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Biomedical subjects

Y Hao

Publications and source records attributed to Y Hao.

At least 19 recordsLinked to original sources
PubMed2001

The effect of fluid shear stress on ICAM-1 expression of rat brain microvascular endothelial cells.

Intercellular adhesion molecule-1 (ICAM-1) is an adherence molecule that is an important factor in many pathophysiological processes such as atherosclerosis, thrombosis and inflammation. It is secretion of endothelial cells by a variety of biochemical stimulations. But hemodynamic forces can also induce various functional changes in vascular endothelium. Some researches have proved that shear stress can modulate the expression of ICAM-1. But most of them examine the regulation of expression of ICAM-1 in human umbilical vein endothelial cells. There is no detail on the effect of shear stress (SS) on ICAM-1 expression of microvascular endothelial cells (RBMECs). In this experiment, we use cultured rat brain microvascular endothelial cells (RBMECs). By using the parallel plate flow chamber method, we give two magnitudes of lamminar shear stresses (0.2 dyn/cm2, 0.4 dyn/cm2) for different perieods of time on the slides of cells. Immunostaining method and image analysis shows a specific upregulation in ICAM-1 expression on RBMECs, which is different from endothelial cells of other species or vascular beds. Expression of ICAM-1 is increased 0.5h after the onset of SS, and reached its highest level 4h after onset of SS, then declines after that. The effect is time-dependent, not force magnitude-dependent. Endothelial cell surface expression of ICAM-1 in the supernatants of RBMECs exposed to SS was not modified excluding the possibility that RBMECs exposed to SS synthesize factors that upregulate ICAM-1. The experiment data are relevant to the current understanding of basic mechanisms that explain the signal transudation pathway occurring inside the endothelial cells under the effect of SS.

Animals↗
PubMed2001

Nitric oxide attenuates alpha(2)-adrenergic receptors by ADP-ribosylation of G(i)alpha in ciliary epithelium.

PURPOSE: To determine the mechanism by which nitric oxide (NO) regulates alpha(2)-adrenergic receptor coupling to adenylyl cyclase in bovine ciliary epithelium. METHODS: Ciliary epithelial explants were dissected, cultured, and labeled with [(3)H]adenine. [(3)H]Adenosine 3',5'-cyclic monophosphate (cAMP) was measured under basal conditions and after exposure to forskolin, isoproterenol, clonidine, yohimbine, pertussis toxin, and the NO donor spermine-NO. Endogenous and NO-stimulated ADP-ribosylation of ciliary epithelial membrane proteins was determined by [(32)P]nicotinamide adenosine diphosphate (NAD) labeling and autoradiography. The three isoforms of the G(i)alpha protein subunit were evaluated by Western blot analysis. RESULTS: Basal [(3)H]cAMP content was 13.4 +/- 1.3 picomoles/mg protein (SEM). Both isoproterenol and forskolin stimulated [(3)H]cAMP accumulation to 36.0 +/- 3.9 and 73.2 +/- 17.5 picomoles/mg protein, respectively. Clonidine did not affect basal [(3)H]cAMP levels, but attenuated both isoproterenol- and forskolin-mediated [(3)H]cAMP accumulation to 23.2 +/- 4.4 and 31.6 +/- 4.6 picomoles/mg protein, respectively. Yohimbine antagonized the clonidine-mediated adenylyl cyclase inhibition. Pertussis toxin blocked the effect of clonidine. In the presence of the NO donor spermine-NO, the clonidine-mediated inhibition of forskolin- and isoproterenol-stimulated cAMP accumulation was attenuated completely. NO significantly stimulated endogenous [(32)P]ADP-ribosylation of a 40-kDa membrane protein. Western blot analysis with specific antibodies revealed expression of all three G(i) subtypes--G(i1)alpha, G(i2)alpha, and G(i3)alpha--in bovine ciliary epithelium. CONCLUSIONS: NO attenuates alpha(2)-adrenergic receptor-mediated inhibition of adenylyl cyclase in ciliary epithelium through ADP-ribosylation of the G(i)alpha subunit. The findings demonstrate heterologous regulation between the NO and cAMP signaling pathways in ciliary epithelium.

Adenosine Diphosphate Ribose↗
PubMed2000

Early loss of synaptic protein PSD-95 from rod terminals of rhodopsin P347L transgenic porcine retina.

Retinitis pigmentosa (RP), a type of retinal degeneration involving first rod and then slow cone photoreceptor degeneration, can be caused by any of a number of mutations in different genes. In the cases of mutations affecting rod-specific genes such as rhodopsin, it is unclear how the mutations may cause degeneration of cones. We have used the porcine retina, which is rod-dominated and has an abundance of cones, to study the mutation-induced changes in both rod and cone photoreceptors. Like patients with the same mutation, rhodopsin P347L transgenic swine manifest rod-cone degeneration. In addition, the rod bipolar cells fail to form synaptic connections with rods; instead, they form ectopic synapses with cones. The mechanisms that prevent the formation of the rod-rod bipolar cell synaptic connection are not known. We used specific antibodies and immunocytochemistry to show that the synaptic protein, PSD-95, is present in both normal and transgenic porcine retinas. During neonatal development, however, PSD-95 is lost from rod terminals in the transgenic swine. This loss is virtually complete (90%) by postnatal day 5, at a time when greater than 80% of rod cell bodies still remain. Furthermore, the remaining rods retain their outer segments and their gross morphology appears relatively normal. In contrast, PSD-95 expression continues in cone terminals, even in 10-month-old transgenic swine, where the rods have all disappeared and the cones show signs of severe degeneration. These results suggest that loss of PSD-95 may not be a general consequence of the deteriorating cell. Rather, the very early and selective loss of PSD-95 from the rod terminals may be causally related to the absence of rod-rod bipolar cell synapses in the rhodopsin P347L transgenic retina.

Animals↗
PubMed2000

BAG-1 promotes apoptosis induced by N-(4-hydroxyphenyl)retinamide in human cervical carcinoma cells.

N-(4-hydroxyphenyl)retinamide (4-HPR) is a synthetic apoptosis-inducing retinoid with cancer chemopreventive properties and lower toxicity than all-trans retinoic acid. BAG-1 is an antiapoptotic gene that is overexpressed in cervical and other cancers. In this study, we examined whether BAG-1 can inhibit 4-HPR-induced apoptosis in the C33A cervical carcinoma cell line. Surprisingly, although it inhibited apoptosis induced by five different apoptotic stimuli, overexpression of BAG-1 enhanced apoptosis induced by 4-HPR, producing a 2.5-fold lower IC(50) of 4-HPR. The effects of BAG-1 on 4-HPR-induced apoptosis were mediated by enhancing the caspase-3 activation pathway. Deletion mutation experiments showed that the central ubiquitin homology domain of BAG-1 protein was necessary for its promotion of 4-HPR-induced apoptosis, whereas its C-terminal Hsp70/Hsc70-interacting domain was required for its inhibition of staurosporine-induced apoptosis. These in vitro results suggest that the effectiveness of 4-HPR against the development of malignancy may be due to the overexpression of BAG-1 in cancer cells.

Antineoplastic Agents↗
PubMed2000

Serotonin released from intestinal enterochromaffin cells mediates luminal non-cholecystokinin-stimulated pancreatic secretion in rats.

BACKGROUND & AIMS: Similar to cholecystokinin (CCK), non-CCK-dependent duodenal factors stimulate vagal mucosal afferent fibers to mediate pancreatic enzyme secretion via a common cholinergic pathway. We tested the hypothesis that 5-hydroxytryptamine (5-HT) released from enterochromaffin (EC) cells plays an important role in the transduction of luminal information to the central nervous system via vagal afferent fibers to mediate pancreatic secretion. METHODS: Pancreatic secretions were examined in conscious rats after intragastric administration of chopped rodent chow in the presence and absence of CCK or 5-HT(3) and 5-HT(2) antagonists. Pancreatic responses to intraduodenal administration of maltose, hyperosmolar NaCl, and light mucosal stroking were examined in rats pretreated with various pharmacological antagonists or after surgical or chemical ablation of vagal and 5-HT neural pathways. RESULTS: Administration of L364, 718 inhibited 54% of pancreatic protein secretion evoked by intragastric administration of rodent chow. L364,714 and ICS 205-930, a 5-HT(3) antagonist, combined produced a 94% inhibition. Vagal afferent rootlet section eliminated pancreatic secretions evoked by intraduodenal stimuli. p-Chlorophenylalanine, a 5-HT synthesis inhibitor, but not 5,7-hydroxytryptamine, a 5-HT neurotoxin, also eliminated the pancreatic response to these luminal stimuli. The 5-HT(3) antagonist markedly inhibited pancreatic secretion induced by maltose and hyperosmolar NaCl. 5-HT(2) and 5-HT(3) antagonists combined inhibited the pancreatic response to light stroking of the mucosa. CONCLUSIONS: Luminal factors such as osmolality, disaccharides, and mechanical stimulation stimulated pancreatic secretion via intestinal vagal mucosal afferent fibers. It is likely that 5-HT originating from intestinal EC cells activated 5-HT(3) and 5-HT(2) receptors on vagal afferent fibers to mediate luminal factor-stimulated pancreatic secretion.

5,7-Dihydroxytryptamine↗
PubMed2000

Ectopic synaptogenesis in the mammalian retina caused by rod photoreceptor-specific mutations.

In addition to rod photoreceptor loss, many mutations in rod photoreceptor-specific genes cause degeneration of other neuronal types. Identifying mechanisms of cell-cell interactions initiated by rod-specific mutations and affecting other retinal cells is important for understanding the pathogenesis and progression of retinal degeneration. Here we show in animals with rod and cone degeneration due to mutations in the genes encoding rhodopsin and cGMP phosphodiesterase beta-subunit (PDE-beta) respectively, that rod bipolar cells received ectopic synapses from cones in the absence of rods. Thus, synaptic plasticity links certain rod-specific mutations to retina-wide structural alterations that involve different types of neurons.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed2000

Cell signaling in bovine ciliary epithelial organ culture.

The ciliary epithelium secretes aqueous humor, an intraocular fluid whose production is regulated in part by transmembrane signaling pathways including those mediated by G protein-coupled receptors. Many drugs, such as beta-adrenergic receptor (AR) antagonists and alpha2-AR agonists, are used to lower intraocular pressure by presumably decreasing fluid transport across this epithelium. Hence, our purpose was to establish a ciliary epithelial organ culture system suitable for the study of cell signaling pathways. A trypsin-mediated dissection method was established to isolate bovine ciliary epithelial sheets. These sheets were cultured in a 5% CO2 incubator. The quality was assessed by light microscopy, by protein analysis, and by the evaluation of epinephrine-mediated phosphoinositide turnover. The cultured epithelial explants were viable as evidenced by minimal trypan blue staining. The explants were composed primarily of nonpigmented cells and some pigmented cells, but no other ciliary body tissues were present on histology. Membrane preparations showed proteins with a distribution from 31 to 116 kDa. Epinephrine caused a dose-dependent increase in [3H]inositol phosphates (InsPs) accumulation with a maximal increase of two- to three-fold over basal levels. This epinephrine-mediated increase was inhibited by prazosin. We established an organ culture system of isolated bovine ciliary epithelium suitable for the study of transmembrane signaling pathways.

Adrenergic Agonists↗
PubMed2000

Identification of antiangiogenic and antiinflammatory proteins in human amniotic membrane.

PURPOSE: To identify the potential antiangiogenic and antiinflammatory proteins expressed in human amniotic membrane tissue. METHODS: Human amniotic epithelial and mesenchymal cells were isolated from human amniotic membranes by sequential trypsin and collagenase digestion. Total RNAs were harvested from freshly obtained human amniotic epithelial and mesenchymal cells. Antiangiogenic and antiinflammatory proteins were detected by the reverse transcriptase-polymerase chain reaction (RT-PCR) technique and further confirmed by DNA sequencing of PCR-amplified transcripts. The distribution of tissue inhibitors of metalloproteinase (TIMPs) were studied further by immunohistochemistry performed on paraffin-embedded amniotic membrane tissue. RESULTS: RT-PCR results showed that both human amniotic epithelial and mesenchymal cells express interleukin-1 receptor antagonist, all four TIMPs, collagen XVIII, and interleukin-10. Thrombospondin-1 was expressed in all of the epithelial cell specimens and in one out of five mesenchymal cell specimens. Furthermore, immunohistochemistry studies performed on freshly prepared amniotic membrane confirmed that all members of the TIMP family were present in epithelial and mesenchymal cells as well as in the compact layer of the amniotic stroma. In cryopreserved amniotic membranes, positive staining was seen in residual amniotic cells and stroma. CONCLUSIONS: Human amniotic membrane epithelial and mesenchymal cells express various antiangiogenic and antiinflammatory proteins. Some of those proteins also were found in amniotic membrane stroma. These findings may explain in part the antiangiogenic and antiinflammatory effects of amniotic membrane transplantation.

Amnion↗
PubMed2000

Diazepam-binding inhibitor mediates feedback regulation of pancreatic secretion and postprandial release of cholecystokinin.

Recently, we isolated a trypsin-sensitive cholecystokinin-releasing peptide (CCK-RP) from porcine and rat intestinal mucosa. The amino acid sequence of this peptide was determined to be identical to that of the diazepam-binding inhibitor (DBI). To test the role of DBI in pancreatic secretion and responses to feeding, we used pancreaticobiliary and intestinal cannula to divert bile-pancreatic juice from anesthetized rats. Within 2 hours, this treatment caused a 2-fold increase in pancreatic protein output and a >10-fold increase in plasma CCK. Luminal DBI levels increased 4-fold. At 5 hours after diversion of bile-pancreatic juice, each of these measures returned to basal levels. Intraduodenal infusion of peptone evoked a 5-fold increase in the concentration of luminal DBI. In separate studies, we demonstrated that intraduodenal administration of antiserum to a DBI peptide specifically abolished pancreatic secretion and the increase in plasma CCK levels after diversion of bile-pancreatic juice. To demonstrate that DBI mediates the postprandial rise in plasma CCK levels, we showed that intraduodenal administration of 5% peptone induced dramatic increases in pancreatic secretion and plasma CCK, effects that could be blocked by intraduodenal administration of anti-DBI antiserum. Hence, DBI, a trypsin-sensitive CCK-RP secreted from the proximal small bowel, mediates the feedback regulation of pancreatic secretion and the postprandial release of CCK.

Acyl Coenzyme A↗
PubMed2000

The effect of the prostaglandin I2 analogue OP-2507 on adrenaline-induced pulmonary edema in rabbits and analysis of hemodynamic changes.

This study was carried out to understand the onset mechanism of adrenaline (ADR)-induced pulmonary edema (PE) and the effect of drugs related to the arachidonate cascade in a rabbit model. ADR was administered intravenously by a bolus injection to the rabbits at 50, 75 and 100 microg/kg. To evaluate the severity of PE, the lung-water ratio (LWR) was calculated as a ratio of the difference between wet and dry lung weight to dry lung weight. The PE incidence and LWR exhibited a dose-dependent increase, and LWR correlated with the left atrial pressure (LAP). The involvement of the arachidonate cascade was evaluated by the co-administration of flurbiprofen, a cyclooxygenase inhibitor; ozagrel, a thromboxane synthase inhibitor; and OP-2507 (15-cis-(4-n-propylcyclohexyl)-6,17,18, 19,20-pentanor-9-deoxy-6,9-alpha-nitriloprostaglandin F1 methyl ester), a prostaglandin I2 analogue. Co-treatment of the rabbits with ADR and flurbiprofen resulted in an increase in LAP and the incidence of PE, whereas co-administration of ozagrel did not exhibit any significant changes in the measured parameters. Conversely, OP-2507 reduced the LAP, PE incidence and LWR when co-administered with ADR. Rabbits co-treated with OP-2507 displayed an improved cardiac function. The results of these studies demonstrated the effectiveness of OP-2507 in protecting the lung and cardiac function from the ADR-induced PE.

Animals↗
PubMed1999

Overexpression of anti-apoptotic gene BAG-1 in human cervical cancer.

Apoptosis is a programmed cell death process in which cells commit suicide under certain environmental conditions. Recent studies suggest that apoptosis is controlled by a variety of cellular genes, and dysregulation of these genes plays an important role in the pathogenesis of human diseases, including cancer. BAG-1 is a novel anti-apoptotic protein isolated by its interaction with another anti-apoptotic protein, Bcl-2. It binds to several hormone receptors and growth factor receptors and modulates their function in apoptosis. However, the role of BAG-1 in the oncogenesis of human cervical cancer has yet to be illustrated. In this study, we examined the expression of BAG-1 in cervical normal and carcinoma cultured cells and tissues. BAG-1 was overexpressed in human cervical carcinoma cell lines and tissues. Overexpression was regulated at the transcriptional level. The increased expression of BAG-1 was correlated with enhanced resistance of cervical carcinoma cells to apoptosis induced by a DNA-damaging reagent. In addition, overexpression of BAG-1 enhanced the resistance of cervical cells to apoptosis. This study provided the first evidence that BAG-1 is upregulated in human cervical cancer and may play an important role in apoptosis and human cervical carcinogenesis.

Apoptosis↗
PubMed1999

Evolutionary relationship between K(+) channels and symporters.

The hypothesis is presented that at least four families of putative K(+) symporter proteins, Trk and KtrAB from prokaryotes, Trk1,2 from fungi, and HKT1 from wheat, evolved from bacterial K(+) channel proteins. Details of this hypothesis are organized around the recently determined crystal structure of a bacterial K(+) channel: i. e., KcsA from Streptomyces lividans. Each of the four identical subunits of this channel has two fully transmembrane helices (designated M1 and M2), plus an intervening hairpin segment that determines the ion selectivity (designated P). The symporter sequences appear to contain four sequential M1-P-M2 motifs (MPM), which are likely to have arisen from gene duplication and fusion of the single MPM motif of a bacterial K(+) channel subunit. The homology of MPM motifs is supported by a statistical comparison of the numerical profiles derived from multiple sequence alignments formed for each protein family. Furthermore, these quantitative results indicate that the KtrAB family of symporters has remained closest to the single-MPM ancestor protein. Strong sequence evidence is also found for homology between the cytoplasmic C-terminus of numerous bacterial K(+) channels and the cytoplasm-resident TrkA and KtrA subunits of the Trk and KtrAB symporters, which in turn are homologous to known dinucleotide-binding domains of other proteins. The case for homology between bacterial K(+) channels and the four families of K(+) symporters is further supported by the accompanying manuscript, in which the patterns of residue conservation are demonstrated to be similar to each other and consistent with the known 3D structure of the KcsA K(+) channel.

Amino Acid Sequence↗
PubMed1999

Management of allogeneic bone marrow transplant recipients at risk for cytomegalovirus disease using a surveillance bronchoscopy and prolonged pre-emptive ganciclovir therapy.

BACKGROUND: Patients undergoing allogeneic bone marrow transplant (BMT) are considered to be at increased risk of cytomegalovirus (CMV) disease if they and/or their donor are CMV seropositive pre-transplant. Although several pre-emptive strategies have been shown to be effective in preventing early CMV disease, the ability of pre-emptive strategies using prolonged ganciclovir therapy to reduce the incidence of late-onset CMV infection, disease and mortality has not been fully evaluated. OBJECTIVE: To assess the efficacy of 18 weeks of pre-emptive ganciclovir therapy in preventing late-onset (> 100 days post-transplant) CMV disease when administered to asymptomatic BMT patients found to have CMV in bronchoalveolar lavage (BAL) fluid obtained during a surveillance bronchoscopy approximately 35 days post-transplant. To determine whether or not survival of BMT recipients is influenced by pre-transplant donor and recipient CMV serostatus in the context of this pre-emptive ganciclovir strategy. STUDY DESIGN: Consecutive patients undergoing allogeneic BMT were assessed for their risk of developing CMV disease based on their pre-transplant CMV serostatus and that of their donor. Patients who were CMV seropositive and/or received marrow from a CMV seropositive donor underwent a surveillance bronchoscopy and BAL approximately 35 days post-transplant. Patients with positive BAL fluid for CMV received pre-emptive ganciclovir therapy for 18 weeks at decreasing dose levels. Patients considered to be at low risk for the development of CMV disease (donor and recipient CMV seronegative) were followed without intervention. RESULTS: Of 98 consecutive patients, 55 were considered to be at risk for CMV disease and underwent a surveillance bronchoscopy. Sixteen (29%) patients had a positive BAL fluid for CMV and were started on pre-emptive ganciclovir therapy. Two patients progressed and died with CMV-related pneumonia. One additional patient developed CMV-related enteritis on day 42 post-transplant and recovered with continuing ganciclovir treatment. Of the 39 patients with a negative BAL fluid for CMV, one developed a fatal CMV pneumonia 150 days post-transplant and two additional patients developed gastrointestinal CMV disease 28 and 57 days post-BMT, respectively. None of the patients in the low risk group developed CMV disease. CONCLUSIONS: The strategy utilizing a surveillance bronchoscopy for CMV and initiating prolonged (18 weeks) pre-emptive ganciclovir therapy for patients with a positive BAL fluid for CMV resulted in a low incidence of CMV-related post-transplant complications. After a minimum follow-up of 16 months, late CMV reactivations (occurring > 100 days post-transplant) were not observed in the group of individuals pre-emptively treated with ganciclovir. This observation suggests that prolonged therapy with a reduced dose of ganciclovir may be important in the prevention of CMV reactivation. The CMV serostatus of donors and recipients prior to BMT did not correlate with survival.

Adult↗
PubMed1999

Differential expression of antiapoptotic gene BAG-1 in human breast normal and cancer cell lines and tissues.

BAG-1 is an antiapoptotic protein that binds to and enhances the antiapoptotic activity of Bcl-2. It binds several growth factor and hormone receptors and modulates their function. BAG-1 was also shown recently to be expressed as four protein isoforms, p50, p46, p33, and p29, through alternative translation initiation. Although many apoptosis-associated genes have been linked to oncogenesis of human breast cancer, the role of BAG-1 has not been fully elucidated. In this study, we examined the expression of BAG-1 RNA or protein isoforms and its interacting antiapoptotic proteins, Bcl-2 and BcI-X(L), in breast normal and tumor cell lines and tissues by Northern or Western blot analysis. We provide convincing evidence that both BAG-1 RNA and protein are overexpressed in human breast cancer cell lines. More importantly, we found that the expression of two isoforms of BAG-1, p46 and p33, was also much higher in breast primary tumors. The expression of Bcl-2 and Bcl-X(L) correlated with that of BAG-1 in breast normal and carcinoma cell lines but not tissues. Our study suggests that BAG-1 isoforms may serve as a molecular marker, independent of Bcl-2 and Bcl-X(L), for human breast cancer.

Adenocarcinoma↗
PubMed1999

Killing effect of interleukin-2 and interferon-alpha activated leukemic bone marrow in remission on K562 leukemic cells.

OBJECTIVE: To evaluate the killing effect of interleukin-2 (IL-2) and interferon-alpha (IFN-alpha) activated bone marrow cells on K562 cells. METHODS: Semi-solid colony and 3H-TdR incorporating method were used. RESULTS: Bone marrow from leukemia patients in remission was activated in vitro with IL-2 for 3 days. The activated bone marrow (ABM) displayed killing effects of 0.31-2.30 logs on K562 cells. This killing effect was further increased to 0.30-3.15 logs when IFN-alpha added with IL-2 to the marrow for activation. IL-2 alone or in combination with IFN-alpha showed no inhibition of CFU-GM and K562 cells. Compared with IL-2 or IFN-alpha alone, the combination of the two cytokines could more effectively maintain the killing effect of ABM on leukemic cells. CONCLUSIONS: IFN-alpha can augment the purging effect of IL-2 ABM and combination of the two cytokines can effectively maintain the cytotoxicity of ABM.

Acute Disease↗
PubMed1999

[Refractory anemia and preleukemia: an analysis of 92 cases].

OBJECTIVE: To investigate the relationship between MDS-RA (refractory anemia subtype of myelodysplastic syndromes) and preleukemia (PL). METHODS: Hematological parameters of 86 RA and 6 PL patients were retrospectively analyzed. RESULTS: Thirty-four RA cases (39.53%) transformed into acute leukemia (AL), RA with excess blasts (RAEB), or RAEB in transformation (RAEB-t). As compared with 52 non-transformed RA cases, the transformed cases showed the following hematological features: 1. higher frequencies of immature granulocytes (P < 0.005), erythroblasts (P < 0.05) and megaloerythrocytes (P < 0.05), and higher granulocyte nuclear lobulation (P < 0.001) in peripheral blood; 2. higher percentages of early erythroid and granulocytic lineages (P < 0.05), and higher frequencies of erythroblasts with multiple nuclei (P < 0.05), pseudo Pelger-Huet abnormality (P < 0.05), and micromegakaryocytes (P < 0.005) in bone marrow. CONCLUSION: There is a higher overlap between RA and PL; the above hematological features may be useful for predicting the transformation of RA patients. Based on those findings, a score system for predicting the transformation of RA was proposed.

Adolescent↗