7 research outputs found

    Determinants of high somatic-cell count prevalence in dairy herds practicing teat dipping and dry cow therapy and with no evidence of Streptococcus-agalactiae on repeated bulk tank milk examination

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    PT: J; CR: 1982, SAS USERS GUIDE STAT BODOH GW, 1976, J DAIRY SCI, V59, P1119 BRAMLEY AJ, 1984, J DAIRY RES, V51, P481 BUSHNELL RB, 1984, 23RD P ANN M NAT MAS, P31 BUSHNELL RB, 1985, 24TH P ANN M NAT MAS, P45 DOHOO IR, 1982, CAN VET J, V23, P119 GALTON DM, 1984, 17TH P ANN C AM ASS, P108 GOODHOPE RG, 1980, CAN J COMP MED, V44, P351 HARVEY WR, 1982, J ANIM SCI, V54, P1067 HOARE RJT, 1979, AUST J DAIRY TECHNOL, V34, P91 HUESTON WD, 1987, PREV VET MED, V4, P447 KIRK JH, 1984, COMP CONT EDUC PRACT, V6, S237 LESLIE KE, 1983, COMPEND CONTIN ED P, V5, S601 LINDSTROM UB, 1983, ACTA AGR SCAND, V33, P389 MEIN GA, 1977, AUST J DAIRY TECHNOL, V32, P81 MINETT FC, 1933, J COMP PATH THERAP, V46, P131 MOXLEY JE, 1978, J DAIRY SCI, V61, P1637 NEWMAN LE, 1973, AM J VET RES, V34, P979 PEARSON JKL, 1972, VET REC, V91, P615 POSTLE DS, 1968, AM J VET RES, V29, P669 POSTLE DS, 1971, J MILK FOOD TECH, V34, P517 SMITH KL, 1983, J DAIRY SCI, V66, P1790 STABLEFORTH AW, 1935, J COMP PATHOL, V48, P300; NR: 23; TC: 11; J9: PREV VET MED; PG: 12; GA: DU955Source type: Electronic(1

    Traumatic posterior shoulder dislocation: A case with modification of Gerber procedure for humeral head reconstruction at 10-year follow-up

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    We report a case of acute traumatic posterior shoulder dislocation in a 41-year-old patient, which we treated surgically by a modification of the procedure described by Gerber for humeral head reconstruction in such cases. The diagnosis was confirmed by CT scan, which also helped us to assess the size of the antero-medial humeral head defect or impaction secondary to the dislocation; the size of this defect being a determinant element for the indication. Because the shoulder was unstable after closed reduction and almost 50percent of the humeral head was impacted, we carried out a surgical treatment using an original technique as mentioned above. Radiologic and surgical features of acute traumatic posterior shoulder dislocation are discussed with special emphasis on diagnosis, indications and surgical aspects of this rare lesion, which represent 2-4percent of acute traumatic shoulder dislocations. © 2008 Springer-Verlag.ARNDT JH, 1965, AMER J ROENTGENOL RA, V94, P639; BLOOM MH, 1967, J BONE JOINT SURG AM, VA 49, P943; CISTERNINO SJ, 1978, AM J ROENTGENOL, V130, P951; CONSTANT CR, 1987, CLIN ORTHOP RELAT R, P160; Dubousset J, 1967, Rev Chir Orthop Reparatrice Appar Mot, V53, P65; FINKELSTEIN JA, 1995, J ORTHOP TRAUMA, V9, P190; Gerber C, 1991, CAHIERS ENSEIGNEMENT, V40, P223; GERBER C, 2006, J BONE JOINT SURG AM, V87, P1739; GERBER C, 1988, CAHIERS ENSEIGNEMENT, V33, P51; Gerber C, 1996, J BONE JOINT SURG AM, V78A, P376; HAWKINS RJ, 1987, J BONE JOINT SURG AM, V69A, P9; Kaar TK, 1999, J BONE JOINT SURG AM, V81A, P708; MANSAT M, 1988, REV CHIR ORTHOP, V74, P257; MCLAUGHLIN HL, 1952, J BONE JOINT SURG AM, V34-A, P584; PICARD F, 1993, JOURN LYONN EP LYON; Picard F, 1998, REV CHIR ORTHOP, V84, P217; RANDELLI M, 1988, 2 C EUR SOC SHOULD E; RICHARDS RH, 1989, INJURY, V20, P297, DOI 10.1016-0020-1383(89)90174-5; Samilson R L, 1964, Clin Orthop Relat Res, V32, P69; STABLEFORTH PG, 1992, J BONE JOINT SURG BR, V74, P579; Swamy G, 1998, J TRAUMA, V44, P377, DOI 10.1097-00005373-199802000-00026; VANDENBUSCHE E, 1996, CAHIER SOFCOT, V56, P238; VANDENBUSSCHE E, 1994, CAHIERS ENSEIGNEMENT, V49, P75; VASTAMAKI M, 1980, ACTA ORTHOP SCAND, V51, P479, DOI 10.3109-17453678008990827; VICHARD P, 1981, REV CHIR ORTHOP, V67, P71; VICHARD P, 1988, CAHIERS ENSEIGNEMENT, V31, P179; WALCH G, 1990, REV CHIR ORTHOP, V76, P5460

    Monoclonal Antibodies to Migraine: Witnesses to modern biomedicine, an A-Z

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    The History of Modern Biomedicine Research Group hosted its first Witness Seminar, on monoclonal antibodies, in 1993. Since then more than sixty such meetings have been held, the most recent on migraine in 2013. These all sought to go behind-the-scenes of contemporary biomedicine to find out ‘what really happened’. In this, the Group’s twenty-first anniversary year, we are delighted to present our fiftieth Witness Seminar volume Monoclonal Antibodies to Migraine: Witnesses to modern biomedicine, an A–Z. Comprising a series of extracts from previous volumes, contributors include clinicians, scientists, patients and numerous others involved in modern biomedicine, in the UK and beyond. Topics range from ‘age discrimination’ to ‘Zantac’, and feature memories from every decade between the 1930s and the present.The History of Modern Biomedicine Research Group hosted its first Witness Seminar, on monoclonal antibodies, in 1993. Since then more than sixty such meetings have been held, the most recent on migraine in 2013. These all sought to go behind-the-scenes of contemporary biomedicine to find out ‘what really happened’. In this, the Group’s twenty-first anniversary year, we are delighted to present our fiftieth Witness Seminar volume Monoclonal Antibodies to Migraine: Witnesses to modern biomedicine, an A–Z. Comprising a series of extracts from previous volumes, contributors include clinicians, scientists, patients and numerous others involved in modern biomedicine, in the UK and beyond. Topics range from ‘age discrimination’ to ‘Zantac’, and feature memories from every decade between the 1930s and the present.The History of Modern Biomedicine Research Group hosted its first Witness Seminar, on monoclonal antibodies, in 1993. Since then more than sixty such meetings have been held, the most recent on migraine in 2013. These all sought to go behind-the-scenes of contemporary biomedicine to find out ‘what really happened’. In this, the Group’s twenty-first anniversary year, we are delighted to present our fiftieth Witness Seminar volume Monoclonal Antibodies to Migraine: Witnesses to modern biomedicine, an A–Z. Comprising a series of extracts from previous volumes, contributors include clinicians, scientists, patients and numerous others involved in modern biomedicine, in the UK and beyond. Topics range from ‘age discrimination’ to ‘Zantac’, and feature memories from every decade between the 1930s and the present.The History of Modern Biomedicine Research Group hosted its first Witness Seminar, on monoclonal antibodies, in 1993. Since then more than sixty such meetings have been held, the most recent on migraine in 2013. These all sought to go behind-the-scenes of contemporary biomedicine to find out ‘what really happened’. In this, the Group’s twenty-first anniversary year, we are delighted to present our fiftieth Witness Seminar volume Monoclonal Antibodies to Migraine: Witnesses to modern biomedicine, an A–Z. Comprising a series of extracts from previous volumes, contributors include clinicians, scientists, patients and numerous others involved in modern biomedicine, in the UK and beyond. Topics range from ‘age discrimination’ to ‘Zantac’, and feature memories from every decade between the 1930s and the present.The History of Modern Biomedicine Research Group hosted its first Witness Seminar, on monoclonal antibodies, in 1993. Since then more than sixty such meetings have been held, the most recent on migraine in 2013. These all sought to go behind-the-scenes of contemporary biomedicine to find out ‘what really happened’. In this, the Group’s twenty-first anniversary year, we are delighted to present our fiftieth Witness Seminar volume Monoclonal Antibodies to Migraine: Witnesses to modern biomedicine, an A–Z. Comprising a series of extracts from previous volumes, contributors include clinicians, scientists, patients and numerous others involved in modern biomedicine, in the UK and beyond. Topics range from ‘age discrimination’ to ‘Zantac’, and feature memories from every decade between the 1930s and the present.Wellcome Trust

    The Liverpool alcohol‐related liver disease algorithm identifies twice as many emergency admissions compared to standard methods when applied to Hospital Episode Statistics for England

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    BACKGROUND: Emergency admissions in England for alcohol-related liver disease (ArLD) have increased steadily for decades. Statistics based on administrative data typically focus on the ArLD-specific code as the primary diagnosis and are therefore at risk of excluding ArLD admissions defined by other coding combinations. AIM: To deploy the Liverpool ArLD Algorithm (LAA), which accounts for alternative coding patterns (e.g., ArLD secondary diagnosis with alcohol/liver-related primary diagnosis), to national and local datasets in the context of studying trends in ArLD admissions before and during the COVID-19 pandemic. METHODS: We applied the standard approach and LAA to Hospital Episode Statistics for England (2013-21). The algorithm was also deployed at 28 hospitals to discharge coding for emergency admissions during a common 7-day period in 2019 and 2020, in which eligible patient records were reviewed manually to verify the diagnosis and extract data. RESULTS: Nationally, LAA identified approximately 100% more monthly emergency admissions from 2013 to 2021 than the standard method. The annual number of ArLD-specific admissions increased by 30.4%. Of 39,667 admissions in 2020/21, only 19,949 were identified with standard approach, an estimated admission cost of £70 million in under-recorded cases. Within 28 local hospital datasets, 233 admissions were identified using the standard approach and a further 250 locally verified cases using the LAA (107% uplift). There was an 18% absolute increase in ArLD admissions in the seven-day evaluation period in 2020 versus 2019. There were no differences in disease severity or mortality, or in the proportion of admissions with decompensation of cirrhosis or alcoholic hepatitis. CONCLUSIONS: The LAA can be applied successfully to local and national datasets. It consistently identifies approximately 100% more cases than the standard coding approach. The algorithm has revealed the true extent of ArLD admissions. The pandemic has compounded a long-term rise in ArLD admissions and mortality

    Hetrocyclic methacrylate systems as vehicles for the release of active species.

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    PhDThe room temperature polymerising heterocyclic polymer system, poly(ethyl methacrylate)/tetrahydrofurfuryl methacrylate (PEM/THFM) has been shown previously to be biocompatible and supported tissue repair, specifically for bone and cartilage, and biologically inert when in contact with the dental pulp. It proved more effective, than other glassy methacrylates in the release of active species. The PEM/THFM system is a rigid material. The aim of this study was to develop and characterise the use of this system as a flexible patch, for application and retention to the buccal mucosa, thus facilitating sustained regulated release. Model species, dextrans, were used to represent macromolecular drugs whereby the effect of molecular weight could be studied. N-methyl pyrrolidone was added to the polymer system as a biocompatible plasticiser to enhance molecular mobility, and hence the transport of species. The effect of the addition of chitosan was also studied, due to its bioadhesiveness and permeation enhancing ability. A range of systems was investigated both in terms of water and species release. The release of the agent was measured by a fluorometer, the leachable components by HPLC and Confocal microscopy demonstrated the transport of water and active species through the system. Immunological and viability studies established whether the leachants or released components of the polymeric systems had an inflammatory or irritant action on `in vitro' stratified epithelium. The addition of N-methyl pyrrolidone, dextran and chitosan substantially increased water uptake, thus affecting the release kinetics. Analysis of the kinetics of water uptake showed Case I, combination of Case I and Case II, and Case II kinetics, depending on the systems studied. Dextran release was largely diffusion controlled, from which diffusion coefficients were calculated; the amount released varied between the systems studied

    Pretreatment prediction of response to ursodeoxycholic acid in primary biliary cholangitis: development and validation of the UDCA response score

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    BACKGROUND: Treatment guidelines recommend a stepwise approach to primary biliary cholangitis: all patients begin treatment with ursodeoxycholic acid (UDCA) monotherapy and those with an inadequate biochemical response after 12 months are subsequently considered for second-line therapies. However, as a result, patients at the highest risk can wait the longest for effective treatment. We determined whether UDCA response can be accurately predicted using pretreatment clinical parameters. METHODS: We did logistic regression analysis of pretreatment variables in a discovery cohort of patients in the UK with primary biliary cholangitis to derive the best-fitting model of UDCA response, defined as alkaline phosphatase less than 1·67 times the upper limit of normal (ULN), measured after 12 months of treatment with UDCA. We validated the model in an external cohort of patients with primary biliary cholangitis and treated with UDCA in Italy. Additionally, we assessed correlations between model predictions and key histological features, such as biliary injury and fibrosis, on liver biopsy samples. FINDINGS: 2703 participants diagnosed with primary biliary cholangitis between Jan 1, 1998, and May 31, 2015, were included in the UK-PBC cohort for derivation of the model. The following pretreatment parameters were associated with lower probability of UDCA response: higher alkaline phosphatase concentration (p<0·0001), higher total bilirubin concentration (p=0·0003), lower aminotransferase concentration (p=0·0012), younger age (p<0·0001), longer interval from diagnosis to the start of UDCA treatment (treatment time lag, p<0·0001), and worsening of alkaline phosphatase concentration from diagnosis (p<0·0001). Based on these variables, we derived a predictive score of UDCA response. In the external validation cohort, 460 patients diagnosed with primary biliary cholangitis were treated with UDCA, with follow-up data until May 31, 2016. In this validation cohort, the area under the receiver operating characteristic curve for the score was 0·83 (95% CI 0·79-0·87). In 20 liver biopsy samples from patients with primary biliary cholangitis, the UDCA response score was associated with ductular reaction (r=-0·556, p=0·0130) and intermediate hepatocytes (probability of response was 0·90 if intermediate hepatocytes were absent vs 0·51 if present). INTERPRETATION: We have derived and externally validated a model based on pretreatment variables that accurately predicts UDCA response. Association with histological features provides face validity. This model provides a basis to explore alternative approaches to treatment stratification in patients with primary biliary cholangitis. FUNDING: UK Medical Research Council and University of Milan-Bicocca

    Pretreatment prediction of response to ursodeoxycholic acid in primary biliary cholangitis: development and validation of the UDCA Response Score

    No full text
    Background: Treatment guidelines recommend a stepwise approach to primary biliary cholangitis: all patients begin treatment with ursodeoxycholic acid (UDCA) monotherapy and those with an inadequate biochemical response after 12 months are subsequently considered for second-line therapies. However, as a result, patients at the highest risk can wait the longest for effective treatment. We determined whether UDCA response can be accurately predicted using pretreatment clinical parameters. Methods: We did logistic regression analysis of pretreatment variables in a discovery cohort of patients in the UK with primary biliary cholangitis to derive the best-fitting model of UDCA response, defined as alkaline phosphatase less than 1·67 times the upper limit of normal (ULN), measured after 12 months of treatment with UDCA. We validated the model in an external cohort of patients with primary biliary cholangitis and treated with UDCA in Italy. Additionally, we assessed correlations between model predictions and key histological features, such as biliary injury and fibrosis, on liver biopsy samples. Findings: 2703 participants diagnosed with primary biliary cholangitis between Jan 1, 1998, and May 31, 2015, were included in the UK-PBC cohort for derivation of the model. The following pretreatment parameters were associated with lower probability of UDCA response: higher alkaline phosphatase concentration (p<0·0001), higher total bilirubin concentration (p=0·0003), lower aminotransferase concentration (p=0·0012), younger age (p<0·0001), longer interval from diagnosis to the start of UDCA treatment (treatment time lag, p<0·0001), and worsening of alkaline phosphatase concentration from diagnosis (p<0·0001). Based on these variables, we derived a predictive score of UDCA response. In the external validation cohort, 460 patients diagnosed with primary biliary cholangitis were treated with UDCA, with follow-up data until May 31, 2016. In this validation cohort, the area under the receiver operating characteristic curve for the score was 0·83 (95% CI 0·79–0·87). In 20 liver biopsy samples from patients with primary biliary cholangitis, the UDCA response score was associated with ductular reaction (r=–0·556, p=0·0130) and intermediate hepatocytes (probability of response was 0·90 if intermediate hepatocytes were absent vs 0·51 if present). Interpretation: We have derived and externally validated a model based on pretreatment variables that accurately predicts UDCA response. Association with histological features provides face validity. This model provides a basis to explore alternative approaches to treatment stratification in patients with primary biliary cholangitis. Funding: UK Medical Research Council and University of Milan-Bicocca
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