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Biomedical subjects

K L Jensen

Publications and source records attributed to K L Jensen.

32 records · Page 2Linked to original sources
PubMed1990

The distribution of mesenchyme proteoglycan (PG-M) during wing bud outgrowth.

This study utilizes immunofluorescence to describe the distribution of several extracellular matrix molecules in the chick embryo during the process of limb outgrowth and the formation of precartilage condensations. A large chondroitin sulfate proteoglycan (PG-M) is detected at the wing level at Hamburger and Hamilton stage 14 in and under the dorsal ectoderm, and is associated with the basement membranes around the neural tube, notochord and pronephros, but not with other basement membranes. The galactose-specific lectin, peanut agglutinin (PNA), has a similar distribution except that it also binds to the dorsal side of the neural tube. PG-M is not detected in the limb mesenchyme until after stage 17, when it is present in the distal region, as is PNA-binding material. With further development of the wing bud, PG-M is present in the subectodermal mesenchyme, the mesenchyme at the distal tip and in the prechondrogenic core. After stage 22 PNA-binding material becomes localized in the prechondrogenic core, the basement membranes under the apical ectodermal ridge, and the ventral sulcus. The distribution of these components (PG-M and PNA binding material) overlaps, but differs from that of type I collagen and fibronectin and basement membrane components, such as laminin, basement membrane heparan sulfate proteoglycan, and type IV collagen. Tenascin, on the other hand, is not detected in the limb bud until stage 25, after the appearance of cartilage matrix components such as type II collagen and cartilage proteoglycan (PG-H). These results are considered in relation to the formation of precartilage aggregates, and indicate that PNA binds to components in precartilage aggregates other than PG-M or tenascin.

Aggrecans↗
PubMed1990

Transient expression of a cell surface heparan sulfate proteoglycan (syndecan) during limb development.

Syndecan is an integral membrane proteoglycan that contains both heparan sulfate and chondroitin sulfate chains and that links the cytoskeleton to interstitial extracellular matrix components, including collagen and fibronectin. Immunohistochemistry with a monoclonal antibody directed to the core protein of the syndecan ectodomain has been used to analyze the distribution of this proteoglycan in the developing mouse limb bud and in high-density cultures of limb mesenchyme cells. By Day 9 of gestation when the limb buds are just apparent, syndecan is detected on cells throughout the limb region, including both ectodermal and mesenchymal components. This distribution does not change as the limb bud elongates along its proximodistal axis, except for its reduction in the apical ectodermal ridge. By Day 11, the intensity of immunofluorescence in the central core decreases relative to other regions. By Day 13 immunostaining is lost in the regions destined for chondrogenesis and myogenesis but persists in the limb ectoderm and peripheral and distal mesenchyme. In the limb mesenchyme cell cultures, syndecan is initially undetected, but is found throughout the culture by 24 hr. With further culture the antigen becomes reduced in chondrogenic foci and in association with myogenic cells. When chick limb ectoderm is placed on the high-density cultures, immunoreactivity in the mouse mesenchyme is enhanced suggesting that epithelial-mesenchymal interactions modulate syndecan expression in the limb bud. Based on analysis of 35S-labeled syndecan from the cultures, syndecan from limb mesenchyme cells contains more glycosaminoglycan chains and is larger in size than the previously described polymorphic forms of syndecan from various epithelia. The high affinity of syndecan for components of the extracellular matrix and its distribution in the early limb bud are consistent with a role in maintaining the morphologic integrity of the limb bud during the period of initiation and rapid outgrowth, and in preventing the onset of chondrogenesis.

Animals↗
PubMed1989

[The effect of anabolic androgenic steroids on muscle strength, body weight and lean body mass in body-building men].

A review of the effects of anabolic-androgenic steroids (AAS) on muscle strength, body weight and lean body mass in body-building men is presented. In about half of the placebo-controlled studies, a significant effect on the above mentioned response variables is found. In all cases where an effect was achieved, the drug used was methandrostenolone or stanozolol. Whether this is connected with a special quality of these AAS or whether the negative results achieved with the other AAS are caused by type 2 error is not yet known. The use of AAS as ergogenic drugs must be deprecated because of their marginal effects, the risks of side effects and the unsporting, unethical aspects.

Adult↗
PubMed1988

The accumulation of basement membrane components during the onset of chondrogenesis and myogenesis in the chick wing bud.

The study describes the distribution of several basement membrane molecules in the embryonic chick wing bud from stages 23 to 26, during the onset of myogenesis and chondrogenesis, and then later at stage 28. Laminin is localized as early as stage 23, prior to the onset of myogenesis, in regions corresponding to the position of the future dorsal and ventral myogenic areas. Other matrix components, including fibronectin, do not differentially accumulate in these same regions. Fibronectin, basement membrane heparan sulphate proteoglycan and type IV collagen are more widespread in their distribution than laminin, and are even present between mesenchymal cells. These results suggest a role for laminin in the initial differentiation of the muscle masses and emphasize that components of basement membrane can also be associated with mesenchymal cells.

Animals↗
PubMed1986

Environmental regulation of type X collagen production by cultures of limb mesenchyme, mesectoderm, and sternal chondrocytes.

We have examined whether the production of hypertrophic cartilage matrix reflecting a late stage in the development of chondrocytes which participate in endochondral bone formation, is the result of cell lineage, environmental influence, or both. We have compared the ability of cultured limb mesenchyme and mesectoderm to synthesize type X collagen, a marker highly selective for hypertrophic cartilage. High density cultures of limb mesenchyme from stage 23 and 24 chick embryos contain many cells that react positively for type II collagen by immunohistochemistry, but only a few of these initiate type X collagen synthesis. When limb mesenchyme cells are cultured in or on hydrated collagen gels or in agarose (conditions previously shown to promote chondrogenesis in low density cultures), almost all initiate synthesis of both collagen types. Similarly, collagen gel cultures of limb mesenchyme from stage 17 embryos synthesize type II collagen and with some additional delay type X collagen. However, cytochalasin D treatment of subconfluent cultures on plastic substrates, another treatment known to promote chondrogenesis, induces the production of type II collagen, but not type X collagen. These results demonstrate that the appearance of type X collagen in limb cartilage is environmentally regulated. Mesectodermal cells from the maxillary process of stages 24 and 28 chick embryos were cultured in or on hydrated collagen gels. Such cells initiate synthesis of type II collagen, and eventually type X collagen. Some cells contain only type II collagen and some contain both types II and X collagen. On the other hand, cultures of mandibular processes from stage 29 embryos contain chondrocytes with both collagen types and a larger overall number of chondrogenic foci than the maxillary process cultures. Since the maxillary process does not produce cartilage in situ and the mandibular process forms Meckel's cartilage which does not hypertrophy in situ, environmental influences, probably inhibitory in nature, must regulate chondrogenesis in mesectodermal derivatives. (ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Extracellular matrix mediates epithelial effects on chondrogenesis in vitro.

It has been previously observed that single chick embryonic limb mesenchymal cells can differentiate into chondrocytes without cell-cell interactions when cultured in collagen or agarose gels. In the present study, limb ectoderm, but not dermis, inhibits chondrogenesis when placed on such collagen gel cultures. The inhibitory influence can be transmitted extensive distances in the gel, even when the ectoderm is placed on a porous filter. Collagen gels, preconditioned with limb ectoderms, are also inhibitory to chondrogenesis. On the other hand, chondrogenesis is less inhibited by ectoderm when the mesenchymal cells are placed in agarose. These results suggest that the antichondrogenic effect of limb ectoderm is mediated through alterations of the collagenous extracellular matrix and support the idea that the extracellular matrix must be considered as an organized, functional unit capable of regulating cell differentiation.

Animals↗
PubMed1983

Histiomonocytic malignancy. A spectrum of disease in an 11-month-old infant.

The initial pathologic diagnosis in an 11-month-old girl presenting with a suprarenal mass was true histiocytic lymphoma. The histiocytic nature of the cells was verified by ultrastructural, histochemical, and immunologic studies. The subsequent course featured widespread dissemination as both tumorous masses and diffuse tissue infiltrates, including extensive soft tissue, leptomeningeal, and bone marrow involvement, with a terminal histiomonocytic leukemic phase. Subsequently, this tumor was reclassified as malignant histiocytosis with atypical features, and this case exemplifies the difficulties in classifying some malignant histiomonocytic neoplasms. The overlapping clinical, pathologic, and theoretic features of true histiocytic lymphoma, malignant histiocytosis, and histiomonocytic leukemia are discussed in the context of this case.

Autopsy↗
PubMedDate not supplied

Shoulder arthroplasty in recreational golfers.

A retrospective review of 24 patients who had shoulder arthroplasty revealed that 23 were able to resume playing golf. The 23 patients (mean age 52.4 years, range 26.4 to 71.9 years) underwent 26 shoulder arthroplasties, 20 total shoulder arthroplasties, and 6 hemiarthroplasties. The average follow-up was 53.4 months (range 24.4 to 127.2 months). The average length of time from shoulder arthroplasty to playing an entire round of golf was 4.5 months. Eighteen patients were able to report their preoperative handicap and noted an average improvement after surgery of almost 5 strokes. Playing golf did not result in increased radiographic evidence of component loosening, and no increase occurred in lucent lines when the golfers were compared with a control group of 76 patients with osteoarthritis who had 103 shoulder arthroplasties (P < .05). Fifty members of the American Shoulder and Elbow Society were mailed a standardized questionnaire of 11 questions concerning patients who had shoulder arthroplasty and played golf. Most surgeons (91%) encouraged such patients to resume playing golf. The average length of time members of the Society recommended that patients should wait after shoulder arthroplasty before resuming golf was 4.3 months. Approximately 60% of surgeons believed that no limit should be placed on the number of golf rounds played weekly, and 91% denied an increase in complications among those who returned to playing golf after undergoing shoulder arthroplasty. Fewer than one third of the surgeons (29.5%) believed that component wear would be a problem in patients who undergo shoulder arthroplasty and play golf frequently and would recommend a hemiarthroplasty for an active golfer because of concern about future glenoid problems.

Adult↗
PubMedDate not supplied

Prospective randomized comparison of two types of pressure therapy garments.

A prospective randomized study was undertaken to compare compliance efficacy and cost of the elastic nylon pressure garment (Jobst Institute, Inc., Toledo, Ohio) with the cotton elastic pressure garment (Tubigrip, SePro Healthcare Inc., Montgomeryville, Penn.). Of 110 patients enrolled, 54 received Jobst pressure garments and 56 received Tubigrip pressure garments. Time spent in pressure-therapy garments was the same for both groups. Comparable clinical results were achieved with either Tubigrip or Jobst garments. A significantly greater percentage of patients were compliant with Tubigrip pressure-garment therapy than with Jobst pressure-garment therapy. The cost of the Tubigrip garments was significantly lower than that of Jobst garments. These data suggest that the use of elasticized cotton pressure garments results in significantly better patient compliance, a lower cost, and equal therapeutic efficacy when compared with the elasticized nylon pressure garments.

Adolescent↗