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J R Neff

Publications and source records attributed to J R Neff.

At least 37 records · Page 2Linked to original sources

Comparison of the Nebraska collar, a new prototype cervical immobilization collar, with three standard models.

OBJECTIVES: To determine whether a novel immobilization collar called the Nebraska collar would restrict motion of the cervical spine better than three traditional designs: the Philadelphia collar, the sterno occipital mandibular immobilizer (S.O.M.I.), and the Lehrman-Minerva cervical orthosis. DESIGN: Cervical spine radiographs and a compass were used to assess motion allowed by four separate cervical collars placed on volunteers. SETTING: University-affiliated level one trauma center. PATIENTS/PARTICIPANTS: Fourteen paid volunteers (six females and eight males) between the ages of twenty and thirty-five years (mean twenty-five years) were recruited. MAIN OUTCOME MEASUREMENTS: The maximum amount of flexion, extension, and lateral bending permitted by each collar was assessed by cervical radiographs taken of the volunteers while wearing each of the four collars. Maximum rotation was measured with a compass positioned on the top of the head of the volunteers and oriented in the horizontal plane. RESULTS: The Nebraska collar restricted rotation (p < 0.0001) and lateral bending (p < 0.0001) significantly more than did the other three orthoses. In total maximum extension from occiput to C7, the Nebraska collar was found to be more restrictive than the Philadelphia collar (p < 0.05) and the S.O.M.I. (p < 0.05). In total maximum flexion, there was no statistically significant difference among the four collars. When the total maximum flexion-to-extension motion was measured, both the Nebraska and Lehrman-Minerva cervical collars were found to be more restrictive than the Philadelphia collar (p < 0.05). CONCLUSION: The new Nebraska collar provides stabilization that is significantly more rigid than the other models tested, with no difference in patient comfort.

Adult↗

Characterization of a variant SYT-SSX1 synovial sarcoma fusion transcript.

Synovial sarcoma is characterized cytogenetically by an X;18 translocation [t (X;18) (p11;q11)] that results in the fusion of the SYT gene from chromosome 18 to either of two highly homologous genes at Xp11, SSX1 or SSX2. Heterogeneity within the synovial sarcoma fusion junctions is rare. Examination of a primary monophasic synovial sarcoma for an SYT-SSX fusion transcript by reverse-transcription polymerase chain reaction revealed a smaller-than-expected product. Direct sequencing of the product disclosed a novel SYT-SSX1 fusion transcript that contained an additional 51 bp of normal SSX1 sequence but lost 135 bp of the SYT sequence. Detection of synovial sarcoma hybrid transcripts is useful for diagnosis and should include the recognition of distinct variants.

Amino Acid Sequence↗

Chromosomal abnormalities in low grade chondrosarcoma and a review of the literature.

In this study, cytogenetic analysis of two low-grade chondrosarcomas revealed relatively simple chromosomal complements with structural rearrangements involving chromosomes 1, 6, and 12 [46,XY,add(16)(q24)[3]/46,XY,t(1;20)(q21;q11),t(6;17)(q23;q23)[3]/46,XY, t(4;14)(q12;q24),t(5;6)(q12;p21) [2] and 45,XY,t(12;16)(q13;q24),-14[17]/44,idem,add(4)(p16),-17,[2] respectively]. Previously published reports of chondrosarcoma have revealed structural abnormalities of chromosomes 1, 6, 9, 12, and 15 as common. Also, a correlation between the simplicity or complexity of the abnormalities seen and histologic grade has been suggested. The findings of the current study support these earlier observations.

Chondrosarcoma↗

Chromosomal anomalies in a case of proliferative myositis.

Proliferative myositis, a reactive lesion similar to proliferative fasciitis and nodular fasciitis, has only been cytogenetically described in one other report to date. This previously described case showed trisomy 2. Cytogenetic analysis and fluorescence in situ hybridization (FISH) of a proliferative myositis lesion in the present study did not reveal trisomy 2 but the following clonal translocation was observed: 46,XX,t(6;14)(q23;q32).

Chromosomes, Human, Pair 14↗

Characterization of a human myxoid malignant fibrous histiocytoma cell line, OH931.

Malignant fibrous histiocytoma (MFH), the most common soft-tissue sarcoma of late adult life, includes several histopathologic subtypes. The myxoid MFH subtype is characterized by the presence of abundant mucopolysaccharide within a loose connective tissue stroma. Although the myxoid variant is typically distinguished clinically by its better prognosis, we report a case of myxoid MFH that exhibited an aggressive phenotype with early metastases and death. A cell line, OH931, was established from this myxoid MFH. The primary tumor, OH931 cell line, and cells recovered from tumors generated in nude mice shared similar morphologic features, including the continued production of abundant mucopolysaccharide. Cytogenetic analysis of the primary tumor and a subsequently established cell line (OH931) revealed a complex hypertriploid mainline. Chromosomal breakpoints involved in all three specimens analyzed (diagnostic biopsy, definitive surgical, and cell line) included 1p33, 1q21, 2p14, 4p15, 5q13, 12q13, 14p13, 15p13, 19q13 and 20q13.1. The OH931 cell line, which appears to maintain its peculiar characteristics in vitro, should be useful in studies investigating the role of mucopolysaccharide production in the process of neoplasia.

Aged↗

Cytogenetic findings in 73 osteosarcoma specimens and a review of the literature.

Tumor-specific chromosomal abnormalities have been identified in several histologic subtypes of sarcomas. Characterization of recurrent chromosomal abnormalities has provided direction for molecular investigations of pathogenetically important genes. Cytogenetic reports of osteosarcoma, the most common primary malignant bone tumor, are relatively rare. In this study, 73 osteosarcoma specimens from 51 patients were cytogenetically analyzed following short-term culture. Clonal chromosomal abnormalities were detected in 47 and included one haploid specimen, 18 near-diploid specimens, 17 near-triploid, 8 near-tetraploid, 1 near-hexaploid, and 2 specimens with multiple clones of different ploidy levels. Examination of the present data and previously published data (111 clonally abnormal osteosarcoma specimens) reveals that chromosomal bands or regions 1p11-13, 1q10-12, 1q21-22, 11p15, 12p13, 17p12-13, 19q13, and 22q11-13 are most frequently rearranged and the most common numerical abnormalities are +1, -9, -10, -13, and -17. Partial or complete loss of the long arm of chromosome 6 also was seen in all cases of the present study and all previously published cases describing structural abnormalities of 6q. Parosteal osteosarcoma, a prognostically favorable osteosarcoma subtype, was characterized by the presence of a ring chromosome accompanied by no or few other abnormalities. Complex karyotypes were seen nearly exclusively in the high-grade lesions. These findings indicate that specific chromosomal bands and/or regions are nonrandomly involved in osteosarcoma and may provide useful clinical information.

Adolescent↗

Regulation of MMP-9 (92 kDa type IV collagenase/gelatinase B) expression in stromal cells of human giant cell tumor of bone.

Matrix metalloproteinases (MMPs) play an important regulatory role in tissue morphogenesis, cell differentiation, tumor invasion and metastasis. Several authors have reported a direct correlation between the production of 72 kDa (MMP-2) and 92 kDa (MMP-9) type IV collagenases/gelatinases and the metastatic potential of cancer cells. Recently, we have identified the expression of both MMP-2 and MMP-9 in primary cultures of human giant cell tumor (GCT) of bone in vitro, and in tissue extracts in vivo. Interestingly, MMP-9 is not secreted by late-passaged GCT cells. It is possible that the production of MMP-9 is regulated by certain factor(s) secreted by the multinucleated giant cells in the primary culture. In order to test this hypothesis, the effect of primary-culture-conditioned medium on the expression of MMP-9 by late-passaged mononuclear stromal cells was examined. Adding conditioned medium from the primary GCT culture to the late-passaged stromal cells induced MMP-9, as evidenced by the presence of lytic bands at M(r) 92,000 and 72,000 on a gelatin zymogram. These enzyme activities were inhibited by EDTA, a well-known inhibitor of the MMPs. We confirmed these results by Western blotting using specific antibodies and RT-PCR for MMP-2 and MMP-9. Immunofluorescence studies with specific antibodies to MMP-9 further confirmed its expression by the passaged stromal cells cultured in the primary-culture-conditioned medium. The data indicate that MMP-2 and MMP-9 are produced by the mononuclear stromal cells when cultured in GCT primary-culture-conditioned medium. This suggests that multinucleated giant cells in primary cultures secrete a factor(s) that stimulates stromal cells to produce MMP-9, which, in turn, may contribute to the aggressive behavior of GCT.

Adolescent↗

Arthrodesis of the knee with a modular titanium intramedullary nail.

We retrospectively studied the results of arthrodesis of the knee with a modular titanium intramedullary nail that couples at the knee. The study group consisted of thirteen patients who had a malignant tumor around the knee, five who had failure of a total knee arthroplasty, and three who had a locally destructive benign tumor about the knee. All of the patients were followed for a minimum of two years. Through a single incision at the knee, one nail was inserted retrograde into the femur and the other, antegrade into the tibia; the two nails were joined at the level of the knee by a conical couple and were secured with locking screws. The diameters of the nails were different, to accommodate the dissimilar sizes of the tibial and femoral intramedullary canals. A solid osseous fusion was achieved in nineteen (90 per cent) of the twenty-one patients (sixteen who had had resection of a tumor and three who had had a failed arthroplasty), at an average of 8.4 months (range, three to nineteen months) after the operation. One patient had a delayed union, but fusion was achieved after additional bone-grafting. Of the sixteen patients who were available for clinical and radiographic evaluation at the time of the study, fifteen were satisfied with the over-all outcome and thirteen had either less pain or the same amount of pain as they had had preoperatively. There were no mechanical failures of the implant and no recurrences of tumor. Complications occurred in eight (38 per cent) of the twenty-one patients: three patients had a stress fracture, three had a peroneal nerve palsy (one of which was transient), one had a superficial wound infection, and one had reflex sympathetic dystrophy.

Adolescent↗

Cytogenetic analysis of a malignant triton tumor and a malignant peripheral nerve sheath tumor and a review of the literature.

Cytogenetic analyses of malignant peripheral nerve sheath tumors (MPNST) and malignant triton tumors (MTT) are few to date. Two separate triton tumor specimens from one patient and a MPNST specimen from another patient, both with peripheral neurofibromatosis (NF-1, von Recklinghausen disease), showed complex near-triploid complements and partial deletion of the short arm of chromosome 1. Notably, a structural abnormality of chromosome 17 was detected in the MPNST, and loss of chromosome 22 was detected in the MTT. The genes for peripheral neurofibromatosis (NF-1) and central neurofibromatosis (NF-2) have been mapped to these two chromosomes respectively.

Adolescent↗

Cytogenetic analysis of dedifferentiated chondrosarcoma.

Cytogenetic analysis of a dedifferentiated chondrosarcoma with a fibrosarcomatous component revealed the following chromosomal complement: 47,XX,i(1)(q10), add(6)(q13),+7,+8,t(10;12) (p11.2;q11.2),+14,-15,-17, add(19)(q13,4). Chromosome studies of dedifferentiated chondrosarcoma are sparse. Three of the anomalies in the present study are similar to those previously described in dedifferentiated chondrosarcoma.

Chondrosarcoma↗

Translocation (X;18) in primary synovial sarcoma of the lung.

Primary sarcomas of the lung are extremely rare. Among the most common to occur in this location are leiomyosarcoma, fibrosarcoma, and hemangiopericytoma. Many difficulties are encountered when establishing these sarcoma diagnoses, or one of another pathologic type, because of overlapping histologic features and morphologic similarities between primary and metastatic lesions. In this study, the diagnosis of a primary monophasic synovial sarcoma of the lung was aided by the observation of the X;18 translocation characteristic of this neoplasm. To the best of our knowledge, this is the first cytogenetic report of a primary pulmonary synovial sarcoma.

Chromosomes, Human, Pair 18↗

Chromosomal anomalies exclusive of telomeric associations in giant cell tumor of bone.

The occurrence of telomeric associations in giant cell tumor of bone is well recognized. However, there has been little emphasis on clonal structural abnormalities that may be seen in addition to or in the absence of telomeric associations. Two cases of giant cell tumor of bone are presented in this study demonstrating clonal karyotypic anomalies other than telomeric association with a review of previously reported cases showing similar findings.

Adult↗

Translocation t(3;12)(q28;q14) in parosteal lipoma.

Parosteal lipoma is a rare primary benign bone tumor demonstrating histopathologic features similar to those seen in the commonly occurring lipoma of soft tissue. Cytogenetic studies of soft tissue lipoma have demonstrated frequent abnormalities of 12q13-15. To the best of our knowledge the cytogenetic findings in parosteal lipoma have not yet been described. Cytogenetic analysis of a parosteal lipoma of the femur of a 51-year-old female revealed a t(3;12)(q28;q14), indicating that bone and soft tissue lipomas are cytogenetically similar and likely share a common histopathogenesis.

Chromosome Mapping↗

Expression of 72 kDa and 92 kDa type IV collagenases from human giant-cell tumor of bone.

Basement membrane forms widespread barriers to tumor invasion. It has been shown that tumor-secreted, basement membrane-degrading enzymes, namely metalloproteinases (MMPs) play an important role in tumor invasion and metastasis. In this study, we determined the enzymatic activity, content, and mRNA of both the 72 kDa (MMP-2) and 92 kDa (MMP-9) MMPs in primary cultures of human giant-cell tumor of bone (GCT) in vitro and in tissue extracts (in vivo). Gelatin zymography showed the presence of lytic bands at M(r) 121,000, 92,000, and 72,000, and these enzymatic activities were inhibited by EDTA, an inhibitor of MMPs. Western blots with antibodies specific for MMP-2 and MMP-9 confirmed the presence of MMP-2 and MMP-9 both in vitro and in vivo, but GCT cells at late passage showed only MMP-2. Northern blots using labeled cDNA probes specific for these molecules revealed the presence of 3.1 kb transcript for MMP-2 and a 2.9 kb transcript for MMP-9. Using specific antibodies to 72 kDa and 92 kDa type IV collagenases, we studied their cellular distribution by immunohistochemical means. Stronger immunoreactivity was found for 92 kDa type IV collagenase than 72 kDa type IV collagenase in the giant cells. It appears, therefore, that MMP-9 may play an important role in the malignant behavior of GCTs and suggests a potential therapeutic role for protease inhibitors in attempting to minimize the invasive behavior of GCTs.

Bone Neoplasms↗

Cytogenetic and molecular cytogenetic analysis of sacral chordoma.

A specific or characteristic anomaly has not yet been identified in chordoma. Cytogenetic analysis of a sacral chordoma from a 70-year-old male revealed the following chromosomal complement: 42,XY,add(1)(p11), -3,der(4)t(4;?;?18;?)(q12;?;?;), -6, -9, -14,der(16) t(4;?;16)(q12;?;q11), der(17)add(17)(p12) t(17;18)(q11;p11),der(18)del(18)(p11)add(18)(q?)[6]/42, idem,der(9)t(6;9)(q11;p11)[4]/46,XY[10]. In situ hybridization with chromosome-specific paint probes assisted in identifying several of the rearrangements formerly designated as marker chromosomes. Although some of the anomalies observed appear unique to this case, others are similar to those previously reported in chordoma.

Aged↗

Clonal chromosomal abnormalities in osteofibrous dysplasia. Implications for histopathogenesis and its relationship with adamantinoma.

BACKGROUND: The pathogenesis of osteofibrous dysplasia, a rare fibroosseous lesion occurring almost exclusively in the tibia of children younger than 10 years of age, is not known. One theory is that osteofibrous dysplasia results from excessive resorption of bone with fibrous repair of the defect. Alternatively, osteofibrous dysplasia has been considered a congenital lesion or a variant of fibrous dysplasia. It has been hypothesized that osteofibrous dysplasia is a secondary reactive process to adamantinoma. Cytogenetic analysis is one form of investigation that has been instrumental in determining the origin of many disorders. METHODS: Short-term cultures of two separate osteofibrous dysplasia specimens (approximately 1 year apart) from the tibia of an 11-year-old boy and 2 separate specimens (approximately 2 years apart) from the tibia of a 16-year-old boy were cytogenetically examined using standard procedures. Additionally, fluorescence in situ hybridization (FISH) studies were performed on uncultured cells of both specimens of the first patient using an alpha-satellite probe for chromosome 12. RESULTS: Cytogenetic and FISH analysis revealed trisomy 12 in both specimens of the first patient. Trisomy for chromosomes 7, 8, and 22 was seen in both specimens of the second patient. CONCLUSIONS: Osteofibrous dysplasia has not previously been subjected to cytogenetic analysis. Trisomy 7 and 12, however, have been reported in a clonally aberrant adamantinoma, potentially providing further support for a relationship between these two lesions. Most importantly, these findings demonstrate a clonal and possibly neoplastic origin for osteofibrous dysplasia of long bone.

Adolescent↗

Cytogenetic findings in malignant triton tumor.

Malignant triton tumor is a rare histologic variant of malignant schwannoma that shows both neural and skeletal muscle differentiation. In this study, cytogenetic analysis of a recurrent malignant triton tumor of the forearm from a 26-year-old female and a primary paraspinal malignant triton tumor from a 27-year-old female revealed complex karyotypes displaying multiple numerical and structural abnormalities. Abnormalities shared by both tumors included three copies of chromosome 22 and structural rearrangements of chromosomes 2, 7, and 21 at identical or closely located breakpoints.

Adult↗