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Biomedical subjects

B Berman

Publications and source records attributed to B Berman.

At least 19 recordsLinked to original sources
PubMed1997

Identification of glypican as a dual modulator of the biological activity of fibroblast growth factors.

Heparan sulfate moieties of cell-surface proteoglycans modulate the biological responses to fibroblast growth factors (FGFs). We have reported previously that cell-associated heparan sulfates inhibit the binding of the keratinocyte growth factor (KGF), but enhance the binding of acidic FGF to the KGF receptor, both in keratinocytes, which naturally express this receptor, and in rat myoblasts, which ectopically express it (Reich-Slotky, R., Bonneh-Barkay, D., Shaoul, E., Berman, B., Svahn, C. M., and Ron, D. (1994) J. Biol. Chem. 269, 32279-32285). The proteoglycan bearing these modulatory heparan sulfates was purified to homogeneity from salt extracts of rat myoblasts by anion-exchange and FGF affinity chromatography and was identified as rat glypican. Affinity-purified glypican augmented the binding of acidic FGF and basic FGF to human FGF receptor-1 in a cell-free system. This effect was abolished following digestion of glypican by heparinase. Addition of purified soluble glypican effectively replaced heparin in supporting basic FGF-induced cellular proliferation of heparan sulfate-negative cells expressing recombinant FGF receptor-1. In keratinocytes, glypican strongly inhibited the mitogenic response to KGF while enhancing the response to acidic FGF. Taken together, these findings demonstrate that glypican plays an important role in regulating the biological activity of fibroblast growth factors and that, for different growth factors, glypican can either enhance or suppress cellular responsiveness.

Animals↗
PubMed1997

Teledermatology.

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Confidentiality↗
PubMed1997

Teledermatology and underserved populations.

BACKGROUND: The dermatologic needs of many communities in the United States and worldwide are underserved. Telemedicine enables physicians and non-physician primary care providers to use modern telecommunications devices to gain access to specialist consultations promptly and with much less travel. The independently developed telemedicine programs described herein support 3 traditionally underserved populations: Pacific Islanders, migrant farmworkers, and prison inmates. OBSERVATIONS: In 3 independently designed telemedicine programs, dermatology emerged as the specialty most used by remote practitioners. Patients were presented for both diagnosis and treatment and in the setting of initial evaluation and as part of follow-up care. CONCLUSION: Teledermatology is a useful way to provide dermatologic support to remote or underserved communities.

Dermatology↗
PubMed1997

Timing of the expression of enamel gene products during mouse tooth development.

In order to understand the mechanisms involved in tooth development it is important to define the timing for tissue-specific gene expression. A consequence of ameloblast cell differentiation is the sequential expression of tissue-specific genes whose products form the enamel extracellular matrix. The ameloblast phenotype has been characterized as consisting of two major classes of proteins: amelogenins and non-amelogenin proteins such as anionic enamel proteins (enamelins, tuft proteins, tuftelin, sulfated proteins) and enamel proteases. The postulated functions for the anionic enamel proteins are as nucleators for hydroxyapatite crystal formation while amelogenins control the crystal size, growth and orientation. While the amelogenins have been well characterized, detailed knowledge for anionic enamel proteins has been sparse. In the present study, we designed experiments to characterize one of the anionic enamel proteins from mouse molars, tuftelin, and to determine the timing of expression of this protein during molar tooth development. Our results showed the initial detection of tuftelin transcripts within proliferating inner enamel epithelial cells at very early stages of tooth development (13 days of embryonic development equivalent to the bud stage of tooth development). These data provide direct evidence that invalidates previous dogmas that enamel proteins were synthesized by polarized, non-dividing, fully differentiated ameloblast cells. In addition, tuftelin was found to be synthesized also by dental papilla mesenchyme cells suggesting that this protein is not enamel-specific. These data taken together open the possibility that the tuftelin present in the dentino-enamel junction could be secreted by both, preodontoblast cells and preameloblast cells. It might also suggest a possible different role for tuftelin than nucleator of hydroxyapatite crystals.

Amelogenin↗
PubMed1996

Adjunct therapies to surgical management of keloids.

BACKGROUND: The literature describing surgical treatments, with or without supplementary nonsurgical treatments for keloids, offers a confusing picture of widely variable "success" rates, recurrence rates, patient populations, and follow-up periods. OBJECTIVE: A review of the surgical treatment of keloids with emphasis on surgery combined with nonsurgical therapies is presented. RESULTS: Surgery alone leads to recurrence rates ranging from 45 to 100%. When surgery is combined with intradermal corticosteroids the recurrence rate in the majority of studies falls below 50%. Surgery combined with button compression therapy on earlobes led to no recurrences. External radiation following excision, often combined with other therapies, has been associated with recurrence rates of less than 10%. Various lasers have been used in the treatment of keloids with great variability in the recurrence rate but in general result in similar recurrence rates as conventional surgery. As with cryodestruction, laser ablation recurrence rates often are improved when combined with other treatments. Inferon-alpha 2b injected after keloid excision demonstrated, in a small series of patients an 8% recurrence rate. CONCLUSION: Presently, it appears that a combined therapeutic approach offers the most propitious possibility for preventing keloid recurrence.

Combined Modality Therapy↗
PubMed1995

Chimeric molecules between keratinocyte growth factor and basic fibroblast growth factor define domains that confer receptor binding specificities.

Basic fibroblast growth factor (FGF) and keratinocyte growth factor (KGF) are structurally related fibroblast growth factors, yet they exhibit distinct receptor binding specificity. Basic FGF binds with high affinity to FGFR1, FGFR2, and FGFR4, whereas KGF does not interact with these receptors and can only bind an isoform of FGFR2 known as the KGFR. Basic GFG binds KGFR but with lower affinity than KGF. In order to identify domains that confer this specificity, four reciprocal chimeras were generated between the two growth factors and were analyzed for receptor recognition and biological activity. The chimeras are designated BK1 (bFGF1-54:KGF91-194), BK2 (bFGF1-74:KGF111-194), KB1 (KGF31-90:bFGF55-155), and KB2 (KGF31-110:bFGF75-155). The two BK chimera similarly interacted with FGFR1 and FGFR4 but differed from each other with respect to KGFR recognition. BK1 displayed a slightly better affinity for KGFR than BK2 and induced a higher level of DNA synthesis in keratinocytes compared with bFGF and BK2. A neutralizing monoclonal antibody directed against bFGF specifically neutralized the biological activity of the BK chimeras. The reciprocal chimeras, KB1 and KB2, exhibited KGF-like receptor binding and activation properties. However, KB2 displayed higher affinity for KGFR and was significantly more potent mitogen that KB1. Altogether, our results suggest that the amino-terminal part of KGF and bFGF plays an important role in determining their receptor binding specificity. In addition, the results point to the contribution of a segment from the middle part of KGF (residues 91-110) for recognition and activation of the KGFR, as the two chimeras containing these residues (BK1 and KB2) displayed an enhanced interaction with the KGFR.

3T3 Cells↗
PubMed1995

Fibroblast growth factor receptors display both common and distinct signaling pathways.

We compared the mitogenic and signaling pathways of three Fibroblast Growth Factor Receptors (FGFRs), FGFR1, KGFR and FGFR4 in the same cell line. Each receptor was expressed in L6E9 rat myoblasts that do not normally express detectable levels of FGFRs and clones that express comparable levels of each receptor were selected. Our results show that FGFs induce an effective survival and growth of FGFR1 and KGFR expressing cells. In addition, these cells exhibit a morphology that is reminiscent of that of malignantly transformed cells and display anchorage independent growth in a ligand dependent manner. Unlike KGFR and FGFR1, FGFR4 mediates a less effective growth, and cells overexpressing this receptor do not undergo any morphological changes nor do they display an anchorage independent growth in response to FGFs. All three receptors exhibit both quantitative and qualitative differences in their ability to induce tyrosine phosphorylation of cellular substrates. Both FGFR1 and KGFR induce strong phosphorylation of phospholipase C-gamma and a 90 kDa protein, while FGFR4 induces a relatively weak phosphorylation of phospholipase C-gamma and completely fails to induce phosphorylation of the 90 kDa. The three receptors also induce phosphorylation of the mitogen activated protein kinases (MAPK) but the effect of FGFR1 is far stronger than that of the other two receptors. Since FGFR4 is expressed in myoblasts in vivo, we examined whether this receptor can function in the differentiation pathway of myoblasts. Contrary to its weak mitogenic activity, FGFR4 effectively mediates the inhibition of myogenic differentiation in L6E9 cells and also suppresses the expression of the myogenic regulatory protein myogenin. Taken together, our results suggest that the signaling mechanism of FGFR4 differs from that of FGFR1 and KGFR, and that the primary role of FGFR4 in myoblasts may be the maintenance of their non differentiated state.

Animals↗
PubMed1995

Keloids.

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Humans↗
PubMed1995

Risk of recurrent stroke in patients with sickle cell disease treated with erythrocyte transfusions.

OBJECTIVE: To determine the effect of a transfusion program on risk of stroke recurrence in children with sickle cell disease. DESIGN: The clinical course and experience with transfusion therapy at eight centers were reviewed for subjects whose initial stroke occurred after January 1988. RESULTS: Sixty subjects were observed for 191.7 patient-years. Eight had a single recurrent stroke (two intracranial hemorrhages and six infarctions) for a prevalence of 13.3%, or one recurrence for each 24 patient-years of observation. Thirteen subjects had 15 transient neurologic events; two of these had subsequent strokes, but the overall risk was similar for those who did and those did not have transient events. Hemoglobin S levels were greater than the desired maximum of 30% at the time of 7 of 16 transient events and five of six recurrent infarctions. The stroke recurrence rate was similar to those in previous reports of children receiving long-term transfusion therapy but significantly less than that reported for children who did not receive transfusions (p < 0.001). CONCLUSIONS: We conclude that maintenance of hemoglobin S at a level less than 30% appears to be effective in reducing the rate of recurrent infarction but does not prevent transient neurologic events. Transient neurologic events are common but do not appear to be related to recurrent stroke.

Adolescent↗
PubMed1995

Efficacy of Chinese acupuncture on postoperative oral surgery pain.

One of the challenges of acupuncture research is designing appropriate control groups. To address this problem, after surgical third molar extractions 19 patients were randomly assigned to an acupuncture group (n = 11) or a placebo acupuncture group (n = 8). The length of time for reaching moderate pain and pain intensity after oral surgery were recorded by standard patient self-report. The results indicated that subjects treated with acupuncture reported longer pain-free duration times (mean, 181 versus 71 minutes; p < or = 0.046) and experienced less pain intensity than those who received placebo acupuncture. This study provides a model for an acupuncture control that could examine the placebo effect in clinical acupuncture research.

Acupuncture Analgesia↗
PubMed1995

Long-term central venous access in patients with sickle cell disease. Incidence of thrombotic and infectious complications.

PURPOSE: Central venous access devices (CVAD) have been used with increasing frequency in recent years among pediatric patients. We retrospectively reviewed our experience in 25 children and young adults with sickle cell disease (SCD) over a 4 1/2 year period in an attempt to define occurrence rates of perioperative complications, thrombosis requiring catheter removal, and infectious episodes. PATIENTS AND METHODS: The setting was a university-associated tertiary children's hospital. Patients were 25 children and young adults (ages 8 months to 23 years) with SCD who required CVAD placement between February 1987 and April 1992. A total of 31 catheters (totally implantable ports and partially implanted catheters) were placed for 17,444 patient catheter days. RESULTS: Rates of significant perioperative complications, thrombotic events requiring catheter removal, and infectious episodes were recorded. No perioperative complications were noted. Five episodes of catheter occlusion requiring replacement occurred in two patients (0.29 per 1,000 catheter patient days, involving 8% of patients and 16% of catheters). Fifteen episodes of catheter-associated bacteremia occurred in eight patients (0.86 per 1,000 catheter patient days involving 32% of patients and 26% of catheters). Three catheters required removal because of infection unresponsive to antibiotic therapy. CONCLUSION: The occurrence of thrombosis requiring catheter removal and infection in our population of patients with SCD was comparable to that reported in patients with malignant disease, cystic fibrosis and acquired immune deficiency syndrome. CVAD represents an effective, reliable, and reasonably safe means of establishing and maintaining venous access for a selective group of children and young adults with SCD who have limited peripheral venous access and require intravenous therapies.

Adolescent↗
PubMed1995

Pentoxifylline, pentifylline, and interferons decrease type I and III procollagen mRNA levels in dermal fibroblasts: evidence for mediation by nuclear factor 1 down-regulation.

Pentoxifylline (PTX) is a methylxanthine that exhibits multiple biologic activities, including the inhibition of collagen synthesis by dermal fibroblasts. Because some PTX activities have recently been linked to transcription factor-mediated regulation of gene transcription, we have investigated if PTX acts to inhibit collagen synthesis at a transcriptional locus by measuring procollagen mRNA levels by assaying for the presence of an activator of procollagen gene promoters, nuclear factor (NF)-1. The effects of another methylxanthine, pentifylline (PTF), shown herein to be a tenfold more potent inhibitor of collagen synthesis than PTX, and interferon-alpha, -beta, and -gamma were studied in parallel. Analysis of extracellular protein and RNA from 48-h-treated fibroblasts showed that PTX, PTF, and interferons decreased alpha 1(I), alpha 2(I), and alpha 1(III) procollagens by reducing the steady-state levels of the corresponding procollagen mRNA transcripts. Reduction of procollagen mRNA levels appeared to be dependent on new protein synthesis, as it was prevented by treatment with cycloheximide. Assay for the presence of nuclear NF-1 by gel mobility shift analysis showed that extracts from interferon, PTX, and PTF-treated fibroblasts lacked proteins recognizing the consensus DNA binding sequence for NF-1. Taken together, these observations suggest interferons and methylxanthines may inhibit fibroblast collagen synthesis by a common mechanism requiring new protein synthesis that suppresses procollagen gene transcription through down-regulation of NF-1.

Adult↗
PubMed1995

Oncostatin M stimulates collagen and glycosaminoglycan production by cultured normal dermal fibroblasts: insensitivity of sclerodermal and keloidal fibroblasts.

It is thought that normal fibrotic repair progresses to dermal fibrosis when fibroblasts are activated persistently by chronic exposure to cytokines such as transforming growth factor-beta. However, additional cytokines and mechanisms may play a role in the development of fibrosis. Thus, we examined a recently described T-lymphocyte/macrophage-derived cytokine, oncostatin M, for its effect on the production of collagen and glycosaminoglycan by microcultures of normal dermal, sclerodermal, and keloidal fibroblasts. Treatment with oncostatin M for 48 h induced dose-dependent (1-100 ng/ml) increases in the collagen and glycosaminoglycan production of nine normal fibroblast strains, which in the absence of fetal bovine serum at 100 ng/ml averaged 196% and 244%, respectively. Oncostatin M treatment increased both types I and III procollagens and their mRNA transcripts, as well as levels of hyaluronic acid, chondroitin-4/6 sulfates, and dermatan sulfate, but not fibronectin or general noncollagenous protein synthesis. In contrast, the collagen production of six of eight sclerodermal and keloidal fibroblast strains was essentially unresponsive to oncostatin M treatment, with 100 ng/ml inducing an average increase of only 34% for the eight fibrotic strains. Oncostatin M stimulation of fibrotic fibroblast glycosaminoglycan production was also hyporesponsive, as 100 ng/ml of oncostatin M induced an average increase of only 101%. These results indicate that oncostatin M could function as a stimulator of normal fibrotic repair via activation of fibroblast collagen and glycosaminoglycan synthesis and that the persistent activation of sclerodermal and keloidal fibroblasts is accompanied by a loss of sensitivity to oncostatin M stimulation.

Adult↗
PubMed1995

Fulminant head and neck congestion in advanced cutaneous T cell lymphoma: a poor prognostic indicator.

BACKGROUND: Clinical factors associated with a poor prognosis in patients with cutaneous T cell lymphoma (CTCL) include the extent and type of skin involvement and the presence and extent of lymphadenopathy. MATERIALS: We report retrospectively the clinical course and survival time of four patients with advanced CTCL after the development of fulminant head and neck congestion. METHODS: All four patients presented with marked erythema and edema of the head and neck with marked cervical adenopathy. Treatment with multidrug chemotherapy and radiation induced only brief remissions. The clinical picture was felt to be due to extensive tumor infiltration of the skin as well as lymphatic compression due to cervical adenopathy rather than venous compression at the level of the mediastinum. Survival from onset of this fulminant head and neck congestion was 1-5 months. CONCLUSION: Development of this fulminant head and neck congestion in patients with advanced CTCL heralds a progressively deteriorating clinical course with a poor prognosis.

Adult↗