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Listeriosis is a rare but serious foodborne disease caused by Listeria monocytogenes. This matched case–control study (1:1 ratio) aimed to identify the risk factors associated with food consumption and food-handling habits for the occurrence of sporadic listeriosis in Beijing, China. Cases were defined as patients from whom Listeria was isolated, in addition to the presence of symptoms, including fever, bacteraemia, sepsis and other clinical manifestations corresponding to listeriosis, which were reported via the Beijing Foodborne Disease Surveillance System. Basic patient information and possible risk factors associated with food consumption and food-handling habits were collected through face-to-face interviews. One hundred and six cases were enrolled from 1 January 2018 to 31 December 2020, including 52 perinatal cases and 54 non-perinatal cases. In the non-perinatal group, the consumption of Chinese cold dishes increased the risk of infection by 3.43-fold (95% confidence interval 1.27–9.25, χ2 = 5.92, P = 0.02). In the perinatal group, the risk of infection reduced by 95.2% when raw and cooked foods were well-separated (χ2 = 5.11, P = 0.02). These findings provide important scientific evidence for preventing infection by L. monocytogenes and improving the dissemination of advice regarding food safety for vulnerable populations.
Based on a scanning electron microscope operated at 30 kV with a homemade specimen holder and a multiangle solid-state detector behind the sample, low-kV scanning transmission electron microscopy (STEM) is presented with subsequent electron tomography for three-dimensional (3D) volume structure. Because of the low acceleration voltage, the stronger electron-atom scattering leads to a stronger contrast in the resulting image than standard TEM, especially for light elements. Furthermore, the low-kV STEM yields less radiation damage to the specimen, hence the structure can be preserved. In this work, two-dimensional STEM images of a 1-μm-thick cell section with projection angles between ±50° were collected, and the 3D volume structure was reconstructed using the simultaneous iterative reconstructive technique algorithm with the TomoJ plugin for ImageJ, which are both public domain software. Furthermore, the cross-sectional structure was obtained with the Volume Viewer plugin in ImageJ. Although the tilting angle is constrained and limits the resulting structural resolution, slicing the reconstructed volume generated the depth profile of the thick specimen with sufficient resolution to examine cellular uptake of Au nanoparticles, and the final position of these nanoparticles inside the cell was imaged.
The potential relationship between the establishment of Foot-and-mouth disease virus (FMDV) persistent infection and gene variation was identified by investigating the variation of VP1 and 3ABC genes from yellow cattle persistent infection isolates. Five yellow cattle were inoculated on their tongue with 1.0×104 ID50/ml of FMDV O/Akesu/58 strain. After displaying clinical or subclinical signs, they probably became asymptomatic carriers. Oesophageal–pharyngeal fluids were collected monthly from the carriers with a probang and inoculated into a baby hamster kidney cell line (BHK-21); 12 FMDV isolates were obtained. The VP1 and 3ABC genes of the 12 isolates were then amplified by reverse-transcriptase polymerase chain reaction (RT-PCR). Cloning and sequencing revealed that the homology of the VP1 nucleotide and amino-acid sequence of all the isolates was above 98%, with no base deletion or insertion. When compared with the O/Akesu/58 FMDV strain, the homology of the VP1 nucleotide sequence of the isolates was only 85%, and that of the deduced amino-acid sequence only 90%.There were several nucleotide mutations in the VP1 gene of the isolates, including 16 consistent nucleotide mutations, with only two of them leading to a change in amino acid (I56→T, A210→E). Moreover, it was found that four nucleotide points and three amino-acid points had transversions among all isolates. The 3ABC gene had only 13 nucleotide transversions and five amino-acid mutations. It was presumed that persistent FMDV infection might have little connection with variation in the VP1 and 3ABC genes, and was probably related to other structural protein gene and key factors.
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