Biomedical subjects

L Xue

Publications and source records attributed to L Xue.

At least 37 records · Page 2Linked to original sources

PubMed2001

[The value of medical thorascopy].

OBJECTIVE: To study the practicality and feasibility for a physician to diagnose and treat pleural diseases through thoracoscopy. METHODS: To perform open thoracoscopy on 345 patients with a fibrobronchoscope or a hard thoracoscope under local anesthesia and evaluate the safety and tolerance of patients during the operation. RESULTS: (1) Determination of etiology: in 92.7% (227/245 cases) of pleural effusion cases, 75.0% (69/92) of pneumothorax cases, etiologic causes have been determined and 8 cases of pleural tumors were diagnosed. (2) Therapeutic effectiveness: the response rate of malignant pleural effusions was 78.4% (80/102 cases), the cure rate of pneumothorax was 81.5% (75/92 cases) and for empyema, the cure rate was 92.9% (26/28 cases). (3) SAFETY: during operation the ECG, SaO(2), BP, R, P of 98 patients did not show important changes. In 345 patients, 4.3% (15/345) complained a fransceis cheot stiffin. 7% (24/345) showed sinus tachycardia. CONCLUSIONS: (1) Through thoracoscopy, we can observe the whole pleural cavity and can take biopsy specimen under direct observation. It is a good method to get the etiological diagnosis in cause-underdetermined pleural diseases. (2) It is effective and practical to treat difficult pleural effusion, the obstinate pneumothorax, or one that is not suitable for thoracic surgery. (3) It is safe and simple to apply the thoracoscopy under local anesthesia.

Adolescent↗

PubMed2001

Desensitization of adrenomedullin and calcitonin gene-related peptide receptors in vascular smooth muscle cells--effects of receptor activity-modifying protein.

Recent researches suggest that adrenomedullin (ADM) and calcitonin gene-related peptide (CGRP) bind to the same calcitonin receptor-like receptors (CRLR), with receptor specificity being determined by a receptor activity-modifying protein (RAMP). Our objective was to explore the significance of CRLR/RAMP hypothesis in cardiovascular tissues through experiments on the phenomenon of desensitization of both ADM and CGRP receptors using cultured rat aortic vascular smooth muscle cells (VSMCs). VSMCs were incubated for 20 min either in serum-free medium (SFM) alone or in the SFM containing vasoactive agonist [10(-8) mol/L ADM, CGRP and proadrenomedullin (PAMP)]. Cells were washed twice and incubated for another 20 min in SFM containing a repetitive agonist ADM or CGRP and 0.5 mmol/L isobutyryl methylxant (an inhibitor of phosphodiesterase). VSMCs were harvested and assayed for cAMP. Exposure of VSMCs to ADM, CGRP, or PAMP alone increased intracellular cAMP generation by 191% (P < 0.01), 385% (P < 0.01) and 67% (P < 0.05), respectively, compared with SFM group. Pre-treatment of VSMCs to ADM or CGRP decreased cAMP generation in response to subsequent stimulation with CGRP by 44% (P < 0.05) and 48% (P < 0.01), respectively. Pre-treatment of VSMCs with 100 nmol/L H-89, a protein kinase A (PKA) inhibitor, abolished the desensitization of CGRP-acting receptor, implying that this desensitization was mediated through PKA. In contrast, there was no attenuation in cAMP response to stimulation with ADM by pre-exposure to ADM or CGRP. Identical results were seen with or without PKA inhibition by H-89. Pre-exposure of VSMCs to PAMP resulted in no change in cAMP generation in response to subsequent stimulation with ADM or CGRP. These results indicate that ADM receptors do not desensitize in VSMCs in contrast to CGRP-receptors, which are desensitized by pre-exposure to ADM or CGRP. These data also suggest that the desensitization phenomenon of ADM is different from that of CGRP.

Adrenomedullin↗

PubMed2001

[Influence of interleukin-10 on nitric oxide /nitric oxide synthase system of the aorta].

To study the influence of the inflammatory factor---interleukin-10 on nitric oxide (NO) and nitric oxide synthase system of rat aorta, Griess assay, production of (3)H-citrulline and Western blot were used to determine the release of NO, and the activity and expression of nitric oxide synthase, respectively. The results showed that lipopolysaccharide (LPS) stimulated the activity of inducible nitric oxide synthase (iNOS) and the release of NO. 10(-10) 10(-8) g/ml of IL-10 induced the activity and expression of endothelial nitric oxide synthase (eNOS), but not of iNOS. 10(-9) 10(-8) g/ml of IL-10 also downloaded the release of NO, and the activity and expression of iNOS induced by LPS, while 10(-7) g/ml of IL-10 significantly stimulated the activity and expression of iNOS but not eNOS. In summary, IL-10 presents a duple role in NO/NOS system. On the one hand, IL-10 inhibits the activity and expression of iNOS induced by inflammatory factor; on the other hand, IL-10 stimulates the release of endothelial NO.

Animals↗

PubMed2000

Inhibition of JNK by overexpression of the JNL binding domain of JIP-1 prevents apoptosis in sympathetic neurons.

Studies in non-neuronal cells show that c-Jun N-terminal kinases (JNK) play a key role in apoptotic cell death. In some neurons JNK is also thought to initiate cell death by the activation of c-Jun. JNK inhibition has been achieved pharmacologically by inhibiting upstream kinases, but there has been no direct demonstration that inhibition of JNK can prevent neuronal death. We have therefore examined whether the JNK binding domain (JBD) of JNK-interacting protein-1 (JIP-1, a scaffold protein and specific inhibitor of JNK) can inhibit c-Jun phosphorylation and support the survival of sympathetic neurons deprived of NGF. We show that expression of the JBD in >80% of neurons was sufficient to prevent the phosphorylation of c-Jun and its nuclear accumulation as well as abrogate neuronal cell death induced by NGF deprivation. JBD expression also preserved the capacity of mitochondria to reduce MTT. Interestingly, although the PTB domain of JIP was reported to interact with rhoGEF, expression of the JBD domain was sufficient to localize the protein to the membrane cortex and growth cones. Hence, JNK activation is a key event in apoptotic death induced by NGF withdrawal, where its point of action lies upstream of mitochondrial dysfunction.

Adaptor Proteins, Signal Transducing↗

PubMed2000

Death commitment point is advanced by axotomy in sympathetic neurons.

Axotomized neurons have several characteristics that are different from intact neurons. Here we show that, unlike established cultures, the axotomized sympathetic neurons deprived of NGF become committed to die before caspase activation, since the same proportion of NGF-deprived neurons are rescued by NGF regardless of whether caspases are inhibited by the pan-caspase inhibitor Boc-Asp(O-methyl)-CH(2)F (BAF). Despite prolonged Akt and ERK signaling induced by NGF after BAF treatment has prevented death, the neurons fail to increase protein synthesis, recover ATP levels, or grow. Within 3 d, all the mitochondria disappear without apparent removal of any other organelles or loss of membrane integrity. Although NGF does rescue intact BAF-treated 6-d cultures after NGF deprivation, rescue by NGF fails when these neurons are axotomized before NGF deprivation and BAF treatment. Moreover, cytosolic cytochrome c rapidly kills axotomized neurons. We propose that axotomy induces signals that make sympathetic neurons competent to die prematurely. NGF cannot repair these NGF-deprived, BAF-treated neurons because receptor signaling (which is normal) is uncoupled from protein renewal, and the mitochondria (which are damaged) go on to be eliminated. Hence, the order of steps underlying neuronal death commitment is mutable and open to regulation.

Adenosine Triphosphate↗

PubMed2000

Drosophila female sexual behavior induced by sterile males showing copulation complementation.

Females of most animal species are usually inseminated by more than one male, which allows sperm from different males to compete for fertilization. To prevent invasion of sperm from other males, Drosophila males elicit a rejection behavior in their mates after copulation. Using paired mutant males that, for the lack of accessory glands, are sterile, we show that this rejection behavior is induced exclusively by the secreted accessory gland products transferred to the female during copulation. Moreover, the activities of sperm and accessory gland products are complementary and interdependent: both sperm fertility and rejection behavior depend on accessory gland products whose prolonged activities, in turn, require the presence of sperm. Fertility of sperm from paired males can be restored by accessory gland products of spermless males in "copulation complementation" experiments. Our observations may have important implications for the role of sexual behavior in evolution and for the treatment of male sexual dysfunction in humans.

Animals↗

PubMed2000

The Ras/phosphatidylinositol 3-kinase and Ras/ERK pathways function as independent survival modules each of which inhibits a distinct apoptotic signaling pathway in sympathetic neurons.

Ras promotes robust survival of many cell systems by activating the phosphatidylinositol 3-kinase (PI3-kinase)/Akt pathway, but little is understood about the survival functions of the Ras/ERK pathway. We have used three different effector-loop mutant forms of Ras, each of which activates a single downstream effector pathway, to dissect their individual contributions to survival of nerve growth factor (NGF)-dependent sympathetic neurons. The PI3-kinase pathway-selective protein Ras(Val-12)Y40C was as powerful as oncogenic Ras(Val-12) in preventing apoptosis induced by NGF deprivation but conferred no protection against apoptosis induced by cytosine arabinoside. Identical results were obtained with transfected Akt. In contrast, the ERK pathway-selective protein Ras(Val-12)T35S had no protective effects on NGF-deprived neurons but was almost as strongly protective as Ras(Val-12) against cytosine arabinoside-induced apoptosis. The protective effects of Ras(Val-12)T35S against cytosine arabinoside were completely abolished by the ERK pathway inhibitor PD98059. Ras(Val-12)E37G, an activator of RalGDS, had no survival effect on either death pathway, similar to RasS17N, the full survival antagonist. Thus, Ras provides two independent survival pathways each of which inhibits a distinct apoptotic mechanism. Our study presents one of the few clear-cut cases where only the Ras/ERK, but not the Ras/PI3K/Akt pathway, plays a dominant survival signaling role.

Animals↗

PubMed2000

Carbon monoxide and nitric oxide as coneurotransmitters in the enteric nervous system: evidence from genomic deletion of biosynthetic enzymes.

Nitric oxide (NO) and carbon monoxide (CO) seem to be neurotransmitters in the brain. The colocalization of their respective biosynthetic enzymes, neuronal NO synthase (nNOS) and heme oxygenase-2 (HO2), in enteric neurons and altered intestinal function in mice with genomic deletion of the enzymes (nNOS(Delta/Delta) and HO2(Delta/Delta)) suggest neurotransmitter roles for NO and CO in the enteric nervous system. We now establish that NO and CO are both neurotransmitters that interact as cotransmitters. Small intestinal smooth muscle cells from nNOS(Delta/Delta) and HO2(Delta/Delta) mice are depolarized, with apparent additive effects in the double knockouts (HO2(Delta/Delta)/nNOS(Delta/Delta)). Muscle relaxation and inhibitory neurotransmission are reduced in the mutant mice. In HO2(Delta/Delta) preparations, responses to electrical field stimulation are nearly abolished despite persistent nNOS expression, whereas exogenous CO restores normal responses, indicating that the NO system does not function in the absence of CO generation.

Animals↗

PubMed2000

The cysteine-free fibroblast growth factor 1 mutant induces heparin-independent proliferation of endothelial cells and smooth muscle cells.

BACKGROUND: The structure/function relationships of fibroblast growth factor 1 (FGF-1) are being investigated using site mutation, yielding novel structures with potential clinical applicability for modulating tissue responses to vascular interventions. We generated a mutant FGF-1 in which all three cysteines were converted to serines and then tested the relative mitogenic activities on endothelial cells (ECs) and smooth muscle cells (SMCs) and the molecular stability of the protein to thrombin-induced degradation. METHODS: The dose responses of wild-type FGF-1 and the Cys-free mutant in the absence or presence of heparin were tested on ECs and SMCs. Cell proliferation was measured by [(3)H]thymidine incorporation. Data were normalized by positive control (20% fetal bovine serum) and expressed as percentage of positive control for comparison. The molecular stability was examined by exposure of the cytokines to thrombin at 37 degrees C for 0.5-24 h and then analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. RESULTS: Unlike wild-type FGF-1 which induced only minimal DNA synthesis at concentrations as high as 100 ng/ml, the Cys-free mutant induced a dose-dependent proliferation starting at 1 ng/ml on both ECs and SMCs in the absence of heparin. At 100 ng/ml, Cys-free mutant induced 4-fold more proliferation than wild-type FGF-1 on ECs (76.64 +/- 13.39% vs 14.58 +/- 1.38%, P < 0.01) and 12-fold more proliferation on SMCs (143.52 +/- 9.96 vs 11.25 +/- 3.32, P < 0.01). Heparin 5 U/ml potentiated the mitogenic activity of the Cys-free mutant at low dose range. Both proteins were degraded by thrombin progressively. But the Cys-free mutant showed more susceptibility with accelerated appearance of lower-molecular-weight fragment bands after incubation with thrombin. CONCLUSIONS: Conversion of cysteine residues to serine changed the heparin dependency of the growth factor and increased its mitogenic activity and its susceptibility to thrombin-induced degradation.

Animals↗

PubMed2000

Evolution of Hoxa-11 in lineages phylogenetically positioned along the fin-limb transition.

HOXA11 is a transcription factor implicated in paired appendage development. To identify signatures of evolutionary change in the structural, and putative functional, domains of HOXA11, we studied its evolution in tetrapod and nontetrapod lineages that represent approximately 1.5 billion years of evolutionary time. Here, Hoxa-11 gene proper sequences were determined for frog (Xenopus tropicalis), coelacanth (Latimeria chalumnae), common zebrafish (Danio rerio; Hoxa-11a and Hoxa-11b paralogs), and giant zebrafish (D. aequipinnatus; Hoxa-11b) and aligned against previously published Hoxa-11 sequences of human, mouse, chick, and newt. Based on aligned Hoxa-11 amino acid sequences, the protein was demarcated into three segments: Domains I (N-terminal) and III (homeobox + C-terminal), which varied slightly in rates and patterns of evolution, and a variable, overall hydrophilic region (HyD), which partially overlaps with Domain I. As judged by character reconstructions of HOXA11 Domains I and III, no significant changes in rates of coding sequence evolution occurred in tetrapods (frog and chick), relative to coelacanth (a lobe-finned fish), i.e., across the fin-limb transition. Accelerated rates of Hoxa-11 coding sequence evolution were observed for the mammalian and newt lineages. This was shown to be a gene-specific phenomenon. The duplicated Hoxa-11a and Hoxa-11b genes of zebrafish exhibited accelerated rates of evolution and accumulated substitutions at sites that are conserved among coelacanth and all tetrapods examined. Amino acid sequence comparisons of the HyD of HOXA11 suggested that a putative repressor subdomain, containing stretches of consecutive alanine residues, emerged within the tetrapods. A high degree of nucleotide conservation in the 5' half of the Hoxa-11 intron was observed for tetrapod and nontetrapod lineages. Using electrophoretic mobility shift assays, a 35-bp intron sequence, which is 100% conserved in all Hoxa-11 loci except for the zebrafish Hoxa-11a paralog, was found to bind protein(s) in HeLa and chick whole-cell extracts.

Alanine↗

PubMed2000

The S130K fibroblast growth factor-1 mutant induces heparin-independent proliferation and is resistant to thrombin degradation in fibrin glue.

OBJECTIVE: Site-directed mutagenesis is an important technique that can alter cytokine function, thereby eliciting desired responses. S130K is a mutation of fibroblast growth factor-1 (FGF-1), with lysine replacing serine in the heparin-binding site. We measured molecular stability and mitogenic activity of FGF-1 and S130K, both in the media and when suspended in fibrin glue (FG), on smooth muscle cells (SMCs) and endothelial cells (ECs) to determine if the mutation altered the function and potential clinical applicability. METHODS: EC and SMC proliferation of soluble FGF-1 or S130K at 0, 0. 1, 1, 10, or 100 ng/mL with heparin at 0, 5, 50, or 500 units (U)/mL was measured on growth-arrested cells in serum-free media. EC and SMC proliferation assays with cells on FG containing either FGF-1 or S130K at 0, 1, 10, 100, or 1000 ng/mL in combination with heparin at 0, 5, 50 or 500 U/mL were also performed during the exponential growth phase. Molecular degradation by thrombin was measured by sodium dodecylsulfate-polyacrylamide gel electrophoresis. RESULTS: S130K induces greater EC and SMC proliferation in the absence of heparin than FGF-1 does (P <.0001 for both the 10 and 100 ng/mL doses). S130K is also significantly more potent than FGF-1 in the presence of heparin. Heparin in the media enhances cytokine-induced SMC and EC proliferation at doses of 5 U/mL, but inhibits SMC proliferation at concentrations of 500 U/mL. For the FG data, unlike FGF-1, S130K induces EC and SMC proliferation in the absence of heparin. The addition of 5 U/mL of heparin enhances the proliferation induced by S130K. For ECs, as the heparin dose increases to 50 U/mL, proliferation decreases, as compared with the 5 U/mL concentration when either FGF-1 or S130K in the FG was compared at concentrations of 10, 100, and 1000 ng/mL (P <.01). S130K is more potent in FG than is FGF-1 both with and without heparin and exhibits maximal EC and SMC proliferation at 10 ng/mL, whereas FGF-1 activity is maximal at 100 ng/mL. Gel electrophoresis demonstrated that S130K was relatively more resistant to thrombin degradation than FGF-1. CONCLUSIONS: Site-directed mutagenesis changed the potency and the heparin dependency on cellular proliferation of FGF-1 in vitro. These techniques should allow the delivery of mutant growth factors to areas of vascular intervention to induce specific, desired responses. We believe that these studies will enhance our knowledge of the function of various regions of the FGF-1 molecule, allowing us to more precisely design increasingly more useful FGF-1 mutants.

Animals↗

PubMed2000

Combinatorial preferences affect molecular similarity/diversity calculations using binary fingerprints and Tanimoto coefficients

A combinatorial method was developed to calculate complete distributions of the Tanimoto coefficient (Tc) for binary fingerprint (FP) representations of specified length, regardless of the chemical parameters they reflect. Theoretical Tc distributions were calculated for FPs consisting of up to 67 bit positions which revealed significant statistical preferences of certain Tc values. Calculation of Tc distributions in a large compound database using different FPs mirrored the effects identified by our general analysis. On the basis of these findings, an average Tc is biased by statistically preferred values.

Journal Article↗

PubMed2000

Searching for molecules with similar biological activity: analysis by fingerprint profiling.

We have recently developed a mini-fingerprint (MFP) representation for small molecules that performs well in database searches for compounds with similar biological activity. The MFP consists of only 54 bit positions that account for numerical ranges of three two-dimensional (2D) descriptors or the presence or absence of defined structural fragments. Here we present an analysis method, termed fingerprint profiling, to systematically compare bit patterns of compounds belonging to different biological activity classes. Some but not all bit positions were variably occupied in seven different activity classes and responsible for the detection of structure-activity differences. The analysis has made it possible to rank bit positions and encoded molecular descriptors according to their importance for our similarity search calculations. Fingerprint profiling can be applied to any keyed bit string representation and should be helpful, for example, to analyze descriptor distributions in large compound databases.

Computer-Aided Design↗

PubMed2000

Effect of exogenous ATP on canine jejunal smooth muscle.

Intracellular recordings were made from the circular smooth muscle cells of the canine jejunum to study the effect of exogenous ATP and to compare the ATP response to the nonadrenergic, noncholinergic (NANC) inhibitory junction potential (IJP) evoked by electrical field stimulation (EFS). Under NANC conditions, exogenous ATP evoked a transient hyperpolarization (6.5 +/- 0.6 mV) and EFS evoked a NANC IJP (17 +/- 0.4 mV). Omega-conotoxin GVIA (100 nM) and a low-Ca(2+), high-Mg(2+) solution abolished the NANC IJP but had no effect on the ATP-evoked hyperpolarization. The ATP-evoked hyperpolarization and the NANC IJP were abolished by apamin (1 microM) and N(G)-nitro-L-arginine (100 microM). Oxyhemoglobin (5 microM) partially (38.8 +/- 5.5%) reduced the amplitude of the NANC IJP but had no effect on the ATP-evoked hyperpolarization. Neither the NANC IJP nor the ATP-evoked hyperpolarization was affected by P2 receptor antagonists or agonists, including suramin, reactive blue 2, 1-(N, O-bis-[5-isoquinolinesulfonyl]-N-methyl-L-tyrosyl)-4-phenylpiperazine , pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid, alpha, beta-methylene ATP, 2-methylthioadenosine 5'-triphosphate tetrasodium salt, and adenosine 5'-O-2-thiodiphosphate. The data suggest that ATP evoked an apamin-sensitive hyperpolarization in circular smooth muscle cells of the canine jejunum via local production of NO in a postsynaptic target cell.

Adenosine Triphosphate↗

PubMed2000

Expression and regulation of a molecular marker, SPR1, in multistep bronchial carcinogenesis.

A small proline-rich protein, SPR1, is overexpressed in squamous metaplasia of bronchial epithelium. We studied the expression and regulation of SPR1 in a series of human bronchial epithelial cell lines representing a model of multistep bronchial carcinogenesis. These cell lines included a primary culture of tracheobronchial epithelial cells (HTBE), a papilloma virus-transformed tracheobronchial epithelial cell line (HBE1), a cell line selected from HBE1 by a tobacco carcinogen and a phorbol ester (HBE1-C), a simian virus-transformed bronchial epithelial cell line (BEAS-2B), and a lung carcinoma cell line (H460). Different tumorigenic potentials of these cell lines were indicated by graded levels of telomerase activity. Concomitant with squamous transformation, there was an increase in SPR1 expression in HTBE, HBE1, and HBE1-C that was reversible by vitamin A. With progression of tumorigenicity, there was a marked reduction in SPR1 expression in BEAS-2B and a total loss of expression in H460. In these latter cell lines representing advanced malignant transformation, there was a loss of up- and downregulation, respectively, by the phorbol ester and vitamin A. Transfection study with chimeric constructs of the SPR1 promoter and a reporter gene showed that the dysregulation of SPR1 expression in malignant transformation was a result of perturbation of the basal and enhancer elements of the first 162 nucleotides in the 5'-flanking promoter region of the SPR1 gene. These findings suggest an association of transcriptional dysregulation of the SPR1 gene with multistep bronchial carcinogenesis.

Animals↗

PubMed2000

Molecular descriptors in chemoinformatics, computational combinatorial chemistry, and virtual screening.

Many contemporary applications in computer-aided drug discovery and chemoinformatics depend on representations of molecules by descriptors that capture their structural characteristics and properties. Such applications include, among others, diversity analysis, library design, and virtual screening. Hundreds of molecular descriptors have been reported in the literature, ranging from simple bulk properties to elaborate three-dimensional formulations and complex molecular fingerprints, which sometimes consist of thousands of bit positions. Knowledge-based selection of descriptors that are suitable for specific applications is an important task in chemoinformatics research. If descriptors are to be selected on rational grounds, rather than guesses or chemical intuition, detailed evaluation of their performance is required. A number of studies have been reported that investigate the performance of molecular descriptors in specific applications and/or introduce novel types of descriptors. Progress made in this area is reviewed here in the context of other computational developments in combinatorial chemistry and compound screening.

Algorithms↗

PubMed2000

Molecular typing of Trichomonas vaginalis isolates by HSP70 restriction fragment length polymorphism.

Subtyping isolates of Trichomonas vaginalis is an essential tool for understanding the epidemiology of this common sexually-transmitted disease. Restriction fragment length polymorphism (RFLP) analysis employing a probe from the heat-inducible cytoplasmic HSP70 gene family hybridized with EcoR I-digested genomic DNA was used in the molecular typing of Trichomonas isolates. Analysis of five American Type Culture Collection (ATCC) reference strains and 31 Jackson, Mississippi, isolates from six male and 21 female patients, revealed 10 distinct RFLP pattern subtypes of Trichomonas. The subtypes were temporally stable and cosmopolitan. The RFLP profiles seen in Maryland, Ohio, Massachusetts, and New York ATCC strains were identical to those of some Mississippi isolates, even though the samples were isolated 10-35 years apart. There was no correlation between metronidazole resistance and RFLP subtype with resistant isolates from eight patients distributed among six different subtypes.

Animals↗

PubMed2000

[Effect of chuanwu and baishao used separately or in combination on adjuvant arthritis in rats].

OBJECTIVE: To study the effect of Chuanwu(Aconitum carmichaeli) and Baishao(Paeonia lactiflora) used separately or in combination on the adjuvant arthritis in rats. METHOD: Chuanwu-Baishao decoctions of different proportions were orally administered to three different rat models with adjuvant arthritis to observe the preventing and curing actions on the primary and secondary adjuvant arthritis in rats. RESULT: The curing action on the primary adjuvant arthritis appeared the same whether the two ingredients were used separately or in combination, while on the secondary adjuvant arthritis the combination, produced significant preventing effect. Chuanwu was proved weaker in action when used alone Chuanwu and Baishao were very efficacious in curing adjuvant arthritics when used in combination other than separately. CONCLUSION: In preventing and curing the secondary adjuvant arthritis in rats Chuanwu and Baishao work better in combination.

Aconitum↗