Objective To understand the elonal expansion and genetic diversity of Salmonella en-terica semtype Paratyphi A (SPA) and to construct a typing method to determine the epidemic clones of the isolates. Methods Antimicrobial susceptibility testing was performed with 3980 SPA isolates by the cen-trolled Kirby-Bauer disc diffusion technique on Muller-Hinton agar plates. A total of 15 SPA with nalidixie acid resistance for mutations in gyrA, gyrB, gyrC and gyrE genes within the quinolone-resistant determina-tion region (QRDR) were examined. Subtyping of 121 isolates of SPA from seven counties in Yuxi were studied using pulsed-field gel eleetrophoresis (PFGE) analysis following digestion of chromosomal DNA with restriction endanucleases Spe Ⅰ and Xba Ⅰ. PFGE patterns were analyzed by duster analysis. Results The nalidixic acid-susceptible isolates predominated in 1999 but was replaced by nalidixic acid -resistant (NAR) isolates after 2000. Amplification by PCR and sequencing of the genes with subsets of 15 NAR strains re-vealed that the resistance mechanisms had resulted from single point mutations in the gyrA gene. Spe Ⅰ and Xba Ⅰ digestion of 121 isolates gave five and four different PFGE patterns with the predominance of the Spe Ⅰ 01 and Spe Ⅰ 02 (or the Xba Ⅰ 01) epidemic patterns, respectively. Spe Ⅰ 01 and Spe Ⅰ 02 consisted of 37.2% and 57.9% of isolates, respectively, or Xba Ⅰ 01 consisted of 95.0% of isolates. Conclusion The incidence of resistance to nalidixic acid of the isolates increased during the study period. PFGE patterns Spe Ⅰ 01 and Spe Ⅰ 02 (or Xba Ⅰ 01), the main clones of the epidemics, are highly prevalent in Yuxi. PFGE with Spe Ⅰ and Xba Ⅰ is a useful technique to differentiate SPA.

Many people affected by fragile X syndrome (FXS) and autism spectrum disorders have sensory processing deficits, such as hypersensitivity to auditory, tactile, and visual stimuli. Like FXS in humans, loss of Fmr1 in rodents also cause sensory, behavioral, and cognitive deficits. However, the neural mechanisms underlying sensory impairment, especially vision impairment, remain unclear. It remains elusive whether the visual processing deficits originate from corrupted inputs, impaired perception in the primary sensory cortex, or altered integration in the higher cortex, and there is no effective treatment. In this study, we used a genetic knockout mouse model (Fmr1^KO), in vivo imaging, and behavioral measurements to show that the loss of Fmr1 impaired signal processing in the primary visual cortex (V1). Specifically, Fmr1^KO mice showed enhanced responses to low-intensity stimuli but normal responses to high-intensity stimuli. This abnormality was accompanied by enhancements in local network connectivity in V1 microcircuits and increased dendritic complexity of V1 neurons. These effects were ameliorated by the acute application of GABA_A receptor activators, which enhanced the activity of inhibitory neurons, or by reintroducing Fmr1 gene expression in knockout V1 neurons in both juvenile and young-adult mice. Overall, V1 plays an important role in the visual abnormalities of Fmr1^KO mice and it could be possible to rescue the sensory disturbances in developed FXS and autism patients.
Animals ; Disease Models, Animal ; Fragile X Mental Retardation Protein/metabolism* ; Fragile X Syndrome/metabolism* ; Humans ; Mice ; Mice, Knockout ; Neurons/metabolism*