[Commentary on the article of C. Smola: about the problem of radial tunnel syndrome or "where does the tennis elbow end and where does the radial tunnel syndrome begin?"].
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Denervation↗
Biomedical subjects
A Wilhelm
Publications and source records attributed to A Wilhelm.
Residual kidney function after donor nephrectomy. Assessment by 99mTc-MAG3-clearance.
AIM: We evaluated the long-term residual renal function after donor nephrectomy using 99mTc-mercaptoacetyltriglycin (MAG3)-clearance. DONORS, METHODS: Altogether 49 kidney donors were examined using 99mTc-MAG3-clearance after nephrectomy for donation to a relative (m:f = 11:38; age 55+/-27 years). The donors were examined 16+/-8 years postoperatively (1.5-26 years). 42 donors (86%) showed normal creatinine values, whereas the other seven (14%) exhibited slightly elevated levels. 20 donors were examined pre- and postoperatively and compared intraindividually. The kidney function was compared to the age adapted normal values of healthy persons with two kidneys (67-133% of age related mean). RESULTS: After nephrectomy all donors showed a normal perfusion, good secretion, merely physiological intrarenal transit and a normal elimination from the kidneys. The 99mTc-MAG3-clearance was 69+/-15% of the normal mean value of healthy carriers of two kidneys regardless of the gender. 20 donors with a preoperative examination showed a significantly reduced total renal function from 84+/-15% of the mean normal value preoperatively to 60+/-15% postoperatively (p <0.0005). 15 donors of this group exhibited a significant functional increase of the residual kidney from 40% initially to 60% after nephrectomy (p = 0.003). No correlation was found between the initial-99mTc-MAG3-clearance measured prior to nephrectomy and the clearance levels after nephrectomy. Also, no correlation between the preoperative 99mTc-MAG3-clearance and the postoperative serum creatinine values could be observed. Altogether, 22% of the donors (11/49) developed arterial hypertension 10+/-8 years after donation (1-23 years). This corresponds to the normal age prevalence of hypertension in the carriers of two kidneys. Three donors suffered from arterial hypertension prior to the operation. CONCLUSION: Kidney donors with normal or slightly elevated creatinine values postoperatively show a 99mTc-MAG3-clearance value of 69% of the mean value of healthy carriers of two kidneys. This may serve as a reference value for healthy carriers of one kidney. In our study we demonstrated a good compensation of the contralateral kidney via renal scintigraphy by means of 99mTc-MAG3-clearance.
Adult↗
Acute impairment of hepatic microcirculation and recruitment of nonparenchymal cells by intrasplenic hepatocyte transplantation.
BACKGROUND/PURPOSE: Over the last 20 years, hepatocyte transplantation (HcTx) has advanced from the experimental to the clinical stage. To date, HcTx has been performed in 30 patients in the United States. Regardless whether hepatocytes are transplanted into the spleen and migrate to the liver or are injected directly into the portal vein, transplanted liver cells will, to some extent, congest the recipient liver microcirculation. The potential negative consequences of intrasplenic HcTx were the subject of this study. METHODS: By using intravital microscopy, the authors investigated whether intrasplenic HcTx of 20 x 10(6) allogenic hepatocytes would influence liver perfusion, excretory liver function, and nonparenchymal cells (Kupffer and Ito cells) in vivo. RESULTS: The sinusoidal perfusion rate declined significantly from 94% (control) to 84% on day 1 and 76% on day 7. Bile acid excretion decreased in a similar fashion from 0.924 mg/h (control) to 0.669 mg/h on day 7. The authors observed a significant increase of Ito cells from 81.1 cells per microscopic field (control) to 97.1 (day 1) and an increase of Kupffer cells (KC; 6.1 cells per microscopic field on day 1 v 3.8 on control). CONCLUSIONS: This study shows an acute impairment of hepatic microcirculation and hepatucellular function along with an recruitment and activation of nonparenchymal cells in the early posttransplantation period after intrasplenic HcTx. Kupffer cell recruitment indicates an activation of local host defense, and Ito cell activation implies the initiation of liver repair mechanisms owing to ischemia-related cell damage.
Animals↗
Growth rate of potash alum crystals: comparison of silent and ultrasonic conditions.
The influence of power ultrasound on the growth rate of potash alum was investigated. The experiments on growth of potash alum crystals were carried out in a stirred double jacket tank in silent conditions as well as in the presence of power ultrasound (20 kHz) at 32 degrees C, with different initial crystal sizes. It was observed that the mass growth rate of potash alum was faster under ultrasound compared to that under silent conditions. The shape was not modified by ultrasound but the size of crystals, which are grown under ultrasound, are smaller and with higher density compared to those grown under silent conditions.
Journal Article↗
The hemicholinium-3 sensitive high affinity choline transporter is internalized by clathrin-mediated endocytosis and is present in endosomes and synaptic vesicles.
Synthesis of acetylcholine depends on the plasma membrane uptake of choline by a high affinity choline transporter (CHT1). Choline uptake is regulated by nerve impulses and trafficking of an intracellular pool of CHT1 to the plasma membrane may be important for this regulation. We have generated a hemagglutinin (HA) epitope tagged CHT1 to investigate the organelles involved with intracellular trafficking of this protein. Expression of CHT1-HA in HEK 293 cells establishes Na+-dependent, hemicholinium-3 sensitive high-affinity choline transport activity. Confocal microscopy reveals that CHT1-HA is found predominantly in intracellular organelles in three different cell lines. Importantly, CHT1-HA seems to be continuously cycling between the plasma membrane and endocytic organelles via a constitutive clathrin-mediated endocytic pathway. In a neuronal cell line, CHT1-HA colocalizes with the early endocytic marker green fluorescent protein (GFP)-Rab 5 and with two markers of synaptic-like vesicles, VAMP-myc and GFP-VAChT, suggesting that in cultured cells CHT1 is present mainly in organelles of endocytic origin. Subcellular fractionation and immunoisolation of organelles from rat brain indicate that CHT1 is present in synaptic vesicles. We propose that intracellular CHT1 can be recruited during stimulation to increase choline uptake in nerve terminals.
Animals↗
[Ultrasound diagnosis of Meckel diverticulitis in adults].
Meckel's diverticulitis is a rare disease. In addition to physical examination, abdominal ultrasound can help to pinpoint the diagnosis. By presenting a case report we would like to demonstrate the typical ultrasonographic findings in acute Meckel's diverticulitis and differentiate it from acute appendicitis. A 60-year-old patient was admitted to our hospital with the diagnosis of acute appendicitis. Abdominal ultrasound was performed and a blind ending, liquid-filled segment of small bowel in the right lower quadrant of the abdomen found. This segment was not compressible, no peristalsis was evident, nor was there any anatomical association with the cecum. Locally we found free fluid and hints of inflamed mesenteric fatty tissue. A perforated Meckel's diverticulum was diagnosed and confirmed intraoperatively. The major ultrasonographic difference between an inflamed Meckel's diverticulum and acute appendicitis is its anatomical location. In contrast to the appendix there is no association with the cecum. A diameter of up to 40 mm and a well-defined wall of small bowel with 3 definite layers visible by ultrasound may help to distinguish between a Meckel's diverticulum and the appendix.
Acute Disease↗
Denervation of the wrist.
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Journal Article↗
The MAPK kinase kinase TAK1 plays a central role in coupling the interleukin-1 receptor to both transcriptional and RNA-targeted mechanisms of gene regulation.
Mechanisms of fulminant gene induction during an inflammatory response were investigated using expression of the chemoattractant cytokine interleukin-8 (IL-8) as a model. Recently we found that coordinate activation of NF-kappaB and c-Jun N-terminal protein kinase (JNK) is required for strong IL-8 transcription, whereas the p38 MAP kinase (MAPK) pathway stabilizes the IL-8 mRNA. It is unclear how these pathways are coupled to the receptor for IL-1, an important physiological inducer of IL-8. Expression of the MAP kinase kinase kinase (MAPKKK) TAK1 together with its coactivator TAB1 in HeLa cells activated all three pathways and was sufficient to induce IL-8 formation, NF-kappaB + JNK2-mediated transcription from a minimal IL-8 promoter, and p38 MAPK-mediated stabilization of a reporter mRNA containing IL-8-derived regulatory mRNA sequences. Expression of a kinase-inactive mutant of TAK1 largely blocked IL-1-induced transcription and mRNA stabilization, as well as formation of endogenous IL-8. Truncated TAB1, lacking the TAK1 binding domain, or a TAK1-derived peptide containing a TAK1 autoinhibitory domain were also efficient in inhibition. These data indicate that the previously described three-pathway model of IL-8 induction is operative in response to a physiological stimulus, IL-1, and that the MAPKKK TAK1 couples the IL-1 receptor to both transcriptional and RNA-targeted mechanisms mediated by the three pathways.
Adaptor Proteins, Signal Transducing↗
The p38 MAP kinase pathway signals for cytokine-induced mRNA stabilization via MAP kinase-activated protein kinase 2 and an AU-rich region-targeted mechanism.
Stabilization of mRNAs contributes to the strong and rapid induction of genes in the inflammatory response. The signaling mechanisms involved were investigated using a tetracycline-controlled expression system to determine the half-lives of interleukin (IL)-6 and IL-8 mRNAs. Transcript stability was low in untreated HeLa cells, but increased in cells expressing a constitutively active form of the MAP kinase kinase kinase MEKK1. Destabilization and signal-induced stabilization was transferred to the stable beta-globin mRNA by a 161-nucleotide fragment of IL-8 mRNA which contains an AU-rich region, as well as by defined AU-rich elements (AREs) of the c-fos and GM-CSF mRNAs. Of the different MEKK1-activated signaling pathways, no significant effects on mRNA degradation were observed for the SAPK/JNK, extracellular regulated kinase and NF-kappaB pathways. Selective activation of the p38 MAP kinase (=SAPK2) pathway by MAP kinase kinase 6 induced mRNA stabilization. A dominant-negative mutant of p38 MAP kinase interfered with MEKK1 and also IL-1-induced stabilization. Furthermore, an active form of the p38 MAP kinase-activated protein kinase (MAPKAP K2 or MK2) induced mRNA stabilization, whereas a negative interfering MK2 mutant interfered with MAP kinase kinase 6-induced stabilization. These findings indicate that the p38 MAP kinase pathway contributes to cytokine/stress-induced gene expression by stabilizing mRNAs through an MK2-dependent, ARE-targeted mechanism.
3' Untranslated Regions↗
Effects of the endogeneous cannabinoid, anandamide, on neuronal activity in rat hippocampal slices.
1. The arachidonic acid derivative arachidonylethanolamide (anandamide) is an endogeneous ligand of cannabinoid receptors that induces pharmacological actions similar to those of cannabinoids such as delta9-tetrahydrocannabinol (THC). We examined whether anandamide can influence excessive neuronal activity by investigating stimulation-induced population spikes and epileptiform activity in rat hippocampal slices. For this purpose, the effects of anandamide were compared with those of the synthetic cannabinoid agonist WIN 55,212-2 and its inactive S(-)-enantiomer WIN 55,212-3. 2. Both anandamide (1 and 10 microM) and WIN 55,212-2 (0.1 and 1 microM) decreased the amplitude of the postsynaptic population spike and the slope of the field excitatory postsynaptic potential (field e.p.s.p.) without affecting the presynaptic fibre spike of the afferents. At a concentration of 1 microM, WIN 55,212-2 completely suppressed the postsynaptic spike, whereas the S(-)-enantiomer WIN 55,212-3 produced only a slight depression. The CB1 receptor antagonist SR 141716 blocked the inhibition evoked by the cannabinoids. SR 141716 had a slight facilitatory effect on neuronal excitability by itself. 3. Anandamide shifted the input-output curve of the postsynaptic spike and the field e.p.s.p. to the right and increased the magnitude of paired-pulse facilitation indicating a presynaptic mechanism of action. 4. Anandamide and WIN 55,212-2, but not WIN 55,212-3, attenuated both stimulus-triggered epileptiform activity in CA1 elicited by omission of Mg2+ and spontaneously occurring epileptiform activity in CA3 elicited by omission of Mg2+ and elevation of K+ to 8 mM. The antiepileptiform effect of these cannabinoids was blocked by SR 141716. 5. In conclusion, cannabinoid receptors of the CB1 type as well as their endogeneous ligand, anandamide, are involved in the control of neuronal excitability, thus reducing excitatory neurotransmission at a presynaptic site, a mechanism which might be involved in the prevention of excessive excitability leading to epileptiform activity.
Animals↗
[Scaphoid pseudarthrosis of the proximal third--results of treatment with the Herbert screw].
Purpose of this study was to assess the value of the Herbert screw used with iliac crest cancellous bone graft for treatment of scaphoid nonunion in the proximal third. From 1986 to 1996, 75 patients underwent this procedure. We followed-up on 67 of them using the Martini score, which covers pain, grip strength and social activities, range of motion, X-ray results, individual, clinical and overall assessment. We found 57 patients (85.1%) with a good to excellent outcome, eight patients (11.9%) with satisfactory results and two patients with a poor result. We conclude that the Herbert screw with or without cancellous bone graft should be the first choice for surgical treatment of non-union located in the proximal third of the scaphoid bone.
Adult↗
[Treatment of therapy refractory epicondylitis lateralis humeri by denervation. On the pathogenesis].
PURPOSE: The pathogenesis of tennis elbow is still debated, the question of proper surgical treatment as well. Because the area of pain in tennis elbow and the concomitant spots of pain together with sensibility disorders of the hand are supplied entirely by branches of the radial nerve, we suggested a surgical procedure for complete denervation as early as 1962. The main purpose of this paper is to examine the possibilities of improving the surgical technique, thereby shedding light on the pathogenesis of tennis elbow. METHOD AND MATERIAL: Between 1970 and 1994, altogether 166 patients with 172 cases of resistant tennis elbow were treated by denervation. This procedure calls for careful exposure and the severing of only one tiny branch of the radial nerve. Denervation is otherwise accomplished by "blind" dissection by desinsertion of certain muscles, which are reinserted after denervation, however, with exception of the supinator muscle. Until 1990, the original procedure was performed 39 times (Group A). Afterwards, denervation involved only isolated desinsertion of the supinator muscle in 46 cases (Group B) without the temporary incision of the ECRB-origin, as performed previously. In a further series of 87 cases, an evaluation of denervation in combination with a direct decompression of the deep branch of the radial nerve was performed by resection of the supinator arcade (Group C). Postoperative results were evaluated and scored according to Roles and Maudsley (1972). RESULTS: The denervations of Group A were controlled after an average follow-up time of 9.7 years in 36 cases (92.3%), in 91.6% they demonstrated good and excellent results. In Group B, 42 patients (91.3%) were followed-up after an average time of 4.9 years; these cases showed about the same results as in Group A (90.5% good and excellent). The time off work was 2.7 and 5.7 weeks respectively. The results of denervation, however, were not improved by additional direct decompression of the posterior interosseous nerve (Group C); in a follow-up rate of 86% after 3.6 years only 65.3% showed good and excellent results together with an extremely long time off work of up to 11.7 weeks. CONCLUSION: The results in Group A and B prove that the temporary desinsertion of the ECRB, previously regarded as necessary for reasons of dissection, can be discontinued, without worsening of outcome, as long as the anterior and lateral portions of the supinator origin are incised directly, thereby resulting in indirect decompression of the posterior interosseous nerve simultaneously. The results of this procedure emphasize the fact that tennis elbow is the result of a compression syndrome of the radial nerve and its branches, where the pain-triggering nerve irritations are found at one or several localizations that can be treated successfully--as shown in the literature and by our own findings--by direct decompression of this nerve segment.
Adult↗
Alpha-lipoic acid reduces expression of vascular cell adhesion molecule-1 and endothelial adhesion of human monocytes after stimulation with advanced glycation end products.
Advanced glycation end products (AGEs) have been identified as relevant mediators of late diabetic complications such as atherosclerotic disease. The endothelial migration of monocytes is one of the first steps in atherogenesis and monocyte-endothelial interaction itself is linked to the expression of adhesion molecules like vascular cell adhesion molecule-1 (VCAM-1). Recently, stimulation of VCAM-1 by AGEs has been demonstrated. Since endothelial stimulation by AGEs is followed by generation of oxygen free radicals with subsequent activation of nuclear transcription factor kappaB, we investigated the influence of alpha-lipoic acid on the expression of VCAM-1 and monocyte adherence to endothelial cells in vitro by means of cell-associated chemiluminescence assays and quantitative reverse transcriptase polymerase chain reaction using a constructed recombinant RNA standard. We found that alpha-lipoic acid was able to decrease the number of VCAM-1 transcripts from 41. 0+/-11.2 to 9.5+/-4.7 RNA copies per cell in AGE-stimulated cell cultures. Furthermore, expression of VCAM-1 was suppressed in a time- and dose-dependent manner by alpha-lipoic acid as shown by chemiluminescence endothelial cell assay. Pretreatment of endothelial cells with 0.5 mM or 5 mM alpha-lipoic acid reduced AGE-induced endothelial binding of monocytes from 22.5+/-2.9% to 18. 3+/-1.9% and 13.8+/-1.8% respectively. Thus, we suggest that extracellularly administered alpha-lipoic acid reduces AGE-albumin-induced endothelial expression of VCAM-1 and monocyte binding to endothelium in vitro. These in vitro results may contribute to the understanding of a potential antioxidative treatment of atherosclerosis.
Antioxidants↗
Establishment of a quantitative RT-pCR for detection of vascular cell adhesion molecule-1 transcripts in endothelial cells after stimulation with advanced glycation endproducts.
Advanced glycation endproducts (AGE) are supposed to increase endothelial expression of adhesion molecules like vascular cell adhesion molecule-1 (VCAM-1) by inducing an intracellular stress with subsequent activation of nuclear transcription factor NF-kappa-B. Quantitative analysis of VCAM-1-transcription has not been demonstrated concerning this topic. Thus, the aim of this study was to establish quantitative reverse transcription polymerase chain reaction (RT-PCR) assays using a spacer gene in order to measure the amounts of specific mRNA for VCAM-1 in human umbilical vein endothelial cells (HUVEC) which were stimulated with AGE-albumin (AGE-BSA). A recombinant RNA-standard was synthesized and used as internal RT-PCR standard. The amount of VCAM-1-mRNA in unstimulated HUVEC was found to be 2.2 +/- 2.7 copies per cell. After stimulation with AGE-BSA, mRNA-levels were elevated to 38.9 +/- 10.9 copies per cell. Positive controls (stimulated with lipopolysaccharide) revealed mRNA-levels of 78.7 +/- 27.5 copies per cell. We conclude that quantitative RT-PCR using the spacer gene technique is a valid and reliable method for the measurement of small amounts of specific
Cells, Cultured↗
[Rare cause of acute pancreatitis: phytobezoar in an intraluminal diverticulum in type I duodenal atresia, intestinal malrotation and rudimentary pancreas anulare].
A 28-year-old woman was hospitalized because of the third episode of acute pancreatitis. No hint for an extrinsic cause was evident. Under conservative treatment pancreatitis and signs of intestinal obstruction were persisting. Imaging procedures showed an undefinite mass in the neighbourhood of the pancreatic caput. Endoscopy revealed a phytobezoar in a wind sock web, a special form of congenital duodenal atresia. Obstructing the papilla of Vater the bezoar had caused acute pancreatitis. After endoscopical removal the symptoms of pancreatitis disappeared immediately. Web excision and duodenoduodenostomy were performed. At operation further anomalies of the gastrointestinal tract frequently associated with duodenenal atresia were found.
Acute Disease↗
[Nerve compression in the lateral neck triangle].
Among the compression neuropathies associated with the lateral cervical neck region the thoracic outlet syndrome has received special attention during the last decades. In resistant cases, the transaxillary decompression of the neurovascular bundle according to Roos proved to be very successful for us. Since 1982, a total of 185 procedures of this kind were performed with the following results: excellent and good 76%, fair 16%, and not successful 8%.--As the symptoms of Sudeck's dystrophy resemble the clinical findings of a severe thoracic outlet and inlet syndrome, a transaxillary decompression together with sympathectomy was performed in nine resistant dystrophies as well. Thus, in seven patients an excellent result was obtained, and a good and a fair result in one case each. According to our findings, the individual predisposition for Sudeck's dystrophy is based on an impairment of the venous run-off due to a stenosis of the subclavian vein with simultaneous increase of sympathetic activity.
Adult↗
Syndesmotic screw placement: a biomechanical analysis.
At the present time, syndesmotic screw fixation is recommended when there is a tibiofibular diastasis, a Maisonneuve fracture, or syndesmotic instability after fixation of distal tibia-fibula fractures. The aim/purpose of this study was to demonstrate the optimal level of syndesmotic screw placement before creation of a Maisonneuve fracture. Legs of 17 embalmed cadavers underwent knee disarticulation. The legs were then dissected to expose the syndesmosis/interosseous membrane. The paired cadaver legs were tested in two groups. In group I (10 pairs), the left legs were tested without any syndesmotic fixation and the right legs were tested with the syndesmosis fixed at 2.0 cm above the tibiotalar joint. In group II (7 pairs), the syndesmosis in each left leg was fixed at 3.5 cm above the tibiotalar joint and the right leg syndesmosis was fixed at 2.0 cm above the tibiotalar joint. After ligament section and syndesmosis fixation, each leg was then jig mounted with transfixing wires through the proximal tibia and calcaneus. The ankle was placed in neutral with 15 degrees of pronation and a load of 150 pounds and a strain gauge anchored medially and laterally. The proximal tibia was internally rotated while the ankle was held fixed until syndesmotic, bony, or hardware failure occurred. Torsional force, the degree of rotation and the amount of syndesmotic widening were quantitated. Two-tailed t-test comparing no fixation with fixation at 2.0 cm indicated less syndesmotic widening with screw placed at 2.0 cm (P = 0.04). Two-tailed t-test comparing screw fixation at 2.0 cm and 3.5 cm indicated less syndesmotic widening with screw placed at 2.0 cm (P = 0.07). It would seem reasonable to place a syndesmotic screw at 2.0 cm above tibiotalar joint.
Ankle Injuries↗
[Surgical treatment of therapy refractory Sudeck's dystrophy by transaxillary decompression of the neurovascular bundle and sympathectomy. On the pathogenesis of Sudeck's disease].
Since 1984, altogether nine cases of otherwise untreatable reflex sympathetic dystrophy (RSD) of the upper extremity were treated by transaxillary decompression of the neurovascular bundle with resection of the upper thoracic ganglia. This resulted in an immediate improvement of the local findings and the entire post-operative course of treatment as well as significantly improved functional results (seven excellent, one good, one fair). Average follow-up was 7.5 years. All patients returned to their original work. Clinical as well as intraoperative studies show that the acute edema of RSD is caused by a stenosis of the subclavian vein, which was proven in all cases by preoperative phlebography. Surgical decompression of the subclavian vein thus can result in an essential improvement of venous backflow and also significant improvement of the lesion-caused misproportion between increased arterial inflow and venous outflow with all resulting consequences for peripheral edema, subfascial pressure, microcirculation, perfusion of tissue and metabolism. By decompression of the subclavian artery and the lower plexus roots as well as by simultaneous transaxillary sympathectomy, the sympathetic efferents are drastically reduced or rather interrupted, leading to immediate improvement of the acute pain-syndrome. The so-called "individual predisposition" for RSD can mainly be attributed to a venous stenosis in the area of the subclavian vein and to an increase in sympathetic tonus by irritation of the lower parts of the brachial plexus and the postganglionic fibres accompanying the subclavian artery. The consequences for the pathogenesis of RSD are discussed in detail.
Adult↗