Biomedical subjects
Publications and source records attributed to P Gruber.
We report on three patients who were operated on peripheral nerve compression syndromes in the hand and forearm caused by a lipoma. After surgical removal of the lipoma, distinct improvement or even recovery of symptoms was observed.
OBJECTIVE: Arterial switch is the operation of reference for the surgical treatment of transposition of the great arteries. In cases of late referral, perinatal complications or early left ventricular (LV) dysfunction, the one stage arterial switch is contra indicated. Anatomical repair remains possible in these patients following a LV retraining. METHODS: From January 1992 to January 2000, a LV retraining was attempted in 22 patients with transposition of the great arteries with intact ventricular septum (TGA IVS), whereas 470 direct arterial switch and 2 Senning were performed. Indication for LV retraining was based on a combination of factors including: an age older than 3 weeks, a "banana shape" aspect of the inter-ventricular septum and mainly a LV mass <35G/m(2). RESULTS: The mean age at LV retraining was 3.2 months ranging from 9 days to 8 months. Usually conducted by sterntomy, it associated a loose PA banding with a LV/RV at 65% with a systemico-pulmonary shunt. The first stage was associated with frequent LV dysfunction and the LV retraining was discontinued in two patients in favor of one Senning and one early switch followed by ECMO. One patient died at first stage from a mediastinitis. Nineteen patients underwent a second stage arterial switch that was performed when the LV mass had reached 50 G/m(2) after a mean delay of 10 days, ranging from 5 days to 6 weeks. After a mean follow up of 25 months, there was one non-cardiac late death. The 17 patients followed and leaving with an arterial switch are in NYHA class I, with a mean LV shortening fraction of 39%. CONCLUSIONS: Arterial switch following LV retraining in TGA IVS is a satisfactory option. The inferior limit of 35 G/m(2) adopted, to indicate LV retraining, seems a safe landmark. The quality of the myocardium generated and the respective roles played by the LV afterload, LV wall shear stress, LV inflow and outflow to induce the LV remodeling remain under debate.
Cell death by apoptosis is exerted by the coordinated action of many different gene products. Mutations in some of them, acting at different levels in the apoptosis process, have been identified as cause or contributing factor for human diseases. Defects in the transmembrane tumor necrosis factor receptor 1 (TNF-R1) lead to the development of familial periodic fever syndromes. Mutations in the homologous receptor Fas (also named CD95; Apo-1) are observed in malignant lymphomas, solid tumors and the autoimmune lymphoproliferative syndrome type I (ALPS I). A mutation in the ligand for Fas (Fas ligand; CD95 ligand, Apo-1 ligand), which induces apoptosis upon binding to Fas, was described in a patient with systemic lupus erythematodes and lymphadenopathy. Perforin, an other cytotoxic protein employed by T- and NK-cells for target cell killing, is mutated in chromosome 10 linked cases of familial hemophagocytic lymphohistiocytosis. Caspase 10, a representative of the caspase family of proteases, which plays a central role in the execution of apoptosis, is defect in autoimmune lymphoproliferative syndrome type II (ALPS II). The intracellular pro-apoptotic molecule bcl-10 is frequently mutated in mucosa-associated lymphoid tissue (MALT) lymphomas and various non-hematologic malignancies. The p53, an executioner of DNA damage triggered apoptosis, and Bax, a pro-apoptotic molecule with the ability to perturb mitochondrial membrane integrity, are frequently mutated in malignant neoplasms. Anti-apoptotic proteins like bcl-2, cellular-inhibitor of apoptosis protein 2 (c-IAP2) and neuronal apoptosis inhibitory protein 1 (NAIP1) are often altered in follicular lymphomas, MALT lymphomas and spinal muscular atrophy (SMA), respectively. This article reviews the current knowledge on mutations of apoptosis genes involved in the pathogenesis of human diseases and summarises the gradual transformation of discoveries in apoptosis research into benefits for the clinical management of diseases.
Carcinogenesis encompasses a prolonged accumulation of injuries at several different biological levels and include both genetic and biochemical changes in the cells. At each of these levels, there are several possibilities of intervention in order to prevent, slow down or even halt the gradual march of healthy cells towards malignancy. Diet modification is one such possibility. A number of natural foodstuffs, especially fruits and vegetables contain substantial quantities of molecules that have chemopreventive potential against cancer development. Such compounds include vitamins, trace elements and a variety of other molecules with antioxidant properties. Carotenoids, flavanoid polyphenols, isoflavones, catechins, and several other components that found in cruciferous vegetables are molecules that are known to protect against the deleterious effect of reactive oxygen species. A number of epidemiological and experimental studies have shown that vitamin C and E, Beta-carotene and the essential trace element selenium can reduce the risk of cancer. Consistent observations during the last few decades that cancer risk is reduced by a diet rich in vegetables, fruits, legumes, grains and green tea have encouraged research to identify several plant components especially phytochemicals that protect against DNA damage. Many of these substances block specific carcinogen pathways. Dietary supplements are part of an overall health program, along with a high intake of fruits and vegetables that help to combat damage to cells, which in turn may initiate cancer development. This paper will review current knowledge concerning diet modification and cancer prevention with special reference to minerals and trace elements.
Both radial tunnel syndrome and posterior interosseous nerve compression syndrome are caused by compression of the posterior interosseous nerve. Posterior interosseous nerve (PIN) compression syndrome is a rare condition--less than 10 percent of our cases of PIN-compression showed signs of palsy--and must be differentiated from tendinous lesions. From 1992 to 1997, we decompressed the PIN using an anterior approach in nine cases because of palsy without a history of trauma. Only one patient was lost to follow-up. Our study indicates that the results of operative decompression of the PIN depend on the time interval between first symptoms of palsy and operation. On the other hand, some cases of posterior interosseous nerve compression syndrome show spontaneous recovery. We recommend operative decompression of the PIN if incomplete palsy worsens or if complete palsy persists for more than 12 weeks.
Both radial tunnel syndrome and posterior interosseous nerve (PIN) compression syndrome are caused by compression of the posterior interosseous nerve. There is a controversy about certain features of PIN compression especially with regard to diagnostic criteria and therapy as well as differentiation from tennis elbow. From 1992 to 1997, we operated 110 patients because of PIN compression. Diagnosis was based on clinical examination only. As a rule, we decompressed the PIN directly using an anterior approach. With regard to radial tunnel syndrome, we could review 69 from 103 operations with an average follow-up of 41 months. Using the criteria originally proposed by Roles and Maudsley, only 60% showed excellent or good results. The mean DASH score was 32. Recompression of the PIN by scarring was found in as much as 17% of patients and proved to be a serious complication of direct decompression of the PIN. Furthermore, 52% of our patients operated on because of PIN compression suffered from tennis elbow as well. We therefore believe that radial tunnel syndrome is a specific form of tennis elbow. From an anatomical point of view, the inseparable origin of the radial wrist extensors and supinator muscle seems to link tennis elbow and radial tunnel syndrome. To avoid recompression of the PIN by scarring, we have abandoned direct decompression and now routinely use Wilhelm's denervation procedure for the treatment of tennis elbow as well as radial tunnel syndrome. This procedure indirectly decompresses the PIN by cutting the superficial origin of the supinator muscle with consecutive relaxation of Frohse's arcade. Preliminary results are promising and show improvement of preoperative neurologic status by indirect decompression.
OBJECTIVE: To determine the time it takes for O2 saturation measured by pulse oximetry to equilibrate after a change is made in supplemental O2 administered by nasal cannula in patients with cardiac and pulmonary disease. METHODS: A prospective, observational study of a convenience sample of 51 patients treated in a university-affiliated ED with nasal cannula O2. Patients were placed on and/or subsequently taken off O2 via nasal cannula set at 2 or 4 L/min based on clinical indications. Oxygen saturation was measured at 1-minute intervals over a 30-minute period using finger-probe pulse oximetry. Of the 51 patients in the study, 43 were monitored while O2 treatment was initiated and 18 were monitored when it was discontinued. RESULTS: Most (95%) of the patients placed on O2 attained equilibration of O2 saturation within 3.5 minutes. Most (95%) of the patients taken off supplemental O2 attained equilibration of O2 saturation within 4.5 minutes. CONCLUSION: The interval to equilibration of O2 saturation in patients receiving O2 by nasal cannula is considerably shorter than the 20-30 minutes generally suggested. Adequacy of O2 supplementation should be assessable much sooner than was previously taught.
A modified light-weight intestinal cannula, based on the modified Thomas type (Thomas, 1941; Jones et al., 1971) was fabricated and tested. The design extends the useful life of the cannula and expands the versatility of the canine gastrointestinal (GI) system for pharmaceutical and physiological research. The cannula permits easy administration of pharmaceutical dosage forms directly into or access to ingested substances anywhere along the small intestine.
Gastric emptying of nondigestible solid particles was studied in the fasted dog. Particles of varying sizes (0.5-6.4 mm), density (0.5-2.9 gm/cm3), and surface characteristics were coadministered orally with 50 mL of saline and collected from a permanent duodenal cannula implanted approximately 15 cm from the gastroduodenal junction. The phase of the motility pattern was ascertained by the appearance of bile, which occurs during phase II, as well as by mucus discharge, which stops at the onset of phase I. A lag phase, due to the 'quiet' phase I, was observed in the gastric emptying of coadministered saline. This is in contrast with gastric processing of large volumes (i.e., greater than 200 mL) which can usually be approximated by first-order discharge. Most coadministered saline was discharged before the solid particles. The pH of the duodenal effluent was elevated approximately 1 pH unit during mucus discharge and its pH can be as high as 8.3. In the fasted dog, gastric emptying of nondigestible particles closely followed the gastric motility patterns. The onset of discharge of the particles correlated with the late phase II and the phase III activity. Except for a few cases, which took two migrating motor complexes (MMC), greater than 90% of administered particles was discharged from the stomach after one MMC. The discharged particles were entrapped within mucous plugs. In the fasted state, gastric emptying of nondigestible particles appeared to be independent of size, density, and surface characteristics. Mucus seems to play a significant role in the distribution and discharge of the administered particles.
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Electron-microscopic analysis of iris biopsy material was carried out paying particular attention to vessels and infiltrating cells. Characteristic changes of vessels and cells were found in two cases. One showed abundant lymphodiapedesis, perivascular infiltration, and vessels appearing morphologically normal. The other showed diffuse infiltration of cells and numerous fenestrated newly formed vessels. In the latter, three different types of opening in the endothelium were observed: (1) separation of intercellular junctions; (2) small pores or defects in the endothelium, and (3) large holes or defects in the endothelium. Cell leakage from normal and newly formed vessels was considered. We concluded that lymphocytes may migrate through the cytoplasm within membrane-bounded vesicles in normal vessels, whereas in newly formed fenestrated vessels cells, including small lymphocytes, may pass through three different types of opening in the endothelium.
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Explore the source record for details and available documents.