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Biomedical subjects

N Yokota

Publications and source records attributed to N Yokota.

At least 55 records · Page 3Linked to original sources
PubMed1999

What can predict postoperative "endocrinological cure" in Cushing's disease?

OBJECTIVE: The goal of surgical treatment for Cushing's disease is "endocrinological cure." The purpose of this study was to determine predictors for postoperative endocrinological cure in Cushing's disease. METHODS: Postoperative endocrinological studies were evaluated in 18 patients with Cushing's disease who underwent transsphenoidal surgery for selective adenomectomy. Serum adrenocorticotropic hormone (ACTH) levels were measured by radioimmunoassay during the first week after surgery. One week after surgery, a test using corticotropin-releasing hormone (CRH) was performed on each patient to check the reserve function of normal ACTH-secreting cells. RESULTS: In eight patients, postoperative ACTH levels were below the measurable level for 1 week, and ACTH showed no response to the CRH test. In these patients, serum ACTH and cortisol levels were kept in the normal range with a normal diurnal variation during long-term follow-up. These patients can be defined as endocrinologically cured. In seven patients, the ACTH level returned to within normal range on the day after surgery, but ACTH was provoked by the CRH test. Five of these seven patients showed subsequent re-elevation of ACTH above the normal range. ACTH levels were never normalized in the remaining three patients, and medical treatments were unavoidable. CONCLUSION: The most reliable indicators for predicting endocrinological cure in Cushing's disease are no response of ACTH to the CRH test in the early postoperative stage and an unmeasurably low ACTH level in the week after surgery. Obtaining a normal range of ACTH level postoperatively is insufficient to define endocrinological cure.

Adenoma↗
PubMed1999

Plasma and urine levels of uroguanylin, a new natriuretic peptide, in nephrotic syndrome.

Uroguanylin, a new natriuretic peptide originally isolated from urine, stimulates the membrane guanylate cyclase C receptor. No information, however, is available on the plasma and urine levels of uroguanylin in nephrotic syndrome (NS), the state associated with sodium and water retention. Using a sensitive radioimmunoassay, we measured the plasma and urine concentrations of immunoreactive (ir-)uroguanylin in NS patients and compared them with those of patients with non-nephrotic glomerulonephritis. Plasma ir-uroguanylin, blood pressure and the cardiothoracic ratio were higher, and urine excretion of ir-uroguanylin was lower in the NS patients. Plasma ir-uroguanylin in the NS patients significantly decreased during remission as compared with findings on admission. There was a significant inverse correlation between the concentration of plasma ir-uroguanylin and that of serum total protein or albumin. Moreover, fluid retention in the NS patients was correlated with the changes in plasma ir-uroguanylin between admission and remission, indicative that the plasma concentration increases with the severity of the nephrotic state. Taking into account its potent natriuretic effect, these findings suggest that uroguanylin may function in the pathophysiological mechanism in NS.

Adult↗
PubMed1999

Neurovascular decompression for trigeminal neuralgia in elderly patients.

The operative findings and outcomes of neurovascular decompression for trigeminal neuralgia were compared between patients aged 75 years and older (elderly group, 17 patients) and patients aged under 75 years (nonelderly group, 115 patients). There were no statistically significant differences in the operative findings or outcomes between the two groups, except in the percentage of patients who had been treated with carbamazepine. Neurovascular decompression for trigeminal neuralgia can be performed in elderly patients with the same operative results as in nonelderly patients. If other treatments (especially carbamazepine treatment) prove ineffective, neurovascular decompression should be considered in elderly patients before they become too old to undergo surgery. However, neurovascular decompression in elderly patients requires great care, as the venous system, including the superior petrosal vein, should be preserved and retraction of the cerebellum should be avoided whenever possible to maintain correct blood circulation in the cerebellum and brainstem.

Aged↗
PubMed1999

Prefrontal dysfunction following unilateral posteroventral pallidotomy in Parkinson's disease.

OBJECT: Pre- and postoperative cognitive function was evaluated in 25 patients with Parkinson's disease (PD) who underwent unilateral posteroventral pallidotomy (PVP) to clarify the effects of this operation on cognitive function. METHODS: Cognitive function was assessed before surgery and 1 month and 3 months afterward by using a battery of neuropsychological tests consisting of orientation, digit span (forward and backward), digit learning, 5-minute memory of five words, similarities, serial sevens, animal name listing, and the kana pick-out test, as well as the Japanese version of the Mini-Mental State. Preoperative evaluation revealed that patients experienced difficulties in performing the neuropsychological tasks of reasoning and abstraction, working memory of numerals, word fluency, and concept formation compared with 36 healthy volunteers (p < 0.05). A simple regression analysis showed strong relationships in a negative fashion between preoperative (r = 0.81, p = 0.002) and 1-month (r = 0.79, p = 0.0059) and 3-month (r = 0.85, p = 0.0016) postoperative gross-total scores and Hoehn and Yahr staging. Preoperative and postoperative scores at 1 month and 3 months were analyzed by analysis of variance, but only the Fisher's post hoc test revealed the source of difference. All tasks except orientation (p = 0.0292) were unchanged in the 10 patients who underwent surgery on the right side. The scores for this task at 1 month postsurgery were significantly lower (p = 0.0203) but improved to preoperative values by 3 months. In the 15 patients who underwent surgery on the left side significant differences among tasks were revealed for serial sevens (p = 0.0471) and animal naming (p = 0.0425). The scores for these tasks were significantly lower at 1 month postoperatively (p = 0.0431 for serial sevens and p = 0.0408 for animal naming), but improved by 3 months after the operation. CONCLUSIONS: The present data revealed that cognitive dysfunction in patients with PD relates to advancement of Hoehn and Yahr stage, but PVP is not associated with significant long-lasting cognitive deficits.

Aged↗
PubMed1999

[Exercise-induced acute renal failure associated with renal vasoconstriction].

Exercise-induced acute renal failure without rhabdomyolysis is not a rare condition. We experienced 6 cases (5 men and a woman) during last the 8 years. All cases complained of severe loin pain and nausea after mild to moderate exercises (for example, a track race in an athletic meeting). The elevation of serum and urinary myoglobin was undetected. In 4 of 5 patients with abdominal CT, renal patchy vasoconstriction (wedge-shaped low-density lesion) was observed. This was diagnosed as exercise-induced acute renal failure with loin pain (serum creatinine levels: 1.7-8.6 mg/dl). The renal function in 5 of the 6 cases normalized in about three weeks by fluid replacement therapy and hemodialysis support, which one patient received for 3 days. One patient required a long time for improvement of renal function and renal insufficiency persisted (serum creatinine 1.8 mg/dl). In 2 patients, the concentration of serum uric acid became very low after the recovery of renal function. These two patients were diagnosed as an isolated hyperuricosuric hypouricemia. More than half of the 6 patients had previously experienced the same episodes (loin pain and nausea) after exercise. Exercise-induced acute renal failure, probably due to renal patchy vasoconstriction, seems to be not a rare disease. The etiology of renal patchy vasoconstriction after exercises remains to be elucidated. The occurrence of acute renal failure must be taken into consideration when the youngster, especially with renal hypouricemia, complains of severe loin pain and nausea after exercise such as a track race.

Acute Kidney Injury↗
PubMed1999

Increased plasma levels of mature form of adrenomedullin in patients with chronic renal failure.

BACKGROUND: Adrenomedullin (AM), a novel vasodilator peptide, is produced by C-terminal amidation reaction of AM-glycine. AM-glycine, an intermediate form of AM (iAM), is processed from pro AM. AM circulating in the human blood stream was found to consist of an amidated mature form (mAM) and iAM. Biological activity is exerted only by mAM. METHODS: To investigate the pathophysiological role of mAM in renal disease, we measured plasma concentrations of mAM as well as total AM (tAM), representing both mAM and iAM, in patients with various renal diseases. In addition, plasma ANP level was measured in all patients. RESULTS: The concentrations of plasma mAM in renal failure with dialysis (2.1 +/- 0.2 fmol/ml, mean +/- SEM) and without dialysis (1.2 +/- 0.2) were significantly (p < 0.05) higher than those in control group (0.5 +/- 0.1). However, the plasma ANP level was increased only in renal failure patients with dialysis. Plasma mAM levels were significantly correlated positively with serum creatinine levels and negatively with hematocrit. No significant difference was noted in the ratio of mAM/tAM between renal failure patients and healthy subjects. CONCLUSION: These results suggest that plasma mAM is increased in renal failure in relation to deterioration of renal function, while the amidation process of AM seems to be unaffected in patients with renal failure.

Adrenomedullin↗
PubMed1998

LolA-dependent release of a lipid-modified protein from the inner membrane of Escherichia coli requires nucleoside triphosphate.

The outer membrane-directed lipoproteins are released from the inner membrane of Escherichia coli as a complex with LolA, a periplasmic chaperone. The LolA-dependent release of lipoproteins is critical for lipoprotein sorting as it depends on the outer membrane-specific sorting signal. To clarify molecular events involved in the LolA-dependent lipoprotein release, we attempted to establish an in vitro assay system. The major outer membrane lipoprotein (Lpp) was found to lose its release competence soon after being processed to mature Lpp in the inner membrane and therefore could not be used as a substrate for an in vitro system. An Lpp derivative, L10P, was constructed and found to retain the release competence long after its maturation. L10P was synthesized and radiolabeled in spheroplasts in the absence of LolA; therefore, it remained anchored to the inner membrane of spheroplasts. Right-side out membrane vesicles containing L10P were then prepared and used to examine the release of L10P. In addition to LolA, L10P release absolutely required nucleoside triphosphate (NTP). A non-hydrolyzable NTP analogue strongly inhibited the NTP-dependent release. The outer membrane-specific sorting signal was essential for the in vitro release of L10P. Furthermore, L10P released in vitro was specifically incorporated into the outer membrane. These results indicate that the in vitro release of L10P represents an in vivo reaction and requires energy.

Amino Acid Sequence↗
PubMed1998

Genetic analyses of the in vivo function of LolA, a periplasmic chaperone involved in the outer membrane localization of Escherichia coli lipoproteins.

The major outer membrane lipoprotein (Lpp) of Escherichia coli is released from the cytoplasmic membrane into the periplasm as a complex with LolA, a periplasmic chaperone, prior to the localization in the outer membrane. To determine whether or not LolA is generally involved in the outer membrane localization of lipoproteins in vivo, the chromosomal lolA gene was manipulated so as to be controlled by the lac promoter-operator. Depletion of LolA caused a severe growth defect, and impaired the outer membrane localization of Lpp and Pal, another outer membrane lipoprotein. Although LolA depletion did not immediately arrest the growth of cells lacking Lpp, disruption of the chromosomal lolA gene was lethal to the lpp strain, indicating that LolA is generally required for the outer membrane localization of lipoproteins, and therefore essential irrespective of the presence or absence of Lpp.

Bacterial Proteins↗
PubMed1998

Obligatory roles of protein kinase C and nitric oxide in the regulation of cerebral vascular tone: an implication of a pathogenesis of vasospasm after subarachnoid haemorrhage.

We previously showed that a canine basilar artery manifested tonic and potent, protein kinase C (PKC)-dependent contractions when nitric oxide (NO) was inhibited. We also reported a linear correlation between chronological changes in the angiographic severity of vasospasm, enhanced PKC, and attenuated guanosine, 13',15'-cyclic monophosphate (cGMP) activity in a canine subarachnoid haemorrhage model. The activity of cGMP is an indicator of NO-function. Based on this evidence, we have hypothesized that PKC and NO regulate cerebral vascular tone. We particularly focused on the role of NO in a negative feedback mechanism on PKC activity in the maintenance of vascular tone. To further confirm our hypothesis, we investigated the effect of PKC down-regulation on the tonic vascular contraction induced by NO-inhibition. Canine basilar artery was used in the experiment. Significant down-regulation of PKC activity in vascular smooth muscle cells was obtained by incubation with 10(-5) mole/L of phorbol 12-myristate 13-acetate (PMA) for 24 hours. The tonic and potent contraction induced by NO-inhibition was completely suppressed in the PKC down-regulated artery, even though the artery manifested a significant contraction in high-K+ solutions. These results indicate an obligatory role of PKC activity in tonic contraction when NO is inhibited, and support our previous data. Nitric oxide induces vascular relaxation by inhibiting PKC activity. Subarachnoid haemorrhage impairs this inhibition, resulting in PKC-dependent vascular contraction, such as vasospasm.

Animals↗
PubMed1998

Neural activity of the subthalamic nucleus in Parkinson's disease patients.

The neural activity pattern of the subthalmic nucleus (STN) was investigated in five patients with Parkinson's disease who were scheduled for electrode implantation for chronic stimulation of the STN. The initial target was placed 8 mm or 10 mm lateral to the midline, 3 mm to 4 mm posterior to the midcommissural point, and 5 mm to 6 mm below the intercommissural (AC-PC) line. The STN was identified by semi-microelectrode recordings with a trajectory moving laterally in 2-mm steps. The amplitudes of multi-unit activities were relatively low at depths from 8 mm to 5 mm above and from 1 mm to 4 mm below the target, while those 4 mm to 0 mm above the target were significantly higher than at the other sites (ANOVA, Fisher's test, p < 0.05), with the highest amplitude at 2 mm above the target (91.0 +/- 23.3 mu v, n = 15). In the mediolateral direction, amplitudes were relatively higher in the lateral portion, and amplitudes at 14 mm lateral to the midline were significantly higher than at the other sites (ANOVA, Fisher's test, p < 0.05). The target for chronic electrical stimulation was determined to be at the midpoint of the hyperactive STN, i.e., 12 mm lateral to the midline in three patients and 13 mm lateral in two patients. Movement-related neural activity was observed at 5 sites, i.e., 3 sites responded to passive movement of the contralateral wrist and 2 sites to passive knee and/or ankle movement. In conclusion, our data show that the lateral part of the STN is hyperactive in PD, and recordings of neural activities contributed greatly to identifying the STN and determining the target for chronic stimulation within it.

Aged↗
PubMed1998

Plasma dehydroepiandrosterone sulfate in unipolar major depression. Short communication.

We investigated plasma dehydroepiandrosterone sulfate (DHEAS) and cortisol levels in 12 patients with unipolar depression and 11 matched normal controls. The depressed patients showed significantly higher values of plasma DHEAS and cortisol than the controls. After 4 weeks of treatment with antidepressants (mainly clomiplamine), the high plasma DHEAS levels recovered. This finding showed the possible relationship between plasma DHEAS levels and depression, as well as cortisol levels.

Adult↗
PubMed1998

Effect of dantrolene on K(+)- and caffeine-induced dopamine release in rat striatum assessed by in vivo microdialysis.

Recently, dantrolene has been reported to affect the central nervous system in addition to peripheral targets such as skeletal muscle. We examined effects of dantrolene on K(+)- and caffeine-induced dopamine release in rat striatum using in vivo microdialysis. Perfusion with KCl via the dialysis probe for 20 min induced immediate increase in DA release. Either chelation of extracellular calcium or addition of dantrolene for 120 min preceded reapplication of 100 mM KCl for 20 min. Calcium chelation attenuated the increase in DA release induced by KCl. Application of dantrolene enhanced the KCl-induced increase in DA release, but this effect disappeared at 100 microM. Caffeine caused a dose-dependent increase in dopamine release, independently of extracellular calcium. Treatment with 100 microM dantrolene for 120 min reduced the increase in DA release induced by caffeine. These findings that dantrolene modulates dopamine release in rat striatum indicate that conventionally administered dantrolene is likely to act on the central nervous system.

Animals↗
PubMed1998

Differential regulation by pregnenolone sulfate of intracellular Ca2+ increase by amino acids in primary cultured rat cortical neurons.

We investigated the effects of pregnenolone sulfate (PS) on the [Ca2+]i increase induced by gamma-aminobutyric acid (GABA) and N-methyl-D-aspartate (NMDA) using fluorescence imaging. PS inhibited the 50 microM GABA-induced increase in [Ca2+]i in a dose-dependent manner with an IC50 of 30 microM. The inhibitory effect of PS was apparent within 5 min and was in a non-competitive manner, suggesting that PS may act directly to the membrane level but indirectly to the GABA binding sites. Our previous study has already shown that the GABA-induced Ca2+ increase involves GABAA receptors and the similar pathway to a high K(+)-induced Ca2+ response (Takebayashi et al., 1996). Because 50 microM of PS could not inhibit a 25 mM K(+)-induced Ca2+ increase, it seems likely that the site of the inhibitory action of PS on the GABA-induced Ca2+ increase may be independent of the pathway of the high K(+)-induced Ca2+ response, but rather at GABAA receptor complex. In contrast, PS potentiated the 50 microM NMDA-induced increase in [Ca2+]i in a dose-dependent manner. The magnitude of the NMDA response was approximately doubled in the presence of 100 microM of PS. However, PS did not affect the acetylcholine(Ach)-induced increase in [Ca2+]i. Furthermore, corticosterone had little effect on the GABA- and NMDA-induced Ca2+ increases, indicating that the alteration of the Ca2+ response is specific for PS. In conclusion, it is suggested that PS modulates differentially [Ca2+]i increase induced by GABA and NMDA.

Acetylcholine↗
PubMed1998

Simvastatin suppresses glomerular cell proliferation and macrophage infiltration in rats with mesangial proliferative nephritis.

Inhibition of 3-hydro-3-methylglutaryl coenzyme A reductase inhibits the production of mevalonate and has been shown to suppress proliferation in many cell types. Therefore, 3-hydro-3-methylglutaryl coenzyme A reductase inhibitors may have a beneficial effect in glomerular disease, because glomerular cell proliferation is a central feature in the active glomerular injury. This study examines the effect of simvastatin on glomerular pathology in a rat mesangial proliferative glomerulonephritis (GN) induced by anti-thymocyte antibody (anti-Thy 1.1 GN). There was no difference in the degree of the antibody and complement-mediated initial injuries between simvastatin-treated and control GN rats. The most pronounced feature of simvastatin-treated GN was the suppression of the early glomerular cell proliferation. The proliferative activity was maximal at day 4 after disease induction (26.5+/-7.0 of proliferating cell nuclear antigen-positive cells/glomerulus); however, approximately 70% of proliferation was suppressed by simvastatin treatment. At day 4 after disease induction, simvastatin administration also decreased alpha-smooth muscle actin expression in the glomerulus, which is a marker for mesangial cell activation. Inhibition of monocyte/macrophage recruitment into glomeruli by simvastatin was also a prominent feature. There was a 30% decrease in the number of glomerular ED-1+ cells by simvastatin treatment at day 2 after disease induction. Furthermore, simvastatin remarkably suppressed subsequent mesangial matrix expansion and type IV collagen accumulation in glomeruli. We also found that the platelet-derived growth factor expression was reduced in simvastatin-treated nephritic rats, which might simply reflect the reduction in mesangial cell proliferation and mesangial cellularity. There was no significant difference in plasma cholesterol or triglyceride levels between simvastatin- and vehicle-treated nephritic rats at day 2 and day 4, which corresponded to the times when simvastatin treatment resulted in a reduction in mesangial cell proliferation. In conclusion, this is the first report to find that mesangial cell proliferation and matrix expansion have been blocked by simvastatin in vivo. The protective effect of simvastatin in the matrix expansion in anti-Thy1.1 GN was partly by inhibition of mesangial cell proliferation and monocyte/ macrophage recruitment into glomeruli, which were independent of a change in circulating lipids.

Actins↗
PubMed1998

An isolated case of nephronophthisis: medullary cystic disease without typical onset.

A 16-year-old girl with renal failure was transferred to our hospital for an extensive renal examination. Computerized tomography and ultrasonography showed multiple small cysts throughout the medulla of both kidneys. Histological findings revealed tubular atrophy and dilatation and marked periglomerular fibrosis, all of which were compatible with nephronophthisis. Her development and growth were normal. A prior urinalysis, as well as her symptoms and family history were not helpful for making a diagnosis. As early diagnosis of nephronophthisis is difficult in some cases, more detailed screening is needed for children and adolescents.

Adolescent↗