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Biomedical subjects

H Schmalbruch

Publications and source records attributed to H Schmalbruch.

At least 73 records · Page 4Linked to original sources
PubMed1987

Loss of sensory neurons after sciatic nerve section in the rat.

In this study, the loss of sensory neurons in the rat was assessed after sciatic nerve section at birth and at 4 weeks of age. The neuronal deficit in ganglia L4-L6, 39-89 weeks after neonatal denervation, was 10,000-17,000. The nerve contains about 19,000 afferent axons, so some axotomized neurons survived. Degenerating perikarya were absent, probably because all surviving neurons had reestablished target contacts. Sectioning the nerve at age 4 weeks, in five rats, after 19-92 weeks had caused the death of 7,000-11,500 neurons. Whether the nerve regenerated or not in these rats apparently did not influence the extent of neuron death. Nevertheless, no deficit was observed in a sixth rat in which muscle reinnervation was very good. Therefore, the results are inconclusive with respect to the effect of axonal regeneration. Ganglia of rats operated at age 4 weeks regularly contained perikarya with axonal reaction; this supports the notion that some mature neurons are able to permanently survive without target contact. There was no evidence for selective loss of large or small neurons after nerve section at birth or at age 4 weeks. The extent of cell loss in individual ganglia varied, indicating varying contributions of the three ganglia to the nerve. Hence, it is not possible to quantify the effect of experimental conditions on the number of sensory neurons when only one of the several ganglia contributing to the nerve is investigated.

Animals↗
PubMed1987

Benign congenital muscular dystrophy with autosomal dominant heredity: problems of classification.

A family with autosomal dominant congenital muscular dystrophy affecting members of both sexes in three generations is described; a father and his two sons were studied. The onset of symptoms was in early childhood and progression, if any, was slow. The proximal limb muscles, the sternocleidomastoid and anterior tibial muscles were affected. One patient had torticollis and all had heel-cord shortening. An electrophysiological examination showed myopathy. There was no cardiomyopathy. Creatine kinase (CK) was elevated, and a histological study revealed a necrotizing myopathy with pronounced regeneration and formation of aberrant myofibrils (ringbinden) and fibrosis.

Adolescent↗
PubMed1987

Abnormalities in spinal neurons and dorsal root ganglion cells in Tangier disease presenting with a syringomyelia-like syndrome.

A woman with homozygous Tangier disease had progressive syringomyelia-like neuropathy. She died with cardiac failure at age 61. A sural nerve biopsy taken at age 60 had shown lipid storage in Schwann and interstitial cells, and a pronounced loss of unmyelinated fibers. The neurons of the L5 spinal ganglion and, to a lesser extent, all neurons of the sacral spinal cord, contained large lipid inclusions which in electron micrographs differed from those in Schwann and satellite cells. There was no storage material in glial cells. The neuronal inclusions were membrane-bound and consisted of electron-dense and electron-lucent components. There was evidence of neuronal death in the spinal ganglion, and a diameter histogram showed that small cytons had preferentially been lost. The inclusions probably were secondary lysosomes or residual bodies, and resembled giant lipofuscin granules. Nevertheless, they were uncolored and displayed weak autofluorescence as compared to the aging pigment in control ganglia. It is tentatively suggested that the syringomyelia-like neuropathy in Tangier disease represents a lysosomal storage disorder preferentially affecting small dorsal root ganglion cells.

Diagnosis, Differential↗
PubMed1987

Early fatal nemaline myopathy: case report and review.

A newborn girl with atonia and arthrogryposis multiplex required mechanical ventilation; she died on the 14th day. Postmortem muscle histology disclosed nemaline myopathy with a lack of myofibrils. Peripheral nerves appeared to be normal. The parents are first cousins. The findings for 13 other patients who died from nemaline myopathy within the first year of life are reviewed. It is suggested that early fatal cases, in contrast to patients with the 'benign' childhood form, are homozygotic for the disease gene, and that the myopathy results from abnormal myosin synthesis.

Biopsy↗
PubMed1986

Fiber composition of the rat sciatic nerve.

The rat sciatic nerve originates from the spinal segments L4-L6. It is unifascicular at the trochanter; 5-7 mm distally, the nerve splits into two and then into four fascicles. The tibial portion gives rise to the tibial and the sural nerves, and the peroneal portion gives rise to the peroneal nerve and a cutaneous branch that perforates the lateral hamstring muscles to innervate the proximolateral face of the calf. The number and type of the axons in these branches were determined in light and electron micrographs of normal nerves, and after de-efferentation or sympathectomy. Deafferentation was technically not feasible because spinal ganglia and ventral roots were supplied by the same vascular plexus. The tibial nerve contained 1,000 motor and 3,500 myelinated afferent axons, 3,700 sympathetic axons, and 5,400 unmyelinated afferent axons. The peroneal nerve contained 600 motor and 1,300 myelinated afferent axons, 1,100 sympathetic axons and 3,000 unmyelinated afferent axons. The sural nerve contained 1,100 myelinated and 2,800 unmyelinated afferent axons; in addition, there were 1,500 unmyelinated sympathetic axons. The cutaneous branch consisted of 400 myelinated and 1,800 unmyelinated afferent axons. Thus, the entire sciatic nerve at midthigh is composed of about 27,000 axons; 6% are myelinated motor axons, 23% and 48% are myelinated and unmyelinated sensory axons, respectively, and 23% are unmyelinated sympathetic axons. The techniques used did not demonstrate sympathetic axons in the cutaneous branch and did not reveal the few motor axons contained in the sural nerve.

Adrenergic Fibers↗
PubMed1984

The eggs of the freshwater fish Epiplatys dageti have tight plasma membranes without intramembranous particles.

The plasma membrane of fish (Epiplatys dageti) eggs, which are capable of developing in salt-free water despite intracellular osmolarity corresponding to a pressure gradient of 7 to 8 atmospheres, is almost devoid of intramembrane particles. The specific membrane resistance is at least 3 orders of magnitude larger than that of nerve or muscle cells of different species indicating that the membrane is tight. These findings support the view that intramembranous particles are involved in transmembrane transport of ions, and indicate that the ionic concentration gradient in this cell is maintained by a tight membrane rather than by active transport.

Animals↗
PubMed1984

Regenerated muscle fibers in Duchenne muscular dystrophy: a serial section study.

Muscle fibers from two boys with Duchenne muscular dystrophy and one normal boy were, for 6 mm, traced in serial sections. In normal muscle, we saw no branching or terminating fibers, and fiber diameters varied in different levels by +/- 5%. Dystrophic muscles showed signs of regeneration after segmental necrosis: multiple branchings, caliber variations, and short noninnervated fibers. In rats, muscle fibers regenerate without innervation but eventually they are replaced by fat cells. In Duchenne muscles, some regenerates lack innervation and possibly vanish as well; this may explain why regeneration finally fails.

Child↗
PubMed1981

Gap junctions on CA3 pyramidal cells of guinea pig hippocampus shown by freeze-fracture.

In freeze-fracture replicas of the hippocampus of guinea pig, gap junctions were found on membranes identified as belonging to the apical dendrites or somata of the CA3 pyramidal cells. The junctions were not part of mixed synapses. It is concluded that adjacent pyramidal cells, which in places lacked an interposed glial sheath are electrically coupled.

Animals↗
PubMed1980

The early changes in experimental myopathy induced by chloroquine and chlorphentermine.

In soleus muscles of rats treated for 2 to 11 days with high doses of chloroquine or chlorphentermine, muscle fibres showed autophagocytosis followed by segmental contracture and necrosis. Vascuolar degeneration, "splitting", and internal nuclei were absent. At variance with findings in progressive muscular dystrophy, the incidence of intramembrane particles was unchanged and membrane defects in necrotizing fibres were absent. Autophagic vacuoles were formed by cup-shaped cisternae derived from tubules that often enclosed single mitochondria. Golgi complexes occurred in the centre of the fibres; dilated vesicles of the sarcoplasmic reticulum contained an electrondense substance, possibly lysosomal enzymes. Exocytosis of autophagic vacuoles and of almost undigested mitochondria was observed. The changes in the plasma membrane were as in other cells: a bulge was formed that was cleared of intramembrane particles; the membrane fused with the limiting membrane of the autophagic vacuole, the content of which was expelled through an orifice. Inside autophagic vacuoles, persisting phospholipids arranged themselves into protein-free lipid bilayers, that formed concentric membranes or single-layered vesicles. Both drugs are known to inhibit degradation of phospholipids; the findings indicate that the rate of autophagocytosis and exocytosis were enhanced as well. Fibre necrosis was probably due to the fact that fibres eventually became unable to maintain their integrity.

Animals↗
PubMed1979

'Square arrays' in the sarcolemma of human skeletal muscle fibres.

Fast twitch fibres of rat and rabbit show rectangular patterns of intramembrane particles in freeze-fracture preparations of the sarcolemma. These 'square arrays' are almost totally absent in the slow twitch coleus muscle of rat. I report here differences in the incidence of square arrays in human fetal and adult muscle and in different fibres within a human muscle. Square arrays probably classify fast and slow twitch fibres in freeze-fracture preparations of mixed muscles.

Humans↗