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Well-known thesis that productive capacities constraints can be a strong obstacle to economic growth is discussed in the article. Basing on the Russian Economic Barometer data the author shows that the impact of such a factor upon economic growth in Russia is not as strong as many researchers think.

`The book is an excellent example of the application of modern econometric techniques to Chinese data, some of which was especially collected for the research. The results throw new light on aspects of industrial sector reform in China. The book deserves wide attention from those interested in the economic reforms in China, especially those interested in the implications of the reforms for industrial sector efficiency and productivity growth.' - Christopher Findlay, University of Adelaide As the rural township, village and private enterprises are becoming more and more significant in the Chinese economy, this book focuses on the comparison of the rural (non-state) and state firms in terms of performance. The analysis is based on the empirical results from estimating various production functions applied to cross-section and panel data. Both aggregate and firm-specific efficiencies are examined in the case studies, exploring potential sources of efficiency differentials such as ownership, scale, factor intensity, location and economic reforms. Special attention is also paid to the regional comparison of industrial development and performance. The implications of the findings in the book for economic and reform policy are thus highlighted.

In discussing the productive efficiency of public enterprises, the expert group meeting convened by ICPE in November 1981, noted that in the imperfect market conditions prevailing in developing countries, where different factors, including price distortions, have to be taken into consideration, indicators of productive efficiency represent a necessary evaluative tool compensating for the inadequacy of profitability indicators. This need is often highlighted in those instances where public enterprises are entrusted with social goals, particularly in the underpricing of products, which run counter to commercial objectives. The rationale of this paper is that unless some systematic means of measuring the output and productivity of public enterprises is found, a large proportion of economic activity will remain unaccountable. It is inconceivable that the "efficiency" measures expected of public enterprises by concerned citizens and administrators in developing countries are either non-existent or are so primitive as to give misleading information. Notwithstanding the number of conceptual and methodological problems which abound in this area, it must be realized that parallel attempts are being made by governments and research institutions of advanced industrial countries to measure the productivity of non- commercial public sector activity. ; peer-reviewed

Abstract Huntington's disease (HD) is a progressive neurodegenerative hereditary disease clinically characterised by the presence of involuntary movements, behavioural problems and cognitive decline. The disease-onset is usually between 30 and 50 years of age. HD is a rare disorder affecting approximately 1.3 in 10,000 people in the European Union. It is caused by an expanded CAG repeat in the first exon of the Huntingtin ( HTT) gene, leading to an abnormal form of the Huntingtin protein (Htt) (polyQHtt), containing N-terminus, enlarged polyglutamine strands of variable length that stick together to form aggregates and nuclear inclusions in the damaged brain cells. Treatments currently used for Huntington's disease are symptomatic and aimed at temporally relieving the symptoms of the disease; although some promising therapies are on study, there is no drug capable of stopping disease progression either in the form of delaying onset or slowing disability progression. The utilization of peptides interacting with polyQ stretches or with Htt protein to prevent misfolding and aggregation of the expanded polyQ protein is a fascinating idea, because of low potential toxicity and ability to target very initial steps in the pathophysiological cascade of the disease, such as aggregation or cleavage process. Indeed, several therapeutic peptides have been developed and were found to significantly slow down the progression of symptoms in experimental models of Huntington's disease. This review is essentially focusing on the latest development concerning peptide strategy. In particular, we focused on a 23aa peptide P42, which is a part of the Htt protein. It is expected to work principally by preventing the abnormal Htt protein from sticking together, thereby preventing pathological consequences of aggregation and improving the symptoms of the disease. In the meantime, as P42 is part of the Htt protein, some therapeutic properties might be linked to the physiological actions of the peptide itself, considered as a functional domain of the Htt protein.

International audience ; Huntington's disease (HD) is a progressive neurodegenerative hereditary disease clinically characterised by the presence of involuntary movements, behavioural problems and cognitive decline. The disease-onset is usually between 30 and 50 years of age. HD is a rare disorder affecting approximately 1.3 in 10,000 people in the European Union. It is caused by an expanded CAG repeat in the first exon of the Huntingtin (HTT) gene, leading to an abnormal form of the Huntingtin protein (Htt) (polyQHtt), containing N-terminus, enlarged polyglutamine strands of variable length that stick together to form aggregates and nuclear inclusions in the damaged brain cells. Treatments currently used for Huntington's disease are symptomatic and aimed at temporally relieving the symptoms of the disease; although some promising therapies are on study, there is no drug capable of stopping disease progression either in the form of delaying onset or slowing disability progression. The utilization of peptides interacting with polyQ stretches or with Htt protein to prevent misfolding and aggregation of the expanded polyQ protein is a fascinating idea, because of low potential toxicity and ability to target very initial steps in the pathophysiological cascade of the disease, such as aggregation or cleavage process. Indeed, several therapeutic peptides have been developed and were found to significantly slow down the progression of symptoms in experimental models of Huntington's disease. This review is essentially focusing on the latest development concerning peptide strategy. In particular, we focused on a 23aa peptide P42, which is a part of the Htt protein. It is expected to work principally by preventing the abnormal Htt protein from sticking together, thereby preventing pathological consequences of aggregation and improving the symptoms of the disease. In the meantime, as P42 is part of the Htt protein, some therapeutic properties might be linked to the physiological actions of the peptide itself, considered as ...

International audience ; Huntington's disease (HD) is a progressive neurodegenerative hereditary disease clinically characterised by the presence of involuntary movements, behavioural problems and cognitive decline. The disease-onset is usually between 30 and 50 years of age. HD is a rare disorder affecting approximately 1.3 in 10,000 people in the European Union. It is caused by an expanded CAG repeat in the first exon of the Huntingtin (HTT) gene, leading to an abnormal form of the Huntingtin protein (Htt) (polyQHtt), containing N-terminus, enlarged polyglutamine strands of variable length that stick together to form aggregates and nuclear inclusions in the damaged brain cells. Treatments currently used for Huntington's disease are symptomatic and aimed at temporally relieving the symptoms of the disease; although some promising therapies are on study, there is no drug capable of stopping disease progression either in the form of delaying onset or slowing disability progression. The utilization of peptides interacting with polyQ stretches or with Htt protein to prevent misfolding and aggregation of the expanded polyQ protein is a fascinating idea, because of low potential toxicity and ability to target very initial steps in the pathophysiological cascade of the disease, such as aggregation or cleavage process. Indeed, several therapeutic peptides have been developed and were found to significantly slow down the progression of symptoms in experimental models of Huntington's disease. This review is essentially focusing on the latest development concerning peptide strategy. In particular, we focused on a 23aa peptide P42, which is a part of the Htt protein. It is expected to work principally by preventing the abnormal Htt protein from sticking together, thereby preventing pathological consequences of aggregation and improving the symptoms of the disease. In the meantime, as P42 is part of the Htt protein, some therapeutic properties might be linked to the physiological actions of the peptide itself, considered as ...

International audience ; Huntington's disease (HD) is a progressive neurodegenerative hereditary disease clinically characterised by the presence of involuntary movements, behavioural problems and cognitive decline. The disease-onset is usually between 30 and 50 years of age. HD is a rare disorder affecting approximately 1.3 in 10,000 people in the European Union. It is caused by an expanded CAG repeat in the first exon of the Huntingtin (HTT) gene, leading to an abnormal form of the Huntingtin protein (Htt) (polyQHtt), containing N-terminus, enlarged polyglutamine strands of variable length that stick together to form aggregates and nuclear inclusions in the damaged brain cells. Treatments currently used for Huntington's disease are symptomatic and aimed at temporally relieving the symptoms of the disease; although some promising therapies are on study, there is no drug capable of stopping disease progression either in the form of delaying onset or slowing disability progression. The utilization of peptides interacting with polyQ stretches or with Htt protein to prevent misfolding and aggregation of the expanded polyQ protein is a fascinating idea, because of low potential toxicity and ability to target very initial steps in the pathophysiological cascade of the disease, such as aggregation or cleavage process. Indeed, several therapeutic peptides have been developed and were found to significantly slow down the progression of symptoms in experimental models of Huntington's disease. This review is essentially focusing on the latest development concerning peptide strategy. In particular, we focused on a 23aa peptide P42, which is a part of the Htt protein. It is expected to work principally by preventing the abnormal Htt protein from sticking together, thereby preventing pathological consequences of aggregation and improving the symptoms of the disease. In the meantime, as P42 is part of the Htt protein, some therapeutic properties might be linked to the physiological actions of the peptide itself, considered as ...

International audience ; Huntington's disease (HD) is a progressive neurodegenerative hereditary disease clinically characterised by the presence of involuntary movements, behavioural problems and cognitive decline. The disease-onset is usually between 30 and 50 years of age. HD is a rare disorder affecting approximately 1.3 in 10,000 people in the European Union. It is caused by an expanded CAG repeat in the first exon of the Huntingtin (HTT) gene, leading to an abnormal form of the Huntingtin protein (Htt) (polyQHtt), containing N-terminus, enlarged polyglutamine strands of variable length that stick together to form aggregates and nuclear inclusions in the damaged brain cells. Treatments currently used for Huntington's disease are symptomatic and aimed at temporally relieving the symptoms of the disease; although some promising therapies are on study, there is no drug capable of stopping disease progression either in the form of delaying onset or slowing disability progression. The utilization of peptides interacting with polyQ stretches or with Htt protein to prevent misfolding and aggregation of the expanded polyQ protein is a fascinating idea, because of low potential toxicity and ability to target very initial steps in the pathophysiological cascade of the disease, such as aggregation or cleavage process. Indeed, several therapeutic peptides have been developed and were found to significantly slow down the progression of symptoms in experimental models of Huntington's disease. This review is essentially focusing on the latest development concerning peptide strategy. In particular, we focused on a 23aa peptide P42, which is a part of the Htt protein. It is expected to work principally by preventing the abnormal Htt protein from sticking together, thereby preventing pathological consequences of aggregation and improving the symptoms of the disease. In the meantime, as P42 is part of the Htt protein, some therapeutic properties might be linked to the physiological actions of the peptide itself, considered as ...

Based on the last national livestock census in 2013, the population number of cattle and buffalo have reduced by 15% compared to that in 2011. The highest reduction happened in Java that reached around 24-27%, while that in Bali and Nusa Tenggara was 25%. One of the reasons was caused by decreasing number of cows due to the increase of productive cows slaughtered every year. Number of cows slaughtered in Bali, Nusa Tenggara, and South Sulawesi had reached on average of 72% from total slaughtered, where more than 90% were productive cows. Reasons for slaughtering productive cows were due to: (1) Lower cows price; (2) Limited bulls supply; (3) Local government regulation on inter-island trade; (4) Weak and inconsistent law enforcement; and (5) Lack of understanding on criteria for productive cows by farmers. Increased rate of slaughtered cattle and increasing rate of inter-island trade volumes that higher than the rate of cattle population had caused the decrease of national cattle population. There are currently needs to improve and develop operation slaughter-houses under management of local state enterprise. The management applies on certain mechanisms that sort of incoming productive females according to different grades into allowable to be slaughtered and selected for breeding females, which could be further traded inter-island as supplier of cows for other regions. This strategy may help the central government to meet the demand for productive cows, particularly in Sumatera and Kalimantan which have abundance of feed biomass resources. Policy support is needed as instruments for all interested stakeholders including those who are willing to invest in cattle development such as oil-palm estates.

The M. H. Ross Papers contain information pertaining to labor, politics, social issues of the twentieth century, coal mining and its resulting lifestyle, as well as photographs and audio materials. The collection is made up of five different accessions; L2001-05, which is contained in boxes one through 104, L2002-09 in boxes 106 through 120, L2006-16 in boxes 105 and 120, L2001-01 in boxes 120-121, and L2012-20 in boxes 122-125. The campaign materials consist of items from the 1940 and 1948 political campaigns in which Ross participated. These items include campaign cards, posters, speech transcripts, news clippings, rally materials, letters to voters, and fliers. Organizing and arbitration materials covers labor organizing events from "Operation Dixie" in Georgia, the furniture workers in North Carolina, and the Mine-Mill workers in the Western United States. Organizing materials include fliers, correspondence, news articles, radio transcripts, and some related photos. Arbitration files consist of agreements, decisions, and agreement booklets. The social and political research files cover a wide time period (1930's to the late 1970's/early 1980's). The topics include mainly the Ku Klux Klan, racism, Communism, Red Scare, red baiting, United States history, and literature. These files consist mostly of news and journal articles. Ross interacted with coal miners while doing work for the United Mine Workers Association (UMWA) and while working at the Fairmont Clinic in West Virginia. Included in these related files are books, news articles, journals, UMWA reports, and coal miner oral histories conducted by Ross. Tying in to all of the activities Ross participated in during his life were his research and manuscript files. He wrote numerous newspaper and journal articles on history and labor. Later, as he worked for the UMWA and at the Fairmont Clinic, he wrote more in-depth articles about coal miners, their lifestyle, and medical problems they faced (while the Southern Labor Archives has many of Ross's coal mining and lifestyle articles, it does not have any of his medical articles). Along with these articles are the research files Ross collected to write them, which consist of notes, books, and newspaper and journal articles. In additional to his professional career, Ross was adamant about documenting his and his wife's family history in the oral history format. Of particular interest are the recordings of his interviews with his wife's family - they were workers, musicians, and singers of labor and folk songs. Finally, in this collection are a number of photographs and slides, which include images of organizing, coal mining (from the late 19th through 20th centuries), and Appalachia. Of note is a small photo album from the 1930s which contains images from the Summer School for Workers, and more labor organizing. A few audio items are available as well, such as Ross political speeches and an oral history in which Ross was interviewed by his daughter, Jane Ross Davis in 1986. All photographic and audio-visual materials are at the end of their respective series. ; Myron Howard "Mike" Ross was born November 9, 1919 in New York City. He dropped out of school when he was seventeen and moved to Texas, where he worked on a farm. From 1936 until 1939, Ross worked in a bakery in North Carolina. In the summer of 1938, he attended the Southern School for Workers in Asheville, North Carolina. During the fall of 1938, Ross would attend the first Southern Conference on Human Welfare in Birmingham, Alabama. He would attend this conference again in 1940 in Chattanooga, Tennessee. From 1939 to 1940, Ross worked for the United Mine Workers Non-Partisan League in North Carolina, working under John L. Lewis. He was hired as a union organizer by the United Mine Workers of America, and sent to Saltville, Virginia and Rockwood, Tennessee. In 1940, Ross ran for a seat on city council on the People's Platform in Charlotte, North Carolina. During this time, he also married Anne "Buddie" West of Kennesaw, Georgia. From 1941 until 1945, Ross served as an infantryman for the United States Army. He sustained injuries near the Battle of the Bulge in the winter of 1944. From 1945 until 1949, Ross worked for the International Union of Mine, Mill and Smelter Workers, then part of the Congress of Industrial Organizations (CIO), as a union organizer. He was sent to Macon, Georgia, Savannah, Georgia and to Winston-Salem, North Carolina, where he worked with the United Furniture Workers Union. He began handling arbitration for the unions. In 1948, Ross ran for United States Congress on the Progressive Party ticket in North Carolina. He also served as the secretary for the North Carolina Progressive Party. Ross attended the University of North Carolina law school from 1949 to 1952. He graduated with honors but was denied the bar on the grounds of "character." From 1952 until 1955, he worked for the Mine, Mill and Smelter Workers as a union organizer, first in New Mexico (potash mines) and then in Arizona (copper mines). From 1955 to 1957, Ross attended the Columbia University School of Public Health. He worked for the United Mine Workers of America Welfare and Retirement Fund from 1957 to 1958, where he represented the union in expenditure of health care for mining workers. By 1958, Ross began plans for what would become the Fairmont Clinic, a prepaid group practice in Fairmont, West Virginia, which had the mission of providing high quality medical care for miners and their families. From 1958 until 1978, Ross served as administrator of the Fairmont Clinic. As a result of this work, Ross began researching coal mining, especially coal mining lifestyle, heritage and history of coal mining and disasters. He would interview over one hundred miners (coal miners). Eventually, Ross began writing a manuscript about the history of coal mining. Working for the Rural Practice Program of the University of North Carolina from 1980 until 1987, Ross taught in the medical school. M. H. Ross died on January 31, 1987 in Chapel Hill, North Carolina. ; Digitization of the M. H. Ross Papers was funded by the National Historical Publications and Records Commission.