Reparative effects of sodium alginate (Alloid G) on radiation stomatitis

Discontinuation or alteration of the schedule of radiation therapy is often necessary in patients with tumors of the parotid gland and pharynx because of the development of stomatitis. Alloid G (Sodium alginate; AL-G) is an agent with a promotive effect on healing of inflammation of the gastric and esophageal mucosa. In this study, we orally administered the agent in irradiated mice to examine its healing effect against radiation stomatitis. ICR mice (5-week-old males) were subjected to gamma-irradiation at 17-32 Gy, and followed by oral administration with either AL-G, polyvinyl pyrrolidone (PVP), or water twice daily for 20 days. The effects of the treatments on radiation stomatitis were examined according to the survival of the animals and histological findings in the oral mucosa. After irradiation at 32 Gy, it was found that the epidermal basal layer was present in the AL-G group. In both PVP and water-treated groups, however, it was not found. The dose modification factor (DMF) of 1.12 was calculated from oral radiation death of LD50/20 and radiation dose with or without AL-G. These results suggest that AL-G probably have a pharmacologically reparative effect on radiation injury of the oral mucosa, in addition to the physical epidermal protective effect due to its viscosity such as that of PVP.     

Study of levels of latamoxef in prostatic tissue and bladder mucosal tissue

The concentration of Latamoxef (LMOX) in the serum, prostatic tissue and bladder mucosal tissue of 20 patients with benign prostatic hypertrophy and bladder cancer was measured after intravenous infusion of 1 g or 2 g of LMOX. Serum, prostatic tissue and bladder mucosal tissue levels of LMOX responded satisfactorily to the dose of LMOX. The bladder mucosal tissue level was higher than the prostatic tissue levels. Judging from the inhibitory concentration of LMOX (MIC 80), the concentration was sufficiently effective against infections caused by gram-negative, gram-positive and anaerobic bacilli.     

Synaptosomal T3 binding sites in rat brain: their localization on synaptic membrane and regional distribution

Previous studies have shown the existence of specific high affinity T3 binding sites in rat cerebrocortical synaptosomes. In this study, to define the localization of the binding sites, T3 binding to disrupted synaptic membrane fractions was compared with the binding to intact synaptosomes obtained from the rat cerebral cortex. Scatchard analysis revealed two orders of T3 binding sites with almost identical apparent dissociation constant (Kd) in synaptosomes and synaptic membrane fractions. However, the maximal binding capacity (MBC) of the higher affinity binding sites for synaptic membrane fractions was significantly greater than that for intact synaptosomes (4.2 +/- 0.2 vs 3.0 +/- 0.3 pg T3/mg protein). Regional distribution of the synaptosomal T3 binding sites in various areas of the rat brain was also studied. The Kd values were not significantly different in discrete brain regions. On the other hand, the MBCs of the higher affinity binding sites were greater in the cerebral cortex and hypothalamus (72.8 +/- 1.4 and 64.8 +/- 9.5 pg T3/g tissue) than in the cerebellum (22.1 +/- 1.6 pg T3/g tissue). Similar difference was also observed in the lower affinity sites. These results indicate that the specific T3 binding sites in brain synaptosomes are localized mainly on synaptic membranes and that the MBC is different in discrete brain regions.     

Effects of divalent cations on vitamin B12 adsorption to brush borders of rat intestine.

A brush border preparation from rat intestine was incubated with rat intrinsic factor-vitamin B12 complex in 0.01 M Tris-HCl buffer, pH 7.4. The 57Co-B12 uptake to brush borders was proportional to the amount of protein or to alkaline phosphatase activity in the preparations. The uptake increased with time of incubation. At 37degreesC, the uptake after incubation for 15 min was 80-85% of that for one hr. The uptake at 4degreesC was approximately 70% of that at 37degreesC. Ther was no difference as a result of adding glucose to the incubation medium. The uptake was observed in the alkaline environment above pH 6.3. Maximum uptake occurred at pH 8.0. Brush borders washed with Krebs-Ringer bicarbonate buffer (pH 7.4) exhibited no difference in B12 uptake, whether in the presence or absence of calcium ion. But brush borders washed with ethylenediaminetetraacetate exhibited no uptake when incubated in calcium-free medium. The uptake reached a maximum by addition of calcium ion at a concentration of 0.3 mM, and was not alter up to 10 mM. Addition of magnesium ion exhibited no uptake. Calcium-dependent B12 uptake was markedly inhibited by manganese ion. Magnesium ion seemed to slightly inhibit the calcium-dependent uptake.     

Heterogeneous distribution of beta-adrenoceptors and muscarinic receptors in the sinoatrial node and right atrium of the dog

1. The pacemaker site is known to shift away from the sinoatrial (SA) node in response to autonomic stimuli. 2. To test whether the shifting of the impulse-initiation site that occurs during autonomic nerve stimulation can be explained by the spatial distributions of beta-adrenoceptor and muscarinic receptors, we obtained densities (B(max)) and dissociation constants (K((d)) for these receptors in three regions along the sulcus terminalis (the SA node itself and regions superior and inferior to it) and a region of the right atrial appendage in the dog. 3. The Bmax values for [(125)I]-iodocyanopindolol binding to beta-adrenoceptors were not different among the four regions. The Bmax value for [(3)H]-quinuclidinyl benzilate binding to muscarinic receptors was significantly higher in the SA node area than in any other region (P < 0.01), although there was no difference among the other three regions. 4. For each receptor, K(d) values were similar among the four regions. 5. These results suggest that spatial variations in the densities of beta-adrenoceptors and muscarinic receptors are not important for shifting the impulse-initiation site and that other factors, such as non-uniform innervation by autonomic nerve fibres, may be mainly responsible for the pacemaker shift induced by autonomic nerve stimulation.