Biomedical subjects
Publications and source records attributed to S Yamada.
We report a case of blunt abdominal trauma in which delayed ischaemic ileal stenosis occurred. A 24-year-old man presented with symptoms and signs of bowel obstruction 2 weeks after blunt abdominal trauma. Enhanced CT clearly demonstrated a stenotic ileal loop with mural thickening, associated with a mesenteric haematoma. This abnormal ileal loop was resected.
A criticality accident occurred on September 30, 1999, at the uranium conversion plant in Tokai-mura (Tokai-village), Ibaraki Prefecture, Japan. When the criticality occurred, three workers saw a "blue-white glow," and a radiation monitor alarm was sounded. They were severely exposed to neutron and gamma-ray irradiation, and subsequently developed acute radiation syndrome (ARS). One worker reported vomiting within minutes and loss of consciousness for 10-20 seconds. This worker also had diarrhea an hour after the exposure. The other worker started to vomit almost an hour after the exposure. The three workers, including their supervisor, who had no symptoms at the time, were brought to the National Mito Hospital by ambulance. Because of the detection of gamma-rays from their body surface by preliminary surveys and decreased numbers of lymphocytes in peripheral blood, they were transferred to the National Institute of Radiological Sciences (NIRS), which has been designated as a hospital responsible for radiation emergencies. Dose estimations for the three workers were performed by prodromal symptoms, serial changes of lymphocyte numbers, chromosomal analysis, and 24Na activity. The results obtained from these methods were fairly consistent. Most of the data, such as the dose rate of radiation, its distribution, and the quality needed to evaluate the average dose, were not available when the decision for hematopoitic stem cell transplantation had to be made. Therefore, prodromal symptoms may be important in making decisions for therapeutic strategies, such as stem-cell transplantation in heavily exposed victims.
We describe a case of severe gastric insufflation in a patient with amyotrophic lateral sclerosis who was receiving bilevel nasal positive airway pressure (BNPAP) ventilation (BiPAP; Respironics; Murrysville, PA). The injection of inspiratory flow into the esophagus, aerophagia, and air trapping below the gastroesophageal junction after a meal are probably the major causes. We suggest that BNPAP ventilation can be a cause of serious gastric insufflation in a patient who lies supine, especially after a meal, and attention should be paid to avoiding this complication by having the patient sit up for about half an hour after a meal.
Insulinotropic action of glucose can be categorized as 1) triggering of release, 2) augmentation of exocytosis elicited by Ca2+, and 3) time-dependent potentiation (TDP) of the exocytotic machinery. Glucose-induced closure of ATP-sensitive K+ (K+ATP) channel is required for the first but not for the latter two. We examined the legitimacy of a novel hypothesis that glutamate is a conveyer of the K+ATP channel-independent glucose action, using intact rat pancreatic islets. To this end, we compared glucose and cell permeable glutamate donors such as dimethylglutamate and glutamine for their potency of augmentation and TDP in the presence of diazoxide (250 micromol/l), a K+ATP channel opener. One millimolar leucine was employed as an activator of glutamate dehydrogenase (GDH) as needed. A high concentration (16.7 mmol/l) of glucose applied simultaneously with a depolarizing concentration (50 mmol/l) of K+ augmented (5.80 fold) insulin release elicited by the latter. Pretreatment of the islets with 16.7 mmol/l glucose caused TDP so that insulin release subsequently elicited by 50 mmol/l K+ alone was enhanced (4.70 fold). The augmentation and TDP caused by dimethylglutamate and glutamine (10 mmol/l each), respectively, were very weak (12% of the glucose effect utmost), and dramatically enhanced upon activation of GDH by leucine. Insulinotropic effect of the glutamate donors, but not that of 50 mmol/l K+, was eliminated by 2 mmol/l NaN3, a mitochondrial poison. Glutamate per se serves as a weakly metabolizable mitochondrial fuel, but not a direct conveyer of the K+ATP channel-independent glucose action in the islet beta cell.
Inhibition of insulin release by norepinephrine has been attributed to activation of ATP-sensitive K+ channels, inactivation of voltage-dependent Ca2+ channels, and inhibition of adenylyl cyclase. However, direct inhibitory action of norepinephrine at a distal site of stimulus-secretion coupling has also been suggested. To obtain more direct evidence for norepinephrine inhibition of insulin release at a distal site, we performed experiments in intact, non-permeabilized beta cells. In rat pancreatic islets, a combination of glucose, phorbol ester and forskolin under stringent Ca2+-free conditions was used as a trigger of insulin exocytosis at a distal site. Norepinephrine inhibited this Ca2+-independent insulin release in a concentration-dependent manner, with an IC50 of 50 nM. The inhibition was complete, reversible, and pertussis toxin-sensitive, and not associated with any reduction of cAMP content in the islet cells. In conclusion, norepinephrine strongly, yet reversibly, inhibits insulin release in intact beta cells at a late step of exocytosis, through pertussis toxin-sensitive, G protein-mediated mechanism(s).
BACKGROUND: Periodontopathic bacteria induce inflammation of periodontal tissues. The cytokines and nitric oxide released in periodontal lesions have been reported to play a protective role in bacterial infection and to relate to the process of inflammation. To clarify the relationship between colonization of periodontopathic bacteria and cytokines, we evaluated profiles of inflammatory cytokines, chemokine, anti-inflammatory cytokines, and inducible nitric oxide synthase (iNOS) and colonization by Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans, which are major pathogens of periodontitis. METHODS: mRNA expression of cytokines and iNOS in inflamed and healthy gingival tissue was determined using reverse transcription-polymerase chain reaction (RT-PCR), and the relationship between their profiles and the detection of specific bacteria was analyzed. RESULTS: The relative expression of interleukin (IL)-6 and iNOS mRNAs in periodontal lesions was significantly higher than those in healthy individuals. IL-6 mRNA expression was also significantly higher at bleeding on probing (BOP)-positive sites than at BOP-negative sites. The expressions of IL-1alpha and IL-8 increased, but IL-10 expression decreased at sites where A. actinomycetemcomitans was detected. We found no correlation between the expression of cytokine and iNOS mRNA and infection by P. gingivalis. CONCLUSIONS: The expression of IL-6 may reflect inflammation in gingival tissue, and iNOS may be involved in the inflammatory process in periodontitis. The presence of A. actinomycetemcomitans or P. gingivalis might relate to the different cytokine profiles of IL-1alpha, IL-8, and IL-10.
It has been confirmed from circular dichroism (CD) spectral changes of aqueous solutions of deltaLLL-fac(S)-[Co(L-cys-N,S)3]3- that the absolute configurational inversion to the ALLL isomer is remarkably accelerated by zinc(II), while it is retarded by cadmium(II). In the diluted solutions of these metal ions containing excess deltaLLL-fac(S)-[Co(L-cys-N,S)3]3-, the observed inversion rate constant linearly depends on the zinc(II) concentration with an intercept, while it is not affected by the cadmium(II) concentration. The kinetic behavior has been explained by difference between zinc(II)- and cadmium(II)-interactions with lone pairs on sulfur donor atoms of fac(S)-[Co(L-cys-N,S)3]3-. It has also been proposed that concentrations of zinc(II) and cadmium(II) can be simultaneously determined by the kinetic measurements.
A 59-year-old man who had received chronic hemodialysis developed left occipital pain and hypoglossal nerve palsy. He was diagnosed as having skull base metastasis from renal cell carcinoma related to acquired cystic kidney. Retrospective analysis revealed the patient had had elevated serum C-reactive protein and alkaline phosphatase levels before the symptoms appeared. Radiotherapy to the skull base relieved the pain. Finally he died with generalized metastases. Serum interleukin-6 levels measured during admission had been elevated, and interleukin-6 mRNA was detected in the autopsy specimen of renal cell carcinoma. Interleukin-6 might be involved in the etiology of paraneoplastic signs.
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OBJECTIVE: The majority of type 1 diabetes is considered to be autoimmune with, for the most part, abrupt development. However, type 1 diabetes with slow onset, or the so-called slowly progressive type 1 diabetes or latent autoimmune diabetes in adults, has been recently recognized and is considered to be autoimmune-related. Although some investigators tried to explain the difference in onset pattern by the genetic background, including HLA type, it has not been established thus far. We hypothesized that the difference in onset pattern may relate to regeneration or differentiation of pancreatic beta-cells, and we therefore focused on the NeuroD/BETA2 gene, which encodes a transcription factor for the insulin gene and beta-cell differentiation. RESEARCH DESIGN AND METHODS: We examined the NeuroD/BETA2 gene polymorphism in 105 Japanese type 1 diabetic patients and in 122 nondiabetic Japanese subjects in a case-control study, and we stratified the patients according to their onset pattern and islet-associated autoantibody positivity. RESULTS: Regardless of the existence of islet-associated autoantibody, we found a significant difference in A allele frequency between type 1 diabetic patients with acute-onset type and control subjects. However, no difference was found between type 1 slow-onset diabetic patients and control subjects. CONCLUSIONS: These results support our hypothesis that NeuroD/BETA2 may affect the ability of regeneration of beta-cells, leading to a difference in the onset pattern and clinical course of type 1 diabetes.
A morphological and immunohistochemical study of the ultimobranchial body of reptiles Japanese lizard and snake was carried out. The ultimobranchial body of the Japanese lizard was located adjacent to the left arch of the aorta between the trachea and esophagus. It was found as a cluster or group of cells with no capsule. Grimelius' silver impregnation and lead-hematoxylin staining produced positive reactions in some of the clustered cells and follicular cells. The same reaction pattern was observed with anti-calcitonin using the PAP method. The PAP reactions were positive to antiserum against pig calcitonin, but negative to antiserum against synthesized human calcitonin. Furthermore, the PAP reactions were negative to antiserum against tyrosine hydroxylase. The immunofluorescent study of the snake ultimobranchial body revealed that most of the clustered cells and some of the follicular cells were calcitonin-immunoreactive but none was tyrosine hydroxylase-immunoreactive. Certain histological similarities exist between the Japanese lizard ultimobranchial body and snake ultimobranchial body, but the distribution of calcitonin-positive cells were slightly different. In the Japanese lizard, the positive cells were scattered between the foliicles and the number was small. However, most of the cells which formed the cluster in the ultimobranchial body of snake were positive. The findings suggest that the configuration of amino acid in the Japanese lizard calcitonin and snake calcitonin are similar to that of pig calcitonin, and the reptile and the birds is a boundary of the tyrosine hydroxylase existence.
Susceptibility to insulin-dependent (type 1) diabetes mellitus is determined by both environmental and genetic factors. The primary gene associated with predisposition to type 1 diabetes is the human leukocyte antigen (HLA) class II gene (IDDM1). Recent studies have described linkage and association of type 1 diabetes to the cytotoxic T lymphocyte antigen-4 (CTLA-4) gene (IDDM12)in Caucasians. CTLA-4 is a candidate gene for T-cell-mediated autoimmune diseases because it is a negative regulator of T-cell proliferation. We investigated distribution of a CTLA-4 (AT)n microsatellite marker in 118 Japanese patients with type 1 diabetes and 195 control subjects. We also investigated association between this CTLA-4 gene polymorphism and GAD65 antibody positivity in 103 of the patients. CTLA-4 microsatellite marker loci were determined by polymerase chain reaction amplification of genomic DNA and resolution of the products on sequencing gels. GAD65 antibody was detected by radioligand binding assay. There was no significant difference in the distribution of CTLA-4 alleles between patients and controls, and no difference was observed in the prevalence of CTLA-4 alleles when GAD65 antibody-positive and -negative individuals with the type 1 diabetes were compared. The present study did not support an association between the CTLA-4 microsatellite marker and type 1 diabetes in our Japanese study population.
The details of calcium flux during growth were examined in female rats. Twenty-eight 53-d-old rats were equally divided into 4 groups. Rats were given a purified diet (0.5% Ca and 0.35% Pi) throughout the experiment. Calcium balance and 45Ca kinetics studies using an open two-compartment model were performed over a 3-d period when rats were 60 (control), 74 , 88 and 116 d old. A simple calcium balance study, using the last group, was carried out at the age of 102 d. Compared with the control group, true intestinal calcium absorption was significantly increased at 74 d, but then decreased in a time-dependent manner up to 116 d. The apparent intestinal calcium absorption began to decrease at 88 d, and decreased further with age. An increase in urinary calcium output was observed at 74 and 88 d in phase with calcium excretion into the intestine, and both variables returned to the control level at 116 d. Calcium into bone was decreased at 74 and 116 d. Calcium from bone similarly changed with Vo+ at 74 d: however the highest value was observed at 88 d. Thereafter, Vo- reached the control level at 116 d. Calcium balance rapidly decreased at 88, 102 and 116 d, but still remained positive. Calcium intake remained steady until 102 d, but was significantly decreased at the end of the experiment. The changes in calcium flux with age can be summarized as follows: 1) bone turnover decreased, calcium excretion into the urine and feces began to increase, and true intestinal calcium absorption increased, 2) apparent intestinal calcium absorption decreased, while calcium from bone and calcium excretion into the urine and feces increased, and 3) calcium intake and calcium into bone decreased.
Recently, titanium-tantalum alloys have been studied as implant materials for dental and orthopedic surgery. However, titanium and tantalum are difficult to mix by common arc melting and induction melting, because of their high melting point and the marked difference between their densities (Ti: 1,680 degrees C, 4.5 g/cm3, Ta: 2,990 degrees C, 16.6 g/cm3). Thus, the Cold Crucible Levitation Melting (CCLM) method was chosen to produce a Ti-30 wt%Ta binary alloy in the present study. The CCLM furnace, with 1 kg capacity, consisted of a water-cooled crucible comprising oxygen-free high purity copper segments and coils wrapped around the crucible and connected to a frequency inverter power supply. A qualified ingot of 1.0 kg of Ti-30 wt%Ta alloy was obtained. The ingot was characterized from the surface quality, chemical composition distribution and microstructure, and finally the melting process was discussed.
OBJECTIVES: This study attempted to clarify the health effects of implementing a 12-hour shift in place of the traditional 8-hour shift in work in a clean room in an electronic parts producing factory. METHODS: Health-check records during a year or longer before and after the shift change were reviewed regarding subjective symptoms, height, body weight, and blood pressure for 189 male workers who had moved to a 12-hour shift and for 16 male workers who remained on an 8-hour shift. RESULTS: The workers changing to a 12-hour shift showed significant increases in subjective symptoms, particularly psychological symptoms defined as related to fatigue and bodyweight gain, 1 kg on average, in the year after the shift change. Increased symptoms and body weight remained high even another year later. The workers remaining in the 8-hour shift did not show significant changes in symptoms or body weight during the observation. No changes in blood pressure were observed in relation to the shift move. CONCLUSIONS: The results suggested that implementing a 12-hour shift caused marked psychological fatigue and unhealthy weight gain among some cleanroom workers and that the adaptation to the new work shift did not seem easy for these workers. Working in a clean room can be considered a job in which special caution is needed regarding increased fatigue when a compressed working schedule is implemented. Attention should also be paid to possible weight gain among persons working 12-hour shifts.
A 54-year-old woman presented with a 6-month history of left back pain. She had undergone left mastectomy for breast cancer in 1993 and hysterectomy for cervical cancer in 1997. Excretory urography showed no abnormality in the left collecting system, but right hydronephrosis caused by a midureteral stone. She was treated by transurethral ureterolithotripsy first. Computerized tomography showed a 4 x 3 cm. mass enhanced slightly by contrast medium at the left renal hilus. The tumor was bordered laterally by the left kidney and posteriorly by the left renal vein which appeared normal on magnetic resonance imaging. Selective left renal angiography revealed no abnormality. Radical en bloc excision of the tumor with the left kidney and adrenal gland was performed. Pathological examination showed a well differentiated leiomyosarcoma arising from the renal vein; the tumor cells stained positive for alpha-smooth muscle actin, vimentin and desmin and negative for S 100-protein. She was free of symptoms and there was no evidence of local recurrence or distant metastases 22 months postoperatively.
PURPOSE: We report the clinical results and efficacy of laparoscopic radical prostatectomy for localized prostate cancer. PATIENTS AND METHODS: Between December, 1999 and June, 2000 we performed transperitoneal laparoscopic radial prostatectomy on 10 patients with T1 or T2 organ confined prostate cancer according to the techniques as described by Guillonneau et al. Different points were as follows: 1) We placed double J catheters during surgery to prevent ureteral injury. 2) We treated dorsal vein complex using an Endo-GIA-stapler. 3) We dissected the bladder neck from the prostate using an ultrasound scalpel in the manner to preserve the bladder neck. RESULT: We could not completed laparoscopic prostatectomy on two patients because of massive bleeding from dorsal vein and consuming too much time to suture urethra-bladder anastomosis. The average operating time in all cases was 8.1 hours including 1.8 hours in laparoscopic pelvic lymphadenectomy. The average estimated blood loss in all cases was 859 ml. There were 2 surgical complications with bladder injury and port site hernia. The histological examination revealed prostate cancer; pT2pNO in 8, pT3pNO in 2. The surgical margin and lymph nodes were negative in all patients. The duration of an indwelling catheter ranged from 5 to 40 days mean 17 days. The duration to recovery of normal micturition was 6 to 90 days, mean 40 days. CONCLUSION: Long-term follow-up and extensive studies are necessary to evaluate the efficacy of this procedure. It might provide shorter duration of an indwelling catheter and earlier recovery of normal micturition as compared with the conventional open surgery.
The present study was undertaken to characterize the in vivo alpha(1)-adrenoceptor binding of KMD-3213, a novel selective antagonist of alpha(1A)-adrenoceptors, in rat tissues by using a tritiated ligand with high specific activity, in comparison with that of [(3)H]prazosin. A significant degree of in vivo specific binding of [(3)H]KMD-3213 after i.v. injection of the radioligand (1. 4 nmol/kg) was seen in most rat tissues, except the cerebral cortex, spleen, and liver, which showed a little or no specific binding. There was a notable difference among tissues in the time course of specific [(3)H]KMD-3213 binding after i.v. injection of the ligand. The specific binding in the lung, kidney, and spleen was greatest at 10 min and declined rapidly with the disappearance of the ligand from the plasma. On the other hand, [(3)H]KMD-3213 binding in the submaxillary gland, vas deferens, and prostate attained peak levels at 60 min, and a considerable degree of binding was present even at 240 min. After i.v. injection of a similar dose (1.2 nmol/kg) of [(3)H]prazosin in rats, the in vivo specific binding in the submaxillary gland was greatest at 10 min and then it fell rapidly, whereas [(3)H]prazosin binding in the spleen attained a peak level at 60 min, and this was maintained even at 120 min. The AUC(0-120) values of the specific binding for [(3)H]KMD-3213, compared with those of [(3)H]prazosin, were markedly lower in the rat aorta, spleen, and liver, whereas the prostate, submaxillary gland, and lung showed significantly higher AUC(0-120) values of [(3)H]KMD-3213 compared with [(3)H]prazosin. Furthermore, the in vivo specific binding of [(3)H]KMD-3213 at dose ranges of 1.4 to 13.6 nmol/kg increased linearly in the prostate and submaxillary gland, but did not increase in a dose-dependent manner in the spleen. On the other hand, there was a dose-dependent increase in the in vivo specific binding of [(3)H]prazosin at doses of 1.2 to 10.6 nmol/kg in all tissues. The in vivo specific binding of [(3)H]KMD-3213 in rat tissues was reduced by concomitant i.v. injection of low doses of prazosin in a dose-dependent manner, but not by even a relatively high dose of yohimbine. In conclusion, the present study shows that KMD-3213 binds to the alpha(1A)-adrenoceptor subtype with a higher affinity than to the alpha(1B)- and alpha(1D)- subtypes under in vivo condition, thus leading to prostate selectivity.