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Biomedical subjects

S Endo

Publications and source records attributed to S Endo.

At least 145 records · Page 8Linked to original sources
PubMed2000

[A case of recurrent pancreatic cancer brought into a complete response by a multimodal treatment with intraarterial chemotherapy and radiotherapy].

We achieved a complete response of recurrent pancreatic cancer using a multimodal treatment with intravenous, oral and intraarterial chemotherapies and radiotherapy. A 55-year-old female patient had a recurrent pancreatic cancer, which had invaded the portal vein, 2 years after pancreatoduodenectomy. Angiography demonstrated prominent stenosis of the portal vein, which was enlarged by the insertion of a metalic stent to maintain blood flow to the liver. Chemotherapy included intravenous mitomycin C, 5-FU and 4'-epirubicin (EPI), oral UFT and cyclophosphamide, and intraarterial cisplatin, 5-FU and EPI through a catheter inserted into the celiac artery. Furthermore, the patient received a total of 50 Gy radiotherapy. Four months after the initiation of therapy, a computed tomography image demonstrated a complete disappearance of the recurrent tumor and a prominent decrease in the serum CA19-9 level. At present, 11 months have passed after the initiation of therapy, and she has been followed at our outpatient department without any symptoms of recurrence.

Adenocarcinoma↗
PubMed2000

[Continuous monitoring to detect brain ischemia during carotid endarterectomy and aortic arch replacement by near infrared spectrophotometory--a case report].

We report two cases in which continuous monitoring was used to detect brain ischemia by 8-channel electroencephalograph (EEG), transcranial Doppler (TCD) of middle cerebral blood flow velocities and near infrared spectrophotometric monitoring (NIR) of bifrontal area simultaneously. The symptom of brain ischemia was indicated by NIR and TCD but not by EEG following temporary cross-clamping of the common carotid artery during carotid endarterectomy. According to this sign we successfully used temporary shunt during CEA. On the other hand, these methods of monitoring did not show abnormal findings of cerebral blood flow disorders during aortic arch replacement. Nevertheless, neurologic disorders were complicated postoperatively. In conclusion, these methods monitor carotid artery blood flow but not vertebral artery blood flow.

Aged↗
PubMed2000

[SIRS in surgical stress].

It has been suggested that SIRS are triggered by superfluous pro-inflammatory cytokine production, and that organ injury is caused by uncontrolled inflammatory responses. However, the results of clinical studies, on the usefulness of specific cytokine antagonists and anti-TNF antibodies for the treatment of septic shock, have been unsatisfactory. The reason for this might have been that when uncontrolled inflammatory reactions progressed locally, anti-inflammatory reactions were elevated in the circulated blood by way of CARS, thus the timing of administration and pharmacokinetics did not match clinical course. Recent research has shown that SIRS is always accompanied by CARS, and since it seems to do the amplitude of SIRS and CARS to each other so that there may be a deep valley, if there is a high mountain. We introduce the recent knowledge which indicates that SIRS is a preliminary alert for not only organ dysfunction but also immunosuppression after severe injury or major surgery.

Cytokines↗
PubMed2000

Interleukin 18 (IL-18) levels in patients with sepsis.

IL-18 levels in the blood of 13 sepsis patients were assessed. The IL-18 values were significantly correlated with their Acute Physiology and Chronic Health Evaluation (APACHE) II scores, and they were a good reflection of the severity of the disease. There was also a strong correlation between the IL-18 values and the patients' inflammatory cytokine levels. The results suggested strong involvement of IL-18 in the pathogenesis of sepsis.

APACHE↗
PubMed2000

[Sensory nerve action potentials in the evaluation of diabetic polyneuropathy].

In order to clarify the suitability of sensory nerve action potential(SNAP) in the evaluation of diabetic polyneuropathy, we studied measurements of SNAPs in the median, ulnar and sural nerves. Subjects were 253 patients with non-insulin dependent diabetes mellitus; 167 men and 86 women, aged 58.2 +/- 12.8(mean +/- SD) years old. Their diabetic history was 10.2 +/- 8.6 years. SNAPs were recorded antidromically from index finger, little finger and lateral to the Achilles tendon, respectively. Twenty-eight patients, in whom any one of the SNAPs couldn't be obtained, were already excluded from this study. The polyneuropathy index (PNI) was calculated from 12 indices concerning to the velocity or long distance latency in motor nerve conduction studies of 4 nerves. The PNI is known to be an excellent index to express the degree of diabetic polyneuropathy. Amplitude and conduction velocity in each nerve was 28.6 +/- 15.6 microV and 46.2 +/- 7.4 m/sec in the median nerve, 26.7 +/- 15.8 microV and 47.0 +/- 6.5 m/sec in the ulnar nerve, 13.1 +/- 6.5 microV and 43.1 +/- 6.0 m/sec in the sural nerve, respectively. The coefficient of correlation of the measurements between median and ulnar nerves was larger than other assortment of nerves. The coefficient of correlation of each measurement with PNI was around 0.40 in the amplitude and around 0.55 in the conduction velocity. Nevertheless, the mean value of the 3 nerves had a higher coefficient of correlation with PNI; 0.48 in the amplitude and 0.60 in the conduction velocity. SNAP measurements of a single nerve are often largely affected by the inter-individual differences, inter-nerve differences or measuring errors. But the mean value of the 3 nerves will be better in exploring the degree of diabetic polyneuropathy. Evaluation of diabetic polyneuropathy by SNAPs will be best achieved by using the mean value of these 3 nerves.

Action Potentials↗
PubMed2000

Nuclear matrix protein (NMP) levels in patients with acute pancreatitis.

Nuclear matrix protein (NMP) is an index of apoptosis. We measured NMP in 22 patients with acute pancreatitis and investigated the relationship between severity and NMP. We also measured tumor necrosis factor-alpha (TNF-alpha) and investigated the relationship between NMP and TNF-alpha. The NMP value increased significantly as the pancreatitis became more increasingly severe, and the NMP values were significantly higher in the group with multiple organ dysfunction syndrome (MODS) than in the group without MODS. A comparison of the NMP values in the group that survived and the group that died revealed higher NMP values in the former. A significant correlation was found between the NMP values and the TNF-alpha values, suggesting that apoptosis may contribute to the pathophysiology of acute pancreatitis.

Acute Disease↗
PubMed2000

Soluble Fas and soluble Fas L levels in patients with acute pancreatitis.

The FasL-Fas system is an apoptosis induction system and plays an important role in homeostasis and biophylaxis. The present study was conducted to investigate soluble Fas (sFas), soluble Fas ligand (sFasL), and tumor necrosis factor alpha (TNF-alpha) in patients with acute pancreatitis. As acute pancreatitis became severe, the levels of sFas in the serum increased significantly, while those of sFasL decreased significantly. A significant inverse correlation was observed between the serum levels of sFas and those of sFasL. Also, a significant positive correlation was observed between the levels of TNF-alpha and sFas. A greater increase in serum sFas and decrease in serum sFasL levels was observed in patients with complicating multiple organ dysfunction syndrome (MODS) than in those without it. The results of the study suggest that the pathological aggravation of acute pancreatitis could be related to changes in the Fas-FasL system.

Acute Disease↗
PubMed1999

Correlation of glutamate-induced apoptosis with caspase activities in cultured rat cerebral cortical neurons.

In cultured rat cortical neurons lactate dehydrogenase (LDH) activity in the medium, a cell-death marker, increased gradually after exposure to glutamate (100 microM to 1 mM) for 60 min and reached a plateau at 24 to 30 h. Neuronal death was mainly apoptotic as suggested by typical electron microscopic findings, fluorescent double staining with membrane-permeating and nonpermeating chromatin dyes, nick end labeling, and assessment of DNA fragmentation by agarose gel electrophoresis. After 1 mM glutamate exposure, a rise of interleukin-1beta converting enzyme (ICE)-like protease activity in neurons was parallel to cysteine protease p32 (CPP32)-like protease activity and declined before CPP32-like protease activity reached the peak (at 6 h). LDH activity in the medium of glutamate-exposed neurons was decreased by specific ICE and/or CPP32 inhibitors, acetyl-L-tyrosyl-L-valyl-L-alanyl-L-aspart-1-al (Ac-YVAD-CHO) and acetyl-L-aspartyl-L-glutamyl-L-valyl-L-aspart-1-al (Ac-DEVD-CHO), respectively, in a dose-dependent manner. Fluorescent double staining of nuclei also demonstrated that at 100 microM each inhibitor prevented neuronal apoptosis and that this effect was additive. Among agonists corresponding to various glutamate receptor subtypes, N-methyl-D-aspartate (NMDA) and kainate induced apoptosis in cortical neuronal cultures while alpha-amino-3-hydroxy-5-methylisoxazole-4-propinate (AMPA) did not. The metabotropic glutamate receptor agonist, 1-aminocyclopentane-1S, 3R-dicarboxylate (ACPD) prevented apoptosis. Interestingly, apoptosis at 24 h after agonist or antagonist exposure correlated closely with caspase activity 6 h after exposure.

Animals↗
PubMed1999

Possible mechanism for the decrease of mitochondrial aspartate aminotransferase activity in ischemic and hypoxic rat retinas.

Glutamate is believed to be an excitatory amino acid neurotransmitter in the retina. Enzymes for glutamate metabolism, such as glutamate dehydrogenase, ornithine aminotransferase, glutaminase, and aspartate aminotransferase (AAT), exist mainly in the mitochondria. The abnormal increase of intracellular calcium ions in ischemic retinal cells may cause an influx of calcium ions into the mitochondria, subsequently affecting various mitochondrial enzyme activities through the activity of mitochondrial calpain. As AAT has the highest level of activity among enzymes involved in glutamate metabolism, we investigated the change of AAT activity in ischemic and hypoxic rat retinas and the protection against such activity by calpain inhibitors. We used normal RCS (rdy+/rdy+) rats. For the in vivo studies, we clamped the optic nerve of anesthetized rats to induce ischemia. In the in vitro studies, the eye cups were incubated with Locke's solution saturated with 95% N2/5% CO2. The activity of cytosolic AAT (cAAT) was about 20% of total activity, whereas mitochondrial AAT (mAAT) was about 75% in rat retina. Ninety minutes of ischemia or hypoxia caused a 20% decrease in mAAT activity, whereas cAAT activity remained unchanged. To examine the contribution of intracellular calcium ions to the degradation of mAAT, we used Ca2+-free Locke's solution containing 1 mM EGTA, ryanodine (Ca2+ channel blocker), and thapsigargin (Ca2+-ATPase inhibitor). In the present study, thapsigargin in Ca2+-free Locke's solution, but not ryanodine in this solution, was found to prevent AAT degradation. AAT degradation was also prevented by calpain inhibitors (Ca2+-dependent protease inhibitor) such as calpeptin at 1 nM, 10 nM, 0.1 microM, 1 microM and 10 microM, and by calpain inhibitor peptide, but not by other protease inhibitors (10 microM leupeptin, pepstatin, chymostatin). Additionally, we determined the subcellular localization of calpain activity and examined the change of calpain activity in ischemic rat retinas. Our results suggest that decreased activity of mAAT in ischemic and hypoxic rat retinas might be evoked by the degradation by calpain-catalyzed proteolysis in mitochondria.

Animals↗
PubMed1999

Spatial- and task-dependent neuronal responses during real and virtual translocation in the monkey hippocampal formation.

Neuropsychological data in humans demonstrated a pivotal role of the medial temporal lobe, including the hippocampal formation (HF) and the parahippocampal gyrus (PH), in allocentric (environment-centered) spatial learning and memory. In the present study, the functional significance of the monkey HF and PH neurons in allocentric spatial processing was analyzed during performance of the spatial tasks. In the tasks, the monkey either freely moved to one of four reward areas in the experimental field by driving a cab that the monkey rode (real translocation task) or freely moved a pointer to one of four reward areas on the monitor (virtual translocation task) by manipulating a joystick. Of 389 neurons recorded from the monkey HF and PH, 166 had place fields that displayed increased activity in a specific area in the experimental field and/or on the monitor (location-differential neurons). More HF and PH neurons responded in the real translocation task. These neurons had low mean spontaneous firing rates (0.96 spikes/sec), similar to those of rodent HF place cells. The remaining nonresponsive neurons had significantly higher mean firing rates (8. 39 spikes/sec), similar to interneurons or theta cells in the rodent HF. Furthermore, most location-differential neurons showed different responses in different tasks. These results suggest that the HF and PH are crucial in allocentric information processing and, moreover, that the HF can encode different reference frames that are context or task-dependent. This may be the neural basis of episodic memory.

Animals↗
PubMed1999

Molecular identification of human G-substrate, a possible downstream component of the cGMP-dependent protein kinase cascade in cerebellar Purkinje cells.

G-substrate, an endogenous substrate for cGMP-dependent protein kinase, exists almost exclusively in cerebellar Purkinje cells, where it is possibly involved in the induction of long-term depression. A G-substrate cDNA was identified by screening expressed sequence tag databases from a human brain library. The deduced amino acid sequence of human G-substrate contained two putative phosphorylation sites (Thr-68 and Thr-119) with amino acid sequences [KPRRKDT(p)PALH] that were identical to those reported for rabbit G-substrate. G-substrate mRNA was expressed almost exclusively in the cerebellum as a single transcript. The human G-substrate gene was mapped to human chromosome 7p15 by radiation hybrid panel analysis. In vitro translation products of the cDNA showed an apparent molecular mass of 24 kDa on SDS/PAGE which was close to that of purified rabbit G-substrate (23 kDa). Bacterially expressed human G-substrate is a heat-stable and acid-soluble protein that cross-reacts with antibodies raised against rabbit G-substrate. Recombinant human G-substrate was phosphorylated efficiently by cGMP-dependent protein kinase exclusively at Thr residues, and it was recognized by antibodies specific for rabbit phospho-G-substrate. The amino acid sequences surrounding the sites of phosphorylation in G-substrate are related to those around Thr-34 and Thr-35 of the dopamine- and cAMP-regulated phosphoprotein DARPP-32 and inhibitor-1, respectively, two potent inhibitors of protein phosphatase 1. However, purified G-substrate phosphorylated by cGMP-dependent protein kinase inhibited protein phosphatase 2A more effectively than protein phosphatase 1, suggesting a distinct role as a protein phosphatase inhibitor.

Amino Acid Sequence↗
PubMed1999

Sequence analysis of an 800-kb genomic DNA region on chromosome 8q21 that contains the Nijmegen breakage syndrome gene, NBS1.

An 800-kb region on chromosome 8q21, which complements the phenotype of cells from Nijmegen breakage syndrome patients, is a candidate for the locus of the underlying gene, termed NBS1. The sequence of this 800-kb region of DNA indicated that the size of this segment is 755,832 bp with an additional 36-kb gap. From this region, we identified four genes including NBS1, a gene coding for a 27-kDa vitamin D-dependent calcium-binding protein (27-kDa calbindin), the mitochondrial 2,4-dienoyl-CoA reductase gene, and a novel gene, C8orf1/hT41. All four genes were aligned in a 250-kb centromeric portion of the region, and no gene was found in the remaining telomeric portion containing 500 kb. The genomic organization of the C8orf1/hT41 and NBS1 genes has been analyzed using the computer programs GRAIL 2 and GENSCAN. They predicted and successfully found more than 93% of the exons, even a small 54-bp exon, indicating that one or more exons in any gene can be identified by these programs. GENSCAN was more efficient at locating the four genes than GRAIL 2 and identified 15 of the 16 exons of the NBS1 gene. This 800-kb region contained repetitive sequences, including 179 copies of the Alu sequence (1 copy/4.2 kb), 123 copies of the L1 sequence (1 copy/6.1 kb), 107 copies of the LTR sequence (1 copy/7.1 kb), and 63 copies of the MER sequence (1 copy/12 kb). There was a slight but not significant difference in the repetitive content of the gene-rich region and the remaining noncoding region. Our results indicate that computer-assisted methods are useful and powerful for identifying exons of both known and novel genes.

Abnormalities, Multiple↗
PubMed1999

Guideline of surgical management based on diffusion of descending necrotizing mediastinitis.

BACKGROUND: Descending necrotizing mediastinitis resulting from oropharyngeal abscess, is a serious, life-threatening infection. Exisiting strategies for surgical management, such as transcervical mediastinal drainage or aggressive thoracotomic drainage, remain controversial. METHODS: Four patients, (three males and one female) were treated for descending necrotizing mediastinitis resulting from oropharyngeal infection. Two had peritonsillar abscesses, while the others experienced dental abscess and submaxillaritis. Descending necrotizing mediastinitis received its classification according to the degree of diffusion of infection diagnosed by computed tomography. Mediastinitis in two cases, (Localized descending necrotizing mediastinitis-Type I), was localized to the upper mediastinal space above the carina. In the others, infection extended to the lower anterior mediastinum (Diffuse descending necrotizing mediastinitis-Type IIA), and to both anterior and posterior lower mediastinum (Diffuse descending necrotizing mediastinitis-Type IIB). The spread of infection to the pleural cavity occurred in three cases. RESULTS: The surgical outcome concerning each of the patients was successful. Radical cervicotomy (unilateral in three patients, bilateral in the other) in conjunction with mechanical ventilation with continuous postoperative positive airway pressure, was performed in all cases. Tracheostomy was established in three patients and pharyngostomy in two. The two descending necrotizing mediastinitis-Type I cases were successfully managed with transcervical mediastinal drainage. The descending necrotizing mediastinitis-Type IIA case received treatment through transcervicotomy and anterior mediastinal drainage through a subxiphoidal incision. The patient with descending necrotizing mediastinitis-Type IIB required posterior mediastinal drainage through a right standard thoracotomy followed by left minimal thoracotomy. CONCLUSIONS: The mediastinal infection, the extent of which has been accurately determined by computed tomograms, necessitates radical cervicotomy followed by pleuromediastinal drainage. Situations where infection has spread to posterior medisatinum, particularly when it reaches in the level of the carina (descending necrotizing mediastinitis-type I), may not always require aggressive mediastinal drainage. In comparison, diffuse descending necrotizing mediastinitis-Type IIB demands complete mediastinal drainage with debridement via thoracotomy. Subxiphoidal mediastinal drainage without sternotomy may provide adequate drainage in diffuse descending necrotizing mediastinitis-Type IIA.

Abscess↗
PubMed1999

Argatroban, an attractive anticoagulant, for left heart bypass with centrifugal pump for repair of traumatic aortic rupture.

Systemic heparinization often increases the risk of fatal bleeding from other injured organs in surgical repair of the aorta using extracorporeal circulation in patients with traumatic aortic rupture associated with multisystem injuries. We used an antithrombin agent, argatroban, as an alternative anticoagulant in left heart bypass with the Bio-Medicus centrifugal pump in 7 of 9 recent patients who underwent aortic repair using left heart bypass. All these patients survived without obvious evidence of systemic thromboembolization. Surgical treatments for other organ injuries were carried out in 3 patients concomitantly or immediately after aortic repairs without undue blood loss. Argatroban may have a complementary effect for preventing thrombus formation without aggravating bleeding tendency because of its monotarget specificity to thrombin. We believe intravenous administration (0.5 to 2 micrograms/kg/min) of argatroban is a safe anticoagulant for left heart bypass in repairs of traumatic aortic rupture associated with multiple organ injuries.

Adolescent↗
PubMed1999

Recurrent cardiac tamponade treated using a pericardio-venous shunt.

A 49-year-old woman was admitted because of recurrent cardiac tamponade. She had undergone radical mastectomy and radiotherapy for left breast cancer four years previously. In the following two years, she felt short of breath on exertion due to cardiac tamponade. Repeated conservative therapy with diuretics and pericardial drainage were ineffective in terminating pericardial effusion. The therapeutic procedure of a pericardio-venous shunt was then employed and was effective for improving the recurrent symptoms.

Breast Neoplasms↗