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Biomedical subjects

X Q Liu

Publications and source records attributed to X Q Liu.

At least 37 records · Page 2Linked to original sources

Absolute requirement for an active immune response involving B cells and Th cells in immunity to Plasmodium yoelii passively acquired with antibodies to the 19-kDa carboxyl-terminal fragment of merozoite surface protein-1.

Vaccination of mice with the leading malaria vaccine candidate homologue, the 19-kDa carboxyl terminus of merozoite surface protein-1 (MSP119), results in sterile immunity to Plasmodium yoelii, with no parasites detected in blood. Although such immunity depends upon high titer Abs at challenge, high doses of immune sera transferred into naive mice reduce parasitemia (and protect from death) but do not result in a similar degree of protection (with most mice experiencing high peak parasitemias); this finding suggests that ongoing parasite-specific immune responses postchallenge are essential. We analyzed this postchallenge response by transferring Abs into manipulated but malaria-naive mice and observed that Abs cannot protect SCID, nude, CD4+ T cell-depleted, or B cell knockout mice, with all mice dying. Thus, in addition to the Abs that develop following MSP119 vaccination, a continuing active immune response postchallenge is required for protection. MSP119-specific Abs can adoptively transfer protection to strains of mice that are not protected following vaccination with MSP119, suggesting that the Ags targeted by the immune response postchallenge include Ags apart from MSP119. These data have important implications for the development of a human malaria vaccine.

Animals↗

Characterization of a self-splicing mini-intein and its conversion into autocatalytic N- and C-terminal cleavage elements: facile production of protein building blocks for protein ligation.

The determinants governing the self-catalyzed splicing and cleavage events by a mini-intein of 154 amino acids, derived from the dnaB gene of Synechocystis sp. were investigated. The residues at the splice junctions have a profound effect on splicing and peptide bond cleavage at either the N- or C-terminus of the intein. Mutation of the native Gly residue preceding the intein blocked splicing and cleavage at the N-terminal splice junction, while substitution of the intein C-terminal Asn154 resulted in the modulation of N-terminal cleavage activity. Controlled cleavage at the C-terminal splice junction involving cyclization of Asn154 was achieved by substitution of the intein N-terminal cysteine residue with alanine and mutation of the native C-extein residues. The C-terminal cleavage reaction was found to be pH-dependent, with an optimum between pH6.0 and 7.5. These findings allowed the development of single junction cleavage vectors for the facile production of proteins as well as protein building blocks with complementary reactive groups. A protein sequence was fused to either the N-terminus or C-terminus of the intein, which was fused to a chitin binding domain. The N-terminal cleavage reaction was induced by 2-mercaptoethanesulfonic acid and released the 43kDa maltose binding protein with an active C-terminal thioester. The 58kDa T4 DNA ligase possessing an N-terminal cysteine was generated by a C-terminal cleavage reaction induced by pH and temperature shifts. The intein-generated proteins were joined together through a native peptide bond. This intein-mediated protein ligation approach opens up novel routes in protein engineering.

Amino Acid Sequence↗

Molecular characterization of a new excitatory insect neurotoxin with an analgesic effect on mice from the scorpion Buthus martensi Karsch.

Besides the neurotoxins active on mammals, a new excitatory insect selective toxin with a mice analgesic activity was found and purified from the venom of the scorpion Buthus martensi Karsch (BmK) (Ji, Y.H., Mansuelle, P., Terakawa, S., Kopeyan, C., Yanaihara, N., Hsu, K., Rochat, H., 1996. Toxicon 34, 987; Luo, M.J., Xiong, Y.M., Wang, M., Wang, D.C., Chi, C.W., 1997. Toxicon 35, 723.). This peptide (designated as BmK IT-AP) is composed of 72 amino acid residues. Its primary structure was determined by automated Edman degradation of the N-terminal part of the reduced and S-carboxamidemethylated protein and its lysylendopeptidase degraded fragments. Based on the determined sequence, the gene specific primers were designed and synthesized for 3' and 5' RACE (rapid amplification of cDNA ends). Their partial cDNA fragments obtained by 3' and 5' RACEwere cloned and sequenced and the full length cDNA sequence of BmK IT-AP was then completed by overlapping their two partial cDNA sequences. It encodes a precursor of 90 amino acid residues: a signal peptide of 18 residues and a mature peptide of 72 residues which are consistent with the determined protein sequence of BmK IT-AP. The genomic DNA of the peptide was also amplified by PCR from the scorpion genomic DNA and sequenced, which is a first report on the genomic structure of a scorpion toxin specific for insects. Its sequence revealed an intron of 590 bp inserted in the end part of the signal peptide. The peptide caused a fast excitatory contraction paralysis on house fly larvae. Furthermore, the peptide also showed an obvious analgesic effect on mice, as assayed by using a twisting test model. This effect of BmK IT-AP well characterized at molecular level is first reported among the known scorpion insect neurotoxins.

Amino Acid Sequence↗

Predictive chemotherapy of advanced breast cancer directed by MTT assay in vitro.

In order to investigate the predictive value of in vitro MTT assay for directing chemotherapy of breast cancer patients, from 1992 to 1995, 156 advanced breast cancer patients who had evaluable lesions were recruited for a prospective study. Of them 83 had MTT assay before chemotherapy; the 73 patients in the MTT sensitive group received chemotherapy according to the result of the MTT assay. The other 10 patients in the MTT resistant group and 73 patients in the control group were given chemotherapy according to clinicians' discretion. The response rate in the MTT sensitive group was 76.7% (56/73). There was statistically significant difference as compared with 0 (0/10) in the MTT resistant group and 43.8% (32/73) in the control group. Between in vitro and in vivo, the overall coincident rate was 79.5% [(56 + 10)/83]. In the MTT sensitive group, the response rate of the subgroups of lesions and the chemotherapy regiments tended to be higher than that in the control group. Patients in the MTT sensitive group had longer response and survival than those in the control group. However, there was no statistical difference in the median response duration and the median survival between the two groups. Further exploration of in vitro chemosensitivity testing by MTT assay for patients with advanced breast cancer is warranted.

Antineoplastic Combined Chemotherapy Protocols↗

A novel method for increasing production of mature proteins in the periplasm of Escherichia coli.

A novel strategy to obtain high-level production of mature proteins exported to the periplasm of Escherichia coli is described. It is based on a modified signal sequence generated by insertion of a coding sequence of the polypeptide precursor of interest at the BamHI site of the commercial vector pQE-30 resulting in an addition of a dodeca-peptide (MRGSH6GS) at the N-terminus of the precursor. The modification does not affect correct processing of the modified signal nor proper folding of the target protein, resulting in an untagged native product. The method is simple for avoiding onerous optimization of translation initiation and screening of host stains. The usefulness of this method is illustrated by overexpression of DsbC and DsbA. Induced by 0.01 mM IPTG at 37 degrees C, proteins were overproduced to comprise 20-30% of the total cellular proteins, and more than 95% of the expressed proteins were correctly processed and exported into the periplasm with yields of more than 100 mg per liter culture.

Amino Acid Sequence↗

Overexpression and accumulation of apolipoprotein E as a cause of hypertriglyceridemia.

The molecular mechanisms of hypertriglyceridemia (HTG), a common lipid metabolic disorder in humans, often of genetic origin, are not well understood. In studying the effect of apolipoprotein (apo) E on the metabolism of triglyceride-rich lipoproteins, we found that expressing high plasma levels of human apoE3 in transgenic mice lacking endogenous mouse apoE caused HTG. These transgenic animals had 3-fold higher plasma triglyceride levels, higher very low density lipoproteins (VLDL), and lower high density lipoproteins than did nontransgenics. Removing one or both low density lipoprotein receptor alleles in the apoE3-overexpressing mice caused severe HTG (8-11-fold over nontransgenics) and increased VLDL and decreased low and high density lipoproteins, and apoE3-enriched VLDL were markedly depleted in apoC-II. At least two mechanisms could explain HTG associated with apoE3 overexpression: stimulated VLDL triglyceride production and impaired VLDL lipolysis. The apoE3 mice with HTG had a 50% increase in hepatic VLDL triglyceride production. Furthermore, overexpression of apoE (E2, E3, or E4) in cultured hepatocytes (McA-RH7777 cells) correlated positively with secretion of VLDL into the medium. However, apoE3 overexpression-associated HTG was only partially explained by VLDL overproduction, as lipoprotein lipase-mediated VLDL lipolysis was also decreased 20-86% depending on apoE3 levels, most likely by displacing or masking apoC-II on the particles. In human subjects, HTG correlated positively with increased VLDL triglyceride and plasma and VLDL apoE levels. However, plasma and VLDL apoE correlated negatively with VLDL apoC-II levels and lipoprotein lipase-mediated VLDL lipolysis. Thus, optimal expression of apoE is crucial for normal metabolism of triglyceride-rich lipoproteins, and overexpression and/or accumulation of apoE may contribute to HTG by stimulating VLDL triglyceride production and by impairing VLDL lipolysis. The apoE3-overexpressing mice will be useful for studying the pathophysiology of this disorder.

Animals↗

Protein trans-splicing and functional mini-inteins of a cyanobacterial dnaB intein.

A 429 aa theoretical intein is encoded in the dnaB gene (DNA helicase) of the cyanobacterium Synechocystis sp. strain PCC6803. This intein is shown to be capable of protein splicing with or without its native exteins when tested in E. coli cells. A centrally located 275 amino acid sequence (residues 107-381) of this intein can be deleted without loss of the protein splicing activity, resulting in a functional mini-intein of 154 aa in size. Efficient in vivo protein trans-splicing was observed when this mini-intein was split into a 106 aa N-terminal fragment containing intein motifs A and B, and a 48 aa C-terminal fragment containing intein motifs F and G. These results indicate that the N- and C-terminal regions of the Ssp DnaB intein, whether covalently linked with each other or not, can come together through non-covalent interaction to form a protein splicing domain that is functionally sufficient and structurally independent from the centrally located endonuclease domain of the intein.

Amino Acid Sequence↗

Protein trans-splicing by a split intein encoded in a split DnaE gene of Synechocystis sp. PCC6803.

A split intein capable of protein trans-splicing is identified in a DnaE protein of the cyanobacterium Synechocystis sp. strain PCC6803. The N- and C-terminal halves of DnaE (catalytic subunit alpha of DNA polymerase III) are encoded by two separate genes, dnaE-n and dnaE-c, respectively. These two genes are located 745,226 bp apart in the genome and on opposite DNA strands. The dnaE-n product consists of a N-extein sequence followed by a 123-aa intein sequence, whereas the dnaE-c product consists of a 36-aa intein sequence followed by a C-extein sequence. The N- and C-extein sequences together reconstitute a complete DnaE sequence that is interrupted by the intein sequences inside the beta- and tau-binding domains. The two intein sequences together reconstitute a split mini-intein that not only has intein-like sequence features but also exhibited protein trans-splicing activity when tested in Escherichia coli cells.

Amino Acid Sequence↗

Apolipoprotein E2 reduces the low density lipoprotein level in transgenic mice by impairing lipoprotein lipase-mediated lipolysis of triglyceride-rich lipoproteins.

Apolipoprotein (apo) E2 is often associated with low levels of low density lipoprotein (LDL) cholesterol and high levels of plasma triglycerides in humans. Mice expressing apoE2 also have low LDL levels. To evaluate the possible role of the LDL receptor in the cholesterol-lowering effect of apoE2, we bred transgenic mice expressing low levels of apoE2 with LDL receptor-null mice (hE2(+/0), LDLR-/-). Even in the absence of the LDL receptor, plasma total and LDL cholesterol levels decreased progressively with increasing levels of plasma apoE2. At plasma apoE2 levels >20 mg/dl, LDL cholesterol was approximately 45% lower than in LDLR-/- mice. Thus, the LDL cholesterol-lowering effect of apoE2 is independent of the LDL receptor. In contrast, plasma triglyceride levels increased (mostly in very low density lipoproteins (VLDL) and intermediate density lipoproteins (IDL)) progressively as apoE2 levels increased. At plasma apoE2 levels >20 mg/dl, triglycerides were approximately 150% higher than in LDLR-/- mice. Furthermore, in apoE-null mice (hE2(+/0), mE-/-), apoE2 levels also correlated positively with plasma triglyceride levels, suggesting impaired lipolysis in both hE2(+/0),LDLR-/- and hE2(+/0),mE-/- mice. Incubating VLDL or IDL from the hE2(+/0),LDLR-/- or the hE2(+/0),mE-/- mice with mouse postheparin plasma inhibited lipoprotein lipase-mediated lipolysis of apoE2-containing VLDL and IDL by approximately 80 and approximately 70%, respectively, versus normal VLDL and IDL. This observation was confirmed by studies with triglyceride-rich emulsion particles, apoE2, and purified lipoprotein lipase. Furthermore, apoE2-containing VLDL had much less apoC-II than normal VLDL. Adding apoC-II to the incubation partially corrected the apoE2-impaired lipolysis in apoE2-containing VLDL or IDL and corrected it completely in apoE2-containing emulsion particles. Thus, apoE2 lowers LDL cholesterol by impairing lipoprotein lipase-mediated lipolysis of triglyceride-rich lipoproteins (mostly by displacing or masking apoC-II). Furthermore, the effects of apoE2 on both plasma cholesterol and triglyceride levels are dose dependent and act via different mechanisms. The increase in plasma cholesterol caused by apoE2 is due mostly to impaired clearance, whereas the increase in plasma triglycerides is caused mainly by apoE2-impaired lipolysis of triglyceride-rich lipoproteins.

Animals↗

A topA intein in Pyrococcus furiosus and its relatedness to the r-gyr intein of Methanococcus jannaschii.

A new intein coding sequence was found in a topA (DNA topoisomerase I) gene by cloning and sequencing this gene from the hyperthermophilic Archaeon Pyrococcus furiosus. The predicted Pfu topA intein sequence is 373 amino acids long and located two residues away from the catalytic tyrosine of the topoisomerase. It contains putative intein sequence blocks (C, E, and H) associated with intein endonuclease activity, in addition to intein sequence blocks (A, B, F, and G) that are necessary for protein splicing. This DNA topoisomerase I intein is most related to a reverse gyrase intein from the methanogenic Archaeon Methanococcus jannaschii. These two inteins share 31% amino acid sequence identity and, more importantly, have the same insertion sites in their respective host proteins. It is suggested that these two inteins are homologous inteins present in structurally related, but functionally distinct, proteins, with implications on intein evolution and intein homing.

Amino Acid Sequence↗

Mutation analysis of the 6-pyruvoyl-tetrahydropterin synthase gene in Chinese hyperphenylalaninemia caused by tetrahydrobiopterin synthesis deficiency.

Hyperphenylalaninemia (HPA) may be caused by deficiency of phenylalanine hydroxylase or tetrahydrobiopterin (BH4), the essential cofactor for the aromatic amino acid hydroxylases. 6-Pyruvoyl-tetrahydropterin synthase (PTPS) deficiency is a major cause of BH4 deficient HPA. In this study, seven single base mutations at nucleotides 73 (C>G), 155 (A>G), 166 (G>A), 209 (T>A), 259 (C>T), 286 (G>A), and 317 (C>T) on PTPS cDNA were detected in Chinese PTPS-deficient HPA by polymerase chain reaction and solid phase DNA sequencing. These nucleotide alterations result in R25G, N52S, V56M, V70D, P87S, D96N, and T106M amino acid substitutions, respectively. The R25G, V56M, V70D, and T106M were novel mutations found in PTPS gene. By analysis of 38 PTPS mutant alleles from 19 unrelated Chinese PTPS-deficient HPA families, the allele frequency of these mutations in Chinese PTPS-deficient HPA were determined to be approximately 5.3% (R25G), 34.2% (N52S), 7.9% (V56M), 2.6% (V70D), 36.8% (P87S), 7.9% (D96N), and 2.6% (T106M), respectively. Two common mutations, N52S and P87S, were found to account for 71% of the Chinese PTPS mutant alleles. The N52S mutation accounts for 48% of the southern Chinese PTPS mutation, but only one (9%) of the northern Chinese PTPS mutant allele was found to be N52S, which suggested that the N52S mutation might be southern Chinese. Clinically, the V56M mutation was found to associate with the mild form of PTPS deficiency. However, the R25G, N52S, P87S, and D96N were found mainly in the patients with severe clinical symptom. Using polymerase chain reaction-based mutation analysis, a fetus at risk of PTPS deficiency was diagnosed prenatally to be a carrier of N52S mutation.

Alcohol Oxidoreductases↗

Accelerated cholesteryl ester transfer in patients with essential hypertension and the effect of ramipril treatment.

Although the transfer of cholesteryl ester (CE) from high-density lipoprotein (HDL) to the apolipoprotein B-containing lipoproteins (very-low-density lipoproteins + low-density lipoproteins) has been shown to be abnormally increased in a number of conditions associated with increased cardiovascular risk, it has not been studied in patients with essential hypertension (EH). To determine whether subjects with EH have increased CE transport, CE transfer (CET) was estimated isotopically and lipoprotein lipid and phospholipid composition determined in a group of 14 untreated normolipidemic (triglycerides 116+/-46, cholesterol 185+/-30, HDL 38+/-10 mg/dl) otherwise healthy ethnically diverse EH subjects. CET was significantly increased in EH subjects compared to a similar group of normotensive controls (EH: k = 0.27+/- 0.09 vs. control k = 0.11+/-0.02: P < 0.01). Lipoprotein concentration and composition were comparable in the two groups and closely resembled that of an age- and sex-matched reference group. The abnormal increase in CET persisted (k = 0.25+/-0.12) after 3 months of treatment with the angiotensin converting enzyme (ACE) inhibitor ramipril without a change in either plasma or lipoprotein lipids. Thus, CET is increased in normolipidemic subjects with EH and is not affected by the ACE inhibitor ramipril.

Adult↗

Evaluation of in vitro chemosensitivity of antitumor drugs using the MTT assay in fresh human breast cancer.

Practical criteria were developed in this paper for the purpose of evaluating chemosensitivity of fresh human breast cancer by the MTT assay. The survival rates at maximum inhibition (Imax %) and the concentrations of drugs which caused fifty percent reduction in absorbance compared to baseline values (IC50) of 175 samples of 10 anti-tumor drugs were evaluated by logistic analyses of the dose-response curves. Distributions of Imax% appeared as normal curves, while those of the IC50 significantly deviated from normal distribution (p < 0.0001). We assessed the in vitro chemosensitivity by comparing the Imax % of each drug on individual samples with the mean Imax % + SD which was obtained from the Imax% of 175 samples. If the individual Imax % > mean Imax % + SD. we thought the tumor sample was resistant to this drug. If the Imax % < or = mean Imax % + SD, we would compare its IC50 with Q50 which was used as a cutoff point for in vitro chemosensitivity of anti-tumor drugs. The in vitro chemosensitivity could be graded as sensitive (Q1-Q25), intermediate (Q26-Q75), and resistant (Q76-Q100) by means of percentile method. If the individual IC50 > or = Q76, the tumor sample would be defined as resistant. If the individual IC50 < or = Q25, it would be defined as sensitive. In the range of Q26-Q75, we used Q50 as a cutoff point between relative sensitivity and relative resistance. Preliminary results showed that the in vitro chemosensitivity to different anti-tumor drugs determined by these criteria were consistent with the clinical response in 83 advanced breast cancer patients.

Antineoplastic Agents↗

Effect of Na+ and K+ ions on the initial crystallization process of lysozyme in the presence of D2O and H2O.

In the initial stage of the crystallization of egg-white lysozyme, monomeric lysozyme aggregated rapidly to form a nucleus in the presence of high salt concentrations. In the present studies, we examined the initial aggregation process of lysozyme (initial crystallization process of lysozyme) in D2O/H2O with sodium ions or potassium ions, and investigated the relationship between the surface hydrophobicity and the aggregation rate of lysozyme. The effect of sodium ions or potassium ions on the initial aggregation process of lysozyme in D2O was clearly different from H2O. The initial aggregation rate of lysozyme in H2O was slower than in D2O. In the case of H2O, the initial aggregation rate was about the same in both ions. But in the case of D2O, the initial aggregation rate was affected by the ion species and the value was lower in potassium ions than in sodium ions. These results suggest that the interaction between lysozyme molecules is stronger in D2O than in H2O. Furthermore, sodium ions have a stronger effect on the interaction than potassium ions in the case of D2O. There was a good correlation among the initial aggregation rate, surface hydrophobicity, and zeta-potential of lysozyme. The hydrophobic interaction may be an important active force in the initial aggregation process of lysozyme.

Cations, Monovalent↗

Kinetic studies on the initial crystallization process of lysozyme in the presence of D2O and H2O.

In the initial stages of the crystallization of egg-white lysozyme, monomeric lysozyme aggregates rapidly and forms a nucleus in the presence of high salt concentrations. The formation process of the aggregates was examined to make clear the difference between the situations in heavy water and in water at the same sodium ion concentration. The aggregation in both cases was observed at unsaturated and/or saturated lysozyme concentrations. The turbidity at 350 nm of lysozyme increased remarkably within 60 min under each experimental condition and showed no appreciable changes over 60 min. The increase of turbidity in H2O was much slower than in D2O at the same salt concentration (3%). Lysozyme showed a critical concentration for nucleus formation whose value in H2O was lower than in D2O at 3% salt concentration. There are two different aggregation models, depending on the concentration of lysozyme. However, similar results were not obtained at 3% sodium ions in H2O. The initial aggregation rate was also dependent on the concentrations of both lysozyme and NaCl. Therefore, the effect of lysozyme concentration on the aggregation process in H2O may be smaller than in D2O.

Chemical Phenomena↗

Effect of thyroid hormone on plasma apolipoproteins and apoA- and apoB-containing lipoprotein particles.

METHODS: Apolipoprotein and apoB- and apoA-containing lipoprotein particle concentrations were determined in 10 athyreotic patients 4 weeks after withdrawal of Synthroid replacement therapy [T4, 0.96 +/- 0.66 microgram mL-1; thyroid-stimulating hormone (TSH), 62.7 +/- 22.8 muIU mL-1] and again 4 weeks after reinstitution of treatment. RESULTS: Thyroid hormone replacement was associated with significant decreases in plasma cholesterol (TC), triglyceride (TG), apolipoprotein B and apolipoprotein C-III (P < 0.01). Both the cholesterol ester-rich LP-B particles and triglyceride-rich LP-Bc particles declined significantly in response to thyroid hormone (LP-B withdrawal 81.6 +/- 24.0 vs. replacement 65.1 +/- 22.0; LP-Bc withdrawal 14.3 +/- 6.0 vs. replacement 10.9 +/- 4.8 mg%, P < 0.01). ApoC-III also decreased in high-density lipoprotein (HDL) (apoC-III-HS), and in very low-density lipoprotein (VLDL) + low-density lipoprotein (LDL) (apoC-III-HP), but this reduction was proportionate so that the apo-C-III-HS/apoC-III-HP ratio, an indirect estimate of the efficiency of lipoprotein lipase (LPL), was unchanged. Apolipoprotein A-I concentrations also decreased significantly (withdrawal 140.7 +/- 27.0 vs. replacement 127.1 +/- 30.0 mg%, P < 0.01) in parallel with the changes in LP-A-I and LP-A-I:A-II particles (LP-A-I withdrawal 35.8 +/- 7.7 vs. replacement 31.5 +/- 6.3; LP-A-I:AII withdrawal 104.9 +/- 20.0 vs. replacement 95.5 +/- 26.0; P < 0.05). CONCLUSION: These findings indicate that thyroid hormone influences the transport not only of both TG-rich and cholesterol-rich apoB-containing lipoprotein particles but also of those that contain apoAI.

Apolipoproteins A↗

Intranasal immunization with yeast-expressed 19 kD carboxyl-terminal fragment of Plasmodium yoelii merozoite surface protein-1 (yMSP119) induces protective immunity to blood stage malaria infection in mice.

Variable protection against malaria blood-stage infection has been demonstrated in mice following parenteral immunization with the highly conserved 19 kD carboxylterminal fragment of the merozoite surface protein-1 (MSP119) using CFA/IFA and other adjuvants. Here we show that intranasal immunization of BALB/C mice with yeast expressed Plasmodium yoelii MSP119 plus a mixture of native and recombinant cholera toxin B subunit, could induce serum MSP119-specific antibodies at titres ranging from 20 000 to 2 560 000. The Ig subclass responses were predominantly G1 and G2b. Intranasal immunization led to protection following challenge (peak parasitaemia < 1%) in mice with the highest MSP119-specific titre (>/= 640 000). In two of the three protected mice, a peak parasitaemia of 0.1%-1% was followed by a boost of the antibody response whereas one of the three protected mice did not boost its antibody response after a peak parasitaemia of 0.02%. In unprotected mice, antibody levels rose, then fell, following the detection of parasites in the peripheral blood. CD4+ T cell-depletion abrogated the ability of the mice to boost their antibody response following challenge. These data demonstrate the potential for intranasal immunization with MSP119 to protect against malaria.

Adjuvants, Immunologic↗

Circadian and septadian variation in the occurrence of acute myocardial infarction in a Chinese population.

To investigate whether circadian or any other temporal pattern(s) exist in the occurrence of acute myocardial infarction (AMI) in a Chinese population, we analyzed 428 patients with confirmed AMI for temporal patterns of AMI occurrence. The patients admitted to the Affiliated Hospital of Shandong Medical University during 1991-95 were from Jinan, the capital city of Shandong Province of China, which has a population of 2.5 million. The chi-square test for goodness of fit was used to test the difference among the frequencies of AMI occurrence in 4 equal intervals (01.00-07.00 h, 07.00-13.00 h, 13.00-19.00 h, 19.00-01.00 h) during the day and among those on 7 days during the week. The results showed that AMI occurrence exhibited significant circadian (p<0.001) and septadian (day of the week) (p=0.046) periodicity, with a peak at 01.00-07.00 h and a trough at 13.00-19.00 h during the day, and a peak on Saturday and a trough on Wednesday during the week. The peak to trough ratio of risk was 2.7 during the day and 2.1 during the week. It is concluded that there were circadian and septadian biorhythms in AMI occurrence in the Chinese population and that these were different from those observed in Western populations. Further investigation of the underlying mechanisms may shed further light on the trigger mechanisms of AMI and thus be helpful in the prevention and treatment of AMI.

Acute Disease↗