TCR-Vbeta repertoire analysis with RT-PCR was useful for the early detection of pulmonary relapsed T-cell lymphoma after autologous peripheral blood stem cell transplantation

Pulmonary recurrence of malignant lymphoma is a rare event after stem cell transplantation. We report here a 45-year-old male who was successfully diagnosed with relapsed pulmonary T-cell lymphoma using an RT-PCR method. Clonal expansion of T cells expressing identical TCR V-D-J junction size (Vbeta5-Jbeta1.5) was demonstrated in lymphocyte groups obtained from both bronchoalveolar lavage fluid at relapse, and paraffin embedded lymph node samples resected when he was first diagnosed with angioimmunoblastic T-cell lymphoma. This method provided evidence to diagnose relapsed pulmonary angioimmunoblastic T-cell lymphoma in its early phase.     

Autoradiographic demonstration of target cells for 1,25-dihydroxycholecalciferol in the chick embryo chorioallantoic membrane,duodenum, and parathyroid glands

Sixteen-day-old chick embryos were injected with tritiated 1,25-dihydroxycholecalciferol (1,25-DHCC) and sacrificed 2 hr later. Portions of the chorioallantoic membrane, duodenum, yolk sac, and parathyroid glands were frozen and processed for thaw-mount autoradiography. High concentration of radioactivity was found in nuclei of the chorionic epithelium; their spatial distribution suggests, although does not prove, that these nuclei correspond to “calcium-absorbing” cells. Radioactivity was also demonstrated in nuclei of the duodenal epithelial cells and the cords of parathyroid glands. No localization was found in the wall of the yolk sac after 150 days of exposure. The injection of nonradioactive 1,25-DHCC 30 min before the administration of the radiocctive hormone prevented in all cases the nuclear concentration, probably by saturating receptors. The results are interpreted as demonstrating the presence of target cells for the hormone in chorionic epithelium, duodenum, and parathyroid glands, structures all believed to be involved in calcium metabolism in the embryo.     

Hyaluronic acid stimulates tumor-cell proliferation at wound sites

BACKGROUND: For EMR, the submucosal injection of sodium hyaluronate has become popular, because this substance creates a more prominent and longer-lasting mucosal protrusion than normal saline solution. However, the effects of sodium hyaluronate on tumor growth at wound sites remain unclear. METHODS: For these experiments, a murine model with artificial wounds was used. Forty mice were randomly divided into two groups according to the substance to be injected into a wound: a sodium hyaluronate group and a control group. Tumors were created by inoculation of transplantable adenocarcinoma cell line colon 26. Two weeks later, the size, weight, proliferating cell nuclear antigen-labeling index, and CD44 expression of the subcutaneous tumors were compared between the two groups of mice. RESULTS: There were significantly greater increases in the growth and the weight of subcutaneous tumors in the sodium hyaluronate group compared with the control group. The PCNA-labeling index of cancer cells also was higher in the sodium hyaluronate group. Immunohistochemistry and Western blot analysis demonstrated that the CD44 protein expression of cancer cells was higher in the sodium hyaluronate group vs. the control group. CONCLUSIONS: In this study, sodium hyaluronate enhanced both tumor growth and CD44 expression of cancer cells at wound sites, suggesting that the use of sodium hyaluronate for EMR might stimulate the growth of residual tumor cells.     

Rectal cancer associated with chronic lymphocytic leukemia

It has been reported that chronic lymphocytic leukemia (CLL) often occurs concomitantly with other malignant neoplasms. However, because CLL is rare in Japan, there are only a limited number of reports of the occurrence of malignant neoplasia in Japanese patients with CLL. We report here the simultaneous occurrence of rectal cancer and CLL in a 57-year-old man. Because the clinical stage of CLL was Rai system I, we decided, in accordance with the National Cancer Institute–Sponsored Working Group guidelines, to monitor him without therapy for CLL until evidence of disease progression, and we performed abdominoperineal resection of the rectum for the cancer. The small rectal tumor was associated with aggressive lymphangiosis carcinomatosa, and multiple nodal metastases were observed in the pool of CLL cells. He died of rectal cancer 7 months after the operation, and autopsy revealed extensive metastases of the cancer. Cellular and humoral immunity is often impaired in patients with CLL, and the defective immunity in this patient may have had an etiological role in the development and rapid progression of the cancer. In the follow-up of CLL patients, we must always be aware of the possible existence of a second malignant disease. Particular attention should be paid to those with defective immunity, and screening should be performed, especially for pulmonary and gastrointestinal malignancies.     

A single bout of exercise at higher intensity enhances glucose effectiveness in sedentary men

OBJECTIVE: Previous studies have shown that glucose effectiveness and insulin sensitivity are acutely enhanced by exercise at various intensities. The aim of this study was to determine the effects of a single bout of exercise at intensities recommended by the American Diabetes Association (ADA) and the American College of Sports Medicine (ACSM) on glucose uptake-specific glucose effectiveness (S(G)(2)*) and insulin sensitivity (S(I)(2)*). S(G)(2)* and S(I)(2)* were estimated by a two-compartment minimal model. DESIGN: Six healthy men (age, 28.5 +/- 2.0 yr) performed a stable-labeled frequently sampled iv glucose tolerance test (FSIGT) under three separate conditions: without any prior exercise, and immediately after single 20-min bouts of cycle ergometer exercise at an intensity of 50% and 70% of maximal oxygen uptake (Vo(2max)). The exercise intensities were close to the lower and upper boundaries recommended by the ADA and ACSM. RESULTS: Glucose disappearance constant (K(G)), S(G)(2)*, and S(I)(2)* increased after exercise in an intensity-dependent manner. Increases in S(G)(2)* (+237.1 +/- 50.5%), S(I)(2)* (+225.6 +/- 51.9%), and K(G) (+151.7 +/- 16.5%) following exercise at 70% Vo(2max) were statistically significant (P < 0.05), whereas those at 50% Vo(2max) were not. CONCLUSIONS: In conclusion, a single bout of exercise acutely improves S(I)(2)* and S(G)(2)* in individuals with normal glucose tolerance in an intensity-dependent manner.     

Smoking is associated with silent cerebrovascular disease in a high-risk Japanese community-dwelling population.

We aimed to investigate the relationships between smoking and silent cerebrovascular damage. We performed brain MRI to evaluate silent cerebral infarct (SCI) and periventricular hyperintensity (PVH), and carotid-ultrasonography to investigate carotid atherosclerotic plaque in 170 high-risk community-dwelling subjects (mean age: 67.2 years; men: 28.7%) who met more than 3 of the following 9 criteria: 1) high blood pressure (BP); 2) hypercholesterolemia; 3) left ventricular hypertrophy; 4) high hemoglobin A1c; 5) proteinuria; 6) high waist-to-hip ratio; 7) smoking > or =30 cigarettes/day; 8) heavy alcohol intake; 9) family history of stroke. The subjects with SCI (SCI group) were older (70 years vs. 66 years, p=0.004) and had higher systolic BP (SBP) (160 vs. 148 mmHg, p <0.001) and higher carotid plaque score (2.3 vs. 1.5/person, p <0.05) than those without SCI. Among the variables, smoking status (r =0.34, p <0.001), SBP (r =0.28, p <0.001), male gender (r =0.29, p <0.001), left ventricular mass index (r =0.25, p =0.001), and serum creatinine (r =0.20, p =0.006) were significantly correlated with the number of SCIs. Among smokers, the number of SCIs was significantly higher in current smokers than in past smokers (1.9+/-2.2 vs. 0.5+/-0.8, p <0.01). In multiple regression analysis, smoking status (beta =0.183, p =0.045) and SBP (beta =0.196, p =0.011) were independent determinants of the increased number of SCIs. In conclusion, smoking status was an independent determinant of multiple SCIs in a high-risk Japanese community-dwelling population.     

Inhibition of peptic ulcer relapse by ranitidine and ecabet independently of eradication of Helicobacter pylori: a prospective,controlled study versus ranitidine

BACKGROUND/AIMS: The recent increase in resistant strains of Helicobacter pylori has become a serious problem. Ecabet is a novel anti-ulcer agent that acts directly on the gastric mucosa, has bactericidal activity, and inhibits adhesion of Helicobacter pylori to the gastric mucosa. These actions result from inhibition of urease and ATPase in Helicobacter pylori, a mechanism distinct from that of antibiotics. METHODOLOGY: Sixty-three patients positive for Helicobacter pylori who had been cured of gastric ulcers and duodenal ulcers were randomly assigned to receive maintenance therapy with ranitidine alone or a combination of ranitidine and ecabet. Ulcer relapse was studied in these patients. RESULTS: The cumulative relapse rates in the ranitidine group and the ecabet plus ranitidine group were respectively, 29.6% and 4.4% after 1 year of treatment and 66.1% and 13.0%, after 2 years. These differences were significant (p = 0.006). Multivariate analysis of factors potentially related to relapse showed that outcome was significantly related only to treatment (p = 0.020) and not to other characteristics, such as age, diagnosis, or sex. CONCLUSIONS: We conclude that maintenance therapy with a combination of ranitidine and ecabet prevents ulcer relapse in Helicobacter pylori-positive patients. Controlled studies comparing ulcer relapse rates between eradication treatment and maintenance therapy with ranitidine and ecabet are awaited.     

Significance of Decreased Plasma D-Dimer Levels following Lipopolysaccharide-Induced Disseminated Intravascular Coagulation in Rats

Plasma D-dimer (DD) is considered to be one of the most useful markers in the diagnosis and assessment of disseminated intravascular coagulation (DIC). The present study was performed to clarify the role of DD in a rat model of lipopolysaccharide (LPS)-induced DIC in which low-molecular-weight heparin (LMWH) and tranexamic acid (TA) were used. We investigated whether a relationship exists between plasma DD levels and severity of DIC. Experimental DIC was induced in rats by a sustained 4-hour infusion of 30 mg/kg LPS administered via the tail vein (LPS group). Rats received either LPS alone (LPS group) or LPS combined with 200 U/kg LMWH (LPS+LMWH group) or 50 mg/kg TA (LPS+TA group) from -30 minutes to 4 hours. Blood was drawn from each rat at 4, 8, and 12 hours. Plasma levels of thrombin-antithrombin complex (TAT) and creatinine were suppressed in the LPS+LMWH group, and less glomerular fibrin deposition was observed compared with the LPS group. On the other hand, an increased level of creatinine and increased glomerular fibrin deposition were observed in the LPS+TA group compared with the LPS group. LMWH demonstrated a protective effect against LPS-induced DIC, resulting in increased survival at 12 hours, whereas TA had the opposite effect. From these results, it appears that LMWH protects against LPS-induced DIC, but TA exacerbates LPS-induced DIC. It was interesting that plasma levels of DD were almost completely suppressed by concurrent administration of either TA or LMWH in this LPS-induced DIC model. This finding suggested that plasma levels of DD were suppressed by inhibition of coagulation (reduced deposition of fibrin) in the LPS+LMWH group and that DD levels were also suppressed by inhibition of fibrinolysis (reduced degradation of fibrin by plasmin) in the LPS+TA group. Thus care should be taken when evaluating the significance of plasma DD levels, because suppressed levels can occur with progressive fibrin deposition and worsening organ dysfunction or improvement in the course of DIC.