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Biomedical subjects

V Stein

Publications and source records attributed to V Stein.

At least 19 recordsLinked to original sources
PubMed2003

[Mechanisms and prevention of windsurfing injuries].

Aim of this study was to analyse the mechanisms of windsurfing injuries. For this purpose we performed a internet based survey among 327 windsurfers in Germany. Overall 630 accidents have been registered among all 327 athletes during the 2000 season. The majority of injuries were classified as minor injury. The most common injury was the bruise. 70 participants reported fractures, 26 participants ruptured a ligament. 280 injuries required medical treatment; in 67 cases even surgical treatment was necessary. The majority of accidents happened at wind power of 5-6 Beaufort after 2 hour exercise. A technical mistake was the most frequent cause for the accident. The most dangerous manoeuvres were difficult jumps (e. g. front loop, backward loop, 70 injuries). In 46 cases the weather conditions were underestimated. Only 10 windsurfers reported about broken material as cause for the injury. One half of the injuries happened in wave conditions. The analysis of injury mechanisms allows conclusions regarding injury prevention. A longer break after 60 minutes windsurfing might help to prevent injuries due to poor physical fitness. After one hour windsurfing without a break training of difficult manoeuvres should not be performed. The use of a helmet might prevent head injuries during training of difficult jumps. "Overpower situations" should be prevented by choosing the right board and sail size.

Adult↗
PubMed2002

The blood supply of the posterior tibial tendon.

We studied the vascular pattern of human posterior tibial tendons by injection techniques and immunohistochemically using antibodies against laminin. The intravascular volume of the posterior tibial tendon was determined using a new method of injection of a solution of 99mTc and gelatin ink into the lower legs of cadavers. Three segments of 1 cm length from different regions of the human posterior tibial tendon were measured using a gamma well counter. The main blood supply arises from the posterior tibial artery. Blood vessels enter the paratenon of the posterior tibial tendon via a mesotenon from the posterior aspect. From the paratenon, the blood vessels penetrate the posterior tibial tendon and anastomose with a longitudinally orientated intratendinous network. The number of vessels in the substance of the tendon is consistently less than that in the surrounding paratenon. The distribution of blood vessels within the posterior tibial tendon is not homogeneous. In the retromalleolar region the intravascular volume was significantly reduced with a mean value of 15 microl/g of tendon tissue. There was no significant difference between the mean intravascular volumes of the proximal and distal areas (distal, 27.7 microl/g tendon tissue; proximal, 30 microl/g tendon tissue). The immunohistochemical investigation showed that there was no immunostaining for laminin in the anterior part of the tendon in the region where it passes behind the medial malleolus. This region is avascular. The most frequent site of rupture of the posterior tibial tendon is in the region behind the medial malleolus. A potential endogenous risk factor may be the limited healing potential of avascular tissue.

Aged↗
PubMed2001

Barttin is a Cl- channel beta-subunit crucial for renal Cl- reabsorption and inner ear K+ secretion.

Renal salt loss in Bartter's syndrome is caused by impaired transepithelial transport in the loop of Henle. Sodium chloride is taken up apically by the combined activity of NKCC2 (Na+-K--2Cl- cotransporters) and ROMK potassium channels. Chloride ions exit from the cell through basolateral ClC-Kb chloride channels. Mutations in the three corresponding genes have been identified that correspond to Bartter's syndrome types 1-3. The gene encoding the integral membrane protein barttin is mutated in a form of Bartter's syndrome that is associated with congenital deafness and renal failure. Here we show that barttin acts as an essential beta-subunit for ClC-Ka and ClC-Kb chloride channels, with which it colocalizes in basolateral membranes of renal tubules and of potassium-secreting epithelia of the inner ear. Disease-causing mutations in either ClC-Kb or barttin compromise currents through heteromeric channels. Currents can be stimulated further by mutating a proline-tyrosine (PY) motif on barttin. This work describes the first known beta-subunit for CLC chloride channels and reveals that heteromers formed by ClC-K and barttin are crucial for renal salt reabsorption and potassium recycling in the inner ear.

Absorption↗
PubMed2001

Male germ cells and photoreceptors, both dependent on close cell-cell interactions, degenerate upon ClC-2 Cl(-) channel disruption.

The functions of some CLC Cl(-) channels are evident from human diseases that result from their mutations, but the role of the broadly expressed ClC-2 Cl(-) channel is less clear. Several important functions have been attributed to ClC-2, but contrary to these expectations ClC-2-deficient mice lacked overt abnormalities except for a severe degeneration of the retina and the testes, which led to selective male infertility. Seminiferous tubules did not develop lumina and germ cells failed to complete meiosis. Beginning around puberty there was a massive death of primary spermatocytes and later also of spermatogonia. Tubules were filled with abnormal Sertoli cells, which normally express ClC-2 in patches adjacent to germ cells. In the retina, photoreceptors lacked normal outer segments and degenerated between days P10 and P30. The current across the retinal pigment epithelium was severely reduced at P36. Thus, ClC-2 disruption entails the death of two cell types which depend on supporting cells that form the blood-testes and blood-retina barriers. We propose that ClC-2 is crucial for controlling the ionic environment of these cells.

Animals↗
PubMed2001

Disruption of KCC2 reveals an essential role of K-Cl cotransport already in early synaptic inhibition.

Synaptic inhibition by GABA(A) and glycine receptors, which are ligand-gated anion channels, depends on the electrochemical potential for chloride. Several potassium-chloride cotransporters can lower the intracellular chloride concentration [Cl(-)](i), including the neuronal isoform KCC2. We show that KCC2 knockout mice died immediately after birth due to severe motor deficits that also abolished respiration. Sciatic nerve recordings revealed abnormal spontaneous electrical activity and altered spinal cord responses to peripheral electrical stimuli. In the spinal cord of wild-type animals, the KCC2 protein was found at inhibitory synapses. Patch-clamp measurements of embryonic day 18.5 spinal cord motoneurons demonstrated an excitatory GABA and glycine action in the absence, but not in the presence, of KCC2, revealing a crucial role of KCC2 for synaptic inhibition.

Action Potentials↗
PubMed2001

Mutations in CAV3 cause mechanical hyperirritability of skeletal muscle in rippling muscle disease.

Hereditary rippling muscle disease (RMD) is an autosomal dominant human disorder characterized by mechanically triggered contractions of skeletal muscle. Genome-wide linkage analysis has identified an RMD locus on chromosome 3p25. We found missense mutations in positional candidate CAV3 (encoding caveolin 3; ref. 5) in all five families analyzed. Mutations in CAV3 have also been described in limb-girdle muscular dystrophy type 1C (LGMD1C; refs. 6,7), demonstrating the allelism of dystrophic and non-dystrophic muscle diseases.

Caveolin 3↗
PubMed2000

Structure of the human tibialis anterior tendon.

The structure and vascular pattern of the human tibialis anterior tendon was investigated using injection techniques, light and transmission electron microscopy and immunohistochemistry. From the well vascularised peritenon, blood vessels penetrate the tendon tissue and anastomose with a longitudinally oriented intratendinous network. The distribution of blood vessels within the tibialis anterior tendon was not homogenous. The posterior part of the tendon had a complete vascular network that extends from the musculotendinous junction to the insertion at the first metatarsal and medial cuneiform bones. In the anterior half, the tissue was avascular in a zone with a length of 45-67 mm. This zone was covered by a single layer (approximately 30 microm) of oval shaped cells. Transmission electron microscopy showed that these cells have the characteristics of chondroid cells. This region was stained by Alcian blue at pH 1 which indicates a high concentration of acid glycosaminoglycans and immunohistochemical staining for chondroitin-4-sulphate, chondroitin-6-sulphate and aggrecan was positive. However, immunostaining for the typical cartilage specific type II collagen within this zone was negative. The location of the avascular zone corresponds to the region where the tibialis anterior tendon wraps around the superior and inferior retinacula which serve as fibrous pulleys. This is the region where most spontaneous ruptures of the tibialis anterior tendon occur. The presence of fibrocartilage within gliding tendons is a functional adaptation to compressive and shearing forces. In contrast to reports from the literature about the structure of gliding tendons wrapping around a bony pulley, the gliding zone of the tibialis anterior tendon has only a narrow layer of chondroid cells and proof of type II collagen is lacking.

Adult↗
PubMed2000

Blood supply of the peroneal tendons: injection and immunohistochemical studies of cadaver tendons.

We studied the vascular pattern of human peroneal tendons with injection techniques and immunohistochemically by using antibodies against laminin The main blood supply arises from the peroneal artery. The distal part of the peroneus longus tendon is supplied by branches of the medial tarsal artery. Blood vessels enter the peritenon of both tendons via a mesotenon from the posterior aspect. From the peritenon, the blood vessels penetrate the peroneus brevis and peroneus longus tendons and anastomose with a longitudinally-oriented intratendinous network. The amount of vessels in the tendon substance is consistently less than in the surrounding peritenon. The distribution of blood vessels in the peroneal tendons is not homogeneous. In the region where the peroneus brevis tendon passes through the fibular groove, the longitudinally-oriented intratendinous vascular network is interrupted and the tendon is almost avascular. In this region, the tendon is squeezed between the peroneus longus tendon and the bony slide bearing of the lateral malleolus. The peroneus longus tendon has two avascular zones. In the region where the peroneus longus tendon curves around the lateral malleolus and the peroneal trochlea of the calcaneus, the anterior part of the tendon which is directed towards the pulley is avascular. A second avascular zone is located more distally in the region where the tendon changes direction and wraps around the cuboid.

Adult↗
PubMed2000

Quantitative assessment of intravascular volume of the human Achilles tendon.

The pathogenesis of Achilles tendon rupture remains unclear, but vascular patterns may play an important role. We determined the intravascular volume of the Achilles tendon using a new method with injection of radioisotopes. A solution of Tc-99m and gelatin-ink was injected into the lower limbs of body donors. The intravascular volume of each 1 cm section of the Achilles tendon was measured using a gamma well counter. We found that the distal part of the Achilles tendon (0-2 cm above the calcaneus) had an intravascular volume of 59-98 microL/g tendon tissue. In the middle part of the tendon (3-6 cm above the calcaneal insertion), the intravascular volume was much less: 2743 microL/g tissue. The proximal part of the tendon (7-9 cm) had an intravascular volume between 51-100 microL/g tendon tissue. The reduced vascularization in the middle part of the human Achilles tendon may play a role in degeneration and spontaneous rupture of the tendon.

Achilles Tendon↗
PubMed1999

Chloride dependence of hyperpolarization-activated chloride channel gates.

1. ClC proteins are a class of voltage-dependent Cl- channels with several members mutated in human diseases. The prototype ClC-0 Torpedo channel is a dimeric protein; each subunit forms a pore that can gate independently from the other one. A common slower gating mechanism acts on both pores simultaneously; slow gating activates ClC-0 at hyperpolarized voltages. The ClC-2 Cl- channel is also activated by hyperpolarization, as are some ClC-1 mutants (e.g. D136G) and wild-type (WT) ClC-1 at certain pH values. 2. We studied the dependence on internal Cl- ([Cl-]i) of the hyperpolarization-activated gates of several ClC channels (WT ClC-0, ClC-0 mutant P522G, ClC-1 mutant D136G and an N-terminal deletion mutant of ClC-2), by patch clamping channels expressed in Xenopus oocytes. 3. With all these channels, reducing [Cl-]i shifted activation to more negative voltages and reduced the maximal activation at most negative voltages. 4. We also investigated the external halide dependence of WT ClC-2 using two-electrode voltage-clamp recording. Reducing external Cl- ([Cl-]o) activated ClC-2 currents. Replacing [Cl-]o by the less permeant Br- reduced channel activity and accelerated deactivation. 5. Gating of the ClC-2 mutant K566Q in normal [Cl-]o resembled that of WT ClC-2 in low [Cl-]o, i.e. channels had a considerable open probability (Po) at resting membrane potential. Substituting external Cl- by Br- or I- led to a decrease in Po. 6. The [Cl-]i dependence of the hyperpolarization-activated gates of various ClC channels suggests a similar gating mechanism, and raises the possibility that the gating charge for the hyperpolarization-activated gate is provided by Cl-. 7. The external halide dependence of hyperpolarization-activated gating of ClC-2 suggests that it is mediated or modulated by anions as in other ClC channels. In contrast to the depolarization-activated fast gates of ClC-0 and ClC-1, the absence of Cl- favours channel opening. Lysine 556 may be important for the relevant binding site.

Animals↗
PubMed1999

[Blood supply of the quadriceps tendon].

Degenerative changes have been considered to be a cause for spontaneous quadriceps tendon rupture. Aim of this study is to investigate the microvasculature of the quadriceps tendon by injection techniques and immunohistochemical methods (antibodies against laminin) with regard to the pathogenesis of tendon degeneration. The blood supply of the quadriceps tendon arises from descending branches of the lateral circumflex femoral artery, by branches of the descending geniculate artery and by branches of the medial and lateral superior geniculate arteries. Blood vessels penetrate the tendon from the surrounding connective tissue and anastomose with a longitudinally orientated intraligamentous network. Compared to the surrounding synovial layer, the amount of vessels in the tendon substance is greatly reduced. The distribution of blood vessels within the quadriceps tendon is not homogenous. The anterior or superficial part of the tendon has a complete vascular network that extends from the musculo-tendinous junction to the patella. Within the deep portion of the quadriceps tendon there is an oval shaped avascular area which measures app. 30 mm in length and app. 15 mm in width. Within this area the immunohistochemical proof of laminin is negative. An explanation for the absence of blood vessels may be compressive stress caused by the patellar groove which serves as hypomochlion for the quadriceps tendon when the knee is flexed. The occurrence of an avascular zone within the deep layer of the tendon that is directed to the joint cavity may explain the frequency of degenerative changes in this region.

Adult↗
PubMed1999

[Bilateral spontaneous rupture of the quadriceps tendon in a patient with Wilson disease. A case report].

A 58-year old man with Wilson's disease sustained a bilateral spontaneous rupture of the quadriceps tendon. The histological investigation showed advanced degeneration of tendon structure and copper deposits. After tenosuture the patient had complete cure with full range of movement. We discuss about relation of Wilson's disease, copper deposits and degenerative changes of tendon tissue.

Calcium↗
PubMed1999

Blood supply of the tibialis anterior tendon.

Injection techniques and immunohistochemical methods (antibodies against laminin) were performed to uncover the vascular pattern of the human tibialis anterior tendon with regard to spontaneous rupture of this tendon. Proximally, the blood supply of the tibialis anterior tendon mainly arises from the anterior tibial artery. Distally, the tendon is supplied by branches of the medial tarsal artery. Blood vessels enter the peritenon via vinculae from the posterior side. From the peritenon, the blood vessels penetrate the tendon and anastomose with a longitudinally orientated intratendinous network. Compared with the surrounding peritenon, the number of vessels in the tendon substance is greatly reduced. The distribution of blood vessels within the anterior tibial tendon is not homogenous. The posterior part of the tendon has a complete vascular network that extends from the musculotendinous junction to the insertion at the bone. In the anterior half of the tendon, there is an avascular zone between 45 and 67 mm in length. The location of the avascular zone correlates well with the location of the most frequent site of spontaneous rupture of the tibialis anterior tendon reported in the literature. Hypovascularity has to be considered as an etiological cofactor for spontaneous rupture of the tibialis anterior tendon.

Aged↗
PubMed1998

Moderate loss of function of cyclic-AMP-modulated KCNQ2/KCNQ3 K+ channels causes epilepsy.

Epilepsy affects more than 0.5% of the world's population and has a large genetic component. It is due to an electrical hyperexcitability in the central nervous system. Potassium channels are important regulators of electrical signalling, and benign familial neonatal convulsions (BFNC), an autosomal dominant epilepsy of infancy, is caused by mutations in the KCNQ2 or the KCNQ3 potassium channel genes. Here we show that KCNQ2 and KCNQ3 are distributed broadly in brain with expression patterns that largely overlap. Expression in Xenopus oocytes indicates the formation of heteromeric KCNQ2/KCNQ3 potassium channels with currents that are at least tenfold larger than those of the respective homomeric channels. KCNQ2/KCNQ3 currents can be increased by intracellular cyclic AMP, an effect that depends on an intact phosphorylation site in the KCNQ2 amino terminus. KCNQ2 and KCNQ3 mutations identified in BFNC pedigrees compromised the function of the respective subunits, but exerted no dominant-negative effect on KCNQ2/KCNQ3 heteromeric channels. We predict that a 25% loss of heteromeric KCNQ2/KCNQ3-channel function is sufficient to cause the electrical hyperexcitability in BFNC. Drugs raising intracellular cAMP may prove beneficial in this form of epilepsy.

Amino Acid Sequence↗
PubMed1989

NERVTRACK--a neuroanatomical data bank.

To provide the neurologist with a detailed and easily accessible neuroanatomical reference, we have developed a data bank including all relevant efferent and many afferent neuroanatomical pathways. NERVTRACK contains 4000 anatomical data items arranged in a tree-like manner reflecting structural and functional relationships. The program is able to address problems like the following: (1) What is the spinal, radicular, and peripheral innervation of a given muscle? (2) Which muscles are affected by a lesion of a given peripheral nerve, a root, or a segment of the spinal cord? (3) For a given muscle, what are synergists and antagonists, and which clinical test is applicable to evaluate its strength? NERVTRACK runs on IBM-compatible microcomputers, even on lap tops. It is a fast and comfortable reference for clinical practice and serves as a readily accessible teaching aid.

Expert Systems↗
PubMed1989

Thermally induced formation of polychlorinated dibenzofurans from Aroclor 1254-contaminated mineral oil.

Numerous laboratory simulations and real-world events have demonstrated the thermal conversion of neat or high concentration of PCBs into the much more toxic PCDFs. Since millions of mineral oil transformers currently in service contain PCB concentrations in the 50 to 5000 ppm range, the thermal behavior of dilute PCB solutions is of practical and regulatory significance. In this work, neat Aroclor 1254 and 5000 ppm Aroclor 1254 in mineral oil were subjected to pyrolysis and combustion under a range of experimental conditions to define parameters resulting in maximal PCDF yields. The dependence of PCDF yield on Aroclor 1254 concentrations was then investigated in the 5000 to 50 ppm range. Combustion experiments demonstrated that PCDF yields expressed as micrograms PCDF/gram PCB were independent of concentration range, confirming that the process is kinetically first order in PCB. Much lower yields of PCDF were observed in the open tube pyrolysis experiments, as compared to combustion experiments and to earlier and concurrent sealed tube experiments. Slightly improved yields were observed in the pyrolysis experiments at lower concentrations, suggesting the existence of a PCB or PCDF destruction process of higher than first order kinetics. In all cases, yields expressed as micrograms PCDF/gram mixture were sharply and monotonically lower as concentrations decreased between neat or 5000 ppm Aroclor 1254 and 50 ppm Aroclor 1254.

Aroclors↗