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The aim of this study was to clarify the factors influencing the dietary behavior of patients with diabetic nephropathy. One hundred twenty-two patients with type 2 diabetes were recruited from the outpatients of Okayama University Hospital in Okayama, Japan. We performed a cross-sectional study using a questionnaire including 206 items among 18 categories as follows:background factors, coping behavior (coping scale), degree of uncertainty in illness (uncertainty scale), and dietary behavior. The data were analyzed by correlation analysis, t-test, one-way analysis of variance, Pearson correlation analysis, and multiple regression analysis. We found that those patients with microalbuminuria alone tended to recognize more mild about their kidney status than those with macroalbuminuria and chronic renal failure. We also found that common factors influencing the dietary behavior of diabetic patients with and without nephropathy are as follows:1. coping with the problem (beta0.342, p0.01);2. anxiety about prognosis (beta0.344, p0.01);3. sex (beta0.234, p0.05);4. uncertainty regarding treatment (beta0.377, p0.01);5. negative coping (beta0.354, p0.01);and 6. employment status (beta0.367, p0.01). Coping and uncertainty in illness had a significant relation to positive support and lack of support. To maintain appropriate dietary behavior in diabetic patients, medical staff need to determine what the social supports are important for the patient, and also to ensure good communication among healthcare personnel as well as positive support for patients and families.

For the purpo3e to determine exactly what stage of cell specialization the DNA level of erythroid cell nuclei begins to decline, the author observed the DNA level of erythroblasts in mitosis by microspectrophotometry and the DNA synthesis by flash labeling with H3-thymidine. The cell samples were obtained from the bone marrow of normal, blood-depleted and phenylhydrazine-treated animals, and the anemic animals received a mass red cell transfusion, all the animals being injected with colchicine 4 hours before obtaining the bone marrow sample. DNA level was measured on the smeared cells stained by Feulgen reaction and DNA synthesis by autoradiography on the smeared cells. Besides these, chromosome number was observed on the anemic rat erythroblasts at metaphase by air dry method. The observations indicated that the DNA level begins to decrease at polychromatic stage being accompanied by a decrease in TDH3-incorporation into DNA, reaching minimum level at orthochromatic cell both in DNA contents and synthesis. Chromosome numbers of erythroblasts of rat were irregular being distri buted between 42 to 20. The data have suggested that the DNA level of erythroblasts decreases only in the later stages of cell specialization, and at polychromatic stage the chromosome number may also decrease in rabbit at polychromatic stage by the cell division with an incomplete DNA replication. The high DNA level of the erythroblasts of rabbit, in severe anemia where most of the cells are denucleated at polychromatic and late basophilic stages, has been discussed from the view point of the insufficient DNA replication at polychromatic stages.

The appearance of sideroblasts in hypoplastic anemia (HAl and acute myelocytic leukemia (AML), together with their sideroblastograms, was studied. Hematological studies on cases with type III sideroblast dominance by sideroblastograms produced the following results. Type III sideroblast dominant HA was observed in three of 63 cases. Two of the above three cases had what we call "atypical factor", while the remaining one became AML in its clinical course and could be considered to be leukemia in a hypoplastic preleukemic stage. Type III sideroblast dominant AML was noted in five of 32 cases. Three of these five cases are compatible with low percentage leukemia, and one of the above three cases showed ringed sideroblasts exhibiting erythroleukemia in the terminal stage. In HA and AML, type III sideroblast dominant cases have to be examined in relation to atypical HA and atypical leukemia. Changes of iron meta. bolism in erythroblasts with preleukemic stage will be attributable to disturbance of erythropoiesis such as erythroid hyperplasia in bone marrow and also, in part, to disturbance of hemoglobin synthesis.

The present experiment was undertaken to study what types of human cancers are responsive to the antiproliferative effects of suramin. The human malignant cells used were as follows: cervical cancer (HeLa), mammary cancer (MCF-7), bladder cancer (EJ), hepatoma (HuH-7, PLC/PRF/5), embryonal carcinoma (PA-1), in vitro transformed fibroblasts (KMST-6, SUSM-1, VA-13), five myeloma cell lines (KMM-1, KMS-5, KMS-11, KMS-12, RPMI 8226), Burkitt's lymphoma (Raji), acute promyelocytic leukemia (HL-60), chronic myelocytic leukemia (K562), Epstein-Barr virus nuclear antigen positive lymphoblastoid cells (KMS-9). The cells were treated with 25 to 100 micrograms/ml suramin for 72h. Proliferation of HuH-7 and two human myeloma cells (KMS-11 and KMS-12) was remarkably inhibited, and that of PA-1, PLC/PRF/5, KMST-6, two other myeloma cell lines (KMM-1 and KMS-5), Raji and HL-60, was moderately inhibited. In order to confirm part of the results obtained from in vitro experiments, in vivo experiments were also undertaken. The growth of HuH-7 cells transplanted subcutaneously into nude mice was significantly suppressed by intravenous injection of suramin. We discussed the possibility that certain types of human cancers, the growth of which seemed to be more or less dependent on polypeptide growth factors, might be sensitive to the antiproliferative effects of suramin.

When cultured cells are used in experiments, It is very important to know from what kinds of cells the cultured cells are originated, and what characteristics the cultured cells maintain continuously in vitro Some properties of rat liver cells in long-term cultivation were examined for the purpose of identifying the cultured cells with parenchymal liver cells by investigating their functions. The production of rat serum albumin and α-globulin which is regarded as specific functions of liver parenchymal cells was detected in these cultured rat liver cells with the method of immunoelectrophoresis. Histochemically, acid phosphatase, glucose-6-phosphate dehydrogenase, succinic dehydrogenase, lactic dehydrogenase, and adenosine triphosphatase were demonstrated in the cultured rat liver cells which were morphologically epithelial. Alkaline phosphatase showed little activity in these cells. Glycogen was recognized by the periodic acid-Schiff technique, when bovine serum concentration in the culture fluid was reduced to 5 per cent. These histochemical findings of cultured rat liver cells were identical with those of parenchymal liver cells in vivo. These facts suggest that there is a possibility of the continuous cultivation of liver cells by the present methods and of the identification of the cultured cells with the parenchymal liver cells from their functions.

With a certain fixed methods of analyses, we carried out the determination of flavins and cytochromes in the mitochondria (Mt) and electron transfer particles (ETP) of the heart and liver of rats and cows, and made a comparison of the data with one another. Our findings may briefly be summarized as follows. 1. The concentration of each component of the beef heart mitochondria proved to be 0.47 for acid extractable flavins; 0.22 for acid nonextractable flavin; O. 75 for cytochrome (cyt.) a; 0.58 for cyt. b; and O. 51 for cyt. C + Cl, all units being mμ mole per mg of protein. 2. In the beef liver mitochondria it was 0.46 for acid extractable flavins; 0.18 for acid non-extractable flavin; 0.092 for cyt. a; 0.089 for cyt. b; and 0.122 for cyt. C+Cll likewise all units in term of mμ mole per mg of protein. 3. In the case of rat heart mitochondria, it was found to be O. 42 for acid extractable flavins; 0.22 for acid non-extractable flavin; 0.88 for cyt. a; 0.41 for cyt. b; and 0.62 for cyt. C + Cll all in mμ mole per mg of protein. 4. In the rat liver mitochondria it was 0.56 for acid extractable flavins; 0.19 for acid non-extractable flavin; 0.20 for cyt. a; 0.14 for cyt. b; and 0.19 for cyt. C+Cl. 5. The concentration ratios of Fs, cyt. a and cyt. b of the mitochondria, what are considered to be intrinsic and fixed components of the mitochondrion. to those of the electron transfer particles were 1. 3 in both the beef heart and the rat heart, while 2.2 in the beef liver and 2.1 in the rat liver. 6. These findings were compared with the data reported by other workers, and also a discussion was made on the molecular organization of the mitochondrial inner membrane.

Brugada syndrome is increasingly being recognized in clinical medicine. What started as an electrocardiographic curiosity has become an important focus of attention for individuals working in the different disciplines related to sudden cardiac death, from basic scientists to clinical cardiac electrophysiologists. In just 12 years, since the description of the disease, clinically relevant information is continuously being provided to physicians to help protect the individuals with Brugada syndrome to the best of our ability. And this information has been gathered thanks to the effort of hundreds of basic scientists, physicians and patients who continue to give their time, effort and data to help understand how the electrocardiographic pattern may cause sudden cardiac death. There are still many unanswered questions, both at the clinical and basic field. However, with the further collection of data, the longer follow-up and the continued interest from the basic science world we will have the necessary tools to the successful unraveling of the disease.

A report is made of a 52-year-old male whose main complaint was a painless tumor at the right side of the palate resulting in speech disturbance. He was diagnosed as a case of what Stout called benign mesenchymoma. Some discussion is also made of the tumor pathology in terms of genetic factors, predirective sites, age range, sex differences and therapy.

It has been documented that the serum complement activities measured by hemolytic assay (CH50) are decreased after storage of sera at a low temperature in some patients with chronic hepatitis C. However, the mechanism of this phenomenon has not been identified yet. Here, we tried to elucidate factors involved in the cold activation of complement (CAC). To clarify what pathway is activated in CAC, we measured complement cleavage products after cold storage of sera. C4d increased significantly after 12 h-storage at cold temperatures in 5 CAC (+) sera compared with 5 CAC (-) (P < 0.01) and 3 control sera (P < 0.05), while Bb did not increase in any of the groups. In order to determine whether IgG or IgG complex is necessary for CAC, 8 CAC (+) sera were incubated with Protein G Sepharose gel beads, and all of them retained hemolytic activities to some extent after cold storage. Column chromatography through Superose 6HR of CAC-positive serum identified the fractions containing molecules that induced CAC in normal serum, which were depleted by treatment with protein G Sepharose. In conclusion, CAC in hepatitis C seems to occur via a classical or lectin pathway, and the IgG complex produced in hepatitis C virus infection may be an important factor in inducing CAC, a common extrahepatic manifestation of hepatitis C.