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At least 937 records · Page 52Linked to original sources
PubMed2004

Beneficial influence of platelets on antibiotic efficacy in an in vitro model of Staphylococcus aureus-induced endocarditis.

Platelets contribute to antimicrobial host defense against infective endocarditis (IE) by releasing platelet microbicidal proteins (PMPs). We investigated the influence of thrombin-stimulated human platelets on the evolution of simulated IE in the presence and absence of vancomycin or nafcillin. Staphylococcus aureus strains differing in intrinsic susceptibility to PMPs or antibiotics were studied: ISP479C (thrombin-induced PMP-1 [tPMP-1] susceptible; nafcillin and vancomycin susceptible), ISP479R (tPMP-1 resistant; nafcillin and vancomycin susceptible), and GISA-NJ (tPMP-1 intermediate-susceptible; vancomycin intermediate-susceptible). Platelets were introduced and thrombin activated within the in vitro IE model 30 min prior to inoculation with S. aureus. At 0 to 24 h postinoculation, bacterial densities in chamber fluid and simulated endocardial vegetations (SEVs) were quantified and compared among groups. Activated platelets alone, or in combination with antibiotics, inhibited the proliferation of ISP479C in chamber fluid or SEVs over the initial 4-h period (P < 0.05 versus controls). Moreover, nafcillin-containing regimens exerted inhibitory effects beyond 4 h against ISP479C in both model phases. By comparison, activated platelets inhibited GISA-NJ proliferation in SEVs but not in chamber fluid. The combination of platelets plus nafcillin or vancomycin significantly inhibited proliferation of the GISA-NJ strain in SEVs compared to the effect of platelets or antibiotics alone (P < 0.05). In contrast, platelets did not significantly alter the antistaphylococcal efficacies of nafcillin or vancomycin against ISP479R. These data support our hypothesis that a beneficial antimicrobial effect may result from the interaction among platelets, PMPs, and anti-infective agents against antibiotic-susceptible or -resistant staphylococci that exhibit a tPMP-1-susceptible or -intermediate-susceptible phenotype.

Animals↗
PubMed1999

Assessment of coronary stenoses by Doppler wires: a validation study using in vitro modeling and computer simulations.

The present study evaluates the use of intracoronary velocity measurements by Doppler guidewires for assessing coronary obstructions. In vitro experiments were performed in a flow model using acrylic phantoms of coronary stenoses with different configurations (stenosis area: 56%, 75% and 89%; stenosis length: 1 and 5 mm; stenosis border: tapering or abrupt). Nonpulsatile laminar flow conditions of a test fluid were established at flow rates ranging from 0.5 to 2.0 mL/s to simulate baseline flow and flow after vasodilation. Peak Doppler velocity was measured proximal to, within and distal to the model stenoses. Computer simulations were employed to calculate radial flow profiles with and without a Doppler wire aligned with the vessel center. In 84 in vitro flow experiments, peak Doppler velocity correlated well with the average flow velocity as calculated from the actual flow rate and the vessel's cross-sectional area proximal to (r = 0.98, SEE = 1.4, p < 0.001) and within (r = 0.97, SEE = 16.4, p < 0.001) the stenosis. However, the ratio of calculated average velocity to Doppler-measured peak velocity was significantly different from 0.5, the expected value for a parabolic flow profile (0.76+/-0.08, 0.81+/-0.14; p < 0.001). Acceptable accuracy was found for the Doppler estimation of stenosis severity using the continuity equation (error: 0.9+/-1.2% and -4.6+/-3.5% for stenosis with a length of 5 mm and 1 mm, respectively). Doppler velocity reserve significantly underestimated the true flow reserve for the 56% and 75% stenoses (p < 0.01). Computer simulations demonstrated significant alterations of flow profiles by the wire, which explained the observed underestimation of the true flow reserve by the Doppler velocity reserve. Thus, Doppler guidewire measurements of intracoronary flow velocities are useful to assess the severity of coronary stenoses. However, the in vitro results and computer simulations indicate that guidewires alter the flow profile, so that Doppler velocity reserve may underestimate the true flow reserve.

Analysis of Variance↗
PubMed1992

[Significance of the combined treatment with isepamicin and piperacillin in an in vitro model for complicated cystitis operated by automatic simulator apparatus for urinary concentration].

Isepamicin (ISP) and piperacillin (PIPC) were shifted to the urinary concentration by employing an in vitro complicated cystitis model operated by a computer-controlled automatic simulator for urinary concentration, and administrated to bacteria in the urinary bladder model (Pseudomonas aeruginosa: P. aeruginosa, initial cell concentration: 10(7) cfu/ml). In this case, effects by single treatment with ISP or PIPC on cell number curves were examined. Further, significance of the combined treatment with ISP and PIPC were investigated by changing the order of each treatment. And following the results were obtained. 1. In a single treatment with PIPC the cell concentration was minimum (10(4) cfu/ml) at 9th hour after its treatment and thereafter, regrowth to the same level as the initial concentration was observed at 16th hour. 2. In the case of single treatment with ISP, the cell concentration became minimum (10(2) cfu/ml) at 13th hour after the treatment and raised to the same concentration as the initial one at 25th hour. 3. In the combined treatment, the cell concentration was minimum (less than 10(1) cfu/ml) at 26th hour in the case of prior treatment with ISP. Thereafter, regrowth was observed and the cell concentration at 42nd hour reached to the initial cell concentration. 4. In simultaneous treatment with ISP and PIPC, the cell concentration at 24th hour was minimum (10(1) cfu/ml) and reached to the same level as the initial one after regrowth. From these results, it was found that the combined treatment with ISP and PIPC caused more reduction of the cell concentration than either single treatment. Further, regrowth of the cells was suppressed for longer duration.(ABSTRACT TRUNCATED AT 250 WORDS)

Computer Simulation↗
PubMed2003

Prediction of precipitation-induced phlebitis: a statistical validation of an in vitro model.

To avoid phlebitis, new intravenous (IV) parenterals are often screened by injection into animals. This method is not only expensive and time consuming, it is also detrimental to the animals. An alternate method, focusing on precipitation as the cause, uses an in vitro dynamic injection model that requires less money and time and reduces the need for live models. Validation of the dynamic injection apparatus, for predicting mechanical phlebitis, is established. Twenty-one currently marketed IV products were injected into isotonic Sorenson's phosphate buffer flowing at 5 mL/min. The resulting opacities, produced by precipitation, are measured in an ultraviolet flow cell. These opacity data, coupled with literature reports on phlebitis occurrence, were used to generate a logistic regression that indicates the probability of phlebitis given an opacity value measured by the apparatus. Regression results are supported by a receiver operator characteristic curve that establishes the most ideal cut-off opacity value. This opacity value provides the highest combined sensitivity (statistical power) and specificity while minimizing false-positive and false-negative results. Both analyses show that an opacity value of 0.003 best delineates phlebitic and nonphlebitic products. Measures of sensitivity (0.83), specificity (0.93), positive predictive value (0.93), and negative predictive value (0.78) indicate the model's predictive accuracy and reliability. These results support the use of the dynamic model in place of animals for preliminary phlebitis testing of new IV injectables.

Chemical Precipitation↗
PubMed1995

Vesicle dynamics during regulated secretion in a novel pancreatic acinar cell in vitro model.

Neonatal rat pancreatic acinar cells were isolated in long-term culture to study vesicular trafficking in a regulated secretory epithelial cell. These cultured cells are of a reduced thickness to facilitate cell biological applications, yet have maintained a differentiated state capable of manufacturing and releasing zymogen from defined cellular locations in response to physiological concentrations of secretagogues. Cells observed with video and electron microscopy display numerous dense zymogen-containing granules which are interconnected by fine filamentous strands. Exposure of 6-day cultured cells to 2 x 10(-9) M of the hormone agonist cholecystokinin octapeptide (CCK-8), or 2 to 5 microM 12-O-tetradecanoylphorbol-13-acetate (TPA), stimulates an increase in directed granule movements to a defined perinuclear region of the cell where they undergo exocytosis. This dramatic exocytic event can be observed readily by video microscopy or measured with enzymatic amylase assays. High voltage electron and scanning electron microscopy reveal that these stimulated cells undergo pronounced changes in shape. Concomitantly, secreting cells insert the integral zymogen granule membrane protein (GP-2) into a defined region of the apical plasmalemma while forming numerous membranous surface projections; both are processes consistent with a regulated exocytic event. These acinar cells provide a novel, fully functional, differentiated exocrine epithelial cell model which possess a receptor signaling cascade capable of stimulating the release of zymogen. To our knowledge, the observations presented here provide the first direct evidence that a) secretory agonists initiate directed transport and polarized delivery of zymogen granules to a defined cellular location for subsequent release, b) zymogen granules are physically interconnected in both resting and activated cells, c) cells undergo active changes in shape and form during secretion, and d) membranous blebs accumulate at a region of the cell surface where exocytosis occurs. The potential contributions of this in vitro cell model to the study of regulated vesicular transport, exocytosis, and membrane retrieval are discussed.

Animals↗
PubMedDate not supplied

Anatomically shaped internal carotid artery aneurysm in vitro model for flow analysis to evaluate stent effect.

BACKGROUND AND PURPOSE: Stent implantation alone might not be sufficient to produce definitive treatment of cerebral aneurysms. Therefore, extended experimental work is needed to improve results. We show the feasibility of using an in vitro anatomically shaped elastic model for flow evaluation before and after stent implantation. METHODS: Based on human vascular casting, an anatomic elastic internal carotid artery model, including an aneurysm on the supraclinoid portion, was manufactured. The model was connected to a circulatory loop to simulate physiological flow. After visualization of the flow by using glass particles and laser sheet translumination, the digitally recorded data were transferred for computer analysis. Intra-saccular flow pattern changes and the vortex velocity reduction induced by the stent were investigated qualitatively and quantitatively. RESULTS: The distal neck of the aneurysm behaved as a flow divider. Therefore, it was directly exposed to the hemodynamic stress. Inside the sac, a well-defined vortex formed and progressed along the wall toward the proximal neck. After stent implantation this pattern changed significantly; the vortex appeared more dispersed and its residence time increased. The velocity reduction was 32%. Velocity peak was observed close to the distal neck in both cases. CONCLUSION: In vitro anatomic elastic models are feasible for flow evaluation with laser sheet translumination. In our model, stent implantation resulted in hemodynamic changes that might favor the exclusion of the aneurysm from the circulation and can prevent regrowth of the aneurysmal sac.

Carotid Artery Diseases↗
PubMed1997

NOD fetal thymus organ culture: an in vitro model for the development of T cells involved in IDDM.

This paper introduces a model which incorporates fetal thymus organ culture (FTOC) from NOD mice to replicate thymic development of diabetogenic T cells. NOD fetal pancreas organ culture (FPOC) co-cultured with 13-16 day NOD FTOC for an additional 14-21 days produced less insulin than FPOC cultured alone. Insulin production from the FTOC of non-diabetic strains C57BL/6 and BALB/c was not inhibited by co-culture with FTOC from their syngeneic counterparts. Sections of the NOD co-cultures showed peri-islet infiltration with lymphocytes. Insulin reduction by FTOC/FP co-culture was prevented by co-culture of the NOD FT with FT from immunologically incompetent C.B-17 SCID/SCID mice. Co-culture of NOD FP with NOD FT prior to the development of T cells prevented generation of diabetogenic FTOC. Thus, early exposure of NOD T cell precursors to the thymic stromal elements of C.B-17 SCID/SCID FT or to islet antigens can negatively select for diabetogenic T cells or activate immuno-regulatory cells that can suppress diabetogenic T cell activity. The addition of blocking F(ab')2 fragments of anti-CD3epsilon monoclonal antibody to NOD FTOC/FP co-cultures prevented insulin reduction, implicating a role for TcR-mediated recognition in this "in vitro IDDM" model. The addition of activating whole anti-CD3epsilon caused the complete ablation of insulin production in FTOC/FP co-cultures from all strains tested. Transfer of unprimed syngeneic FTOC cells to prediabetic NOD mice prevented the onset of IDDM while transfer of islet-cell primed FTOC/FP cells slightly increased disease incidence. These data suggest that while diabetogenic T cells are present in the FT, they are normally suppressed, even after organ culture. However, these cells can induce the destruction of islet cells, in vitro and in vivo, if they are appropriately activated with pancreatic tissue.

Adoptive Transfer↗
PubMed2003

Developmental aspects of blood-brain barrier (BBB) and rat brain endothelial (RBE4) cells as in vitro model for studies on chlorpyrifos transport.

The mammalian central nervous system (CNS) is characterized by the blood-brain barrier (BBB), a restrictive barrier endowed with the maintenance of homeostatic control of an optimal milieu within the brain. Whereas in tissues other than the CNS, concentrations of various metabolites (amino acids, K+) can undergo frequent fluctuations, the CNS must keep rigorous control over the extracellular cerebral fluid composition, preventing the mirroring of transient fluctuations in blood, because abrupt changes in these metabolites can translate to aberrant CNS function. The BBB is a specialized structure accomplished by individual endothelial cells that are continuously linked by tight junctions. This brief review will address pertinent issues to development of the BBB. Particular emphasis will be directed at the role of astrocytes in the induction and maintenance of the restrictive properties of this barrier, and the utility of in vitro culture models in surveying transport kinetics, exemplified by recent studies with the pesticide, chlorpyrifos.

Animals↗
PubMed2005

Enhancement of transformed foci and induction of prostaglandins in Balb/c 3T3 cells by palytoxin: in vitro model reproduces carcinogenic responses in animal models regarding the inhibitory effect of indomethacin and reversal of indomethacin's effect by exogenous prostaglandins.

Cell transforming activity of palytoxin, a non-TPA type tumor-promoter, was investigated with the two-stage transformation assay using Balb/c 3T3 cells. Palytoxin showed potent promoting activity; treatment at 1.9 pM or more increased the number of transformed foci after initiation by 3-methylcholanthrene (MCA). Determination of prostaglandin (PG) E2 and PGF(2alpha) concentrations in the culture medium revealed that palytoxin (1.9-3.7 pM for 24 h) stimulated the production of PG in Balb/c 3T3 cells (the concentration reached 3-4 microM), and treatment with PGE2 or PGF(2alpha) itself increased the number of transformed foci of Balb/c 3T3 cells after initiation by MCA. Neither palytoxin nor PGs showed initiating activity. Indomethacin suppressed the promoting activity of palytoxin, but not that of PGE2 and PGF(2alpha). Interestingly, concomitant treatment with PGE2 or PGF(2alpha) in addition to indomethacin markedly reversed the suppressive effect of indomethacin. These findings indicated that the in vitro transformation model could reproduce experiments that have been performed in animal models regarding the inhibitory effect of indomethacin on carcinogenic responses and reversal of indomethacin's effect by exogenous prostaglandin and, therefore, may provide insight into molecular modes of action of palytoxin. In the present study, palytoxin also induced prostaglandin synthesis, and therefore, the Balb/c 3T3 cell model should provide insight into the molecular mechanism by which palytoxin regulates prostaglandin biosynthesis.

Acrylamides↗
PubMed2006

Directing adenovirus across the blood-brain barrier via melanotransferrin (P97) transcytosis pathway in an in vitro model.

Adenovirus serotype 5 (Ad5) is widely used in the development of gene therapy protocols. However, current gene therapy strategies involving brain are mostly based on intra-cranial injection. A major obstacle for systemically administered vectors to infect brain tissue is the blood-brain barrier (BBB). One strategy to cross the BBB is transcytosis, a transcellular transport process that shuttles a molecule from one side of the cell to the other side. Recently, melanotransferrin (MTf)/P97 was found to be able to cross the BBB and accumulate in brain. We thus hypothesize that re-directing Ad5 vectors to the MTf transcytosis pathway may facilitate Ad5 vectors to cross the BBB. To test this hypothesis, we constructed a bi-specific adaptor protein containing the extracellular domain of the coxsackie-adenovirus receptor (CAR) and the full-length melanotransferrin (sCAR-MTf), and investigated its ability to re-direct Ad5 vectors to the MTf transcytosis pathway. We found this adaptor protein could re-direct Ad5 to the MTf transcytosis pathway in an in vitro BBB model, and the transcytosed Ad5 viral particles retained their native infectivity. The sCAR-MTf-mediated Ad5 transcytosis was temperature- and dose dependent. In addition, we examined the directionality of sCAR-MTf-mediated Ad5 transcytosis, and found the efficiency of apical-to-basal transcytosis was much higher than that of basal-to-apical direction, supporting a role of this strategy in transporting Ad5 vectors towards the brain. Taken together, our study demonstrated that re-directing Ad5 to the MTf transcytosis pathway could facilitate gene delivery across the BBB.

Adenoviridae↗
PubMed1993

Development of an in vitro model of Toxoplasma gondii cyst formation.

Toxoplasma gondii tissue cyst reactivation is a major pathogenic mechanism in ocular toxoplasmosis, disease associated with AIDS and organ transplantation. The mechanisms associated with cyst formation and reactivation have not been elucidated. The complexity of studying these issues in animal models has led to the development of in vitro tissue culture strategies for cyst formation. In the present study we have adopted the human embryonic lung fibroblast (HEL) as the host cell and have compared the cyst forming abilities of eight clinical isolates. We describe by transmission electron microscopy and quantitative light microscopy the development of cysts in vitro. The numbers of in vitro cysts increased with time for all isolates. Cyst cultures were stabilised by manipulation of the free parasite load, an observation not previously recorded. Thus, in this paper we describe a viable model for the analysis of the mechanisms of Toxoplasma cyst development.

Animals↗
PubMed1992

In vivo and in vitro models of the human colonic flora.

The study of colonic flora composition and metabolism presents considerable methodological problems. Attempts to circumvent these problems have led to the development of numerous in vitro and in vivo models to simulate the human colon and its microbial population. In terms of in vivo models, conventional laboratory animals have many limitations. Data of greater relevance to man can be obtained by using germ-free rodents associated with human colonic bacteria. The applications of such animals to studies of toxicity of chemicals and gastrointestinal infections are discussed. The advantages and disadvantages of the various in vitro systems for studying gut microflora and its metabolic activity (from simple static cultures to the more sophisticated continuous and semicontinuous flow models) are reviewed. The apparatus involved is described together with practical information on media, running conditions, and sampling. The bacteriological and metabolic criteria for establishing the similarity of the models to the in situ colonic flora are also discussed. The final sections of the review are devoted to the major applications (current and future) of the models, including fermentation studies on dietary fiber, metabolism of nutrients and foreign compounds (including carcinogens) in food, and the investigation of colonization resistance.

Anaerobiosis↗
PubMed1986

An in vitro model for polymorphonuclear-leukocyte-induced injury to an extracellular matrix. Relative contribution of oxidants and elastase to fibronectin release from amnionic membranes.

Alteration of the extracellular matrix by inflammatory cells is believed to be important in both lung injury and the subsequent restoration of lung architecture. Here we describe the results of the interaction between an acellular human amnionic membrane model and stimulated human polymorphonuclear neutrophils (PMN) in vitro. Polymorphonuclear neutrophil suspensions were placed on one surface of the amnion, and either the chemotactic peptide FMLP or the cell membrane activator phorbol myristate acetate (PMA) was placed on the opposite side of the amnion. Stroma and basement membrane sides of the amnion were separately exposed to the PMN. The PMN suspension was removed and centrifuged, and the supernatant was assayed for superoxide anion (O2-.) and for elastase activity. Injury to the acellular amnion was evaluated by transmission electron microscopy and by measurement of fibronectin (FN) released from the membrane matrix. Although both stimulants cause a concentration-dependent release of O2-., only PMA stimulated elastase release. These effects were similar when either the stroma or the basement membrane side was exposed to PMN. PMA-stimulated cells and supernatants from PMA-stimulated cells caused solubilization of membrane at different incubation times. Electron microscopy confirmed the disruption of the basement membrane of the amnion by PMA-stimulated PMN. Oxidant scavengers (SOD and catalase) did not prevent matrix degradation, and elastase inhibition by a specific chloromethylketone inhibitor diminished FN release on both sides of the amnion by activated PMN supernatants, but only on the basement membrane side by intact PMN. We conclude that in this model, elastase rather than oxygen radicals solubilizes FN from the matrix.

Amnion↗
PubMed2005

Activation of cerebral endothelium is required for mononuclear cell recruitment in a novel in vitro model of brain inflammation.

Brain inflammation is a common event in the pathogenesis of several neurological diseases. It is unknown whether leukocyte/endothelium interactions are sufficient to promote homing of blood-borne cells into the brain compartment. The role of mononuclear cells and endothelium was analyzed in a new experimental model, the isolated guinea-pig brain maintained in vitro by arterial perfusion. This preparation allows one to investigate early steps of brain inflammation that are impracticable in vivo. We demonstrate by confocal microscopy analysis that in vitro co-perfusion of pro-inflammatory agents and pre-activated fluorescent mononuclear cells induced endothelial expression of selectins and intracellular adhesion molecule-1 in correspondence of arrested mononuclear cells, and correlates with a moderate increase in blood-brain barrier permeability. Separate perfusion of pro-inflammatory agents and mononuclear cells induced neither mononuclear cell adhesion nor adhesion molecule expression. We demonstrate that co-activation of mononuclear cells and cerebral endothelium is an essential requirement for cell arrest and adhesion in the early stages of experimental cerebral inflammation.

Animals↗
PubMed2003

Pancreatic precursors and differentiated islet cell types from murine embryonic stem cells: an in vitro model to study islet differentiation.

Embryonic stem (ES) cells differentiating in vitro reproduce many facets of early embryonic development, including the expression of developmentally regulated transcription factors and the differentiation of multipotent precursor cells. ES cells were evaluated for their ability to differentiate into pancreatic and islet lineage-restricted stages including pancreatic duodenal homeobox 1 (PDX1)-positive pancreatic precursor cells, early endocrine cell progenitors, and islet hormone-producing cells. Following growth and differentiation in nonselective medium containing serum, murine ES cells spontaneously differentiated into cells individually expressing each of the four major islet hormones: insulin, glucagon, somatostatin, and pancreatic polypeptide. PDX1 immunostaining cells appeared first, before hormone-positive cells had emerged. Hormone-positive cells appeared within focal clusters of cells coexpressing PDX1 and the nonclassical hormone markers peptide YY (YY) and islet amyloid polypeptide (IAPP) in combination with the definitive hormones, characteristic of endocrine cells appearing during early pancreaticogenesis. This system allows the investigation of many facets of islet development since it promotes the appearance of the complete range of islet phenotypes and reproduces important developmental stages of normal islet cytodifferentiation in differentiating ES cell cultures.

Amyloid↗
PubMed1986

Insulin resistance in uremia: in vitro model in the rat liver using human serum to study mechanisms.

We have previously demonstrated in a rat model of chronic uremia that the liver is resistant to insulin. To further investigate the mechanism(s) of insulin resistance in uremia, primary cultures of normal rat hepatocytes were incubated with varying dilutions (1/10 to 1/10,000) of sera from undialyzed end stage uremic and normal humans for 20 hours. We then studied insulin action, binding, and postbinding events. Dilutions of uremic sera as low as 1/1,000 rendered the hepatocytes resistant to maximal concentrations of insulin with regard to [14C]acetate incorporation into lipids. The dose response curve for insulin-stimulated [14C]aminoisobutyric acid uptake demonstrated a shift to the right in hepatocytes incubated with uremic sera when compared with those incubated with normal sera. The 125I-insulin binding sites and affinity, 125I-insulin internalization and degradation, insulin receptor structure, autophosphorylation of the insulin receptor, and its tyrosine-specific kinase activity were normal in the hepatocytes rendered resistant to insulin by uremic sera. However, these cells failed to generate the chemical mediator or second messenger of insulin action, as assessed by its ability to stimulate pyruvate dehydrogenase (PDH) in liver mitochondria from normal rats. We concluded that uremic sera renders normal rat hepatocytes resistant to insulin. Insulin resistance is a postinsulin receptor kinase defect possibly due to lack of the generation of the chemical mediator of insulin action. This in vitro cell model may be useful to further define the mechanism(s) and the serum factor(s) responsible for insulin resistance in uremia in the absence of complicating hormonal and substrate changes that occur in vivo.

Adult↗
PubMed1989

Growth of osteoblasts on porous calcium phosphate ceramic: an in vitro model for biocompatibility study.

Biomaterial implantation in animals is commonly used for biocompatibility studies as well as examination of long-term interaction between tissue and the test material. An in vitro cell culture model is proposed as an alternative which will save animal lives and reduce the pain and discomfort of animals used for such studies. In this study the biomaterial was matched to the cell types typical of the implant site of the particular material: porous calcium phosphate ceramic, used as dental and orthopaedic implants, with periosteal fibroblasts, osteoblasts and chondrocytes. All three cell types attached on to the ceramic and formed multicellular layers. Numbers of periosteal fibroblasts, osteoblasts and chondrocytes increased 29-, 23- and 17-fold, respectively, during the 10 wk period. Osteoblasts retained their phenotypic expression by producing only Type I collagen. Parathyroid hormone (PTH, 50 nM) suppressed the alkaline phosphatase activity of osteoblasts by over 50% and increased cAMP by more than 10-fold over control cultures.

Alkaline Phosphatase↗