Craniofacial morphological characteristics of Japanese adults with various malocclusions were investigated. Cephalometric radiographs of 100 Class I, 100 Class II, and 100 Class III cases were selected and subjected to counterpart analysis as described by Enlow. Results of individuals with normal Class I occlusion revealed a mean value of 39.5 degrees for the angle of the middle cranial fossa relative to the posterior maxillary plane alignment (MCF/PM). This value was used as the basis for intrinsic alignment comparisons for all other skull points. Class I and II malocclusions were classified as either type A or B, depending on whether point A or B was protrusive in the functional occlusal plane (FOP). We found that type B was more common for both Class I and Class II malocclusion. Further, in both Classes, type B cases exhibited an underlying Class III character. We also noted that both B groups had different structural craniofacial patterns relative to those seen in A groups. Both dental Class IA and Class IB had a skeletal Class II tendency. The difference between Class IA and Class IIA, or between Class IB and Class IIB was slight but quantitative. Class III and Class IIA individuals had distinctly different and essentially opposite underlying patterns. Most compensatory effects were ineffective in both Class IIA and Class III groups. However, the composite compensatory result in Class IB case was, for the most part, effective.

Adolescent↗

PubMed1993

Cloning and sequencing of the cDNA encoding the murine mammary gland long-form prolactin receptor.

The nucleotide sequence of a 1992-bp cDNA encoding the long form of the murine mammary prolactin receptor (PRL-R) has been determined. The deduced 68-kDa protein has high sequence identity with long forms of prolactin receptors from rat ovary and rabbit mammary gland.

Amino Acid Sequence↗

PubMed1993

Fatal Epstein-Barr virus-associated hemophagocytic syndrome.

A virus-associated hemophagocytic syndrome is characterized by high fever, liver dysfunction, coagulation abnormalities, pancytopenia, and a benign histiocytic proliferation with prominent hemophagocytosis in bone marrow, lymph node, spleen, and liver. We describe six Japanese children with fatal Epstein-Barr virus (EBV)-associated hemophagocytic syndrome. Five of the six patients had serologic evidence of primary EBV infection at the onset of their diseases. EBV genomes were detected in all the patients by Southern blot hybridization or the polymerase chain reaction. Furthermore, clonality analysis of the EBV genome showed that EBV-infected cells proliferated monoclonally or biclonally in three examined patients. In situ hybridization study using EBV-encoded RNA 1 (EBER1) showed that EBER1 was detected in one of two examined liver tissues, which localized in hepatocytes.

Base Sequence↗

PubMed1993

Intracerebroventricular injection of interleukin-1 beta induces hyperalgesia in rats.

To determine whether interleukin-1 beta (IL-1 beta) in the brain may modulate nociception, recombinant human IL-1 beta (rhIL-1 beta) (1 pg/kg to 1 microgram/kg) was microinjected into the lateral cerebral ventricle of rats and the latency before initiating the licking of their hindpaws after being placed on a hot plate (50.0 +/- 0.1 degrees C) was measured. A significant reduction of the paw-lick latency was observed after injections of nonpyrogenic doses (10 pg/kg to 1 ng/kg) of rhIL-1 beta, showing a maximal response at a dose of 100 pg/kg which began to appear 5 min after injection, reached a peak within 30 min and then gradually subsided. An increase in the amount of rhIL-1 beta to > 1 ng/kg (up to 1 microgram/kg) had no effect on the nociceptive threshold. The rhIL-1 beta-induced hyperalgesia was completely abolished by pretreatment with an IL-1 receptor antagonist (IL-1ra) or Na salicylate. Similar pretreatment with alpha-melanocyte-stimulating hormone (alpha-MSH) also inhibited the rhIL-1 beta-induced hyperalgesia. However, pretreatment with alpha-helical corticotropin-releasing factor (CRF)9-41 failed to affect it. The results suggest that IL-1 beta in the brain produces hyperalgesia by its receptor-mediated and prostaglandin-dependent action which is sensitive to alpha-MSH. The hyperalgesic action of central IL-1 does not appear to depend on the CRF system.

Animals↗

PubMed1993

Differential responses of intestinal glucose transporter mRNA transcripts to levels of dietary sugars.

Dietary sugars are known to stimulate intestinal glucose transport activity, but the specific signals involved are unknown. The Na(+)-dependent glucose co-transporter (SGLT1), the liver-type facilitative glucose transporter (GLUT2) and the intestinal-type facilitative glucose transporter (GLUT5) are all expressed in rat jejunum [Miyamoto, Hase, Taketani, Minami, Oka, Nakabou and Hagihira (1991) Biochem. Biophys. Res. Commun. 181, 1110-1117]. In the present study we have investigated the effects of dietary sugars on these glucose transporter genes. A high-glucose diet stimulated glucose transport activity and increased the levels of SGLT1 and GLUT2 mRNAs in rat jejunum. 3-O-Methylglucose, D-galactose, D-fructose, D-mannose and D-xylose can mimic the regulatory effect of glucose on the SGLT1 mRNA level in rat jejunum. However, only D-galactose and D-fructose increased the levels of GLUT2 mRNA. The GLUT5 mRNA level was increased significantly only by D-fructose. Our results suggest that the increase in intestinal transport activity in rats caused by dietary glucose is due to an increase in the levels of SGLT1 and GLUT2 mRNAs, and that these increases in mRNA may be caused by an enhancement of the transcriptional rate. Furthermore, for expression of the SGLT1 gene, the signal need not be a metabolizable or transportable substrate whereas, for expression of the GLUT2 gene, metabolism of the substrate in the liver may be necessary for signalling. Only D-fructose is an effective signal for expression of the GLUT5 gene.

Animals↗

PubMed1993

Widespread distribution of free D-aspartate in rat periphery.

We have identified and quantified free D-aspartate in adult rat peripheral organs using gas chromatographic-mass spectrometric and high-performance liquid chromatographic techniques. The level of free D-aspartate was highest in the adrenal, testis, spleen and pituitary, followed by the thymus, lung, ovary, placenta, pancreas and heart, and below the detection limit in the kidney, liver, brain, muscle and serum. These data provide the first evidence that a high level of free D-aspartate widely occurs in the adult rat periphery and suggest that the D-amino acid may be an endogenous substrate for D-aspartate oxidase.

Animals↗

PubMed1993

Vitamin B6 deficiency causes activation of RNA polymerase and general enhancement of gene expression in rat liver.

The effect of vitamin B6 deficiency on the activity of RNA polymerase and expression of several mRNAs in rat liver was investigated. The activities of RNA polymerase I and II in the liver of vitamin B6-deficient rats were found to be higher than the control rats by 30%. The expression of several mRNAs, including mRNAs for beta-actin and glyceraldehyde-3-phosphate dehydrogenase, and the content of poly(A)+ RNA were also increased in vitamin deficiency. These observations suggest that vitamin B6 influences gene expression in the liver, at least in part, by modulating the activity of RNA polymerase.

Actins↗

PubMed1993

Tumors in hepatobiliary tract and pancreatic islet tissues of transgenic mice harboring gastrin simian virus 40 large tumor antigen fusion gene.

Gastrin is expressed in the gastric antrum and in fetal pancreatic islets but not in adult islets. We have now identified the hepatobiliary tract as another, previously unknown, potential site of gastrin gene expression. Two human gastrin simian virus 40 large tumor antigen (SV40 T antigen) fusion genes containing 1.5 kb of 5' flanking sequence and 10.5 kb that included 5.5 kb upstream, 1.5 kb downstream, and the entire transcribed region were used to generate transgenic mice. Analysis of several transgenic lines, derived from both fusion genes, revealed development of transmissible hepatobiliary tract tumors and pancreatic islet cell tumors. Analysis of each of the tumor cells demonstrates expression of SV40 T antigen but no expression of gastrin. Of the two fusion genes, only the 10.5-kb sequence induces hyperplasia of gastrin-producing cells in the antrum. Analysis of these cells demonstrates expression of SV40 T antigen and gastrin, suggesting that the 10.5-kb sequence is sufficient for gastrin cell hyperplasia in the antrum. These data raise the possibility that gastrin is transiently expressed in the hepatobiliary tract.

Adenoma, Islet Cell↗

PubMed1993

Esophagectomy for metastatic carcinoma of the esophagus from lung cancer.

A patient with metastatic carcinoma of the esophagus from lung cancer is reported. The patient was a 54-year-old woman who underwent a left lower lobectomy for lung cancer 5 years previously. The authors performed a thoracic esophagectomy, dissection of mediastinal lymph nodes, and reconstruction of the esophagus; the surgery was followed by chemotherapy. Because the histologic pattern of the esophageal tumor was similar to that of lung cancer and mucosal involvement was not seen, the esophageal tumor was interpreted to be a metastasis from lung cancer. The patient is well without recurrence of disease 23 months after operation. This is the first report of a successful esophagectomy for metastatic carcinoma of the esophagus from lung cancer.

Adenocarcinoma↗

PubMed1993

DNA-binding proteins and their cis-acting sites controlling hormonal induction of a mouse beta-casein::CAT fusion protein in mammary epithelial cells.

Transcription of the mouse beta-casein (beta CAS)-encoding gene (casB) is regulated by the synergistic actions of insulin, glucocorticoid and prolactin in the mammary gland (MG). To delineate its regulatory sequence(s), we examined the hormonal inducibility of various chimeric constructs containing the promoter sequence of casB and the cat reporter gene in primary MG epithelial cells. A DNA fragment from bp -258 to +7 of casB was sufficient for the hormonal induction. Using a series of 5'- and internal deletions of the casB promoter region, at least three DNA elements were found to be necessary for full induction. These were located at bp positions -258 to -180, -154 to -136, and -98 to -62. DNase I footprinting analysis with a partially purified extract from lactating MG cells detected at least seven protected sequences, I(-242 to -219), II(-213 to -202), III(-151 to -139), IV(-125 to -110), V(-98 to -90), VI(-79 to -70) and VII(-59 to -45). Regions I/II, III and V/VI were included in the three DNA elements required for the hormonal induction, and the IV region corresponded to the MG consensus sequences of several milk protein-encoding genes. Competition gel retardation assays using nuclear extracts of lactating mouse MG revealed the presence of specific binding proteins for regions I, II, IV and VI, as well as specific protein(s) binding to both regions III and V. The binding activities of these proteins, except that associated with region IV, were increased from the virgin to lactating periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Free D-serine, D-aspartate and D-alanine in central nervous system and serum in mutant mice lacking D-amino acid oxidase.

We have examined whether D-amino acid oxidase (DAO) regulates free D-serine content using mutant ddY/DAO- mice lacking DAO activity. We find that the content of D-serine in the serum and cerebellum of mutant mice is much higher than that of normal mice, whereas a slight but significant difference in the cerebral D-serine level is observed between the two strains. These results suggest that, although DAO may participate in the catabolism of D-serine in the cerebellum and periphery, there appears to be other mechanisms for catabolism of endogenous D-serine in the brain.

Alanine↗

PubMed1993

Lisinopril reduces cardiac hypertrophy and mortality in rats with aortocaval fistula.

We evaluated the effects of lisinopril (1 mg/kg per day) on hemodynamics, cardiac hypertrophy, and neurohumoral factors in Wistar rats with an abdominal aortocaval fistula. After 4 weeks of treatment, the results were compared with values obtained for untreated rats with a fistula and for sham-operated rats. Volume loading induced biventricular hypertrophy, hemodynamic signs of high-output heart failure (increased cardiac output, left ventricular end-diastolic pressure, and pulse pressure), and impaired renal function (decreased renal blood flow and kidney weight; increased blood urea nitrogen). Lisinopril did not affect these cardiorenal hemodynamics, but decreased left ventricular mass and mortality rate (both P < 0.05). Lisinopril attenuated the increase in plasma norepinephrine, and increased plasma renin activity (both P < 0.05). Thus, lisinopril reduced left ventricular mass and mortality in rats with high-output heart failure without changing the cardiorenal hemodynamics. Neurohumoral inhibition may play a role in the beneficial effects of lisinopril.

Angiotensin-Converting Enzyme Inhibitors↗