[Influence of Age on the Susceptibility of Anopheles stephensi to Plasmodium berghei Infection].

Objective: To investigate the ability of Anopheles stephensi at different ages to transmit Plasmodium berghei and elucidate the possible mechanisms. Methods: To study and compare the susceptability of A. stephensi of different ages to P. berghei, 4-day and 25-day female A. stephensi were fed with P. berghei infected BALB/c mouse blood with parasitaemia 4%-8%. At 8 days after infection, the mosquitoes were dissected and the number of intestinal Plasmodium oocysts was counted under microscope. Difference in the susceptability to Plasmodium infection was analyzed between the two age groups. To study the intestinal bacteria load in A. stephensi, LB plate culture was used to detect the intestinal bacteria in the mosquitoes of the two groups before infection, and real-time quantitative PCR (qPCR) was performed to check the culturable bacteria and the total bacteria load. The expression levels of major immune response effectors cecropin（CEC1, CEC3）, defensin (DEF), gambicin (GAM), attacin (ATT), nitric oxide synthase (NOS), dual oxidase (DUOX), and thioester protein 1（TEP1） in 4-day and 25-day mosquitoes were determined by qPCR. Results: At 8 days after infection, the median of oocyst number in 4-day mosquitoes was 139, which was nearly 46 times of that in 25-day mosquitoes (median, 3)（P<0.01）. There was a significant difference in the intestinal bacteria load between 4-day and 25-day mosquitoes. The results of qPCR showed that the total bacteria load in 25-day mosquitoes was 1.5 times of that in 4-day mosquitoes (P<0.05). By LB plate culture, proliferation of 28 889 colony forming units (cfu) bacteria was found for 25-day mosquitoes, which was 9 times of that for 4-day mosquitoes（3 200 cfu）（P<0.05）. In addition, the NOS expression level in 25-day mosquitoes was 2.4 times of that in 4-day mosquitoes (P<0.01）, while the expression levels of antimicrobiota peptides ATT, DEF, CEC3, and CEC1 in 25-day mosquitoes were only 27%, 48%, 14%, and 61% of those in 4-day mosquitoes, respectively (P<0.05). The expression levels of GAM, DUOX, TEP1 showed no difference between the two groups. Conclusion: The antimicrobiota peptides in A. stephensi are significantly downregulated with age increase, together with increased intestinal bacteria load and NOS expression, resulting in enhanced resistance to Plasmodium.

3-Chloro-4-dimethyl-amino-5-[(1R,2S,5R)-2-isopropyl-5-methyl-cyclo-hex-yloxy]furan-2(5H)-one.

The title compound, C(16)H(26)ClNO(3) contains one almost planar furan-one ring [maximum deviation of 0.021 (2) Šfor the O atom] with a stereogenic center (S) and one cyclo-hexane ring which displays a chair conformation and has three stereogenic centers [S at the C atom bearing the isopropyl group, R at the C atom attached to the O atom and R at the C atom bearing the methyl group].

2,2'-(p-Phenyl-ene)bis-(4,5-dihydro-1H-imidazol-3-ium) bis-(3-nitro-benzoate).

In the title compound, C(12)H(16)N(4) (+)·2C(7)H(4)NO(4) (-), the complete 2,2'-(p-phenyl-ene)bis-(4,5-dihydro-1H-imidazol-3-ium) (bib) dication is generated by crystallographic inversion symmetry. The bib cations reside on crystallographic inversion centers, which coincide with the centroids of the respective benzene rings. In the cation, the imidazole ring adopts an envelop conformation with the flap atom displaced by 0.082 (3) Šfrom the plane through the other ring atoms. In the crystal, the cations and anions are linked through inter-molecular N-H⋯O hydrogen bonds, forming chains running along the a axis. C-H⋯O inter-actions also occur. Weak π-π contacts between the imidazole rings of bib and between the benzene rings of NB [centroid-centroid distances = 3.501 (1) and 3.281 (2) Å, respectively] may further stabilize the structure.

2-[4-(4,5-Dihydro-1H-imidazol-2-yl)phen-yl]-4,5-dihydro-1H-imidazol-3-ium 4-amino-benzoate.

In the cation of the title compound, C(12)H(15)N(4) (+)·C(7)H(6)NO(2) (-), the benzene ring makes dihedral angles of 30.51 (9) and 25.64 (9)° with the imidazole and imidazolinium rings, respectively. In the crystal, inter-molecular N-H⋯O and N-H⋯N hydrogen-bonding inter-actions link the mol-ecules into a three-dimensional network.

[Analysis of flap thickness created with mechanical microkeratome in LASIK by using anterior segment optical coherence tomography].

OBJECTIVE: To evaluate the accuracy, uniformity and relevant factors of LASIK flaps created with a mechanical microkeratome Moria II (90, 110 and 130 heads). METHODS: It was a case-control study. Eighty-seven patients underwent LASIK in both eyes using Moria II 90 head (52 eyes, 26 cases), 110 head (58 eyes, 29 cases), or 130 head (64 eyes, 32 cases). One week after surgery, anterior segment optical coherence tomography was performed four times on each eye to measure flap thickness at 20 points in four meridians. The results were assessed for accuracy, uniformity and relevant factors. RESULTS: The central thickness of corneal flaps was (119.23±15.65), (140.42±12.26), and (165.92±17.00) µm by Moria II 90, 110 and 130 heads, respectively. The shape of the corneal flaps in the three groups resembled a concave lens, the central zone was significantly thinner than the paracentral and peripheral zones. The central flap thicknesses were statistically significantly more accurate and regular than the flap in the peripheral zone (F=212.419, P<0.05). The mean difference of right eye (19.58±0.44) µm was higher than that of the left eye (16.55±0.44) µm. The mean difference of knife in-side (21.30±0.55) µm was higher than the knife out-side (14.36±0.64) µm (F=25.341, 44.461; P<0.05). CONCLUSIONS: The central flap thicknesses were more accurate as compared with the expected value. The mean flap thickness in the three groups was not uniform. Variation of the thickness in corneal flaps was greater in thicker flaps. The flap thickness in right eye was greater than that in left eye, according to the surgical sequence between two eyes. The flap thickness of blade in-side was thicker than that of out-side.

N-[(2S)-4-Chloro-2-(l-menth-yloxy)-5-oxo-2,5-dihydro-furan-3-yl]-l-valine.

The title compound, C(19)H(30)ClNO(5), was obtained by the tandem asymmetric Michael addition-elimination reaction of (5S)-3,4-dichloro-5-(l-menth-yloxy)furan-2(5H)-one and l-valine in the presence of potassium hydroxide. The furan-one unit is approximately planar (r.m.s. deviation = 0.0204 Å) and the six-membered cyclo-hexane ring adopts a chair conformation. The crystal structure is stabilized by a network of O-H⋯O and N-H⋯O hydrogen bonds.

N-{4-Bromo-2-[(S)-menth-yloxy]-5-oxo-2,5-dihydro-3-fur-yl}-l-valine.

The title compound, C(19)H(30)BrNO(5), was obtained via a tandem asymmetric Michael addition-elimination reaction of 3,4-dibromo-5-[(S)-l-menth-yloxy]furan-2(5H)-one and l-valine in the presence of potassium hydroxide. The mol-ecular structure contains an approximately planar (r.m.s. deviation = 0.0204 Å) five-membered furan-one ring and a six-membered menth-yloxy ring adopting a chair conformation. The crystal packing is stabilized by inter-molecular O-H⋯O and N-H⋯O hydrogen bonding.

N-[(2S)-4-Chloro-2-(l-menthyloxy)-5-oxo-2,5-dihydro-3-furyl]-l-alanine.

The title compound, C(17)H(26)ClNO(5), was prepared via a tandem asymmetric Michael addition-elimination reaction of (5S)-3,4-dichloro-5-(l-menth-yloxy)furan-2(5H)--one and l-alanine in the presence of potassium hydroxide. The five-membered furan-one ring is approximately planar while the six-membered menth-yloxy ring adopts a chair conformation. The crystal packing is stabilized by inter-molecular O-H⋯O and N-H⋯O hydrogen bonds.

3,3'-Dibromo-5,5'-bis-[(S)-l-menth-yloxy]-4,4'-(hexane-1,6-diyldiimino)difuran-2(5H)-one.

The title compound, C(34)H(54)Br(2)N(2)O(6), was obtained by the Michael addition-elimination reaction of (5S)-5-(l-menthyl-oxy)-3,4-dibromo-furan-2(5H)-one with 1,6-hexa-nediamine in the presence of triethyl-amine. The crystal structure contains two chiral five-membered furan-one rings, in twist and envelope conformations, and two six-membered cyclo-hexane rings in chair conformations.