor below this level (BC group). RESULTS: The number of T4 tumor was significantly larger in the AC group (P < 0.001). Survival curve for all patients in the AC group was significantly worse than the BC group (P < 0.001). Survival in patients who underwent any treatment other than esophagectomy was equally bad in the two groups. However, survival in patients undergoing esophagectomy was similar in the two groups (P = 0.64), with the cumulative 5-year survival rates of 44.5% and 43.1%, respectively. Even in patients with metastatic disease in the lymph nodes, the cumulative 5-year survival rates after radical esophagectomy were similar. CONCLUSIONS: The prognosis of patients in the AC group is generally worse than the BC group because of the close anatomical relationship with the tracheobronchial tree. However, radical esophagectomy is recommended for patients at stages less advanced than T4.
Adenocarcinoma↗
Second primary carcinoma in the residual cervical esophagus after thoracic esophagectomy: report of five cases.
BACKGROUND AND OBJECTIVES: Development of second primary carcinomas after thoracic esophagectomy has become of much concern, because recently the prognosis of thoracic esophageal carcinoma after esophagectomy with extended lymph node dissection has been improving. We report our experience of diagnosing and treatment second primary carcinomas arising in the remaining esophagus after thoracic esophagectomy. METHODS: Among 253 patients who underwent esophagectomy for thoracic esophageal carcinoma more than 2 years previously, second primary esophageal carcinomas developed in five (2.0%), and these five patients were examined. RESULTS: All second primary carcinomas were found by endoscopy, and were diagnosed as superficial carcinoma (Tis or T1) of the residual cervical esophagus. One patient underwent laser irradiation, another endoscopic mucosal resection, two had surgical mucosectomy, and one segmental resection of the esophagus. After the second treatment, three patients were disease free for 37-38 months, one died of recurrent disease of the first carcinoma 36 months later, and one died of distant metastases of the second carcinoma 8 months later. There have been no local recurrences after treatments for the second primaries. CONCLUSIONS: A variety of low-trauma treatments were employed for the second carcinomas because they were found at an early stage. Endoscopic follow-up is proposed to detect second lesions at an early stage.
Carcinoma, Squamous Cell↗
Monoclonal antibodies to purified cortical Lewy bodies recognize the mid-size neurofilament subunit.
Lewy bodies (LBs) are filamentous intraneuronal inclusions that are hallmark lesions of Parkinson's disease, and LBs have been shown, by immunohistochemistry, to contain cytoskeletal as well as other cellular proteins. Similar LBs also occur in the cortical neurons of a subset of patients with Alzheimer's disease (AD), and cortical LBs are the predominant or sole lesions in the brains of patients with an AD-like dementia known as diffuse Lewy-body disease (DLBD). To gain insight into the biochemical composition of LBs, we generated monoclonal antibodies (mAbs) to LBs purified from the brains of patients with DLBD. Here, we describe three of these new mAbs (LB48, LB202, and LB204) that stained LBs by immunohistochemistry and recognized the medium molecular mass neurofilament (NF) protein in western blots. These results support the hypothesis that NF subunits are integral components of LBs. Continued efforts to clarify the composition of LBs are likely to lead to novel strategies for the antemortem diagnosis of LB disorders as well as to insight into the role LBs play in the degeneration of affected neurons in these disorders.
Antibodies, Monoclonal↗
Different expressions of sialyl Tn antigen between polypoid and flat-type early colorectal cancers.
PURPOSE: Sialyl Tn (STn) antigen is a cancer-associated carbohydrate antigen expressed in cancers of the digestive tract. We compared the proportion of specimens of flat-type colorectal cancers expressing STn with that of polypoid cancers, by examining the immunohistochemical reactivity of STn in various morphologic types of early and advanced colorectal cancers. METHODS: A total of 111 biopsies from the colorectal area were examined for STn expression, including 11 adenomas, 58 early cancers, and 42 advanced cancers. Each section was stained immunohistochemically for STn antigen. In each section, we examined STn expression in the cancer area, adjacent mucosa, and normal epithelium. RESULTS: STn expression was detected in 90.9 percent of adenomas, 36.2 percent of early cancers (T1), 64.3 percent of advanced cancers (>T1), and 52 percent of mucosa adjacent to cancer. The morphology of cancer tissue did not influence the number of specimens exhibiting STn antigen expression in mucosa adjacent to cancer cells. STn antigen was rarely expressed in flat or depressed-type early cancers (T1; 7.1 percent), and the expression was higher in moderately than in well-differentiated adenocarcinomas. In advanced cancers (>T1), a similar proportion of protruding and small ulcerative cancers expressed STn. CONCLUSION: Our results suggest that the low expression of STn antigen in flat-type cancers may be the result of different mechanisms of cellular transformation during carcinogenesis from the usual adenoma-carcinoma sequence in colorectal neoplasms.
Adenocarcinoma↗
Microglial activation in early stages of amyloid beta protein deposition.
The present study was undertaken to investigate the relationship of microglial activation to amyloid beta protein (A beta) deposition, particularly at the early stage. Using single and double immunostaining methods with a panel of microglia markers and antibodies against A beta and amyloid beta protein precursor (APP), we examined the cerebrum and cerebella of both Alzheimer's disease (AD) and non-demented subjects obtained at autopsy. In nondemented, middle-aged subjects that had small amounts of cerebral A beta deposits, approximately 70% of the diffuse plaques contained ramified microglia. However, no evidence of microglial activation was found in diffuse plaques in any of the non-demented subjects. Dual immunostaining of sections of cerebral cortex using antibodies against A beta and major histocompatibility complex class II antigen showed that in AD subjects, approximately 20% of total diffuse plaques contained a few, activated microglia. Most of these plaques were defined as a transitional from between diffuse and primitive plaques. Both primitive and classic plaques in the cerebral cortex of AD subjects consistently contained clusters of activated microglia. Subpial A beta deposits without neuritic changes lacked microglial activation. In the cerebellum, all of the diffuse plaques lacked microglial activation, and activated microglia in the compact plaques were not as hypertrophic as those in cerebral primitive/classic plaques. Our findings indicate that microglial reactions are absent in the early stages of A beta deposition, and it occurs during the transition from diffuse to primitive plaques, when amounts of A beta deposits and the degree of neuritic changes increase.
Aged↗
Blood flow in the carotid artery during breath-holding in relation to diving bradycardia.
The present study investigated the mechanism of diving bradycardia. A group of 14 healthy untrained male subjects were examined during breath-holding either out of the water (30-33 degrees C), in heat-out immersion, or in whole-body submersion (27-29 degrees C) in a diving pool. Blood velocity, blood volume flow in the carotid artery, diastolic blood pressure and electrocardiogram were measured and recorded during the experiments. The peak blood velocity increased by 13.6% (P < 0.01) and R-wave amplitude increased by 57.1% (P < 0.005) when the subjects entered water from air. End-diastolic blood velocity (Ved) in the carotid artery increased significantly during breath-holding, e.g. Ved increased from 0.20 (SD 0.02) m.s-1 at rest to 0.33 (SD 0.04) m.s-1 (P < 0.001) at 50.0 s in breath-hold submersion to a 2.0-m depth. Blood volume flow in the carotid artery increased by 26.6% (P < 0.05) at 30 s and 36.6% (P < 0.001) at 40 s in breath-hold submersion to a 2.0-m depth. Diastolic blood pressure increased by 15.4% (P < 0.01) at 60 s during breath-holding in head-out immersion. Blood volume flow, Ved and diastolic blood pressure increased significantly more and faster during breath-holding in submersion than out of the water. There was a good negative correlation with the heart rate: the root mean square correlation coefficient r was 0.73 (P < 0.001). It was concluded that an increased accumulation of blood in the aorta and arteries at end-diastole and decreased venous return, caused by an increase in systemic peripheral resistance during breath-holding, underlies diving bradycardia.
Adult↗
Extracellular matrix is reduced by inhibition of transforming growth factor beta1 in pancreatitis in the rat.
BACKGROUND & AIMS: Regeneration from cerulein-induced pancreatitis is accompanied by a transient synthesis and deposition of extracellular matrix components in the rat pancreas. The pleiotropic transforming growth factor (TGF)-beta1 has been suggested to regulate extracellular matrix remodeling during regeneration from acute pancreatitis. The present study was designed to verify this hypothesis by investigating the effect of TGF-beta1 inhibition. METHODS: Experimental acute pancreatitis was induced in rats by supramaximal doses of cerulein. The biological activity of TGF-beta1 was inhibited by injections of neutralizing TGF-beta1 antibody. Changes in the content of extracellular matrix proteins, TGFs, and their messenger RNA concentrations were monitored. RESULTS: TGF-beta1 expression in pancreatic cells was suppressed after induction of acute pancreatitis by the application of neutralizing TGF-beta1 antibody. Immunochemical analysis showed a clear reduction of extracellular matrix formation during the regeneration of the pancreas in antibody-treated animals. The hydroxyproline content and the concentration of collagen types I and III, fibronectin on protein, and messenger RNA level were significantly reduced in the pancreas of treated animals. CONCLUSIONS: These results provide evidence that TGF-beta1 is involved in the regulation of extracellular matrix remodeling in the rat pancreas during regeneration from acute pancreatitis.
Acute Disease↗
Pure red cell aplasia during carbamazepine monotherapy.
A 7-year-old girl developed pure red cell aplasia during carbamazepine (CBZ) monotherapy for epilepsy. She developed generalized clonic convulsions at the age of 7 years and 8 months. Treatment with CBZ was begun. Two months later she was admitted to our hospital because of severe anemia. Bone marrow examination revealed the almost complete absence of erythroblasts, with normal myelopoiesis and megakaryocytopoiesis, indicating pure red cell aplasia. Following the discontinuation of CBZ, she developed brisk reticulocytosis within 1 week and her hemoglobin level rose to a normal one within 1 month. Although the hematological toxicity of CBZ is well documented, isolated cessation of red cell production is uncommon. A patient who is undergoing treatment with CBZ should be carefully monitored, especially for serious adverse reactions including pure red cell aplasia.
Anticonvulsants↗
Effectiveness of an antioxidant in preventing restenosis after percutaneous transluminal coronary angioplasty: the Probucol Angioplasty Restenosis Trial.
OBJECTIVES: The Probucol Angioplasty Restenosis Trial was a prospective, randomized, controlled study that investigated the effectiveness of probucol therapy in reducing the rate of restenosis after percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND: Antioxidants have an inhibitory effect on smooth muscle cell growth in experiments in vitro and in vivo, which suggests a possible pharmacologic effect on restenosis after PTCA. METHODS: One hundred one patients were randomly assigned to receive 1,000 mg/day of probucol or control (no lipid-lowering) therapy 4 weeks before PTCA. After 4 weeks of premedication, both groups underwent PTCA. Probucol was continued until follow-up angiography 24 weeks after PTCA. Angiographic results were analyzed at a core laboratory by quantitative coronary angiography. RESULTS: Dilation was successful in 46 of 50 patients in the probucol group and 45 of 51 in the control group. At follow-up angiography 24 weeks after angioplasty, angiographic restenosis occurred in 9 (23%) of 40 patients in the probucol group and 22 (58%) of 38 in the control group (p = 0.001). Minimal lumen diameter was 1.49 +/- 0.75 mm (mean +/- SD) in the probucol group and 1.13 +/- 0.65 mm in the control group (p = 0.02). Percent diameter stenosis at follow-up angiography in the probucol group was significantly lower than that in the control group (43.9% vs. 56.4%, p = 0.009). The late loss was 0.37 +/- 0.69 mm in the probucol group and 0.60 +/- 0.62 mm in the control group (p = 0.13). The loss/gain ratio was 0.32 +/- 0.74 in the probucol group and 0.56 +/- 0.81 in the control group (p = 0.059). Net gain was greater in the probucol group than in the control group (0.77 +/- 0.70 vs. 0.48 +/- 0.59 mm, p = 0.053). CONCLUSIONS: Probucol administered beginning 4 weeks before PTCA appears to reduce restenosis rates.
Aged↗
Flow cytometric analysis for adhesion of Vibrio cholerae to human intestinal epithelial cell.
The adhesion of Vibrio cholerae O1 strains to human intestinal epithelial cell, Intestine 407, was analyzed by flow cytometer. According to positive percentages of Intestine 407 cells adhered by V. cholerae, two groups of V. cholerae strains were classified as follows: more adhesive (more than 50%), less adhesive (less than 50%) strains. In addition, the fluorescence intensity after attachment of V. cholerae was directly correlated to the number of the microorganisms. It was concluded that flow cytometry is a useful and objective method for analyzing adhesion of V. cholerae to cultured cells.
Bacterial Adhesion↗
Gain of chromosome 20 is a frequent aberration in liver metastasis of colorectal cancers.
To investigate the characteristics of the numerical chromosome aberrations in liver metastasis of colorectal cancers, fluorescence in situ hybridization (FISH) for chromosomes 8, 18, 14/22, and 20 was performed in 18 specimens of primary regions and 18 of metastatic regions in liver metastasis of colorectal cancers compared with 15 of non-liver metastatic cancers. Among these numerical aberrations, the gain of chromosome 20, especially copy numbers exceeding three, was frequently observed in primary and metastatic cancers. Among these numerical aberrations, the gain of chromosome 20, especially copy numbers exceeding three, was frequently observed in primary and metastatic regions of liver metastasis groups compared with that of the non-liver metastasis group (P < 0.05). The incidences of gain of chromosome 20 in both regions of the liver metastasis group were higher than that of the non-liver metastasis group (P < 0.05). The gain of chromosome 20 is a frequent aberration in primary and metastatic regions in patients with liver metastatic colorectal cancers and may be available as a genetic marker for the diagnosis or prediction of liver metastasis.
Case-Control Studies↗
Augmentation of production of TNF-alpha and anti-tumour activity by an amphotericin B preparation for clinical use in mice.
Effects of amphotericin B on production of endogenous tumour necrosis factor alpha (TNF-alpha) and anti-tumour activity in mice was examined. Intravenous administration of Fungizone, an amphotericin B preparation complexed with deoxycholate, augmented the induction of endogenous TNF in response to a second stimulus with intravenous doses of FK23 (heat-killed Enterococcus faecalis). This augmentation was observed when more than 1.8 microg of Fungizone was injected intravenously before intravenous dosing of FK23. The time interval between priming injection of Fungizone and secondary injection of FK23 for the maximal effect was 3 h. Similar augmentation of TNF production was also observed in amphotericin B-primed and FK23-injected mice. Correspondingly, anti-tumour activity of the combined, intravenous injection of Fungizone and FK23 with a 3-h interval was examined. Growth of Meth A fibrosarcoma was clearly inhibited by this combination but not by administration of either one alone. These results suggest that amphotericin B is able to elicit anti-tumour activity, perhaps through activation of the immune system, and in particular augmentation of the induction of endogenous TNF.
Amphotericin B↗
Urine and plasma levels of uroguanylin and its molecular forms in renal diseases.
Uroguanylin activates the intestinal and possibly the renal guanylate cyclase C receptor, and stimulates Cl- secretion. We developed a sensitive radioimmunoassay (RIA) for human uroguanylin and measured its concentration in the urine and plasma. Twenty-four-hour urinary excretion of immunoreactive (ir-) uroguanylin for persons with a high-salt diet (10 g/day) was 137.8 +/- 14.4 pmol/day, significantly higher than that for persons with a low-salt diet (7 g/day, 95.1 +/- 16.3 pmol/day, P < 0.05). There were significantly positive correlations between the urinary excretion of ir-uroguanylin and Na+, Cl-, K+ or cyclic GMP (cGMP). We demonstrated the presence of messenger RNA of guanylate cyclase C in the medulla of human kidney. The concentration of plasma ir-uroguanylin significantly correlated with that of serum creatinine (r = 0.71, P < 0.001). Biologically active uroguanylin-16 accounted for 99% of the endogenous uroguanylin molecules in normal urine and 60% in plasma, the remainder being the 10 kDa precursor. The precursor content increased in the urine and plasma as the severity of renal impairment increased. These findings suggest that bioactive uroguanylin-16 is involved in the regulation of electrolyte homeostasis and that the kidney participates in the metabolism and excretion of uroguanylin.
Circadian Rhythm↗
Heterogenous expression of bcr-abl fusion mRNA in a patient with Philadelphia-chromosome-positive acute lymphoblastic leukaemia.
We performed molecular and cytogenetic analysis on a 56-year-old woman with Philadelphia chromosome (Ph1)-positive acute lymphoblastic leukaemia (ALL) having two types of major and minor bcr-abl (M-bcr-abl, m-bcr-abl/fusion mRNA at diagnosis. In the course of her disease, unexpected heterogenous bcr-abl fusion mRNA was detected by sequential analysis using the reverse transcription and polymerase chain reaction (RT-PCR). The RT-PCR analysis showed both M-bcr-abl (b2-a2 type) and m-bcr-abl at diagnosis. Although b2-a2 type M-bcr-abl disappeared after complete remission (CR) was achieved with intensive induction chemotherapy, expression of both m-bcr-abl and a new type of M-bcr-abl mRNA (b1-a2 type), which may have been produced through splicing out of exon b2, was detected in the early stage of CR. The leukaemic cells contained these heterogenous bcr-abl mRNAs in both the CR and relapsed state, and showed more stable expression of the m-bcr-abl type mRNA than that of the b2-a2 type. These findings of heterogenous bcr-abl mRNA due to alternative or missplicing during the disease course in the present ALL case may provide important evidence of disease progression.
Alternative Splicing↗
Defective response to thrombopoietin and impaired expression of c-mpl mRNA of bone marrow cells in congenital amegakaryocytic thrombocytopenia.
Congenital amegakaryocytic thrombocytopenia (CAMT) is an uncommon disorder in newborns and infants, characterized by isolated thrombocytopenia and megakaryocytopenia in the first year without physical anomalies. The defect of thrombopoiesis is not well understood. Recently, thrombopoietin (TPO), the ligand for the c-mpl receptor, was cloned. Accumulating evidence from in vitro and in vivo studies indicate that TPO plays a key role in the regulation of megakaryocytopoiesis. In this study we examined the effect of TPO on megakaryocyte colony formation from a patient with CAMT using a plasma-containing methylcellulose clonal culture. The in vitro results demonstrated a defective response to TPO in megakaryocyte colony formation from bone marrow mononuclear cells (MNC) of the patient. although interleukin-3 (IL-3) but not stem cell factor (SCF) induced only a small number of megakaryocyte colonies. These findings indicated that thrombocytopenia in CAMT could not be corrected by administration of TPO in vitro. Additionally, clonal cultures containing SCF, IL-3, IL-6 and erythropoietin showed decreased numbers of erythroid and myelocytic progenitors in the bone marrow of the patient. The serum TPO level measured by enzyme-linked immunosorbent assay was significantly higher than that in healthy controls. By PCR, marrow MNC from healthy children and from a patient with essential thrombocytosis expressed c-mpl mRNA, whereas no c-mpl mRNA was detected in marrow MNC from the patient with CAMT. There was no difference in the CD34 expression and c-kit mRNA between the CAMT patient and healthy children. The results of this study suggest that the pathophysiology in CAMT may be a defective response to TPO in haemopoietic cells through impaired expression of c-mpl mRNA.
Bone Marrow↗