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S Dekel

Publications and source records attributed to S Dekel.

At least 55 records · Page 3Linked to original sources
PubMed1988

Bilateral suprascapular nerve entrapment syndrome due to an anomalous transverse scapular ligament.

A rare case is reported of a young woman who suffered from suprascapular nerve entrapment syndrome (SNES) of the right side and two years later developed the same syndrome on the left. At the first operation an anomalous bifid transverse ligament was found and cut. The combination of pressure effect from the congenital defect together with frequent protraction of the shoulder due to her work as a physical education teacher caused triggering of the SNES. The clinical course, electromyographic findings, and differential diagnosis are reported. Cutting of the anomalous ligament on both sides brought relief from pain, weakness, and atrophy of the shoulder muscles, enabling the patient to return to work.

Adult↗
PubMed1987

Healing of rachitic lesions in chicks by 24R,25-dihydroxycholecalciferol administered locally into bone.

In an attempt to further define the nature of the active metabolite in bone formation, a series of experiments were conducted whereby vitamin D metabolites were administered locally in vivo into the proximal epiphyseal growth plate of the tibiae of rachitic chicks. Local administration of 3 micrograms of 24,25(OH)2D3 in vivo to D-deficient chicks resulted in disappearance of the rachitic lesions in the same leg. Administration of 1 microgram 1,25(OH)2D3 in a similar manner failed to show any sign of healing. Injection of 5 micrograms 25(OH)D3 was followed by recovery from rickets in both the injected right leg and in the vehicle-injected left tibia, although the recovery was more pronounced in the injected leg. Lower doses of 0.3 or 1 microgram 24,25(OH)2D3 failed to reverse the rachitic lesions and induced only minimal recovery. These findings suggest that 24,25(OH)2D3 at the higher doses has a direct local effect on cartilage and bone, while 1,25(OH)2D3 has no such effect in chicks. 25(OH)D3 is probably absorbed from the epiphyses into the blood stream and converted into the active metabolites, which were indeed detected in the blood to exert its systemic effects.

24,25-Dihydroxyvitamin D 3↗
PubMed1987

The metabolism of vitamin D3 during fracture healing in chicks.

The metabolism of vitamin D3 was studied in chicks after experimental fractures were performed on their tibiae. The chicks were fed for 3 weeks a vitamin D-deficient diet but were supplemented with radioactive labeled vitamin D3. The chicks were then divided into two groups. In the first group the right tibia was fractured, whereas the second group served as nonfractured control group. During the following days of fracture healing, the metabolites of [3H]vitamin D3 were measured in callus, epiphysis, diaphysis, plasma, duodenum, and kidney. Histological examination of calluses and bones, measurements of intestinal absorption of calcium, and renal production of dihydroxylated metabolites of vitamin D3 were performed as well. The levels of the dihydroxylated metabolites were increased in the calluses and the levels of [3H]24,25-dihydroxyvitamin D3 were found to coincide with the formation of cartilaginous tissue and with the renal production of this steroid. In the duodenum of the fractured chicks, the levels of [3H]1,25-dihydroxyvitamin D3 dropped significantly during the first week after fracture, coinciding with reduction in the intestinal absorption of calcium. In the plasma during those 3 weeks of healing process the levels of [3H]1,25-dihydroxyvitamin D3 were far below normal. These findings indicate that during the process of fracture repair, changes in the metabolism and expression of vitamin D are taking place in order to meet the new requirements of the body under stress condition of skeletal fracture.

Animals↗
PubMed1987

Levels of active metabolites of vitamin D3 in the callus of fracture repair in chicks.

The levels of the active metabolites of vitamin D were measured in the callus and in the epiphyseal growth plate of chicks given radioactive cholecalciferol during fracture healing. Those levels were correlated with the histological findings. Three groups of chicks were studied: a control group with no fracture, chicks with fractures fixed by Kirschner wire, and chicks with unfixed fractures. A significant increase in the levels of the active metabolites was found in the callus during the first few days after fracture. The levels of 25-hydroxycholecalciferol [25(OH)D3] and of 24,25-dihydroxycholecalciferol [24,25(OH)2D3] were higher when there was no fixation, while those of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] were higher after fixation. The concentrations of these metabolites in the proximal epiphysis of the tibia were similar to those found in the callus. Based on these findings it is suggested that the active metabolites of vitamin D are directly involved in the process of fracture repair.

Animals↗
PubMed1983

The effect of vitamin D and its metabolites on fracture repair in chicks.

One-day-old chicks were depleted of vitamin D. At 3 weeks their right tibiae, and those of a control group given vitamin D3, were fractured and pinned. After fracture the controls were kept on vitamin D3. Another group was left vitamin D-deficient. The remaining depleted chicks, divided into four groups, were given vitamin D3, 24,25-dihydroxyvitamin D3 [24,25(OH)2D3], 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] or a combination of 24,25(OH)2D3 and 1,25(OH)2D3. The callus obtained after 9 and 14 days was subjected to torsional stress. The callus of chicks given vitamin D continuously showed the greatest resistance, whereas that of vitamin D-deficient chicks showed the smallest resistance. Repletion with either vitamin D3 or its metabolites increased the strength of the callus. Repletion with the combination of 24,25(OH)2D3 and 1,25(OH)2D3 produced the most marked results, in that the callus was even stronger than that of chicks replete with vitamin D3. It is concluded that 24,25(OH)2D3 is essential for bone formation in addition to the known active vitamin D metabolite 1,25(OH)2D3, and the possible clinical implications of these findings are discussed.

24,25-Dihydroxyvitamin D 3↗
PubMed1983

Fracture repair in the Snell dwarf mouse.

Snell dwarf mice are deficient in the somatomedin peptides which are mediators of growth hormone action on the skeleton. Tibial fractures in dwarf mice united within 6 weeks, however chondroid differentiation and osteogenesis at the fracture site were retarded in the first few weeks after fracture compared with normal mice. Administration of bovine growth hormone (5 micrograms daily) accelerated the repair process and 2 micrograms thyroxine daily resulted in rapid callus formation and ossification indistinguishable from normal controls. Normal somatomedin levels are not therefore essential for adequate fracture healing in Snell dwarf mice. The acceleration resulting from growth hormone and thyroxine administration may be due to an increased production of somatomedins locally or systemically or by direct action on connective tissue.

Animals↗
PubMed1981

Haematogenous osteomyelitis and Staphylococcus aureus.

Some 80 - 90% of all acute haematogenous osteomyelitis is caused by staphylococcus aureus. We suggest that this is due to the special ability of staphylococci to synthesise prostaglandins from appropriate precursors such as arachidonic acid. Prostaglandins, especially of the E series, are potent stimulators of bone resorption. Establishment of osteomyelitis could thus result from minor bone trauma and local release of prostaglandins and their precursors, followed by adventitious infection. Infection by staphylococcus aureus, but not by other bacteria, could then lead to a sudden surge in prostaglandin production and so bone destruction, facilitating the formation of an osteomyelitic focus.

Adolescent↗
PubMed1981

The treatment of osteomyelitis of the tibia with sodium salicylate. An experimental study in rabbits.

Osteomyelitis was induced in the tibiae of rabbits by injecting a suspension of Staphylococcus aureus and sodium tetradecylsulphate, a sclerosing agent. These rabbits were then divided into two groups: one group remained untreated and the other was fed a diet containing sodium salicylate. Two and four weeks after induction of osteomyelitis the tibiae taken from untreated rabbits with osteomyelitis and incubated in vitro released significantly more prostaglandin E and F than the control uninjected or uninfected tibiae. Tibiae taken from rabbits treated with sodium salicylate showed minimal radiographic changes and a significantly decreased release of prostaglandin E and F compared to the untreated rabbits. Prostaglandins are known to be potent bone resorbing agents and the results of this study suggest that they may also be involved in the destruction of bone which is characteristic of osteomyelitis. The treatment of rabbits with osteomyelitis using anti-inflammatory drugs, which block synthesis of prostaglandins, in addition to antibiotics, may prevent the destruction of bone and possible sequestration thereby decreasing the risk of chronic disease.

Animals↗
PubMed1981

Release of prostaglandins from bone and muscle after tibial fracture. An experimental study in rabbits.

The release of prostaglandins E and F from the tibiae of rabbits and the surrounding muscle in vitro after fracture and pinning, or pinning alone, has been compared to the release from unoperated tissues. The fractured tibiae released significantly more prostaglandins E and F than the control tibiae three to 14 days after operation. The pinned tibiae also released more of the two prostaglandins, although this was significant only after 14 days. Consequently it was only around the third day that the fractured tibiae released significantly more prostaglandin E than the tibiae which had been pinned, but not fractured. Similar results were obtained for the release from the muscles surrounding the tibiae. Prostaglandins are important mediators of inflammation as well as potent stimulators of bone resorption. Their increased formation in response to fracture and pinning may stimulate the vascular changes, bone resorption and the proliferation of osteogenic cells observed after trauma to bone.

Animals↗
PubMed1980

Idiopathic carpal tunnel syndrome caused by carpal stenosis.

Computed tomography was used to measure the cross-sectional area of the carpal canals in normal controls of both sexes and in women with idiopathic carpal tunnel syndrome. The women controls had significantly smaller carpal canals than the men controls both proximally and distally. In the patients both the proximal and distal cross-sectional areas were significantly reduced compared with the women controls. The measurements showed that carpal canal stenosis is associated with idiopathic carpal tunnel syndrome, narrowing of the canal is bilateral in patients who have unilateral symptoms, and narrowing is greater in the proximal carpal canal. There was no correlation between age and the size of the canal. The difference in the size of the carpal canal between normal men and women might explain the tendency of women to develop carpal tunnel syndrome. The lack of correlation between age and the size of the canal suggests that stenosis of the carpal canal is inherited rather than acquired. Symptoms arise only later in life, when degenerated changes in the content or the walls of the carpal canal compete with the median nerve for space and its function becomes impaired by compression.

Adult↗