Gastric emptying after gastric interposition for esophageal carcinoma: comparison between the anterior and posterior mediastinal approaches

BACKGROUND/AIMS: Close observation and evaluation of the function of the transposed stomach after esophagectomy is essential. The present study uses the sulfamethizole capsule meal test to evaluate differences in gastric emptying between the anterior and posterior mediastinal approaches in patients undergoing esophagectomy. METHODOLOGY: Thirty-eight patients who underwent the esophagectomy and esophagogastrostomy for esophageal cancer were randomly divided into 2 groups: Group 1: anterior mediastinal approach, and Group 2: posterior mediastinal approach. Gastric emptying was studied using the sulfamethizole capsule meal test. Patients received sulfamethizole food capsules, 65 g of bread, and 150 ml of water. Plasma sulfamethizole levels were determined by high performance liquid chromatography (HPLC). RESULTS: Gastric emptying in both groups was significantly accelerated compared to healthy volunteers. Gastric emptying did not differ significantly between groups 1 and 2. CONCLUSIONS: The present data show that the sulfamethizole capsule meal test is an effective means of evaluating the emptying of the transposed stomach. Furthermore, when the stomach is used as an esophageal substitute following esophagectomy, gastric emptying does not differ according to the access route.     

Preparation of pyrochlores. A1−xHxTaO3·nH2O (A=Na,K)

Pyrochlores of A_1?xH_xTaO₃·nH₂O (A=Na,K) were prepared under the hydrothermal conditions. The values of x for these compounds were increased from 0.3 to 0.5 for A=Na and from 0.2 to 0.5 for A=K by treatment with the distilled water. The compounds with x<0.5 were decomposed to a mixture of NaTaO₃ and Na₂Ta₄O₁₁ for A=Na, or to a mixture of KTaO₃ and a tetragonal tungsten bronze phase, and those with x=0.5 to a single phase of A₂Ta₄O₁₁ at elevated temperatures. Below the decomposition temperatures, defect pyrochlores with oxygen vacancies, $\text{A}{}_{\mathrm{<mtext>1?</mtext><mtext>x</mtext>}}\text{TaO}{}_{\mathrm{<mtext>3?</mtext><mtext>x</mtext><mtext>2</mtext>}}$, were produced. They were hygroscopic, and in the case of A=K and x=0.5 the original phase was recovered by leaving in air for several hours.     

Determination of a cleavage site of presenilin 2 protein in stably transfected SH-SY5Y human neuroblastoma cell lines

Mutations in the presenilin 1 (PS1) and presenilin 2 (PS2) genes are associated with early-onset autosomal dominant familial Alzheimer's disease, and the gene products are endoproteolytically processed to yield N-terminal fragments (NTF) and C-terminal fragments (CTF). We have studied the cleavage site of the PS2 protein in stably transfected human neuroblastoma cells. The 23 kD PS2-CTF was isolated by a combination of anion exchange chromatography and affinity chromatography and directly sequenced. The N-terminus of the PS2-CTF started at residue 307, which indicated that the cleavage occurs between Lys306 and Leu307 in the proximal portion of the large hydrophilic loop. This site is close to the cleavage positions observed in the PS1 protein.     

Chronic loss of glucocorticoids following adrenalectomy down-regulates the expression of glucocorticoid receptor mRNA in the rat forebrain

In the negative feedback model, loss of endogenous glucocorticoids up-regulates the expression of glucocorticoid receptor mRNA. To elucidate further the effect of chronic lack of glucocorticoids on the expression of glucocorticoid receptor mRNA and protein, in situ hybridization and immunohistochemical methods were used to examine the long-term alteration of glucocorticoid receptor mRNA and its immunoreactivity in the forebrain of adrenalectomized rats. Constant lack of glucocorticoids resulted in marked decrease in the expression of glucocorticoid receptor mRNA and disappearance of glucocorticoid receptor immunoreactivity in many forebrain structures. In particular, in the suprapyramidal blade of the hippocampal granule cell layer and cerebral cortex, many cells showed almost no glucocorticoid receptor mRNA signals. These results suggest that long-term loss of endogenous glucocorticoids down-regulates the levels of glucocorticoid receptor mRNA, leading to reduction in the synthesis of glucocorticoid receptors in the rat forebrain. Therefore, the presence of endogenous glucocorticoids is vital to the continued expression of glucocorticoid receptor mRNA.     

Functional differentiation of human naive helper T cells

Here we report a case of a 56-year-old male with post-poliomyelitis muscular atrophy (PPMA), who presented with cranial nerve signs and widespread atrophy of the extremities. He had suffered from poliomyelitis at the age of 2 years. After recovery from the acute stage, the paralysis remained in his left arm. He noticed muscle weakness of the right upper and lower extremities at the age of 45 years and the muscle atrophy progressed to his arms, hip and thigh at the age of 55 years. Neurological examination revealed muscle atrophy of the neck and disturbance of left V, VIII, IX, X and bilateral XI cranial nerves. We diagnosed this case as PPMA from his history and electromyographic and muscle biopsy findings which suggested chronic denervation. Among the 21 PPMA cases in the past in which the acute poliomyelitis had resulted in paralysis of the only one limb, ours was the only case that had muscle atrophy of all the limbs. Cranial nerve involvement is known to occur in acute poliomyelitis; therefore, there is a possibility that the involvement of the cranial nerves in our case might be a delayed progressive symptoms.     

Enhancing effect of nonionic surfactant on the inactivation of lipopolysaccharide by steam-heat treatment II

n-alkylpolyoxyethylene surfactants (CnH2n+1O(CH2CH2O)mH; CnEm) showed a strong enhancing effect on the inactivation of lipopolysaccharide (LPS) by heat treatment over a wide range of temperatures. The effect of CnE8 (n = 10-16) was observed above the critical micelle concentration (CMC) and above the cloud point, and was influenced by the length of the alkyl chains. The efficacy of the surfactants was in the order C10E8 < C12E8, C16E8 < C14E8. However, the hydrophilic moiety seemed to have no influence. An 80-95% solution of n-butanol showed a similar effect, indicating that LPS was more effectively inactivated in the oily phase of the surfactants than in water. The effect of surfactant on the hydrodynamic diameter of LPS was the same before and after steam-heat treatment for 20 minutes at 121 degrees C. Each surfactant disaggregated LPS without alteration of the activity of LPS before the heat treatment. We consider that the surfactants interact with LPS in the region of lipid A in a manner that favors loss of the activities of LPS during heating.     

Late phase II trial of oral etoposide administered for 21 consecutive days in patients with cervical cancer. ETP 21 Study Group--Cervical Cancer Group

We conducted a multi-site late phase II trial of oral etoposide administered for 21 consecutive days in patients with cervical cancer in cooperation with 32 institutes. Fifty mg/body of oral etoposide was administered daily for 21 consecutive days. Treatment cycles were to be repeated at 4- to 5-week intervals. Eighty patients were enrolled and 70 patients were evaluated. The overall response rate (95% CI), including one complete response patient and 18 partial response patients, was 27.1% (19/70). The most commonly observed toxicity was myelosuppression such as leukopenia, neutropenia, hemoglobin decrease and thrombocytopenia. Other adverse effects were gastrointestinal toxicities such as anorexia, nausea, stomatitis and vomiting, as well as fatigue and alopecia. These adverse effects were well tolerated and controlled with medications. From these results we concluded oral etoposide administered for 21 consecutive days was an effective drug against cervical cancer.     

Intracellular retention and degradation of tissue-nonspecific alkaline phosphatase with a Gly317-->Asp substitution associated with lethal hypophosphatasia

One point mutation which converts glycine-317 to aspartate of tissue-nonspecific alkaline phosphatase (TNSALP) was reported to be associated with lethal hypophosphatasia (Greenberg, C. R., et al. Genomics 17, 215-217, 1993). In order to define the molecular defect of TNSALP underlying the pathogenesis of hypophosphatasia, we have examined the biosynthesis of TNSALP with a Gly317-->Asp substitution. When expressed in COS-1 cells, the mutant did not exhibit alkaline phosphatase activity at all, indicating that the replacement of glycine-317 with aspartate abolishes the catalytic activity of TNSALP. Pulse-chase experiments showed that the newly synthesized mutant failed to acquire Endo H-resistance and to reach the cell surface. Interestingly, this TNSALP mutant was found to form a disulfide-bonded high-molecular-mass aggregate and was rapidly degraded within the cell, though the mutant protein was modified by glycosylphosphatidylinositol (GPI). Lactacystin, an inhibitor of the proteasome, obstructed the degradation of the mutant protein, suggesting the involvement of proteasome as a part of quality control of TNSALP.