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The present study was performed to clarify the influences of anesthetic methods and insufflating gases on arterial blood gas and ventilation during laparoscopy. Forty five women undergoing laparoscopy for gynecological procedure were studied after dividing into four groups; general anesthesia with control ventilation or epidural anesthesia with spontaneous breathing, plus insufflation with carbon dioxide (CO2) or nitrous oxide (N2O). After CO2 insufflation, PaCO2 increased significantly in the patients who were mechanically ventilated, but not in the patients breathing spontaneously. After N2O insufflation, the decrease in tidal volume (VT) and the increase in VD/VT were significant, but minute ventilation was well maintained by the compensatory increase in respiratory frequency during spontaneous breathing. On the other hand, after CO2 insufflation VE and VD/VT increased significantly without any change in VT. PaO2 decreased significantly after both insufflation and Trendelenburg tilt in all groups, probably secondary to the decrease in functional residual capacity. These findings suggest that during laparoscopy, ventilation could be well maintained by spontaneous breathing, although the increase in VD/VT and costal breathing indicate the increase in respiratory work load. We recommend that ventilation and oxygenation should be closely monitored during laparoscopy to avoid hypercapnia and hypoxia.

Inositol 1,4,5-trisphosphate (IP3) functions as a second messenger for many neurotransmitters, hormones and growth factors. It causes the release of Ca2+ from intracellular stores by binding to specific receptors that are coupled to Ca2+ channels. Recent studies have shown that there is a family of IP3 receptors, and the complete sequences of two members of this family and partial sequences of two others have been reported. We have determined the complete sequence of a third IP3 receptor, designated IP3R-3, and characterized its pharmacological properties and sites of expression. Rat IP3R-3 is 2670 amino acids in size, has 62 and 64% identity with IP3R-1 and IP3R-2, and is predicted to have a similar structure including a region of eight potential membrane-spanning segments at its COOH terminus, which presumably functions as a Ca2+ channel. Expression of recombinant rat IP3R-3 in COS-7 cells showed that it bound IP3 as well as inositol 1,3,4,5-tetrakisphosphate and inositol hexakisphosphate. Immunohistocytochemical studies of cells expressing recombinant IP3R-3 indicated that it has a preferential cellular distribution in the endoplasmic reticulum. RNA and protein blotting studies indicate that IP3R-3 is expressed in a number of different cultured cell lines including insulin-secreting RINm5F cells. The IP3R-3 is also expressed in adult pancreatic islets, kidney, gastrointestinal tract, and brain. Reverse transcriptase-polymerase chain reaction amplification of IP3R-1, -2, and -3 mRNAs in adult rat pancreatic islets indicated that IP3R-3 was the predominant subtype expressed in this tissue and thus may be responsible for mediating the effects of IP3 on insulin secretion.

The enzyme glucokinase catalyzes the phosphorylation of glucose and plays a key role in the regulation o f insulin secretion by pancreatic beta cells and glucose disposal in hepatocytes. Recent studies have shown that mutations in the gene encoding this key regulatory enzyme of glycolysis are a common cause of an autosomal dominant form of non-insulin-dependent (type 2) diabetes mellitus that has an onset often during childhood. The association of mutations in the glucokinase gene with impaired pancreatic cell function underscores the importance of glycolysis in the regulation of insulin secretion and suggests that mutations in other genes expressed in the beta-cell that also control rate-limiting steps in glucose metabolism may lead to diabetes.

The influence of prostaglandin E1 (PGE1) on PaO2 at doses that produced slight hypotension was evaluated in 176 patients scheduled for surgery. When systolic blood pressure was stabilized after induction of anesthesia, PGE1 infusion was started until 20% reduction of systolic blood pressure was achieved. Arterial blood gases were analyzed before infusion of PGE1 and 30 min after the completion of this hypotensive level respectively. The reductions in both PaO2 [from 177 +/- 64 mmHg to 164 +/- 65 mmHg (mean +/- SD) (P0.01)] and PaO2/FIO2 [from 486.5 +/- 144.4 to 437.6 +/- 121.6 (P0.01)] were observed with PGE1 infusion of 0.079 +/- 0.068 micrograms.kg-1.min-1. The results of this study show that PaO2 decreases during induced hypotension with PGE1 infusion, but this decrease is not clinically significant.

To evaluate the interaction of amrinone with inhalational anesthetics, cardiovascular effects of amrinone were investigated in nine mongrel dogs anesthetized with enflurane. Each dog received enflurane and amrinone in the following sequence: 1) 2% enflurane alone, 2) continuous infusion of 20 micrograms.kg-1.min-1 during enflurane, 3) 40 micrograms.kg-1.min-1 infusion during enflurane. Amrinone 40 micrograms.kg-1.min-1 during enflurane anesthesia improved the maximum left ventricular dP/dt, stroke volume and decreased effective arterial elastance (Ea) without changes in left ventricular end-diastolic pressure and heart rate. Left ventricular pressure (LVP) and systolic femoral arterial pressure were stable, but diastolic femoral arterial pressure decreased significantly from enflurane anesthesia alone. These parameters at 20 micrograms.kg-1.min-1 of amrinone infusion during enflurane showed the same tendency with 40 micrograms.kg-1.min-1 infusion but not significantly different from enflurane alone. This result suggests that amrinone may be beneficial in the patients with depression of cardiac performance during anesthesia.

The change in electroencephalographic (EEG) activity during sevoflurane anesthesia was quantitatively evaluated by using zero-crossing analysis in 10 adult patients. The deceleration of EEG activity was significant and dose-dependent. Such change was not significantly different among the regions. Burst suppression appeared at 2-2.5 MAC in all patients. The significant decrease in both alpha and beta activities and the significant increase in delta activity disappeared with 1% or less of sevoflurane. Toward the emergence from anesthesia, EEG activity accelerated and there was no significant difference in its activity between the emergence period and control period. The results demonstrated that the effect of sevoflurane on EEG activity is similar to that of other inhalation anesthetics, but the difference among anesthetics should be clarified in a further study.

We have investigated the cell kinetic effect of four carcinostatic agents (MMC, CDDP, ADR and 5-FU) on the human gastric cancer cell line (KATO-III; signet ring cell carcinoma) by means of flow cytometry (FCM), using bromodeoxyuridine (BrdU) and its monoclonal antibody. Cancer cells in the S phase were first labelled with BrdU and then the bivariate DNA/BrdU distribution was examined to analyze the effect on the cell cycle. Furthermore, cells were reincubated at 24 hours after labelling to evaluate the cell turnover during FCM. MMC, CDDP and ADR assembled the cells into late S phase and G2M phase, while 5-FU assembled them into S phase. after 24 hours, cells with cessation of cell cycle had inhibited their proliferation. We conclude that this technique can be usefully applied as a susceptibility test of carcinostatic agents, since it could define the phase where carcinostatic agents acted on cancer cells.

Prognosis following surgery for gastric cancer has markedly improved as a result of early diagnosis, advances in operative techniques, and perioperative management. However, gastrointestinal surgery in patients with hepatic cirrhosis has continued to be associated with a high operative morbidity and mortality. On the basis of a detailed classification of the preoperative hepatic conditions into three risk groups, we have established a preoperative means of assessing surgical indication. Depending on the preoperative assessment, 40 gastric cancer patients with hepatic cirrhosis underwent surgical exploration. Thirty-seven patients (92.5%) received gastric resection, while 3 patients (7.5%) were non-resectable. Postoperative complications occurred in only 8 patients (20%), and no anastomotic leakage occurred; the overall operative mortality was zero. The five-year-survival rate following a curative resection, as calculated by Kaplan-Meier statistical analysis, was 51.4% (n = 30).

In recent studies we have identified PC2 and PC3, members of a family of serine proteases that are related structurally to subtilisin, and have provided evidence that these are involved in the tissue-specific processing of prohormones and neuropeptides. PC2 is expressed at high levels in the islets of Langerhans, where it participates in the processing of proinsulin to insulin (S.P.S. and D.F.S., unpublished data). To evaluate the regulated expression of the human PC2 (hPC2) gene we have analyzed its structure and characterized its promoter. A map of the gene was constructed by using 11 clones isolated from two human genomic DNA libraries. The gene spans greater than 130 kilobase pairs and consists of 12 exons. Comparison with the structure of the gene encoding human furin, another member of this superfamily, revealed a high degree of conservation of exon-intron junctions. The hPC2 gene was localized to chromosome 20, band p11.2. The 5' flanking region of the hPC2 gene is very G+C-rich and contains six potential Sp1 binding sites but no TATA or CAAT box. Expression of chloramphenicol acetyltransferase reporter fusions containing the putative promoter region was observed to occur in beta TC-3 mouse insulinoma cells but not in HepG2 human hepatoma cells, consistent with the known tissue-specific pattern of expression of the hPC2 gene. Analysis of the level of chloramphenicol acetyltransferase activity with several deletion mutants identified the region from -1100 to -539 from the translation start site as essential for hPC2 promoter activity.

Operative ultrasonography was performed during operations to improve the accuracy of diagnosing the extent of the spread of carcinoma of the stomach in the following areas: tumor invasion in the gastric wall (31 patients), para-aortic lymph node metastasis (30 patients) and hepatic metastasis (30 patients). The over-all diagnostic accuracy rates of operative ultrasonography were 81 per cent for determining the depth of tumor invasion, 80 per cent for carcinoma of the mucosa, 70 per cent for carcinoma of the submucosa, 83 per cent for carcinoma of the proper muscle, 80 per cent for carcinoma of the subserosa and 100 per cent for carcinoma of the extraserosa. The over-all accuracy of operative ultrasonography in diagnosing para-aortic lymph node metastasis was 93 per cent. In comparison with the results of preoperative studies, the accuracy (sensitivity) of operative ultrasonography was significantly superior in diagnosing metastasis to the lymph nodes. In three of 30 operations, preoperatively unrecognized and nonpalpable (occult) hepatic metastases were identified by operative ultrasonography. Operative ultrasonography provides more accurate information regarding the spread of carcinoma of the stomach, and thus may be helpful in deciding upon the type of surgical procedure or in avoiding unnecessary tissue dissection.

The relation between the patient's consciousness level and the change in electroencephalographic (EEG) activity during general anesthesia has not been well understood. In the present study, we evaluated such relationship quantitatively during the induction of high-dose fentanyl anesthesia in adult open-heart cases. There are significant increase in delta activity and significant decrease in alpha and beta activity in response to the induction of anesthesia. The loss of consciousness coincided with the sharp reduction in delta ratio and edge frequency (80%). Such reduction was more prominent in delta ratio than in edge frequency. These findings suggest that delta ratio could indicate the consciousness level during the induction of high-dose fentanyl anesthesia. Further study is needed to clarify the EEG response during inhalation and intravenous anesthesia in relation to EEG activity.

C5 convertase of the classical complement pathway is a protein complex consisting of C4b, C2a, and C3b. Within this complex C3b binds to C4b via an ester linkage. We now present evidence that the covalent C3b-binding site on human C4b is Ser at position 1217 of C4. We also show that formation of the covalently linked C4b.C3b complex occurs in the mouse complement system and that the C3b-binding site on mouse C4b is Ser at position 1213 which is homologous to Ser-1217 of human C4. Therefore, covalent binding of C3b to a single specific site on C4b within the classical pathway C5 convertase is likely a common phenomenon in the mammalian complement system. Specific noncovalent association of metastable C3b with C4b would occur first, leading to reaction of the thioester with a specific hydroxy group. This is supported by two lines of experimental evidence, one which shows that a mutant C4 that does not make a covalent linkage with C3b is still capable of forming C5 convertase and a second in which the C4b.C3b complex has been demonstrated by cross-linking erythrocytes bearing this C5 convertase.

Between 1970 and 1990, a total of 2,189 patients with gastric cancer underwent resection in the First Department of Surgery, Kurume University Hospital. Of these, 54 patients had previously undergone a partial gastrectomy. The time interval between the initial partial gastrectomy and the resection of the remnant-stump gastric cancer was more than 10 years in 25 patients and less than 10 years in 29 patients. Those with a time interval of more than 10 years we have termed remnant-stump cancer. The original pathology was a gastric ulcer in 13, a duodenal ulcer in 5, a gastric polyp in 1, and a gastric cancer in 6 patients. Of the 19 patients that had undergone an initial operation for benign disease (Group 1), 15 (79%) patients had received initial reconstruction by B-II and 4 (21%) by B-I. On the other hand, of the 6 patients with an initial operation for gastric cancer (Group 2), 3 (50%) had undergone reconstruction by B-I and the other 3 (50%) had received a B-II procedure. Twenty-three of 25 (92%) remnant-stump gastric cancers underwent total gastrectomy, while the other 2 (8%) were early remnant-stump cancers in the stoma and underwent partial gastrectomy. In group 1, only 5 out of 19 (26.3%) patients are alive, while in group 2 all 6 patients are alive, including the 2 (33.3%) early-stage cancers that were found through periodical endoscopic follow-up examinations.

MATURITY-ONSET diabetes of the young (MODY) is a form of non-insulin-dependent (type 2) diabetes mellitus (NIDDM) which is characterized by an early age at onset and an autosomal dominant mode of inheritance1. Except for these features, the clinical characteristics of patients with MODY are similar to those with the more common late-onset form(s) of NIDDM. Previously2 we observed tight linkage between DNA polymorphisms in the glucokinase gene on the short arm of chromosome 7 and NIDDM in a cohort of sixteen French families having MODY. Glucokinase is an enzyme that catalyses the formation of glucose-6-phosphate from glucose and may be involved in the regulation of insulin secretion and integration of hepatic intermediary metabolism3. Because the glucokinase gene was a candidate for the site of the genetic lesion in these families, we scanned this gene for mutations. Here we report the identification of a nonsense mutation in the gene encoding glucokinase and its linkage with early-onset diabetes in one family. To our knowledge, this result is the first evidence implicating a mutation in a gene involved in glucose metabolism in the pathogenesis of NIDDM.

The most difficult and important thing in dynamic design of structures subjected to impulsive loadings is to take into consideration of rate effects, especially unfavorable rate effects, for example brittlely rapid propagation of cracks in concrete which is newly found in experimental study. This paper deals with the rate effects on concrete and structural members and the study on the prediction of unfavorable rate effects on concrete.

CRE-BP1 is a transcriptional regulator binding to the cyclic AMP response element (CRE). To understand the role of CRE-BP1 in vivo, we studied the expression of the CRE-BP1 gene in monkey tissues including the central nervous system, in rat regenerating liver, and in human cancer tissues compared with normal tissues. The CRE-BP1 mRNA was detected in all tissues examined, and was fairly abundant in brain. The CRE-BP1 mRNA was expressed in monkey brain tissues with different region specificities. In the hippocampus, frontal lobe, and parietal lobe, the CRE-BP1 mRNA was abundant and two mRNA species 4.0 kb and 3.7 kb in length were expressed. In rat liver, the expression of the CRE-BP1 gene was increased up to 4- to 5-fold of the normal level within 12-24 h after partial hepatectomy. Furthermore, the levels of CRE-BP1 mRNA in some clinical samples of human tumors were apparently higher than that in normal tissues. These results suggest that CRE-BP1 may be important for both the signal transduction in brain and cellular proliferation.

The difference in the uptake rate through the lungs between nitrous oxide and oxygen has been shown to represent the pulmonary capillary blood flow (Qc). The pulsatility of Qc, defined as the ratio of maximum Qc and mean Qc (Qc max/Qc), the ratio of Qc max and stroke volume (Qc max/SV), and the ratio of systolic Qc and SV (Vsyst/SV), has been also shown to indicate the pulmonary vasodilation as well as vasoconstriction. We measured Qc by means of body plethysmography in dogs with pulmonary air embolism, in order to evaluate its effect on the pulmonary vasculature. Ten adult dogs were anesthetized with pentobarbital and pancuronium, and were mechanically ventilated. A volume of air (0.5 ml/kg) was injected into the central vein. Although there was no significant change in systemic blood pressure, cardiac output, heart rate, and airway pressure after the injection of air, pulmonary arterial pressure and pulmonary vascular resistance increased significantly. Qc, Qc max, Qc max/Qc, and Qc max/SV decreased significantly after the air injection. Since these findings suggest that the pulmonary air embolism provoked pulmonary vasoconstriction, and attenuated the pulsatility of Qc, optimal pulmonary vasodilation therapy would be recommended to improve the pulmonary hypertension secondary to pulmonary air embolism.

Publisher Summary This chapter presents an analysis of tachykinin peptide family gene expression patterns by combined high-performance liquid chromatography-radioimmunoassay (HPLC-RIA). The tachykinins are a family of structurally related peptides originally discovered on the basis of their smooth muscle contractile activity. It is now appreciated from peptide biochemical and molecular cloning experiments that the multiple tachykinin peptides are produced as a result of transcription of two specific genes, alternative precursor RNA splicing, and differential posttranslational processing of individual precursor proteins. The identification and quantitation of tachykinin peptides and an analysis of secretion of specific tachykinin peptides is essential to understanding the roles of these peptides as neurotransmitter or neuromodulatory substances. The chapter summarizes the strategies and methods used for the HPLC analysis of tachykinin peptides isolated from mammalian cell and tissue extracts. It focuses particularly on the analysis of the multiple neurokinin A-related peptides. The chapter also illustrates the precursor–product relationships of mammalian tachykinin precursors and the multiple tachykinin peptides.

This study was designed to clarify the mechanisms underlying the antihypertensive action of oral calcium supplementation in SHR. Four-week-old SHR and age-matched WKY were divided into calcium-supplemented and control groups. Calcium supplementation was carried out by giving 1.2% CaCl2 solution as drinking water ad libitum. Distilled water was given to the control group. After 3 weeks of treatment, plasma NE, pressor response to NE in isolated mesenteric artery, platelet cytosolic free calcium concentration and membrane fluidity of erythrocytes were evaluated. The elevation of blood pressure were retarded in calcium supplemented SHR. Calcium supplementation reduced the augmented pressor response to NE and the high level of cytosolic free calcium concentration in SHR. WKY showed no significant changes of these parameters by calcium supplementation. In conclusion, calcium supplementation reduces blood pressure through the reduction of sympathetic and vascular tone in SHR.

We report on the fabrication of highly uniform hexagonal nanopillars with single InGaAs/GaAs quantum wells (QW) on GaAs(111)B substrate by selective-area metal–organic vapour phase epitaxy. The standard size deviation of the fabricated nanopillars with single InGaAs/GaAs QW is about 2% and the standard deviation in their height about 5%. With a decrease in temperature, the peak position shifts to shorter wavelength, the peak intensity increases and the peak width decreases. The calculated well width based on the finite square potential well model taking account of the strain effect and the piezoelectric effect is smaller than the value determined from the growth rate and the growth time, which is mainly due to indium segregation and its incorporation into the subsequent GaAs layer grown at the higher temperature.

Hexagonal nanopillars with a single InGaAs/GaAs quantum well (QW) were fabricated on a GaAs (111) B substrate by selective-area metal-organic vapor phase epitaxy. The standard deviations in diameter and height of the nanopillars are about 2% and 5%, respectively. Zincblende structure and rotation twins were identified in both the GaAs and the InGaAs layers by electron diffraction. The excitation-power-density-dependent micro-photoluminescence (mu-PL) of the nanopillars was measured at 4.2, 50, 100 and 150 K. It was shown that, with increasing excitation power density, the mu-PL peak's positions shift to a higher energy, and their intensity and width increase, which were rationalized using a model that includes the effects of piezoelectricity, photon-screening and band-filling. It was also revealed that the rotation twins significantly reduce the diffusion length of the carriers in the nanopillars, compared to that in the regular semiconductors.

Serum levels of beta-Sm (a component of human seminal plasma) were measured in patients with breast cancer or mastopathy by RIA method. 9.4 +/- 9.5 ng/ml in control healthy adult women and 11.7 +/- 15.7 ng/ml in 8 patients with mastopathy were observed. Whereas, in 30 patients with breast cancer including 28 pre-operation and 2 recurrence 64.5 +/- 52.3 ng/ml were observed. Especially, high levels of beta-Sm (135.8 and 182.3 ng/ml) in the recurrence were detected. Each case of 8 post-operation was below 50 ng/ml. Fifty-seven percent of patients with breast cancer including pre-operation and recurrence were showed over 50 ng/ml. In histological typing, the beta-Sm levels of papillotubular carcinoma were higher than that of scirrhous carcinoma. In tubular carcinoma, 45% of stage I, 67% of stage II and 100% of stage III, IV and recurrence cases were over 50 ng/ml. The evidence suggests that serum levels of beta-Sm is useful for the diagnosis of breast cancer.

The present study was performed to evaluate postoperative hoarseness quantitatively by means of acoustic wave form analysis. Pitch and amplitude perturbation (PPQ, and APQ), and normalized noise energy (NNE) were measured along with the frequency characteristics in 51 adult patients undergoing elective surgery. The normal values for these acoustic parameters were less than 0.5%, less than 2.0%, and less than -10 dB, respectively. Vowel sound "E" was recorded and evaluated before the induction of anesthesia and on the morning of the day after the surgery. PPQ increased from 0.39% to 1.00% (P less than 0.05), APQ increased from 3.34% to 6.62% (P less than 0.05), and NNE increased from -9.19 dB to -4.74 dB (P less than 0.05). Eighteen percent of the patients showed abnormal values in all parameters preoperatively, but 45% of the patients postoperatively (P less than 0.05). These findings suggest that even the short term intubation resulted in the postoperative hoarseness, and this method is a useful and non-invasive bed-side test to evaluate postoperative hoarseness quantitatively.

A male case of Swyer-James syndrome, who had been followed for bronchiectasis for a long time, detected at age 70 and diagnosed by radiological studies was reported. The movement of his left diaphragm was impaired. Arterial oxygen tension was 68 torr while breathing room air. Pulmonary function tests showed mixed ventilatory impairment, increase of residual volume, and uneven gas distribution, but diffusing capacity was normal with the single breath method. Chest radiograph revealed hyperlucency of the left lung and the right middle lung field. In these areas, pulmonary angiography showed marked hypovascularity and diffuse vascular atrophy, and perfusion and inhalation scans also showed marked decreased perfusion and ventilation. Pulmonary hypertension was not detected by right heart catheterization. Fiberoptic bronchoscopy was performed and showed no abnormality of the left bronchial tree, and bronchography demonstrated diffuse cylindrical bronchiectasis of the left lung with no alveolar filling. He had suffered from chronic sinusitis for a long time, which might suggest that he had sinobronchitis due to congenital abnormality of the airway and this caused continuous respiratory infection, which could cause this syndrome. Including our own case, about 80 cases of Swyer-James' syndrome have been reported in Japan. But only 4 cases were above 70 years of age and all of them were male, and there has been no female cases above age 50. Males predominate over females, and in both sexes the left lung was more commonly affected than the right.

A 59-year-old female was admitted to our institute with coughing. A primary tumor of the diaphragm was suspected by chest X-ray, CT and angiograms preoperatively. Intraoperative findings also suggested a large primary tumor in the diaphragm with invasion to the lung, pericardium and liver. Therefore, we performed partial resection of the diaphragm, lung, pericardium and liver all together through a right thoraco-abdominal approach and the diaphragm was reconstructed using polyglycolic acid mesh. Histologically, the large tumor located mainly in the diaphragm was sarcomatous, with transposition from the carcinomatous cells to the sarcomatous cells. A large cell tumor of the lung was also confirmed. Immunohistologically, the diaphragm tumor was positively stained by keratin and by epithelial membrane antigen. In addition, desmosomes were demonstrated under electron microscopy studies. The tumor of this case was sarcoma in the diaphragm developed from a minor large cell tumor in the lung. Though commonly thought difficult to prove sarcomatous change development from large cell tumor in the lung, we were able to determine this clearly with immunohistology and electron microscopy.

In order to clarify the surgical aspects for parasternal lymphnode dissection to improve prognosis in patients with breast cancer, we have retrospectively investigated a total of 319 patients with breast cancer who underwent radical mastectomy with parasternal lymphnode dissection. During the 13 years from 1974 to 1986, 418 patients with breast cancer underwent radical mastectomy. Of these, 319 underwent combined dissection of the parasternal lymphnodes. Among these 319 cases, 36 (11.3%) showed pathologically-confirmed positive lymphnode metastasis. In those cases involving a tumor of diameter greater than 5 cm and more than 4 positive metastatic axillar lymphnodes, then the positive parasternal lymphnode metastasis was higher than 30%. The 5-year survival rate was 88.9% for negative parasternal lymphnode metastasis and 44.7% for positive cases (p less than 0.01 logrank test). The standard adjuvant chemotherapy, chemo-endocrine therapy and radiation therapy, each did not significantly affect or improve prognosis. We conclude that parasternal lymphnode positivity is an important factor in radical mastectomy affecting prognosis and a more powerful adjuvant chemotherapy must be developed to improve prognosis.

1) Aggregates of eosinophils closely related to the enlarged endothelial cells in the capillary vessels were recognized in 64% of 28 cases in biopsied specimens of the major bronchus of patients with sarcoidosis. 2) Electron microscopy revealed the vacuolated central cores or matrix in the specific granules of the eosinophils adjacent to the swollen vascular endothelial cells, frequent findings with attachment of the blood platelets to the damaged plasma membrane of the endothelial cells eventually becoming occluded in the lumen with platelet thrombosis, and multilayer formation of the basement membrane of the capillary vessels. 3) Sarcoidosis is suggested to be a pathological process producing both granuloma formation in each organ and vascular endothelial cell changes in the capillary vessels accompanied by aggregation of eosinophils in some periods of the disease process due to unidentified etiological factors.

The oxidation of glucose represents a major source of metabolic energy for mammaliancells. However, because the plasma membrane is impermeable to polar molecules such as glucose, the cellular uptake of this important nutrient is accomplished by membrane-associated carrier proteins that bind and transfer it across the lipid bilayer. Two classes of glucose carriers have been described in mammalian cells: the Na+-glucose cotransporter and the facilitative glucose transporter. The Na+-glucose cotransporter transports glucose against its concentration gradient by coupling its uptake with the uptake of Na+ that is being transported down its concentration gradient. Facilitative glucose c rriers accelerate the transport of glucose down its concentration gradient by facilitative diffusion, a form of passive transport. cDNAs have been isolated from human tissues encoding a Na+-glucose-cotransporter protein and five functional facilitative glucosetransporter isoforms. The Na+-glucose cotransporter is expressed by absorptive epithelial cells of the small intestine and is involved in the dietary uptake of glucose. The same or a related protein may be responsible for the reabsorption of glucose by the kidney. Facilitative glucose carriers are expressed by most if not all cells. The facilitative glucose-transporter isoforms have distinct tissue distributions and biochemical properties and contribute to the precise disposal of glucose under varying physiological conditions. The GLUT1 (erythrocyte) and GLUT3 (brain) facilitative glucose-transporter isoforms may be responsible for basal or constitutive glucose uptake. The GLUT2 (liver) isoform mediates the bidirectional transport of glucose by the hepatocyte and is responsible, at least in part, for the movement of glucose out of absorptive epithelial cells into the circulation in the small intestine and kidney. This isoform may also comprise part of the glucosesensing mechanism of the insulin-producing β-cell. The subcellular localization of the GLUT4 (muscle/fat) isoform changes in response to insulin, and this isoform is responsible for most of the insulin-stimulated uptake of glucose that occurs in muscle and adipose tissue. The GLLJT5 (small intestine) facilitative glucose-transporter isoform is expressed at highest levels in the small intestine and may be involved in the transcellular transport of glucose by absorptive epithelial cells. The exon-intron organizations of the human GLUT1, GLUT2, and GLUT4 genes have been determined. In addition, the chromosomal locations of the genes encoding the Na+-dependent and facilitative glucose carriers have been determined. Restriction-fragment-length polymorphisms have also been identified at several of these loci. The isolation and characterization of cDNAs and genes for these glucose transporters will facilitate studies of their role in the pathogenesis of disorders characterized by abnormal glucose transport, including diabetes mellitus, the glucose-galactose malabsorption syndrome, and benign renal glycosuria.

The authors report the fabrication of the nanopillars with single InGaAs∕GaAs quantum well by selective-area metal organic vapor phase epitaxy. The standard diameter deviation of the nanopillars is about 8% and the standard deviation in their height about 5%. Their photoluminescence peak positions shift to the longer wavelength with an increase in the diameter of the nanopillars, which is not due to the quantum confinement effect in the radial or axial direction but due to the stoichiometry difference of the indium content in the nanopillars with different diameters.

Somatostatin is a 14-amino-acid polypeptide that is widely distributed throughout the central nervous system and peripheral tissues. It potently inhibits basal and stimulated secretion from a wide variety of endocrine and exocrine cells and functions as a neurotransmitter/neuromodulator in the central nervous system with effects on locomotor activity and cognitive function. Somatostatin also has antiproliferative effects and may be an important hormonal regulator of cell proliferation and differentiation. Recent studies have shown that the physiological effects of somatostatin are mediated by a family of somatostatin receptors. They are all predicted to be membrane glycoproteins with seven {alpha}-helical membrane-spanning regions and members of the G-protein-coupled receptor superfamily. The receptors have been named, chronologically, sst{sub 1}, sst{sub 2}, and sst{sub 3}. However, the sequence of a fourth subtype was determined simultaneously by two different groups, and sst{sub 4} was assigned to two proteins of different sequence and functional properties. The nomenclature of these two proteins has been resolved, with the sst{sub 4} and the sst{sub 5} receptors denoting the proteins cloned by Bruno et. al. and O`Carroll et. al., respectively. 9 refs., 1 fig.

Using the cloned mouse kappa opioid receptor cDNA clone as a probe, screened a human genomic library and isolated a clone containing part of the human kappa opioid receptor gene (OPRK1), designated [lambda]hSR4-1. To determine the chromosomal localization of OPRK1, [lambda]hSR4-1 DNA was labeled with biotin by nick-translation in the presence of bio-11-dUTP and hybridized to human metaphase cells prepared from phytohemagglutinin-stimulated peripheral blood lymphocytes as described previously. Hybridization of the OPRK1-specific probe [lambda]hSR4-1 DNA to normal human metaphase chromosomes resulted in specific labeling only of chromosome 8. Specific labeling of 8q11 was observed on all 4 (6 cells), 3 (9 cells), 2 (9 cells), or 1 (1 cell) chromatid of the chromosome 8 homologs in 25 cells examined. Of 72 signals observed, 70 were located at 8q11. 1 signal was located at 7q11 and at 12p11. In most cells, the signal on 8q was located at 8q11.2. 7 refs., 1 fig.

Ossification of the posterior longitudinal ligament of the spine (OPLL) is characterized by ectopic ossification in the spinal ligaments leading to a various degree of myelopathy by a compression of the spinal cord. OPLL is commonly observed among Japanese and throughout other Asian populations. The incidence of OPLL in the general Japanese population was reported to be 1.9 - 4.3% over 30 years of age. Although its etiology is thought to involve a multiplicity of factors, epidemiological and family studies strongly implicate genetic susceptibility in the pathogenesis of OPLL. The disease has a substantial genetic component, a risk in siblings compared to general population risk (λs) of 10. Previously, we have reported of suggestive evidence of linkage to a candidate gene, collagen 11A2, where only a candidate region (HLA region at 6p21.3) was tested for linkage. To define the genetic causalities of OPLL in more extensive manner, we performed a genome-wide scan with 138 affected sib-pairs. Non-parametric linkage analysis was performed with affected sib-pairs by the use of two different programs. Identical by descent (IBD) was tested for possible linkage with SIBPAL from S.A.G.E. package (single point analysis). Multipoint affected sib-pairs linkage analysis was performed using GENEHUNTER. We found that five principal loci of possible linkage were identified on chromosome 1, 6, 13. 16, 21 (p < 0.01) And the most significant evidence of linkage was observed with D21S263 at chromosome 21q (P=0.000009). Multipoint linkage analysis revealed that the peak linkage was also located close to D21S263 (maximum lod score = 3.4). These mapping results could be an important step towards identifying susceptible genes for OPLL.