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Background Kidney transplantation is performed as a useful treatment to improve the quality of life (QOL) of patients with end-stage renal failure; however, the correlation between mood status and QOL among recipients post-kidney transplantation have yet to be clarified. Methods Sixty-eight post-kidney transplantation patients who visited our institution between March and December 2016 were enrolled in this study. The QOL of the participants as measured by the Short Form-36 Health Survey Version 2 (SF-36v2) questionnaire was compared to results gathered from hemodialysis patients in a previous study. To identify the factors associated with QOL, a multiple regression analysis was performed, including some physical, mental, and socioeconomic characteristics as well as the Profile of Mood States as independent variables. Results The QOL of the transplantation group was significantly higher for all 8 subscales of SF-36v2 compared to the hemodialysis group. Among the factors, greater age and higher Confusion levels were related to lower physical QOL. In addition, higher Vigor and lower Fatigue levels were related to higher mental QOL, while the condition of having an occupation was related to higher role/social QOL. Conclusion The QOL of recipients after kidney transplantation was better than that of hemodialysis patients. It is important to pay attention to mood status, especially confusion and fatigue, in order to maintain and improve the QOL of the recipient after kidney transplantation. Kidney transplantation can be a beneficial treatment not only physically but also psychologically and socially.

大腸癌では,血行性・リンパ行性の膣壁転移は極めてまれであり,これまでに詳細な報告例は,本邦ではわずか5例しかない.今回,我々は,膣壁転移を伴ったS状結腸癌の1切除例を経験した.症例は74歳,女性.不正性器出血を主訴に当院産婦人科を受診した.内診にて膣壁に2cm大の腫瘍が認められ,生検にて腺癌と診断された.大腸内視鏡にてS状結腸に1/2周性の2型進行癌が認められた.手術時,腹水や腹膜播種は認められなかった.S状結腸癌は漿膜面へは露出しておらず,膣とは接していなかった.S状結腸切除術の後,経膣的膣壁腫瘍切除術が施行された.S状結腸癌は径28mm,中分化腺癌,sslylvln(-)と診断された.膣壁腫瘍は径23mmで,S状結腸癌と極めて類似した癌病巣が平滑筋層と横紋筋層の間にまで浸潤していた.病理組織学的所見の詳細な検討より,膣壁腫瘍はS状結腸癌からの脈管性転移と診断された.

Summary Objectives: To improve insight into age and gender related distributions of serum lipids and their correlation with body mass index (BMI). Methods: Serum lipids embracing atherogenic index (AI) and BMI were analyzed from the results obtained in 19,823 men and 14,788 women undergoing a health examination between 1986 and 1996. Results: The changes in total cholesterol (TC), triglyceride (TG), AI and BMI differed regarding gender. Although high-density lipoprotein-cholesterol (HDL-C) showed a flat pattern for all ages in both genders, its level in women was higher than in men. The ratio of the number in the unsuitable range to those in the suitable range increased with age as to TC in both sexes, then more than half of the population have an unsuitable level in the sixth decade. As for the correlation between serum lipids and BMI: TC, TG and AI correlated positively, but HDL-C correlated negatively. There were significant gaps between both age and gender. Conclusions: We suggest that the normal range of values of serum lipids needs to be revised according to gender and age to evaluate the risk status for a cardio-cerebrovascular disease more precisely in the field of preventive medicine. Simpler guidelines are preferable in specialized care as well as in general practice, particularly since computer technology is not yet universally adapted. In the near future, when computed information technology will be as common as the electricity and the telephone are current on the whole earth, all guidelines will have to be computed on the spot and personally.

The pathogenesis of pericyte loss, an initial deficit in the early stage of diabetic retinopathy, remains unclear. Polyol pathway hyperactivity has been implicated in the pathogenesis of diabetic retinopathy, and recent studies have suggested that apoptosis may be involved in pericyte loss. The present study was conducted to investigate whether high glucose induces apoptosis in cultured bovine retinal pericytes. The effect of an aldose reductase inhibitor, SNK-860, was also examined. After a 5 day incubation with various concentrations of glucose (5.5–40 m M ) in the presence or absence of SNK-860, the cell viability and the percentages of dead cells were measured, and staining with the TUNEL method and Hoechst 33342, and DNA electrophoresis were performed. High glucose reduced the viability and increased the percentages of dead cells. TUNEL-positive cells were observed in pericytes under high glucose, but not in those under 5.5 m M glucose. In the staining of nuclei with Hoechst 33342, the percentage of apoptotic cells in total cells counted under high glucose was higher than that under 5.5 m M glucose. DNA electrophoresis of pericytes cultured with high glucose demonstrated a ‘ladder pattern’. Hyperosmolarity also induced apoptosis in pericytes, but less than that by high glucose. SNK-860 inhibited the glucose-induced apoptosis in pericytes. These observations suggest that the pericyte loss in diabetic retinopathy involves an apoptotic process, and that the polyol pathway hyperactivity plays an important role in inducing apoptosis in pericytes by high glucose.

Aims/hypothesis. Although increased polyol pathway activity has been implicated in the pathogenesis of diabetic microangiopathy, the relation with diabetic macroangiopathy remains unclear. Galactose feeding is known to stimulate the polyol pathway and to develop abnormalites similar to those in diabetic microangiopathy. Our study was conducted to investigate whether an activation of polyol pathway by long-term treatment with galactose produced morphological changes in coronary arteries of dogs and the effect of an aldose reductase inhibitor, epalrestat, was also studied. Methods. Dogs received either normal chow or chow containing 30 % galactose with or without epalrestat given orally (20 or 50 mg◊ kg ‐1 ). After 44 months, morphometric analyses of coronary arteries were carried out and the galactitol contents in aortas were measured. Results. The ratio of areas of the intimal layer to those of the medial layer, an indicator of intimal thickening, was statistically significantly increased in galactosefed dogs compared with control dogs. Galactose-fed dogs had a remarkable accumulation of galactitol in their aortas. These morphological and biochemical deficits were reduced by treatment with epalrestat. Conclusion/interpretation. This report morphologically shows diabetes-like macrovascular abnormalities in galactosaemic animals, suggesting that polyol pathway hyperactivity is closely related to the development of diabetic macroangiopathy, which could be prevented by aldose reductase inhibition. [Diabetologia (1999) 42: 1404‐1409]

To examine the role of platelet-derived growth factor (PDGF) and the polyol pathway in the growth activity of smooth muscle cells (SMCs), [(3)H]-thymidine incorporation, [(125)I]-PDGF-BB binding and expression of PDGF-beta receptor protein were measured in rat aortic SMCs cultured with 5.5 or 20 mM glucose with or without anti-PDGF antibody or an aldose reductase inhibitor, epalrestat. SMCs cultured with 20 mM glucose demonstrated an accelerated thymidine incorporation compared with SMCs cultured with 5.5 mM glucose, which was prevented by anti-PDGF antibody. This acceleration of growth activity by 20 mM glucose was accompanied by an increase in PDGF-BB binding, which was due to the increased number of PDGF-beta receptors and the overexpression of PDGF-beta receptor protein. Epalrestat prevented all these abnormalities. These observations suggest that polyol pathway hyperactivity plays an important role in the proliferation of SMCs which may be mediated through the accelerated expression of PDGF-beta receptor protein.

Pour examiner les caracteristiques physiopathologiques du diabete noninsulinodependant, on a examine le metabolisme de l'alanine dans des hepatocytes isoles de gros rats Wistar-Kyoto (WKY) mâles (genetiquement obeses et hyperglycemiques) et de rats maigres de meme portee. On a aussi examine les effets du glucagon et des biguanides, metformine et buformine, sur le metabolisme de l'alanine, en mesurant la capture de l'alanine et la synthese lipidique liee a l'alanine. A 5 et 12 semaines, les gros rats WKY ont eu de plus fortes concentrations de lipides et d'insuline plasmatique que les rats maigres. A 12 semaines, la capture d'alanine dans les hepatocytes a augmente chez les gros rats uniquement, tout comme la synthese lipidique liee a l'alanine, a 5 et 12 semaines. Le glucagon a augmente la capture d'alanine, mais n'a pas eu d'effet sur la synthese lipidique liee a l'alanine et ce, chez les deux groupes de rats. De faibles concentrations (0,1 mM) de biguanides ont diminue la synthese lipidique liee a l'alanine, sans inhiber la capture d'alanine, chez les gros rats uniquement. Ces observations suggerent que la synthese lipidique liee a l'alanine dans les hepatocytes des rats obeses WKY augmente avant l'apparition du diabete, ce qui pourrait faire partie de l'evolution de ce dernier, et que l'une des actions pharmacodynamiques des biguanides se manifeste par une inhibition de l'augmentation de la synthese lipidique.

SUMMARYInvasive pneumococcal disease (IPD) is of concern in Japan, where the heptavalent pneumococcal conjugate vaccine (PCV7) is unavailable. We determined serotypes, genotypes indicating β-lactam resistance, and antibiotic susceptibilities of 496 isolates from normally sterile sites in patients (193 children, 303 adults) from 186 institutions between August 2006 and July 2007. Disease presentations included sepsis (46·2%), pneumonia (31·5%), and meningitis (17·5%). Mortality was 1·4% in children and 22·1% in adults, many of whom had underlying diseases. In children, serotype 6B (22·5%) was followed by 19F (14·1%), and 14 (13·1%); potential coverages of PCV7 and PCV13 were 75·4% and 93·7%, respectively. In adults, serotype 12F (14·3%) was followed by 3 (11·3%), and 6B (10·3%); 23-valent polysaccharide vaccine (PPV23) coverage was 85·4%. Most serotype 12F strains were gPISP, withpbp2bgene alteration; carbapenem had an excellent MIC90.PCV7 is recommended for children and PPV23 for adults to increase prevention against IPD.

The metabolic effects of a biguanide, metformin, on glycemic control and eating behavior were investigated in 16 type 2 diabetic subjects with mental retardation who were habitual overeaters and had difficulty in controlling their appetites. The subjects (n = 16) received metformin (750 mg/day) for 6 months and body weight, body mass index (BMI) were measured monthly. They had repetitive metabolic and hormonal studies. Their eating behavior was analyzed by questionnaires given by their guardians before and after treatment. Metformin treatment significantly reduced their body weights (p < 0.01), body mass index (BMI) (p < 0.01), the levels of HbA1c (p < 0.001), fasting blood glucose (FBG) (p < 0.05), serum insulin (p < 0.05), C-peptide (p < 0.01), triglyceride (p < 0.01), and total cholesterol (p < 0.05). Insulin resistance index (FBG (mg/dl) x serum insulin levels ( micro U/ml) x 1/405) was significantly reduced after 1-month treatment. The serum leptin levels were significantly decreased after 4 month's treatment and thereafter (p < 0.05). Analysis of the questionnaires before and after treatment showed that the daily intake of regular and additional foods significantly decreased after treatment (p < 0.01 and p < 0.001, respectively) with improvements of eating behavior. We conclude that metformin may have beneficial effects not only to control glycemia but also to correct eating behavior in obese type 2 diabetic patients with the difficulty in controlling their appetites. The improvement was related to the reduction of insulin resistance and serum leptin levels.

Involvement of the lingual muscle is considered one of the exclusion criteria of facioscapulohumeral muscular dystrophy (FSHD). In a series of 151 Japanese patients with 4q35-FSHD, seven patients (4.6%) had tongue atrophy with abnormal MRI findings and typical myogenic patterns of electromyography. All seven patients belong to a group of early-onset FSHD with large gene deletions on chromosome 4q35. Our result suggests that the patients with 4q35-FSHD could have myopathic tongue atrophy.

OBJECTIVE: To clarify the role of the polyol pathway in the intracellular formation of advanced glycation end products in human tissues, we examined the effects of epalrestat, an aldose reductase inhibitor, on the level of Nepsilon-(carboxymethyl)lysine (CML) along with 3-deoxyglucosone (3-DG) and triosephosphates in erythrocytes from diabetic patients. Plasma thiobarbituric acid-reactive substances (TBARS) were also determined as indicators of oxidative stress. RESEARCH DESIGN AND METHODS: Blood samples were collected from 12 nondiabetic volunteers, 38 untreated type 2 diabetic patients, and 16 type 2 diabetic patients who had been treated with 150 mg epalrestat/day. Blood samples were also collected from 14 of the untreated type 2 diabetic patients before and after the administration of epalrestat for 2 months. The amount of erythrocyte CML was determined by a competitive enzyme-linked immunosorbent assay, and 3-DG was measured by high-performance liquid chromatography RESULTS: In diabetic patients not treated with epalrestat, the erythrocyte CML level was significantly elevated above levels seen in nondiabetic individuals (49.9 +/- 5.0 vs. 31.0 +/- 5.2 U/g protein, P < 0.05) and was significantly lower in patients receiving epalrestat (33.1 +/- 3.8 U/g protein, P < 0.05). Similar results were observed with 3-DG. The treatment of patients with epalrestat for 2 months significantly lowered the level of erythrocyte CML (46.2 +/- 5.6 at baseline vs. 34.4 +/- 5.0 U/g protein, P < 0.01) along with erythrocyte 3-DG (P < 0.05), triosephosphates (P < 0.05), fructose (P < 0.05), sorbitol (P < 0.05), and plasma TBARS (P < 0.05) without changes in plasma glucose and HbA(1c) levels. A positive correlation was evident between the erythrocyte CML and sorbitol (r = 0.49, P < 0.01) or fructose (r = 0.40, P < 0.05) levels in diabetic patients. CONCLUSIONS: The results indicate that epalrestat administration lowers CML and associated variables and that polyol metabolites are correlated with CML in the erythrocytes of diabetic patients. The observed results suggest that aldose reductase activity may play a substantial role in the intracellular formation of CML in the mediation of reactive intermediate metabolites and oxidative stress.

We report the case of a patient whose periods of periodic catatonia were abolished by thyroid hormone and reserpine. A ratio of fractions in the urinary 17-ketosteroids was a good indicator for the treatments.

We investigated the mechanisms of the effects of the biguanides metformin and buformin on hepatic gluconeogenesis in hepatocytes isolated from normal rats. Both 10 nM glucagon and 50 microM dibutyryl cAMP increased [3H]alanine uptake in isolated hepatocytes of normal rats by about 150% and 55%, respectively, compared with the effect of 5 mM alanine alone. Metformin (3 mM) reduced glucagon-stimulated [3H]alanine uptake to the level seen with alanine alone; buformin (3 mM) inhibited glucagon-stimulated [3H]alanine uptake by about 69%. The effects of biguanides on dibutyryl cAMP-stimulated [3H]alanine uptake were similar, but of smaller magnitude compared with those observed in the presence of glucagon. Ouabain (3 mM) had a stronger inhibitory effect on [3H]alanine uptake than the biguanides. However, 3 mM tolbutamide failed to suppress [3H]alanine uptake in the presence or absence of glucagon or dibutyryl cAMP. Our results suggest that the inhibition of alanine uptake, related to a reduction in the Na+/L-alanine transport system, is a possible mechanism of biguanide-related inhibition of hepatic gluconeogenesis.

The effect of buformin, a biguanide, on gluconeogenesis from 10 mM alanine in the presence of 143 nM glucagon were studied using isolated rat liver perfusions. In addition, to investigate possible mechanisms of biguanide action, alanine utilization in isolated rat liver perfusion and [3H]alanine uptake in isolated hepatocytes were observed. Buformin (1.85 mM) strongly inhibited gluconeogenesis from alanine in the presence of glucagon in both normal and streptozocin-induced diabetic rat livers. This inhibition was followed by a decrease in alanine utilization. Both of these inhibitory effects of buformin were dose-dependent. [3H]Alanine uptake was significantly inhibited by buformin. The effect of this agent was similar to but weaker than that of ouabain. However, tolbutamide failed to reduce either alanine utilization or [3H]alanine uptake, although this drug significantly inhibited gluconeogenesis from alanine. These data suggest that biguanides may reduce hepatic alanine utilization via the inhibition of Na+/L-alanine transport activity as one possible mechanism, resulting the inhibition of gluconeogenesis from alanine in the presence of glucagon.

Thirteen consecutive Japanese patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) were studied by MRI, evoked potentials, and EEG. We found 3 of these patients exhibited symptoms of CNS disorders. Of these 3, 2 with abnormal MRI and visual evoked potentials, and one with abnormal brainstem auditory evoked potentials were detected. Another case without clinical CNS signs showed abnormal EEG findings. The subclinical CNS abnormalities found in the Japanese patients were considered to be less frequent than in cases from Western countries reported previously.

An autopsy case of human T lymphotropic virus I-associated myelopathy (HAM) of a duration of 28 years in a 61-year-old man with serological confirmation of HTLV-I infection was reported. The spinal cord was grossly atrophic. There was severe symmetrical degeneration of the lateral funiculi, particularly of the bilateral pyramidal tracts, involving all levels of the spinal cord, but anterior horn cells were relatively well preserved. In the most severely damaged middle and lower thoracic segments, the white matter degeneration also involved the anterior funiculi. In the degenerated white matter, both the myelin and axons were equally lost and had been replaced by glial scars. Marked adventitial fibrosis was commonly seen in small parenchymal vessels in both the white and gray matter. Although there was no evidence of inflammation in the spinal cord, mild lymphocytic infiltration was occasionally observed in the subarachnoid and perivascular spaces in the brain stem, cerebellum and cerebrum. This case was considered as a burnt-out case of HAM.

Tanaka and Fillmore treated the swelling of a gel as a process where a crosslinked polymer network having been initially under uniform stress is expanded by osmotic pressure, sucking up the surrounding fluid medium. We point out that their physical reasoning is unnatural and leads to an unacceptable conclusion; we propose a more sound approach to the same problem. Our treatment assumes that the gel network is extended not by the osmotic pressure of the gel, but rather by the swelling pressure which is generated by the excess fluid penetrating in against the real nature of a polymer network that tends to shrink. The diffusion equation of the fluid, hence, plays a dominant role and gives the distribution of fluid concentration in contrast to Tanaka-Fillmore's scheme. The expression for the distribution of local strain in a spherical gel is deduced from the relation of mechanical balance between two forces, the one is due to the elasticity of the network and the other due to the gradient in the chemical potential of the fluid. The results obtained have forms analytically similar to Tanaka-Fillmore's, but are differ in the physical meanings.

The swelling process of sodium acrylate gel is experimentally investigated. It is found that sodium acrylate gels weakly crosslinked with N,N′-methylene-bis-acrylamide may undergo volume phase transition and that different kinds of mechanical instabilities occur in sequence at the transition. Peculiar wrinkle patterns appear on the free surface of an unstable gel and are changed in geometry as swelling proceeds. Cellular patterns seen at various instances in the late period of swelling are ascertained to be geometrically similar to each other and different only in size. The radii of spherical acrylate gels allowed to swell in water are measured as functions of time. The results are discussed and compared with the kinetic theories of swelling. As a result, these theories are proved to be unsatisfactory to fully describe the experimental facts.

High density lipoprotein (HDL) and low density lipoprotein (LdL) cholesterol levels were measured in fasting blood samples from 950 healthy subjects and 188 aged patients by a new simple method. The HDL-cholesterol levels and HDL/LDL-cholesterol ratios are significantly higher in females than in males. In the healthy subjects, there are slight decreases in the levels of HDL-cholesterol and HDL/LDL-cholesterol ratio with aging in both sexes. The patients with myocardial infarction had significantly lower HDL-cholesterol levels and HDL/LDL-cholesterol ratios as compared to those of the group without infarction. On the contrary, no differences in total lipoprotein cholesterol levels were observed in the patients with cerebral infarction. The results, obtained in respect of electrocardiographic findings after the isoproterenol stress test, suggest that the HDL-cholesterol levels and HDL/LDL-cholesterol ratios may be related not only to the established myocardial infarction, but also to the presence of coronary atherosclerosis and stenosis.