Factors affecting the acceptance of deoxyguanosine-treated thymus allografts

dGuo-treated mouse embryo thymus lobes depleted of lymphoid and dendritic cells are not rejected by normal allogeneic mice despite expression of class I and class II major histocompatibility (MHC) antigens on thymic epithelial cells. Our results suggest that host mice are not tolerant to donor antigens, but treated lobes survive because thymic epithelial cells are not immunogenic. Multiple grafts of dGuo-treated lobes are rejected perhaps because numbers of residual dendritic cells reach a threshold necessary for priming. Mice previously primed by injection of spleen cells reject dGuo-treated thymus lobes, and crossreactions between major and minor histocompatibility antigens can be demonstrated. The acceptance of dGuo-treated thymus allografts by normal mice provides a system for investigating the requirements for priming.     

Ruthenium red selectively inhibits oedema formation and increased blood flow induced by capsaicin in rabbit skin.

It has been suggested that ruthenium red has a selective inhibitory effect on capsaicin-induced nociceptor stimulation. We have investigated the effect of ruthenium red on oedema formation and vasodilatation induced by intradermal (i.d.) injection of capsaicin in the rabbit in vivo. Responses induced by capsaicin were inhibited by ruthenium red, but responses induced by bradykinin, N-formyl-methionyl-leucyl-phenylalanine (FMLP), platelet activating factor (PAF), histamine and calcitonin gene-related peptide (CGRP) were not affected. These results suggest that ruthenium red selectively inhibits capsaicin-induced local plasma protein leakage and vasodilatation in the rabbit skin microvasculature.     

31P NMR spectra of intact red blood cells: Quantitation of UDPGlucose and UDPGalactose

The combined levels of uridine diphosphogalactose (UDPGal) and uridine diphosphoglucose (UDPGlu) were measured directly by ³¹P NMR spectroscopy in intact fully oxygenated erythrocytes. Quantitative analysis was obtained using a sealed capillary of methylene diphosphonate (MDP) calibrated with standard solutions of UDPGlu and UDPGal of known concentration prepared in KRB/BSA. The combined peaks of UDPGlu and UDPGal were integrated after subtraction of the underlying broad component originating from membrane phospholipids. The average concentration of 27.16 ± 5.18 nmole/ml or 8.08 ± 1.36 μmole/100 g hemoglobin obtained for these metabolites correlated well with their total determined by HPLC of trichloracetic acid (TCA) extracts of the same samples.     

Mutagenicity and toxicity of the DNA alkylation carcinogens 1, 2-dimethylhydrazine and azoxymethane in Escherichia coli and Salmonella typhimurium

DNA alkylating agents such as 1, 2-dimethylhydrazine (SDMH)and azoxymethane (AOM) are potent carcinogens and are widelyused to induce colon tumors in experimental animals. However,standard bacterial mutagenesis assays have failed to detectthe mutagenic effects of these chemicals. Using derivativesof a set of Escherichia coli test strains developed by Cupplesand Miller (Proc. NatL Acad. Set USA, 86, 5345, 1989), we havedemonstrated that under two conditions, SDMH and AOM inducedpoint mutations by several-fold in a dose-dependent manner:(i) of six possible base substitutions, they only induced GC     

Echinococcal disease of the kidney presenting as a renal filling defect

We report a unique case of renal echinococcal disease. The patient presented with only a left renal pelvic filling defect without hepatic, pulmonary or other renal involvement. Management consisted of successful exploration and removal of the hydatid mass without sacrifice of renal tissue. The pathogenesis, diagnosis and treatment of echinococcal disease are reviewed.     

Efficacy of antimicrobial treatment in non-dysenteric persistent diarrhoea in a community setting

Objectives : To determine the efficacy of antimicrobial treatment in non-dysenteric persistent diarrhoea in a community setting. Methods : In this double-blind field trial, 156 children aged 4 36 months with persistent diarrhoea not associated with Giardia lamblia infestation seeking treatment in a community outpatient clinic, were randomized to receive a combination of nalidixic acid and metronidazole, metronidazole alone, or placebo for 7 days. Results : In comparison with placebo, metronidazole treatment did not result in a significant reduction in the mean post-enrolment diarrhoeal duration and stool frequency, increase in the proportion of patients recovered by days 3, 5 and 7 of treatment, and increase in weight gain at days 7 and 14. Comparing the combination of nalidixic acid and metronidazole with metronidazole alone, 17.5% more children treated with the combination recovered by day 3 of treatment ( p = 0.08) and the mean stool frequency ascertained on day 7 for the previous 24 h was 26.8% less in them ( p = 0.05). The weight gains at days 7 and 14 were similar in the two groups. Conclusions : These findings indicate that metronidazole offers no therapeutic benefit in persistent diarrhoea not associated with Giardia lamblia and nalidixic acid has only a modest clinical benefit, which is not substantial enough to warrant its routine use.     

Comparison of the beta-adrenoceptor affinity and selectivity of cetamolol, atenolol, betaxolol, and ICI-118,551

The objective of the present study was to compare the quantitative differences in the beta 1- vs. beta 2-adrenoceptor affinity and selectivity of cetamolol and its enantiomers to the reference compounds atenolol, betaxolol, and ICI-118,551, using isolated tissues obtained from the dog, guinea pig, and rat. Cetamolol antagonized the beta-adrenoceptor-mediated responses induced by isoproterenol, epinephrine, norepinephrine, and salbutamol, in tissues from both the dog and guinea pig, in a concentration-dependent manner. For a given tissue, the beta-adrenoceptor antagonist activity of cetamolol (measured as a pA2 or pKB value) was independent of the agonist used. In the dog tissues, cetamolol was more potent at inhibiting responses in the coronary artery (beta 1-adrenoceptors) than in the saphenous vein (beta 2-adrenoceptors). In the guinea pig tissues, the potency of cetamolol was approximately the same in the trachea (mixed beta 1- and beta 2-adrenoceptors) and atria (predominately beta 1-adrenoceptors), but lower in the soleus muscle (beta 2-adrenoceptors). Studies with the S-(-) and R-(+) enantiomers of cetamolol demonstrated that the S-(-) enantiomer was approximately 100-fold more potent at beta 1-adrenoceptors than the R-(+) enantiomer. In rat brain, cetamolol displaced [3H]-dihydroalprenolol bound to homogenates of cortex (beta 1-adrenoceptor binding sites) and cerebellum (beta 2-adrenoceptor binding sites). The potency of cetamolol at beta 1-adrenoceptors was found to be similar to that of betaxolol but greater than that of atenolol. However, the magnitude of the beta 1-adrenoceptor selectivity displayed by atenolol and betaxolol was greater than that displayed by cetamolol. In contrast, ICI-118,551 was found to possess potent and selective affinity for beta 2-adrenoceptors.