Transformation of the Rice Marketing System and Myanmar's Transition to a Market Economy

Creating a rice marketing system has been one of the central policy issues in Myanmar's move to a market economy since the end of the 1980s. Two liberalizations of rice marketing were implemented in 1987 and 2003. This paper examines the essential aspects of the liberalizations and the subsequent transformation of Myanmar's rice marketing sector. It attempts to bring into clearer focus the rationale of the government's rice marketing reforms which is to maintain a stable supply of rice at a low price to consumers. Under this rationale, however, the state rice marketing sector continued to lose efficiency while the private sector was allowed to develop on condition that it did not jeopardize the rationale of stable supply at low price. The paper concludes that the prospect for the future development of the private rice marketing sector is dim since a change in the rice market's rationale is unlikely. Private rice exporting is unlikely to be permitted, while the domestic market is approaching the saturation point. Thus, there is little momentum for the private rice sector to undertake any substantial expansion of investment.

Diário da Constituinte [gravação de vídeo] : [programa n. 611]

Ainda não há acordo sobre a votação da anistia aos microempresários. Diante disso a votação do tema segue indefinida. O plenário retomou a votação das disposições transitórias, votando temas que já foram acordados entre as lideranças. A votação sobre a anistia aos micros e pequenos empresários urbanos e aos pequenos e médios empresários rurais continua em impasse. O texto prevê o não pagamento da correção monetária dos empréstimos concedidos aos microempresários na época do Plano Cruzado. O governo alega que a anistia prejudicaria os bancos e provocaria o aumento dos impostos. A negociação entre governo e os constituintes já dura mais de uma semana A expectativa é que ocorra um entendimento para que haja justiça aos microempresários prejudicados. Havendo um acordo pode-se mudar radicalmente o previsto na emenda da anistia.

Ms.Ff.F.Stoltze 3. 33 - Brief von Jacob Daltroff an Friedrich Stoltze

Friedrich Stoltze II: Grab

(Table 1) Age and sedimentation rates of Pleistocene/Holocene sequences at DSDP Sites 86-580 and 94-611

The recovery from the North Atlantic (Site 611) of a continuous Pleistocene sedimentary record with a siliceous microfaunal component made it possible to compare the high-latitude abundance pattern of the radiolarian species Cycladophora davisiana in the Atlantic with that produced from analyses of a high-latitude record (Site 580) from the northwest Pacific. Previous studies had shown that the late Pleistocene (0-0.45 Ma) abundance variations of this species in these high-latitude regions were similar. Cycladophora davisiana maxima in the North Atlantic record reach abundance levels three to four times higher than C. davisiana maxima registered in sediments from the northwest Pacific site. This difference in magnitude of abundance peaks is most likely an effect of the more northerly location of Site 611 (53°N) compared with that of Site 580 (42°N), since high-latitude time-slice studies have shown a direct relationship between increasing latitude and C. davisiana abundance. Discontinuous preservation of radiolarians in sediments from North Atlantic Site 611 allows only tentative correlation of the North Atlantic and northwest Pacific C. davisiana abundance curves. These correlations are confined to those portions of the cores where ages are tightly constrained by magnetic boundaries, and to intervals with comparable sedimentation rates.

Association of a disintegrin and metalloprotease 33 (ADAM33) gene polymorphisms with the risk of COPD: An updated meta-analysis of 2,644 cases and 4,804 controls

A series of observational studies have been made to investigate the association of the ADAM33 gene polymorphisms with the risk of COPD, but their results were conflicting. Therefore, we performed an updated meta-analysis to quantitatively summarize the associations of ADAM33 gene polymorphisms with the risk of COPD. Thirteen case–control studies referring to nine SNPs were identified: V4 (rs2787094), T+1 (rs2280089), T2 (rs2280090), T1 (rs2280091), S2 (rs528557), S1 (rs3918396), Q−1 (rs612709), F+1 (rs511898) and ST+5 (rs597980). A dominant model (AA+Aa vs. aa), recessive model (AA vs. Aa+aa), additive model (AA vs. aa) and allelic model (A vs. a) were used to evaluate the association of ADAM33 polymorphism with the risk of COPD. The results indicated that significant associations were found for ADAM33 T1, T2, S1, Q−1, F+1 and ST+5 polymorphisms associated with the risk of COPD in different populations. However, no significant associations were found for V4, T+1 and S2 polymorphisms with the risk of COPD in all genetic models, even in the subgroup analysis by ethnicity. This meta-analysis provided evidence that the ADAM33 T1, T2, S1, Q−1, F+1 and ST+5 six locus polymorphisms association with the risk of COPD. Furthermore, T2, Q−1 and ST+5 indicated an association with the risk of COPD in the European populations, whereas T1, T2, S1, F+1 and Q−1 indicated an association with the risk of COPD in the Asian populations.

Identification of the Meckel syndrome gene (MKS1) exposes a novel ciliopathy

Meckel syndrome (MKS, MIM 249000) is an autosomal recessive developmental disorder causing death in utero or shortly after birth. The hallmarks of the disease are cystic kidney dysplasia and fibrotic changes of the liver, occipital encephalocele with or without hydrocephalus and polydactyly. Other anomalies frequently seen in the patients are incomplete development of the male genitalia, club feet and cleft lip or palate. The clinical picture has been well characterized in the literature while the molecular pathology underlying the disease has remained unclear until now. In this study we identified the first MKS gene by utilizing the disease haplotypes in Finnish MKS families linked to the MKS1 locus on chromosome 17q23 (MKS1) locus. Subsequently, the genetic heterogeneity of MKS was established in the Finnish families. Mutations in at least four different genes can cause MKS. These genes have been mapped to the chromosomes 17q23 (MKS1), 11q13 (MKS2), 8q22 (MKS3) and 9q33 (MKS4). Two of these genes have been identified so far: The MKS1 gene (this work) and the MKS3 gene. The identified MKS1 gene was initially a novel human gene which is conserved among species. We found three different MKS mutations, one of them being the Finnish founder mutation. The information available from MKS1 orthologs in other species convinced us that the MKS1 gene is required for normal ciliogenesis. Defects of the cilial system in other human diseases and model organisms actually cause phenotypic features similar to those seen in MKS patients. The MKS3 (TMEM67) gene encodes a transmembrane protein and the gene maps to the syntenic Wpk locus in the rat, which is a model with polycystic kidney disease, agenesis of the corpus callosum and hydrocephalus. The available information from these two genes suggest that MKS1 would encode a structural component of the centriole required for normal ciliary functions, and MKS3 would be a transmembrane component most likely required for normal ciliary sensory signaling. The MKS4 locus was localized to chromosme 9q32-33 in this study by using an inbred Finnish family with two affected and two healthy children. This fourth locus contains TRIM32 gene, which is associated to another well characterized human ciliopathy, Bardet Biedl syndrome (BBS). Future studies should identify the MKS4 gene on chromosome 9q and confirm if there are more than two genes causing MKS Finnish families. The research on critical signaling pathways in organogenesis have shown that both Wnt and Hedgehog pathways are dependent on functional cilia. The MKS gene products will serve as excellent model molecules for more detailed studies of the functional role of cilia in organogenesis in more detail.

Plan poselkov Nº Nº 5, 6 uchastku 33 - 58

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Plan zemelʻnogo uchastka poselka N 33

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High-level expression of biologically active glycoprotein hormones in Pichia pastoris strains—selection of strain GS115, and not X-33, for the production of biologically active N-glycosylated 15N-labeled phCG

The methylotrophic yeast Pichia pastoris is widely used for the production of recombinant glycoproteins. With the aim to generate biologically active 15N-labeled glycohormones for conformational studies focused on the unravelling of the NMR structures in solution, the P. pastoris strains GS115 and X-33 were explored for the expression of human chorionic gonadotropin (phCG) and human follicle-stimulating hormone (phFSH). In agreement with recent investigations on the N-glycosylation of phCG, produced in P. pastoris GS115, using ammonia/glycerol-methanol as nitrogen/carbon sources, the N-glycosylation pattern of phCG, synthesized using NH4Cl/glucose–glycerol–methanol, comprised neutral and charged, phosphorylated high-mannose-type N-glycans (Man8–15GlcNAc2). However, the changed culturing protocol led to much higher amounts of glycoprotein material, which is of importance for an economical realistic approach of the aimed NMR research. In the context of these studies, attention was also paid to the site specific N-glycosylation in phCG produced in P. pastoris GS115. In contrast to the rather simple N-glycosylation pattern of phCG expressed in the GS115 strain, phCG and phFSH expressed in the X-33 strain revealed, besides neutral high-mannose-type N-glycans, also high concentrations of neutral hypermannose-type N-glycans (Manup-to-30GlcNAc2). The latter finding made the X-33 strain not very suitable for generating 15N-labeled material. Therefore, 15N-phCG was expressed in the GS115 strain using the new optimized protocol. The 15N-enrichment was evaluated by 15N-HSQC NMR spectroscopy and GLC-EI/MS. Circular dichroism studies indicated that 15N-phCG/GS115 had the same folding as urinary hCG. Furthermore, 15N-phCG/GS115 was found to be similar to the unlabeled protein in every respect as judged by radioimmunoassay, radioreceptor assays, and in vitro bioassays.

Studies of phosphazenes. Part 33. Thermal rearrangement of alkoxy(p-methylphenoxy)cyclophosphazenes: a synthetic route to oxocyclophosphazanes, phosphazadienes and phosphaz-1-enes

The aryloxy(alkoxy)cyclotriphosphazenes N3P3(OR)6�m(OC6H4Me-p)n(R = Me, n= 1�3; R = Et or CH2Ph, n= 3) rearrange on heating to give trioxocyclotriphosphazanes; the di- and mono-methoxy derivatives, N3P3(OMe)6�n(OC6H4Me-p)n(n= 4 or 5), yield dioxophosphaz-1-enes and an oxophosphazadiene respectively. The 1H, 13C and 31P NMR data for the starting materials and the products are presented. No evidence has been found for partially rearranged products. The geometrical disposition of the aryloxy groups in the starting material is retained in the rearranged products. Some aspects of the mechanism of the thermal rearrangement are discussed.

Ukrainan vuosien 1932-33 nälänhädän historiapolitiikka

Ukrainan presidentiksi nousi ns. oranssin vallankumouksen nosteessa Viktor Justsenko. Hänen presidenttikaudellaan (2005-2010) vuosien 1932-33 nälänhätä (holodomor) nousi keskeiseksi sekä sisä-, että ulkopolitiikan teemaksi. Holodomor, joka viittaa nälällä aiheutettuun tuhoon, pyrittiin tuomaan osaksi ukrainalaista kollektiivista muistia. Justsenkon aloitteesta säädettiin laki, jonka mukaan holodomor oli ukrainalaisten kansanmurha. Vuosina 1932-33 ympäri Neuvostoliittoa vallitsi nälänhätä. Ukrainalainen maaseutu kärsi pahoin nälänhädän seurauksista, sillä eri arvioiden mukaan 3,5-10 miljoonaa ukrainalaista menehtyi joko suoranaisesti tai välillisesti nälänhädän seurauksena. Ukrainan itsenäistyttyä nälänhätä, jota oli diasporassa alettu kutsua holodomoriksi (nälkätuho), nousi kansallisen historian keskeiseksi teemaksi. Ukrainalainen historioitsija Georgi Kasjanov on nimittänyt tätä uutta vaihetta historian kansallistamiseksi. Tässä työssä pohditaan sitä, miksi holodomor nostettiin keskeiseen asemaan presidentti Viktor Justsenkon valtakaudella. Keskeinen vastakkainasettelun lähtökohta on ollut itsenäisen Ukrainan ja Neuvostoliiton seuraajavaltion Venäjän suhtautuminen nälänhätään 1932-33. Ukrainalaisissa näkökulmissa on painottunut stalinistisen järjestelmän kritiikki, mikä toisaalta on saatettu tulkita myös koko kommunistisen aikakauden tuomitsemiseksi. Venäjällä taas nälänhätä on tulkittu useimmiten yleisneuvostoliittolaiseksi tragediaksi, joka ei kohdistunut erityisesti mitään tiettyä kansallisuutta vastaan. Tutkimuksen keskeinen lähtökohta on tarkastella ukrainalaisten ja venäläisten tulkintojen eroja ja sitä, millä tavoin holodomorilla on tehty politiikkaa. Tutkimusaineistona on käytetty ukrainalaisten osalta presidentti Justsenkon puheita, lakialoitteita ja muita julkilausumia, sekä eräiden yhteiskunnallisten toimijoiden ja historioitsijoiden kannanottoja. Venäläisen osapuolen tulkintoja on pyritty luomaan muutamien tutkimusten ja yhteiskunnallisten toimijoiden, sekä poliitikkojen lausumien pohjalta. Suurin osa aineistosta on kerätty venäjänkielisistä verkkolehdistä. Presidentti Justsenkolle vuosien 1932-1933 historiasta muodostui ase, jolla hän kävi omaa poliittista taisteluaan lännen puolesta itää vastaan. Välit Venäjään olivat viileät koko hänen presidenttikautensa ajan. Lähimmäksi presidentin kantaa holodomor-kysymyksessä tulivat diasporaukrainalaiset. Venäjällä kritisoitiin ankarasti Justsenkon tanssia haudoilla eli hänen tapaansa käyttää nälänhädän uhreja oman politiikkansa välineenä. Venäläiset korostivat nälänhädän tragediaa kaikkien Neuvostoliiton kansojen tragediana. Holodomor oli osa kansallisen historian uudelleenkirjoitusta ja kansakunnan rakentamisen prosessia. Justsenkon päämääränä oli lähentää Ukrainaa länteen, jolloin ukrainalaisen kansakunnan uhriasema antoi oikeutuksen sanoutua irti neuvostoajasta. Tietyssä mielessä holodomor-projekti oli venäläisvastainen, sillä se implisiittisesti tuki käsitystä venäläisistä rikollisina, kansanmurhan toimeenpanijoina.