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J Hua

Publications and source records attributed to J Hua.

At least 19 recordsLinked to original sources
PubMed2006

Aerosol delivery of Akt controls protein translation in the lungs of dual luciferase reporter mice.

Lung cancer has emerged as a leading cause of cancer death in the world; however, most of the current conventional therapies are not sufficiently effective in altering the progression of disease. Therefore, development of novel treatment approaches is needed. Although several genes and methods have been used for cancer gene therapy, a number of problems such as specificity, efficacy and toxicity reduce their application. This has led to re-emergence of aerosol gene delivery as a noninvasive method for lung cancer treatment. In this study, nano-sized glucosylated polyethyleneimine (GPEI) was used as a gene delivery carrier to investigate the effects of Akt wild type (WT) and kinase deficient (KD) on Akt-related signaling pathways and protein translation in the lungs of CMV- LucR-cMyc-IRES-LucF dual reporter mice. These mice are a powerful tool for the discrimination between cap-dependent/-independent protein translation. Aerosols containing self-assembled nano-sized GPEI/Akt WT or GPEI/Akt KD were delivered into the lungs of reporter mice through nose-only-inhalation-chamber with the aid of nebulizer. Aerosol delivery of Akt WT caused the increase of protein expression levels of Akt-related signals, whereas aerosol delivery of Akt KD did not. Furthermore, dual luciferase activity assay showed that aerosol delivery of Akt WT enhanced cap-dependent protein translation, whereas a reduction in cap-dependent protein translation by Akt KD was observed. Our results clearly showed that targeting Akt may be a good strategy for prevention as well as treatment of lung cancer. These studies suggest that our aerosol delivery is compatible for in vivo gene delivery which could be used as a noninvasive gene therapy in the future.

Aerosols↗
PubMed2006

Measurement of liver fat by magnetic resonance imaging: Relationships with body fat distribution, insulin sensitivity and plasma lipids in healthy men.

AIM: We compared the use of magnetic resonance imaging (MRI) as a test for liver fat content (LFAT) with proton magnetic resonance spectroscopy (MRS) and investigated its relationship with body fat distribution, insulin sensitivity, plasma lipids and lipoproteins. METHODS: LFAT was quantified by MRI and MRS in 17 free-living, healthy men with a wide range of body mass indexes. Fasting adiponectin was measured by immunoassay and insulin resistance by homeostasis assessment (HOMA) score. Intraperitoneal, retroperitoneal, anterior subcutaneous and posterior subcutaneous abdominal adipose tissue masses (ATMs) were determined by MRI. RESULTS: Measurements of LFAT by MRI and MRS were highly correlated (r = 0.851, p < 0.001). In univariate regression analysis, LFAT by MRI was also significantly correlated with plasma triglycerides (TGs), insulin, HOMA score, carbohydrate intake and the masses of all abdominal adipose tissue compartments (p < 0.05). LFAT was inversely correlated with plasma adiponectin (r = -0.505, p < 0.05). In multivariate linear regression analysis including plasma adiponectin and age, intraperitoneal ATM was an independent predictor of LFAT (beta-coefficient = 0.587, p = 0.024). Moreover, intraperitoneal ATM was also an independent predictor of HOMA score after adjusting for LFAT, plasma adiponectin and age (beta-coefficient = 0.810, p = 0.010). Conversely, LFAT was a significant predictor of plasma TG concentration after adjusting for adiponectin, intraperitoneal ATM, HOMA and age (beta-coefficient = 0.751, p = 0.007). Similar findings applied with LFAT measured by MRS. CONCLUSIONS: These data suggest that MRI is as good as MRS to quantify liver fat content. Our data also suggest that liver fat content could link intraabdominal fat with insulin resistance and dyslipidaemia.

Adiponectin↗
PubMed2006

The use of hydroxyapatite-coated CAD-CAM femoral components in adolescents and young adults with inflammatory polyarthropathy: ten-year results.

Between June 1991 and January 1995, 42 hydroxyapatite-coated CAD-CAM femoral components were inserted in 25 patients with inflammatory polyarthropathy, 21 of whom had juvenile idiopathic arthritis. Their mean age was 21 years (11 to 35). All the patients were reviewed clinically and radiologically at one, three and five years. At the final review at a mean of 11.2 years (8 to 13) 37 hips in 23 patients were available for assessment. A total of four femoral components (9.5%) had failed, of which two were radiologically loose and two were revised. The four failed components were in patients aged 16 years or less at the time of surgery. Hydroxyapatite-coated customized femoral components give excellent medium- to long-term results in skeletally-mature young adults with inflammatory polyarthropathy. Patients aged less than 16 years at the time of surgery have a risk of 28.5% of failure of the femoral component at approximately ten years.

Adolescent↗
PubMed2005

Correlation of radiographic and telemetric data from massive implant fixations.

One proximal femoral replacement (PFR) and two distal femoral replacements (DFR) used in tumoural limb salvage were instrumented to measure axial force in the femoral shaft and at the tip of the intramedullary stem in vivo. The prostheses were implanted in suitable subjects and regular recording sessions held over 2 years for each subject. The ratio of the tip force to the shaft force increased with time in all 3 subjects, albeit at different rates, indicating that a greater proportion of the load was being transmitted along the prosthesis stem. The aim of this study was to correlate these changes with bone remodelling observed radiographically over the same period. Radiographs were analysed using a computer-assisted method to quantify bone width, radiolucent line width and relative bone density. The analysis showed the development of radiolucent lines at the bone-cement interface and a decrease in the lateral to medial ratio of bone density near the transection site. For the PFR, the mean width of the radiolucent area alongside the proximal fifth of the stem on the lateral side increased from 0 to 0.67 mm over the 2 years. The tip to shaft ratio correlated significantly with radiolucency on the lateral side of the stem. Both the DFRs became loose within 2 years but the PFR has remained in situ for 13 years to date. The correlations found thus far suggest that it may be possible to establish relationships between load transfer (and therefore loosening in the fixation) and radiographic data, with possible application to advance warning of clinical loosening in stemmed implants.

Adult↗
PubMed2005

Preventive actions of a high dose of glucosamine on adjuvant arthritis in rats.

OBJECTIVE: Glucosamine, a naturally occurring amino monosaccharide has been used to treat or prevent osteoarthritis in humans. In this study, we evaluated the effect of glucosamine on rat adjuvant arthritis, a model of rheumatoid arthritis. MATERIALS AND METHODS: Adjuvant arthritis was induced in male Wistar rats by injection of Freund's complete adjuvant (FCA) into the right hind paw, and 300 mg/kg of glucosamine, an extra-dose compared with a regular dose for osteoarthritis patients (1.5 g/day, approximately 25 mg/kg), was orally administered once a day to the arthritic rats for 22 days. RESULTS: Glucosamine significantly suppressed the increase in arthritis score (p < 0.05) after day 10 of adjuvant injection, and inhibited the swelling of FCA-injected right and -uninjected left hind paws (p < 0.01) after day 18. In addition, histopathological examination of the arthritic joints revealed that glucosamine suppressed synovial hyperplasia, cartilage destruction and inflammatory cell infiltration. Furthermore, glucosamine reduced the production of nitric oxide and prostaglandin E(2) in plasma (p < 0.05). CONCLUSIONS: These observations suggest that glucosamine is able to suppress the progression of adjuvant arthritis in rats. Glucosamine may be expected as a novel anti-inflammatory agent for treatment of rheumatoid arthritis.

Animals↗
PubMed2005

Inhibitory action of glucosamine on platelet activation in guinea pigs.

OBJECTIVE: Glucosamine, a naturally occurring amino monosaccharide, has been used to treat or prevent osteoarthritis in humans. Recently, we have revealed that glucosamine inhibits platelet activation in vitro. However, the effect of in vivo administration of glucosamine has not yet been clarified. In this study, we administered glucosamine orally to guinea pigs and examined its effects on platelet functions. MATERIALS AND METHODS: Glucosamine hydrochloride solution (0.5%, 5 mg/ml) was administered orally to guinea pigs ad libitum for 22 days, and platelet rich plasma was collected to evaluate platelet functions in vitro. Guinea pigs received an average of 400 mg glucosamine/animal/day. RESULTS: Glucosamine-administration suppressed platelet aggregation in response to ADP by 51% (p < 0.01), but not platelet aggregation induced by collagen. Furthermore, glucosamine-administration inhibited the ADP-induced extracellular release of ATP and production of thromboxane A(2) by 91% and 96%, respectively (p < 0.001). In contrast, glucosamine did not affect the body-weights, platelet counts and bleeding time in guinea pigs after the administration. CONCLUSIONS: These observations suggest that glucosamine is likely to exert an inhibitory action on platelets in vivo by suppressing platelet aggregation, ATP release, and thromboxane A(2) production. Thus, glucosamine could be expected as a novel and safe anti-platelet agent.

Adenosine Diphosphate↗
PubMed2004

CD44 regulates arteriogenesis in mice and is differentially expressed in patients with poor and good collateralization.

BACKGROUND: Arteriogenesis refers to the development of collateral conductance arteries and is orchestrated by circulating monocytes, which invade growing collateral arteries and act as suppliers of cytokines and growth factors. CD44 glycoproteins are involved in leukocyte extravasation but also in the regulation of growth factor activation, stability, and signaling. Here, we explored the role of CD44 during arteriogenesis. METHODS AND RESULTS: CD44 expression increases strongly during collateral artery growth in a murine hind-limb model of arteriogenesis. This CD44 expression is of great functional importance, because arteriogenesis is severely impaired in CD44-/- mice (wild-type, 54.5+/-14.9% versus CD44-/-, 24.1+/-9.2%, P<0.001). The defective arteriogenesis is accompanied by reduced leukocyte trafficking to sites of collateral artery growth (wild-type, 29+/-12% versus CD44-/-, 18+/-7% CD11b-positive cells/square, P<0.01) and reduced expression of fibroblast growth factor-2 and platelet-derived growth factor-B protein. Finally, in patients with single-vessel coronary artery disease, the maximal expression of CD44 on activated monocytes is reduced in case of impaired collateral artery formation (poor collateralization, 1764+/-572 versus good collateralization, 2817+/-1029 AU, P<0.05). CONCLUSIONS: For the first time, the pivotal role of CD44 during arteriogenesis is shown. The expression of CD44 increases during arteriogenesis, and the deficiency of CD44 severely impedes arteriogenesis. Maximal CD44 expression on isolated monocytes is decreased in patients with a poor collateralization compared with patients with a good collateralization.

Aged↗
PubMed2004

Glucosamine, a naturally occurring amino monosaccharide, suppresses the ADP-mediated platelet activation in humans.

OBJECTIVE: To evaluate the anti-thrombotic action of glucosamine, a naturally occurring amino monosaccharide, platelets were stimulated with ADP in the presence of glucosamine, and its effects on platelet functions were examined. MATERIALS AND METHODS: Human platelet-rich plasma was stimulated with 2.5 microM ADP in the presence of glucosamine (0.01 approximately 1 mM) or other aminosugars (N-acetyl-glucosamine, galactosamine or N-acetyl-galactosamine, 1 mM), and platelet aggregation was monitored. Furthermore, the effects of glucosamine on the thromboxane A2 production, release of granule contents, intracellular calcium mobilization and phosphorylation of Syk (a 72 kD protein tyrosine kinase) were evaluated following ADP-stimulation. In addition, the binding of [3H] ADP to its receptors was examined. RESULTS: Glucosamine (>0.01 mM) dose-dependently suppressed platelet aggregation in response to ADP (p < 0.05), whereas N-acetyl-glucosamine, galactosamine or N-acetyl-galactosamine (1 mM) did not affect the ADP-induced platelet aggregation. Furthermore, glucosamine (>0.1 mM) inhibited the extracellular release of granule contents (ATP and platelet factor 4) and production of thromboxane A2 from ADP-stimulated platelets (p < 0.05). Moreover, glucosamine significantly repressed the intracellular calcium mobilization at >0.1 mM and phosphorylation of Syk at >0.01 mM upon ADP-stimulation (p < 0.05). In addition, glucosamine (>0.1 mM) inhibited the binding of ADP to its receptors (p < 0.05). CONCLUSION: Glucosamine is able to suppress platelet aggregation, release of granule constituents, thromboxane A2 production, calcium mobilization and phosphorylation of Syk possibly via the inhibition of ADP-binding to the receptors. Glucosamine could be expected as a novel anti-platelet agent for thrombotic disorders due to its suppressive actions on platelets.

Adenosine Diphosphate↗
PubMed2003

Protein interaction for an interferon-inducible systemic lupus associated gene, IFIT1.

OBJECTIVE: To identify disease-related genes and immune-regulatory pathways in the pathogenesis of systemic lupus erythematosus (SLE) by using gene expression profiling and protein-protein interaction analysis. METHODS: Peripheral white blood cell gene expression profiles of 10 SLE patients were determined by oligonucleotide microarray analysis. Clustering of the gene expression profile was compared with the clinical immune phenotype. SLE-induced genes that were over- or under-expressed were determined and independently validated using a real-time polymerase chain reaction (PCR) method. To study their potential function and the possible pathways involved, a candidate gene was cloned and a GST (glutathione S-transferase) fusion protein was expressed in Escherichia coli. The fusion protein was further purified using the glutathione Sepharose 4B system, and was treated as bait to capture prey from SLE peripheral white blood cell lysate. MALDI-TOF (matrix-assisted laser desorption/ionization-time-of-flight) mass spectrometry was then performed to determine the prey protein. RESULTS: Similarity was found between the gene expression profile and the immune phenotype clusters of the SLE patients. More than 20 disease-associated genes were identified, some of which have not been related to SLE previously. Of these genes, a cluster of interferon-induced genes were highly correlated. IFIT1 (interferon-induced with tetratricopeptide repeats 1) was one of these genes, and overexpression of its mRNA was confirmed independently by real-time PCR in a larger population (40 SLE patients and 29 normal controls). An IFIT1 protein- protein interaction study showed that IFIT1 may interact with Rho/Rac guanine nucleotide exchange factor. CONCLUSION: The gene expression profile seems to be the molecular basis of the diverse immune phenotype of SLE. On the basis of the SLE-related genes found in this study, we suggest that the interferon-related immune pathway is important in the pathogenesis of SLE. IFIT1 is the first gene described as a candidate gene for SLE, and may function by activating Rho proteins through interaction with Rho/Rac guanine nucleotide exchange factor. IFIT1 and the interferon-related pathway may provide potential targets for novel interventions in the treatment of SLE.

Adaptor Proteins, Signal Transducing↗
PubMed2003

Local monocyte chemoattractant protein-1 therapy increases collateral artery formation in apolipoprotein E-deficient mice but induces systemic monocytic CD11b expression, neointimal formation, and plaque progression.

Monocyte chemoattractant protein-1 (MCP-1) stimulates the formation of a collateral circulation on arterial occlusion. The present study served to determine whether these proarteriogenic properties of MCP-1 are preserved in hyperlipidemic apolipoprotein E-deficient (apoE-/-) mice and whether it affects the systemic development of atherosclerosis. A total of 78 apoE-/- mice were treated with local infusion of low-dose MCP-1 (1 microg/kg per week), high-dose MCP-1 (10 microg/kg per week), or PBS as a control after unilateral ligation of the femoral artery. Collateral hindlimb flow, measured with fluorescent microspheres, significantly increased on a 1-week high-dose MCP-1 treatment (PBS 22.6+/-7.2%, MCP-1 31.3+/-10.3%; P<0.05). These effects were still present 2 months after the treatment (PBS 44.3+/-4.6%, MCP-1 56.5+/-10.4%; P<0.001). The increase in collateral flow was accompanied by an increase in the number of perivascular monocytes/macrophages on MCP-1 treatment. However, systemic CD11b expression by monocytes also increased, as did monocyte adhesion at the aortic endothelium and neointimal formation (intima/media ratio, 0.097+/-0.011 [PBS] versus 0.257+/-0.022 [MCP-1]; P<0.0001). Moreover, Sudan IV staining revealed an increase in aortic atherosclerotic plaque surface (24.3+/-5.2% [PBS] versus 38.2+/-9.5% [MCP-1]; P<0.01). Finally, a significant decrease in the percentage of smooth muscle cells was found in plaques (15.0+/-5.2% [PBS] versus 5.8+/-2.3% [MCP-1]; P<0.001). In conclusion, local infusion of MCP-1 significantly increases collateral flow on femoral artery ligation in apoE-/- mice up to 2 months after the treatment. However, the local treatment did not preclude systemic effects on atherogenesis, leading to increased atherosclerotic plaque formation and changes in cellular content of plaques.

Animals↗
PubMed2001

Plant growth homeostasis is controlled by the Arabidopsis BON1 and BAP1 genes.

Wild-type Arabidopsis plants maintain a relatively constant size over a wide range of temperatures. Here we show that this homeostasis requires the BONZAI1 (BON1) gene because bon1 null mutants make miniature fertile plants at 22 degrees C but have wild-type appearance at 28 degrees C. The expression of BON1 and a BON1-associated protein (BAP1) is modulated by temperature. Thus BON1 and BAP1 may have a direct role in regulating cell expansion and cell division at lower temperatures. BON1 contains a Ca(2+)-dependent phospholipid-binding domain and is associated with the plasma membrane. It belongs to the copine gene family, which is conserved from protozoa to humans. Our data suggest that this gene family may function in the pathway of membrane trafficking in response to external conditions.

Animals↗
PubMed2001

Evaluation of the expression of NADPH oxidase components during maturation of HL-60 clone 15 cells to eosinophilic lineage.

OBJECTIVE: Superoxide-generating NADPH oxidase consists of the membrane-bound cytochrome b558 (gp91phox and p22Phox) and the cytosolic components (p67phox, p47phox, p40phox and rac). In this study, we evaluated the superoxide-generating activity and the expression of NADPH oxidase components during eosinophilic maturation using HL-60 clone 15 cell line. MATERIALS AND METHODS: HL-60 clone 15 cells were matured to eosinophils by incubation with 0.5 mM butyrate for 7 days, and NADPH oxidase components were detected by Northern blot, Western blot analyses and immunocytochemical staining. Moreover, superoxide-generating activity was examined by nitro blue tetrazolium (NBT) assay. RESULTS: Northern blot and Western blot analyses revealed that mRNAs and proteins for gp91phox, p67phox and p47phox were expressed after eosinophilic myelocyte stages, whereas mRNAs and proteins for p40phox and rac-2 were expressed from the promyelocyte stage. Interestingly, p22phox mRNA was expressed from the promyelocyte stage, but its protein was expressed after eosinophilic myelocyte stages. Consistent with the results of Western blotting, immunocytochemical staining of butyrate-induced HL-60 clone 15 cells indicated that gp91phox, p22phox, p67phox and p47phox were detected after eosinophilic myelocyte stages (eosinophilic myelocytes, eosinophilic metamyelocytes, eosinophilic band cells and eosinophilic-segmented cells), whereas p40phox and rac-2 were expressed from the promyelocyte stage. Moreover, almost the same results as those with butyrate-treated HL-60 clone 15 cells were obtained using human bone marrow cells by immunocytochemical staining. Furthermore, nitro blue tetrazolium (NBT) assay indicated that superoxide could be produced after eosinophilic myelocyte stages but not produced before the promyelocyte stage. CONCLUSIONS: Together these observations indicate that all the components for NADPH oxidase are expressed, and the superoxide-producing activity is obtained after myelocyte stages during eosinophilic maturation.

Amino Acid Sequence↗
PubMed2001

Simple geometric characteristics fail to reliably predict abdominal aortic aneurysm wall stresses.

PURPOSE: The treatment of patients with abdominal aortic aneurysms (AAAs) is typically based on the potential for rupture. Current rupture assessments are in turn based on statistics from aggregate populations and are incapable of providing precise risk estimates for individual AAAs. Significant benefit could be realized if rupture potential for individual AAAs could be reliably determined on the basis of simple geometric characteristics or the results of symmetric thin-shell analysis. This study seeks to determine whether it is possible to estimate wall stresses by use of these simple measures. METHODS: Linear finite element analysis was used to estimate the distribution of von Mises stresses in a series of homogeneous, isotropic, three-dimensional AAA models subject to static loading and assumed to have zero residual stresses. The magnitude of the peak stress was tabulated for each model along with the following characteristics: aneurysm volume; maximum diameter; maximum radius; maximal wall distention; aspect ratio (ratio of greatest anteroposterior diameter to transverse diameter); local radii of curvature (in both longitudinal and circumferential directions); and maximum symmetric thin-shell stress estimates (on the basis of the meridional contour). The relationship between peak stress and each of the characteristics was assessed by use of Spearman rank correlation coefficients, with values less than 0.95 interpreted as signifying unreliable associations. RESULTS: Peak stresses in the individual models ranged from 1.79 x 10(6) dyne/cm2 to 15.1 x 10(6) dyne/cm2. The circumferential and longitudinal radii of curvature were frequently able to predict the locations of high stress, but were unreliable in predicting the magnitude of peak stress. The aspect ratio showed the strongest correlation with peak wall stress (r = 0.88, 95% CI, 0.68-0.96), whereas the other characteristics showed even less correlation. Symmetric thin shell analysis accurately predicted stresses in axially symmetric models, but it was incapable of predicting either the location or magnitude of peak stress in asymmetric models. CONCLUSIONS: Simple geometric criteria and symmetric thin shell analyses are unreliable in predicting AAA stresses. Future attempts to estimate wall stress and assess risk of rupture for individual AAAs may require detailed three-dimensional modeling.

Aorta, Abdominal↗
PubMed2001

Identification of virulence mutants of the fungal pathogen Cryptococcus neoformans using signature-tagged mutagenesis.

Cryptococcus neoformans var. neoformans is an important opportunistic fungal pathogen of patients whose immune system has been compromised due to viral infection, antineoplastic chemotherapy, or tissue transplantation. As many as 13% of all AIDS patients suffer a life-threatening cryptococcal infection at some time during the course of their HIV disease. To begin to understand the molecular basis for virulence in Cryptococcus neoformans var. neoformans serotype A, we have employed signature-tagged mutagenesis (STM) to identify mutants with altered virulence in a mouse model. The critical parameters of signature-tagged mutagenesis in C. neoformans are explored. Data are presented showing that at least 100 different strains can be mixed together in a single animal with each participating in the infection and that there is no apparent interaction between a virulent strain and an avirulent strain in our animal model. Using signature-tagged mutagenesis, we identified 39 mutants with significantly altered growth in a competitive assay. Molecular analyses of these mutants indicated that 19 (49%) contained an insertion in the actin promoter by homologous recombination from a single crossover event, creating a duplication of the actin promoter and the integration of single or multiple copies of the vector. Analysis of the chromosomal insertion sites of those mutants that did not have an integration event in the actin promoter revealed an approximately random distribution among the chromosomes. Individual challenge of the putative mutants in a mouse model revealed five hypovirulent mutants and one hypervirulent mutant.

Actins↗
PubMed2001

Involvement of cytosolic prolyl endopeptidase in degradation of p40-phox splice variant protein in myeloid cells.

Our previous studies indicated that an alternatively spliced variant mRNA of p40-phox, a cytosolic component of NADPH oxidase, is expressed but its protein is hardly detected in myeloid cells such as promyelocytic HL-60 cells and neutrophils. Here, we have examined the stability of p40-phox variant protein in undifferentiated HL-60 cells. When in vitro-translated proteins were incubated with subcellular fractions of HL-60 cells, p40-phox variant protein but not native p40-phox was degraded by the cytosol and granule fractions. The degradation of variant protein by the granule fraction was observed using sonicated but not intact granules, suggesting that the variant protein is unlikely to be degraded by the granules in intact cells. To identify the enzyme(s) involved, we examined the effects of various enzyme inhibitors on the degradation of variant protein by the cytosol fraction. Degradation was completely inhibited by proline-specific serine protease (prolyl endopeptidase) inhibitors but not by proteasome, calpain, and metalloprotease inhibitors. Furthermore, the variant protein was degraded by a purified prolyl endopeptidase, and the degradation was protected by treating HL-60 cells with a cell-permeable inhibitor (S17092-1) for prolyl endopeptidase. These observations suggest that a cytosolic prolyl endopeptidase is involved in the degradation of p40-phox variant protein in myeloid cells.

Alternative Splicing↗
PubMed2001

[The inhibitory effect of oxymatrine on hepatitis C virus in vitro].

OBJECTIVE: To study the inhibitory effect of oxymatrine on HCV in vitro. METHODS: SMMC-7721 cells transfected with pBK-HCV using lipofectin transfection protocal were treated with oxymatrine. bDNA signal amplification assay and MTT colorimetric assay were used for intracellular HCV RNA and cytotoxicity. RESULTS: The stable HCV expression cell model established here could be used as a tool for medicine screen. Oxymatrine at the concentration of 100~1000 mug/ml could significantly decrease the level of intracellular HCV RNA. No cytotoxicity was shown in such concentrations. CONCLUSIONS: Oxymatrine has an anti-HCV potential activity in vitro.

Alkaloids↗