Expression of mRNAs for Gal, GalR1, and GalR2 in DRG and SDH.

<p>Panel A: Gal mRNA levels in DRG after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel B: Gal mRNA levels in SDH after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel C: GalR1 mRNA levels in DRG after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel D: GalR1 mRNA levels in SDH after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel E: GalR2 mRNA levels in DRG after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. Panel F: GalR2 mRNA levels in SDH after sciatic nerve-pinch injury at day 8, 16, and 24 without or with Gal treatment. The mRNA level was expressed as the ratio of control. The data are presented as mean ± SD (n = 7). *<i>P<</i>0.05, **<i>P<</i>0.01, ***<i>P<</i>0.001.</p

The thermal threshold alterations with different treatment from day 0 to day 24.

<p>The data are presented as means ± SD (n = 7). *<i>P<</i>0.05 <i>vs</i>. control, **<i>P<</i>0.01 <i>vs</i>. control, ***<i>P<</i>0.001 <i>vs</i>. control, ^#<i>P<</i>0.05 <i>vs</i>. pinch + Gal group, ^##<i>P<</i>0.01 <i>vs</i>. pinch + Gal group, ^###<i>P<</i>0.001 <i>vs</i>. pinch + Gal group.</p

The NCV alterations at different experimental conditions.

<p>Panel A: MNCV decreased significantly after sciatic nerve-pinch injury at day 16 and 24 as compared with that in sham-operated control animals. Gal treatment improved MNCV significantly at the same experimental time point. Panel B: SNCV decreased significantly after sciatic nerve-pinch injury at day 16 and 24 as compared with that in sham-operated control animals. Gal treatment improved SNCV significantly at the same experimental time point. The data are presented as mean ± SD (n = 7). *<i>P<</i>0.05, **<i>P<</i>0.01, ***<i>P<</i>0.001.</p

Semi-thin cross sections of sciatic nerve with toluidine blue staining.

<p>Panel A1, A2 and A3: The dystrophy appearance of nerve fibers after sciatic nerve-pinch injury at day 8, 16, and 24, respectively. The internal structure of the nerve was severely disorganized, sometimes with apparently enlarged nerve fibers (arrows) in Panel A1 or A2. Panel B1 and B2: The dystrophy appearance improved at day 8 and 16, respectively, after sciatic nerve-pinch injury with Gal treatment as compared with that in Panel A1 and A2. Panel B3: Most of the nerve fibers recovered to almost normal status at day 24 after sciatic nerve-pinch injury with Gal treatment. Panel C1, C2, and C3: Normal appearance of the sciatic nerve, with small and large diameter myelinated fibers regularly distributed in sham-operated control animals at day 8, 16 and day 24, respectively, after sham operation. Scale bar = 10 µm.</p

The mechanical threshold alterations with different treatment from day 0 to day 24.

<p>The data are presented as means ± SD (n = 7). *<i>P<</i>0.05 <i>vs</i>. control, **<i>P<</i>0.01 <i>vs</i>. control, ***<i>P<</i>0.001 <i>vs</i>. control, ^#<i>P<</i>0.05 <i>vs</i>. pinch + Gal group, ^##<i>P<</i>0.01 <i>vs</i>. pinch + Gal group, ^###<i>P<</i>0.001 <i>vs</i>. pinch + Gal group.</p

Table_1_A cluster of Psittacosis cases in Lishui, Zhejiang Province, China, in 2021.docx

IntroductionPsittacosis, caused by Chlamydia psittaci, is widespread throughout the world. In humans, C. psittaci infection may lead to severe conditions and complications, including sepsis and multiple organ failure. We report a cluster of cases caused by C. psittaci in Zhejiang Province, 2021, which led to one death and three cases of hospitalization.MethodsThe cases were confirmed by nest-PCR, RT-PCR, and mNGS.ResultsThe four cases were related and the sequences obtained from the samples were closely correlated with those from Taiwan.DiscussionThis study is the first to report on the case of death from psittacosis in Zhejiang Province, and our results help to assess the disease and recommend effective measures to prevent further spread of C. psittaci.</p

The Effect of Pre-Condition Cerebella Fastigial Nucleus Electrical Stimulation within and beyond the Time Window of Thrombolytic on Ischemic Stroke in the Rats

<div><p>Objective</p><p>To investigate the effect of neurogenic neuroprotection conferred by cerebellar fastigial nucleus stimulation (FNS) and the role of PPARγ- mediated inflammation in a rat model of cerebral ischemia reperfusion.</p><p>Methods</p><p>After a continuous 1 hour fastigial nucleus electric stimulation, the male Sprague Dawley (SD) rats were given middle cerebral artery occlusion (MCAO) for 1, 3, 6, 9, 12 and 15 hours undergoing reperfusion with intravenous recombinant tissue plasminogen activator (rt-PA), while the control group received without FNS. After 72h of reperfusion, the neurological deficits, infarct volume and brain edema were evaluated. The brain tissue in ischemic penumbra was determined the myeloperoxidase (MPO) activity by a spectrophotometer and expression of PPARγ was measured by Rt-PCR and Western blotting.</p><p>Results</p><p>Our findings showed that FNS group had significantly reduced infarct volume and brain edema, and improved neurological deficits compared with the control group, especially in 6h and 9h reperfusion subgroups(p<0.05). The expression levels of PPARγ increased gradually and the peak may be before and after 9h reperfusion, the 3h, 6h, 9h, 12h and 15h reperfusion subgroups were higher than each control group(p<0.05). The MPO activity of 6h, 12h and 15h reperfusion subgroups were higher than each control group(p<0.05).</p><p>Conclusions</p><p>The neuroprotective effects of FNS have been shown to prolong the therapeutic window in cerebral ischemia/reperfusion, which might be related to the PPARγ mediated-inflammation in penumbral region.</p></div

The scores of two groups.

<p>FNS group were significantly decreased compared to the control group. Results are expressed as the mean ± SD. *p < 0.05, vs the control group, n = 10.</p

Brain water content of two groups.

<p>(A) The percentage of ischemic lesion area was represented as the ratio of the infarction area to the whole slice area. (B)Water content was calculated by (wet weight −dry weight) /wet weight × 100%. Results are expressed as the mean ± SD. *p < 0.05, vs the control group, n = 5.</p

The protein expressions of PPARγ in cerebral ischemic penumbra.

<p>Results are expressed as the mean ± SD. *p < 0.05, vs the control group, n = 5.</p