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Biomedical subjects

J Martinell

Publications and source records attributed to J Martinell.

At least 37 records · Page 2Linked to original sources
PubMed1987

Prosthetic valve endocarditis caused by Brucella melitensis. A report of four cases successfully treated with tetracycline, streptomycin, and sulfamethoxazole and trimethoprim plus valve replacement.

Optimal treatment of prosthetic valve endocarditis due to Brucella melitensis is unknown. The presence of ring abscess makes extensive surgical débridement and valve replacement essential steps of management. Antimicrobial therapy with tetracycline hydrochloride plus streptomycin sulfate or sulfamethoxazole and trimethoprim can achieve the sterilization of infected cardiac tissue. Late bland periprosthetic leaks occur frequently. Reoperation can be safely performed after a period of antimicrobial therapy. Prolonged treatment with doxycycline hyclate seems advisable.

Adult↗
PubMed1986

Comparative clinical results with Omniscience (STM1), Medtronic-Hall, and Björk-Shiley convexo-concave (70 degrees) prostheses in mitral valve replacement.

The intermediate clinical results of 289 patients undergoing isolated mitral valve replacement with three different low-profile mechanical prostheses have been retrospectively analyzed and compared. Between June, 1980, and September, 1983, 70 patients received the Omniscience prosthesis, 159 patients the Medtronic-Hall valve, and 60 patients the convexo-concave 70 degree Björk-Shiley prosthesis. Hospital mortality was 15% for the Björk-Shiley group, 4.4% for the Medtronic-Hall group, and 7.1% for the Omniscience group. Cumulative follow-up was 88 years (mean 1.7 years) for the Björk-Shiley, 229 years (mean 1.5 years) for the Medtronic-Hall, and 223 years (mean 3.3 years) for the Omniscience group. All patients were placed on a program of anticoagulant therapy (dicumarol) postoperatively. Actuarial survival rates (+/-SE) 2 years postoperatively were comparable for the three groups: Björk-Shiley, 90% +/- 4.7%; Medtronic-Hall, 93% +/- 2.2%; and Omniscience, 88% +/- 4.1% (p = NS). Late mortality, expressed at linearized rates (percent patient-year +/-SE), was 3.4% +/- 1.9% for the Björk-Shiley group, 1.7% +/- 0.8% for the Medtronic-Hall group, and 3.6% +/- 1.2% for the Omniscience group (p = NS). Actuarially determined rates of freedom from thromboembolic complications (systemic embolism and valvular thrombosis) 2 years postoperatively were 97% +/- 2.2% for the Björk-Shiley group, 94% +/- 2.1% for the Medtronic-Hall, and 84% +/- 4.7% for the Omniscience group (p = 0.05, Omniscience versus Medtronic-Hall; p = 0.02, Omniscience versus Björk-Shiley) The actuarial probability of being free from reoperation 2 years postoperatively was 92 +/- 3.5 for the Björk-Shiley group, 92 +/- 2.9 for the Medtronic-Hall group, and 82 +/- 3.9 for the Omniscience group (p = 0.04). The major cause for reoperation in the Omniscience group was valve thrombosis (seven patients), yielding a linearized incidence (+/-SE) of 3.1 +/- 1.1 (p = 0.01). No statistically significant differences were obtained regarding the incidence of prosthetic infective endocarditis or perivalvular leak. Overall rates of anticoagulant-related hemorrhage were comparable for the three groups.

Actuarial Analysis↗
PubMed1985

Long-term comparative analysis of the Björk-Shiley and Hancock valves implanted in 1975.

The long-term results in all patients undergoing isolated mitral, aortic, or double mitral-aortic heart valve replacement operated upon in 1975 has been retrospectively analyzed. A total of 153 patients received the standard Björk-Shiley (flat pyrolytic disc) mechanical prostheses and 150 patients received the noncomposite Hancock porcine xenograft. Overall operative mortality was not significantly different between groups. All patients receiving a Björk-Shiley prosthesis, but none in the Hancock group, received long-term anticoagulant therapy. Medium and long-term actuarial survival rates (5 and 10 years postoperatively) were comparable for the two groups (88% for Björk-Shiley and 84% for Hancock [NS] at 5 years; 86% for Björk-Shiley and 80% for Hancock at 10 years [NS]). The incidence of systemic embolism was similar in the two groups (1.6% +/- 0.4% per patient-year for the Björk-Shiley group and 1.3% +/- 0.3% per patient-year for the Hancock group [NS]). Also the incidence of endocarditis was similar (0.6% +/- 0.2% per patient-year for the Björk-Shiley group and 0.8% +/- 0.3% per patient-year for the Hancock group [NS]). In the Hancock group the overall incidence of reoperations was significantly higher than in the Björk-Shiley group (4.2% +/- 0.6% per patient-year versus 0.9% +/- 0.3% per patient-year (p = 0.001). The major cause for reoperation in the Hancock group was primary tissue failure (3% +/- 0.5% per patient-year). In the Björk-Shiley group the major cause of reoperation was valve thrombosis (0.5% +/- 0.2% per patient-year). Therefore, accepting the fact that other bioprostheses may behave differently from the Hancock noncomposite xenograft, we currently restrict our indications for valve replacement with bioprostheses.

Actuarial Analysis↗
PubMed1984

Results and complications with the Omniscience prosthesis.

A clinical trial with the Omniscience heart valve was conducted from June, 1980, until May, 1981. In this period 166 patients underwent heart valve replacement: mitral valve replacement (MVR) 70 patients, aortic valve replacement (AVR) 37, and combined mitral-aortic valve replacement (M/AVR) 59 patients. There were 20 hospital deaths, for a mortality of 12%. Total follow-up was 226 patient-years (range 6 to 28 months, mean 18 months). There were eight late deaths (MVR 4.6%, AVR 3.1%, and M/AVR 8.1%). All patients were taking oral anticoagulants. The incidence of valve-related complications (expressed as events per 100 patient-years) was as follows: Systemic embolism--MVR 2, AVR 4.7, and M/AVR 2.5; and anticoagulant complications--MVR 1.9, AVR 2.3, and M/AVR 0. The incidence of valvular dysfunction (expressed as events per 100 patient-years) was as follows: valvular thrombosis--MVR 4.8, AVR 0, and M/AVR 1.2; perivalvular leakage--MVR 1.9, AVR 2.3, and M/AVR 2.5; and infective endocarditis--MVR 0.96, AVR 0, and M/AVR 1.2. The actuarial probability of being free of valvular dysfunction 30 months postoperatively is 73% for the MVR group, 90% for the AVR group, and 71% for the M/AVR group. Despite a short follow-up, the incidence of valvular dysfunction has been significant. For this reason, we have discontinued using these prostheses for heart valve replacement.

Aortic Valve↗
PubMed1983

Early surgical results of the Medtronic-Hall valve.

A clinical trial with the Medtronic-Hall (M-H) valve was started in November 1981. From then until December 1982, 157 patients underwent heart valve replacement: Mitral valve replacement (MVR) 63 patients, isolated aortic valve replacement (MVR) 41 patients, and 53 underwent combined mitral-aortic valve replacement (MVR + AVR). Hospital mortality was 2.5% overall (4/157). The total follow-up was 147 patient-years (range 1 to 12 months). Late mortality was 3.2% for MVR, 2.5% for AVR and 1.9% for double MVR + AVR. Oral anticoagulation therapy (Dicumarol) was administered to all patients included in this study. There were no anticoagulant complications and no prosthetic bacterial endocarditis registered in this series of patients up to date. The incidence of systemic embolism was 2.5 events per 100 patient-years in the AVR group. No embolic episodes have been registered in the other 2 groups. The incidence of valvular dysfunction (expressed as events per 100 patient-years) were: --Perivalvular leak (0 MVR, 0 AVR and 2 MVR + AVR) --Valve thrombosis (1.7 MVR, 0 AVR and 0 MVR + AVR) --Mechanical dysfunction (1.7 MVR, 0 AVR and 0 MVR + AVR) Despite a short follow-up, the results with the Medtronic-Hall valve are encouraging and compare favorably with other mechanical prostheses.

Adult↗
PubMed1981

Deletions in the alpha-globin gene complex in alpha-thalassemic mice.

Three induced, heritable mutations in the mouse cause alpha-thalassemias. The adult alpha-globin genes on each mutant chromosome are no longer expressed. Embryos heterozygous for one normal and any of the three mutant chromosomes also seem to be deficient in embryonic alpha-globin-like x-globin, suggesting that the x-globin gene is nearby and also inactivated. A normal genetic polymorphism for a specific EcoRI site in or around the mouse alpha-globin gene complex has been used here to show that each of the three mutated chromosomes has a deletion that includes the segment of a 12-kilobase EcoRI band which normally carries one of the two adult alpha-globin genes. The deletion of the comparable part of the second alpha-globin gene site is also inferred. Nonetheless, a 4.7-kilobase EcoRI segment which carries a characterized alpha-globin-like pseudogene is still present in each mutant. These mutations were recovered after triethylenemelamine or x-ray treatments.

Animals↗
PubMed1981

Three mouse models of human thalassemia.

Three types of mice with globin gene mutations, called 352HB, 27HB, and Hbath-J, appear to be true animal models of human thalassemia. Expression of the alpha-globin genes in three stocks of mice, each one heterozygous for one of the alpha-globin mutations, was examined at the polypeptide, RNA, and DNA levels. alpha-Globin polypeptide chains, relative to beta-globin chains in heterozygous thalassemic mice, are present at approximately 80% of normal. The ratios of alpha-globin to beta-globin RNA sequences are also 75-80% of normal, exactly reflecting the alpha-globin to beta-globin chain ratios. In the case of mutant 352HB, at least one alpha-globin gene is deleted. Thalassemic mouse erythroid cells appear to compensate partially for the loss of half of their alpha-globin genes.

Animals↗
PubMed1980

Liver function during treatment with cefuroxime.

The liver function was studied in 15 patients before and during treatment with cefuroxime. Four elderly patients had a prolonged half-life of galactose at admission but they all showed declining values during the cefuroxime treatment. Only in one patient did the galactose half-life increase during treatment (from 14 to 25 min.). This patient was an old diabetic who also had prostatic cancer. Cefuroxime treatment seems to be well tolerated also in patients with signs of impaired metabolic liver function at start of treatment.

Adult↗
PubMed1979

Thrombotic obstruction of the Björk-Shiley aortic valve prosthesis. Report of four cases.

We present four cases of late thrombotic obstruction of the Björk-Shiley aortic valve prosthesis. The incidence of this complication reported in the literature to vary from 0.7% to 5%. In our experience of a total of 623 Björk-Shiley aortic valve replacements, we observed this complication in only 4 patients (0.6%). Two of them had poorly controlled anticoagulation therapy. The clinical presentation was subacute in all four patients. Surgical treatment, thrombectomy and debridement, was performed in all of them. The diagnosis was made upon abrupt and progressive onset of dyspnoea, physical examination data and echocardiographic and radioscopic findings. Angiocardiographic studies were needed in two patients.

Adult↗
PubMed1976

Potentiation of glucagon secretion by serotonin antagonists in man.

To study the possible implication of endogenous serotonin in the control of glucagon secretion in man, normal volunteers were subjected to alpha-cell stimulation before and after oral treatment with serotonin antagonists (cyproheptadine and methysergide) and with an inhibitor of serotonin synthesis (para-chlorophenylalanine, PCPA). After administration of cyproheptadine (16 mg daily, for two days) the glucagon responses to arginine (N=12) and to insulin-induced hypoglycemia (N=9) were more marked than in the control experiments (differences between maximal elevations: +165 pg/ml, P less than 0.0001, and +197 pg/ml, P less than 0.02, respectively). After methysergide treatment (9 mg daily, for two days), a potentiation of arginine-provoked glucagon secretion was also observed (+260 pg/ml, P less than 0.002; N=7). Similarly, after PCPA administration (2 g daily, for four days) the alpha-cell responsiveness to both aminogenic (N=12) and hypoglycemic (N=7) stimuli was enhanced (+108 pg/ml, P less than 0.05, and +164 pg/ml, P less than 0.05, respectively). Since glucagon secretion is potentiated by treatment with drugs which either antagonize serotonin action or inhibit its synthesis, the suggestion can be made that endogenous serotonin modulates alpha-cell function in man by acting as an inhibitor.

Arginine↗
PubMed1975

Identification and purification of collagen-synthesizing polysomes with anti-collagen antibodies.

Antibodies against embryonic chick bone collagen were prepared in rabbits and were purified by affinity and ion exchange chromatography until collagen-specific and RNase-free. 125I-anti-collagen antibodies were used to locate the collagen-synthesizing polysomes of 8-day chick embryo wings and legs on sucrose gradients by measuring the polysome associated radioactivity. The 125I-anti-collagen antibodies bound predominantly to polysomes in the heavy region of sucrose gradients. These binding sites could only be saturated with homologous anti-collagen antibodies. Further evidence for the specificity of this reaction was provided by a correlation of the amount of anti-collagen antibodies bound in the heavy regions of sucrose gradients with the amount of collagen being synthesized by a particular tissue. The validity of this immunochemical method was confirmed by localizing collagen-synthesizing polysomes by an independent method which utilizes their ability to incorporate [3H]proline into collagen peptides in a cell-free system. The collagen-synthesizing polysomes are found in a single, rather broad peak in these gradients. The results of shortening the centrifugation time indicate that larger species of collagen-synthesizing polysomes are not present in these tissues. Partial purification of the collagen-synthesizing polysomes may be achieved by specifically sedimenting them after treatment with anti-collagen antibodies followed by goat anti-rabbit antibodies.

Animals↗
PubMedDate not supplied

The Swedish version of the Childhood Health Assessment Questionnaire (CHAQ) and the Child Health Questionnaire (CHQ).

We report herein the results of the cross-cultural adaptation and validation into the Swedish language of the parent's version of two health related quality of life instruments. The Childhood Health Assessment Questionnaire (CHAQ) is a disease specific health instrument that measures functional ability in daily living activities in children with juvenile idiopathic arthritis (JIA). The Child Health Questionnaire (CHQ) is a generic health instrument designed to capture the physical and psychosocial well-being of children independently from the underlying disease. The Swedish CHAQ CHQ were already published and therefore were revalidated in this study. A total of 129 subjects were enrolled: 69 patients with JIA (13% systemic onset, 39% polyarticular onset, 25% extended oligoarticular subtype, and 23% persistent oligoarticular subtype) and 60 healthy children. The CHAQ clinically discriminated between healthy subjects and JIA patients, with the systemic, polyarticular and extended oligoarticular subtypes having a higher degree of disability, pain, and a lower overall well-being when compared to their healthy peers. Also the CHQ clinically discriminated between healthy subjects and JIA patients, with the systemic onset, polyarticular onset and extended oligoarticular subtypes having a lower physical and psychosocial well-being when compared to their healthy peers. In conclusion the Swedish version of the CHAQ-CHQ are reliable, and valid tools for the functional, physical and psychosocial assessment of children with JIA.

Adolescent↗