The amino acid sequence of human chorionic gonadotropin. The alpha subunit and beta subunit.

The amino acid sequences of both the alpha and beta subunits of human chorionic gonadotropin have been determined. The amino acid sequence of the alpha subunit is: Ala - Asp - Val - Gln - Asp - Cys - Pro - Glu - Cys-10 - Thr - Leu - Gln - Asp - Pro - Phe - Ser - Gln-20 - Pro - Gly - Ala - Pro - Ile - Leu - Gln - Cys - Met - Gly-30 - Cys - Cys - Phe - Ser - Arg - Ala - Tyr - Pro - Thr - Pro-40 - Leu - Arg - Ser - Lys - Lys - Thr - Met - Leu - Val - Gln-50 - Lys - Asn - Val - Thr - Ser - Glu - Ser - Thr - Cys - Cys-60 - Val - Ala - Lys - Ser - Thr - Asn - Arg - Val - Thr - Val-70 - Met - Gly - Gly - Phe - Lys - Val - Glu - Asn - His - Thr-80 - Ala - Cys - His - Cys - Ser - Thr - Cys - Tyr - Tyr - His-90 - Lys - Ser. Oligosaccharide side chains are attached at residues 52 and 78. In the preparations studied approximately 10 and 30% of the chains lack the initial 2 and 3 NH2-terminal residues, respectively. This sequence is almost identical with that of human luteinizing hormone (Sairam, M. R., Papkoff, H., and Li, C. H. (1972) Biochem. Biophys. Res. Commun. 48, 530-537). The amino acid sequence of the beta subunit is: Ser - Lys - Glu - Pro - Leu - Arg - Pro - Arg - Cys - Arg-10 - Pro - Ile - Asn - Ala - Thr - Leu - Ala - Val - Glu - Lys-20 - Glu - Gly - Cys - Pro - Val - Cys - Ile - Thr - Val - Asn-30 - Thr - Thr - Ile - Cys - Ala - Gly - Tyr - Cys - Pro - Thr-40 - Met - Thr - Arg - Val - Leu - Gln - Gly - Val - Leu - Pro-50 - Ala - Leu - Pro - Gin - Val - Val - Cys - Asn - Tyr - Arg-60 - Asp - Val - Arg - Phe - Glu - Ser - Ile - Arg - Leu - Pro-70 - Gly - Cys - Pro - Arg - Gly - Val - Asn - Pro - Val - Val-80 - Ser - Tyr - Ala - Val - Ala - Leu - Ser - Cys - Gln - Cys-90 - Ala - Leu - Cys - Arg - Arg - Ser - Thr - Thr - Asp - Cys-100 - Gly - Gly - Pro - Lys - Asp - His - Pro - Leu - Thr - Cys-110 - Asp - Asp - Pro - Arg - Phe - Gln - Asp - Ser - Ser - Ser - Ser - Lys - Ala - Pro - Pro - Pro - Ser - Leu - Pro - Ser-130 - Pro - Ser - Arg - Leu - Pro - Gly - Pro - Ser - Asp - Thr-140 - Pro - Ile - Leu - Pro - Gln. Oligosaccharide side chains are found at residues 13, 30, 121, 127, 132, and 138. The proteolytic enzyme, thrombin, which appears to cleave a limited number of arginyl bonds, proved helpful in the determination of the beta sequence.     

T cell requirement for development of chronic ulcerative dermatitis in E- and P-selectin-deficient mice

C57BL/6 mice deficient in E- and P-selectin (E(-/-)P(-/-)) kept under specific pathogen-free barrier conditions have high circulating neutrophil counts and develop hypercellular cervical lymph nodes with substantial plasma cell infiltrates, severe ulcerative dermatitis, conjunctivitis, and lung pathology, which eventually lead to premature death. To test the hypothesis that the pathology in E(-/-)P(-/-) mice may be caused by dysfunctional lymphocyte activity, we crossed E(-/-)P(-/-) mice with recombination activation gene (Rag)-1(-/-) mice to generate E(-/-)P(-/-)Rag-1(-/-) mice lacking mature T and B lymphocytes. E(-/-)P(-/-)Rag-1(-/-) mice had circulating neutrophil counts and plasma G-CSF levels similar to E(-/-)P(-/-) mice. Remarkably, none of the E(-/-)P(-/-)Rag-1(-/-) mice developed conjunctivitis or ulcerative dermatitis typical of E(-/-)P(-/-) mice. These mice were overall healthier in appearance than E(-/-)P(-/-) mice, and histopathologic changes in the lung were reduced. Cervical lymph nodes in E(-/-)P(-/-)Rag-1(-/-) mice were much smaller than those of E(-/-)P(-/-) mice, containing few mononuclear cells and no plasma cells. These data show that the severe disease phenotype of E(-/-)P(-/-) mice depends on lymphocyte function. We conclude that a dysregulated immune response in E(-/-)P(-/-) mice causes disease development, but is not necessary for elevated neutrophil counts.     

Protection of atherogenesis in thromboxane A2 receptor-deficient mice is not associated with thromboxane A2 receptor in bone marrow-derived cells

In the previous study, we generated mice lacking thromboxane A2 receptor (TP) and apolipoprotein E, apoE(-/-)TP(-/-) mice, and reported that the double knockout mice developed markedly smaller atherosclerotic lesions than those in apoE(-/-) mice. To investigate the mechanism responsible for reduced atherosclerosis in apoE(-/-)TP(-/-) mice, we examined the role of TP in bone marrow (BM)-derived cells in the development of the atherosclerotic lesions. When we compared the function of macrophages in apoE(-/-) and in apoE(-/-)TP(-/-) mouse in vitro, there was no difference in the expression levels of cytokines and chemokines after stimulation with lipopolysaccharide. We then transplanted the BM from either apoE(-/-) or apoE(-/-)TP(-/-) mice to either apoE(-/-) or apoE(-/-)TP(-/-) mice after sublethal irradiation. After 12 weeks with high fat diet, we analyzed the atherosclerotic lesion of aortic sinus. When the BM from apoE(-/-) or apoE(-/-)TP(-/-) mice was transplanted to apoE(-/-) mice, the lesion size was almost the same as that of apoE(-/-) mice without BM transplantation. In contrast, when the BM from apoE(-/-) or apoE(-/-)TP(-/-) mice was transplanted to apoE(-/-)TP(-/-) mice, the lesion size was markedly reduced. These results indicate that the protection of atherogenesis in TP(-/-) mice is not associated with TP in BM-derived cells.     

Monoterpene ketones in the synthesis of optically active insect pheromones

This review considers the synthetic possibilities of monoterpene ketones, such as (R)-(+)- and (S)-(-)-pulegones, (-)-menthone, (R)-(-)- and (S)-(+)-carvones, (2R,5S)-dihydrocarvone, (S)-(+)- and (R)-(-)-camphors, (R)-(-)-nopinone, (R)-(+)- and (S)-(-)-verbenones by the examples of synthesis of optically pure and enantiomerically enriched insect pheromones.     

Genetic mapping and characterization of Pseudomonas aeruginosa mutants defective in the formation of extracellular proteins.

We isolated 15 mutants of Pseudomonas aeruginosa PAO which were defective in the formation of certain extracellular proteins, such as elastase, staphylolytic enzyme, and lipase ( Xcp mutants). The mutations were mapped on the chromosome by conjugation and transduction. The locations were xcp -1 near 0', with the gene order cys-59- xcp -1- proB , and loci xcp -2, xcp -3, and xcp -31 at 35', with the gene order trpC , D- xcp -3/ xcp -31- xcp -2- argC . Loci xcp -4 and xcp -41 through xcp -44 were cotransducible with proA at 40'; loci xcp -5, xcp -51, xcp -52, and xcp53 were located at 55', with the gene order leu-10- trpF -met-9010- xcp -53- xcp -5/ xcp -51/ xcp+ ++-52, and xcp -6 was located at 65' to 70', between catA and mtu-9002. Nine mutations ( xcp -2, xcp -3, xcp -31, xcp -4, and xcp -41 through xcp -45) caused decreased production of extracellular enzymes. Six strains with mutations xcp -1, xcp -5, xcp -51, xcp -52, xcp -53, and xcp -6 produced cell-bound exoproteins and had defective release mechanisms. The regulation of production of alkaline phosphatase and phospholipase C is different from other exoproteins , such as elastase, but they all seem to share a common release mechanism. Alkaline protease had separate mechanisms for regulation and release, since this protease was found in culture supernatants of all but one of the mutants, and none of the strains had cell-bound enzyme.     

Fluorogenic substrates of glycogen debranching enzyme for assaying debranching activity

Glycogen debranching enzyme (GDE) degrades glycogen in concert with glycogen phosphorylase. GDE has two distinct active sites for maltooligosaccharide transferase and amylo-1,6-glucosidase activities. Phosphorylase limit dextrin from glycogen is debranched by cooperation of the two activities. Fluorogenic branched dextrins were prepared as substrates of GDE from pyridylaminated maltooctaose (PA-maltooctaose) and maltotetraose, taking advantage of the synthetic action of Klebsiella pneumoniae pullulanase. Their structures were as follows: Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-4(Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-6)Glcalpha1-4Glcalpha1-4GlcPA (B3), Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-4(Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-6)Glcalpha1-4Glcalpha1-4Glcalpha1-4GlcPA (B4), Glcalpha1-4Glcalpha1-4Glcalpha1-4(Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-6)Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-4GlcPA (B5), Glcalpha1-4Glcalpha1-4(Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-6)Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-4GlcPA (B6), Glcalpha1-4(Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-6)Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-4GlcPA (B7), and Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-6Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-4Glcalpha1-4GlcPA (B8). These dextrins were incubated with porcine skeletal muscle GDE. No fluorogenic product was found in the digest of B8. The fluorogenic products from B3, B4, and B5 were PA-maltooctaose only. PA-maltooctaose, PA-maltoundecaose, and 6(7)-O-alpha-glucosyl-PA-maltooctaose were from B7. PA-maltooctaose and 6(6)-O-alpha-glucosyl-PA-maltooctaose were from B6. These results indicate that the maltooligosaccharide transferase removed the maltotriosyl residues from the maltotetraosyl branches by hydrolysis or intramolecular transglycosylation to expose 6-O-alpha-glucosyl residues, and then the amylo-1,6-glucosidase hydrolyzed the alpha-1,6-glycosidic linkages of the products rapidly. Probably, 6-O-alpha-glucosyl-PA-maltooctaoses from B7 and B6 were less susceptible to the amylo-1,6-glucosidase than were those from B3, B4, and B5. Taking this into account, B3, B4, and B5 are suitable substrates for GDE assay.     

Germitorosone and methylgermitorosone,two hydroanthracene derivatives from seedlings of Cassia torosa

Two new yellow pigments, germitosone and methylgermitorosone, were isolated from the seedling of Cassia torosa. The structures of these substances were established as 3,7 dimethyl - 6 - methoxy - 1 - oxo - 2,3,8,9 - tetrahydroxy - 1,2,3,4 - tetrahydroanthracene and 6,9 dimethoxy - 3,7 - dimethyl - 1 - oxo - 2,3,8 - trihydroxy - 1,2,3,4 - tetrahydroanthracene respectively.     

Functional relation among RecQ family helicases RecQL1, RecQL5, and BLM in cell growth and sister chromatid exchange formation

Human RECQL1 and RECQL5 belong to the RecQ family that includes Bloom syndrome, Werner syndrome, and Rothmund-Thomson syndrome causative genes. Cells derived from individuals suffering from these syndromes show significant levels of genomic instability. However, neither RECQL1 nor RECQL5 has been related to a disease, and nothing is known about the functions of RecQL1 and RecQL5. We generated here RECQL1(-/-), RECQL5(-/-), RECQL1(-/-)/RECQL5(-/-), RECQL1(-/-)/BLM(-/-), and RECQL5(-/-)/BLM(-/-) cells from chicken B-lymphocyte line DT40 cells. Although BLM(-/-) DT40 cells showed a slow-growth phenotype, a higher sensitivity to methyl methanesulfonate than the wild type, and an approximately 10-fold increase in the frequency of sister chromatid exchange (SCE) compared to wild-type cells, RECQL1(-/-), RECQL5(-/-), and RECQL1(-/-)/RECQL5(-/-) cells showed no significant difference from the wild-type cells in growth, sensitivity to DNA-damaging agents, and the frequency of SCE. However, both RECQL1(-/-)/BLM(-/-) and RECQL5(-/-)/BLM(-/-) cells grew more slowly than BLM(-/-) cells because of the increase in the population of dead cells, indicating that RecQL1 and RecQL5 are somehow involved in cell viability under the BLM function-impaired condition. Surprisingly, RECQL5(-/-)/BLM(-/-) cells showed a higher frequency of SCE than BLM(-/-) cells, indicating that RecQL5 suppresses SCE under the BLM function-impaired condition.     

Physiological expression of macrophage apoE in the artery wall reduces atherosclerosis in severely hyperlipidemic mice

We have previously reported that the introduction of macrophage apoE into mice lacking both apoE and the LDL receptor (apoE(-)(/-)/LDLR(-)(/-)) through bone marrow transplantation (apoE(+)(/+)/LDLR(-)(/-)-->apoE(-)(/-)/LDLR(-)(/-)) produces progressive accumulation of apoE in plasma without affecting lipid levels. This model provides a tool to study the effects of physiologically regulated amounts of macrophage apoE on atherogenesis in hyperlipidemic animals. Ten-week-old male apoE(-)(/-)/LDLR(-)(/-) mice were transplanted with either apoE(+)(/+)/LDLR(-)(/-) (n = 11) or apoE(-)(/-)/LDLR(-)(/-) (n = 14) marrow. Although there were no differences between the two groups in lipid levels at baseline or at 5 and 9 weeks after transplantation, apoE levels in the apoE(+)(/+)LDLR(-)(/-)-->apoE(-)(/-)/LDLR(-)(/-) mice increased to 4 times the apoE levels of normal mice. This resulted in a 60% decrease in aortic atherosclerosis in the apoE(+)(/+)/LDLR(-)(/-)-->apoE(-)(/-)/LDLR(-)(/-) compared with the apoE(-)(/-)/LDLR(-)(/-)-->apoE(-)(/-)/LDLR(-)(/-) controls, (15957 +/- 1907 vs. 40115 +/- 8302 micro m(2) +/- SEM, respectively). In a separate experiment, apoE(+)(/+)/LDLR(-)(/-) mice were transplanted with either apoE(+)(/+)/LDLR(-)(/-) or apoE(-)(/-)/LDLR(-)(/-) marrow and placed on a high-fat diet for 8 weeks. In the absence of macrophage apoE, lesion area was increased by 75% in the aortic sinus and by 56% in the distal aorta. These data show that physiologic levels of macrophage apoE in the vessel wall are anti-atherogenic in conditions of severe hyperlipidemia and can affect later stages of plaque development.     

Die abwandlung des eilegeapparates der bombyliidae (Diptera) Eine funktionsmorphologische studie

Skeleton, muscles, and functioning of the egg-laying systems of 38 species out of 16 subfamilies are studied. A development sequence toward a soil chamber to coat the eggs (b, c) can be characterized by the sternite 8: a) its inward position (Geroninae), b) its erection (9 subfamilies), c) its shell-shaped cavity (Exoprosopinae). Systropodinae and Heterotropinae cannot be fitted into this system.

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Abkürzungen in den Abbildungen VI–X 6.–10. Tergit - 6–8 6.–8. Sternit - A Analöffnung - Ac Acanthophorit 8. Sternits - Ac IX vom 9. Tergit abgetrenntes Acanthophorit - adr 1 schlauchförmige Geschlechtsanhangsdrüse - adr 2 wurstförmige Geschlechts-anhangsdrüse - Af After - AG Apikaler Gangabschnitt des R. sem. - Ak Analkegel - B IX Ausbuchtung am 9. Tergit - BG Basaler Gangabschnitt des R. sem. - Bo Borsten - Br präformierte Bruchstelle am Eideckel - Bu Bursatasche - Ch Chorion - Cö Coecum - D Darm - De Eideckel - Do Dornen - Do VIII Dornen am 8. Tergit - dR-S8 dorsaler Rand von Sternit 8 - Ed Enddarm - EmMG Einmündung der MalpighiGefäße - Er Eierrinne - Ggl 6, 7 Ganglion des 6. bzw. 7. Ab dominalsegments - Gö Geschlechtsöffnung - gOd gemeinsamer Eiergang - HaEr Haarflur entlang der Eierrinne - Ha-S8 Haare am 8. Sternit - Ha-Tv8 Haare an der Unterkante des 8. Tergits - hM häutiges Mittelfeld auf dem 8. Sternit - HPi Haarpinsel am 8. Tergit - Krs Kropfsack - Krst Kropfstiel - Ku Kufen am 8. Tergit - Lö häutige Löffelbildung - IZ lappenartige Zipfel des - M 1,2 Muskel Nr. 1, 2, etc. - MA Muskelapparat im Ductus receptaculi - Md Mitteldarm - Müadr 2 Mündung der Anhangsdrüsen-2 - MüRs Mündung der R. sem. - Od Ovidukt - Ov Ovar - PGP Postgenitalplatte - Pl Pleura - Po verdaute Pollenkörner im Enddarm - R VIII Rostrum am 8. Tergit - Rbl Rectalblase - rEi reifes Ei - Rp Rectalpapille - R. sem. Receptaculum seminis - S Sternit - Sbl Samenkapsel des R. sem. - SGP Subgenitalplatte - Sk Sandkammerbucht - Skl IX Sklerit im Dach der Sandkammerbucht - Spb Spatelborsten - Spdr Speicheldrüsen - Stg Stigma - T Tergit - Tv ventromedial verälangertes Tergit 8 - U IX, U X Zungenfortsatze des 9. bzw. 10. Tergits im Dach der Sandkammerbucht - U Ac Zungenfortsätze des Acan thophorits im Dach der Sandkammerbucht - Vag Vagina - Vag. Ap. Vaginalapodem - Vag-Es Vagina-Einsenkung in die Sternit 8-Schale - Vh Ventralhaut des Analkegels     

Diagnosis of genetic disease using recombinant DNA. Third edition

Summary Recombinant DNA methodology has greatly increased our knowledge of the molecular pathology of the human genome at the same time as providing the means to diagnose inherited disease at the DNA level. Direct detection and analysis of a range of genetic defects are now possible using cloned gene or oligonucleotide probes or by direct sequencing of the disease gene(s). In addition, the use of restriction fragment length polymorphisms (RFLPs) within and around these genes as indirect genetic markers has now potentiated the tracking of disease alleles in affected pedigrees in cases where direct analysis was not feasible. RFLPs associated with linked anonymous segments may also be used not only to diagnose hitherto undetectable disease states, but also for chromosomal localization of the loci responsible. We present here an updated list of reports describing both the direct and the indirect analysis/diagnosis of human inherited disease; it is intended to serve as a guide to current molecular genetic approaches in diagnostic medicine.Abbreviations ADG Annales de Genetique - AHG Ann. Hum. Genet. - AICHG Abstracts Int. Congress Hum. Genet. 7, Berlin, 1986 - AJH Am. J. Haematol. - AJHG Am. J. Hum. Genet. - AJMG Am. J. Med. Genet. - AN Aneuploidy - ANYAS Ann. New York Acad. Sci - APRT Adeninephosphoribosyltransferase - ASHG American Soc. Hum. Genet. Abstracts 34th Ann. Meeting - ATS VII Atherosclerosis VII, Eds. Fidge and Nestel, Elsevier - Arch. Neurol. Archieves of Neurology - Arch. Oph. Arch. Ophthalmol. - Atherosclr. Atherosclerosis - BBRC Biochim. Biophys. Res. Comm. - BJH Brit. J. Haematol. - BMJ Brit. Med. J. - BST Biochem. Soc. Transact. - CCG Cytogenet. Cell Genet. - CDC Carrier detection using clonality - CGC Cancer Genet. Cytogenet. - DEL Deletion - DETECT Mode of Detection - Dis. Marker Disease Markers - DUP Duplication - EJB Eur. J. Biochem. - EJI Eur. J. Immunol. - HGM8 Human Gene Mapping 8 (CCG, Vol. 40, 1–824, 1985) - HGM9 Human Gene Mapping 9 (CCG, Vol. 46, 1–824, 1987) - HGM10 Human Gene Mapping 10 (CCG, Vol. 51, 1–824, 1989) - HPRT Hypoxanthinephosphoibosyltransferase - HVR Hypervariable region - Hos. Prac. Hospital Practice - IMG Immunogenetics - INS Insertion - INV Inversion - IZ Inter-zeta - J. Mol. End. J. Molec. Endocrinol. - JAMA J. Amer. Med. Assoc. - JBC J. Biol. Chem. - JCB J. Cell. Biol. - JCEM J. Clin. Endocrinol. Metab. - JCI J. Clin. Invest. - JMD J. Inher. Metab. Dis. - JIMM J. Immunogenet. - JJCR Jpn. J. Cancer Res. - JJHG Jpn. J. Hum. Genet. - JMG J. Med.Genet. - JNR J. Neurosci. Res. - LH Loss of heterozygosity - MBM Mol. Biol. Med. - MCB Molec. Cell. Biol. - MCKUS McKusick catalogue number - MMP Mismatch pairing analysis - MODY Maturity onset diabetes of the young - MOL. END. Molec. Endocrinol. - MUT Mutation - NAR Nucl. Acids Res. - NEJM New Engl. J. Med. - Neurol. Sup. Neurology Supplement - OLIGO Detection of mutation by oligonucleotide hybridisation - OPG Ophthal. Pediatr. Genet. - PNAS Proc. Natl. Acad. Sci. USA - Ped. Res. Pediatric Res. - PM Point mutation - Pren. Diag. Prenatal Diagnosis - RE Restriction enzyme analysis - REAR Rearrangement - RFLP Indirect analysis using likned RFLP - SEQU Analysis by DNA sequencing - SCMG Somat. Cell Molec. Genet. - Thr. Res. Thrombosis Research - XIA X-inactivation analysis - ar alphoid repeat - atyp. atypical - breakp. breakpoint - def. deficiency - fruct. fructose - haem. haemoglobin - hered. hereditary - minisat. minisatellite - mt mitochondrial - neph. nephritis - persist. persistent - phosph. phosphorylase - resis. resistant - phosph. phosphorylase - resist. resistant - sev. several - synth. synthetase - var various     

Distribution of NT-IR perikarya in the brain of the guinea pig with special reference to cardiovascular centers in the medulla oblongata

Summary The occurrence and distribution of neurotensin-immunoreactive (NT-IR) perikarya was studied in the central nervous system of the guinea pig using a newly raised antibody (KN 1). Numerous NT-IR perikarya were found in the nuclei amygdaloidei, nuclei septi interventriculare, hypothalamus, nucleus parafascicularis thalami, substantia grisea centralis mesencephali, ventral medulla oblongata, nucleus solitarius and spinal cord. The distribution of NT-IR perikarya was similar to that previously described in the rat and monkey. In the gyrus cinguli, hippocampus and nucleus olfactorius, though, no NT-IR neurons were detected in this investigation. Additional immunoreactive perikarya, however, were observed in areas of the ventral medulla oblongata, namely in the nucleus paragigantocellularis, nucleus retrofacialis and nucleus raphe obscurus.The relevance of the NT-IR perikarya within the ventral medulla oblongata is discussed with respect to other neuropeptides, which are found in this area, and to cardiovascular regulation.Abbreviations abl nucleus amygdaloideus basalis lateralis - abm nucleus amygdaloideus basalis medialis - acc nucleus amygdaloideus centralis - aco nucleus amygdaloideus corticalis - ahp area posterior hypothalami - ala nucleus amygdaloideus lateralis anterior - alp nucleus amygdaloideus lateralis posterior - ame nucleus amygdaloideus medialis - atv area tegmentalis ventralis - bst nucleus proprius striae terminalis - CA commissura anterior - CC corpus callosum - cgld corpus geniculatum laterale dorsale - cglv corpus geniculatum laterale ventrale - cgm corpus geniculatum mediale - CHO chiasma opticum - CI capsula interna - co nucleus commissuralis - cod nucleus cochlearis dorsalis - cp nucleus caudatus/Putamen - cs colliculus superior - cu nucleus cuneatus - dmh nucleus dorsomedialis hypothalami - DP decussatio pyramidum - em eminentia mediana - ent cortex entorhinalis - epi epiphysis - FLM fasciculus longitudinalis medialis - fm nucleus paraventricularis hypothalami pars filiformis - FX fornix - gd gyrus dentatus - gp globus pallidus - gr nucleus gracilis - hl nucleus habenulae lateralis - hm nucleus habenulae medialis - hpe hippocampus - ift nucleus infratrigeminalis - io oliva inferior - ip nucleus interpeduncularis - LM lemniscus medialis - MT tractus mamillo-thalamicus - na nucleus arcuatus - nls nucleus lateralis septi - nms nucleus medialis septi - npca nucleus proprius commissurae anterioris - ns nucleus solitarius - n III nucleus nervi oculomotorii - nt V nucleus tractus spinalis nervi trigemini - ntm nucleus mesencephalicus nervi trigemini - osc organum subcommissurale - P tractus cortico-spinalis - PC pedunculus cerebri - PCI pedunculus cerebellaris inferior - pir cortex piriformis - pol area praeoptica lateralis - pom area praeoptica medialis - prt area praetectalis - pt nucleus parataenialis - pvh nucleus paraventricularis hypothalami - pvt nucleus paraventricularis thalami - r nucleus ruber - re nucleus reuniens - rgi nucleus reticularis gigantocellularis - rl nucleus reticularis lateralis - rm nucleus raphe magnus - ro nucleus raphe obscurus - rp nucleus raphe pallidus - rpc nucleus reticularis parvocellularis - rpgc nucleus reticularis paragigantocellularis - sch nucleus suprachiasmaticus - SM stria medullaris thalami - snc substantia nigra compacta - snl substantia nigra lateralis - snr substantia nigra reticularis - ST stria terminalis - tad nucleus anterior dorsalis thalami - tam nucleus anterior medialis thalami - tav nucleus anterior ventralis thalami - tbl nucleus tuberolateralis - tc nucleus centralis thalami - tl nucleus lateralis thalami - tmd nucleus medialis dorsalis thalami - TO tractus opticus - TOL tractus olfactorium lateralis - tpo nucleus posterior thalami - tr nucleus reticularis thalami - trs nucleus triangularis septi - TS tractus solitarius - TS V tractus spinalis nervi trigemini - tvl nucleus ventrolateralis thalami - vmh nucleus ventromedialis hypothalami - vh ventral horn, Columna anterior - zi zona incerta Supported by the Deutsche Forschungsgesellschaft (DFG) SFB 90, Carvas     

Effect of glutaraldehyde fixation on the localization of various oxidative and hydrolytic enzymes in the brain of rhesus monkey, Macaca mulatta

Synopsis Histochemical investigations have been made on the localization of certain oxidative and hydrolytic enzymes in the different areas of rhesus monkey brain using unfixed, freshfrozen tissue and 3% glutaraldehyde-fixed material. After glutaraldehyde fixation, the oxidative enzymes lose most of their activity normally demonstrable in the fresh-frozen section. The hydrolytic enzymes are somewhat resistant to fixation but also lose about half of the enzyme activity observed after no fixing procedure. The glycogen is better preserved in the glutaraldehyde-fixed material compared to fresh-frozen or even formaldehyde-fixed tissue. The significance of these observations is discussed in relation to glutaraldehyde as a fixative of choice in electron histochemistry.List of abbreviations used in the Figures ALH area lateralis hypothalami - APH area posterior hypothalami - AS aquaeductus Sylvii - ATN anterior thalamic nuclei - BC brachium conjunctivum - CC corpus callosum - CD nucleus caudatus - CI capsula interna - CIS cortex insularis - CM centrum medianum thalami - COR corona radiata - CP commissura posterior - CSR colliculus superior - EM eminentia medialis - F fornix - GC substantia grisea centralis - GLM corpus geniculatum laterale, magnocellular part - GLP corpus geniculatum laterale, parvocellular part - GP globus pallidus - LD nucleus lateralis dorsalis thalami - LME lamina medullaris externa thalami - LMI lamina medullaris interna thalami - LP nucleus lateralis posterior thalami - MD nucleus medialis dorsalis thalami - ML nucleus lateralis corpus mammillaris - MM nucleus medialis corpus mammillaris - NC nucleus centralis thalami - NCI nucleus colliculi inferioris - NLL nucleus lemnisci lateralis - NR nucleus ruber - NSTH nucleus subthalamicus - N III nervus oculomotorius - PC nucleus paracentralis thalami - PCR pedunculus cerebri - PUT Putamen - PV nucleus paraventricularis hypothalami - R nucleus reticularis thalami - RU nucleus reuniens thalami - SM stria medullaris thalami - SMH nucleus supramammillaris hypothalami - SMT nucleus submedius thalami - SN substantia nigra - TO tractus opticus - VL nucleus ventralis lateralis thalami - VP nucleus ventralis posterior thalami - ZI zona incerta - II ventriculus lateralis - III ventriculus tertius     

Location of single-stranded and double-stranded regions in rat liver ribosomal 5S RNA and 5.8S RNA.

Rat liver 5S rRNA and 5.8S rRNA were end-labelled with 32P at 5'-end or 3'-end of the polynucleotide chain and partially digested with single-strand specific S1 nuclease and double-strand specific endonuclease from the cobra Naja naja oxiana venom. The parallel use of these two structure-specific enzymes in combination with rapid sequencing technique allowed the exact localization of single-stranded and double-stranded regions in 5S RNA and 5.8 S RNA. The most accessible regions to S1 nuclease in 5S RNA are regions 33-42, 74-78, 102-103 and in 5.8 S RNA 16-20, 26-29, 34-36, 74-80 and a region around 125-130. The cobra venom endonuclease cleaves the following areas in 5S RNA: 7-8, 17-20, 28-30, 49-51, 56-57, 60-64, 69-70, 81-82, 95-97, 106-112. In 5.8S RNA the venom endonuclease cleavage sites are 4-7, 10-13, 21-22, 33-35, 43-45, 51-55, 72-74, 85-87, 98-99, 105-106, 114-115, 132-135. According to these results the tRNA binding sequences proposed by Nishikawa and Takemura [(1974) FEBS Lett. 40, 106-109], in 5S RNA are located in partly single-stranded region, but in 5.8S RNA in double-stranded region.     

Cerebral autoregulation is preserved during orthostatic stress superimposed with systemic hypotension.

We sought to determine whether cerebral autoregulation (CA) is compromised during orthostatic stress superimposed with systemic hypotension. Transient systemic hypotension was produced by deflation of thigh cuffs previously inflated to suprasystolic pressure, combined with or without lower body negative pressure (LBNP). Cardiac output (CO) decreased from a baseline of 5.0+/-0.5 l/min by -8.3+/-1.7, -19.2+/-2.0, and -30.6+/-3.4% during LBNP of -15, -30, and -50 Torr, respectively. Mean arterial pressure (MAP) was maintained during LBNP, despite decreases in systolic and pulse pressures. Middle cerebral arterial blood flow velocity (VMCA) decreased significantly from a baseline of 64+/-3 to 58+/-4 cm/s (-9.7+/-2.4%) at -50 Torr of LBNP. The reduction in VMCA was associated with a decrease in regional cerebral O2 saturation. However, the percent decrease in VMCA was markedly less than that of CO. This suggests that the magnitude of the change in VMCA (an index of cerebral blood flow) is less than would be predicted, given the decrease in CO. Transient systemic hypotension decreased MAP by -21+/-2, -24+/-2, -28+/-3, and -26+/-3% at rest and during LBNP of -15, -30, and -50 Torr, respectively. Likewise, this acute hypotension resulted in decreases in VMCA of -20+/-2, -21+/-2, -24+/-25, and -19+/-2% and regional cerebral O2 saturation of -5+/-1, -6+/-1, -6+/-1, and -7+/-2% at rest and during LBNP of -15, -30, and -50 Torr, respectively. Complete recovery of VMCA to baseline values following transient hypotension (ranging from 5 to 8 s) occurred significantly earlier compared with MAP (from 10 to 12 s). No subjects experienced syncope during acute hypotension. We conclude that CA is preserved during LBNP, superimposed with transient systemic hypotension, despite the decrease in VMCA associated with sustained central hypovolemia in normal healthy individuals. This preserved CA is vital for the prevention of orthostatic syncope.     

Genetic deletion of the tumor necrosis factor receptor p60 or p80 sensitizes macrophages to lipopolysaccharide-induced nuclear factor-kappa B,mitogen-activated protein kinases,and apoptosis

Whether deletion of tumor necrosis factor (TNF) receptor 1 or 2 affects lipopolysaccharide (LPS)-mediated signaling is not understood. In this report, we used macrophages derived from wild type (wt) mice and from mice null for the type 1 receptor (p60-/-), the type 2 receptor (p80-/-), or both (p60-/- p80-/-) to investigate the effect of these receptors on LPS-mediated activation of NF-kappaB, mitogen-activated protein kinases, and apoptosis. LPS activated NF-kappaB by 3-4-fold in wt cells but by 9-10-fold in p60-/-, p80-/-, and p60-/- p80-/- macrophages. These results correlated with the IkappaBalpha kinase activation, which is needed for NF-kappaB activation. LPS-induced cyclooxygenase-2 and inducible NO synthase proteins and NO production were maximum in p60-/- p80-/- macrophages and minimum in wt cells. LPS activated C-Jun N-terminal kinase, p38MAPK, and extracellular signal-regulated kinase in wt cells, but the levels were much higher in p60-/-, p80-/-, and p60-/- p80-/- cells. LPS-induced cytotoxicity, poly(ADP-ribose) polymerase cleavage, and annexin V staining were also highest in p60-/- p80-/- cells and lowest in wt cells. The difference in LPS signaling was unrelated to the expression of LPS receptors, CD14, or toll-like receptor 4. Overall, our studies indicate that deletion of either of the TNF receptors sensitizes the macrophages to LPS and provide evidence for cross-talk between TNF and LPS signaling.     

The distribution of gonadotropin-releasing hormone (GnRH) neurons and fibers throughout the chick brain (Gallus domesticus)

Summary Nerve fibers and perikarya containing gonadotropin-releasing hormone (GnRH-like) immunoreactivity were investigated in the brain of the three-week-old chick, Gallus domesticus using the technique of immunocytochemistry. Six major groups of perikarya were found to include the olfactory bulb, olfactory tubercle/lobus parolfactorius, nucleus accumbens, septal preoptic hypothalamic region (three sub-nuclei), lateral anterior thalamic nucleus and in and about the oculomotor complex. The immunostaining was unusual in the latter group, suggesting that the neurons may contain a GnRH-II like material. Immunoreactive fibers for GnRH were found throughout the entire brain extending from the olfactory bulbs to the caudal brainstem. Two anatomical areas, not emphasized in the past literature, which had distinct GnRH-like immunoreactivity, included the lateral anterior thalamic nucleus and the preoptic recess. The former included a group of GnRH perikarya that is also known to be a retino-recipient area while the latter contained neuronal terminals some of which appeared to be contacting the cerebrospinal fluid of the preoptic recess. An attempt was made to list all anatomical structures that contained or were juxta-positioned to sites that displayed immunoreactive perikarya and fibers including circumventricular organs.Abbreviations used in figure legends Ac Nucleus accumbens - Ap Archistriatum posterior - APH Area parahippocampalis - AVT Area ventralis (Tsai) - BO Bulbus olfactorius - CA Commissura anterior (rostralis) - CDL Area corticoidea dorsolateralis - CO Chiasma opticum - CP Commissura posterior - CPi Cortex piriformis - CPP Cortex praepiriformis - CT Commissura tectalis - CTz Corpus trapezoideum - EW Nucleus of Edinger-Westphal - FV Funiculus ventralis - GCt Substantia grisea centralis - GLv Nucleus geniculatus lateralis, pars ventralis - HD Hyperstriatum dorsale - HM Nucleus habenularis medialis - Hp Hippocampus - ICo Nucleus intercollicularis - IH Nucleus inferior hypothalami - IN Nucleus infundibuli hypothalami - IP Nucleus interpeduncularis - LA Nucleus lateralis anterior (rostralis) thalami - LHy Regio lateralis hypothalami - LPO Lobus parolfactorius - LSO Organum septi lateralis (lateral septal organ) - LT Lamina terminalis - ME Eminentia mediana - INT. Z Internal zone - EXT. Z External zone - ML Nucleus mamillaris lateralis - MM Nucleus mamillaris medialis - nBOR Nucleus opticus basalis (n. of basal optic root) - nCPa Nucleus commissurae pallii - N III Nervus oculomotorius - N V Nervus trigeminus - n V M Nucleus mesencephalicus nervi trigemini - OA Nucleus olfactorius anterior (rostralis) - OMdl Nucleus nervi oculomotorii, pars dorsomedialis - OMv Nucleus nervi oculomotorii, pars ventralis - OVLT Organum vasculosum laminae terminalis - P Glandula pinealis - PA Palaeostriatum augmentatum (caudate putamen) - PHN Nucleus periventricularis hypothalami - POM Nucleus praeopticus medialis - POMn Nucleus praeopticus medianus - POP Nucleus praeopticus periventricularis - PP Palaeostriatum primitivum - PT Nucleus praetectalis - PVN Nucleus paraventricularis magnocellularis - RPaM Nucleus reticularis paramedianus - RPR Recessus praeopticus - b, RPR Basal region, RPR - F, RPR Floor, RPR - R, RPR Roof, RPR - S Nucleus tractus solitarii - SCO Organum subcommissurale - SGP Stratum griseum periventriculare - SHL Nucleus subhabenularis lateralis - SL Nucleus septalis lateralis - SM Nucleus septalis medialis - SO Stratum opticum - SSO Organum subseptale - TO Tuberculum olfactorium - TIO Tractus isthmo-opticus - TPc Nucleus tegmenti pedunculopontinus, pars compacta (substantia nigra) - TrO Tractus opticus - TSM Tractus septomesencephalicus - VeD Nucleus vestibularis descendens - VeM Nucleus vestibularis medialis - VL Ventriculus lateralis - VLT Nucleus ventrolateralis thalami - VO Ventriculus olfactorius - V III Ventriculus tertius (third ventricle)     

Phloroglucinol derivatives from Leucanthemopsis pulverulenta

From roots of Leucanthemopsis pulverulenta, two new phloroglucinol derivatives and (+) sesamin, have been isolated. The new compounds were identified as 1 - acetyl - 4 - isopentenyl - 6 - methylphloroglucinol and 1 - acetyl - 3 - hydroxy - 2,6 - dimethyl - 4 - isopentenylphloroglucinol.     

Suppressor of cytokine signaling 1 stringently regulates distinct functions of IL-7 and IL-15 in vivo during T lymphocyte development and homeostasis

SOCS1(-/-) mice accumulate within the thymus and periphery CD8(+) lymphocytes that express memory cell markers and display heightened in vitro responses to common gamma-chain cytokines. To investigate whether dysregulated homeostasis of T lymphocytes and acquisition of memory phenotype by CD8(+) cells in SOCS1(-/-) mice were mediated by IL-7 and/or IL-15 in vivo, we have generated SOCS1(-/-)IL-7(-/-), SOCS1(-/-)IL-15(-/-) and SOCS1(-/-)IL-7(-/-)IL-15(-/-) mice. We observed that in mice lacking SOCS1, either IL-7 or IL-15 skewed thymocyte development toward CD8 lineage, whereas IL-15 is the principal mediator of dysregulated homeostasis in the periphery. Homeostatic proliferation of SOCS1(-/-) CD8(+) lymphocytes in Rag1(-/-), Rag1(-/-)IL-7(-/-), Rag1(-/-)IL-15(-/-), and Rag1(-/-)IL-7(-/-)IL-15(-/-) mice showed that SOCS1 deficiency did not overcome the requirement for IL-7 and IL-15 to sustain homeostatic expansion. Differential expression of memory phenotype markers CD44, CD122, and Ly6C by SOCS1(-/-)IL-15(-/-) CD8(+) lymphocytes suggest that multiple signals contributed to the memory cell differentiation program. To address whether increased IL-15 responsiveness of SOCS1(-/-) CD8(+) lymphocytes required prior TCR sensitization, we generated SOCS1(-/-) H-Y TCR transgenic (Tg) mice. Using female SOCS1(-/-) H-Y TCR(tg) mice in Rag1(+/+) and Rag1(-/-) backgrounds, we show that acquisition of the memory phenotype by SOCS1-deficient CD8(+) lymphocytes did not require prior antigenic stimulation, but required the presence of activated T cells. SOCS1 deficiency accelerated the maturation of CD8 single-positive thymocytes expressing Tg TCR, but did not compromise negative selection in HY-TCR(tg) males. Our findings illustrate distinct functions for IL-7 and IL-15 in T lymphocyte development and homeostasis, and stringent regulation of these processes by SOCS1.