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Biomedical subjects

K Kaufman

Publications and source records attributed to K Kaufman.

At least 55 records · Page 3Linked to original sources
PubMed1986

Joint ventures revisited: we're all in this together.

Healthcare organizations are finding it advantageous, and in some cases necessary, to join together to offer new services, seek economies of scale, or just stay in business. These partnerships can take various forms including joint ventures, shared service agreements, or multiprovider arrangements. together, they represent new approaches to operating more efficiently and effectively in a changing healthcare industry. This article marks the beginning of a three-part series on the joint venture in health care. The series explores possible joint venture models, explains the legal implications in setting up a joint venture, and shows how to evaluate a potential deal. Together they provide a background and a starting point for the financial manager considering the possibility of a joint venture.

Commerce↗
PubMed1986

Joint ventures in health care: more than a sideline business.

Many times, healthcare joint ventures are considered second class, sideline businesses, and consequently, are not viewed as complex business relationships. However, compared to other small enterprises, the joint venture presents a complex list of legal and practical issues that must be understood and resolved. Such issues as organizational form, antitrust, reimbursement, licensing, and securities laws must be considered to ensure a successful joint venture.

Economic Competition↗
PubMed1986

Joint ventures in health care: what to do before you do the deal.

To be successful, a hospital-physician joint venture must be guided by a strategy that includes a coherent business strategy, an orientation to the specific needs of the potential physician participants, a bias towards closure, and a rigorous process for evaluating, structuring, and implementing transactions. This article focuses on the last characteristic of the strategy--a process for evaluation, structuring, and implementation. Such a process will establish the basic viability of the project, give direction to the approach, provide a fundamental understanding of the transaction, and create an overall businesslike attitude.

Capital Financing↗
PubMed1983

In vitro analysis of allogeneic lymphocyte interaction. VII. I-A-restricted self-reactive and alloreactive helper components of allogeneic effect factor are distinct donor T cell-derived Ia-molecules that recognize Ia determinants on antigen-presenting cells.

An allogeneic effect factor (AEF) derived from mixed lymphocyte reaction (MLR) cultures of alloactivated A.SW (H-2s) responder T cells and irradiated T cell-depleted A/WySn (H-2a) stimulator spleen cells was fractionated on the basis of molecular size and charge into two I-A-restricted helper components. The cellular origin of these components is believed to be an Lyt-1+2- -activated responder T helper (TH) cell. One alloreactive component, TIAH-1, recognizes allo-I-A determinants on an A/WySn antigen-presenting cell (APC). The other self-reactive component, TIAH-2, recognizes self-I-A determinants on an A.SW APC. The interaction of each of these components with the appropriate APC subsequently activates an in vitro primary anti-SRBC PFC response of either stimulator haplotype- or responder haplotype-derived B cells. These data demonstrate that the activity of TIAH-1 and TIAH-2 is dependent on the genotype of the APC and not the B cell, and that the target cell of action of these AEF TH components is an APC. TIAH-1 and TIAH-2 are 68,000 mol wt single polypeptide chains that have an isoelectric point (pI) of 5.8 and 5.5, respectively. Their charge difference is not attributable to altered amounts of sialylation or phosphorylation, but probably is due to other forms of altered glycosylation and/or to changes in their amino acid sequence. They share approximately 80% of their tryptic peptides and likely constitute homologous but nonidentical molecules. Papain cleaves TIAH-1 and TIAH-2 into a 40,000 mol wt fragment. TIAH-1 and TIAH-2 may represent structurally very related but nonidentical secreted forms of activated responder TH cell-derived receptors for allo-I-A and self-I-A determinants, respectively.

Amino Acid Sequence↗
PubMed1983

Taking the mystery out of the consultant selection process.

Underestimating the importance of the selection process for consultants can increase the hospital's chances of receiving unsatisfactory results. In this article, the author discusses techniques for ensuring that the hospital chooses the "right" firm for the "right" job.

Consultants↗
PubMed1983

Deregulation of the health care industry: implications of financial change.

DRG-style prospective reimbursement has the potential to act as a destabilizing and deregulating force in the health care industry. The consequences of deregulation are anticipated to include: corporate capture of the delivery system: increased physician investment in the delivery process; shift in governance from the community to the national marketplace; changes in utilization patterns; re-emphasis on market shares; intensification of ambulatory care strategies; changes in the intensity of diagnostic services; new directions in corporate reorganization; and the rise of the chief financial officer.

Delivery of Health Care↗
PubMed1983

In vitro analysis of allogeneic lymphocyte interaction. VI. I-J-restricted self-reactive and alloreactive components of allogeneic effect factor (AEF) are distinct I-J- molecules that interact with I-J+ T cells and antigen-presenting cells.

An allogeneic effect factor (AEF) generated across an I-J incompatibility was derived from MLR cultures of alloactivated B10.A(3R) responder T cells and irradiated T cell-depleted B10.A(5R) stimulator spleen cells. This AEF consists of two soluble, secreted I-J-restricted helper components. One helper component, TH-I, recognizes self-I-J determinants on an I-J+ B10.A(3R) antigen-presenting cell (APC), whereas the other helper component, TH-II, recognizes allo-I-J determinants on an I-J+ B10.A(5R) APC. TH-I-B10.A(3R) APC interaction and TH-II-B10.A(5R) APC interaction each induce an in vitro primary anti-SRBC PFC response of either B10.A(3R) or B10.A(5R) B cells. Thus, I-J determinants serve as restricting elements during a TH-APC and not an APC-B interaction. TH-II mediates the I-J-restricted allogeneic effect required to activate T suppressor (TS) cells during a contact sensitivity or delayed-type hypersensitivity response to hapten-conjugated syngeneic lymphoid cells. This indicates that TH-II is also involved in a TH-pre-TS type interaction. TH-I and TH-II are I-J-, 68,000 m.w. molecules that differ by about 0.10 units in their pl values. Their charge difference is not due to an altered amount of sialylation or phosphorylation, but may result either from another form of altered glycosylation and/or from a difference in their primary structure. Peptide mapping analyses reveal that TH-I and TH-II possess at least 80% shared peptides and may be structurally homologous but nonidentical molecules; however, the possibility that TH-I and TH-II are structurally identical cannot be eliminated. Papain cleaves TH-I and TH-II into a 40,000 m.w. fragment. No subunit structure of TH-I and TH-II is apparent. It is suggested that TH-I and TH-II are I-J- -activated responder T cell-derived receptors for self-I-J and allo-I-J determinants, respectively.

Amino Acid Sequence↗
PubMed1983

In vivo analysis of allogeneic lymphocyte interaction: activation of suppressor T cells by an I-J-restricted allogeneic effect factor (AEF).

The preceding paper detailed the production and fractionation of a T cell-derived I-J-specific allogeneic effect factor (AEF) and analyzed its ability to provide help in a T cell-depleted, in vitro primary anti-sheep erythrocyte response. The identical AEF fractions were examined in this study for their ability to elicit suppression in a delayed-type hypersensitivity assay. Previous reports showed that low or suboptimal doses of antigen, presented i.v. on a cell surface, induce a precursor or primed set of suppressor T cells (pre Ts). These cells manifested antigen-specific suppression only in the presence of a T cell-mediated I-J-specific allogeneic effect induced in vivo against the pre Ts. The experiments reported here examined the ability of alloactivated T cell-derived I-J-specific AEF components to replace the in vivo I-J allogeneic effect. The results show that certain AEF components can indeed provide the signal(s) necessary for activation of suppression. Size and charge separation of the crude AEF preparation revealed several components, some of which could independently serve as appropriate inductive signals. One of these components proved to be biochemically identical to interleukin 2 (IL 2) and accounted for some of the genetically unrestricted AEF activity observed; other higher m.w. molecules also possessed unrestricted activity. Another component provided the requisite activational signals and this 68,000-dalton, pI 5.6 molecule(s) was I-J restricted. These findings are discussed in terms of models of lymphocyte subset interactions and activation.

Animals↗
PubMed1983

In vitro analysis of allogeneic lymphocyte interaction. VIII. Characterization of helper components of allogeneic effect factor (AEF) that activate Lyb5+ and Lyb5- B cells to respond to thymus-dependent and thymus-independent antigens.

We analyzed the ability of an allogeneic effect factor (AEF), produced using alloactivated A.SW (H-2s) responder T cells and irradiated A/WySN (H-2a) T cell-depleted stimulator spleen cells, to enhance the responsiveness of Lyb5+ and Lyb5- B cells to thymus-dependent (TD) and thymus-independent type 1 (TI-1) and type 2 (TI-2) antigens. We found that normal adult male CBA/CaHN (Lyb5+ + Lyb5-) B cells are activated by unfractionated AEF in primary in vitro IgM antibody responses to the SRBC (TD), TNP-LPS (TI-1), and TNP-Ficoll (TI-2) antigens. Adult male xid CBA/N (Lyb5-) B cells are activated by unfractionated AEF to respond to TNP-LPS but to neither SRBC nor TNP-Ficoll. Gel filtration of AEF on ACA 54 resolves several helper components. One component, which is I-Ak restricted in its activity and may represent a secreted form of an Ia antigen T cell receptor, interacts with histocompatible and functionally competent CBA/CaHN or CBA/N antigen-presenting cells to activate a primary anti-SRBC response of CBA/CaHN B cells but not of CBA/N B cells. A second antigen-nonspecific and H-2-nonrestricted AEF component, which consists of interleukin 2 and possibly also interleukin 1, activates anti-SRBC and anti-TNP-Ficoll responses of both CBA/CaHN B cells and CBA/N B cells. Such CBA/N B cell responses were potentiated by this AEF component only after its biochemical fractionation and only in the presence of a limiting number of T cells. These data indicate that both Lyb5+ and Lyb5- B cells are responsive to TD, TI-1, and TI-2 antigens in the presence of ancillary antigen-nonspecific help. They are also consistent with the notion that T helper cell activation of Lyb5+ B cells is H-2 nonrestricted and that T helper cell activation of Lyb5- B cells is H-2 restricted.

Animals↗
PubMed1982

Role of Ia antigens in graft vs. host reactions. II. Molecular and functional analysis of T cell alloreactivity by the characterization of host Ia antigens on alloactivated donor T cells.

Graft vs. host response (GVHR)-activated donor T cells bind to stimulatory host cell-derived Ia antigens. Radioimmune cell-binding assays demonstrate that activated donor T cells acquire both host I-A and I-E alloantigens on their surface. Approximately threefold to fivefold less I-E products than I-A products are transferred. Immunoprecipitation and one-dimensional and two-dimensional gel electrophoresis analyses show that radioiodinated alpha and beta polypeptide chains of both I-A and I-E-encoded host Ia molecules may be transferred in an apparently structurally unaltered form from host cells to donor cells. Biosynthetic studies indicate that [35S]methionine-labeled activated donor T cells do not synthesize Ia antigens of the donor haplotype. Functional analyses with fluorescence-activated cell sorter sorted donor T cell subpopulations show that donor T cells that bind host I-A antigens preferentially cooperate with nonimmune host B cells. Donor T cells that do not bind detectable amounts of host I-A antigens preferentially help nonimmune donor B cells. By contrast, donor T cells that either bind or do not bind host I-A antigens display no H-2-restricted interaction and help both donor and host immune B cells. These data reveal that the Ia antigen-binding specificity of distinct functional subpopulations of alloactivated donor T cells regulates their I-region-restricted (self or allo) helper activity for nonimmune B cells but not immune B cells. Furthermore, they suggest that T cell-macrophage and T cell-B cell collaboration is mediated by a complementary anti-Ia:Ia receptor:ligand type of interaction in which the receptor of a T cell binds to the ligand of an antigen-presenting macrophage and/or B cell.

Animals↗