Exports, Technical Progress and Productivity Growth in Chinese Manufacturing Industries

Theories suggesting either static or dynamic productivity gains derived from exports often assume the prior existence of a perfect market. In the presence of market failure, however, the competition effect and the resource reallocation effect of exports on productive efficiency may be greatly reduced; and there may actually be disincentives for innovation. This paper analyses the impact of exports on total factor productivity (TFP) growth in a transition economy using a panel of Chinese manufacturing industries over the period 1990-1997. TFP growth is estimated by employing a non-parametric approach and is decomposed into technical progress and efficiency change. We have not found evidence suggesting significant productivity gains at the industry level resulting from exports. Findings of the current study suggest that, for exports to generate significant positive effect on TFP growth, a well?developed domestic market and a neutral, outward-oriented policy are necessary.exports, industrial efficiency, technical progress, productivity

Systematic review of new medics’ clinical task experience by country

OBJECTIVES: There is a need for research which informs on the overall size and significance of clinical skills deficits among new medics, globally. There is also the need for a meta-review of the similarities and differences between countries in the clinical skills deficits of new medics. DESIGN: A systematic review of published literature produced 68 articles from Google/Scholar, of which 9 met the inclusion criteria (quantitative clinical skills data about new medical doctors). PARTICIPANTS: 1329 new medical doctors (e.g., foundation year-1s, interns, PGY1s). SETTING: Ten countries/regions. MAIN OUTCOME MEASURES: 123 data points and representation of a broad range of clinical procedures. RESULTS: The average rate of inexperience with a wide range of clinical procedures was 35.92% (lower CI 30.84%, upper CI 40.99%). The preliminary meta-analysis showed that the overall deficit in experience is significantly different from 0 in all countries. Focusing on a smaller selection of clinical skills such as catheterisation, IV cannulation, nasogastric tubing and venepuncture, the average rate of inexperience was 26.75% (lower CI 18.55%, upper CI 35.54%) and also significant. England presented the lowest average deficit (9.15%), followed by New Zealand (18.33%), then South Africa (19.53%), Egypt, Kuwait, Gulf Cooperation Council countries and Ireland (21.07%), after which was Nigeria (37.99%), then USA (38.5%), and Iran (44.75%). CONCLUSION: A meta-analysis is needed to include data not yet in the public domain from more countries. These results provide some support for the UK General Medical Council’s clear, detailed curriculum, which has been heralded by other countries as good practice

A national register for surveillance of inherited disorders: beta thalassaemia in the United Kingdom

OBJECTIVE: To demonstrate the value of a national register for surveillance of services for an inherited disorder. METHODS: Data from the United Kingdom Thalassaemia Register and the United Kingdom Register of Prenatal Diagnosis for Haemoglobin Disorders were combined in a database; these registers include all fetuses known to have been diagnosed with beta thalassaemia major, beta thalassaemia intermedia, or haemoglobin E/beta thalassaemia in the United Kingdom. Data were extracted to show outcomes (selective abortion or live birth) of all fetuses and the status of those born with a disorder (alive, dead, successful bone marrow transplant, or lost to follow-up) by parents' region of residence and ethnicity. FINDINGS: At the end of 1999 the register included 1074 patients, 807 of whom were alive and residing in the United Kingdom. A successful bone marrow transplant has been performed for 117 out of 581 (20%) patients born since 1975. Residents of Pakistani origin are now the main group at risk in the United Kingdom, replacing residents of Cypriot origin. This has led to a marked shift in the need for services from the south-east of England to the Midlands and the north of England. Despite the acceptability of prenatal diagnosis, the proportion of affected births remains 50% higher than would be expected, reflecting a widespread failure to deliver timely screening and counselling to carriers. Even though effective treatment is available the annual number of deaths is rising, indicating that better tolerated treatments are needed. CONCLUSION: A national diagnosis register is a powerful instrument for monitoring the treatment and prevention of inherited disorders and for highlighting correctable shortcomings. In view of the increasing possibilities for genetic screening there is a strong case for central funding for such databases within modern health services

ANTIGENS OF LEUKEMIAS INDUCED BY NATURALLY OCCURRING MURINE LEUKEMIA VIRUS: THEIR RELATION TO THE ANTIGENS OF GROSS VIRUS AND OTHER MURINE LEUKEMIA VIRUSES

Leukemias can be induced in W/Fu inbred rats by neonatal inoculation of normal thymus cells of C58 mice. These leukemias are not transplantable to C58 mice or to adult W/Fu rats, but they can be kept in passage in W/Fu rats aged 0 to 7 days. Adult W/Fu rats inoculated repeatedly with these isogenic leukemias produce cytotoxic and precipitating antibodies. These antisera are of particular value in the analysis of the antigens of leukemia cells and of leukemia viruses because their mode of preparation precludes the formation of antibody against any normal constituents of the cell. Analysis based on the cytotoxic test indicates the presence of 2 distinct cell surface antigens in leukemias induced by Passage A Gross virus or occurring spontaneously in mice of high-incidence strains. All leukemias and other tissues known to contain G (Gross) leukemia antigen have both determinants, but certain leukemias of low-incidence strains have only 1 of them and so were previously classified G-. Immunoprecipitation with these antisera reveals the presence of a cellular antigen common to G+ cells and absent from G- cells; the same antigen can be demonstrated in ether-treated Gross virus, but not in intact virus. This antigen is present also in ether-treated preparations of the Friend, Moloney, and Rauscher leukemia viruses, but not in Bittner (mammary tumor) virus. Thus it may be regarded as a group-specific antigen of murine leukemia viruses, in contrast to the type-specific cellular antigens demonstrable by the cytotoxic test. Four additional antigens associated with leukemias induced by wild-type Gross virus have been demonstrated by immunoprecipitation, but their relation to viral and cellular antigens has not been determined

SURFACE ALLOANTIGENS OF PLASMA CELLS

A serological study of immunoglobulin-forming cells of the mouse, normal and malignant, shows that they lack all known surface differentiation antigens of the thymocyte-lymphocyte axis: TL, θ, Ly-A, Ly-B, and MSLA. Two systems of normal alloantigens are expressed on these cells, H-2 and a new system named PC. The gene Pca (Plasma cell antigen) which specifies PC.1 alloantigen segregates as a mendelian dominant not closely linked with H-2. This cell surface antigen is absent from thymocytes, leukemias, and very probably from thymus-derived lymphocytes also; it is present on cells of the liver, kidney, brain, and lymph nodes as well as on hemolytic plaque-forming cells of the spleen, and on myelomas. So PC.1 is properly classified as a differentiation alloantigen. The strain distribution of PC.1 does not conform to that of any known immunoglobulin allotype or cell surface alloantigen previously described. Thus the cell surface antigens of immunoglobulin-producing cells are clearly different from those of cells belonging to the thymocyte-lymphocyte axis. Each family of cells has distinctive alloantigens, and the two families share alloantigens of only one known system, H-2. This implies that either immunoglobulin-producing cells are not derived from thymic lymphocytes, or if they are, the program responsible for the transition must include extensive revision of cell surface structure

PRODUCTION OF TL ANTIBODY BY MICE IMMUNIZED WITH TL- CELL POPULATIONS : A POSSIBLE ASSAY FOR THYMIC HORMONE

TL- mice make TL antibody when immunized with spleen or bone marrow cells from TL+ donors, despite the fact that these cells do not express TL antigen. This has been shown to depend on maturation of TL- precursors, contained in the inoculum, into TL+ cells under influence of the recipient's thymus; the differentiated TL+ cells then evoke production of TL antibody

ISOANTIGENS OF THE H-2 AND Tla LOCI OF THE MOUSE : INTERACTIONS AFFECTING THEIR REPRESENTATION ON THYMOCYTES

H-2 and TL isoantigens of the mouse are specified by the closely linked genetic loci H-2 and Tla. A. study of their representation on thymocytes was performed in order to reveal any interactions between the determinant genes or their products affecting the synthesis or disposition of these components of the thymocyte surface. The method employed was quantitative absorption of cytotoxic antibody by viable thymocytes. The phenotypic expression of TL antigens was found to reduce the demonstrable amount of certain H-2 antigens to as little as 34% of the quantity demonstrable on TL- thymocytes. A reduction was observed in all three H-2 types tested, (H-2b, H-2a, and H-2k). As antigenic modulation (change of TL phenotype from TL+ to TL-, produced by TL antibody) is known to entail a compensatory increase in H-2(D) antigen, it is concluded that the TL phenotype, rather than the Tla genotype, influences the surface representation of H-2 antigens. The two known TL+ phenotypes of thymocytes (TL.2 and TL.1,2,3) depress H-2 equally. The H-2 specificities affected are those determined by the D end of the E-2 locus, which is adjacent to Tla; antigens of the K end, which is distal to Tla, are not depressed. The reduction of demonstrable H-2 antigen on the thymocytes of TL+ x TL- progeny is half that of thymocytes of TL+ x TL+ progeny and the reduction affects equally the products of both H-2 alleles (cis and trans in relation to Tla), indicating that the mechanism of H-2 reduction by TL is extrachromosomal. Whether it involves diminished synthesis of H-2 or steric masking by TL at the cell membrane is unknown, but in either case the reciprocal relation of TL and H-2(D) antigens implies that they probably occupy adjacent positions on thymocytes and that the gene order, H-2(K): H-2(D):Tla is reflected in cell surface structure. Extrachromosomal interaction, apparently involving control of synthesis, occurs also within the TL system of antigens. Thymocytes of TL.2 x TL.1,2,3 progeny express the full homozygous quantity of antigens TL.1 and TL.3 (but not of TL.2), in contrast to the half-quantity present in thymocytes of TL- x TL.1,2,3 progeny. Another example of interaction is implicit in the finding that thymocytes of TL-1,2,3 x TL.1,2,3 progeny have more TL.2 antigen than thymocytes of TL.2 x TL.2 progeny, but in this instance there is nothing to indicate whether the mechanism is chromosomal or extrachromosomal. Thus the quantitative surface representation of at least some H-2 and TL antigens is influenced by the cellular complement of H-2:Tla genes as a whole. Comparison of H-2 heterozygous thymocytes with H-2 homozygous thymocytes in quantitative absorption tests shows (a) more than the expected 50% of each parental-type H-2 antigen on heterozygous cells, and (b) a greater suppression of H-2 by TL in H-2 heterozygotes in comparison with H-2 homozygotes. Both results may be explained on the basis of differences in the density of H-2 antigenic sites and consequent differences in the efficiency of absorption of H-2 antibody. These considerations may be useful in other contexts, e.g. in estimating the representation of Rh antigens on the red cells of human subjects homozygous and heterozygous for Rh components

Cannabidiol activates PINK1-Parkin-dependent mitophagy and mitochondrial-derived vesicles

The PINK1/Parkin pathway plays an important role in maintaining a healthy pool of mitochondria. Activation of this pathway can lead to apoptosis, mitophagy, or mitochondrial-derived vesicle formation, depending on the nature of mitochondrial damage. The signaling by which PINK/Parkin activation leads to these different mitochondrial outcomes remains understudied. Here we present evidence that cannabidiol (CBD) activates the PINK1-Parkin pathway in a unique manner. CBD stimulates PINK1-dependent Parkin mitochondrial recruitment similarly to other well-studied Parkin activators but with a distinctive shift in the temporal dynamics and mitochondrial fates. The mitochondrial permeability transition pore inhibitor cyclosporine A exclusively diminished the CBD-induced PINK1/Parkin activation and its associated mitochondrial effects. Unexpectedly, CBD treatment also induced elevated production of mitochondrial-derived vesicles (MDV), a potential quality control mechanism that may help repair partial damaged mitochondria. Our results suggest that CBD may engage the PINK1-Parkin pathway to produce MDV and repair mitochondrial lesions via mitochondrial permeability transition pore opening. This work uncovered a novel link between CBD and PINK1/Parkin-dependent MDV production in mitochondrial health regulation

THE GIX SYSTEM : A CELL SURFACE ALLO-ANTIGEN ASSOCIATED WITH MURINE LEUKEMIA VIRUS; IMPLICATIONS REGARDING CHROMOSOMAL INTEGRATION OF THE VIRAL GENOME

This report concerns a cell surface antigen (GIX; G = Gross) which exhibits mendelian inheritance but which also appears de novo in cells that become productively infected with MuLV (Gross), the wild-type leukemia virus of the mouse. In normal mice, GIX is a cell surface allo-antigen confined to lymphoid cells and found in highest amount on thymocytes. Four categories of inbred mouse strains can be distinguished according to how much GIX antigen is expressed on their thymocytes. GIX- strains have none; in the three GIX+ categories, GIX3, GIX2, and GIX1, the amounts of GIX antigen present (per thymocyte) are approximately in the ratios 3:2:1. A study of segregating populations derived mainly from strain 129 (the prototype GIX3 strain) and C57BL/6 (the prototype GIX- strain) revealed that two unlinked chromosomal genes are required for expression of GIX on normal lymphoid cells. The phenotype GIX+ is expressed only when both genes are present, as in 129 mice. C57BL/6 carries neither of them. At one locus, expression of GIX is fully dominant over nonexpression (GIX fully expressed in heterozygotes). At the second locus, which is linked with H-2 (at a distance of 36.4 ± 2.7 units) in group IX (locus symbol GIX), expression is semidominant (50% expression of GIX in heterozygotes); gene order T:H-2:Tla:GIX. As a rule, when cells of GIX- mice or rats become overtly infected with MuLV (Gross), an event which occurs spontaneously in older mice of certain strains and which also commonly accompanies malignant transformation, their phenotype is converted to GIX+. This invites comparison with the emergence of TL+ leukemia cells in TL- mouse strains which has been observed in previous studies and which implies that TL- → TL+ conversion has accompanied leukemic transformation of such cells. So far the only example of GIX- → GIX+ conversion taking place without overt MuLV infection is represented by the occurrence of GCSA-:GIX+ myelomas in BALB/c (GCSA:GIX-) mice. Unlike the other Gross cell surface antigen described earlier, GCSA, which is invariably associated with MuLV (Gross) infection and never occurs in its absence, GIX antigen sometimes occurs independently of productive MuLV infection; for example, thymocytes and some leukemias of 129 mice are GCSA-:GIX+, and MuLV-producing sarcomas may be GCSA+:GIX-. The frequent emergence of cells of GIX+ phenotype in all mouse strains implies that the structural gene coding for GIX antigen is common to all mice. There is precedent for this in the TL system, in which two of the Tla genes in linkage group IX appear to be ubiquitous among mice, but are normally expressed only in strains of mice carrying a second (expression) gene. It is not yet certain whether either of the two segregating genes belongs to the MuLV genome rather than to the cellular genome. This leaves the question whether MuLV may have a chromosomal integration site still debatable. But there is a good prospect that further genetic analysis will provide the answer and so elucidate the special relationship of leukemia viruses to the cells of their natural hosts