Alsaffar, Fatimah (2017) The Molecular Characterisation of TIMP3 Mutations Responsible for Sorsbys Fundus Dystrophy: is there a link to Age-related Macular Degeneration. PhD thesis, The University of Sheffield. ...
TIMP-3 (Tissue inhibitor of metalloproteinases 3) is a secreted extracellular matrix protein, metalloprotease inhibitor. It forms complexes with metalloproteinases (such as collagenases) and irreversibly inactivates them by binding to their catalytic zinc cofactor. TIMP-3 is critical to the maintenance of tissue homeostasis by suppressing the proliferation of quiescent tissues in response to angiogenic factors and by inhibiting protease activity in tissues undergoing remodelling of the extracellular matrix. Defects in TIMP-3 are the cause of Sorsby fundus dystrophy (SFD). SFD is a rare autosomal dominant macular disorder with an age of onset in the fourth decade. It is characterized by loss of central vision from subretinal neovascularization and atrophy of the ocular tissues. Generally, macular disciform degeneration develops in the patients eye within 6 months to 6 years ...
Sorsby fundus dystrophy (SFD) [MIM:136900]: Rare autosomal dominant macular disorder with an age of onset in the fourth decade. It is characterized by loss of central vision from subretinal neovascularization and atrophy of the ocular tissues. Generally, macular disciform degeneration develops in the patients eye within 6 months to 6 years. {ECO:0000269,PubMed:7550309, ECO:0000269,PubMed:7894485, ECO:0000269,PubMed:8634721, ECO:0000269,PubMed:8728699, ECO:0000269,PubMed:8981947}. Note=The disease is caused by mutations affecting the gene represented in this entry ...
Chemically and conformationally authentic active domain of human tissue inhibitor of metalloproteinases-2 refolded from bacterial inclusion ...
Wyrażam zgodę na otrzymywanie od SFD S.A. z siedzibą w Opolu na podany przeze mnie adres e-mail informacji handlowych, w tym o promocjach, rabatach, wydarzeniach i ofertach. (opcjonalnie ...
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Purpose: Polymorphisms in tissue inhibitor of metalloproteinase 3 (TIMP3) have been associated with Sorsby fundus dystrophy (SFD) and age-related macular degeneration. Toward a molecular understanding of TIMP3 dysfunction, we pursued quantitative proteomic analyses of the retina and choroid from TIMP-3 knockout (KO) mice and knockin (KI) mice expressing the TIMP3 S156C mutation that causes SFD.. Methods: Soluble proteins from isolated retinas and choroid-containing posterior globes from TIMP3 KO mice (n = 5 mice), KI homozygotes (n = 5), KI heterozygotes (n = 4), and wild-type mice (n = 7) were quantified by iTRAQ technology. Protein was digested with trypsin, peptides labeled with iTRAQ tags, fractionated by strong cation exchange chromatography, and peptides were analyzed by LC MS/MS. Proteins were identified using the Swiss-Protein database and quantified using code written in R. Proteins quantified with ≥ 2 unique peptides/protein in ≥ 3 mice/strain were considered significantly altered ...
TY - JOUR. T1 - Tissue inhibitor of metalloproteinases-3 promoter methylation is an independent prognostic factor for bladder cancer. AU - Hoque, Mohammad Obaidul. AU - Begum, Shahnaz. AU - Brait, Mariana. AU - Jeronimo, Carmen. AU - Zahurak, Marianna. AU - Ostrow, Kimberly Laskie. AU - Rosenbaum, Eli. AU - Trock, Bruce. AU - Westra, William H.. AU - Schoenberg, Mark. AU - Goodman, Steven N.. AU - Sidransky, David. PY - 2008/2. Y1 - 2008/2. N2 - Purpose: TIMP-3 (tissue inhibitor of metalloproteinases-3) is 1 of 4 members of a family of proteins that were originally classified according to their ability to inhibit matrix metalloproteinases. We analyzed TIMP-3 methylation in 175 urine sediment DNA samples from patients with bladder cancer with well characterized clinicopathological parameters, including patient outcome. Materials and Methods: We examined urine sediment DNA for aberrant methylation of 9 genes, including TIMP-3, by quantitative fluorogenic real-time polymerase chain reaction. ...
The active forms of all of the matrix metalloproteinases (MMPs) are inhibited by a family of specific inhibitors, the tissue inhibitors of metalloproteinases (TIMPs). Inhibition represents a major level of control of MMP activity. A detailed knowledge of the mechanisms controlling TIMP gene expression is therefore important. We have isolated a genomic clone of the human TIMP-1 gene. A 3 kbp XbaI fragment has been sequenced; this fragment contains 1718 bp 5′ flanking sequences, exon 1, a 929 bp intron 1 and part of exon 2. Computer analysis reveals 10 consensus sequences for Sp1, six for activating protein 1 (AP-1), six for polyoma enhancer A3 (PEA3), 12 for AP-2 and five CCAAT boxes. The region hybridizing with a murine TIMP-1 promoter fragment has been subcloned and analysed further. RNase protection identifies six transcription start points, making exon 1 up to 48 bp in length. Transient transfection of promoter-chloramphenicol O-acetyltransferase reporter constructs into primary human ...
Food Sources Most infant formulas usually contain vegetable oils that provide about 10в15 major fatty acids (43). A3. ПппппDisease basal laminar drusen Doyne honeycomb retinal dystrophy (malattia leventinese) Sorsby fundus dystrophy central areolar choroidal dystrophy AMD-like late-onset maculopathy North Carolina macular dystrophy OMIM Mode of phenotype inheritance number 126700 AR Associated gene CFH EFEMP1 (fibulin-3) TIMP3 peripherinRDS peripherinRDS unknown (MCDR1 locus) Reference(s) this thesis 182 183 this thesis 143 184 пппп126600 136900 215500 - 136550 Kamagra kaufen in der apotheke AD AD AD AD пппппппппAD, autosomal dominant; AMD.
Dr. Eric Capps will have to verify you as a patient. Once you are verified, you can write a patient review. Please only send a request if you already are a patient of Eric Capps ...
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Another thing that I did was to start looking at the CAPPs for this week. I mentioned SAQs and CAPPs before, but I havent really told you much about them yet. You can read the gist about them on the CCLCM portal if you follow the link that I told you about earlier. (Remember to log in as "guest" for both your ID and PW. Then click on the Cardio/Pulmonary block link, and you can read about the SAQs and CAPPs.) The SAQs are multiple choice questions that cover anatomy, physiology, pharmacology, histology, and whatever else weve been covering that week. There are thirty of them, and you have to submit them first before you can submit the CAPPs. However, the SAQs are not available until Friday afternoon, while the CAPP questions are available on Wednesday afternoon. So we are able to start thinking about the CAPPs before we get the SAQs. There are two CAPPs each week, although the two for this week have multiple subparts--I hate when they do that. The CAPPs are essay questions that should take ...
A tissue inhibitor of metalloproteinases (TIMP)-1 was isolated from human polymorphonuclear leukocytes (PMNL) in a complex with latent 95-kDa gelatinase (matrixmetalloproteinase, MMP-9). It was separated from the enzyme by gel fitration in the presence of SDS. Using a competitive ELISA procedure, we determined that 10% of the isolated gelatinase was complexed with TIMP-1. The presence of the inhibitor in isolated PMNL could also be demonstrated by indirect immunofluorescence using a specific antibody against TIMP-1. Cellular mRNA was isolated from PMNL, which were highly purified by separation via formylMet-Leu-Pro-stimulated chemotactic migration in a Boyden chamber. Using reverse-transcription PCR and Northern blotting, TIMP-1 mRNA was shown to be present in PMNL, suggesting that these cells are also capable of synthesizing TIMP-1 ...
A member of the family of TISSUE INHIBITOR OF METALLOPROTEINASES. It is a 21-kDa nonglycosylated protein found in tissue fluid and is secreted as a complex with progelatinase A by human fibroblast and uncomplexed from alveolar macrophages. An overexpression of TIMP-2 has been shown to inhibit invasive and metastatic activity of tumor cells and decrease tumor growth in vivo.
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TY - JOUR. T1 - Cellular distribution of tissue inhibitor of metalloproteimases-1 and-2 transcripts in human hepatocellalar carunoma(共著). AU - Ashida, Kouzou. PY - 1995. Y1 - 1995. M3 - Article. VL - 22. SP - 192. EP - 192. JO - HEPATOLOGY. JF - HEPATOLOGY. IS - 4. ER - ...
MMP-2, MMP-9 and their inhibitors TIMP-2 and TIMP-1 production by human monocytes in vitro in the presence of different forms of hydroxyapatite particles.. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
The Cleveland Indians selected the contract of infielder Jason Giambi on Monday and released reliever Matt Capps.Giambis contract was selected from Triple-A Columbus, but he will begin the season on the 15-day disabled list with a lower back strain and will be eligible to play on April 9
For the first time in more than two years, Carter Capps jogged in from the bullpen to a big league mound. He worked up a sweat. He recorded real outs. The significance of that was not lost on the 27-year-old right-hander even after all three of his runs ...
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TY - JOUR. T1 - The disintegrin-like metalloproteinase ADAM 10 is involved in coinstitutive cleavage of CX3CL1 (fractalkine) and regulates CX3CL1-mediated cell-cell adhesion. AU - Hundhausen, C.. AU - Misztela, D.. AU - Berkhout, Theo. AU - Broadway, N.. AU - Saftig, P.. AU - Reiss, K.. AU - Hartmann, D.. AU - Fahrenholz, F.. AU - Postina, R.. AU - Matthews, J.. AU - Kallen, K.J.. AU - Rose-John, S.. AU - Ludwig, A.. PY - 2003/8/15. Y1 - 2003/8/15. N2 - The CX3C chemokine fractalkine (CX3CL1) exists as a membrane-expressed protein promoting cell-cell adhesion and as a soluble molecule inducing chemotaxis. Transmembrane CX3CL1 is converted into its soluble form by defined proteolytic cleavage (shedding), which can be enhanced by stimulation withphorbol-12-myristate-13-acetate (PMA). PMA-induced CX3CL1 shedding has been shown to involve the tumor necrosis factor-alpha-converting enzyme (TACE), whereas the constitutive cleavage in unstimulated cells remains elusive. Here we demonstrate a role of ...
Balanced expression of proteases and their inhibitors is one prerequisite of tissue homeostasis. Metastatic spread of tumor cells through the organism depends on proteolytic activity and is the death determinant for cancer patients. Paradoxically, increased expression of tissue inhibitor of metalloproteinases-1 (TIMP-1), a natural inhibitor of several endometalloproteinases, including matrix metalloproteinases and a disintegrin and metalloproteinase-10 (ADAM-10), in cancer patients is negatively correlated with their survival, although TIMP-1 itself inhibits invasion of some tumor cells. Here, we show that elevated stromal expression of TIMP-1 promotes liver metastasis in two independent tumor models by inducing the hepatocyte growth factor (HGF) signaling pathway and expression of several metastasis-associated genes, including HGF and HGF-activating proteases, in the liver. We also found in an in vitro assay that suppression of ADAM-10 is in principle able to prevent shedding of cMet, which may be one
The protocol describes a novel, rapid, and no-wash one-step immunoassay for highly sensitive and direct detection of the complexes between matrix metalloproteinases (MMPs) and their tissue inhibitor of metalloproteinases (TIMPs) based on AlphaLISA® technology. We describe two procedures: (i) one approach is used to analyze MMP-9-TIMP-1 interactions using recombinant human MMP-9 with its corresponding recombinant human TIMP-1 inhibitor and (ii) the second approach is used to analyze native or endogenous MMP-9-TIMP-1 protein interactions in samples of human plasma. Evaluating native MMP-9-TIMP-1 complexes using this approach avoids the use of indirect calculations of the MMP-9/TIMP-1 ratio for which independent MMP-9 and TIMP-1 quantifications by two conventional ELISAs are needed. The MMP-9-TIMP-1 AlphaLISA® assay is quick, highly simplified, and cost-effective and can be completed in less than 3 h. Moreover, the assay has great potential for use in basic and preclinical research as it allows direct
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IntroductionThe tissue inhibitors of metalloproteinases (TIMPs) are naturally occurring proteins that specifically inhibit matrix metalloproteinases…
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The proteoglycan aggrecan is an important major component of cartilage matrix that gives articular cartilage the ability to withstand compression. Increased breakdown of aggrecan is associated with the development of arthritis and is considered to be catalyzed by aggrecanases, members of the ADAM-TS family of metalloproteinases. Four endogenous tissue inhibitors of metalloproteinases (TIMPs) regulate the activities of functional matrix metalloproteinases (MMPs), enzymes that degrade most components of connective tissue, but no endogenous factors responsible for the regulation of aggrecanases have been found. We show here that the N-terminal inhibitory domain of TIMP-3, a member of the TIMP family that has functional properties distinct from other TIMPs, is a strong inhibitor of human aggrecanases 1 and 2, with K(i) values in the subnanomolar range. This truncated inhibitor, which lacks the C-terminal domain that is responsible for interactions with molecules other than active metalloproteinases, is
Roswit W.T., McCourt D.W., Partridge N.C., Jeffrey J.J.. Two protein inhibitors of metalloproteinases (TIMP) were isolated from medium conditioned by the clonal rat osteosarcoma line UMR 106-01. Initial purification of both a 30-kDa inhibitor and a 20-kDa inhibitor was accomplished using heparin-Sepharose chromatography with dextran sulfate elution followed by DEAE-Sepharose and CM-Sepharose chromatography. Purification of the 20-kDa inhibitor to homogeneity was completed with reverse-phase high-performance liquid chromatography. The 20-kDa inhibitor was identified as rat TIMP-2. The 30-kDa inhibitor, although not purified to homogeneity, was identified as rat TIMP-1. Amino terminal amino acid sequence analysis of the 30-kDa inhibitor demonstrated 86% identity to human TIMP-1 for the first 22 amino acids while the sequence of the 20-kDa inhibitor was identical to that of human TIMP-2 for the first 22 residues. Treatment with peptide:N-glycosidase F indicated that the 30-kDa rat inhibitor is ...
To the Editor:. It was with great interest that I read the article by Tuomainen et al1 recently published in this journal on the association of matrix metalloproteinase (MMP)-8 and tissue inhibitor of MMP-1 (TIMP-1) with cardiovascular diseases. The authors measured both analytes in serum and concluded from their results that serum MMP-8 and the ratio of MMP-8 to TIMP-1 were useful biomarkers with prognostic and diagnostic significances in men with cardiovascular disease, especially in those with prevalent or subclinical arteriosclerosis.1 Although I am not experienced in this clinical field, I believe it might be meaningful to make the readership of this journal aware of an important issue that was obviously not considered by Tuomainen et al in their study design. It refers to the influence of blood sample processing as essential precondition for the correct determination of circulating MMPs and TIMPs in peripheral blood. The effect of the type of blood sample, either collected as serum with or ...
Cellular pathways for induction of programmed cell death (PCD) have been identified, but little is known about specific extracellular matrix processes that may affect apoptosis along those pathways. In this study, a series of Burkitts lymphoma (BL) cell lines were assayed for their expression of tissue inhibitor of metalloproteinases (TIMP)-1. Results indicate that TIMP-1-positive BL lines show resistance to cold-shock-induced apoptosis. Furthermore, recombinant TIMP-1, but not TIMP-2 or a synthetic metalloproteinase inhibitor (BB-94), confers resistance to apoptosis induced by both CD95-dependent and -independent (cold shock, serum deprivation, and gamma-radiation) pathways in TIMP-1-negative BL lines. TIMP-1 suppression of PCD is not due to metalloproteinase inhibition, as reduction and alkylation of the TIMP-1 did not abolish this activity. Retroviral induction of TIMP-1 not only resulted in cell survival but also in continued DNA synthesis for up to 5 d in the absence of serum, while ...
Badr, A. M., Interleukin-6 induces secretion of tissue inhibitors of metalloproteinases by breast carcinoma cells, Pakistan Journal of Pharmaceutical Sciences, vol. 29, issue 6, pp. 1969-1975, 2016 ...
ADAM (a disintegrin and metalloproteinase) 10 is a key member of the ADAM family of disintegrin and metalloproteinases which process membrane-associated proteins to soluble forms in a process known as shedding. Among the major targets of ADAM10 are Notch, EphrinA2 and CD44. In many cell-based studies of shedding, the activity of ADAM10 appears to overlap with that of ADAM17, which has a similar active-site topology relative to the other proteolytically active ADAMs. The tissue inhibitors of metalloproteinases, TIMPs, have proved useful in the study of ADAM function, since TIMP-1 inhibits ADAM10, but not ADAM17; however, both enzymes are inhibited by TIMP-3. In the present study, we show that, in comparison with ADAM17 and the MMPs (matrix metalloproteinases), the N-terminal domains of TIMPs alone are insufficient for the inhibition of ADAM10. This knowledge could form the basis for the design of directed inhibitors against different metalloproteinases.. ...
Matt Capps, who has pitched seven seasons in the big leagues through 2011, went 9-1 in 2006 on a team that lost 95 games. He served as Pittsburghs closer for two and a half years. Control specialist Capps was taken by the Pittsburgh Pirates in the 7th round of the 2002 amateur draft. He was signed by scout Jack Powell instead of going to Louisiana State University. He debuted with the GCL Pirates, saving one game and winning one in 7 appearances, posting a 0.69 ERA and an uncharasteristic six walks in 13 innings. In 2003, Matt allowed three runs in five innings, walking four with the Lynchburg Hillcats and had a 5-1 record with a 1.87 ERA in 10 starts for the GCL Pirates. He struck out 54, allowed 40 hits and walked nine in 63 innings. He was named the top starting pitcher in the Gulf Coast League and finished fourth in ERA. He led the league in innings pitched. In 2004, Matt struggled with the Hickory Crawdads (2-3, 10.07, a .402 opposing average) and was 3-5, 4.85 for the Williamsport ...
The controversial passenger-profiling system has officially been cancelled, but critics remain appropriately skeptical about what its death means. Below, a brief sampling of perspectives: Edward Hasbrouck @ The Practical Nomad: Hours after announcing that the CAPPS II airline passenger...
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Catalog No :RS01Ab0134Organism- HumanClonality :MonoclonalHost :MouseConcentration :500ug/mlApplication :WB, ICC, IHC-P, IHC-F, ELISA Immunoglobulin Type: IgGPurification: Affinity ChromatographyConjugate: No Conjugate IMMUNOGEN INFORMATIONImmunogen: Recombinant TIMP1 (Thr25~Ala207) expressed in E.coli.ANTIBODY SPECIFI
Based on automated MP annotations supported by experiments on knockout mouse models. Click on icons to go to all Timp3 data for that phenotype. ...
Epic Games CEO Mike Capps is somewhat in awe of the Nintendo Wiis ability to win over consumers despite the consoles shortcomings, calling it kind of like a weird virus. The Wiis virus-like nature comes from its ability to infect new players with instant enthusiasm, Capps explained to IGN. \[Y\]ou buy it and you play \[…\]
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MMPs and TIMPs grouped according to the MFI (low MFI: Goutallier score 0-1 (n = 10); high MFI: Goutallier score 2-4 (n = 20)). qRT-PCR was performed to anal
Tissue inhibitor of metalloproteinase-3 (TIMP-3) is a dual inhibitor of the matrix metalloproteinases (MMPs) and some adamalysins, two families of extracellular and cell surface metalloproteinases that function in extracellular matrix turnover and the shedding of cell surface proteins. The mechanism of inhibition of MMPs by TIMPs has been well characterized, and since the catalytic domains of MMPs and adamalysins are homologous, it was assumed that the interaction of TIMP-3 with adamalysins is closely similar. Here we report that the inhibition of the extracellular region of ADAM-17 (tumor necrosis factor alpha-converting enzyme (TACE)) by the inhibitory domain of TIMP-3 (N-TIMP-3) shows positive cooperativity. Also, mutations in the core of the MMP interaction surface of N-TIMP-3 dramatically reduce the binding affinity for MMPs but have little effect on the inhibitory activity for TACE. These results suggest that the mechanism of inhibition of ADAM-17 by TIMP-3 may be distinct from that for MMPs. The
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Murine tissue inhibitor of metalloproteinases-1 (mTIMP-1) was expressed in baculovirus-infected insect cells (Sf9). The protein secreted into the culture medium was purified to homogeneity by means of heparin-Sepharose CL-6B and FPLC. The purified protein showed metalloproteinase-inhibitory activity in two independent assays: reverse zymography and inhibition of collagenase activity. Digestion of the recombinant TIMP-1 with peptide-N-glycanaseF revealed that both N-glycosylation sites are used. I-125-mTIMP-1 intraveneously injected into a male Sprague Dawley rat disappeared within 2 min from the circulation. 5 min after injection more than 50% of the I-125-mTIMP-1 were found in the liver and 20% in the kidneys. At later times, trichloroacetic-acid-soluble material accumulated in the intestinal tract ...