PURPOSE: To study the epidemiology of adenovirus type 7 (Ad 7) conjunctivitis and adenovirus type 11 (Ad 11) conjunctivitis in the Japanese population by determining the genome type and sub-genome type. METHODS: For Ad 7, we used 12 strains from patients with acute viral conjunctivitis and one strain from a patient with pneumonia. For Ad 11, we used 17 strains from patients with acute viral conjunctivitis and 3 strains from patients with cystitis. For Ad 7 genome typing, we used 11 DNA restriction endonucleases (REs) recognizing 6-or 7-base pair sequences, and for Ad 11 genome typing, we used 7 REs. For Ad 7 and Ad 11 sub-genome typing, we used Taq I and Hinf I that recognize 4- or 5-base pair sequences. RESULTS: The 13 Ad 7 strains all belonged to the same genome type and sub-genome type (Ad 7dH1T1). Adenovirus type 11 strains showed six genome types, with Ad 11p being the most frequent strain. Fifteen Ad 11p strains showed three sub-genome types, but none was the same as the prototype. CONCLUSIONS: Adenovirus type 7 seemed quite stable and an epidemic may occur again. On the other hand, Ad 11 showed several different types. This finding suggests that Ad 11 did not cause an epidemic in Japan during the first half of the 1990s.

Acute Disease↗

PubMedDate not supplied

Hepatocyte growth factor/scatter factor and the placenta.

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Animals↗

PubMedDate not supplied

A single gene for bovine high molecular weight and low molecular weight kininogens.

A potent vasoactive peptide, bradykinin, is liberated from two distinct kininogens designated low molecular weight (LMW) and high molecular weight (HMW) kininogens. We have recently cloned and sequenced cDNAs for bovine LMW prekininogens and indicated that LMW prekininogens are encoded by two very similar but distinct mRNAs. This study concerns the structural basis for the relationship between HMW and LMW prekininogen mRNAs by examination of cDNA clones for bovine HMW prekininogens and a genomic clone. Two types of cDNAs for HMW prekininogens have been identified. The deduced sequences of these two mRNAs are identical with those of two LMW prekininogen mRNAs up to the regions preceding the sequences specifying the divergent C-terminal regions of HMW and LMW kininogens, with one-to-one correspondence. In genomic DNA, the sequence precisely corresponding to the divergent 3'-terminal region of LMW prekininogen mRNA is located after 87 nucleotides downstream from the sequence specifying the 3'-untranslated region of HMW prekininogen mRNA. Based on these findings, we conclude that HMW and LMW prekininogen mRNAs are transcribed from the same gene.

Amino Acid Sequence↗

PubMedDate not supplied

Estimation of coronary flow reserve with the use of dynamic planar and SPECT images of Tc-99m tetrofosmin.

BACKGROUND: We developed a noninvasive method to examine coronary flow reserve with technetium 99m tetrofosmin based on the microsphere model. According to the microsphere model, myocardial blood flow (MBF) can be calculated by MBF = q / integral C(t)dt, where q is myocardial activity and C(t) is tracer concentration in blood. Because the ratio of integral C(t)dt at stress to rest is equal to the ratio of the first transit count in the pulmonary artery (PA) and attenuation factors were canceled out, we calculated the increase ratio of MBF (MBF(IR)). METHODS AND RESULTS: After injection of dipyridamole, tetrofosmin was injected as a bolus and serial dynamic planar images were obtained to measure the first transit count in PA (PAC). Myocardial single photon emission computed tomography was performed to measure the regional myocardial count (RMC). MBF(IR) was calculated as [(RMCs x PACr)/(RMCr x PACs) - 1] x 100, where r and s denote resting and stress conditions, respectively. In contrast, the increase in the myocardial uptake ratio (MUR(IR)) was defined as (RMCs x SCr/RMCr x SCs - 1) x 100, where SC is syringe count of tracer. The results were as follows: (1) The mean MBF of healthy subjects was 46.9% +/- 22.8%. (2) MBF(IR) of the infarcted region and ischemic region was significantly decreased (8.3% +/- 12.2% and 11.2% +/- 11.9%, respectively; P <.001). (3) MUR(IR) was significantly lower than MBF(IR) (14.1% +/- 21.2%; P <.001). (4) MBF(IR) decreased according to the heart rate at rest (r = 0.47; P <.05). CONCLUSIONS: MBF(IR) is a potential parameter with which to evaluate coronary flow reserve when the changes of arterial input function during stress are considered.

Coronary Circulation↗

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Antigenicity of cryopreserved arterial allografts: comparison with fresh and glutaraldehyde treated grafts.

The use of cryopreserved aortic allografts in cardiovascular surgery is widespread and has resulted in excellent outcomes. However, it is controversial whether cryopreservation suppresses the antigenicity of tissue. We designed experimental models to study whether the cryopreservation process alters antigenicity in comparison with that found in fresh and glutaraldehyde treated tissues. Fresh, cryopreserved, and glutaraldehyde treated thoracic aorta from Brown Norway rats were subcutaneously implanted into Lewis rats. Inflammatory cells infiltrating around the grafts were measured on days 7, 14, 28, and 56 after implantation. The glutaraldehyde treated grafts showed significantly less infiltration than the fresh or cryopreserved grafts (p < 0.005). No significant difference was detected between the fresh and cryopreserved grafts. Another study examined the effect of modifications of the aortic allograft on subsequent allogeneic skin graft antigenicity. Subcutaneous implantation of fresh, cryopreserved, and glutaraldehyde treated aortic grafts from Brown Norway into Lewis rats resulted in subsequent skin graft rejection at 4.4+/-0.7, 5.1+/-0.8, and 6.6+/-2.1 days, respectively. There was no significant difference between the fresh and cryopreserved groups; whereas skin grafts in the glutaraldehyde group survived longer than those in the cryopreserved group. These results indicate that cryopreservation had no significant influence on antigenic suppression of arterial allografts.

Animals↗

PubMedDate not supplied

Pretreatment of a Dacron graft with tissue factor pathway inhibitor decreases thrombogenicity and neointimal thickness: a preliminary animal study.

The purpose of this study was to evaluate the effects of locally applied TFPI on the reduction of neointimal thickness in Dacron grafts. Seven millimeter internal diameter 5 cm lengths of albumin coated knitted Dacron grafts were interposed in the infrarenal aorta in 14 mongrel dogs. Before implantation, the grafts were immersed in saline solution containing 200 microg/ml of TFPI (TFPI group, n = 7) or 100 IU/ml of heparin (control group, n = 7) for 15 minutes at room temperature. Three months after implantation, neointimal thickness and percentage of graft stenosis were measured by computerized planimetry. All grafts were patent 3 months after implantation. Thrombus was found in one graft in the TFPI group, but observed in three of seven control grafts. Neointimal thickness in the TFPI group was significantly smaller than that in the control group (mean +/- SD, 0.26 +/- 0.1 mm vs. 0.57 +/- 0.15 mm, p < 0.001). Percentage of graft stenosis was significantly lower in the TFPI group than in the control group (13.4 +/- 5.3% vs. 26.9 +/- 7.0%, p < 0.001). Scanning electron micrographs showed that the neointima of TFPI treated grafts were completely covered by endothelial cells. The present results indicate that locally applied TFPI reduces thrombogenicity and neointimal thickness in albumin coated knitted Dacron grafts.

Animals↗

PubMedDate not supplied

Correlation between CA19-9 production in vitro and histological grades of differentiation in vivo in clones isolated from a human pancreatic cancer cell line (SUIT-2).

The production of carcino-embryonic antigen (CEA) and carbohydrate antigen 19-9 (CA19-9) were investigated in 28 clones isolated from a human pancreatic cancer cell line (SUIT-2) and related to in vitro morphology of the clones and in vivo tumorigenicity. Clones of fusiform and polygonal cells could be morphologically distinguished in confluent cultures. There was no significant difference in CEA production between fusiform-cell clones (2.10 +/- 2.70 ng/L x 10(6) per 24 h) and polygonal-cell clones (6.01 +/- 7.30 ng/L x 10(6) per 24 h), but polygonal-cell clones had higher production of CA19-9 (1176.1 +/- 1628.4 U/L x 10(6) per 24 h) than fusiform (6.0 +/- 7.3 U/L x 10(6) per 24 h; P < 0.01). Production of CA19-9 in vitro correlated with the histological grade of differentiation in vivo in nude mice (r = 0.73, P < 0.001), but CEA production did not. The polygonal-cell clones developed well-differentiated carcinomas in vivo and produced significantly more CA19-9 (P < 0.001) than fusiform-cell clones, which generally developed into poorly differentiated tubular adenocarcinomas in vivo. This cell line may provide an appropriate system for further studies of the biology and therapy of pancreatic cancer.

Adenocarcinoma↗

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Effects of pimobendan, a new cardiotonic agent, on contractile responses in single skeletal muscle fibres of the frog.

Effects of a new cardiotonic agent, pimobendan, on contraction were investigated in single intact skeletal muscle fibres of the frog. Pimobendan increased twitch tension in a concentration-dependent manner regardless of the presence or absence of Ca2+ without any effect on tetanic tension, the resting membrane potential and the shape of the action potential. Pimobendan caused a further increase in twitch tension potentiated by caffeine (1 mM). Adenine, an inhibitor of Ca2+-induced Ca2+ release from the sarcoplasmic reticulum, inhibited twitch tension potentiated by caffeine but not by pimobendan, suggesting that twitch potentiation by pimobendan is not attributed to increases in Ca2+-induced Ca2+ release. Pimobendan failed to increase cAMP levels in the skeletal muscle, though forskolin significantly increased it without any effect on twitch tension. Contractile responses to high concentrations of caffeine and K+ were also potentiated by pimobendan. These results suggest that the potentiating effect of pimobendan on skeletal muscle contraction is mainly due to the increase in Ca2+ sensitivity to the contractile apparatus.

Animals↗

PubMedDate not supplied

Effects of diisopropylamine dichloroacetate on proliferation and differentiation of normal human keratinocytes in vitro.

We found that diisopropylamine dichloroacetate (DADA), known as a vasodilator, enhanced growth of keratinocytes in 4 days culture at 1-30 microg/ml, and such promoting effects of cell proliferation were reconfirmed by measuring DNA synthesis using [(3)H]thymidine incorporation. On the other hand, this substance enhanced synthesis of keratin K1, a potent marker of differentiation in keratinocytes, at 1-100 microg/ml in low calcium (0.1 mM) or high calcium medium (1. 25 mM). Moreover, the formation of cornified envelope, another potent marker of differentiation in keratinocytes, was also promoted by DADA at a concentration of 0.1-10 mM which includes valid concentration of DADA for the enhancement of keratin K1 formation (1-100 microg/ml: 0.05-0.5 mM DADA). These results indicate that DADA has a double function, enhancement of both proliferation and differentiation of cells, which could be linked to the turnover of skin epidermis. Furthermore, in order to analyze the effect of DADA on keratinocytes, we examined the effects of each component of this substance, diisopropylamine (DIA) and dichloroacetate (DCA), on keratinocytes. As the result of these investigations, evidence was found that DCA was effective on enhancement of cell growth, but DIA was ineffective. Moreover, we found that DCA was effective on keratinocyte differentiation by evaluating the enhancement of a differentiation marker, formation of cornified envelopes, within 10 mM, while DIA was not effective. Therefore, we concluded that only DCA was an active component of the DADA molecule for the proliferation and the differentiation of keratinocytes in vitro.

Cell Differentiation↗

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Mutations in the human homologue of the Drosophila segment polarity gene patched in oral squamous cell carcinoma cell lines.

In the present study, we have analyzed tumor deoxyribonucleic acid from oral squamous cell carcinoma (OSCC) cells for patched mutations using an exon-by-exon single strand conformation polymorphism assay and direct sequencing. We found two missense mutations which affected the conserved residue in the transmembrane domains of the gene product and in the intracellular loop at the C-terminal residue implicated in regulating the smoothened molecule. In addition, we demonstrated that the N-terminal fragment of sonic hedgehog (Shh-N) stimulates the growth of normal epithelial cells, the OSCC cell line, NA, and the salivary gland adenocarcinoma cell lines, HSG and HSY, which have no detectable mutation in patched. On the other hand, Shh has no effect on human SCC cells (UE, KA, KO, NI, A431 cells) that have mutations in patched. These results strongly suggest that an Shh-patched signaling is involved in the cell growth of oral epithelial cells and in the tumorigenesis of OSCCs.

Carcinoma, Squamous Cell↗

PubMedDate not supplied

Transmembrane signalling systems in the brain of patients with Parkinson's disease.

The clinical efficacy of dopamine (DA) replacement therapy for patients with Parkinson's disease (PD) depends on the preservation of postsynaptic DA receptors and their intracellular signalling mechanisms in the striatum long after degeneration of the nigrostriatal DA pathway. DA activates adenylyl cyclase (AC) and phospholipase C (PLC) via the D1 receptor, and inhibits through the D2 receptor, thereby regulating the production of intracellular second messengers, cyclic adenosine 3',5'-monophosphate (cAMP), 1,2-diacylglycerol (DAG) and Ca2+. Recent advances in molecular biology have made it possible to monitor the intracellular signal transduction cascade following receptor activation by various transmitters. The authors review the literature addressing this issue, summarized as follows: (1) striatal D1 and D2 receptor densities remain constant, at least in treated and non-demented patients; (2) DA-sensitive AC activity appears to be increased in the putamen of treated patients, although this remains to be confirmed; (3) levels of cAMP-dependent protein kinase (PKA) are normal in non-demented patients, consistent with unchanged levels of DARPP-32 (dopamine- and cAMP-regulated phosphoprotein of M(r) 32,000); (4) levels of Ca2+/phospholipid-dependent protein kinase (PKC) and of inositol 1,4,5-trisphosphate (InsP3) receptor also remain unchanged in non-demented patients; (5) the above three second messenger sites as well as densities of D1 and D2 receptors are decreased in the striatum of demented PD patients (PDD). We tentatively conclude that postreceptor signalling function is intact in the striatum of non-demented PD patients and that there is a clear difference between non-demented patients and PDD, i.e. striatal dopaminoceptive neurons are affected in PDD.

Brain↗

PubMedDate not supplied

Administration of prostaglandin E1 reduces post-operative hepatocellular damage and restores hepatic integrity in patients undergoing hepatectomy.

BACKGROUND/AIMS: The direct protective effects of prostaglandin E1 against hepatic dysfunction are unclear in recent studies. The aim of the present study was to investigate whether post-operative administration of prostaglandin E1 reduces serum concentrations of alpha-glutathione S-transferase, a new indicator of hepatocellular injury, in patients undergoing hepatectomy. METHODOLOGY: The subjects were 15 patients with hepatocellular carcinoma or hilar cholangiocarcinoma undergoing hepatectomy. Prostaglandin E1 was administered to 10 patients (PGE1 group) and was not administered to 5 patients (control group). Prostaglandin E1 was administered for 24 hours from noon on post-operative day 1 to noon on post-operative day 2. Serum concentrations of alpha-glutathione S-transferase, reduced glutathione, cyclic adenosine monophosphate, and total bilirubin, and the concentration of reduced glutathione in bile were measured post-operatively. RESULTS: The serum concentration of alpha-glutathione S-transferase was significantly lower and the serum bilirubin concentration was lower in the PGE1 group than in the control group. The serum concentrations of reduced glutathione and cyclic adenosine monophosphate were significantly higher in the PGE1 group than in the control group. Reduced glutathione in bile was higher in the PGE1 group than in the control group. CONCLUSIONS: The present results show that administration of prostaglandin E1 reduces hepatocellular injury and restores hepatic integrity, post-operatively, in patients undergoing hepatectomy.

Adult↗

PubMedDate not supplied

Chemotherapy-induced apoptosis of lymphocytes in esophageal cancer worsens outcome.

BACKGROUND/AIMS: Chemotherapy has been shown to induce apoptosis in esophageal cancer. However, no windows of opportunity exist to selectively kill tumor cells without killing host cells. Due to the concern that tumor-infiltrating lymphocytes may be killed by chemotherapy, we examined the significance of the effect of treatment on the density of tumor-infiltrating lymphocytes and apoptosis in the tumor itself and in the tumor-infiltrating lymphocytes. METHODOLOGY: In 93 patients with esophageal cancer including 50 with neoadjuvant chemotherapy, esophagectomy specimens were examined for density of tumor-infiltrating lymphocytes and for apoptosis in both tumor cells and tumor-infiltrating lymphocytes. RESULTS: Apoptotic index was increased by neoadjuvant chemotherapy only in tumor-infiltrating lymphocytes, apoptotic index was > or = 4 only in chemotherapy patients. The density of tumor infiltrating lymphocytes was a significant positive prognostic factor in chemotherapy and non-chemotherapy groups, and the high apoptotic index in tumor-infiltrating lymphocytes was an independent negative prognostic factor in the chemotherapy group. CONCLUSIONS: Apoptosis in tumor-infiltrating lymphocytes was induced by chemotherapy in some patients in association with a poor prognosis. Unexpectedly, chemotherapy did not increase apoptosis in tumor cells. Both findings suggest a need for improved regimes and individualized treatment.

Aged↗

PubMedDate not supplied

Predicting initial recurrence pattern of esophageal cancer after neoadjuvant chemotherapy.

BACKGROUND/AIMS: No report has reviewed which clinicopathological factors including 3-field dissection and the response to neoadjuvant chemotherapy can predict the recurrence pattern of an esophageal carcinoma. The aim of this study was to reveal clinicopathological predictors for the initial recurrence pattern of a thoracic esophageal carcinoma. METHODOLOGY: Sixteen parameters derived from 98 patients who underwent a curative esophagectomy with neoadjuvant chemotherapy for a squamous cell carcinoma of the thoracic esophagus were examined using univariate and multivariate logistic regression analyses. RESULTS: Thirty-seven (37.8%) of the 98 patients had recurrences (hematogenous; 16, lymphatic; 13, others; 8). Univariate analyses revealed that the completion of 3-field dissection was the only factor for suppressing the lymphatic recurrence (P = 0.009; odds ratio: 0.2). Multivariate analyses showed that the number of positive nodes was a significant predictor for recurrence including all modalities (P = 0.02; odds ratio: 1.2) and both the number of positive nodes (P = 0.04; odds ratio: 1.1) and the poor response to neoadjuvant chemotherapy (P = 0.02; odds ratio: 6.9) were significant predictors for the hematogenous recurrence. CONCLUSIONS: The number of positive nodes and the response to neoadjuvant chemotherapy could predict the hematogenous recurrence of esophageal carcinoma.

Carcinoma, Squamous Cell↗