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Magistretti J, Ragsdale DS, and Alonso A. Kinetic diversity of single-channel burst openings underlying persistent Na + current in entorhinal cortex neurons. Biophys J 85: 3019-3034, 2003. Mainen ZF, and Sejnowski TJ. Influence of dendritic structure on firing pattern in model neocortical neurons. Nature 382: 363-366, 1996. Mandelblat Y, Etzion Y, Grossman Y, and Golomb D. Period doubling of calcium spike firing in a model of a Purkinje cell dendrite. J Comput. Neurosci 11: 43-62, 2001. Martina A, and Jonas P. Functional differences in Na + channel gating between fast-spiking interneurons and principal neurones of rat hippocampus. J Physiol 505: 593-603, 1997. Martina A, Schultz JH, Ehmke H, Monyer H, and Jonas P. Functional and molecular differences between voltage-activated K + channels of fast-spiking interneourns and pyramidal neurons of rat hippocampus. J Neurosci 18: 8111-8125, 1998. Metz AE, Jarsky T, Martina M, and Spruston N. R-type calcium channels contribute to afterdepolarization and bursting in hippocampal CA1 pyramidal neurons. J Neurosci 25: 57635773, 2005. Mickus T, Jung H, and Spruston N. Properties of slow, cumulative sodium channel inactivation in rat hippocampal CA1 pyramidal neurons. Biophys J 76: 846-860, 1999. Pinsky PF, and Rinzel J. Intrinsic and network rhythmogenesis in a reduced Traub model for CA3 neurons. J Comput Neurosci 1, 39-60, 1994. Pumain R, Menini C, Heinemann U, Louvel J, and Silva-Barrat C. Chemical synaptic transmission is not necessary for epileptic seizures to persist in the baboon Papio papio. Exp Neurol 89, 250-258, 1985. Ranck, JB Jr. Studies on single neurons in dorsal hippocampal formation and septum in unrestrained rats. I. Behavioral correlates and firing repertoires. Exp Neurol 41: 461-531, 1973. Rinzel J, and Ermentrout GB. Analysis of neural excitability and oscillations. In: Methods in neuronal modeling: From ions to networks, 2nd ed. ; , edited by Koch C and Segev I. Cambridge, MA: MIT Press, 1998, pp. 251-291. Rush ME, and Rinzel J. The potassium A-current, low firing rates, and rebound excitation in Hodgkin-Huxley models. Bull Math Biol 57: 899-929, 1995. Sah P, Gibb AJ, and Gage PW. Potassium current activated by depolarization of dissociated.
Transition ; in the 78 position of the apolipoprotein A-I promoter increases transcription efficiency. J Biol Chem. 269: 1737117374. Hixson JE, Powers PK. 1991 Restriction isotyping of human apolipoprotein A-IV: rapid typing of known isoforms and detection of a new isoform that deletes a conserved repeat. J Lipid Res. 32: 1529 1535. Tenkanen H, Koskinen P, Metso J, et al. 1992 A novel polymorphism of apolipoprotein A-IV is the result of an asparagine to serine substitution at residue 127. Biochim Biophys Acta. 1138: 2733. Bennett ST, Lucassen AM, Gough SCL, et al. 1995 Susceptibility to human type 1 diabetes at IDDM2 is determined by tandem repeat variation at the insulin gene minisatellite locus. Nat Genet. 9: 284 292. Forster E. 1994 An improved general method to generate internal standards for competitive PCR. BioTechniques. 16: 18 20. Tang J, Lagace G, Collu R. 1996 Simple method for constructing internal standards for competitive PCR. BioTechniques. 21: 378 380. Vafiadis P, Bennett ST, Todd JA, et al. 1997 Insulin expression in human thymus is modulated by INS VNTR alleles at the IDDM2 locus. Nat Genet. 15: 289 292. Schneid H, Seurin D, Noguiez P, Le Bouc Y. 1992 Abnormalities of insulin-like growth factor IGF1 and IGF2 ; genes in human tumor tissue. Growth Regul. 2: 4554. Schneid H, Seurin D, Vasquez M-P, Gourmelen M, Cabrol S, Le Bouc Y. 1993 Parental allele specific methylation of the human insulin-like growth factor-II gene and Beckwith-Wiedemann syndrome. J Med Genet. 30: 353362. Gicquel C, Bertagna X, Schneid H, et al. 1994 Rearrangements at the 11p15.5 locus and overexpression of insulin-like growth factor-II gene in sporadic adrenocortical tumors. J Clin Endocrinol Metab. 78: 1444 1453. Wagner J, Portwine C, Robin K, Leclerc JM, Narod SA, Malkin D. 1994 High frequency of germline p53 mutations in childhood adrenocortical cancer. J Nat Cancer Inst. 86: 17071710. Esrig D, Spruck CH, Nichols PW, et al. 1993 p53 nuclear protein accumulation correlates with mutations in the p53 gene, tumor grade and stage in bladder cancer. J Pathol. 143: 1389 1397. Ilvesmaki V, Kahri AI, Miettinen PJ, Voutilainen R. 1993 Insulin-like growth factors IGFs ; and their receptors in adrenal tumors: high IGF-II expression in functional adrenocortical carcinomas. J Clin Endocrinol Metab. 77: 852 858. Boulle N, Logie A, Gicquel C, Perin L, Le Bouc Y. 1998 Increased levels of insulin-like growth factor II IGF-II ; and IGF-binding protein-2 are associated with malignancy in sporadic adrenocortical tumors. J Clin Endocrinol Metab. 83: 17131720. Reincke M, Karl M, Allolio B, Chrousos GP. 1994 p53 Mutations in human adrenocortical neoplasms: immunohistochemical and molecular studies. J Clin Endocrinol Metab. 78: 483 491. Han VK, Lu F, Bassett N, Yang KP, Delhanty PJ, Challis JR. 1992 Insulin-like growth factor-II IGF-II ; messenger ribonucleic acid is expressed in steroidogenic cells of the developing ovine adrenal gland: evidence of an autocrine paracrine role for IGF-II. Endocrinology. 131: 3100 3109. Mesiano S, Mellon SH, Jaffe RB. 1993 Mitogenic action, regulation, and localization of insulin-like growth factors in the human fetal adrenal gland. J Clin Endocrinol Metab. 76: 968 976. Weber MM, Fottner C, Schmidt P, et al. 1999 Postnatal overexpression of insulin-like growth factor II in transgenic mice is associated with adrenocortical hyperplasia and enhanced steroidogenesis. Endocrinology. 140: 15371543. Zhang L, Kashandi F, Zhan Q, et al. 1996 Regulation of insulin-like growth factor II P3 promoter by p53: a potential mechanism for tumorogenesis. Cancer Res. 56: 13671373. Kleihues P, Schauble B, zur Hausen A, Esteve J, Ohgaki H. 1997 Tumors ` associated with p53 germline mutations: a synopsis of 91 families. J Pathol. 150: 113. Zemel S, Bartolomei MS, Tilghman SM. 1992 Physical linkage of two mammalian imprinted genes, H19 and insulin-like growth factor 2. Nat Genet. 2: 61 65. Brannan CI, Dees EC, Ingram RS, Tilghman SM. 1990 The product of the H19 gene may function as an RNA. Mol Cell Biol. 10: 28 36. Joubel A, Curgy J-J, Pelczar H, Begue A, Lagrou C, Stehelin D, Coll J. 1996 The 5 part of the human H19 RNA contains cis-acting elements hampering its translatability. Cell Mol Biol. 42: 1159 1172. Hurst LD, Smith NG. 1999 Molecular evolutionary evidence that H19 mRNA is functional. Trends Genet. 15: 134 135. Hao Y, Crenshaw T, Moulton T, Newcomb E, Tycko B. 1993 Tumoursuppressor activity of H19 RNA. Nature. 365: 764 767. Cui H, Hedborg F, He L, Nordenskjold A, Sandstedt B, Pfeifer-Ohlsson S, Ohlsson R. 1997 Inactivation of H19, an imprinted and putative tumor repressor gene, is a preneoplastic event during Wilms' tumorogenesis. Cancer Res. 57: 4469 4473. Zhang Y, Tycko B. 1992 Monoallelic expression of the human H19 gene. Nat Genet. 1: 40 44. Leighton PA, Ingram RS, Eggenschwiler J, Efstratiadis A, Tilghman SM. 1995 Disruption of imprinting caused by deletion of the H19 gene region in mice. Nature. 375: 34 39. Liu J, Kahri AI, Heikkila P, Ilvesmaki V, Voutilainen R. 1995 H19 and.
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ABSTRACT: The purpose of this investigation was to evaluate the role of cytochrome P450 CYP ; 3A4 in human liver microsomal bupropion BUP ; hydroxylation. Across the BUP concentration range of 0.075 to 12 mM, cDNA-expressed CYP3A4 demonstrated BUP hydroxylase activity only when incubated with concentrations 4 mM. When assayed at 12 mM BUP, cDNA-expressed CYP3A4 catalyzed BUP hydroxylation at a 30-fold lower rate than cDNA-expressed CYP2B6 0.2 versus 7 pmol min pmol of P450 ; . Among a panel of 16 human liver microsomes HLMs ; , BUP hydroxylase activity varied 80-fold when assayed at 500 M and did not strongly correlate with testosterone 6 -hydroxylase activity when assayed at 250 M testosterone r2 0.39 ; , nor with CYP3A4 protein expression. A selective CYP3A4 inhibitor, troleandomycin TAO ; , did not significantly alter rates of BUP hydroxylation when assayed in a moderate activity HLM at 10 to 2000 M BUP, as reflected by a similarity in the kinetic parameters of BUP hydroxylation in the absence or presence of TAO. In addition, the same range of TAO concentrations 0.025100 M ; that inhibited testosterone 6 -hydroxylation in a concentration-dependent manner 4681% ; in pooled HLMs produced negligible inhibition 7% ; of BUP hydroxylation when assayed at 500 M BUP. These results suggest that CYP3A4 does not significantly catalyze BUP hydroxylation. Furthermore, these results complement recent data supporting selectivity of BUP hydroxylation for CYP2B6 at 500 M BUP.
A symposium held December 7, 2003, in conjunction with the ASHP Midyear Clinical Meeting Planned and conducted by ProCE, Inc. and supported by an educational grant from Scios.
The bv- and adv-mediated gene transfer. The location of the tissue damage is not known nor to what extent the cerebral operation itself had affected the elevated LDH levels. Bvs did not markedly evoke any microglial response, in contrast to the situation after adv transduction. This is very important finding because any inflammatory reaction in the brain after adv-mediated gene transfer could be considered as a safety problem Driesse et al., 1998; Goodman et al., 1996; Ohmoto et al., 1999 ; . The delivery of viral vectors into the brain ventricles usually releases cytokines and induces an adaptive immune response. This kind of reaction was not studied after bv intracerebral injections but it will need to be analyzed before the safety of bv vectors can be fully assessed Lowenstein and Castro, 2003 ; . Injection with bv lead to short time transgene expression. The peak expression was diminished from 80 % of the cells at day 5 ; to 30% at day 10 and had almost vanished 14 days after the bv gene transfer. The reasons for the short-term gene expression are not known. The transgene expression of adv was seen 5 days after the gene delivery and thought it had decreased by 3 weeks, but still remained detectable with 30 % transduction efficiency in corpus callosum and in ependyma. The formation of anti-adv antibodies after adv injections has been shown in study I which may explain partly the transient transgene expression. Biodistribution analyses showed that both virus vectors were detectable in ectopic organs when tissue samples were analysed with RT-PCR 5 days after the gene transfer. Study reports of systemic leakage of adv vector have been published previously by other researchers Lohr et al., 2001 ; . Bvs seemed to have a more pronounced biodistribution, which may be related to their efficient transduction of choroid plexus cells which are a part of the BBB. The bv expression was also occasionally noted in the subarachnoidal space, indicating that viruses had been distributed along the neuraxis via the cerebrospinal fluid. The viruses probably escaped through the arachnoid villi into the systemic circulation and bvs were found in heart, lung, and spleen. After adv injections, transgene expression was seen in brain and in heart. In summary, bv is suitable to be used as an in vivo gene transfer vector with a broad range of target tissues. However, the systemic leakage after intracerebral bv injections does point to the need of further experiments to evaluate the safety and biodistribution of the bv vectors. It is concluded that utilizing the naturally restricted cell tropism, bv may provide an efficient tool for gene delivery to cerebral choroid and tarceva.
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To provide Canadians with: assurance that manufacturers' prices for patented medicines sold in Canada are not excessive achievement to be demonstrated by: review of the manufacturer's prices of 100% of the new and existing patented medicines sold in Canada each year. an annual percentage change in the Patented Medicine Price Index PMPI ; that is not greater than the annual percentage change in the Consumer Price Index CPI ; . manufacturers' prices for new and existing patented medicines no greater than manufacturers' prices charged in other countries. level of compliance as show by the percentage of patented medicines priced within the guidelines. the enforcement measures taken in accordance with the Patent Act to ensure that prices are not excessive information on trends in manufacturers' prices of all medicines in Canada comprehensive reports on: ! trends in manufacturers' prices and volume of patented drug products sold; ! trends in manufacturers' prices of all drug products -- patented and nonpatented; and ! the comparison of Canadian patented drug prices to international prices. comprehensive reports of: ! the ratio of R&D expenditures to sales revenues for each patentee and the industry as a whole based on information supplied by patentees; and ! R&D expenditure by location and by type of research. ongoing consultations with a representative cross-section of stakeholders achievement reported in: See 7.1 7.2 7.4.1.
Notes that the training itself and most related expenses are being paid completely by the Board. Moreover, section 9 of the act 71 P. S. 2109 ; requires the Commission to reimburse counties for the regular salary of deputy sheriffs in training at a 50% rate. Finally, due to other training certifications held, a large percentage of new deputies seeking Board certification are able to obtain required training through the abbreviated waiver course rather than the full basic training course. However, in response to the concerns raised, the Board asked the Commission to undertake a feasibility study regarding whether projected revenues from surcharges assessed under section 8 of the act 71 P. S. 2108 ; could accommodate an increase of the 50% salary reimbursement rate. That study culminated in action taken by the Commission at its September 2001 meeting to endorse legislative action to raise the reimbursement rate to 100%. In response to these comments, the Board reexamined its position on the issue of mandatory versus optional training. Among other things, the Board conducted a meeting on July 10, 2001, with the associations that had submitted comments on the proposed rulemaking. With its approval of this final-form rulemaking, the Board signals its continuing commitment to the concept of uniform training for all new deputies. A uniform standard of training will generate a cadre of professionals who, having undergone the expanded training, will share the same set of enhanced skills. These enhanced skills will provide each deputy with increased employment opportunities, allowing a deputy to move to a county that uses deputies for vehicle patrol even if the current employer does not do so. The Montgomery County Sheriff also noted concern about the Board's practices regarding newly-hired deputies who were eligible for a partial waiver of basic training based on previous completion of a municipal public officers training program. At the time that the proposed rulemaking was published, the Board was requiring candidates for partial waiver to pass a Board waiver test to be able to forego full basic training and take an abbreviated waiver course instead. The commentator pointed out that the additional 200 hours training would be a particular burden for counties whose deputies did not pass the Board's waiver test and, consequently, would be required to take a 760 hour course instead of a waiver course of approximately 100 hours. The sheriff's concerns are no longer pertinent, however, because subsequent to the publication of the proposed rulemaking the Board eliminated the test requirement as a condition for entry into the waiver course. Specific comments of IRRC The Board received several comments from IRRC. The Board will address IRRC's comments in the order in which the regulatory sections appear. 421.1. Definitions In the proposed definition of ``continuing education, '' IRRC considered the term ``periodically'' too vague to describe the frequency of required training, and suggested it be replaced with ``2-years.'' The Board sees merit in this suggestion. However, rather than specifying the time frame, the Board has chosen to redraft the definition by making reference to the applicable statutory cite. The same approach is being taken with the definition of ``basic training.'' The proposed definitions of ``school'' and ``waiver'' are being deleted for stylistic purposes and, in and targretin.
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Under current law, you can pay for eligible dependent care expenses with after-tax dollars. In addition, you can apply some or all of those expenses to the after-tax dependent care tax credit when you file your federal income tax return. Even though you may not apply the same expense to both tax-savings methods, you may apply a portion to the credit and then reimburse yourself from your FSA for any remaining amounts. You are encouraged and directed to talk with your own tax advisor, but as a general rule: If your family's total annual adjusted gross income is above , 000, you probably will save more if you use the dependent care FSA. If your family's total annual adjusted gross income is at or below , 000, the best method to use will vary according to your individual circumstance. You may want to estimate your tax savings using both methods and compare the results. For the care of one dependent, you can generally take a tax credit of up to , 400 in expenses each year. For two or more dependents, the credit is , 800. The tax credit amount varies depending on your income. And, if you use your FSA and the tax credit, the maximum amount deducted through the tax credit is reduced by any amount you receive as reimbursement from the dependent care FSA.
M. Ruiz-Ortega et al. 27. Klahr S, Schreiner G, Ichikawa I. The progression of renal disease. N Engl J Med 1988; 318: 16571666 Wolf G, Neilson EG. Molecular mechanism of tubulointerstitial hypertrophy and hyplerplasia. Kidney Int 1991; 39: 401420 Strutz F. Novel aspects of renal fibrogenesis. Nephrol Dial Transplant 1995; 10: 15261532 Wiggins R, Goyal M, Merritt S, Killen PD. Vascular adventitial cell expression of collagen type I messenger ribonucleic acid in antiglomerular membrane antibody-induced crescentic nephritis in rabbit. Lab Invest 1993; 68: 557565 Rodemann HP, Muller GA. Characterization of human renal fibroblast in health and disease, II, in vitro growth, differentiation, and collagen synthesis of fibroblast from kidneys with intrestitial fibrosis. J Kidney Dis 1991; 17: 684686 Yurchenco PD, Schittny JC. Molecular architecture of basement membranes. FASEB J 1990; 4: 15771590 Ignotz RA, Massague J.Transforming growth factor-b stimulates the expression of fibronectin and collagen and their deposition into the extracellular matrix. J Biol Chem 1986; 261: 43374345 Alvarez RJ, Sun MJ, Haverty TP, Iozzo RV, Myers JC, Neilson EG. Biosynthetic and proliferative characteristics of tubulointerstitial fibroblast probed with paracrine cytokines. Kidney Int 1992; 41: 1423 Ruiz-Ortega M, Egido J. Angiotensin II modulates cell growthrelated events and synthesis of matrix proteins in renal interstitial fibroblasts. Kidney Int 1997; 52: 000000 36. Egido J. Vasoactive hormones and renal sclerosis. Kidney Int 1996; 49: 578597 Gillery P, Marquat FX, Borel JP. Fibronectin dependence of the contraction of collagen by human skin fibroblast. Exp Cell Res 1986; 167: 2937 Bruggeman LA, Horigan EA, Horikoshi S, Ray PE, Klotman PE. Thromboxane stimulates synthesis of extracellular matrix proteins in vitro. J Physiol 1991; 261: F488F494 39. Bruggeman LA, Pellicoro JA, Horigan EA, Klotman PE. Thromboxane and prostacyclin differentially regulate murine extracellular matrix gene expression. Kidney Int 1993; 43: 12191225 Bazan H, Tao Y, Bazan NG. Platelet-activating factor induces collagenase expression in corneal epithelial cells. Proc Natl Acad Sci USA 1993; 90: 86788682 Gutierrez S, Miguelez R, Sanchez-Pernaute O, Palacios I, Egido J, Herrero-Beaumont G. Involvement of platelet-activating factor in fibronectin deposition. Studies in vivo and in vitro. Br J Rheumatol 1997; 36: 1S96 Cross F, Roberts J, Weintraub H. Simple and complex cell cycles. Ann Rev Cell Biol 1989; 5: 341395 Fine L. The biology of renal hypertrophy. Kidney Int 1986; 29: 619634 Received for publication: 25.4.97 Accepted in revised form: 19.12.97 and tarka.
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II clinical trials--in which drugs are examined for efficacy, dosage, and side effects--and phase III clinical trials--in which drugs are further tested against current standards of care and for rare side effects--could decrease by "enriching" the study population with people having the candidate genotypes. As a result, fewer participants would be needed to achieve the anticipated effect, and the time spent on these stages of drug development would decrease. The drug would then be labeled for use only by people with the genotypes in question. Although such approaches may prove to be efficacious, the question remains of whose genotypes will be the foci of interest for these newly tailored therapeutics. Unless the entire population is genotyped, how will race and ethnicity influence decisions to selectively enroll individuals into clinical trials? What are the scientific, economic, and medically relevant issues that will inform such decisions? And how will such decisions affect current health disparities?.
Bypass for massive obesity. Int J Obes Relat Metab Disord. 1997; 21: 38792. Westerterp-Plantenga MS, Lejeune MP, Nijs I, van Ooijen M, Kovacs EM. High protein intake sustains weight maintenance after body weight loss in humans. Int J Obes Relat Metab Disord. 2004; 28: 57 Ranganath L, Norris F, Morgan L, Wright J, Marks V. The effect of circulating non-esterified fatty acids on the entero-insular axis. Eur J Clin Invest. 1999; 29: 2732. Rissanen P, Franssila-Kallunki A, Rissanen A. Cardiac parasympathetic activity is increased by weight loss in healthy obese women. Obes Res. 2001; 9: 637 Herrmann C, Goke R, Richter G, Fehmann HC, Arnold R, Goke B. Glucagon-like peptide-1 and glucose-dependent in sulin-releasing polypeptide plasma levels in response to nutrients. Digestion. 1995; 56: 11726. Mersebach H, Svendsen OL, Holst JJ, Astrup A, FeldtRasmussen U. Comparisons of leptin, incretins and body composition in obese and lean patients with hypopituitarism and healthy individuals. Clin Endocrinol Oxf ; . 2003; 58: 65 Goldstone AP, Morgan I, Mercer JG, et al. Effect of leptin on hypothalamic GLP-1 peptide and brain-stem pre-proglucagon mRNA. Biochem Biophys Res Commun. 2000; 269: 3315. Naslund E, Gutniak M, Skogar S, Rossner S, Hellstrom PM. Glucagon-like peptide 1 increases the period of postprandial satiety and slows gastric emptying in obese men. J Clin Nutr. 1998; 68: 52530. Anderson JW, Konz EC. Obesity and disease management: effects of weight loss on comorbid conditions. Obes Res 2001; 9 Suppl 4 ; : 326S34S. Landry N, Bergeron N, Archer R, et al. Whole-body fat oxidation rate and plasma triacylglycerol concentrations in men consuming an ad libitum high-carbohydrate or low-carbohydrate diet. J Clin Nutr. 2003; 77: 580 and taxol.
Chinh sach kinh t6 6 dja phucmg duqc ujr thac cho cac cAp chinh q u y dia ph~rcmg.C i hai nu& d2u co doanh thu thug tr n GDP suy giim, trong khi tf 1e thu chi d o chinh q u y dja phucmg ki6m soht lai tiing. Cic thoi thusn chia s&t.hu6 tao ra cic hi h g dong ccr khuysn khich quan trong 6 c i hai qu6c gia. 6Nga, Lust v6 cic nguysn tic ca b i cfia thug khoi quy d w phdn bd thug t6i cic cap chinh quyan dia phucmg kh6c nhau duqc ban h i n 1991, h u n g khbng duqc thi hhnh mot chch nhit quhn. Tren thuc t&, thim quy&ndhnh thu6 c i a chinh quy6n cic cap v i mirc dQ phdn chia doanh thu thug duqc xac djnh th8ng qua chc cuoc dam phan li n tqc, v6i kst q u i ph&n anh s u thay ddi c2n bing q u y luc chinh tri.'9 Cic tip chinh quy&n thip hcm thu d t q thhnh cbng trong tiing doanh thu thu6 dia phucmg c i k g thubng bi cit giim tucmg h g cic khoin chuyin nhugng tir thba thuan chia s6 thug &a cic tip cao hcm. Mot nghi nc h nhsn thAy, d6i v6i mot s8 thhnh ph8 6 Nga, s u cgt giim nhy vh s u gia t5ng doanh thu thus dia phucmg cb m6i quan h nhu mot - mop. Nghi6n c h nhy c i k thAy mirc 68 tai 66 cic chinh quy&n dja p h u ki6m soht duqc doanh thu thug gia tZng co vai trb quan trong d6i v6i hoat dong kinh t s b dia phucmg. N ~ U nhu mirc cgt giim chuyi!n nhuqng nhy vh di k6m v& doanh thu thus gia tiing c i a thhnh ph6 chng cao thi tjr 1e thhnh l$p doanh nghi pm6i chng thip. b Trung Qu8c trong thsp ni n1980, chinh quy$n trung ucmg xhc l$p cac 9 1e vh dua ra ccr s b cho n h i loai thus, h u n g viec thu thu6 duqc u? thic cho chinh quysn tinh. Doanh thu thus duqc chia sP theo mot he th8ng "khoin thus". Trong thlri gian giiia n i m 1985 vh 1988, n h k g qui dinh nhy cho phkp cic tinh thdm hut thi khoa duqc giCi lai doanh thu thu6 cao hcm vh c6c tinh thgng d u thi khoh duqc gifi lai thAp hcm. ~ i 6 nhy lhm suy ysu dong ccr thu thus vh u d$n dsn vi ct8c do gia t h g doanh thu thu6 cham lai b cic tinh giiu nhit. I36 d8i ph6 lai, trong thbi gian gitia nZm 1988 vh 1993, h th6ng niy duqc thay ddi nhim cho phkp chinh quy&n.
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In both groups of rats, BrdU-positive nuclei could be distinguished on the basis of their different patterns of labelling Fig. 9 ; . Nuclei intensely and diffusely labelled corresponding to type 1 of Takahashi et al. 1992 ; were the minority and showed the sharpest radial distribution Fig. 10a, c, e, g ; . In normal P40 rats, type 1 cells labelled after E14, 15, 16 injections Fig. 10a ; were mostly located in layers V and VI. The number of cells in layers II, III and IV increased gradually, from dorsal to ventral, and was maximal near the rhinal sulcus. Type 1 cells labelled after E17, 18, 19 injections Fig. 10c ; were mostly distributed throughout layers II and III although several were also in layers IV, V and, dorsally, in layer VI. In hypothyroid rats, the distribution of type 1 cells was much more widespread than that described above. Indeed, these animals could be distinguished from normal ones on simple inspection of the histological preparations in double-blind tests, and irrespective of the age at injection. Cells labelled after E14, 15, 16 injections Fig. 10b ; were also mainly located in layers V and VI, but some were also found in all the other layers. A particularly striking finding was the high number of labelled cells in the subcortical white matter, including locations corresponding to the subplate of the developing neocortex Figs 9 and 10e ; . Similarly, cells labelled after E17, 18, 19 injections were found in all layers, including the white matter, although the majority were in layers IIIV Fig. 10g ; . In both normal and hypothyroid rats, the distribution of diffusely labelled nuclei but lighter than type 1 and with clumped chromatin type 2 of Takahashi et al., 1992 ; was comparable to that described for type 1 cells although the radial distributions were less sharp Fig. 10b, d, f, h ; . The proportion of type 1 and 2 nuclei plotted along radially oriented probes see Materials and Methods ; was calculated for radial sectors, roughly corresponding to the cortical layers Fig. 11 ; . After E14, 15, 16 injections, in normal rats, 69.8% of labelled cells were in layer VI, 25.7% in layer V, and the remaining 4.5% in the other layers. In hypothyroid rats, the proportion of labelled nuclei in layers VI 62.1% ; and V 17.3% ; , normalized to the cortical layering of normal rats, was lower than in the latter P 0.005 instead, 13.2% of labelled nuclei were found in the subcortical white matter 0.6% in normal rats ; and 1.8% in layers II and III 0.8% in normal rats ; . After E17, 18, 19 injections, in normal rats, labelled nuclei were mostly found in layers IIIII 47.5% ; , IV 22.0% ; , V 22.8% ; and VI 7.0% none were found in the white matter. In hypothyroid rats, the proportion of labelled neurons decreased with respect to normal P 0.005 ; in layers IIIII 35.5% ; and IV 15.0% ; while it increased in layers V 29.8% ; and VI 15.8% ; and in the white matter 1.5.
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