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Biomedical subjects

J Greene

Publications and source records attributed to J Greene.

At least 91 records · Page 5Linked to original sources
PubMed1998

Bound & nagged.

Getting people to take care of their health care by mending unhealthy ways makes cost-saving sense--until you hear about the small percentage that actually manages to kick bad habits for good.

Attitude to Health↗
PubMed1998

The economics of febrile neutropenia: implications for the use of colony-stimulating factors.

The occurrence of fever and neutropenia following cancer chemotherapy generally prompts hospitalisation for evaluation and treatment. Colony-stimulating factors (CSFs) have been shown to reduce the risk of febrile neutropenia (FN) and the need for hospitalisation in such patients. This study was undertaken to obtain estimates of the actual institutional costs associated with FN and the impact of these costs on threshold estimates for the appropriate use of CSFs. Total hospital expenditures for patients admitted with FN over a 2 year period were studied. A cost allocation function was utilised to allocate all direct costs for non-revenue-generating support centres to revenue-generating service centres as indirect costs. A cost accounting function was then utilised to allocate direct and indirect costs for each service centre to the charge code level. Two groups of patients were defined based on diagnostic codes to represent the spectrum of patients with FN. Total hospital costs were estimated and incorporated into a cost model for the use of CSFs. Variation in the total cost of hospitalisation for FN relates primarily to differences in the average length of stay. The daily cost of hospitalisation was comparable in the groups studied, averaging between US$1675 and US$1892. Incorporation of these cost estimates into the cost model yielded FN risk threshold projections for CSF use in the range of 20-25%. Preliminary studies suggest that incorporation of non-medical, indirect and intangible costs into the CSF decision models will further decrease FN risk threshold projections. Total hospitalisation cost estimates for managing patients with FN are greater than those previously reported, reducing projected FN risk thresholds for CSF use.

Adult↗
PubMed1998

A performance indicator of psychosocial services in enhanced prenatal care of Medicaid-eligible women.

OBJECTIVE: Psychosocial services for low-income pregnant women vary widely in practice, and validated indicators of effective performance are lacking. The study presented here aims to determine whether a measure of provider compliance with a psychosocial service delivery guideline is associated with improved birth outcomes and therefore meets an important validity criterion of a performance indicator. METHODS: Data on psychosocial services delivered to 3467 pregnant women came from 27 sites certified by the California Department of Health Services to provide enhanced perinatal services to Medicaid-eligible women. Multivariate regression analyses were used to test the association of adequate service delivery according to a performance guideline with birth outcomes and the dependence of the association on the credentials of the provider and the type of practice setting. RESULTS: Women who received at least one psychosocial assessment each trimester of care according to the guideline were half as likely as women with inadequate services to have a low birthweight (OR = 0.49; CI 0.34, 0.71) or preterm birth (OR = 0.53; CI 0.40, 0.72) outcome. The effect did not depend on the credentials of the provider or the practice setting type. CONCLUSIONS: The indicator of the adequacy of psychosocial services according to a performance guideline appears to meet a fundamental criterion for a performance indicator, an association with improved outcomes. This indicator may be useful in monitoring performance of enhanced perinatal services for continuous quality improvement of services to low-income pregnant women.

Birth Weight↗
PubMed1998

TR1, a new member of the tumor necrosis factor receptor superfamily, induces fibroblast proliferation and inhibits osteoclastogenesis and bone resorption.

A newly identified member of the tumor necrosis factor receptor (TNFR) superfamily shows activities associated with osteoclastogenesis inhibition and fibroblast proliferation. This new member, called TR1, was identified from a search of an expressed sequence tag database, and encodes 401 amino acids with a 21-residue signal sequence. Unlike other members of TNFR, TR1 does not contain a transmembrane domain and is secreted as a 62 kDa glycoprotein. TR1 gene maps to chromosome 8q23-24.1 and its mRNA is abundantly expressed on primary osteoblasts, osteogenic sarcoma cell lines, and primary fibroblasts. The receptors for TR1 were detected on a monocytic cell line (THP-1) and in human fibroblasts. Scatchard analyses indicated two classes of high and medium-high affinity receptors with a kD of approximately 45 and 320 pM, respectively. Recombinant TR1 induced proliferation of human foreskin fibroblasts and potentiated TNF-induced proliferation in these cells. In a coculture system of osteoblasts and bone marrow cells, recombinant TR1 completely inhibited the differentiation of osteoclast-like multinucleated cell formation in the presence of several bone-resorbing factors. TR1 also strongly inhibited bone-resorbing function on dentine slices by mature osteoclasts and decreased 45Ca release in fetal long-bone organ cultures. Anti-TR1 monoclonal antibody promoted the formation of osteoclasts in mouse marrow culture assays. These results indicate that TR1 has broad biological activities in fibroblast growth and in osteoclast differentiation and its functions.

Animals↗
PubMed1998

Outcome states of colorectal cancer: identification and description using patient focus groups.

OBJECTIVE: Utilities for the outcome states of colorectal cancer must be measured to evaluate the cost-utility of screening and surveillance strategies for this disease. We sought to identify these outcome states, define their associated areas of morbidity, and construct representative descriptions of them for use in a utilities assessment instrument. METHODS: We identified candidate colorectal cancer outcome states based on a review of the literature and interviews with health care professionals. We organized patient focus groups from each of the candidate outcome states to examine their homogeneity and define their associated areas of morbidity. After analyzing the focus group transcripts, we identified and described outcome states of colorectal cancer for future incorporation into a utilities assessment instrument. RESULTS: Six candidate outcome states of colorectal cancer were identified based on disease stage and location at diagnosis. Thirty-eight patients then participated in six focus groups. Analysis of the focus group transcripts revealed seven areas of morbidity associated with colorectal cancer. These areas included problems with social interaction and cognition, fear of cancer recurrence, pain, fatigue, changes in bowel habits, and sexual dysfunction. Based on differences in the intensity and frequency of the symptoms reported in each of these areas, seven distinct outcome states of colorectal cancer were identified and described. CONCLUSION: Clinically distinct outcome states of colorectal cancer are determined by the stage and location of the cancer at the time of diagnosis. Descriptions of these outcome states were created using data collected from patient focus groups. These descriptions can be incorporated into a utilities assessment instrument.

Aged↗
PubMed1998

Adenosine deaminase deficiency and purine nucleoside phosphorylase deficiency in common variable immunodeficiency.

The clinical presentations of adenosine deaminase deficiency and purine nucleoside phosphorylase deficiency are widely variable and include clinical and immunologic findings compatible with common variable immunodeficiency. The screening of 44 patients with common variable immunodeficiency failed to identify any individuals with deficiencies of these enzymes.

Adenosine Deaminase↗
PubMed1997

Starting up the upstarts.

Venture capitalists pour $1 billion a year into health care--and that investment may be the most overlooked indicator of new business opportunities. Signs show that companies focused on consolidation and cost-cutting are off the A list for risk capital. Instead, venture capitalists are targeting start-ups that save money on the front lines by truly managing care.

Capital Financing↗
PubMed1997

Preparation and characterization of recombinant tissue inhibitor of metalloproteinase 4 (TIMP-4).

TIMP-4, a novel human tissue inhibitor of metalloproteinase, was identified and cloned (Greene, J., Wang, M., Raymond, L. A., Liu, Y. E., Rosen, C., and Shi, Y. E. (1996) J. Biol. Chem. 271, 30375-30380). In this report, the production and characterization of recombinant TIMP-4 (rTIMP4p) are described. rTIMP4p, expressed in baculovirus-infected insect cells, was purified to homogeneity by a combination of cation exchange, hydrophobic, and size-exclusion chromatographies. The purified protein migrated as a single 23-kDa band in SDS-polyacrylamide gel electrophoresis and in Western blot using a specific anti-TIMP-4 antibody. Inhibition of matrix metalloproteinase (MMP) activities by rTIMP4p was demonstrated in five MMPs. Enzymatic kinetic studies revealed IC50 values (concentration at 50% inhibition) of 19, 3, 45, 8, and 83 nM for MMP-1, MMP-2, MMP-3, MMP-7, and MMP-9, respectively. Purified rTIMP4p demonstrated a strong inhibitory effect on the invasion of human breast cancer cells across reconstituted basement membranes. Thus, TIMP-4 is a new enzymatic inhibitor in MMP-mediated extracellular matrix degradation and may have therapeutic potential in treating cancer malignant progression.

Breast Neoplasms↗
PubMed1997

Inhibition of tumor growth and metastasis of human breast cancer cells transfected with tissue inhibitor of metalloproteinase 4.

We recently identified, cloned, and characterized a novel human tissue inhibitor of metalloproteinases-4, TIMP-4 (Greene et al., 1996). To determine if TIMP-4 can modulate the in vivo growth of human breast cancers, we transfected a full-length TIMP-4 cDNA into MDA-MB-435 human breast cancer cells and studied the orthotopic growth of TIMP-4-transfected (TIMP4-435) versus control (neo-435) clones in the mammary fat pad of athymic nude mice. TIMP4-435 clones expressed TIMP-4 mRNA and produced anti-metalloproteinase (MMP) activity, while neo-435 clones did not express TIMP-4 mRNA or produce detectable anti-MMP activity. Overexpression of TIMP-4 inhibited the invasion potential of the cells in the in vitro invasion assay. When injected orthotopically into nude mice, TIMP-4 transfectants were significantly inhibited in tumor growth by 4-10-fold in primary tumor volumes; and in an axillary lymph node and lung metastasis as compared with controls. These results suggest the therapeutic potential of TIMP-4 in treating cancer malignant progression.

Animals↗