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Biomedical subjects

S Xiong

Publications and source records attributed to S Xiong.

At least 37 records · Page 2Linked to original sources

The role of factor XI in a dilute thromboplastin assay of extrinsic coagulation pathway.

Blood coagulation has been thought to be composed of both intrinsic and extrinsic pathways. Recent evidence strongly supports the critical role of the extrinsic pathway in the initiation of blood coagulation. This investigation established an assay that examines the role of FXI in the thromboplastin-initiated (extrinsic) coagulation based on this new concept. Plasma clotting times were measured at different concentrations of thromboplastin with activated FXII inhibited (FXIIa-inhibited Diluted Thromboplastin Time, FXIIaiDTT). Only at low concentrations of thromboplastin was FXIIaiDTT of FXI-deficient plasma significantly prolonged than that of normal plasma. Depletion of FXI from normal plasma prolonged its FXIIaiDTT and replenishment of FXI shortened it. FXIIaiDTTs of both FVIII-deficient and FIX-deficient plasma were remarkably prolonged, and addition of normal plasma dose-dependently shortened it. Furthermore, earlier alpha-thrombin inhibition was directly correlated with decreasing FXa generation. The amount of FXa production was: platelet-rich plasma > platelet-poor plasma > FXI-deficient plasma. Therefore, our findings from the FXIIaiDTT assays not only support the critical role of extrinsic pathway in blood coagulation initiation, but also demonstrate the importance of FXI as an amplifier of thrombin generation in thromboplastin-initiated coagulation.

Blood Coagulation↗

[Experimental studies on muscle fatigue of human limb motion with FNS].

The basic characteristic of the functional neuromuscular stimulation signals suitable to body is preliminarily determined after the fatigue performance of the biceps, and the physiological reaction to stimulation is investigated using many continuous stimulation signal patterns. The flexion motion of the elbow joint (right hand) of a healthy man was taken as our research objective. The surface electrodes were connected to the biceps and a micro angle sensor was mounted on the elbow joint (right hand). The curves of angular displacement for the elbow joint motion were obtained by using functional neuromuscular stimulation (FNS) limbs motion measurement instruments. The results demonstrate that the biceps are characterized by the non-linear and time-variant no matter what the stimulation patterns are, that continuous slow stimulation signals can reduce the muscle fatigue of the biceps, and that the stimulation frequencies ranging from 30 Hz to 50 Hz are applicable to the neuromuscular system.

Adult↗

[Effect of platelet on procoagulant activity of monocyte].

OBJECTIVE: To investigate the effect of platelet on procoagulant activity of mononcyte(M). METHODS: The procoagulant activity of M lysates was measured by one stage clotting time assay, the tissue factor (TF) activity and the role of P-selectin were confirmed by specific monoclonal antibodies (McAb). RESULTS: 1. Activated M challenged by lipopolysaccharide(LPS) had augmented procoagulant activity and this effect was blocked by TF McAb. 2. Procoagulant activity of M and activated M increased significantly with the presence of activated platelets. 3. The enhancement effect of activated platelet on the procoagulant activity of M was blocked by P-selectin McAb. CONCLUSION: TF expression of M contributes to the procoagulant activity of Ms and activated platelet enhances the procoagulant activity via P-selectin.

Antibodies, Monoclonal↗

Hepatitis B virus S gene mutants in infants infected despite immunoprophylaxis.

OBJECTIVE: To assess the correlation between hepatitis B virus (HBV) surface gene mutant infection and hepatitis B (HB) vaccination failure. METHODS: Using sera from 106 infants who were born to HBV carrier mothers and failed in HB immunoprophylaxis, HBV S gene was amplified by PCR, transferred to nylon membranes for Southern blots, and then hybridized with oligonucleotide probes. Eleven of non-hybridizing samples were used for DNA sequencing. RESULTS: 93.4% (99/106) of the samples were HBV DNA positive, and 30.3% (30/99) failed to hybridize with at least one of the four probes. DNA sequencing confirmed that 10 of the 11 samples had an S gene mutation with amino acid (aa) change. The identified mutants included nucleotide (nt) 546T-->A (aa131N-->T), nt531T-->C (aa1261-->T), nt491A-->C (aa113T-->P), nt491T-->A (aa113S-->T), nt533C-->A (aa127P-->T), nt581T-->A (aa143S-->T), nt636A-->T (aa161Y-->F), and nt679A-->C (aa175L-->F). The sequence in one mother-infant pair was completely the same, with mutations at aa131 and aa161. CONCLUSIONS: The prevalence of HBV surface mutants is about 30% in the children failing in HB vaccination. HBV mutants can infect infants by maternal-infant transmission.

DNA, Viral↗

[A study on the use of traditional Chinese medicine agent in ultrasonic instrumentation of root canals].

OBJECTIVE: To evaluate the bactericidal effect for anaerobes of infected root canals using Chinese medicine agent Jieeryin combing with ultrasonic technique. METHODS: 60 single-rooted teeth in patients with chronic periapical periodotitis were divided into 3 groups randomly, 20 in each. Hand instruments were used for group 1 as control group of traditional treatment. Ultrasound with saline as irrigant were used for group 2 as control group. Ultrasound with Jieeryin as irrigant were used for group 3 as experimental group. The pre-instrumentation and post-instrumentation specimens of each root canal were placed into the anaerobic chambers and incubated. RESULTS: Significant difference was found between hand instruments group and control group of ultrasound (P < 0.05) and even more significant difference was found between control group of ultrasound and experimental group of ultrasound (P < 0.01). CONCLUSIONS: Ultrasound has special superiority on instrumentation and bactericide of root canals. Chinese medicine agent Jieeryin can kill anaerobes in infected root canals effectively. It is an ideal irrigant for ultrasound which conforms to principles of biology.

Adolescent↗

Radiation-induced progressive decreasing in the expression of reverse transcriptase gene of hEST2 and telomerase activity.

OBJECTIVES: In order to identify the relationship between telomerase and the biological effect of radiation injury, and investigate the role of human telomerase catalytic subunit gene (hEST2) reverse transcriptase(RT) segment in the expression of telomerase activity. METHODS: Tumor HeLa cells, KB cells and A431 cells were employed to measure the change in telomerase activity after 60Co-ray irradiation at RNA level and protein level. Quantitative PCR and Northern blotting were used to determine the expression of hEST2 RT segment that encodes seven motifs of the human telomeres, a PCR-based telomeric repeat amplification protocol (TRAP) was used to assay telomerase activity after exposure to radiation. RESULTS: Both of telomerase activity and the expression hEST2 RT segment were decreased with increasing dosage of radiation. In addition, testing the expression of motifs domain is similar to the measurement of telomerase activity. CONCLUSION: The detection of the hEST2 RT segment by Northern blotting and quantitative PCR are new methods for testing telomerase activity. Furthermore, radiation can cause a dose-dependent decrease in telomerase activity. The effect of radiation on telomerase is one possible reason for the death of cancer cells after irradiation.

Catalytic Domain↗

Functional cooperation between T helper cell determinants.

The immune response to T helper (Th) cell determinants of a variety of antigens is often poor and limits severely the potential efficacy of current therapeutic measures through vaccination. Here, we report that an immunologically silent tumor determinant can be rendered immunogenic if linked with a dominant determinant of a parasite antigen, suggesting the existence of functional Th-Th cooperation in vivo. This phenomenon could be mimicked in part by signaling either through CD40 to the antigen-presenting cells or through OX40 to the tumor-determinant reactive T cells, with maximal effects obtained by combined anti-CD40 and anti-OX40 treatment in vivo. The data suggest that CD4 T cells reactive with a dominant determinant provide help to other CD4 T cells through up-regulating the costimulatory ability of antigen-presenting cells, in much the same way as help for CD8 cells. CD4 help for CD4 T cells represents a new immunological principle and offers new practical solutions for vaccine therapy against cancer and other diseases in which antigenic help is limiting.

Amino Acid Sequence↗

Peroxisome proliferator-activated receptors and hepatic stellate cell activation.

The present study examined the roles of peroxisome proliferator-activated receptors (PPAR) in activation of hepatic stellate cells (HSC), a pivotal event in liver fibrogenesis. RNase protection assay detected mRNA for PPARgamma1 but not that for the adipocyte-specific gamma2 isoform in HSC isolated from sham-operated rats, whereas the transcripts for neither isoforms were detectable in HSC from cholestatic liver fibrosis induced by bile duct ligation (BDL). Semi-quantitative reverse transcriptase-polymerase chain reaction confirmed a 70% reduction in PPARgamma mRNA level in HSC from BDL. Nuclear extracts from BDL cells showed an expected diminution of binding to PPAR-responsive element, whereas NF-kappaB and AP-1 binding were increased. Treatment of cultured-activated HSC with ligands for PPARgamma (10 microm 15-deoxy-Delta(12,14)-PGJ(2) (15dPGJ(2)); 0.1 approximately 10 microm BRL49653) inhibited DNA and collagen synthesis without affecting the cell viability. Suppression of HSC collagen by 15dPGJ(2) was abrogated 70% by the concomitant treatment with a PPARgamma antagonist (GW9662). HSC DNA and collagen synthesis were inhibited by WY14643 at the concentrations known to activate both PPARalpha and gamma (>100 microm) but not at those that only activate PPARalpha (<10 microm) or by a synthetic PPARalpha-selective agonist (GW9578). 15dPGJ(2) reduced alpha1(I) procollagen, smooth muscle alpha-actin, and monocyte chemotactic protein-1 mRNA levels while inducing matrix metalloproteinase-3 and CD36. 15dPGJ(2) and BRL49653 inhibited alpha1(I) procollagen promoter activity. Tumor necrosis factor alpha (10 ng/ml) reduced PPARgamma mRNA, and this effect was prevented by the treatment with 15dPGJ(2). These results demonstrate that HSC activation is associated with the reductions in PPARgamma expression and PPAR-responsive element binding in vivo and is reversed by the treatment with PPARgamma ligands in vitro. These findings implicate diminished PPARgamma signaling in molecular mechanisms underlying activation of HSC in liver fibrogenesis and the potential therapeutic value of PPARgamma ligands for liver fibrosis.

Animals↗

Wild-type p53 suppresses angiogenesis in human leiomyosarcoma and synovial sarcoma by transcriptional suppression of vascular endothelial growth factor expression.

Our recent studies (R. Pollock et al., Clin. Cancer Res., 4: 1985-1994, 1998; M. Milas et al., Cancer Gene Ther., in press, 2000) have shown that the restoration of wild-type (wt) p53 enhances cell cycle control in vitro and inhibits the growth of human soft-tissue sarcoma in severe combined immunodeficient mice. We hypothesized that the antitumor effect of wt p53 overexpression in sarcoma cells is attributable not only to enhanced cell cycle control but also to inhibition of angiogenesis. We evaluated the effect of restoring wt p53 function on angiogenesis in human soft-tissue sarcoma harboring mutant p53. Restoration of wt p53 expression in human leiomyosarcoma SKLMS-1 cells that contain mutant p53 markedly inhibited angiogenesis induced by tumor cells in vivo. Angiogenesis assays using an in vivo Matrigel plug assay demonstrated that less neovascularization in severe combined immunodeficient mice was observed with conditioned medium (CM) from human synovial sarcoma cells expressing wt p53 compared with CM from human synovial sarcoma cells expressing mutant p53. Microvessel density and microvessel counts were lower in tumor xenografts from cells containing wt p53 than in tumor xenografts from cells containing mutant p53. The growth and migration of murine lung endothelial cells were decreased when cells were treated with CM from sarcoma cells expressing wt p53 compared with CM from sarcoma cells expressing mutant p53. The introduction of wt p53 into sarcoma cells containing mutant p53 significantly reduced the expression of vascular endothelial growth factor (VEGF), which is a key mediator of tumor angiogenesis. Stimulation of endothelial cell migration by CM from cells expressing mutant p53 was significantly reduced after anti-VEGF neutralizing antibody was added to the CM. Using luciferase as the reporter of VEGF promoter activity, we found that wt p53 inhibited VEGF promoter activity in SKLMS-1 cells. Deletion analysis defined an 87-bp region (bp -135 to -48) in the VEGF promoter that is necessary for inhibiting VEGF promoter activity by wt p53. The transcription factor Sp1 may be involved in the repression of VEGF promoter activity by wt p53 in SKLMS-1 cells. These data indicated that wt p53 can suppress angiogenesis in human soft-tissue sarcomas by transcriptional repression of VEGF expression.

Animals↗

Sterol regulation of human fatty acid synthase promoter I requires nuclear factor-Y- and Sp-1-binding sites.

To understand cholesterol-mediated regulation of human fatty acid synthase promoter I, we tested various 5'-deletion constructs of promoter I-luciferase reporter gene constructs in HepG2 cells. The reporter gene constructs that contained only the Sp-1-binding site (nucleotides -82 to -74) and the two tandem sterol regulatory elements (SREs; nucleotides -63 to -46) did not respond to cholesterol. Only the reporter gene constructs containing a nuclear factor-Y (NF-Y) sequence, the CCAAT sequence (nucleotides -90 to -86), an Sp-1 sequence, and the two tandem SREs responded to cholesterol. The NF-Y-binding site, therefore, is essential for cholesterol response. Mutating the SREs or the NF-Y site and inserting 4 bp between the Sp-1- and NF-Y-binding sites both resulted in a minimal cholesterol response of the reporter genes. Electrophoretic mobility-shift assays using anti-SRE-binding protein (SREBP) and anti-NF-Ya antibodies confirmed that these SREs and the NF-Y site bind the respective factors. We also identified a second Sp-1 site located between nucleotides -40 and -30 that can substitute for the mutated Sp-1 site located between nucleotides -82 and -74. The reporter gene expression of the wild-type promoter and the Sp-1 site (nucleotides -82 to -74) mutant promoter was similar when SREBP1a [the N-terminal domain of SREBP (amino acids 1-520)] was constitutively overexpressed, suggesting that Sp-1 recruits SREBP to the SREs. Under the same conditions, an NF-Y site mutation resulted in significant loss of reporter gene expression, suggesting that NF-Y is required to activate the cholesterol response.

Base Sequence↗

RAR and RXR expression by Kupffer cells.

Retinoids are known to modulate macrophage differentiation, proliferation, and function including cytokine gene expression. However, signaling of retinoic acid (RA), a biologically active metabolite of vitamin A, in Kupffer cells has not been characterized. This study reports mRNA expression by rat Kupffer cells of RA receptor (RAR) and retinoid X receptor (RXR) subtypes and their binding activities to the RA responsive element (RARE) or retinoid X responsive element (RXRE). Total RNA and nuclear proteins were extracted from Kupffer cells immediately following isolation from livers of normal male Wistar rats. Competitive PCR demonstrated relative mRNA expression of RAR and RXR subtypes in the order of beta>alpha>gamma for and alpha>beta>gamma, respectively. It also demonstrated that the RXR alpha and beta mRNA levels were 5- to 10-fold higher in Kupffer cells than in hepatic stellate cells while RAR mRNA expression was shown to be similar for all the subtypes in both cell types. Gel mobility shift assays of nuclear extracts with labeled RARE and RXRE probes showed distinct binding activities for both responsive elements, which were effectively displaced with cold probes in excess but not with an unrelated oligonucleotide. A supershift assay with an antibody against RARalpha or RXRalpha has confirmed the contribution of both receptors to RARE binding and that of the RXRalpha to RXRE binding activity. These results represent the first demonstration of RA signaling at the nuclear level in Kupffer cells.

Animals↗

The change of interleukin-6 and tumor necrosis factor in patients with obstructive sleep apnea syndrome.

The levels of lipopolysaccharide (LPS)-induced interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) expression in culture of peripheral blood mononuclear cells (PBMC) and the plasma levels of IL-6 and TNF-alpha in the patients with obstructive sleep apnea syndrome (OSAS) were measured and the relationship between OSAS and IL-6 or TNF-alpha expression studied. Both IL-6 and TNF-alpha were detected by using ELISA in 22 patients with OSAS and 16 normal controls. The levels of LPS-induced IL-6 (787.82 +/- 151.97 pg/ml) and TNF-alpha (4165.45 +/- 1501.43 pg/ml) expression in the supernatant of the culture of PBMC and plasma level of IL-6 (50.67 +/- 4.70 pg/ml) and TNF-alpha (299.09 +/- 43.57 pg/ml) in the patients with OSAS were significantly higher than those in the normal controls (in the supernatant of the culture of PBMC: 562.69 +/- 197.54 pg/ml and 1596.25 +/- 403.08 pg/ml respectively; in the plasma; 12.69 +/- 2.75 pg/ml and 101.88 +/- 21.27 pg/ml respectively). There were significantly positive correlation between the levels of IL-6 and TNF-alpha and the percentage of time of apnea and hyponea, as well as the percentage of time spending at SaO2 below 90% in the total sleep time. It was concluded that LPS-induced IL-6 and TNF-alpha levels as well as plasma IL-6 and TNF-alpha levels in the patients with OSAS were up-regulated, which may be associated with the pathogenesis of OSAS.

Adult↗

The diagnosis value and its implication of impulse oscillometry in obstructive sleep apnea syndrome patients.

The change of measurements of impulse oscillometry (IOS) in obstructive sleep apnea syndrome (OSAS) patients and its mechanism were observed. The respiratory impedance was measured by using IOS technique and polysomnography (PSG) was monitored synchronously in 36 OSAS patients, 14 patients with chronic obstructive pulmonary disease (COPD) and 12 normal controls. Results showed that R20 in OSAS group was significantly higher than in COPD group and control group (P < 0.01). R5-R20 in OSAS group was lower than that in COPD group, but significantly higher than that in control group (P < 0.01). The levels of R20 and R5-R20 were positively correlated with severity degree of the disease. In addition, apnea-hyponea index (AHI) was positively correlated with R5 and R20 with the correlation index (r)being 0.66 and 0.86 respectively. The lowest SO2 was negatively correlated with R5 and R5-R20, with r being -0.66 and -0.79 respectively. The mean SO2 was negatively correlated with R5 and R5-R20 with r being -0.81 and -0.69 respectively. IOS technique could be used as a valuable tool for assessing the degree of upper airway obstruction in the patients with OSAS, and could help to explore its pathological mechanism.

Adult↗

Angiotensin II increases host resistance to peritonitis.

Studies by other laboratories have shown that angiotensin II (AII) can affect the function of cells which comprise the immune system. In the present study, the effect of AII on the function of peritoneal macrophages and peripheral blood monocytes was assessed. In vitro exposure (4 h prior to assay) of peritoneal macrophages from mice and rats to AII increased the percentage of cells that phagocytosed opsonized yeast and the number of yeast per macrophage. Furthermore, AII increased the respiratory burst capacity of peritoneal macrophages from mice and rats and peripheral blood mononuclear cells from humans. Because of these observations, the effect of AII on host resistance to bacterial infection was assessed. Intraperitoneal administration of AII was shown to increase host resistance (reduced abscess formation) in an animal model of bacterial peritonitis. Studies were then conducted to assess whether parenteral administration of AII, a clinically relevant route, could affect peritoneal host resistance in a manner similar to that observed after peritoneal administration. These studies showed that subcutaneous administration of AII throughout the postinfection interval increased the level of host resistance to bacterial peritonitis. Furthermore, in a study which compared AII and Neupogen, an agent approved for use for the reduction of febrile neutropenia after myeloablative therapy, daily subcutaneous administration of AII reduced abscess size and incidence, whereas Neupogen did not have any therapeutic benefit in this model. These data suggest that AII may be of therapeutic benefit as an immunomodulatory agent.

Angiotensin II↗

Effect of angiotensin II on hematopoietic progenitor cell proliferation.

Angiotensin II (AII) induced the proliferation of hematopoietic progenitor cells (HPC) isolated from murine bone marrow or human cord blood. The formation of colonies with more than 50 cells increased approximately five-sevenfold in cultures of murine lineage-negative (Lin(-)) bone marrow cells both in the presence (day 10) and absence (day 13) of colony-stimulating factors (CSF). This could be blocked with addition of Losartan, an antagonist of AIITR1. The increase in proliferation of early hematopoietic progenitors (Lin(-)Sca l(+) cells) by AII was approximately threefold and occurred only in the presence of CSF, suggesting that AII may affect mesenchymal stromal cells to induce CSF production and might directly affect early HPC. These in vitro studies were replicated with human HPC isolated from cord blood. AII also accelerated the proliferation and formation of colony-forming units (CFU)-granulocyte/erythroid/macrophage/megakaryocyte and CFU-granulocyte/macrophage colonies by CD34(+)CD38(-) enriched progenitors but only in the presence of CSF. Additional studies also indicated that AII can act to increase proliferation in suspension culture. Exposure of CD34(+) cells to AII in suspension culture, prior to placement in a semisolid medium with erythropoietin, increased the formation of colonies with more than 50 cells and erythroid progenitors approximately five- and 20-fold, respectively. Further, mRNA for the AT1a receptor was expressed by human bone marrow CD34(+)CD38(-) cells, CD34(+)CD38(-) cells, and lymphocytes, but not mature myeloid cells. Similarly, mRNA for the AT1a receptor was expressed on human stromal cell clones, offering further support to the hypothesis that AII acts partially through the mesenchymal compartment of the bone marrow. These data suggest that AII may be a factor which stimulates the proliferation of hematopoietic progenitors.

ADP-ribosyl Cyclase↗

Neuronal hypertrophy in acute appendicitis.

OBJECTIVE: The pathogenesis of appendicitis remains poorly understood. However, there is increasing evidence of involvement of the enteric nervous system in immune regulation and in inflammatory responses. This study was set up to characterize the status of the enteric nervous system in normal and in inflamed appendixes. METHODS: S100- and 2',2'-cyclic nucleotide 3' phosphodiesterase-positive Schwann cells, synaptophysin, and neuron-specific, enolase-positive nerve fibers and tryptase-positive mast cells were evaluated with immunohistochemical staining in surgically resected appendixes from 20 children with histologically proven acute appendicitis (HA), 10 histologically normal appendixes (HN) from patients with a clinical diagnosis of appendicitis, and 10 normal appendixes from patients undergoing elective abdominal surgery. Immunostained sections were subjected to quantitative image analysis. The number and size of ganglia and the number of nerve fibers, Schwann cells, and mast cells in each tissue compartment was quantitatively or semiquantitatively measured. RESULTS: Increased numbers of fibers, Schwann cells, and enlarged ganglia, widely distributed in the muscularis externa and submucosa, were seen in all HA appendixes and in 4 of 10 HN appendixes. The number and size of ganglia in muscularis externa and in the submucosa of appendixes with HA were significantly greater compared with those in control appendixes (P <.001). A significantly increased number of individually stained nerve fibers and Schwann cells (P <.05) were present in the muscularis externa in HA appendixes compared with control appendixes. Significantly increased numbers of tryptase-positive mast cells (P <.05) were present in the submucosa, muscularis, and especially in the lamina propria in HA specimens, compared with that of control tissue. CONCLUSIONS: The significant increase in neural components and mast cells in acute appendicitis is unlikely to develop during a single acute inflammatory episode. This suggests an underlying chronic abnormality as a secondary reaction to repeated bouts of inflammation, obstruction, or both. These results challenge our current understanding of the pathophysiological processes that give rise to acute appendicitis.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗

[Skeletal dysplasia and osteoporosis due to inadequate athletic].

Athletic load is an important factor that has an influence on the growth, development and mature of skeleton. In patients who had the functional disorder of hip joint resulting from hip diseases during their teen-ages, skeletal dysplasia and osteoporosis would occur. The present paper reported 30 cases of unilateral hip disorder. The patients were 20 men and 10 women whose age ranged from 2 to 20 years. The course of disease lasted 2 to 49 years. Their primary diseases included suppurant hip arthritis (16 cases), tuberculous arthritis of hip (10 cases), and others (4 cases). The follow-up study revealed fixed hip joint in 18 cases, positive Thomas sign in 22 cases, limited motion of hip joint in 12 cases, and unequal length of lower extremities in 25 cases; at the same time X-ray films showed ankylosis of hip at normal position in 10 patients, dislocation with ankylosis of hip in 13 patients, arthritic disorder of hip in 7 patients, skeletal dysplacia of ischium and pubis in 18 patients, and skeletal dysplasia of femur in 22 patients. All patients had osteoporosis. A discussion about the basic mechanism for skeletal dysplasia and osteoporosis following inadequate athletic load is presented. We believe that the skeletal dysplasia and osteoporosis in our group were caused by the diseases that led to inadequate athletic load. Therefore it is important to provide a thorough treatment and help the patients to their strength to be loaded in time.

Adolescent↗

[Clinical controlled study of shenmai injection and aminophylline on diaphragm fatigue].

OBJECTIVE: To compare the therapeutic effect of Shenmai injection (SM) and aminophylline (AP) on diaphragm fatigue in chronic obstructive pulmonary disease (COPD). METHODS: Sixty-four COPD patients with respiratory failure and diaphragm fatigue were randomly divided into 2 groups: (1) SM group (33 patients), treated with oxygen inhalation and anti-infection agents, and SM injection (SM 40 ml + 10% glucose 100 ml), (2) AP injection group (31 patients), treated with AP 0.25 g plus 10% glucose 100 ml, and the same comprehensive treatment. To investigate the initial time of diaphragm fatigue disappearance, the maintaining effect of 24 hours of drug administration, and the arterial blood gas analysis. RESULTS: The effect in 30 min and maintaining effect in 24 hours in SM group were better than those in the AP group. In both groups, PaO2 increased and PaCO2 decreased. CONCLUSION: The therapeutic effect of SM on COPD patients with respiratory failure and diaphragm fatigue was better than those of AP.

Adult↗