Biomedical subjects

Q Huang

Publications and source records attributed to Q Huang.

At least 199 records · Page 11Linked to original sources

PubMed1997

The morphology and connections of neurons in the gasping centre of adult rats.

Neuronal activities in the intermediate reticular nucleus and adjacent lateral tegmental field are critical for the neurogenesis of the ventilatory pattern of gasping. We report herein the anatomical features of these neurons, their axonal projections and the location of neurons providing afferent inputs. These neuroanatomical evaluations were performed by iontophoretic injection of the tracer Neurobiotin into the region of the intermediate reticular nucleus of the rat. At the site of injection, neurons having soma of 30-50 microns were filled. Labelled axons and terminals were observed in ipsilateral regions which contain neurons having established functions in the control of ventilatory activity. These regions include the nucleus ambiguous and motor nuclei of the hypoglossal and facial nerves. In addition, axonal projections extended to the contralateral region of the intermediate reticular nucleus. From this contralateral region, retrograde tracing revealed projections to the site of injection. Similarly, many ipsilateral regions which received axonal terminals from the region of the intermediate reticular nucleus had reciprocal projections to this region. These anatomical results support the physiological observation that the neurogenesis of gasping involves a synchronized activation of diverse components of the brainstem ventilatory control system.

Animals↗

PubMed1997

Sequencing of a 5.5-kb DNA fragment and identification of a gene coding for a subunit of the helicase/primase complex of avian laryngotracheitis virus (ILTV).

The nucleotide sequence of a 5,520-bp EcoRI restriction fragment of avian infectious laryngotracheitis (ILTV) DNA was reported and submitted to GeneBank with an accession number of AF001078. Computer prediction revealed one large potential open reading frame (ORF) with sequence similar to one subunit of the DNA helicase-primase complex of alpha-herpesviruses. The DNA helicase/primase complex of HSV-1 consists of three sub-units with molecular weights of 12,000, 97,000 and 70,000, encoded by genes UL52, UL5 and UL8, respectively. This enzyme complex is essential for herpesvirus DNA replication. The UL52 and UL5-equivalent genes of ILTV have been reported previously (Fuchs, W. and Mettenleiter, T.C.; J Gen Virol, 1996, 77: 2221-2229; Johnson, M.A. et. al., Arch Virol, 1995, 14: 623-634). Amino acid sequence comparison and homology search revealed that this ORF shares sequence similarity of the UL8-equivalent gene of alpha-herpesviruses, that is, the ORF 52 of vericura-zoster virus (VZV), the ORF 54 of equine herpesvirus type-1 (EHV-1), as well as the equivalent gene of bovine herpesvirus type 1 (BHV-1) and canine herpesvirus (Vlcek, C. et al., Virology, 1995, 210: 100-108; Remond, M. et al., J Gen Virol, 1996, 77: 37-48).

Animals↗

PubMed1997

Growth-inhibitory and differentiation-inducing activity of dimethylformamide in cultured human malignant glioma cells.

OBJECTIVE: To determine the growth-inhibitory and differentiation-inducing activity of dimethylformamide (DMF) on a human glioma cell line (SHG-44). DMF is a type of polar solvent and a potent differentiation-inducing agent in many kinds of human solid tumors, yet its effect on human glioma remains unclear. METHODS: The effects of DMF on cell proliferation using 3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay, cell cycle distribution (with flow cytometry), colony-forming efficiency in double-layer soft agar, tumorigenicity in athymic nude mice, morphological changes, and glial fibrillary acidic protein expression were studied. RESULTS: At dose ranges of 0.25, 0.5, 0.75, and 1.0%, DMF caused a dose-dependent proliferation inhibitory effect in monolayers and a marked dose-dependent suppression of colony-forming efficiency in double-layer soft agar with a complete loss of colony-forming ability in cells exposed to 0.75 and 1.0% DMF. Accumulation of cells in G0/G1 phases was observed in DMF-treated (0.5 and 1.0%) cells, also in a dose-dependent manner. SHG-44 cells exposed to DMF (0.5 and 1.0%) for 15 days changed morphologically from small spindle-shaped to large polygonal and flattened stellate cells with multiple slender processes. These cells were still tumorigenic in athymic nude mice, but the growth of xenografts was remarkably reduced, especially in the 1.0% DMF-treated group. The expression of glial fibrillary acidic protein was notably increased by DMF (0.5 and 1.0%). Washout experiments revealed that the effects of DMF on cell proliferation and cell cycle distribution were reversible. CONCLUSION: Our results suggest that DMF drove the SHG-44 cells to a more mature phenotype with inhibited growth.

Adult↗

PubMed1997

Interleukin-6 and tumor necrosis factor production in an enterocyte cell model (Caco-2) during exposure to Escherichia coli.

Data linking interactions between bacteria and the intestine with elevated serum cytokine levels has led to the concept of the gut as a cytokine-producing organ. An in vitro cell culture model was used to investigate the potential role of intestinal mucosa within this paradigm. Polarized monolayers of human enterocytes (Caco-2) were grown in a two compartment system where the apical and basal aspects of the membrane could be studied. Supernatant was collected at 0, 1, 3, 6, and 24 h after the monolayer was exposed (apically or basally) to 10(2), 10(5), or 10(8) colony-forming units of Escherichia coli C25/mL and saved for interleukin (IL)-6 and tumor necrosis factor (TNF) bioassay analysis. Caco-2 cells (not bacterially challenged) secreted significant amounts of constitutive IL-6, but not TNF, into the apical and basal chambers. Both cytokines levels were increased in a dose-dependent fashion (p < .05) after the E. coli challenge. This stimulated cytokine response was polar, in that the highest cytokine levels were at the side of the bacterial challenge and were most notable at the highest dose (10(8) colony-forming units/mL) of E. coli C25 tested. Caco-2 cells produce IL-6 and TNF in a dose-dependent fashion in response to E. coli C25 and the magnitude of this response is maximal on the side of the bacterial challenge. This data supports the hypothesis that bacterially challenged human enterocytes may be important producers of cytokines.

Caco-2 Cells↗

PubMed1997

An exo-poly-alpha-D-galacturonosidase, PehB, is required for wild-type virulence of Ralstonia solanacearum.

Ralstonia solanacearum, which causes bacterial wilt disease of many plant species, produces several extracellular plant cell wall-degrading enzymes that are suspected virulence factors. These include a previously described endopolygalacturonase (PG), PehA, and two exo-PGs. A gene encoding one of the exo-PGs, pehB, was cloned from R. solanacearum K60. The DNA fragment specifying PehB contained a 2,103-bp open reading frame that encodes a protein of 74.2 kDa with a typical N-terminal signal sequence. The cloned pehB gene product cleaves polygalacturonic acid into digalacturonic acid units. The amino acid sequence of pehB resembles that of pehX, an exo-PG gene from Erwinia chrysanthemi, with 47.2% identity at the amino acid level. PehB also has limited similarity to plant exo-PGs from Zea mays and Arabidopsis thaliana. The chromosomal pehB genes in R. solanacearum wild-type strain K60 and in an endo-PG PehA- strain were replaced with an insertionally inactivated copy of pehB. The resulting mutants were deficient in the production of PehB and of both PehA and PehB, respectively. The pehB mutant was significantly less virulent than the wild-type strain in eggplant virulence assays using a soil inoculation method. However, the pehA mutant was even less virulent, and the pehA pehB double mutant was the least virulent of all. These results suggest that PehB is required for a wild-type level of virulence in R. solanacearum although its individual role in wilt disease development may be minor. Together with endo-PG PehA, however, PehB contributes substantially to the virulence of R. solanacearum.

Amino Acid Sequence↗

PubMed1997

3' processing of human pre-U2 small nuclear RNA: a base-pairing interaction between the 3' extension of the precursor and an internal region.

The spliceosomal small nuclear RNAs U1, U2, U4, and U5 are transcribed by RNA polymerase II as precursors with extensions at their 3' ends. The 3' processing of these pre-snRNAs is not understood in detail. Two pathways of pre-U2 RNA 3' processing in vitro were revealed in the present investigation by using a series of human wild-type and mutant pre-U2 RNAs. Substrates with wild-type 3' ends were initially shortened by three or four nucleotides (which is the first step in vivo), and the correct mature 3' end was then rapidly generated. In contrast, certain mutant pre-U2 RNAs displayed an aberrant 3' processing pathway typified by the persistence of intermediates representing cleavage at each internucleoside bond in the precursor 3' extension. Comparison of the wild-type and mutant pre-U2 RNAs revealed a potential base-pairing interaction between nucleotides in the precursor 3' extension and a sequence located between the Sm domain and stem-loop III of U2 RNA. Substrate processing competition experiments using a highly purified pre-U2 RNA 3' processing activity suggested that only RNAs capable of this base-pairing interaction had high affinity for the pre-U2 RNA 3' processing enzyme. The importance of this postulated base-pairing interaction between the precursor 3' extension and the internal region between the Sm domain and stem-loop III was confirmed by the results obtained with a compensatory substitution that restores the base pairing, which displayed the normal 3' processing reaction. These results implicate a precursor-specific base-paired structure involving sequences on both sides of the mature cleavage site in the 3' processing of human U2 RNA.

Base Composition↗

PubMed1997

Myosin light chain phosphorylation: modulation of basal and agonist-stimulated venular permeability.

We have previously demonstrated that agonists increase microvascular permeability through a phospholipase C-nitric oxide synthase-guanylate cyclase cascade. The aim of this study was to further investigate the downstream end of the signaling pathway with a focus on myosin light chain (MLC) phosphorylation. The apparent permeability coefficient to albumin was measured in isolated coronary venules. Under control conditions, the nitric oxide donor sodium nitroprusside, as well as the guanosine 3',5'-cyclic monophosphate-dependent protein kinase (PKG) activator 8-bromoguanosine 3',5'-cyclic monophosphate, increased venular permeability two- to threefold. Similarly, activation of protein kinase C (PKC) with phorbol 12-myristate 13-acetate significantly elevated permeability. Inhibition of MLC phosphorylation with ML-7 significantly attenuated the hyperpermeability responses to the agonists. Furthermore, ML-7 dose dependently reduced basal venular permeability. Consistently, inhibition of dephosphorylation with the protein phosphatase inhibitor calyculin dramatically increased basal permeability. These results suggest that 1) PKG and PKC play an important signaling role in the regulation of endothelial barrier function and 2) MLC phosphorylation contributes to basal and agonist-stimulated microvascular permeability.

Animals↗

PubMed1997

Interaction of PKC and NOS in signal transduction of microvascular hyperpermeability.

Our previous studies have shown that inflammatory mediators increase microvascular permeability through a phospholipase C-nitric oxide synthase (NOS)-guanylate cyclase cascade. The aim of this study is to delineate in more detail the signaling pathway leading to microvascular hyperpermeability. Endothelial cytosolic calcium and the apparent permeability coefficient of albumin (Pa) were measured in isolated and perfused coronary venules. Histamine stimulated a rapid increase in cytosolic calcium followed by a transient elevation in Pa. The NOS inhibitor NG-monomethyl-L-arginine (L-NMMA) and the guanosine 3',5'-cyclic monophosphate-dependent protein kinase G (PKG) inhibitor KT-5823 abolished the hyperpermeability but did not affect the calcium response to histamine. Similarly, the calcium ionophore ionomycin produced a calcium spike preceding venular hyperpermeability. Blockage of the NOS-PKG cascade inhibited the increase in Pa, whereas the endothelial calcium was still elevated on administration of ionomycin. Furthermore, the relationship between protein kinase C (PKC) and the calcium-NOS-PKG pathway in modulation of venular permeability was investigated. Stimulation of PKC with phorbol 12-myristate 13-acetate (PMA) dramatically increased basal Pa without significantly changing the cytosolic calcium level. The selective PKC inhibitor bisindolylmaleimide abolished the effect of PMA but did not alter the effect of histamines on Pa. In contrast, both L-NMMA and KT-5823 were able to greatly attenuate the increase in Pa caused by PMA. These results suggest that 1) elevation of endothelial cytosolic calcium is an early signaling event preceding nitric oxide (NO) synthesis in the transduction of endothelial hyperpermeability, and 2) activation of PKC may alter the endothelial barrier function partially through the modulation of NO production.

Alkaloids↗

PubMed1997

Lack of linkage between anti-nuclear antibody or clinical features of systemic lupus erythematosus (SLE) and TCR-A/Vbeta loci in families of subjects with SLE.

The role of the TCR-A and TCR-Vbeta genes in the genetic predisposition to SLE expression and anti-nuclear antibody (ANA) production were examined by linkage analysis in eighteen multiplex and forty-three simplex SLE families. All subjects were Caucasian. A significantly increased prevalence of positive ANAs in first-degree relatives of SLE patients from multiplex families was noticed compared to that of simplex families. Linkage between TCR-A/Vbeta genes and SLE expression and ANA production were analysed by affected sib-pair method. Results showed that the haplotypes identical by descent sharing TCR-A and TCR-Vbeta genes in the affected sib-pairs was not different from that expected (P = 0.93 and P = 0.74, respectively). There was no linkage between ANA positivity and TCR-A and TCR-Vbeta genes in ANA positive sib-pairs from both multiplex and simplex families. This study suggests that germline TCR-A and TCR-Vbeta gene loci confer no susceptibility to ANA and SLE expression.

Adult↗

PubMed1997

X-chromosome inactivation in monozygotic twins with systemic lupus erythematosus.

The hypothesis that a low concordance rate in monozygotic (MZ) twins with systemic lupus erythematosus (SLE) may be accounted for by differences in X-chromosome inactivation was examined. Five MZ twin pairs, four discordant and one concordant, were recruited, zygosity confirmed by DNA fingerprinting, and their pattern of X-chromosome inactivation in DNA samples prepared from peripheral blood and buccal cells were examined. X-chromosome inactivation was assessed by the methylation status of the CpG region near trinucleotide repeats in exon 1 of the androgen receptor gene on X-chromosome after digestion with the methylation-sensitive enzyme HpaII or HhaI and PCR amplification. X-chromosome inactivation patterns were found to be the same between affected and non-affected twins in all four discordant twin pairs, with random patterns in two pairs and skewed patterns in the others. The concordant twins demonstrated the same random patterns. X-chromosome inactivation was also examined from buccal smear DNA and shown to have the same pattern as that noted from peripheral blood DNA in one informative twin pair. Differences in X-chromosome inactivation patterns were not observed in these five MZ twin pairs. The results could not support the hypothesis that differences in X-chromosome inactivation is the mechanism accounting for the low concordance rate noted in MZ twins with SLE.

Adult↗

PubMed1997

[Effect of hypoxia on maximal myocardial blood flow in right ventricle].

In order to study the changes of coronary reserve capacity, the effects of hypoxia on hemodynamics and maximal myocardial blood flow in right ventricle were observed. Rats wre divided into 3 groups:normoxic group (control), acute hypoxic group and chronic hypoxic group. Maxmimal myocardial blood flow in the right ventricle was measured with 99 m Tc radiolabelled from RBC during adenosine infusion. The results showed that cardiac output, PaO2 and oxygen delivery were decreased during acute hypoxia, but myocardial blood flow in right ventricle was increased, as compared with the control group. There were no significant change of maximal myocardial blood flow in the right ventricle in acute hypoxic rats. Hematocrit and blood viscosity at different shear rate and RV weight index were augmented, whereas oxygen delivery and myocardial blood flow became normal during chronic hypoxia. Maximal blood flow in RV was significantly decreased whereas arterial wall thickness and collagen in arterial adventitia were increased in chronic hypoxic rats. The above results suggest that the decreased coronary reserve might beresulted from the increasedblood viscosity, arterial wall thickness and collagen in arterial adventitia and right ventricular hypertrophy.

Animals↗

PubMed1997

[Changes of PDGF-alpha and beta receptor gene expression in hypoxic rat pulmonary vessels].

OBJECTIVE: To reveal the role of platelet-derived growth factor-alpha and beta receptor in hypoxic pulmonary vascular remodeling. We investigated the changes of PDGF-alpha and beta receptor gene expression under hypoxic condition. METHODS: Hypoxic pulmonary hypertension rats model was reproduced by normobaric hypoxia. Changes of pulmonary PDGF-alpha and beta mRNA were examined by in situ hybridization. RESULTS: The PDGF-alpha receptor mRNA of the hypoxia group (3 days) declined to 86% compared with that of the control group, and shooting up to 217% of control at day 7, then sustained at 224% until day 14. (all P < 0.001). PDGF-beta receptor mRNA markedly increased at day 3 after hypoxia and maintained this increasing tendency consistently. Its top was 164% at day 14 (P < 0.001). The growth inhibitor, heparin had alleviated the increases of both rat pulmonary arterial pressure and PDGF receptor gene expression. CONCLUSION: Hypoxia led to the increase of PDGF-alpha and beta receptor gene expression in pulmonary vascular endothelial and smooth muscle cells, and might be involved in hypoxic pulmonary vascular remodeling.

Animals↗

PubMed1997

Family and twin studies in systemic lupus erythematosus.

We have estimated how much of the total genetic predisposition to SLE may be attributable to genes outside the HLA region by comparing figures for concordance of SLE in monozygotic twins with those for concordance in HLA identical siblings in Australia. None of six dizygotic co-twins of white Australian SLE probands was concordant for SLE. One of four (25%) monozygotic co-twins of white Australian SLE probands was concordant for SLE which when added to previously published figures for Caucasoid populations gives an overall concordance rate for SLE in monozygotic twins of 25%. None of 18 HLA identical, same sex siblings of SLE probands, had definite SLE by the study criteria (i.e. less than 6%). The comparison of these figures shows that most of the genetic predisposition to SLE is attributable to genes outside the HLA region.

Adolescent↗

PubMed1997

Factor VIIa-tissue factor: functional importance of protein-membrane interactions.

The first enzyme in the blood clotting cascade consists of two distinct protein subunits: a catalytic subunit (factor VIIa; FVIIa) and an essential regulatory subunit (tissue factor; TF). FVIIa is a soluble plasma protease, while TF is a cell-surface, integral-membrane protein. The recently reported X-ray crystal structure of the complex of FVIIa and the isolated extracellular domain of TF has provided important insights into the protein-protein interactions that bind these two subunits together (1). Equally important in the functioning of the TF-FVIIa complex, but much less well understood, are a series of protein-phospholipid interactions involving TF, FVIIa, and the natural substrates of this enzyme, as well as protein-protein interactions important in substrate recognition by TF-FVIIa. Here we review recent studies on the membrane organization and role of protein-phospholipid interactions in the function of TF-FVIIa, the enzyme that triggers blood clotting in hemostasis and thrombosis.

Crystallography, X-Ray↗

PubMed1997

[3H]RY 80: A high-affinity, selective ligand for gamma-aminobutyric acidA receptors containing alpha-5 subunits.

The radiochemical synthesis and pharmacological properties are described of [3H]RY 80 (ethyl-8-acetylene-5, 6-dihydro-5-methyl-6-oxo-4H-imidazo[1,5a][1, 4]benzodiazepine-3-carboxylate, [ethyl-3H]). This compound is one of a series of 8-substituted imidazobenzodiazepines that exhibits both high affinity and selectivity for gamma-aminobutyric acid (GABA)A receptors containing alpha-5 subunits. Saturable, high-affinity (Kd approximately 0.7 nM) binding of [3H]RY 80 was observed in hippocampal membranes. The maximum number (Bmax) of [3H]RY 80 binding sites was approximately 18% of that obtained with [3H]flunitrazepam, a radioligand that labels all "diazepam-sensitive" GABAA receptors. This value is consistent with previous estimates (10-20%) of the proportion of rat hippocampal GABAA receptors containing alpha-5 subunits determined by immunoprecipitation with selective antibodies and competition experiments using an alpha-5-selective ligand. In recombinant GABAA receptors composed of alpha-5 beta-3 gamma-2 subunits, the Kd of [3H]RY 80 (approximately 0.5 nM) was consistent with the value obtained in hippocampus, whereas the Bmax value was not significantly different from that obtained with [3H]flunitrazepam. The potencies of several benzodiazepine site ligands to inhibit [3H]RY 80 binding to hippocampal membranes were in agreement with the values obtained in recombinant (alpha-5 beta-3 gamma-2) GABAA receptors. [3H]RY 80 was used both in a "GABA shift" assay to correctly predict the in vivo actions of a novel, alpha-5-selective ligand and to characterize a population of GABAA receptors containing alpha-5 subunits in neonatal rat cortex. These findings demonstrate that [3H]RY 80 can be used as a radioligand to examine the properties of GABAA receptors containing alpha-5 subunits.

Alkynes↗

PubMed1997

Studies on the transmission potential of surviving microfilaremias after basic control of filariasis.

After filariasis was basically controlled (the microfilarial rate was lower than 1%) in Henan Province in 1987, longitudinal observation of the disease has been carried out in all the province in order to study the regular pattern of growth and decline or the transmission potential of the disease. According to the distribution of filaria species and original microfilarial rate, 7 administrative villages in 7 counties were selected as surveillance sites. From 1988 to 1995, etiological and mosquito vector surveys were made continuously in all sites where no control measure was conducted. 10 surviving microfilaremic individuals became negative gradually over the first 6 years and no new microfilaremia was found. Since then, the microfilarial rate was zero. During the 8 years, 19 vector mosquitos were positive, with a total of 33 filarial larva. Culex pipiens pallens was the predominant mosquito species inside human dwelling in all sites. The man-biting rate of mosquitos for outdoor sleepers fluctuated greatly, the highest was 360.60 mosquitos per man per night and the lowest 7.20. The man-biting rate of mosquitos for sleepers inside mosquito-nets was approximately 1. The proportion of multiparous mosquitos also fluctuated greatly, the highest was 88.10% and the lowest 27.27%. According to the data described above, the man-biting rate of mosquitos which contained filaria L3 was less than 1 mosquito per man per transmission season. It is suggested that after the microfilarial rate was lower than 1%, the surviving microfilaremias became negative gradually in 3-5 years, and the transmission of the disease was blocked. Therefore, in the districts where filariasis was basically controlled, elimination of the disease was attainable.

Animals↗

PubMed1997

Biological and clinical significance of cytogenetic study on 100 acute lymphoblastic leukemia and 219 acute non-lymphoblastic leukemia.

OBJECTIVE: To further investigate the role that cytogenetic may play in the diagnosis and prognosis of leukemia, a study was conducted in 319 acute leukemias. METHODS: 100 patients with acute lymphoblastic leukemia (ALL) and 219 patients with acute non-lymphoblastic leukemia (ANLL) were from Rui Jin Hospital, Xin Hua Hospital, Ren Ji Hospital and Shanghai Children's Hospital. Their cytogenetic data were analyzed together with those of morphology, immunology and clinical prognosis. RESULTS: In ALL group, 48 cases were karyotypically normal whereas 52 cases revealed chromosomal changes, among which 32 had quantitative abnormalities and 20 had qualitative abnormalities. The translocation t(9; 22) was identified in 11 out of 20 cases of structural aberrations (55%). Specific structural aberrations t(9; 22) and t(8; 14) were detected to be related to B-lineage associated differentiation antigens and t(8; 14) also with ALL-L3 according to FAB classification. With regard to clinical prognosis, the survival rate of structural aberration subset decreased significantly compared with the normal karyotype subset (P < 0.05). However, no statistically significant difference was found between hyperdiploidy subset (not including near-triploidy) and normal karyotype subset (P > 0.75). In ANLL group, 80% of de novo patients and relapsed patients had chromosomal abnormalities. Importantly, structural aberrations accounted for 73% of these abnormalities and frequently corresponded to specific types of FAB classification. Relevant prognostic studies demonstrated that t(15; 17) subset had the best overall survival probability, followed by t(8; 21) and normal karyotype subset, while the numerical aberration subset showed a relatively poor prognosis. CONCLUSION: Our data confirmed that cytogenetic study is important for the molecular study of the leukemogenesis. On the other hand, it also provides an independent parameter for prognosis in acute leukemia.

Adolescent↗

PubMed1997

Studies on the transmission potential of filariasis in controlled areas of Henan Province.

OBJECTIVE: To study the regular pattern of growth and declination or the transmission potential of filariasis after the disease was basically (the microfilarial rate was lower than 1%) in Henan Province in 1987. METHODS: According to the distribution of filaria species and original microfilarial rate, in 7 surveillance sites in 7 counties (cities) the etiology and mosquito vector surveys were carried out continuously during 1988-1995 and no control measurement for pathogen was taken. RESULTS: Ten residual microfilaremias became negative gradually in the first 6 years and no new microfilaremias occurred during 1988-1995. During 1993 to 1995, the microfilaremias rate of population in the sites was 0. The natural infection rates of filarial larvae in vector mosquito were 0.1%-0. During the 8 years, 15 vector mosquitos were positive with a total of 18 filarial larvae which were all of first or second-stage larvae. The C. pipiens pallens was the main vector, the second was A. sinensis, with a small number of C. fatigans and A. anthropophagus. The man-biting rates of mosquitoes for outdoor sleepers fluctuated greatly, the highest one was 360.6 mosquitoes/person per night and the lowest, 7.2. The man-biting rates of mosquitoes for sleepers inside mosquito-net was about 1 mosquito/person per night. The proportion of multiparous mosquitoes also fluctuated more greatly, the highest one was 88.1% and the lowest 27. 2% According to the data described above, the man-biting rate of vector mosquito which contained filarial L3 was 0. CONCLUSIONS: The results suggested that after the microfilarial rate was lower than 1%, the residual microfilaremias became negative gradually in 3-6 years, and the transmission of the disease was blocked. Therefore, in the areas where filariasis was basically controlled, elimination of the disease was attainable within sight.

Animals↗