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Biomedical subjects

L Pang

Publications and source records attributed to L Pang.

At least 19 recordsLinked to original sources
PubMed2006

Impact of data quality and model complexity on prediction of pesticide leaching.

Accurate input data for leaching models are expensive and difficult to obtain which may lead to the use of "general" non-site-specific input data. This study investigated the effect of using different quality data on model outputs. Three models of varying complexity, GLEAMS, LEACHM, and HYDRUS-2D, were used to simulate pesticide leaching at a field trial near Hamilton, New Zealand, on an allophanic silt loam using input data of varying quality. Each model was run for four different pesticides (hexazinone, procymidone, picloram and triclopyr); three different sets of pesticide sorption and degradation parameters (i.e., site optimized, laboratory derived, and sourced from the USDA Pesticide Properties Database); and three different sets of soil physical data of varying quality (i.e., site specific, regional database, and particle size distribution data). We found that the selection of site-optimized pesticide sorption (Koc) and degradation parameters (half-life), compared to the use of more general database derived values, had significantly more impact than the quality of the soil input data used, but interestingly also more impact than the choice of the models. Models run with pesticide sorption and degradation parameters derived from observed solute concentrations data provided simulation outputs with goodness-of-fit values closest to optimum, followed by laboratory-derived parameters, with the USDA parameters providing the least accurate simulations. In general, when using pesticide sorption and degradation parameters optimized from site solute concentrations, the more complex models (LEACHM and HYDRUS-2D) were more accurate. However, when using USDA database derived parameters, all models performed about equally.

Adsorption↗
PubMed2006

Identification of Vibrio harveyi using PCR amplification of the toxR gene.

AIMS: The aim of this study was to develop an effective method for the identification of Vibrio harveyi based on using the toxR gene as a taxonomic marker. METHODS AND RESULTS: Primers for the toxR gene were designed for specificity to V. harveyi, and incorporated in a polymerase chain reaction (PCR). The results of the PCR, which took <5 h from DNA extraction to amplification, revealed positive amplification of the toxR gene fragment in 20 V. harveyi isolates including type strains, whereas DNA from 23 other Vibrionaceae type strains and 13 Vibrio parahaemolyticus strains were negative. The detection limit of the PCR was 4.0 x 10(3) cells ml(-1). In addition, the technique enabled the recognition of V. harveyi from diseased fish. CONCLUSIONS: The PCR was specific and sensitive, enabling the identification of V. harveyi within 5 h. SIGNIFICANCE AND IMPACT OF THE STUDY: The PCR allowed the rapid and sensitive detection of V. harveyi.

Animals↗
PubMed2005

Enhanced basal apoptosis in cultured term human cytotrophoblasts is associated with a higher expression and physical interaction of p53 and Bak.

We tested the hypothesis that the expression levels of p53 and the pro-apoptotic mediators from the Bcl-2 family are higher in cytotrophoblasts, when compared to cultures with abundant syncytiotrophoblasts. Cytotrophoblasts isolated from normal term human placentas were cultured in Dulbecco's Modified Eagle medium (DMEM) for 24 h, when the cytotrophoblast phenotype predominates, in DMEM for 72 h, when the syncytiotrophoblast phenotype predominates, or in Ham's-Waymouth medium or DMEM with 1.5% dimethylsulfoxide, each of which maintains the cytotrophoblast phenotype through 72 h of culture. Apoptosis was assessed by detection of cleavage products of poly-ADP-ribose polymerase, by expression of cleaved cytokeratin 18 intermediate filaments, and by assessment of caspase-3 activity. Independent of time in culture, cytotrophoblasts showed higher levels of apoptosis compared to syncytiotrophoblasts. Cytotrophoblasts also expressed a 2-fold higher level of p53, a 2-fold lower level of 60 kDa Mdm-2 protein, a 2-fold higher level of Bak, but no differences in the expression of 90 kDa Mdm-2, Bcl-2, Bcl-X(L), Mcl-1, Bax, Bad, and Bad phosphorylated at the serine(112), serine(136), or serine(155) sites, compared to the syncytiotrophoblasts. Using co-immunoprecipitation, we demonstrated a greater degree of Bak-p53 interaction in cytotrophoblasts than in syncytiotrophoblasts. We also detected Bak-Mcl-1 interaction that was no different between the two phenotypes. Among the proteins studied, enhanced p53 activity, differential Bak expression, and Bak-p53 interactions may contribute to the higher level of constitutive apoptosis in cultures of cytotrophoblasts compared to syncytiotrophoblasts.

Apoptosis↗
PubMed2005

Fibrin enhances differentiation, but not apoptosis, and limits hypoxic injury of cultured term human trophoblasts.

We hypothesized that fibrin enhances apoptosis and modulates differentiation of trophoblast in vitro. Cytotrophoblasts isolated from normal term human placentas were cultured < or =72 h in DMEM-10%-FBS on a fibrin matrix in standard or hypoxic conditions. Trophoblasts were cultured on plastic (control), type I collagen (matrix control), or dishes with fibrinogen, fibrin degradation products (FDP), thrombin, plasma fibronectin or cellular fibronectin. Apoptosis was determined by western analysis of the cleavage products of poly-ADP-ribose polymerase and cytokeratin 18 and caspase 3 activity. Cell cycle regulation was quantified by expression of proliferating cell nuclear antigen (PCNA) and p27 protein. Differentiation was determined by media level of hCG and hPL. Compared to the two controls, fibrin matrix had no effect on trophoblast apoptosis or total cell death in standard conditions. Neither fibrin nor collagen altered expression of PCNA or p27. In contrast, fibrin significantly increased the secretion of both hCG and hPL. Fibrin, but not FDP, thrombin or fibronectins, promoted hormonal differentiation. Fibrin limited the impact of a < or =8h of hypoxia on trophoblast hormone release but did not avert the effects of 24h of low oxygen and did not alter apoptosis in hypoxic trophoblast. We conclude that fibrin provides an environment conducive for trophoblast re-epithelialization of the surface of villi, where injury is marked by fibrin deposition.

Apoptosis↗
PubMed2004

Overexpression of cyclooxygenase-2 in non-small cell lung cancer.

Evidence is accumulating to suggest that the inducible isoenzyme of cyclooxygenase (COX)-2 is up-regulated in human cancers and epidemiological studies indicate that COX inhibitors may have a protective effect on the development of lung cancer. We used immunohistochemistry and Western blotting to investigate COX expression in lung tumour specimens and three lung cancer cell lines. Sixty-five archival lung tissue samples, including 46 squamous cell and 6 adenocarcinoma lung resections, and 13 small cell lung cancer (SCLC) biopsies were studied. Dense and intense cytoplasmic COX-2 staining was found in all 52 resections from non-small cell lung cancer (NSCLC). The staining was diffuse and much stronger than adjacent respiratory epithelium. COX-2 staining was relatively weak in the majority of the SCLC samples. The bronchial and bronchiolar epithelium in the surrounding normal lung structures showed uniform COX immunoreactivity with apical concentration of the stain. There was no increase in COX-1 staining in any tumour type. Western blot analysis of the cancer lines revealed significantly higher expression of COX-1 in CORL23 line and COX-2 in two NSCLC cell lines (MOR/P; A549) compared with the expression of COX-1 and COX-2 in cultured normal bronchial epithelial cells. Our findings demonstrated COX-2 overexpression in NSCLC.

Adenocarcinoma↗
PubMed2002

Inter-test reliability of the anti-RESA indices based on ELISA tests using eluates from whole blood spots dried on filter paper.

The ring-infected erythrocyte surface antigen (RESA), is one of the falciparum malaria vaccine candidates rarely studied in Brazil. Fieldwork logistics to conduct serology studies is simplified when eluates from whole blood dried on filter paper can be used. Therefore, this study aimed to assess the inter-test reliability for the anti-RESA ELISA-based indices using eluates from filter paper and from serum samples. The study population consisted of 210 individuals (Brazil) from whom matched samples were collected. Anti-RESA ELISA-based index means (+/- S.D.) were 15.29% (+/-28.13%) for filter paper and 11.79% (+/-23.67%) for serum samples. The intra-class correlation coefficient was estimated to be 82.38%, indicating high test reliability. However, there was a significant tendency for filter paper test results to have higher values than serum sample test results (P < 0.001). Explanations for this finding may be the presence of haemoglobin in the eluates from filter paper, which may interfere with ELISA testing.

Adolescent↗
PubMed2001

Solutions and verification of a scale-dependent dispersion model.

In this paper, analytical solutions are derived for a one-dimensional scale-dependent dispersion model (SDM), considering linear equilibrium sorption and first-order degradation for continuous and pulse contaminant sources, with a constant input concentration in a semi-infinite uniform porous medium. In the SDM model, dispersivity alpha(x) is replaced with a constant epsilon multiplied by the transport distance x. The solution for a pulse source is verified experimentally in the analysis of tritium data obtained from an 8-m-long homogenous pea-gravel column with multiple sampling locations, and the results are compared with those analysed by a commonly used solution of a constant dispersion model (CDM). The SDM predicts concentrations satisfactorily at all sampling locations, while the CDM fits the experimental data well for only one location. Both models are then calibrated for each individual concentration breakthrough curve, using local values for either epsilon in the SDM or alpha(x) in the CDM. Both models give equally good fits for appropriate choices of individual epsilon and alpha(x) values, and both indicate a linear increase in alpha(x) with distance. The epsilon values tend to change little as x increases and are expected to approach a constant at relatively large distances downstream. Hence, predictions from the SDM should become more accurate as x increases.

Calibration↗
PubMed2001

Effects of angiotensin-converting enzyme inhibition on the development of the atrial fibrillation substrate in dogs with ventricular tachypacing-induced congestive heart failure.

BACKGROUND: Atrial structural remodeling creates a substrate for atrial fibrillation (AF), but the underlying signal transduction mechanisms are unknown. This study assessed the effects of ACE inhibition on arrhythmogenic atrial remodeling and associated mitogen-activated protein kinase (MAPK) changes in a dog model of congestive heart failure (CHF). METHODS AND RESULTS: Dogs were subjected to various durations of ventricular tachypacing (VTP, 220 to 240 bpm) in the presence or absence of oral enalapril 2 mg. kg(-1). d(-1). VTP for 5 weeks induced CHF, local atrial conduction slowing, and interstitial fibrosis and prolonged atrial burst pacing-induced AF. Atrial angiotensin II concentrations and MAPK expression were increased by tachypacing, with substantial changes in phosphorylated forms of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38-kinase. Enalapril significantly reduced tachypacing-induced changes in atrial angiotensin II concentrations and ERK expression. Enalapril also attenuated the effects of CHF on atrial conduction (conduction heterogeneity index reduced from 3.1+/-0.4 to 1.9+/-0.2 ms/mm, P<0.05), atrial fibrosis (from 11.9+/-1.1% to 7.5+/-0.4%, P<0.01), and mean AF duration (from 651+/-164 to 218+/-75 seconds, P<0.05). Vasodilator therapy of a separate group of VTP dogs with hydralazine and isosorbide mononitrate did not alter CHF-induced fibrosis or AF promotion. CONCLUSIONS: CHF-induced increases in angiotensin II content and MAPK activation contribute to arrhythmogenic atrial structural remodeling. ACE inhibition interferes with signal transduction leading to the AF substrate in CHF and may represent a useful new component to AF therapy.

Angiotensin II↗
PubMed2001

Photodynamic effect on cancer cells influenced by electromagnetic fields.

The synergism of low-frequency electromagnetic field treatment and photodynamic effect on killing of human cancer cells is presented. The weak pulsating electromagnetic field (PEMF) generated by Helmholtz coils in the mT range influences the permeability of cell membranes for photosensitizers. Several types of sensitizers were excited by visible light during incorporation without and with two kinds of PEMF treatment. In the first part suitable photosensitizers were selected in the absorption range between 400 and 700 nm against human myeloid leukaemia K562 and human histiocytic lymphoma U937 cells by treatment of PEMF consisting of rectangular pulse groups. In the second part amplitude and frequency dependencies were measured using sinuous PEMF and white light with the result that after 12 min the PEMF treatment enhanced photodynamic effectivity by more than 40% over the control value. Taking into account the influence of many parameters, an additional optimization will be possible by photodynamic PEMF synergism for an increased drug delivery in general.

Cell Membrane Permeability↗
PubMed2001

Subcellular localization of GABA(B) receptor subunits in rat visual cortex.

Although studies in the visual cortex have found gamma-aminobutyric acid B (GABA(B)) receptor-mediated pre- and postsynaptic inhibitory effects on neurons, the subcellular localization of GABA(B) receptors in different types of cortical neurons and synapses has not been shown directly. To provide this information, we have used antibodies against the GABA(B) receptor (R)1a/b and GABA(B)R2 subunits and have studied the localization of immunoreactivities in rat visual cortex. Light microscopic analyses have shown that both subunits are expressed in cell bodies and dendrites of 65-92% of corticocortically projecting pyramidal neurons and in 92-100% of parvalbumin (PV)-, calretinin (CR)-, and somatostatin (SOM)-containing GABAergic neurons. Electron microscopic analyses of immunoperoxidase- and immunogold-labeled tissue revealed staining in the nucleus, cytoplasm and cell surface membranes with both antibodies. Colocalization of both subunits was observed in all of these structures. GABA(B)R1a/b and GABA(B)R2 were concentrated in excitatory and inhibitory synapses and in extrasynaptic membranes. In GABAergic synapses, GABA(B)R1a/b and GABA(B)R2 were more strongly expressed postsynaptically on pyramidal and nonpyramidal cells than presynaptically. In type 1 synapses GABA(B)R1a/b and GABA(B)R2 was found in pre- and postsynaptic membranes. The nuclear localization of GABA(B)R1 and GABA(B)R2 subunits suggests a novel role for neurotransmitter receptors in controlling gene expression. The synaptic colocalization of GABA(B)R1 and GABA(B)R2 indicates that subunits form heteromeric assemblies of the functional receptor in inhibitory and excitatory synapses. Subunit coexpression in GABAergic synapses that include PV-containing and PV-deficient terminals suggests that pre- and postsynaptic GABA(B) receptor activation is provided by several different types of interneurons. The coexpression of both subunits in excitatory synapses suggests a role for GABA(B) receptors in the regulation of glutamate release and raises the question how these receptors are activated in the absence of pre-or postsynaptic GABAergic synaptic inputs to excitatory synapses.

Animals↗
PubMed2001

A field tracer study of attenuation of atrazine, hexazinone and procymidone in a pumice sand aquifer.

A field tracer experiment, simulating point source contamination, was conducted to investigate attenuation and transport of atrazine, hexazinone and procymidone in a volcanic pumice sand aquifer. Preliminary laboratory incubation tests were also carried out to determine degradation rates. Field transport of the pesticides was observed to the significant under non-equilibrium conditions. Therefore, a two-region/two-site non-equilibrium transport model, N3DADE, was used for analysis of the field data. A lump reduction rate constant was used in this paper to encompass all the irreversible reduction processes (e.g. degradation, irreversible adsorption, complexation and filtration for the pesticides adsorbed into particles and colloids) which are assumed to follow a first-order rate law. Results from the field experiment suggest that (a) hexazinone was the most mobile (retardation factor R = 1.4) and underwent least mass reduction; (b) procymidone was the least mobile (R = 9.26) and underwent the greatest mass reduction; (c) the mobility of atrazine (R = 4.45) was similar to that of rhodamine WT (R = 4.10). Hence, rhodamine WT can be used to delimit the appearance of atrazine in pumice sand groundwater. Results from the incubation tests suggest that (a) hexazinone was degraded only in the mixture of groundwater and aquifer material (degradation rate constant = 4.36 x 10(-3) day-1); (b) procymidone was degraded not only in the mixture of groundwater and aquifer material (rate constant = 1.12 x 10(-2) day-1) but also in the groundwater alone (rate constant = 2.79 x 10(-2) and-1); (c) atrazine was not degraded over 57 days incubation in either the mixture of aquifer material and groundwater or the groundwater alone. Degradation rates measured in the batch tests were much lower than the total reduction rates. This suggests that not only degradation but also other irreversible processes are important in attenuating pesticides under field conditions. Hence, the use of laboratory-determined degradation rates could underestimate reduction of pesticides in field conditions.

Algorithms↗
PubMed2001

Effects of paramyxoviral infection on airway epithelial cell Foxj1 expression, ciliogenesis, and mucociliary function.

To elucidate molecular mechanisms underlying the association between respiratory viral infection and predisposition to subsequent bacterial infection, we used in vivo and in vitro models and human samples to characterize respiratory virus-induced changes in airway epithelial cell morphology, gene expression, and mucociliary function. Mouse paramyxoviral bronchitis resulted in airway epithelial cell infection and a distinct pattern of epithelial cell morphology changes and altered expression of the differentiation markers beta-tubulin-IV, Clara cell secretory protein, and Foxj1. Furthermore, changes in gene expression were recapitulated using an in vitro epithelial cell culture system and progressed independent of the host inflammatory response. Restoration of mature airway epithelium occurred in a pattern similar to epithelial cell differentiation and ciliogenesis in embryonic lung development characterized by sequential proliferation of undifferentiated cells, basal body production, Foxj1 expression, and beta-tubulin-IV expression. The effects of virus-induced alterations in morphology and gene expression on epithelial cell function were illustrated by decreased airway mucociliary velocity and impaired bacterial clearance. Similar changes in epithelial cell Foxj1 expression were also observed in human paramyxoviral respiratory infection. Taken together, these model systems of paramyxoviral respiratory infection mimic human pathology and identify epithelial cell Foxj1 expression as an early marker of epithelial cell differentiation, recovery, and function.

Animals↗
PubMed2001

Preoperative high-dose chemotherapy with peripheral blood stem cell support as a primary management of locally advanced breast cancer.

Locally advanced breast cancer (LABC) has a poor prognosis with a high risk of local recurrence and distant metastasis. Preoperative combined chemotherapy with or without granulocyte colony-stimulating factor (G-CSF) support does not improve the long-term survival rate. In our report, two patients with LABC received preoperative high-dose chemotherapy with peripheral blood stem cell support (HDC/PBSCs). Prior to high-dose chemotherapy with peripheral blood stem cell support, they both received induction chemotherapy of cyclophosphamide, epirubicin and 5-fluorouracil (FEC) for two cycles which resulted in a partial response. PBSC mobilization and collection were carried out following the second cycle of induction chemotherapy followed by G-CSF. High-dose cyclophosphamide (2500 mg/m2), carboplatin (600 mg/m2) and etoposide (600 mg/m2) were administered with PBSC support. A radical mastectomy was performed followed by adjuvant chemotherapy with FEC regimen for four cycles, followed by local irradiation, and endocrine therapy with tamoxifen. Both patients achieved a remarkable response in the primary lesion after HDC/PBSCs and tolerated the whole treatment well. Preoperative HDC/PBSCs as a new strategy in the treatment of LABC seems practical but it needs to be studied more deeply.

Adult↗
PubMed2001

Regulation of TNF-alpha-induced eotaxin release from cultured human airway smooth muscle cells by beta2-agonists and corticosteroids.

Eotaxin is a potent eosinophil chemoattractant that contributes to the eosinophilia seen in asthma and other allergic disorders. Recent studies have identified human airway smooth muscle (HASM) as a rich source of eotaxin, but the factors regulating its production are poorly understood. Here we describe for the first time that beta2-agonists can inhibit cytokine-induced eotaxin release. We found that TNF-alpha stimulated eotaxin release (assayed by ELISA) from HASM cells and that the release was partially inhibited by salbutamol and salmeterol. The effect of beta2-agonists was mimicked by forskolin and 8-bromo-cAMP and potentiated by the cAMP-dependent phosphodiesterase inhibitor rolipram, suggesting that it is cAMP dependent. We also found that the cAMP inhibition was likely at the transcription stage, although experiments with the PKA inhibitors H-89 and Rp-cAMP or the PKG inhibitor KT5823 suggested that none of these kinases was involved. Partial inhibition of eotaxin release was also seen with the corticosteroids dexamethasone and fluticasone. The combined use of beta2-agonists, rolipram, and steroids abolished TNF-alpha-induced eotaxin release. These results suggest that the combination of a beta2-agonist, PDE inhibitor, and a corticosteroid may have additive beneficial effects in the treatment of the eosinophilia associated with asthma and other allergic diseases.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2001

Human airway smooth muscle cells secrete vascular endothelial growth factor: up-regulation by bradykinin via a protein kinase C and prostanoid-dependent mechanism.

Bronchial vascular remodeling is an important feature of the pathology of chronic asthma, but the responsible mechanisms and main sources of angiogenic factors are unclear. Here we report that human airway smooth muscle cells express vascular endothelial growth factor (VEGF)121, 165, 189, 206 splice variants and secrete VEGF protein constitutively. VEGF protein secretion was increased by the proinflammatory asthma mediator bradykinin through post-transcriptional mechanisms. Bradykinin-induced VEGF secretion was dependent on the B2 bradykinin receptor, activation of protein kinase C, and generation of endogenous prostanoids. This is the first report that bradykinin can increase VEGF secretion in any biological system and the first to show that airway smooth muscle cells produce VEGF. Our results suggest a novel role for human airway smooth muscle in contributing to bronchial mucosal angiogenesis in chronic asthma by secretion of VEGF and suggest a wider role for mesenchymal cell products in mediating angiogenesis in inflammatory and allergic diseases.

Adult↗
PubMed2001

Attenuation of ischemia-induced mouse brain injury by SAG, a redox-inducible antioxidant protein.

Cerebral ischemia resulting from a disruption of blood flow to the brain initiates a cascade of events that causes neuron death and leads to neurologic dysfunction. Reactive oxygen species are thought, at least in part, to mediate this disease process. The authors recently cloned and characterized an antioxidant protein, SAG (sensitive to apoptosis gene), that is redox inducible and protects cells from apoptosis induced by redox agents in a number of in vitro cell model systems. This study reports a neuroprotective role of SAG in ischemia/reperfusion-induced brain injury in an in vivo mouse model. SAG was expressed at a low level in brain tissue and was inducible after middle cerebral artery occlusion with peak expression at 6 to 12 hours. At the cellular level, SAG was mainly expressed in the cytoplasm of neurons and astrocytes, revealed by double immunofluorescence. An injection of recombinant adenoviral vector carrying human SAG into mouse brain produced an overexpression of SAG protein in the injected areas. Transduction of AdCMVSAG (wild-type), but not AdCMVmSAG (mutant), nor the AdCMVlacZ control, protected brain cells from ischemic brain injury, as evidenced by significant reduction of the infarct areas where SAG was highly expressed. The result suggests a rather specific protective role of SAG in the current in vivo model. Mechanistically, SAG overexpression decreased reactive oxygen species production and reduced the number of apoptotic cells in the ischemic areas. Thus, antioxidant SAG appears to protect against reactive oxygen species-induced brain damage in mice. Identification of SAG as a neuroprotective molecule could lead to potential stroke therapies.

Adenoviridae↗
PubMed2001

Reduction of inflammatory response in the mouse brain with adenoviral-mediated transforming growth factor-ss1 expression.

UNLABELLED: Background and Purpose-Chemokines have been shown to play an important role in leukocyte and monocyte/macrophage infiltration into ischemic regions. The purpose of this study is to identify whether overexpression of the active human transforming growth factor-ss1 (ahTGF-ss1) can downregulate expression of monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1alpha (MIP-1alpha), and intercellular adhesion molecule-1 (ICAM-1) and reduce ischemic brain injury. METHODS: -Overexpression of transforming growth factor-ss1 (TGF-ss1) was achieved through adenoviral gene transfer. Five days after adenoviral transduction, the mouse underwent 30 minutes of middle cerebral artery occlusion followed by 1 to 7 days of reperfusion. TGF-ss1, MCP-1, MIP-1alpha, and ICAM-1 were detected by enzyme-linked immunosorbent assay and immunohistochemistry. Infarct areas and volumes were measured by cresyl violet staining. RESULTS: -MCP-1 and MIP-1alpha expression is increased after middle cerebral artery occlusion, and double-labeled immunostaining revealed that MCP-1 is colocalized with neurons and astrocytes. Viral-mediated TGF-ss1 overexpression was significantly greater at measured time points, with a peak at 7 to 9 days. The expression of MCP-1 and MIP-1alpha, but not ICAM-1, was reduced in the mice overexpressing ahTGF-ss1 (P:<0.05). Furthermore, infarct volume was significantly reduced in the mice overexpressing ahTGF-ss1 (P:<0.05). CONCLUSIONS: -This study demonstrates that MCP-1 and MIP-1alpha expressed in the ischemic region may play an important role in attracting inflammatory cells. The reduction of MCP-1 and MIP-1alpha, but not ICAM-1, in the mice overexpressing ahTGF-ss1 suggests that the neuroprotective effect of TGF-ss1 may result from the inhibition of chemokines during cerebral ischemia and reperfusion.

Adenoviridae↗