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Biomedical subjects

A Hino

Publications and source records attributed to A Hino.

At least 37 records · Page 2Linked to original sources

False localization of rupture site in patients with multiple cerebral aneurysms and subarachnoid hemorrhage.

OBJECTIVE: Patients with subarachnoid hemorrhage and multiple intracranial aneurysms present a unique challenge to the neurosurgeon. Unless all aneurysms can be clipped through a single craniotomy, the surgeon must accurately determine which aneurysm has ruptured. Misjudgment may result in disastrous postoperative rebleeding from the untreated but true ruptured lesion. We assessed the risk of false localization of the rupture site and subsequent rebleeding and documented the problems in predicting the true rupture site when patients have multiple intracranial aneurysms. METHOD: We reviewed the records of a consecutive series of 93 patients treated over a period of 12 years who presented with their first subarachnoid hemorrhage and who had multiple intracranial aneurysms. The rupture site was determined on the basis of computed tomographic and angiographic findings, and the supposed ruptured aneurysm was clipped within 2 days of hemorrhage in each patient. Additional aneurysms that could not be accessed in the same surgical session were operated on at a later stage. All patients' records were reviewed, and all computed tomographic scans and angiograms, including repeat studies performed in some patients, were retrospectively reevaluated by the authors, who had no knowledge of the patients' clinical information. RESULTS: The location of the aneurysm that ruptured was verified at the time of surgery or during the autopsy in 76 patients (82%). The aneurysm that ruptured was the one predicted as ruptured by the surgeon before surgery in 69 patients (91%) and in retrospect in 72 patients (95%). Five of the 6 patients in whom the ruptured aneurysm was not correctly identified were thought to have only a single aneurysm. Four patients rebled after surgery, and 2 patients died as a result of the rebleeding. CONCLUSION: In the reported series, the most common cause of rebleeding soon after aneurysm surgery was failure to obliterate the ruptured aneurysm, usually because it was missed on the initial angiogram. The results support not only meticulous radiological investigation of all intracranial arteries before surgery but also thorough surgical inspection of the target aneurysm in all cases of subarachnoid hemorrhage even after one candidate lesion has been discovered.

Adult↗

An adult case of recurrent arteriovenous malformation after "complete" surgical excision: a case report.

BACKGROUND: Complete surgical excision of arteriovenous malformations (AVM) documented by postoperative angiography is considered a cure. However, recent reports have shown that AVMs in children may recur after negative postoperative angiograms, and some suggest that it may reflect the immaturity of their cerebrovasculature. This case report demonstrates that AVM in adults may also recur, despite postoperative angiograms confirming complete removal. CASE DESCRIPTION: This 28-year-old man presented in 1994 with a focal motor seizure and was found to have an AVM in the right frontal lobe. He underwent surgical excision of the AVM; postoperative angiograms taken immediately after surgery and 15 days later showed no residual AVM. He remained free of symptoms after surgery and it was considered that a complete removal had been achieved. In 1998 he developed a subarachnoid hemorrhage, and subsequent angiograms revealed a small AVM in an adjacent location. CONCLUSION: This is the oldest patient reported in the literature with a recurrence of AVM, despite postoperative angiograms confirming complete removal. Angiographically invisible immature vessels, which might have been left in the surgical field, might have formed a new malformation later. We still believe that such recurrence must be very rare after AVM surgery, but we now recommend follow-up angiography at yearly intervals to our patients.

Adult↗

Double pituitary adenomas: six surgical cases.

While double pituitary adenomas have been found in approximately 1% of autopsy pituitaries, those in surgically resected material have been only rarely reported. We report herein 6 cases of double pituitary adenomas, which consisted of two histologically and/or immunohistochemically different areas among approximately 450 surgical specimens. Five out of 6 patients were men and the age was ranged between 18 and 61 years old. All these 6 patients presented acromegaly or acrogigantism and hyperprolactinemia was noted in 3 patients. In 2 patients (cases 1 and 2) the two adenomas belonged to different adenoma groups (GH-PRL-TSH group and FSH/LH group), while in the remaining 4 patients (cases 3-6) the two adenomas belonged to the same group (GH-PRL-TSH group). Thus, in all patients at least one of the two adenomas was GH-producing adenoma. Reasons for a high incidence of GH-producing adenomas in surgically resected double pituitary adenomas may include the presence of a variety of histologic subtypes among GH-producing adenomas and the advantage of cytokeratin immunostaining to distinguish these subtypes. In regard to pathogenesis of double pituitary adenomas, adenomas in cases 1 and 2 may be of multicentric occurrence, while those in cases 3-6 may occur through different clonal proliferation within originally one adenoma, resulting in diverse phenotypic expressions. Since there were patients with familial MEN 1 (case 2) and familial pituitary adenoma unrelated MEN 1 (case 3), genetic background should be also considered. Double pituitary adenomas in surgically resected material may not be so infrequent. Further molecular analysis will provide new insights into understanding the pathogenesis of pituitary adenomas and their mechanisms of multidirectional phenotypic diffrentiation.

Acromegaly↗

Stress tolerance in doughs of Saccharomyces cerevisiae trehalase mutants derived from commercial Baker's yeast.

Accumulation of trehalose is widely believed to be a critical determinant in improving the stress tolerance of the yeast Saccharomyces cerevisiae, which is commonly used in commercial bread dough. To retain the accumulation of trehalose in yeast cells, we constructed, for the first time, diploid homozygous neutral trehalase mutants (Deltanth1), acid trehalase mutants (Deltaath1), and double mutants (Deltanth1 ath1) by using commercial baker's yeast strains as the parent strains and the gene disruption method. During fermentation in a liquid fermentation medium, degradation of intracellular trehalose was inhibited with all of the trehalase mutants. The gassing power of frozen doughs made with these mutants was greater than the gassing power of doughs made with the parent strains. The Deltanth1 and Deltaath1 strains also exhibited higher levels of tolerance of dry conditions than the parent strains exhibited; however, the Deltanth1 ath1 strain exhibited lower tolerance of dry conditions than the parent strain exhibited. The improved freeze tolerance exhibited by all of the trehalase mutants may make these strains useful in frozen dough.

Carbon Dioxide↗

Identification of a locus for susceptibility to renal cell carcinoma in the Long-Evans Cinnamon rat.

The Long-Evans Cinnamon (LEC) mutant rat shows higher incidence of renal cell carcinomas induced by a treatment with the chemical carcinogen N-diethylnitrosamine, as compared to the normal control rat. We performed the first genome-wide scan for genes responsible for susceptibility to chemically induced renal cell carcinoma in an F2 intercross obtained by mating the LEC and Fischer-344 (F344) rats. The genotype of 71 (F344 x LEC) F2 progenies was determined with the use of 338 simple sequence length polymorphisms (SSLPs) spread over the genome. The F2 rats which carried renal cell carcinoma were shown to possess the incidence of homozygosity of the LEC allele which is higher than that of the other genotypes at SSLP markers on chromosome 5 (chi2 = 17.5 for D5Rat21). Our linkage analysis has led to the revelation of a novel gene that influences susceptibility to renal cell carcinoma on rat chromosome 5.

Alkylating Agents↗

Homolog of a-factor receptor gene in Saccharomyces exiguus.

Homologs of Saccharomyces cerevisiae STE3, a-factor receptor gene were detected from S. exiguus NFRI 3539 by low stringency Southern hybridization. This strain might have at least two types of homolog. One of these homologs, designated as e-STE3 was cloned. Its nucleotide sequence revealed 60% identity to STE3. The putative protein coding region consisted of 453 amino acid residues. The amino acid sequence identity between STE3 and e-STE3 was 62% and that of the N-terminal 303 amino acid residues considered to be the pheromone binding domain was 79%.

Amino Acid Sequence↗

Adenosarcoma of the uterine cervix presenting as a cervical polyp.

A case of adenosarcoma arising from the uterine cervix of a 55-year-old female who complained of vaginal discharge is reported. A polyp, 6 x 2 x 1.5 cm in size, identified in the cervical canal was clinically diagnosed as benign cervical polyp and resected. Histologically, the polyp was composed of benign epithelial components and sarcomatous stroma wherein periglandular hypercellularity and some mitoses including atypical ones were noted. Immunohistochemically, stromal cells were positive for muscle-type actins, desmin and estrogen receptor. Adenosarcoma is a rare, biphasic tumor of the uterus and usually presents as a polypoid mass in the endometrial cavity. When they arise from the cervix, adenosarcomas may be confused with benign cervical polyps clinically and pathologically. As the former often recurs, microscopic differentiation is crucial for further treatment.

Actins↗

Value of repeat angiography in patients with spontaneous subcortical hemorrhage.

BACKGROUND AND PURPOSE: Neuroradiological investigations do not disclose a source of bleeding in some patients with spontaneous subcortical hemorrhage. These patients may harbor undetected vascular malformations and may be at risk of rebleeding in the future. We investigated patients with subcortical hemorrhage with use of repeat angiography and MRI to determine the incidence of occult vascular malformations and the risk of bleeding during follow-up. METHODS: We reviewed a consecutive series of 137 patients with subcortical hemorrhage during a 10-year period (June 1987 through June 1997). If the patient was <65 years old and the first angiogram and/or MRI did not show a source of bleeding, repeat angiography was recommended. All angiographic and MRI studies were reviewed. The relationship between the identified bleeding source and clinical variables such as patient age, sex, and history of hypertension and the size and location of the hematoma were examined. RESULTS: One hundred seven patients (78%) underwent angiography on admission, 10 (7%) had immediate surgery for hematoma without angiography, and 20 (15%) had neither angiography nor surgery. Overall, an etiology for the hemorrhage was found in 55 cases (40%). Vascular malformations were common in young patients without preexisting hypertension. A second angiogram was obtained in 22 patients, and 4 arteriovenous malformations were demonstrated. Rebleeding at the site of the initial hemorrhage was not observed after a mean follow-up of 68 months. CONCLUSIONS: Angiography performed acutely after hemorrhage may not demonstrate vascular malformations. Consideration should be given to repeat angiography in patients who do not have a specific cause for hemorrhage.

Adolescent↗

p53 gene mutation in N-butyl-N-(4-hydroxybutyl)nitrosamine-induced urinary bladder tumors and N-methyl-N-nitrosourea-induced colon tumors of rats.

We analyzed p53 mutations in 17 N-butyl-N-(4-hydroxybutyl) nitrosamine-induced bladder transitional cell carcinomas (TCCs) with or without areas of squamous cell carcinoma (SCC) of Long-Evans Cinnamon (LEC) and F344 rats, and in 7 N-methyl-N-nitrosourea-induced colon adenocarcinomas of LEC rats by polymerase chain reaction-single strand conformation polymorphism analysis and DNA sequencing. Of these bladder tumors, one TCC with moderately differentiated SCC had a T to G transversion mutation at codon 141, leading to a Val to Gly amino acid change. No p53 mutation was found in colon adenocarcinomas. Thus a p53 gene mutation seems infrequent in these rat bladder and colon carcinogenesis models even in the late stage.

Animals↗

Regulation of genes encoding subunits of the trehalose synthase complex in Saccharomyces cerevisiae: novel variations of STRE-mediated transcription control?

Saccharomyces cerevisiae cells show under suboptimal growth conditions a complex response that leads to the acquisition of tolerance to different types of environmental stress. This response is characterised by enhanced expression of a number of genes which contain so-called stress-responsive elements (STREs) in their promoters. In addition, the cells accumulate under suboptimal conditions the putative stress protectant trehalose. In this work, we have examined the expression of four genes encoding subunits of the trehalose synthase complex, GGS1/TPS1, TPS2, TPS3 and TSL1. We show that expression of these genes is coregulated under stress conditions. Like for many other genes containing STREs, expression of the trehalose synthase genes is also induced by heat and osmotic stress and by nutrient starvation, and negatively regulated by the Ras-cAMP pathway. However, during fermentative growth only TSL1 shows an expression pattern like that of the STRE-controlled genes CTT1 and SSA3, while expression of the three other trehalose synthase genes is only transiently down-regulated. This difference in expression might be related to the known requirement of trehalose biosynthesis for the control of yeast glycolysis and hence for fermentative growth. We conclude that the mere presence in the promoter of (an) active STRE(s) does not necessarily imply complete coregulation of expression. Additional mechanisms appear to fine tune the activity of STREs in order to adapt the expression of the downstream genes to specific requirements.

Blotting, Northern↗

Negative feedback mechanism suppresses interleukin-12 production by antigen-presenting cells interacting with T helper 2 cells.

Interleukin-12 (IL-12) has been shown to be produced by monocytes by the ligation of CD40. In the present experiments, IL-12 is shown to be produced by murine spleen antigen-presenting cells (APC) by interaction with T helper 1 (Th1) clones through CD40-CD40 ligand (CD40L) interaction, but not with Th2 clones. The IL-12 production induced by the Th1 clone interaction was inhibited by the addition of exogenous IL-10. Th2 clones were shown to produce a sufficient amount of IL-10 to inhibit the IL-12 production induced by Th1 clones. In the presence of anti-IL-10 monoclonal antibodies splenic APC interacting with Th2 clones produced IL-12. These results indicate that IL-10 produced by Th2 cells stimulated with antigen suppress IL-12 production of APC interacting with Th2 cells. IL-12 is composed of two subunits, p35 and p40. In our experiments, p40 mRNA accumulation was shown to be affected by IL-10 more severely than the accumulation of p35 mRNA, indicating that IL-10 regulates IL-12 production by APC mainly by affecting p40 mRNA accumulation.

Animals↗

Increased expression of endothelin B receptor mRNA following subarachnoid hemorrhage in monkeys.

These studies tested the hypothesis that the cerebral vasospasm that follows subarachnoid hemorrhage (SAH) is due to alterations in endothelin (ET) and ET receptor expression. Eight monkeys underwent cerebral angiography and induction of SAH. Angiography was repeated 7 days later to confirm the presence of cerebral vasospasm, and animals were killed. RNA was isolated from right (vasospastic) and left (control) side middle cerebral arteries and surrounding cerebral cortex. The levels of prepro (PP) ET-1 (ppET-1) and ppET-3 and ETA and ETB receptor MRNAs were determined using a quantitative reverse transcriptase polymerase chain reaction-based assay. ET-1 peptide was also measured in CSF at baseline and after 7 days. Specific agonist binding to ETA and ETB receptors in both middle cerebral arteries and in surrounding brain cortex was measured in three animals by autoradiographic binding assays. Levels of ETB receptor mRNA were 3.4 +/- 2.2-fold higher in the right than in the left cerebral arteries (p < 0.01). There were no significant differences in the levels of ppET-1, ppET-3, or ETA receptor mRNA in cerebral arteries. ET-1 peptide was not elevated in CSF. Levels of ETA and ETB receptor mRNAs were 2.6 +/ 1.1- and 2.1 +/ 1.3-fold higher, respectively, in the right than in the left cerebral cortex, while the level of ppET-3 mRNA was 2.1 +/- 1.0-fold lower. There were no differences in ppET-1 mRNA levels between right and left cerebral cortex. Binding to ETA and ETB receptors in cerebral arteries and cortex did not differ significantly between right and left sides. These results do not support the hypothesis that overexpression of ET-1 is principal cause of vasospasm, but rather they suggest that SAH causes complex changes in the ET system that together are responsible for the cellular response to SAH.

Animals↗

Changes in endothelial nitric oxide synthase mRNA during vasospasm after subarachnoid hemorrhage in monkeys.

OBJECTIVE: We attempt to determine whether changes in messenger ribonucleic acid (mRNA) for nitric oxide synthase (NOS) and soluble guanylate cyclase, enzymes that mediate endothelium-dependent vasodilation in cerebral arteries, occur after subarachnoid hemorrhage (SAH) in monkeys. METHODS: Baseline cerebral angiograms were obtained, and right-sided SAH was induced by microsurgically placing autologous blood clot against the right anterior circle of Willis in seven monkeys. Seven days later, angiographic studies were repeated and the animals were killed. Right (vasospastic) and left (control) middle cerebral arteries and underlying cortex were removed. The competitive reverse transcriptase polymerase chain reaction was used to quantify mRNA for soluble guanylate cyclase and two isoforms of constitutive NOS in these tissues. RESULTS: Comparison of angiograms at baseline and after 7 days showed a 41 +/- 7% (mean +/- standard error of the mean, P < 0.05, Wilcoxon test) decrease in diameter of the right middle cerebral artery. After the animals were killed, comparison of right and left middle cerebral arteries showed a 56 +/- 11% decrease (P < 0.005, paired t test) in endothelial NOS mRNA. There was a 142 +/- 39% (P < 0.05) increase in right cortex endothelial NOS mRNA compared to the left cortex. There were no significant differences between right and left sides in mRNAs for soluble guanylate cyclase or brain NOS. CONCLUSION: Decreased endothelial NOS mRNA in cerebral arteries 7 days after SAH may be caused by endothelial cell damage and could contribute to vasospasm after SAH. Increased endothelial NOS in brain tissue may reflect a compensatory vasodilator mechanism of the brain against the cerebral ischemia associated with vasospasm and SAH.

Animals↗

Preparation of anti-human thymidine phosphorylase monoclonal antibodies useful for detecting the enzyme levels in tumor tissues.

The antitumor activity of cytostatic 5'-deoxy-5-fluorouridine (5'-dFUrd) depends on its being converted to 5-fluorouracil (5-FUra) by the enzyme thymidine phosphorylase (dThdPase, EC 2.42.4). We prepared mouse anti-human dThdPase monoclonal antibodies to serve as tools for clinical studies with this drug. Partially purified dThdPase obtained form HCT116 human colon cancer cells grown in athymic mice was used as and antigen for the immunization of mice. Six hybridomas were cloned which produced anti-human dThdPase antibodies, as detected by Western blot analysis with human dThdPase. With these antibodies, we developed an ELISA method sensitive enough to measure dThdPase levels, even in tumor tissue samples weighing as little as 10 mg. In addition, one monoclonal antibody was suitable for immunologically staining the enzyme in tumor tissues. Thus, these anti-human dThdPase monoclonal antibodies could be used to measure levels of the enzyme in tumor cells, which is essential for the activation of 5'-dFUrd.

Animals↗

Purification, cloning, and expression of murine uridine phosphorylase.

Uridine phosphorylase was purified 10,300-fold from tumors of the murine colorectal adenocarcinoma cell line, Colon-26. Degenerate DNA probes were synthesized corresponding to partial amino acid sequences and used to screen a Colon-26 cDNA library. A cDNA clone of 1327 base pairs that contains a 5' untranslated region, a coding region of 933 base pairs, and a 3' nontranslated region with a polyadenylated tail was identified. The cDNA was confirmed to be uridine phosphorylase by 1) sequence comparison to uridine phosphorylase of Escherichia coli, 2) substrate specificity studies with recombinant protein expressed in COS-7 cells that demonstrated relatively high enzyme activity with uridine as substrate compared low levels when thymidine was used, and 3) inhibition of enzyme activity by the competitive inhibitor 2,2'-anhydro-5-ethyluridine. Northern blot analysis using the cDNA as a probe, demonstrated high levels of mRNA expression in Colon-26. Expression was low in NIH3T3 cells, but high in DMBA-3 and PH-1 cells, which are NIH3T3-derived cells that have been transformed with mutated murine Ha-ras and viral Ha-ras, respectively. Expression of uridine phosphorylase mRNA in these cell lines was further enhanced by treating the cells with the inflammatory cytokines, tumor necrosis factor-alpha, interleukin 1 alpha, and interferon gamma.

Adenocarcinoma↗

An improved source of bryostatin 10, Bugula neritina from the Gulf of Aomori, Japan.

Bryostatins have been isolated from diverse Japanese coastal specimens of Bugula neritina guided by inhibitory activity against fertilized sea urchin egg cell division. B. neritina from the Gulf of Aomori, Japan, has been found to contain bryostatin 10 [1b] in high yield (10(-3)%) for this class of compounds. The 1H- and 13C-nmr signals of bryostatin 10 [1b] were reassigned by 2D nmr techniques. The conformation of bryostatin 10 [1b] in solution was revealed by nmr studies. This compound also exhibited activity in a steroidogenesis assay by increasing the production of adrenocortical hormones nearly twofold.

Animals↗