The Keio Journal of Medicine
Online ISSN : 1880-1293
Print ISSN : 0022-9717
ISSN-L : 0022-9717
Volume 47, Issue 3
Displaying 1-9 of 9 articles from this issue
  • Andrew Y. Finlay
    1998 Volume 47 Issue 3 Pages 131-134
    Published: 1998
    Released on J-STAGE: March 27, 2009
    JOURNAL FREE ACCESS
    Skin diseases cause considerable discomfort, but usually do not affect patients' lifespan. However the effects of skin disease on patients' lives can be profound, as all aspects of life can be interfered with. Methods to measure these effects on life quality are needed for clinical, research, audit and political reasons. General health questionnaires such as the Sickness Impact Profile or the Short Form 36 can be used to compare the impact of skin disease to the impact of diseases of other systems. Disease specific questionnaires such as the Psoriasis Disability Index, dermatology specific measures such as the Dermatology Life Quality Index (DLQI), and utility measures can all be used in derma-tology and have their different specific indications. The use of the DLQI has quantified the major impact that inflammatory skin disease has on patients and has been used to demonstrate the improve-ment resulting from systemic therapy and from inpatient management. A version for use in children has also been described. The information gained from this work can be used to demonstrate the importance of adequately managing skin disease in the community and can help to guide resource allocation.
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  • Michael J. Droller, Elizabeth Kavaler, Jaime Landman, Brian C. S. Liu
    1998 Volume 47 Issue 3 Pages 135-141
    Published: 1998
    Released on J-STAGE: March 27, 2009
    JOURNAL FREE ACCESS
    Voided urine from patients with bladder cancer and from control patients with either hematuria or with no urologic conditions were examined for telomerase activity in order to explore the possibility that this activity could be used as a marker for the detection of bladder cancer. This assay was found to have an overall sensitivity in detecting bladder cancer of 85% (88/104) with 79% (23/29) grade 1 tumors, 84% (32/38) grade 2 tumors, 87.5% (28/32) grade 3 tumors, and 100% (5/5) carcinoma in situ testing positive. This compared favorably with urinary cytology which had an overall sensitivity of 51% and sensitivities of 13%, 44%, 82%, and 100% for grades 1, 2, 3 tumors and carcinoma in situ, respectively. The specificity of telomerase in patients with benign causes of hematuria was 66%, and in normal volunteers without urologic conditions, it was 100%. Assessment of nuclear matrix protein suggested comparable sensitivity and specificity. Evaluation of bladder tumor antigen showed less sensitivity for low-grade disease and less specificity, as it was influenced by inflammation and instrumentation. Telomerase thus seems to be a means whereby low-grade tumors may be detected in examination of voided urine and may offer an advantage in monitoring for recurrent disease.
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  • William I. Rosenblum
    1998 Volume 47 Issue 3 Pages 142-149
    Published: 1998
    Released on J-STAGE: March 27, 2009
    JOURNAL FREE ACCESS
    Evidence from investigations of brain microcirculation (pial arterioles) reveals at least 3 different endothelium (EC) dependent mechanisms for dilation. Only one of the three can be triggered by acetylcholine (ACh) and in this vascular bed it is only this path that is dependent upon endothelial nitric oxide synthase (NOS) which produces nitric oxide (NO) from arginine. In this vascular bed the ACh sensitive path cannot be triggered by bradykinin (BK). This state of affairs appears to differ from that found in other beds or in endothelium cultured from conductance vessels. In the cerebral micro-circulation there is considerable pharmacological evidence that the endothelium derived relaxing factor (EDRF) for ACh is not NO itself but may contain NO. In many experimental vascular settings the release of the NOS dependent EDRF is shear dependent. In the cerebral microcirculation there are several studies suggesting, in vivo, that this is correct. Among these are the following: (1) vessels narrow when shear is reduced after carotid ligation, and remain so along with unresponsiveness to ACh for at least ten minutes following resumption of flow. This may be important in developing stroke. The collapse is not passive due to low pressure. We know this because the narrowed vessels with their low intraluminal shear and pressure are still capable of large dilation by the NO donor, sodium nitroprus-side; (2) the antiplatelet effects of EC which are mediated, in part, by the EDRF for ACh are enhanced for 10 to 20 minutes following the transient increase and return of shear within these vessels. If the reverse is also true, reductions of shear may have important harmful proaggregant effects on platelets (and leukocytes) in the microvascular bed of developing infarcts. However most of the cited work depends upon pharmacological inhibitors of NOS to “prove” that NOS and an EDRF/NO are involved. In the last three years evidence in cats and rats shows that many of the NOS inhibitors also block K channels in cerebrovascular smooth muscle and that arginine, the “antidote” to the NOS inhibitors keeps the channels open. This latter work must force a reexamination of the conclusions reached in many studies.
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  • Tadako Nakatsuji
    1998 Volume 47 Issue 3 Pages 150-156
    Published: 1998
    Released on J-STAGE: March 27, 2009
    JOURNAL FREE ACCESS
    One LEW/Sea (Lewis) strain rat, Rat P-1, had a homozygous defect of the serine protei-nase inhibitor 2 (Spi-2) gene coding for serpin contrapsin. A sibling, Rat P-2, and a rat of the same strain, Rat P-3, had a heterozygous Spi-2 gene defect. The homozygous Spi-2 gene defect of Rat P-1 was diagnosed by the polymerase chain reaction (PCR). The presence of an α1-proteinase inhibitor (PI) gene was confirmed by PCR in all 3 rats. Rat P-1 and the sibling Rat P-2 were sacrificed at 7 days of age because of the severe weakness of Rat P-1, although Rat P-2 appeared healthy. Rat P-3 was sacrificed at 40 days of age because of the severe weakness. Rat P-1's hepatocytes with the homozygous Spi-2 gene defect showed massive accumulation of polymerized α1-antitrypsin (AT) in the rough endoplasmic reticulum (RER). Large, defined accumulations of al-AT were not found in the hetero-zygous rats with the Spi-2 gene defects. Nephrogenesis was retarded in all 3 rats, especially in Rat P-1. Extramedullary hematopoiesis was absent in the liver of Rat P-1 and suppressed in the spleen of Rat P-3, where activated α1-AT synthesis was found. Atelectasis mixed with hyperinfated lung regions and thymic apoptosis were observed in the 2 weak rats. As Spi-2 gene defect had some similar clinical points to platelet-derived growth factor (PDGF) deficiency, it was suggested that increased vaso-constrictor peptide hormones competed with PDGF for binding to the PDGF-receptors.
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  • Jun Iwamoto, Tsuyoshi Takeda, Toshiro Otani, Yutaka Yabe
    1998 Volume 47 Issue 3 Pages 157-161
    Published: 1998
    Released on J-STAGE: March 27, 2009
    JOURNAL FREE ACCESS
    The effect of increased physical activity on bone mineral density (BMD) of the lumbar vertebrae was examined in postmenopausal osteoporotic women. Thirty-five postmenopausal women, aged 53-77 years, whose BMD in the lumbar vertebrae (L2-L4) measured by dual energy x-ray absorptiometry (Norland XR-26) was below (>30%) the young adult mean, were divided into two groups: a control group of 20 women and an exercise group of 15 women. The physical exercise con-sisted of daily outdoor walking and gymnastic training performed for 12 months. During the study period, all subjects were treated with calcium lactate, 2.0g, and 1 α-hydroxyvitamin D3, 1μg, daily. Initial L2-L4 BMD was 0.611±0.045 (mean±SEM) g/cm2 in the control group and 0.606±0.066g/cm2 in the exercise group (NS). In the control group, the BMD changes were -0.54±0.58% (mean±SEM) at 6 months and +1.00±1.29% at 12 months, compared to the baseline (P=0.3424, by one-way ANOVA). In the exercise group, however, the changes were +1.78±0.90% and +4.48±0.93%, respectively (P=0.0305, by two-way ANOVA). These data suggest that increased physical activity consisting of daily outdoor walking and gymnastic training can be useful in increasing lumbar BMD in postmenopausal osteoporotic women on calcium and vitamin D3 supplementation.
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  • Jun Iwamoto, Tsuyoshi Takeda, Shoichi Ichimura
    1998 Volume 47 Issue 3 Pages 162-167
    Published: 1998
    Released on J-STAGE: March 27, 2009
    JOURNAL FREE ACCESS
    The effects of moderate intensity exercise of different duration on the cancellous and corti-cal bone mass of the tibia were investigated in mature ovariectomized rats by bone histomorphometry. A total of twenty 23-week-old female Wistar rats were used in this study. Ovariectomy (OV) was per-formed on 15 animals, and they were divided into three groups of five animals each: an OV group, an OV + exercise for 30min a day (EX30) group and an OV + EX60 group. The other 5 animals served as a sham-operated (SH) control group. The exercise consisted of treadmill running at 16 m/min and was performed 5 days a week for 12 weeks after the operation. After 12 weeks of exercise, bone histo-morphometry was used to evaluate the cancellous bone (secondary spongiosa) of the proximal tibia and the cortical bone of the tibial shaft. The OV group showed a significant decrease in cancellous bone volume, with increased resorption and formation, compared to the SH group (P<0.01). Although the OV + EX30 group showed a significant increase in cancellous bone volume, with decreased resorption and increased osteoblastic activity, compared to the OV group (P<0.05), can-cellous bone volume in the OV + EX30 group remained significantly lower than that in the SH group (P<0.05). There was not a significant difference in cortical bone area between the OV group and the SH group, whereas the OV + EX30 group showed a significant increase in cortical bone area, with decreased resorption on the endosteal surface, compared to the OV group (P<0.05). There were no significant differences in cancellous bone volume or cortical bone area between the OV group and the OV + EX60 group. The data suggest that moderate intensity exercise of appropriate duration may attenuate ovariectomy-induced cancellous bone loss and increase cortical bone mass in mature ovari-ectomized rats.
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  • Yoshiaki Itoh, Takahiro Amano, Takahiro Sasaki, Atsushi Kubo, Jun Hash ...
    1998 Volume 47 Issue 3 Pages 168-173
    Published: 1998
    Released on J-STAGE: March 27, 2009
    JOURNAL FREE ACCESS
    SPECT (single photon emission computed tomography) using iomazenil (IMZ) as a ligand for benzodiazepine receptors has recently been developed. Feasibility of the technique for detecting neuronal damage in the cerebral cortex was evaluated in 17 patients with cerebral infarction, specifi-cally, patients with internal carotid artery (ICA) thrombosis (n=6), middle cerebral artery (MCA) thrombosis (n=5) and embolism (n=6). IMZ SPECT was performed 5 to 17 days after stroke. Fol-lowing the injection of 123I-IMZ 167 or 222 MBq intravenously, images were obtained at 15 minutes (early image) and 180 minutes (late image). In 11 cases, 99mTc-HM-PAO (hexamethyl-propylamine oxime) SPECT was also performed to measure cerebral blood flow (CBF). MRI was performed in all cases to elucidate areas of infarct. Early images from IMZ SPECT correlated well with those from HM-PAO, suggesting that early scans using IMZ SPECT reflect mainly CBF. In late images from IMZ SPECT, observed lesions were consistent with infarcted areas on MRI in most cases. However, in 3 cases of ICA thrombosis, 1 case of MCA thrombosis and 1 case of embolism, late IMZ SPECT imaging showed that the affected area was wider than apparent infarcts on MRI, indicating that the cerebral cortex, which was intact on MRI, was also involved. In these patients, clinical signs of cortical involvement were observed as well. These results suggest that moderately reduced CBF may affect cortical neurons without inducing apparent infarct, and such damage can be detected with IMZ SPECT.
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  • Leonard Hayflick
    1998 Volume 47 Issue 3 Pages 174-182
    Published: 1998
    Released on J-STAGE: March 27, 2009
    JOURNAL FREE ACCESS
    During the first half of this century it was believed that because cultured normal cells were immortal, aging must be caused by extracellular events. Thirty-five years ago we overthrough this dogma when we discovered that normal cells do have a limited capacity to divide and that aging occurs intracellularly. We also observed that only cancer cells are immortal. Normal cells are mortal because telomeres shorten at each division. Immortal cancer cells express the enzyme telomerase that prevents shortening. Recently, it was discovered that the telomerase gene when inserted into normal cells immortalizes them. There appears to be a relationship between these findings and aging, longevity determination and cancer. After performing the miracles that take us from conception to birth, and then to sexual maturation and adulthood, natural selection was unable to favor the development of a more elementary mechanism that would simply maintain those earlier miracles forever. This failure is called aging. Because few feral animals age, evolution could not have favored animals exhibiting age changes. Natural selection favors animals that are most likely to become reproductively successful by developing greater survival skills and reserve capacity in vital systems to better survive predation, dis-ease, accidents and environmental extremes. Natural selection diminishes after sexual maturation because the species will not benefit from members favored for greater development of physiological reserve. A species betters its chances of survival by investing its resources and energy in increasing opportunities for reproductive success rather than on post-reproductive longevity. The level of phy-siological reserve remaining after reproductive maturity determines potential longevity and evolves incidental to the selection process that acts on earlier developmental events. Physiological reserve does not renew at the same rate that it incurs losses because molecular disorder increases. These age changes increase vulnerability to predation, accidents or disease.
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  • 1998 Volume 47 Issue 3 Pages 204
    Published: 1998
    Released on J-STAGE: March 27, 2009
    JOURNAL FREE ACCESS
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