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De-identification is a process to prevent individuals from being identified from original transaction data by processing personal identification information. k-anonymization, which processes data so that at least kusers have the same records, is one of the representative methods of de-identification. One of the methods of k-anonymization is adding dummy records into the data to protect users who have unique histories. For this method, the cost for k-anonymization is the difference in the number of records between the original data and the processed data, and it can be calculated only after deciding the parameter kand processing data. However, we want to calculate the cost before processing and find the optimal value of kbecause processing the big data with various kis very costly. In this paper, we propose a new model of transaction data that gives us a probability distribution and an expected value of values in data under the assumption that all values occur independently with uniform probability. Applying our data model, it is possible to evaluate the cost of k-anonymized data even before processing.

De-identification is a process to prevent individuals from being identified from original transaction data by processing personal identification information. For de-identifying data, we should consider the risk of attackers that try to infer personal information from given de-identified datasets. However, the characteristics of attackers are not known. Attackers could find the weakest records to identify the user who owns them. In the case of big data, there are too many attributes to identify the weakest parts to be protected. To address these issues, we propose a new model of attackers that gain background knowledge from an attribute of the transaction data and estimate the risk of re-identification from the statistics of the dataset, such as the number of records and the background number of users. We present empirical results on evaluating the risks of actual transaction data using our proposed risk model.

In this study, we have attempted to realize different magnetic anisotropy locally on the same substrate, i.e., different directions of the easy axis in each area by combining simple Joule heating (J. H.) and the application of a magnetic field with permanent magnets. Orthogonal arranged thin-film magnetoimpedance elements were fabricated on the same substrate, and the easy axis was successfully induced parallel to the width direction of each element, respectively. Each element shows the double-peak impedance profiles after J. H. which is important to obtain a higher sensitive magnetic field sensor. The results enable local anisotropy control, which has been difficult to realize previously and contribute to the integration of multifunctional thin-film magnetic devices on a substrate.

The regulation of cyclic adenosine monophosphate (cAMP) levels in kidney epithelial cells is important in at least 2 groups of disorders, namely water balance disorders and autosomal dominant polycystic kidney disease. Focusing on the latter, we review genes that code for proteins that are determinants of cAMP levels in cells. We identify which of these determinants are expressed in the 14 kidney tubule segments using recently published RNA-sequencing and protein mass spectrometry data (“autosomal dominant polycystic kidney disease-omics”). This includes G protein–coupled receptors, adenylyl cyclases, cyclic nucleotide phosphodiesterases, cAMP transporters, cAMP-binding proteins, regulator of G protein–signaling proteins, G protein–coupled receptor kinases, arrestins, calcium transporters, and calcium-binding proteins. In addition, compartmentalized cAMP signaling in the primary cilium is discussed, and a specialized database of the proteome of the primary cilium of cultured “IMCD3” cells is provided as an online resource (https://esbl.nhlbi.nih.gov/Databases/CiliumProteome/). Overall, this article provides a general resource in the form of a curated list of proteins likely to play roles in determination of cAMP levels in kidney epithelial cells and, therefore, likely to be determinants of progression of autosomal dominant polycystic kidney disease.

Excellent magnetic features make Co-based materials promising candidates as high-performance microwave absorbers. However, it is still a significant challenge for Co-based absorbers to possess high-intensity and broadband absorption simultaneously, owing to the lack of dielectric loss and impedance matching. Herein, microporous Co@C nanoparticles (NPs) with carbon shell thicknesses ranging from 1.8–4.9 nm have been successfully synthesized by dealloying CoAl@C precursors. All of the samples exhibit high microwave absorption performance. The microporous Co@C sample possessing a carbon shell of 1.8 nm exhibits the highest absorption intensity among these samples with a minimum reflection loss (RL) of −141.1 dB, whose absorption bandwidth for RL ≤ −10 dB is 7.3 GHz. As the thickness of the carbon shell increases, the absorption bandwidth of the NPs becomes wider. For the sample with the carbon shell thickness of 4.9 nm, the absorption bandwidth for RL ≤ −10 dB reaches a record high of 13.2 GHz. The outstanding microwave attenuation properties are attributed to the dielectric loss of the carbon shell, the magnetic loss of the Co core, and the cooperation of the core–shell structure and microporous morphology. The strong wideband microwave absorption of the carbon-coated microporous Co NPs highlights their potential applications in microwave absorbing systems.

The inappropriate over-activation of the with-no-lysine kinase (WNK)–STE20/SPS1–related proline/alanine-rich kinase (SPAK)–sodium chloride cotransporter (NCC) phosphorylation cascade increases sodium reabsorption in distal kidney nephrons, resulting in salt-sensitive hypertension. Although chronic kidney disease (CKD) is a common cause of salt-sensitive hypertension, the involvement of the WNK phosphorylation cascade is unknown. Moreover, the effect of immune systems on WNK kinases has not been investigated despite the fact that immune systems are important for salt sensitivity. Here we demonstrate that the protein abundance of WNK1, but not of WNK4, was increased at the distal convoluted tubules in the aristolochic acid nephropathy mouse model of CKD. Accordingly, the phosphorylation of both SPAK and NCC was also increased. Moreover, a high-salt diet did not adequately suppress activation of the WNK1–SPAK–NCC phosphorylation cascade in this model, leading to salt-sensitive hypertension. WNK1 also was increased in adenine nephropathy, but not in subtotal nephrectomy, models of CKD. By comparing the transcripts of these three models focusing on immune systems, we hypothesized that tumor necrosis factor (TNF)-α regulates WNK1 protein expression. In fact, TNF-α increased WNK1 protein expression in cultured renal tubular cells by reducing the transcription and protein levels of NEDD4-2 E3-ligase, which degrades WNK1 protein. Furthermore, the TNF-α inhibitor etanercept reversed the reduction of NEDD4-2 expression and upregulation of the WNK1–SPAK–NCC phosphorylation cascade in distal convoluted tubules in vivoin the aristolochic acid nephropathy model. Thus, salt-sensitive hypertension is induced in CKD via activation of the renal WNK1– SPAK–NCC phosphorylation cascade by TNF-α, reflecting a link with the immune system.

The kidneys consume a large amount of energy to regulate volume status and blood pressure and to excrete uremic toxins. The identification of factors that cause energy mismatch in the setting of chronic kidney disease (CKD) and the development of interventions aimed at improving this mismatch are key research imperatives. Although the critical cellular energy sensor 5′-adenosine monophosphate (AMP)-activated protein kinase (AMPK) is known to be inactivated in CKD, the mechanism of AMPK dysregulation is unknown. In a mouse model of CKD, metabolome analysis confirmed a decrease in AMPK activation in the kidneys despite a high AMP: ATP ratio, suggesting that AMPK did not sense energy depletion. Similar AMPK inactivation was found in heart and skeletal muscle in CKD mice. Several uremic factors were shown to inactivate AMPK in vitroand in ex vivopreparations of kidney tissue. The specific AMPK activator A-769662, which bypasses the AMP sensing mechanism, ameliorated fibrosis and improved energy status in the kidneys of CKD mice, whereas an AMP analog did not. We further demonstrated that a low-protein diet activated AMPK independent of the AMP sensing mechanism, leading to improvement in energy metabolism and kidney fibrosis. These results suggest that a failure to sense AMP is the key mechanism underlying the vicious cycle of energy depletion and CKD progression and direct AMPK activation may be a novel therapeutic approach in CKD.

This article describes how after the concept of anonymous credential systems was introduced in 1985, a number of similar systems have been proposed. However, these systems use zero-knowledge protocols to authenticate users, resulting in inefficient authentication during the stage of proving credential possession. To overcome this drawback, this article presents a signature scheme that uses partially blind signatures and chameleon hash functions such that both the prover and verifier achieve efficient authentication. In addition to providing a computational cost comparison table showing that the proposed signature scheme achieves a more efficient credential possession proving compared to other schemes, concrete security proofs are provided under a random oracle model to demonstrate that the proposed scheme satisfies the properties of anonymous credentials.

Circadian variability in kidney function is well recognized but is often ignored as a potential confounding variable in physiological experiments. Here, we have created a data resource consisting of expression levels for mRNA transcripts in microdissected proximal tubule segments from mice as a function of the time of day. Small-sample RNA-sequencing (RNA-seq) was applied to microdissected S1 proximal convoluted tubules (PCTs) and S2 proximal straight tubules (PSTs). After stringent filtering, the data were analyzed using JTK-Cycle to detect periodicity. The dataset is provided as a user-friendly webpage at https://esbl.nhlbi.nih.gov/Databases/Circadian-Prox2/. In PCTs, 234 transcripts varied in a circadian manner (4.0 % of total). In PSTs, 334 transcripts varied in a circadian manner (5.3 %). Transcripts previously known to be associated with corticosteroid action and with increased flow were found to be overrepresented among circadian transcripts peaking during the "dark" portion of the day (Zeitgeber Time [ZT] 14-22), corresponding to the peak levels of corticosterone and glomerular filtration rate in mice. To ask whether there is time-of-day dependence of protein abundances in the kidney, we carried out LC-MS/MS-based proteomics in whole mouse kidneys at ZT12 and ZT0. The full data set (n=6546 proteins) is available at https://esbl.nhlbi.nih.gov/Databases/Circadian-Proteome/. Overall, 293 proteins were differentially expressed between ZT12 and ZT0 (197 greater at ZT12; 96 greater at ZT0). Among the regulated proteins, only 9 had been found to be periodic in the RNA-seq analysis, suggesting a high level of post-transcriptional regulation of protein abundances.

The purpose of this study was to generate more concise rule extraction from the Recursive-Rule Extraction (Re-RX) algorithm by replacing the C4.5 program currently employed in Re-RX with the J48graft algorithm. Experiments were subsequently conducted to determine rules for six different two-class mixed datasets having discrete and continuous attributes and to compare the resulting accuracy, comprehensibility and conciseness. When working with the CARD1, CARD2, CARD3, German, Bene1 and Bene2 datasets, Re-RX with J48graft provided more concise rules than the original Re-RX algorithm. The use of Re-RX with J48graft resulted in 43.2%, 37% and 21% reductions in rules in the case of the German, Bene1 and Bene2 datasets compared to Re-RX. Furthermore, the Re-RX with J48graft showed 8.87% better accuracy than the Re-RX algorithm for the German dataset. These results confirm that the application of Re-RX in conjunction with J48graft has the capacity to facilitate migration from existing data systems toward new concise analytic systems and Big Data.

Increasing the number of business operators using anonymously processed information is a critical privacy topic in Japan. To promote the use of the information, an “anonymization dictionary” is proposed and implemented. The dictionary is the system that shares use-cases regarding the manner by which business operators produce and provide anonymously processed information. To develop this system, two technical difficulties are resolved: the lack of (i) a method to acquire the use-cases and (ii) a data structure to store the use-cases. In terms of (i), disclosed statements that specify the production and provisioning processes for anonymously processed information is focused. To recognize the statements described in the business operators’ webpages as the use-cases, a web crawler that acquires the statements is developed. The crawler acquires 331 use-cases (statements) in a short duration. In terms of (ii), to define a concrete data structure to store anonymously processed information use-cases, the structure of the use-cases acquired is analyzed. The use-cases are stored into the structure and then in the DB of the dictionary application. This enables a search function to be provided for identifying the necessary use-cases and organizing use-cases in a readable form to the business operators.

Vasopressin controls renal water excretion through actions to regulate aquaporin-2 (AQP2) trafficking, transcription and degradation. These actions are in part dependent on vasopressin-induced phosphorylation changes in collecting duct cells. Although most efforts have focused on phosphorylation of AQP2 itself, phosphoproteomic studies have identified many vasopressin-regulated phosphorylation sites in proteins other than AQP2. The goal of this bioinformatics-based review is to create a compendium of vasopressin-regulated phosphorylation sites with focus on those that are seen in both native rat inner medullary collecting ducts and cultured collecting duct cells from mouse (mpkCCD), arguing that these sites are the best candidates for roles in AQP2 regulation. This analysis identified 51 vasopressin-regulated phosphorylation sites in 45 proteins. We provide resource web pages at https://esbl.nhlbi.nih.gov/Databases/AVP-Phos/ and https://esbl.nhlbi.nih.gov/AVP-Network/, listing the phosphorylation sites and describing annotated functions of each of the vasopressin-targeted phosphoproteins. Among these sites are 23 consensus protein kinase A (PKA) sites that are increased in response to vasopressin, consistent with a central role for PKA in vasopressin signaling. The remaining sites are predicted to be phosphorylated by other kinases, most notably ERK1/2 which accounts for decreased phosphorylation at sites with a X-p(S/T)-P-X motif. Additional protein kinases that undergo vasopressin-induced changes in phosphorylation are Camkk2, Cdk18, Erbb3, Mink1 and Src, which also may be activated directly or indirectly by PKA. The regulated phosphoproteins are mapped to processes that hypothetically can account for vasopressin-mediated control of AQP2 trafficking, cytoskeletal alterations, and Aqp2 gene expression, providing grist for future studies.

We study the existence and stability of standing wave for the Schrödinger-Poisson-Slater equation in three dimensional space. Let p be the exponent of the nonlinear term. Then we first show that standing wave exists for 1 < p < 5. Next, we show that when 1 < p < 7/3 and p ≠ 2, standing wave is stable for some ω > 0. We also show that when 7/3 < p < 5, standing wave is unstable for some ω > 0. Furthermore, we investigate the case of p = 2. We prove these results by using variational methods.

SUMMARYThis study evaluated the efficacy of adding pioglitazone 30 mg to the therapy of patients with type 2 diabetes mellitus whose glycaemic control was poor on an α-glucosidase inhibitor (α-GI) alone or in combination with a sulphonylurea (SU).The patients (n  20) had a HbA1c level between 7.0 and 12.0 and the fasting plasma glucose was 7.8 mmol l−1or higher. They were treated with 30 mg pioglitazone once daily for 16 weeks.The decrease in HbA1c at week 16 of treatment was 0.8 (7.8 at baseline dropping to 7.1 at week 16; p < 0.01). An increase in leptin was observed 4 weeks after starting the post-study period (p < 0.05). Tumour necrosis factor-α (TNF-α) and body fat percentage did not show anysignificant alterations. Correlations between the decrease in HbA1c at week 16 and characteristic variables of patients were examined. A correlation with leptin (p  −0.5632, p < 0.05) levels was found. Five patients experienced adverse drug reactions, such as oedema, hypoglycaemia and increased creatine phosphokinase (CK), all of which were mild in severity.The addition of pioglitazone in diabetics whose glycaemic control was poor on a α-GI alone or with a α-GI and SU combination resulted in a significant decrease in HbA1c, and the treatment was well-tolerated. Our findings also suggest that leptin levels could be useful for assessing responders to pioglitazone.

Abstract:: The efficacy and safety of microwave coagulation therapy (MCT) in patients with hepatocellular carcinoma (HCC) and impaired hepatic reserve were studied. Preoperative background factors, postoperative results, and prognostic factors were compared in 51 patients who underwent hepatic resection (HR group) and 38 patients who underwent microwave coagulation therapy (MCT group). Before surgery, measures of hepatic function, including level of albumin (P = 0.0072), prothrombin time (P < 0.0001), hepaplastin test (P = 0.0088), and the radioactivity of technetium-99m galactosyl-human serum albumin 15 min in the liver after injection divided by that in both liver and heart (P < 0.0001) were significantly lower in the MCT group than in the HR group. The indocyanine green dye retention rate at 15 min was significantly greater (P < 0.0001) in the MCT group than in the HR group, and a significant difference was noted in Child-Pugh grade between the groups (P < 0.0001). Operative time (P = 0.0014) and blood loss during surgery (P = 0.0005) were significantly lower in the MCT group than in the HR group. In contrast, no significant differences were recognized between the groups in the changes in postoperative liver function, or in the rates of morbidity, mortality, local recurrence, and survival. Moreover, the type of treatment (HR or MCT) was not a prognostic factor. The results indicate that MCT can be used safely as an alternative to hepatic resection in patients with poor liver function without reducing the efficacy of local control.

Abstract: We investigated the antibacterial activity of 12 antibiotics, including 4 carbapenems, against 200 strains of respiratory pathogens isolated in 1997, and compared the results with those obtained in 1993. The strains examined were 38 strains of methicillin-susceptible Staphylococcus aureus (MSSA), 32 strains of methicillin-resistant S. aureus (MRSA), 22 strains of penicillin-susceptible Streptococcus pneumoniae (PSSP), 10 strains of penicillin-resistant S. pneumoniae (PRSP), 53 strains of Pseudomonas aeruginosa, 19 strains of Moraxella catarrhalis, and 26 strains of Haemophilus influenzae. In 1993, 100 strains were examined. The minimal inhibitory concentration data of the present study showed that imipenem and panipenem were more active than the other agents against gram-positive bacteria, and that meropenem and biapenem were more active than the other agents against gram-negative bacteria. By comparing these results with those obtained in 1993, it was found that increase of resistance to carbapenem antibiotics was not observed against all the strains tested in this study. Thus, it can be stated that carbapenem antibiotics retain their position as the drug of first choice for severe infections.

A molecular dynamics (MD) trajectory of 1.0 ns duration has been computed for a methyl-terminated atactic poly(ethyl acrylate) using force field parameters which we determined by ab initio molecular-orbital calculations for small molecules (RHF/6-31G level). Local side chain motions were clarified by analyses of the MD trajectory. The torsional angle autocorrelation functions (TACF) were calculated for each dihedral angle in the side chain. All of the TACF were strongly non-exponential. The entire side chain rotation was an asymmetric 180° jump motion with a rapid torsional oscillation within stable and metastable conformations, while ethyl group motion around the O(non-carbonyl)–CH2bond in the side chain was characterized by rapid torsional motion in the angle range from 60 to 300°involving an obscure three-site jump motion.

Cultured HL‐60, HeLa S3 and WiDr cells grown in male BALB/c nu/numice were studied by conventional and field‐inversion DNA gel electrophoresis (FIGE), as well as by means of cytomorphological approaches, including TdT‐mediated dUTP nick end labeling (TUNEL) assay. Chemosensitivity tests revealed HL‐60 to be sensitive to vindesine (VDS), and HeLa S3 and WiDr to mitomycin C (MMC). Although VDS‐treated HL‐60 exhibited condensation of chromatin and a DNA ladder, MMC‐exposed HL‐60 cells showed apoptotic figures without typical DNA ladders. With MMC‐treated WiDr cells, neither DNA ladders nor apoptotic figures were observed. Cells characterized by chromatin condensation were TUNEL‐positive in both treated and untreated cases with the exception of the MMC‐treated WiDr case, in which many TUNEL‐positive cells were observed without cytomorphological changes. On FIGE, DNA fragments of approximately 50, 300 and 400 kbp were detected in groups treated with both effective and ineffective drugs, as well as in untreated controls. Furthermore, change of the time parameters in FIGE resulted in different sizes (550 and 850 kbp) of DNA fragments. These findings indicate that i) cell death is not always detectable in terms of apoptotic figures or DNA oligonucleosomal fragmentation, ii) only the TUNEL assay is a reliable tool to detect DNA damage and, iii) FIGE does not provide accurate size profiles of macromolecular DNA fragments.

Fecal bile acid and fecal fat were determined in 18 normal subjects and 22 patients with chronic pancreatitis, and the relation of fecal bile acid excretion to exocrine pancreatic dysfunction was studied. In chronic pancreatitis fecal bile acid was approximately three times that of control subjects, and large amounts of primary bile acid were detected. A significant correlation between fecal bile acid excretion and bicarbonate secreted from the pancreas was found. This evidence of bile acid malabsorption was not observed until bicarbonate output was ∼0.05 mEq/h/kg. A slight correlation between fecal bile acid and absorption rates of fat was demonstrated. These results suggest that bile acid malabsorption observed in chronic pancreatitis is related to an impairment of pancreatic bicarbonate secretion.

A new technique for immobilizing enzyme molecules on magnetite particles via the graft polymerization of acrylic acid is presented. The polymerization of acrylic acid was carried out in a redox system consisting of ceric ion and mercapto groups introduced onto magnetite particles. In the course of the polymerization, poly(acrylic acid) was attached to the magnetite particles. Glucose oxidase was covalently immobilized on the magnetite particles by the condensation reaction with the carboxyl groups of the poly(acrylic acid). It was shown that 2.8 mg of glucose oxidase was immobilized on 1 g of the magnetite attached with poly(acrylic acid), and the immobilized glucose oxidase had a specific activity of 81 units/mg, which was 50% of that of the native enzyme. Due to the immobilization, the optimum pH for glucose oxidase was shifted to a higher value and the temperature dependency of activity was diminished. A kinetic study of the glucose oxidation reaction with immobilized enzyme showed that the immobilization limited accessibility of glucose molecules to the active sites of the enzyme and caused a decrease of the maximum reaction rate. Glucose oxidas immobilized on magnetite particles kept 95% of its original activity in water over a period of 9 months.

A determination of caloric consumption based on a dietary survey table, fat and cholesterol intake, and analyses of fecal fatty acids and neutral sterols, and bile acid analysis (gas chromatographic method) were conducted on 33 subjects (including 17 patients with chronic pancreatitis and 16 normal controls). The factors related to hypocholesterolemia in chronic pancreatitis (CP) patients were investigated and the following conclusions were obtained: (1) The total caloric intake and fat consumption by the CP patients were significantly lower with the exception of cholesterol consumption. (2) Significant increases were noted in fecals fat, neutral sterols, and bile acid excretion by the CP patients. (3) A significant positive correlation was noted between the total cholesterol and body mass index (BMI), reaffirming that the cholesterol level can be used as an indicator of nutritional status. (4) A significant negative correlation was noted between the serum total cholesterol and fecal bile acid excretion. These findings indicate that CP patients suffer from neutral sterol malabsorption, in addition to dietary fat maldigestion and bile acid malabsorption. Furthermore, bile acid malabsorption is cited as a factor in the development of hypocholesterolemia in CP patients.

Abstract: Background: The purpose of this study was to determine whether micropore formation caused by application of an electric current can increase the influx of anticancer drugs across cancer cell membranes with a concomitant increase in dose intensity and, therefore, toxicity to cancer cells. Methods: Two cell lines, GCIY and KATO III, both established from human gastric cancers, were used as target cells to assess the effects of combining electroporation and anticancer drug therapy. Results were measured as the proliferation of cells to 50% of the value in control mice (IC50). Results: When GCIY cells were used as targets in vitro, the IC50 value for bleomycin was decreased significantly by the electroporation, to 10−4 of the dose for the chemotherapeutic agent alone, and the IC50 values of cisplatin and 5-fluorouracil were decreased to one tenth of their baseline values. In the case of KATO III cells, the IC50 value for bleomycin was reduced by 10−2, but that of cisplatin did not change. The IC50 value for doxorubicin did not change when GCIY cells, showing multidrug resistance, or when KATO III cells, lacking multidrug resistance, were subjected to electroporation. When GCIY cells were transplanted subcutaneously into nude mice, the resultant tumors decreased to a minimum size at 2 weeks after combined treatment with bleomycin and electroporation. Conclusion: Electroporation seems to be a promising adjunct to cancer chemotherapy.

The study was conducted on five healthy subjects and six patients with calcifying pancreatitis (CP) and steatorrhea. Following overnight fasting, one tube each was placed in the stomach and the upper part of the small intestine, respectively. Through the gastric tube, a test meal that included 30 g of fat (total calories, 625 kcal, 500 mL) was infused over a span of 30 min. Every 30 min (up to 150 min), fluid samples in the upper small intestine were collected and chilled, and the amylase, trypsin, and lipase levels were determined. In addition, in the case of the CP patients, a high-potency pancreatin preparation was infused into the stomach together with the test meal. In order to determine the plasma CCK level, blood sample were collected before test meal infusion and at 10, 20, 30, 45, 60, 90, 120, and 150 min subsequent to infusion. The plasma CCK was extracted using a Sep-Pak C-18 cartridge and analyzed with radioimmunoassay using an OAL-656 antibody. The result was converted to the CCK-8 level and expressed in pg/mL. The enzyme activities in the upper small intestine of the CP patients after test meal administration amounted to 22.8 (amylase), 10.8 (trypsin), and 16.9% (lipase) compared with the corresponding figures for the normal subjects. Following administration of a high-potency pancreatin in patients with CP, enzyme activities in the upper small intestine increased to 132.2 (amylase), 38.7 (trypsin), and 45.3% (lipase) compared with levels in the normal subjects. However, the healthy subjects and the CP patients, both with and without treatment with supplementary exogenous enzymes, all exhibited similar profiles in the plasma CCK response to stimuli. Based on these findings, we concluded that a negative feedback mechanism does not exist between the tryptic activity of the upper small intestine and the CCK secretory response in patients with chronic pancreatitis.

Conclusions: Steatorrhea was almost completely stopped and malabsorption of neutral sterols and shortchain fatty acids was reduced by treatment of high-lipase pancreatin in Japanese patients with pancreatic insufficiency whose dietary fat consumption is low. Methods: Fifteen patients with chronic pancreatitis complicated by steatorrhea who consumed an average of 48 g of dietary fats a day were selected as subjects and given 3 g of high-lipase pancreatin (lipase, 379,800 USP U/g), at each meal (total daily dose is 9 g) for a mean duration of 28.5 d. Fecal output and fecal fat neutral sterol, bile acid, and short-chain fatty acid excretion were determined before and after the course of pancreatin therapy. Results: Pancreatin administration resulted in significant reductions (P&lt;0.01) in fecal output (from 243.2 to 149.1 g), excretion of fecal fat, (from 12.3 to 3.9 g), animal sterols (from 816.3 to 604.6 mg), and shortchain fatty acids (from 52.6 to 18.5 mM). In contrast, no marked changes were recorded in fecal excretion of ß-sitosterol (a plant sterol), bile acids, or the hydroxy fatty acid fraction. Fecal fat and short-chain fatty-acid excretion showed strong correlations with fecal output.

Cultured HL‐60, HeLa S3 and WiDr cells were treated with various doses of ethanol, then subjected to flow cytometry and gel electrophoresis of cellular DNA. On electrophoresis of DNA from HL‐60 cells treated with 0.5 or 1.0 mM ethanol, a ladder pattern was recognized after 3 h. At higher doses of ethanol (2.0 and 5.0 mM), a smear pattern resulted. On flow cytometry, however, A0cells (lower fluorescence level than G0+ G1cells) were noted from 0.5 to 5,0 mMethanol. The observation of A0cells at higher doses indicated loss of DNA after random DNA degradation. HeLa S3 and WiDr cells were partially detached from flasks after administration of ethanol and separated into adherent and non‐adherent categories. In DNA from non‐adherent HeLa S3 cells treated with 0.5 mMethanol, a ladder pattern was observed after 24 h. On flow cytometry, prior to the appearance of A0cells, an accumulation in the G2+M‐phase became obvious after 3 h. Increased mitotic indices indicated that this phenomenon was due to M‐phase arrest. Adherent HeLa S3 cells showed no DNA Oligonucleosomal fragmentation or A0cells. These findings indicate that detection of A0cells by flow cytometry is not proof of cell death by DNA Oligonucleosomal fragmentation.

Abstract: In order to examine the malnutritional condition of outpatients with pancreatitis, a dietary investigation was conducted in Japanese patients with chronic pancreatitis (n=38) and healthy subjects (n=35) of the same age for 3–7 consecutive days, and the characteristics of their food intake were examined. The patients with pancreatitis took in less calories, fat, carbohydrate, and protein than the healthy subjects, by 900 kcal, 20g, 150g, and 20 g, respectively. On the other hand, the fat energy ratio in the patients was 20%, similar to that in the healthy subjects. Also, when the fat intake was classified according to origin, i.e., animal, marine, or plant, the proportions for animal (g) and plant (g) were low, while marine fat accounted for a significantly higher percentage than in the healthy subjects. The intake of cholesterol and Ca in the patients was significantly smaller than that in the healthy subjects, but no significant difference was observed in the intake per body weight of proteins and Ca. It seems, possible that the low calorie, low protein, low fat, and low carbohydrate intake may be factors in the malnutritional condition of the patients with chronic pancreatitis. Analysis of covariance and principal component analysis showed that the body weight of the patients was closely correlated with decreases of caloric intake and intake of carbohydrate. The above results revealed that low body weight in patients with chronic pancreatitis was closely related to the decrease of calorie and carbohydrate intake, in addition to maldigestion and malabosorption of nutrients.

Fecal fat excretion, fecal mass, fecal fat concentration, and the coefficient of fat absorption were evaluated in 31 normal Japanese subjects with a mean fat consumption of 61.8 g and compared with the values in 43 Japanese patients with chronic pancreatitis (CP) with a fat consumption of 40.2g. Fecal fatty acids were analyzed by the gas Chromatographic method. Fecal fat excretion by normal individuals was 1.7±1.0 (Mean±SD) g/day (range, 0.4–4.9 g/day). Steatorrhea was therefore defined as fecal fat excretion that exceeded 5.0 g/day. The patients with CP were divided into three groups: non-steatorrhea (fecal fat «5.0g/day), chemical steatorrhea (fecal fat =5 g/day and no appearance of fatty stool), and manifest steatorrhea (evaluated from the appearance of fatty stool). In addition, we investigated the correlation between fecal fat excretion and pancreatic exocrine function, obtained by the pancreozymin-secretin (or secretin) test in 24 controls and 30 CP patients. Fecal fat excretion by CP patients was 9.1±8.8 g/day, which was significantly higher (P<0.01) than that of controls. There were 28 (65%) CP patients with steatorrhea. Of these, 15 (35%) showed chemical steatorrhea and 13 (30%) manifest steatorrhea. In CP patients, the fecal mass (250.5±133.6 g vs control, 125.6±52.5 g), fecal fat concentration (3.40±2.16g% vs control, 1.48±0.89g%), and coefficient of fat absorption (77.3±20.2% vs control, 97.2±1.7%) all showed significant differences from the controls. Of these three indices—fecal mass, fecal fat concentration, and coefficient of fat absorption—fecal fat concentration was the most useful for identifying pancreatic steatorrhea. In addition, there were significantly different correlations between fecal fat excretion and pancreatic exocrine function in patients' group and control group. Fecal fat excretion was clearly correlated with amylase output. These findings led to the conclusion that steatorrhea indeed exists among Japanese CP patients who consume small amounts of dietary fat; and that fecal fat excretion is closely correlated with pancreatic exocrine dysfunction.

Summary: The study was conducted on five healthy subjects and six patients with calcifying pancreatitis (CP) and steatorrhea. Following overnight fasting, one tube each was placed in the stomach and the upper part of the small intestine, respectively. Through the gastric tube, a test meal that included 30 g of fat (total calories, 625 kcal, 500 mL) was infused over a span of 30 min. Every 30 min (up to 150 min), fluid samples in the upper small intestine were collected and chilled, and the amylase, trypsin, and lipase levels were determined. In addition, in the case of the CP patients, a high-potency pancreatin preparation was infused into the stomach together with the test meal. In order to determine the plasma CCK level, blood sample were collected before test meal infusion and at 10, 20, 30, 45, 60, 90, 120, and 150 min subsequent to infusion. The plasma CCK was extracted using a Sep-Pak C-18 cartridge and analyzed with radioimmunoassay using an OAL-656 antibody. The result was converted to the CCK-8 level and expressed in pg/mL. The enzyme activities in the upper small intestine of the CP patients after test meal administration amounted to 22.8 (amylase), 10.8 (trypsin), and 16.9% (lipase) compared with the corresponding figures for the normal subjects. Following administration of a high-potency pancreatin in patients with CP, enzyme activities in the upper small intestine increased to 132.2 (amylase), 38.7 (trypsin), and 45.3% (lipase) compared with levels in the normal subjects. However, the healthy subjects and the CP patients, both with and without treatment with supplementary exogenous enzymes, all exhibited similar profiles in the plasma CCK response to stimuli. Based on these findings, we concluded that a negative feedback mechanism does not exist between the tryptic activity of the upper small intestine and the CCK secretory response in patients with chronic pancreatitis.

Abstract: Since the role of heparin in hepatic ischemia/ reperfusion (I/R) injury is still not fully understood, we investigated the effects of heparin on hepatic I/R injury in rabbits. Heparin was injected into rabbits after inducing partial hepatic ischemia for 1 h. Thereafter, the serum levels of endothelin-1 (ET-1) and liver transaminase, and tissue levels of oxidized and deoxidized hemoglobin (oxHb, deoxHb) in the reperfused liver were analyzed. Microscopic examinations were also performed. The increased serum levels of ET-1 and liver transaminase after reperfusion were significantly reduced by heparin (P>0.01). Hepatic ischemia reduced oxHb and increased deoxHb. Reperfusion with heparin immediately reduced deoxHb and increased oxHb, and thereafter the balance between the two kinds of Hb also recovered. However, reperfusion without heparin did not demonstrate any similar recovery, but instead gradually exacerbated the dissociation. Microscopically, heparin appeared to normalize I/R-induced activation of hepatic stellate cells which are the target cells for ET-1. These results suggest that heparin improves the hepatic I/R injury caused by sinusoidal microscirculatory disturbances partly via an inhibition of the ET-1 increase.

A new isolated structure for intelligent power ICs was developed using a wafer direct-bonding technique. This structure has partially buried oxide films for dielectric isolation, and gaps are fabricated under them. In this bonding technique, bonding surfaces are crystalline silicon surfaces of the vertical output device region without buried oxide film. This bonding method leads to void-free bonding in the vertical output device region. Electrically perfect bonding was also obtained for the vertical output device in the new structure.

New isolated structures for intelligent power ICs were developed using a wafer bonding technique. These structures have partial buried oxide films for dielectric isolation and buried poly-Si layers for wafer bonding. In this bonding technique, bonding surfaces are a poly-Si layer and a crystalline silicon surface; this combination of bonding surfaces leads to void-free bonding. The electrical perfection of the vertical output device in the new structure was obtained by diffusing antimony into the poly-Si layer. These results indicate that intelligent power ICs can be manufactured by using the new structure.