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Biomedical subjects

S Hofmann

Publications and source records attributed to S Hofmann.

At least 109 records · Page 6Linked to original sources
PubMed1995

Interpretation of sputter depth profiles by mixing simulations.

The interpretation of sputter depth profiles can be simplified by use of computer simulations. Distortions caused by mixing effects and distortions caused by the information depth of the analytical method have to be distinguished. Atomic mixing and the information depth distort the depth profile simultaneously. Therefore, it is necessary to take into consideration a superposition of both distortion effects. The sputtering of a GaAs/A1As multilayer has been calculated on a personal computer with the binary collision approximation code T-DYN by Biersack and with an own layer model. A new computer code LAMBDA has been used for the investigation of the influence of the AES information depth in addition to atomic mixing and preferential sputtering. A comparison of the calculated and the measured depth profile explains the observed effects. Therefore conclusions can be drawn about the original elemental distribution in the sample from the measured depth profile.

Journal Article↗
PubMed1995

Simulation of sputter-induced roughness for depth profiling of thin film structures.

Sputtering induced surface roughening is the dominant factor that degrades depth resolution in sputter profiling of polycrystalline film samples. Due to the dependence of the sputtering yield on the crystallographic orientation, ion beam incidence angle and composition, the local sputtering rate differs from grain to grain. A simple computer program based on a model of Marton and Fine can simulate such a roughness development within one layer, an improved version can even be applied for interfaces. A further extension of the program using a model of Hauffe includes effects like shadowing and enhanced peak erosion leading to surface smoothing.

Journal Article↗
PubMed1995

[Monitoring of bone marrow spilling and cardiopulmonary changes in fat embolism syndrome].

After long bone fractures, as well as hip or knee total arthroplasty, the increase in intramedullary pressure induces bone marrow release into the circulation in more than 90% of patients. Three to four percent of the patients reveal fat embolism syndrome with pulmonary and cerebral involvement and a petechial rash. In about 20% of these patients a fulminant and fatal course is possible. Although fat embolism syndrome was described more than a century ago, there is still no sufficient therapeutic strategy. Because of these facts we try to prevent fat embolism syndrome and monitor patients at risk perioperatively. We have evaluated different diagnostic methods and monitoring facilities and recommend pulse oximetry, capnography, ECG, blood pressure controls and, if indicated, blood gas analyses for perioperative monitoring. Patients at risk and patients who are suffering from fat embolism syndrome require more intensive monitoring, such as transesophageal echocardiography and a pulmonary artery catheter to obtain more detailed information about the hemodynamic and oximetric variables. Furthermore, these patients must be admitted to an intensive care unit.

Blood Gas Analysis↗
PubMed1995

[Modified surgical technique for reduction of bone marrow spilling in cement-free hip endoprosthesis].

Since 1970 the fat embolism syndrome (FES) has been recognised as a severe complication of cemented total hip arthroplasty (THA). Initially and still today the toxicity of bone cement has been though to be responsible for the cardiorespiratory problems. Meanwhile several reports have confirmed the causal relationship between intramedullary pressure (IMP), bone-marrow release into the circulation and subsequent cardiorespiratory deterioration during cemented THA. In recent publications it has been reported that bone-marrow release due to increased IMP also occurs during cementless THA. The clinical implication of these observations is controversial. For this reason in the first part of this paper two autopsy-proven FES deaths and five further clinically manifest FES cases are presented. In the second part of the study, IMP courses during four different surgical techniques (2 conventional, 2 modified) are compared. The aim of the modified surgical technique developed in our department was to minimize IMP peaks and bone-marrow release during cementless THA. Both modified techniques showed significantly lower IMPs during opening of the medullary canal, preparation with rasps, and implantation of the prosthesis than the conventional techniques. The observed FES cases for the first time strongly confirm the clinical relevance of the FES, also during cementless THA. On the basis of the data presented we recommend the modified surgical technique to reduce bone-marrow release during cementless THA.

Aged↗
PubMed1995

[Modified surgical technique for the reduction of bone marrow spilling in knee endoprosthesis].

In the literature 20 cases of fat embolism syndrome (FES) after total knee replacement (TKR) are reported; 16 cases had cemented hinged TKR and 4 resurfacing TKR. Initially, it was believed that the bone cement was responsible for the FES. Since then, however, Fahmy et al. have published extraordinary data, demonstrating the causal relationship between increased intramedullary pressure (IMP) during the insertion of the intramedullary rod (IR) and cardiorespiratory deterioration. The industry responded by developing a fluted IR, disregarding the overdrilling in the distal femur required by Fahmy. In the first part of this paper clinically manifest FES cases after resurfacing TKR are reported. In the second part of the study the conventional surgical technique is compared with a modified technique, which focuses on a reduction of bone-marrow release into the circulation. In the conventional and the modified group, IRs with and without flutes were compared. It was shown that only the opening of the intramedullary canal and insertion of the IR generated relevant IMP peaks during implantation of resurfacing TKR. When compared with the conventional surgical technique, the modified technique revealed significantly lower IMPs, and in neither group was a difference demonstrated between the IR with or without flutes. In 4 patients (2 conventional, 2 modified) transesophageal echocardiography (TEE) was performed for detection of bone-marrow release into the circulation. In the two patients operated on conventionally, TEE showed a markedly higher bone-marrow release than in the patients with modified operations. In conclusion, we recommend the presented modified surgical technique in order to reduce bone-marrow release into the circulation.

Aged↗
PubMed1995

[Therapeutic approach to the management of fat embolism syndrome].

So far, no clinical or experimental study has demonstrated that any drug has a beneficial effect (heparin, cortisone, dextran, etc.) on the course of fat embolism syndrome (FES). Thus, prevention, early diagnosis, and adequate symptomatic treatment are of paramount importance. Besides surgical measures, such as reduction of intraosseous pressure and bone-marrow release during hip or knee replacement, proper treatment of shock in traumatized patients, recognition of risk factors and maintainance of intraoperative cardiorespiratory stability are cornerstones in the prevention of fat embolism syndrome. It is well documented that bone-marrow release into the circulation and pulmonary embolism occurs during any hip or knee arthroplasty. As a result of improvements in anesthesia management, the clinical appearance of FES has moved into the postoperative period. This calls for mandatory cardiorespiratory monitoring up to 24 h postoperatively. When facing a clinically manifest fat embolism syndrome, monitoring and symptomatic treatment must be adapted to the patient's needs in order to ensure adequate oxygenation and acceptable circulatory conditions to protect organ function.

Catheterization, Swan-Ganz↗
PubMed1995

[Pathophysiology of fat embolisms in orthopedics and traumatology].

It is well known that fat embolisms can occur after long bone fractures, and this has been feared for more than 100 years. Since 1970 fat embolisms have also been recognized in endoprosthetic surgery. The clinical manifestation was described as the fat embolism syndrome (FES) by Gurd in 1974. Based on reports in the literature and our own data, a concise pathophysiological model of the FES is presented in this paper. The increase in intramedullary pressure (IMP) in the long bones is the most decisive pathogenic factor for the development of an FES. Any long bone fracture, stabilization of fractures, or implantation of knee or hip endoprostheses can generate IMP peaks leading to bone marrow release into the circulation. Bone marrow itself is a tremendous stimulus for activation of the clotting system. As a result, hypercoagulation and venous stasis in the draining veins generate mixed macroemboli from the initial bone-marrow microemboli. Bone-marrow embolization of the lung in phase I leads to mechanical obstruction of pulmonary arteries. In phase II, release of local mediators, triggered by a systemic inflammatory response (SIR) of the lungs, causes damage to the pulmonary membranes. Disturbed gas exchange and respiratory insufficiency with possible cardiac and cerebral decompensation are the result. In most cases an FES may not be detected clinically, and any mild cardiorespiratory changes are treated easily with oxygen insufflation and usually disappear within 48 h. Of paramount importance for clinical manifestation of an FES are the quantity and duration of bone-marrow release and co-factors (cardiorespiratory compliance and perioperative stability of the patient). Patients with preexisting cardiorespiratory disease in combination with massive intraoperative bone-marrow release may even face a deadly FES event. Increased IMP causes local obstruction of cortical vessels with bone marrow. In combination with the damaged endosteal blood supply, avascular necrosis of the cortical bone occurs. During endoprosthetic procedures, mechanical-and mediator-triggered damage of the intima of big veins, in combination with venous stasis and hypercoagulation may be responsible for the high incidence of proximal thrombosis of femoral veins. As a delayed result of the disseminated intravascular coagulopathy, petechial bleeding in the trunk and subconjunctiva can be seen. A better understanding and recognition of the FES's pathophysiology may help to use prophylactic, diagnostic and therapeutical measures more effectively.

Blood Coagulation↗
PubMed1994

Low-frequency stimulation of rat fast-twitch muscle enhances the expression of hexokinase II and both the translocation and expression of glucose transporter 4 (GLUT-4).

This study followed changes in the capacities of uptake and phosphorylation of glucose in response to contractile activity in low-frequency stimulated (10Hz, 24 h/d) rat fast-twitch muscle. We investigated the intracellular distribution of GLUT-4, the major glucose transporter isoform in muscle, changes in the amounts of its specific mRNA and total cellular protein, as well as changes in its relative synthesis rate. These analyses were complemented by measurements of total hexokinase activity and hexokinase II (HKII) expression at the levels of mRNA content and protein synthesis. Changes in protein synthesis were determined by in vivo labeling with [35S]methionine. Translocation of GLUT-4 into the sarcolemma was an immediate response to contractile activity, whereas changes in its total amount were observed only with ongoing stimulation (5 d and longer). A twofold increase in GLUT-4 content after 5 d and longer stimulation periods was preceded by elevations of its mRNA and by enhanced [35S]methionine incorporation. Conversely, increases in HKII expression with a rise in total hexokinase activity occurred soon after the onset of stimulation (30-fold elevations of HKII mRNA after 12 h and 20-fold increases in [35S]methionine incorporation after 24 h). With ongoing stimulation, HKII mRNA and synthesis returned to lower levels (fivefold elevations). Nevertheless, hexokinase activity continued to rise, stabilizing at fivefold-elevated levels after 3 d. These observation suggested that posttranscriptional mechanisms contributed to the upregulation of HKII, e.g. stabilization by elevated intracellular glucose and mitochondrial binding of the enzyme. This suggestion was supported by experiments with cessation after 24 h where hexokinase activity continued to increase, although the mRNA content and, especially, the [35S]methionine incorporation decayed steeply. The increase in HKII prior to GLUT-4 suggests that phosphorylation may be rate limiting in glucose utilization of glycolytic fibers under conditions of sustained contractile activity. Taken together, the changes in distribution and content of GLUT-4, as well as in HKII represent early metabolic adaptations. In addition, they are related to the overall process of stimulation-induced fiber type transformation.

Acetylcholinesterase↗
PubMed1994

[Osteonecrosis].

The causes of osteonecrosis are varied. The pathogenesis of osteonecrosis subsequent to trauma is well known. Furthermore, an association of this disorder with cortisone, haemoglobinopathies, rare metabolic diseases, and risk factors seems to be evident. However, a sizable proportion of patients have osteonecrosis in which none of these associations exists, referred to as idiopathic osteonecrosis. Generally, intraosseous vascularization represents the common pathway for the various causes of the disease. The prognosis is influenced by the age of the patient, the location of the necrosis and the stage of the disease at the time of diagnosis. In recent times diagnosis has been improved by the use of modern imaging modalities, and MR imaging is now widely accepted as the imaging method of choice. It not only allows early diagnosis but also yields exact staging information in advanced disease, which is a requirement for adequate therapy.

Adult↗
PubMed1994

[The non-traumatic femur head necrosis in the adult. I: pathophysiology, clinical picture and therapeutic options].

Intraosseous vascularization is the common pathway of the multifactorial causes of avascular necrosis of the hip (AVN). Recurring ischemic phases could lead to bone necrosis in the initial stage of the disease, when it is still reversible. A spontaneous repair mechanism can lead to complete healing at this stage. The necrotic area demarcates the superior-anterior aspect from the residual femoral head with a reactive interface in the irreversible early stage of the disease. In this stage damage to the femoral head can only be delayed with core decompression or femoral osteotomy, because a sufficient repair mechanism is no longer possible. When the articular surface collapses the early stage gives way to the late stage. Cartilage incongruence and microfracture lead to progressive destruction of the femoral head and to secondary osteoarthritis. In this late stage femoral osteotomy is only successful in carefully selected patients. Total hip replacement is the last resort for patients with painful destruction of the joint. As clinical symptoms are unspecific, MRI plays an important role for early diagnosis of AVN in the initial or early stages. Conservative treatment is not successful in any of the three stages of the disease.

Adult↗
PubMed1994

[The non-traumatic femur head necrosis in the adult. II: radiologic diagnosis and staging].

In recent years diagnosis, and in particular early diagnosis, of osteonecrosis of the hip has been much improved by modern imaging modalities. Magnetic resonance imaging is widely accepted as the primary imaging modality for the early detection of this disorder and can help to facilitate the therapeutic management in later stages. However, plain radiographs, bone scans and computed tomography are still important techniques, which cannot be avoided in most cases. This paper describes the relative values of the different modalities. The staging system used is the international ARCO system.

Adult↗
PubMed1993

Liver abnormalities associated with chronic mercury accumulation in stranded Atlantic bottlenose dolphins.

Eighteen stranded Atlantic bottlenose dolphins (Tursiops truncatus) examined postmortem were sampled for histologic study. All cases were examined for ferric ion and lipofuscin. Ages were determined from tooth growth layers. Electron microscopic (EM) examination and X-ray spectroscopy (EDAX) were performed. Chemical analysis for mercury was conducted on 12 of the animals by atomic absorption spectrophotometry. Nine animals were found to have excessive lipofuscin in both liver and kidney. Four of these nine animals also exhibited active liver disease (fat globules, central necrosis, lymphocytic infiltrates) whereas, of the animals without the excessive pigment, only one animal had an active liver lesion. EM and EDAX showed electron-dense amorphous material presumably within lysosomes to be Hg with no deposits on mitochondrial or nuclear membranes noted. Age relationship to portal pigment deposition was positive. Liver mercury concentrations ranged from 0.01 to 443 micrograms/g of wet weight with all animals having liver pigment yielding values of or above 61 micrograms/g, whereas all animals lacking pigment had values of or below 50 micrograms/g. The evidence suggests that the excessive pigment accumulation is related to toxic effects of Hg and presents as increased active liver disease.

Age Factors↗
PubMed1993

[Bone marrow edema--an early form of femur head necrosis].

We examined 15 patients (16 hips) with painful hips whose radiographs were either normal (n = 9) or showed a minimal decrease in radiodensity (n = 7). The available bone scintigrams of 9 cases were positive. T1-weighted images visualised a diffuse signal loss of the bone marrow in all hips, with various extensions in the head, neck, and intertrochanteric area. These regions were hyperintensive on T2-weighted images. Focal anomalies were not seen in any of the cases. All patients underwent core decompression treatment. Histology of 13 hips confirmed not only the presence of bone marrow oedema but of bone changes corresponding to those of avascular necrosis. Follow-up examinations with MR after core decompression showed normal signal intensity in all cases. Magnetic resonance represents a viable diagnostic tool for identifying bone marrow oedema. Due to our histological results bone marrow oedema should be included in the differential diagnosis as an early stage of necrosis of the hip.

Adult↗