Search PubMed⌕ Search

Biomedical subjects

J Haines

Publications and source records attributed to J Haines.

At least 109 records · Page 6Linked to original sources
PubMed1987

The importance of trochanteric lag screws to achieve primary stability in cementless fixation of the RM hip prosthesis.

To allow the bony incorporation of a cementless prosthesis it is important to achieve stability at the time of operation. To neutralize tension and torsional stresses the RM-shaft prosthesis is fixed with two lag screws in the trochanteric part of the femur. By measuring the applied torque intraoperatively we could demonstrate that the threads of the screws found a better grip when inserted from the bone to the prosthesis. Thus, the stronger fixation of the screws enhanced the primary stability of the cementless prosthesis.

Bone Cements↗
PubMed1987

Severely comminuted femoral shaft fractures: treatment by bridging-plate osteosynthesis.

We report on 71 severely comminuted femoral shaft fractures that were operated on between 1980 and 1984 at the Berufsgenossenschaftliche Unfallklinik Duisburg-Buchholz. The method of operative stabilization was plate osteosynthesis in two variations: In one group 39 fractures (ten open) were stabilized by plate osteosynthesis after anatomical reduction of the fractured area. The other group comprised 32 fractures (six open) fixed with a bridging-plate osteosynthesis, without preparation of the fracture zone. The rate of postoperative complications was strikingly diminished after bridging-plate osteosynthesis. Fracture healing occurred within 23 (16-32) weeks after bridging-plate osteosynthesis and within 36 (32-40) weeks after anatomical reduction. No special instrumentation or equipment is necessary to perform a bridging-plate osteosynthesis. The patient rests in a supine position. There is no need for intraoperative image-intensifier control. For operative treatment of severely comminuted femoral fractures we consider the technique of bridging-plate osteosynthesis advantageous, especially in multiply injured patients.

Adult↗
PubMed1987

Search for the familial Alzheimer's disease gene.

The application of molecular genetic techniques to the study of autosomal dominantly inherited Familial Alzheimer's Disease may provide a means to determine the chromosomal location of the defective gene causing this form of Alzheimer's disease. Knowledge of the chromosomal location of the defective gene will provide a basis for isolating and characterizing this gene. Preliminary investigations indicate that several candidate genes can be excluded as the site of the defect. Current data also indicate that the defective gene does not reside close to random DNA markers on the distal portion of chromosome 21. Additional DNA markers on the proximal portion of chromosome 21 long arm are currently being investigated.

Alzheimer Disease↗
PubMed1986

The operative treatment of fresh ruptures of the acromioclavicular joint (Tossy III).

We give a preliminary report of ten patients with fresh dislocations of the acromioclavicular joint (Tossy III). All ten were operated with suture of the torn ligaments and indirect fixation of the acromioclavicular joint with a monocerclage wire passed around the coracoid process and the clavicle. Removal of metal was done 8 weeks later. None of the wires broke, and there were no problems with wound healing. Control X-rays under stress revealed stable acromioclavicular joints in all cases.

Acromioclavicular Joint↗
PubMed1986

Immediate mobilization of fractures of the neck of the fifth metacarpal.

Although fractures of the neck of the fifth metacarpal are common injuries, their management remains controversial. In this study we present the results of early mobilization after these fractures in 101 patients. We conclude that if rotational alignment of the finger is maintained, these fractures can be treated by immediate use with good functional and cosmetic results.

Adolescent↗
PubMed1986

Molecular genetics of Huntington's disease.

The discovery of a DNA marker linked to the HD gene has provided new avenues into the investigation of this devastating disorder. Genetic investigations have determined that in most and possibly all HD families, the disease is caused by a defect that maps near the telomere on the short arm of chromosome 4. DNA markers will soon provide presymptomatic diagnosis for this disorder, but this increased capability may be a mixed blessing in the absence of effective treatment. The most hopeful route to developing such treatment lies in cloning and characterization of the primary defect. Precise genetic and physical mapping using DNA markers and improvements in techniques for analyzing large segments of DNA have set the stage for cloning of the disease gene in the near future. It will undoubtedly reveal an interesting mechanism for complete phenotypic dominance in man for comparison with completely dominant mutations in other species, particularly Drosophila. The nature of the defect may provide new insights into the functional organization of the central nervous system. For the sake of the many individuals who are afflicted by HD or who are asymptomatic gene carriers, it is to be hoped that cloning and characterizing the disease gene will also yield the necessary information to develop an effective therapy.

Chromosome Mapping↗
PubMed1985

Myosin heavy chain in avian muscular dystrophy corresponds to the neonatal isozyme.

We have previously demonstrated, based on comparison of homologous amino acid sequences and of two-dimensional CNBr peptide gel patterns, that the myosin heavy chain in pectoralis muscles of Storrs, Connecticut dystrophic chickens is different from that of their normal controls (Huszar, G., Vigue, L., De-Lucia, J. Elzinga, M., and Haines, J. (1985) J. Biol. Chem. 260, 7429-7434). Others have shown, however, that genomic banks and mRNA complements of the control and dystrophic birds are not different. In the present studies, we have examined the hypothesis that the "dystrophic" myosin heavy chain is not a novel gene product, but is a developmental isozyme which is expressed in pectoralis muscles of adult chickens due to the dystrophic process. Two-dimensional maps of myosin heavy chain CNBr peptides were prepared from breast muscles of 17-day in ovo (embryonic), 25-day posthatch (neonatal), and adult birds of the Storrs dystrophic and of two control strains. Also, myosin and actomyosin ATPase enzymatic activities of the various preparations were determined in the pH range of 5.5 to 9.0. Analysis of the peptide maps demonstrates that the embyronic, neonatal, and control adult myosin heavy chain isozymes are distinctly different gene products with only minute variations between the respective developmental isozymes in dystrophic and control muscles. However, the pectoralis myosin heavy chain of adult dystrophic birds, which is a homogeneous isozyme population by amino acid sequences and gel patterns, corresponds to that of the neonatal-type myosin heavy chain. The ATPase properties of the embryonic, neonatal, or adult pectoralis myosins and actomyosins were not different, whether the level of specific activity or the pattern of pH activation is considered. Since the mobility of neonatal chicks (primarily neonatal-type isozymes) is not restricted, the differences in myosin heavy chain structures are part of the syndrome, but not the cause of avian muscular dystrophy.

Adenosine Triphosphatases↗
PubMed1985

Structure of myosin heavy chain in avian muscular dystrophy.

We have studied the structure of myosin heavy chain (MHC) in the pectoralis muscle of genetically dystrophic (Connecticut Strain) and White Leghorn chicks. MHC was alkylated with N-ethylmaleimide, purified by Sepharose-4B chromatography, and cleaved with cyanogen bromide. The MHC CNBr peptides were analyzed by one-dimensional and two-dimensional isoelectric focusing/sodium dodecyl sulfate gradient gels and by amino acid sequencing. Specific changes were detected in the gel patterns which could be correlated with the loss of muscle function as measured by the exhaustion score (the ability of chicks to rise from a reclining position) in three experimental groups (exhaustion scores: less than 3, 10-20, greater than 30). We have also examined the amino acid sequence of a 3-methyl-histidine-containing peptide which originates from the 20-kDa fragment of pectoralis muscle MHC in dystrophic chicks: Val-Leu-Asn-Ala-Ser-Ala-Ile-Pro-Glu-Gly-*Gln-Phe-*Ile-Asp-Ser-Lys-Lys- Ala-Ser-Leu-Gln-Lys-Leu-Gly-Ser-Ile-Asp-Val-(Asp, 3-methylhistidine, Gln). Comparison of the homologous MHC sequences shows two positions at which MHC from dystrophic chicks differs from that of the White Leghorn chicks *(Glu----Gln and Met----Ile). Thus, both the peptide map and sequence analyses demonstrate that in avian muscular dystrophy an abnormal pectoralis MHC is synthesized. It is not yet clear whether the "dystrophic" MHC is a variant MHC or if it arises from the abnormal expression of an earlier developmental form (embryonic or neonatal) of pectoralis muscle MHC.

Amino Acid Sequence↗
PubMed1982

Australia's health system: condition: unstable; prognosis: needs intensive care.

This paper is a discussion of the problems inherent in the development of a health policy in the political arena. Politicians should work towards a consensus health policy, in consultation with health professionals, hospital administrators, health insurance organisations, health care consumers and others. Any consensus health policy must address the issue of health care financing, define the responsibilities of Federal, State and local governments, provide for the special health care needs of disadvantaged groups, and ease the necessary transition from the current emphasis on acute care, to a system which gives high priority to preventive care, health education, individual and community responsibility for health maintenance, and appropriate levels of care.

Australia↗