Academic literature on the topic 'BM 1.0'

AbstractThis paper deals with the existence of positive radial solutions for the quasilinear system $\text{div}(|\nabla u_i|^{p-2}\nabla u_i)+\lambda f^i(u_1,\dots,u_n)=0$, $|x|\lt1$, $u_i(x)=0$, on $|x|=1$, $i=1,\dots,n$, $p\gt1$, $\lambda>0$, $x\in\mathbb{R}^N$. The $f^i$, $i=1,\dots,n$, are continuous and non-negative functions. Let $\bm{u}=(u_1,\dots,u_n)$, $\|\bm{u}\|=\sum_{i=1}^n|u_i|$,$$ f_0^i=\lim_{\|\bm{u}\|\to0}\frac{f^i(\bm{u})}{\|\bm{u}\|^{p-1}}, $$$i=1,\dots,n$, $\bm{f}=(f^1,\dots,f^n)$, $\bm{f}_0=\sum_{i=1}^nf_0^i$. We prove that the problem has a positive solution for sufficiently small $\lambda>0$ if $\bm{f}_0=\infty$. Our methods employ a fixed-point theorem in a cone.

AbstractBreast milk (BM) hormones have been hypothesised as a nutritional link between maternal and infant metabolic health. This study aimed to evaluate hormone concentrations in BM of women with and without gestational diabetes mellitus (GDM), and the relationship between maternal factors, BM hormones and infant growth. We studied ninety-six nulliparous women with (n 48) and without GDM and their exclusively breastfed term singletons. Women with GDM received dietary therapy or insulin injection for euglycaemia during pregnancy. Hormone concentrations in BM, maternal BMI and infant growth were longitudinally evaluated on postnatal days 3, 42 and 90. Mothers with GDM had decreased concentrations of adiponectin (Pcolostrum<0·001; Pmature-milk=0·009) and ghrelin (Pcolostrum=0·011; Pmature-milk<0·001) and increased concentration of insulin in BM (Pcolostrum=0·047; Pmature-milk=0·021). Maternal BMI was positively associated with adiponectin (β=0·06; 95 % CI 0·02, 0·1; P=0·001), leptin (β=0·16; 95 % CI 0·12, 0·2; P<0·001) and insulin concentrations (β=0·06; 95 % CI 0·02, 0·1; P<0·001), and inversely associated with ghrelin concentration in BM (β=–0·08; 95 % CI –0·1, –0·06; P<0·001). Among the four hormones, adiponectin was inversely associated with infant growth in both the GDM (βweight-for-height=–2·49; 95 % CI –3·83, –1·15; P<0·001; βhead-circumference=–0·39; 95 % CI –0·65, –0·13; P=0·003) and healthy groups (βweight-for-height=–1·42; 95 % CI –2·38, –0·46; P=0·003; βhead-circumference=–0·15; 95 % CI –0·27, –0·03; P=0·007). Maternal BMI and GDM are important determinants of BM hormone concentrations. Milk-borne adiponectin is determined by maternal metabolic status and plays an independent down-regulating role in early infant growth.

Background: The long-term effects of eltrombopag on bone marrow (BM) reticulin and/or collagen deposition in previously treated adults with chronic immune thrombocytopenia (ITP) were assessed. Methods: Three BM biopsies were collected at baseline and after 1 and 2 years of eltrombopag treatment. Specimens were centrally processed, stained for reticulin and collagen, independently reviewed by 2 hematopathologists, and rated according to the European Consensus 0-3 scale of marrow fibrosis (MF). Results: Of 162 patients enrolled, 93 completed all 3 protocol-specified BM biopsies. All patients with a baseline assessment were negative for collagen. Of 159 patients assessed at baseline, 150 (94%) had normal reticulin (MF-0) and 9 (6%) had minimally increased reticulin (MF-1). After 2 years, 83/93 patients (89%) with BM biopsies had MF-0, 10 (11%) had MF-1, and none had MF-2 or MF-3. Five out of 127 patients (4%) at 1 year and 1 out of 93 (1%) at 2 years had collagen deposition. None of the patients had clinical symptoms typical of BM dysfunction or abnormalities of clinical concern based on white blood cell count or peripheral blood smear. Conclusion: For most patients with chronic ITP, eltrombopag is not associated with clinically relevant increases in BM reticulin or collagen formation.

1094 Background: The genomics of patients with metastatic breast cancer (MBC) who develop brain metastases (BM) is not well understood given the difficulty in obtaining brain tumor for genotyping. We compared tumor genotyping results via cell-free DNA (cfDNA) collected at MBC diagnosis in patients who developed BM after MBC diagnosis with those who did not develop BM (non-BM). Methods: Patients at an academic institution who had cfDNA testing (Guardant 360/Next generation sequencing, 73 gene assay) at MBC diagnosis between 1/2016-12/2017, with ≥ 6 months of follow-up post testing, were identified. A chart review was done to identify tumor subtype, demographics, cfDNA results, and development of BM at or after MBC diagnosis. Pearson’s chi-squared and Wilcoxon rank sum tests were used to determine differences in clinical and cfDNA characteristics in BM vs. non-BM (p<0.05 for statistical significance). Results: CfDNA results were available for 49 patients, of whom 13 (27%) developed BM (4 with BM at MBC diagnosis). The median time to BM development was 11 months. While patients with BM were younger at MBC diagnosis than non-BM (median age BM 53 vs. non-BM 61, p=0.05), they had similar subtype (BM vs. non-BM: HR+/HER2- 62% vs. 69%, HER2+ 8% vs. 14%, TNBC 23% vs. 17%, unknown 8% vs. 0%, p=0.3), de-novo vs. recurrent disease (BM vs. non-BM: de-novo 8% vs. 14%, recurrent 92% vs. 86%, p=0.6), and visceral disease (BM vs. non-BM: 77% vs. 56%, p=0.2) distributions. All patients with BM had ≥1 detectable cfDNA mutation vs. 88% of non-BM. While the median mutant allele frequency of the most common mutation was similar in BM vs. non-BM (2.4% vs. 3.7%, p=0.5), the mutation pattern varied. Patients with BM more often had mutations in BRCA1 (15% vs. 3%, p=0.1), APC (15% vs. 0%, p=0.02), and CDKN2A (15% vs. 0%, p=0.02), compared to non-BM. In 4 patients with BM at MBC diagnosis, mutations in APC (50%), CDKN2A (50%), and BRCA 1/2 (25%) were noted; 1 had coexisting APC and BRCA1/2 mutations and another had coexisting APC and CDKN2A mutations. Conclusions: Patients with MBC who develop BM may have different cfDNA genomics, particularly BRCA1, APC, and CDKN2A mutations. Further research is needed to determine the predictive value of cfDNA at MBC diagnosis in the identification of patients at higher risk of developing BM. [Table: see text]

There is limited information on the effect of organic fertilizers on seed germination and subsequent transplant growth. The objective of this study was to determine the effects of application rate of blood meal (BM) and feather meal (FM) fertilizers on germination of tomato seeds. Both organic fertilizers were applied as amendments to peat-based organic substrates at rates ranging from 0 to over 50 g·kg−1 N. Tomato ‘Brandywine’ seed were sown in trays. Seed germination was recorded daily until the germination percentage remained unchanged. Ammonia concentration in the substrates (Pro-Mix and Miracle-Gro) increased with increasing rate of substrate N concentration. Ammonia concentration also increased with increasing time after incorporation of BM and FM reaching maximum values (16 ppm) at day 9. Tomato seed germination was little affected at BM and FM rates lower than ≈3 g·kg−1 N (4% w/w for BM or FM), but declined above 3 g·kg−1 N reaching 0% germination rate at ≈14 g·kg−1 N for both BM and FM. Substrates pH was 5.9 in the absence of BM or FM and increased to about pH 7 with addition of low rates of BM (2.7 g·kg−1 N) and FM (2.6 g·kg−1 N). Substrate electrical conductivity (EC) increased with increasing substrate N concentration as supplied by BM and FM; FM, however, had a stronger effect on increasing EC compared with BM. In conclusion, BM and FM had inhibitory effects on tomato seed germination when applied at more than 3 g·kg−1 N (4% w/w for BM or FM). High ammonia concentration in the substrates for the first 2 weeks after incorporation of BM or FM likely caused, at least partially, inhibition of tomato seed germination. Thus, substrate mixed with BM or FM should be allowed to incubate for at least 2 weeks before planting tomato seed.

e15728 Background: BM from PDAC represents a rare clinical entity (<0.6%) of PDAC cases for which the clinical and molecular features are not well described. We reviewed detailed clinical characteristics and molecular profiling performed in a cohort of PDAC pts with BM evaluated at MSKCC. Methods: Patients (pts) with BM from PDAC diagnosed from 01/1990-08/2016 were identified from a prospectively maintained database, following IRB approval. Clinicopathological data including time to BM development, overall survival (OS) from PDAC diagnosis (dx) and OS from BM dx was recorded. Molecular profiling was performed by MSK-IMPACT testing (>340 key cancer genes) or via Seqeunom testing (8 gene panel). Results: We identified n= 24 pts with BM from PDAC. Twenty-three/24 pts had imaging for symptoms. Mean no. of systemic regimens was 3 (range 0-7). Three/24 (13%) had BM at initial dx. Median time from PDAC dx to BM development was 17 months (mths) (range 0-79). Median survival from BM was 50 days (range 7-975). BM treatment included; surgery; n=4, RT; n=13 or supportive care; n=7. Two pts had survival of 21 & 31 months post BM, both had resection. Median OS from PDAC dx was 18 mths (0-82). 10 pts had consent/pathology for molecular testing (MSK-IMPACT n=7, Sequenom n=3). Results are available for 6 pts, 3 by IMPACT. 6/6 pts had KRAS mutations (MUT); G12D (4), G12V (1), Q61K (1). 0/6 pts had ERBB2 AMP or MUT. One tumor arising from an IPMN had concurrent GNAS and KRAS MUT. By MSK-IMPACT; 2/3 pts had MYC AMP, 2/3 TP53 MUT, 1/3 ARID1A loss, 1/3 CDKN2A loss. 5/24 pts had germline testing, 3 had BRCA MUT; BRCA1 (2), BRCA2 (1). Conclusions: The presence of BM portends a poor prognosis. In general pts who develop BM are younger at initial PDAC dx and may have a better OS from dx [median OS 18 mths (all pts); OS de novo stage IV pts; 17 mths]. Somatic profiling identified KRAS MUT in all resulted pts with alterations in TP53 and MYC also detected. Although speculative, germline BRCA MUT occurred in 13% (60% of pts tested). See table. [Table: see text]

Abstract CD34 negative hematopoietic stem cells (CD34− HSCs) were identified in mice and humans. Human HSCs are evaluated as severe combined immunodeficient mouse (SCID)-repopulating cells (SRCs), originally identified by the ability to reconstitute hematopoiesis in nonobese diabetic (NOD)/SCID mouse. CD34− cord blood (CB) cells have been hard to engraft in NOD/SCID mice until recent report of successlul engraftment by intra-bone marrow transplantation (iBMT). However, CD34− bone marrow (BM) cells have not been analyzed precisely. We prepared lineage negative CD34 negative (Lin-CD34−) cells by negative selection using CD2,3,7,14,16,19,20,33,34,36,41,56,127, and GlyA antibody. Lin-CD34− BM cells did not engraft in NOD/SCID mice even by using iBMT (0/6). In the previous study, we reported that Lin-CD34− BM cells were able to differentiate into CD34+ cells accompanied by the emergence of colony forming activity after 7 days of stroma-dependent culture, while SRC activity was not detected. (BMT 28, 587–595, 2001) Here we cultured Lin-CD34− BM cells on stroma cells transfected with human angiopoietin-1 cDNA (AHESS-5), since we detected Tie-2 expression on Lin-CD34− BM cells. AHESS-5 supported induction of CD34 much better than HESS-5 cells or empty vector transfected control cells (EVHESS-5), and the effect was blocked by anti-Tie-2 antibody (Fig.1). Furtheremore, CD34+ cells produced from CD34− BM cells engrafted in NOD/SCID mice (11/12). As previously reported, CD34− CB cells differentiate CD34+ cells and acquire SRC activity by stroma-dependent culture without angiopoietin-1. These results highlighted the characteristic differences of CD34− HSCs of BM from CB and the unique role of BM niche for CD34− HSCs. Fig. 1 CD34 expression on Lin − CD34 − BM cells after 7 days of culture Fig. 1. CD34 expression on Lin−CD34− BM cells after 7 days of culture

Abstract Introduction: In MM pathogenesis, angiogenesis and growth factors have a governing role. VEGF, secreted by malignant bone marrow (BM) plasma cells (PCs) and stroma, acts as an important mediator of tumor angiogenesis. VEGF has been suggested as an adverse prognostic factor, being elevated in advanced and plasmablastic MM. Circulating as well as BM-residing endothelial cells (ECs) have been shown to contribute to angiogenesis in MM as well as other tumors. Moreover, endothelial progenitor cells (EPC) have been demonstrated to contribute to vascular repair and to be decreased in number and function with end-stage renal impairment (RI). Whereas VEGF and/or EPCs have been described in small former analysis in MM, larger comparisons with MGUS pts and healthy donors (HD) are lacking, differences in various MM subsets (such as BM; peripheral blood and apheresis [AP] samples) have not been addressed, nor the role of EPCs and hemangioblasts in advanced vs. mild RI in MM pts. Methods: We sought to characterize ECs (namely VEGF+ cells, EPCs as VEGFR2+/CD133+/CD34+, hemangioblasts as VEGF+/CD34+) and other subtypes (CD34+, CD45+, CD38+, CD45+/CD38+, CD45−/CD38+) via multiparametric flow cytometry. This was performed in MM pts (n=70), MGUS pts (n=8) and HD (n=14). In MM, BM (n=70), PB (n=14) and AP (n=21) specimens were compared, as well as changes in EPCs and hemangioblasts with and without mild or severe RI. Renal function was determined via estimated glomerular filtration rate (eGFR), classifying mild RI as eGFR &lt;90ml/min/1.73m2 and severe RI as eGFR &lt;30ml/min/1.73m2. Results: MM pts’ age, BM-infiltration and serum creatinine were 63 years (range: 35–84), 15% (0–96) and 0.91mg/dl (0.5–8.6), respectively. BM specimens from MM and MGUS pts showed 4-fold and 2-fold higher VEGF levels, respectively as compared to HD (Table 1). EPCs were also elevated in MM as compared to MGUS and HD (Table 1). Hemangioblasts, CD45+/CD38+ and CD45−/CD38+ were increased in MM BM specimens as compared to MGUS and HD, whereas CD45+ and CD34+ cell numbers were decreased in myeloma specimens (Table 1). Table 1. Median endothelial cells and other subtypes in MM, MGUS and healthy donors BM MM (n=70) BM MGUS (n=8) BM healthy donors (n=14) VEGF+ (%) 0.38 (0 – 12.9) 0.18 (0 – 0.7) 0.09 (0 – 0.6) EPCs (%) 0.03 (0 – 0.4) 0.02 (0 – 0.07) 0.01 (0 – 0.2) VEGF+/CD34+ (%) 0.21 (0 – 2.2) 0.11 (0 – 0.4) 0.04 (0 – 0.5) CD34+ (%) 0.65 (0 – 6.6) 1.23 (0.02 – 4.0) 1.50 (0.07 – 2.8) CD45+ (%) 39.54 (2.8 – 99.1) 39.34 (13.8 – 69.7) 51.70 (10.3 – 90.9) CD45+/CD38+ (%) 24.61 (0.9 – 89.7) 21.68 (1.4 – 49.4) 17.20 (2.6 – 56.9) CD45−/CD38+ (%) 1.54 (0 – 77.7) 1.15 (0 – 2.4) 0.62 (0.1 – 5.6) The comparison of BM, PB, AP specimens in MM showed similar VEGF levels in BM and PB with 0.38% which were increased in AP specimens with 0.5%. This was similarly observed for EPCs with 0.03% in BM and PB as compared to 0.04% in AP samples. Other markers showed similar values for CD34, CD45, CD38+ cells in BM and PB; similar hemangioblast numbers in all 3 subsets, and higher CD34+ and CD45+ cells, and lower CD45−/CD38+ cells in AP specimens. Correlation of EPCs and hemangioblasts with renal function revealed that EPCs decreased with RI, whereas hemangioblasts remained comparable (Table 2). Table 2. Median EPCs and hemangioblasts (VEGF/CD34) with and without RI EPCs (%) VEGF+/CD34+ (%) eGFR &gt;90 (n=41) 0.050 (0 – 0.41) 0.195 (0 – 0.86) eGFR &lt;90 (n=46) 0.025 (0 – 0.41) 0.230 (0 – 0.8) eGFR &gt;30 (n=81) 0.030 (0 – 0.41) 0.210 (0 – 2.23) eGFR &lt;30 (n=6) 0.025 (0 – 0.41) 0.190 (0 – 2.23) Conclusions: These results demonstrate that all ECs, namely VEGF+ cells, EPCs and hemangioblasts are higher in MM than MGUS and HD. Lower CD34+ and CD45+ cells in MM suggest this as a result of the disease and most likely also due to anti-MM therapy. We observed differences in BM, PB and AP specimens in MM pts. RI influenced EC numbers. These results suggest that elevated ECs in MM may reflect disease activity and may be useful as MM biomarkers. The quantification of ECs in MM may also be informative to monitor the efficacy of anti-angiogenic treatment, such as thalidomide and lenalidomide. Further analyses will evaluate the prognostic significance of EPCs, hemangioblasts and other markers in MM, their role in mild and severe RI is ongoing, as well the correlation with disease outcome.

Slower weight gain and less visceral fat had been observed when rats fed a high-fat diet were supplemented with freeze-dried bitter melon (BM) juice; the metabolic consequences and possible mechanism(s) were further explored in the present study. In a 4-week experiment, rats were fed a low-fat (70 g/kg) or a high-fat (300 g/kg) diet with or without BM (7·5 g/kg or 0·75%). BM-supplemented rats had lower energy efficiency, visceral fat mass, plasma glucose and hepatic triacylglycerol, but higher serum free fatty acids and plasma catecholamines. In the second experiment, 7-week BM supplementation in high-fat diet rats led to a lowering of hepatic triacylglycerol (P<0·05) and steatosis score (P<0·05) similar to those in rats fed a low-fat diet. BM supplementation did not affect serum and hepatic cholesterol. However, plasma epinephrine and serum free fatty acid concentrations were increased (P<0·05). In the third experiment, BM(7·5 and 15 g/kg) and 1·5 % BM lowered triacylglycerol concentration in red gastrocnemius and tibialis anterior (P<0·05) muscle, but a dose–response effect was not observed. These data suggest that chronic BM feeding leads to a general decrease in tissue fat accumulation and that such an effect is mediated in part by enhanced sympathetic activity and lipolysis. BM or its bioactive ingredient(s) could be used as a dietary adjunct in the control of body weight and blood glucose.

Abstract The major immunological reactions after an allogeneic bone marrow transplantation (BMT) are graft rejection and graft-versus-host disease (GVHD). GVHD can be prevented by T-cell depletion of the allogeneic BM graft, but the beneficial effect of T-cell depletion on the incidence of GVHD is counterbalanced by a higher incidence of graft failure. One option for the prevention of graft rejection after T-cell-depleted BM grafts is the administration of cytokines. Before applying cytokines after an allogeneic BMT, we considered it desirable to learn whether cytokines would alter the susceptibility of donor BM cells to host T cells. An in vitro assay was developed to investigate the role of the cytokines interleukin-1 (IL-1), IL-3, granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage CSF (GM-CSF) on the interaction between allosensitized, cytotoxic-T cells (CTLs) and T-cell- depleted BM cells. CTLs primed against the BM donor suppressed the formation of colonies consisting of granulocytes and macrophages (colony-forming unit GM). Colony formation was not inhibited by CTLs sensitized against a third party. Accordingly, the number of colonies scored in cocultures with CTLs sensitized to third party antigens were designated as 0% inhibition. A 66% inhibition of colony formation was observed for untreated BM cells at an effector:target (E:T) ratio of 1:1. Pretreatment of the BM cells with the cytokines G-CSF, GM-CSF, IL- 1, and IL-3 resulted in a 38% (P = .001), 53%, 66%, and 68% inhibition of colony formation, respectively, at E:T ratios of 1:1. G-CSF reduced the susceptibility of BM cells over a range from 4:1 to 1:16 (E:T ratios). GM-CSF had only significant influence at the lower E:T ratios (1:4 and 1:16). These in vitro data indicate that G-CSF could protect BM cells from killing by allosensitized CTLs and suggest that administration of these cytokines might potentially reduce the susceptibility of T-cell-depleted allogeneic BM grafts to host T-cell- mediated rejection.

An electronic-based business model (BM) is the new paradigm in business model innovation (BMI). In order to adapt to an ever-changing and extremely volatile Internet environment, an enterprise needs a systematic approach and tools to improve its existing business model or create a new one. This study analyzes the issues and system requirements for collaborative business model innovation relating to (1) BM design, (2) BM innovative system design, and (3) moral and intellectual property. Focusing on level (1) BM design, this study develops a systematic business model innovation approach based on the business model canvas (BMC) with nine building blocks and integrates the innovation radar (IR) with twelve key dimensions. Based on level (2), the study proposes a suitable collaborative BMI environment to enable the planning of a BM innovative design support system through virtual innovation teams (VITs), and to understand the system's functional requirements. Using the designed environment, this study develops the architecture of a BM knowledge support service environment based on cloud technology. To verify the proposed method, a bookstore is used as a case study. This study engages in innovative research in order to design a conceptual and systematic BMI approach.

The aquaculture sector stands at a crossroad because of the important changes in the business environment. Demand and competition for food is growing worldwide, fishery sector reached its limits and in this regard farmed fish sector represents a viable solution for food supply. A sustainable development of small business is recommended in order to develop knowledge and skills to support the growth of world population. In this view knowledge management for innovation is crucial to promote sustainable business models (BM) that can achieve a solid economic performance and at the same time take care of the natural environment. The purpose of this chapter is to contribute to the literature about sustainable BMs by an in-depth case study of a small fish farming company which developed competitiveness based on own tacit knowledge. The exemplary case study of a sustainable BM in aquaculture has been analyzed by use of an enhanced BM canvas that links various market oriented elements of a BM with the needs of society.

Effective repair of vascular injury requires assembly of a secure fibrin patch at the injury site. A secure fibrin patch must be anchored to the injury site, else it becomes an embolus. Using enzyme linked immunoassay (ELISA), we have evaluated the binding of fibrinogen (F) to single as well as combinations of the subendothelial BM components including laminin (L), type IV collagen (C), and dermatan sulfate (D). Tests were performed using plates coated over night at either 4°C or 37°C for one hour with individual BM or combinations or BM components. Results indicate that F strongly binds to both D and type IV collagen. Binding of F to L was approximately 50% compared to C or D. Combinations of C, L and D were studied with mole ratios of L and D normalized to C. Thus, when the mole ratio of L was increased from 0.1 to 10 relative to C, the amount of F bound to the plate coated with C and L decreased by 30%. When both D and L were added to C and the binding of F to the coated plate evaluated, increasing the mole ratio of D from 1 to 10 relative to C and L (C:D:L=1:1:0-10), increased the binding of F two fold. If the mole ratio of L was increased by a factor of 10 compare to C, and D varied form 0 to a 10 mole excess compared to C, (C:L:D=1:10:0-10) the increase in F binding was only increased by 1/3. Therefore, L decreases the binding of F by C, while D strongly increases the binding of F. These data suggest that an important interaction between the endothelial basement membrane and fibrin exists and the mole ratio between CLD is critical in determining the extent of the interaction. The interaction between F and C,L,D may underlie the mechanism by which a fibrin clot is anchored and stabilized to the injury site.

In previous studies, we have reported that i) the basement membrane (BM) underlying endothelial cells was initially throm-boresistant; ii) 13-hydroxyoctadecadienoic acid (13-HODE) synthesized by endothelial cells from linoleic acid via the lipoxygenase pathway, contributed to the thromboresistance of the endothelium; and iii) salicylate (SAL) increased injured vessel wall thrombogenecity. Therefore, we performed studies to determine the relationship between injured vessel wall thrombogenecity, vessel wall 13-HODE and cAMP levels, and salicylate treatment. Injured vessel wall thrombogenecity was measured as the number of H-adenine platelet (3H-PLT) adherent to the subendothelial BM exposed by air injury in carotid arteries of rabbits treated with 0 or 100 mg/kg of SAL bid, given orally2. Vessel wall 13-HODE was measured as the amount of 13-HODE/cm produced by the vessel wall following stimulation with 10μ/M linoleic acid, and measured by HPLC. Vessel wall cAMP levels were measured by RIA. Four hours after air injury, there was 25.4 ± 2 3 2H-PLT/cm2 of exposed BM. This was associated with 15.9 ng/cm2 of 13-HODE and 308 pM/cm2 of cAMP (Table 1). In contrast, in rabbits treated with SAL, there was a 2-fold increase in platelet adhesion onto the injured carotid arteries. The increase in platelet adhesion was associated with a 65% decrease in 13-HODE production by the vessel wall and a modest (20%) decrease in cAMP level.We conclude that the lipoxygenase derived linoleic acid metabolite, 13-HODE contributes not only to the thromboresis-tance of the endothelium, but also to its underlying basement membrane.