BACKGROUND： The pathways induced/activated by mercury poisoning that lead to muscle pain remain unclear. The present study addressed the structural changes observed in the peripheral nerve following mercury poisoning...BACKGROUND： The pathways induced/activated by mercury poisoning that lead to muscle pain remain unclear. The present study addressed the structural changes observed in the peripheral nerve following mercury poisoning. OBJECTIVE： To establish the mercury poison rat model, rats were intragastrically administered mercury, The correlation between post-mercury poison-induced muscular pain and tibial nerve morphological changes were observed. DESIGN： Observational contrast animal study. SETTING： Shangdong Academy of Occupational Health and Occupational Medicine. MATERIALS： Thirty adult Sprague Dawley rats of equal gender. Mercury chloride （HgCl2, analytical grade： 99.99%; batch number： 990402） was provided by Shanghai Chemical Reagent Factory, and sodium dimercaptopropanesulfonate （DMPS） injection by Shanghai Harvest Pharmaceutical Co., Ltd. （batch number： 0309011）. METHODS： This study was performed at the Animal Experimental Center of Shangdong Academy of Occupational Health and Occupational Medicine from December 2005 to January 2006. Rats were randomly divided into high-dose mercury, low-dose mercury, and control groups, with 10 rats in each group. Rats in the two mercury groups were intragastrically administered 17 mg/kg and 8.5 mg/kg HgCl2 solution, respectively, once a day to establish a rat model of subacute mercury poisoning. Rats in the control group were intragastrically administered 2 mL saline, once a day. Intragastric administration in the three groups lasted for （20± 2） days. After model establishment, rats in the two mercury groups were injected DMPS once a day to remove mercury. The injection lasted for 3 days after every 4-day interval. Seven days was regarded as one treatment cycle, and there were two treatment cycles in total. MAIN OUTCOME MEASURES： Mercury-induced muscular pain status; ultrastructural changes of the right tibial nerve following model establishment and mercury removal under transmission electron microscope. RESULTS： Thirty rats were included in the final analysis. Muscular pain status： one rat exhibited mercury-induced muscular pain. Red swelling of the skin was observed on the posterior claws, lower limbs, and tail. The rat incessantly licked and scratched the red swelling of the skin, turned over, and occasionally hissed. The axon myelin sheath of the tibial nerve was intact, clear, and dense. The mitochondrial membrane was intact and smooth, and the cristallin was clear. Microfilaments and microtubules were tightly arranged. Axon pathological changes and demyelination lesion occurred in the right tibial nerve in the two mercury groups. However, mercury removal with DMPS for two treatment cycles did not inhibit the peripheral nerve lesion. In the pain model rats, the myelin sheath of the tibial nerve was mottled. Mitochondria in the axoplasm were swollen, the structure was unclear, numbers were decreased, and cristallin disappeared. The mitochondrial membrane was broken, and the microfilament was reduced and unorganized. After two treatment cycles of mercury removal with DMPS, nerve demyelination lesion was aggravated, and the myelin sheath was increasingly mottled. Both rarefaction degeneration and vacuolar transformation were observed in most of the axon myelin sheath. The axonal membrane was damaged to a certain degree. CONCLUSION： Subacute HgCl2 poisoning might result in tibial nerve injury. The myelin sheath of the tibial nerve was mottled in mercury poisoned rats without muscular pain. Nevertheless, the correlation between mercury poisoning and pain remains unclear. The injured tibial nerve of the rats was not repaired after dimercaptopropanesulfonate treatment.展开更多
Human cytomegalovirus(HCMV)is a ubiquitous pathogen belongs to betaherpesvirus subfamily.RNA2.7 is a highly conserved long non-coding RNA accounting for more than 20%of total viral transcripts.In our study,functions o...Human cytomegalovirus(HCMV)is a ubiquitous pathogen belongs to betaherpesvirus subfamily.RNA2.7 is a highly conserved long non-coding RNA accounting for more than 20%of total viral transcripts.In our study,functions of HCMV RNA2.7 were investigated by comparison of host cellular transcriptomes between cells infected with HCMV clinical strain and RNA2.7 deleted mutant.It was demonstrated that RNA polymeraseⅡ(PolⅡ)-dependent host gene transcriptions were significantly activated when RNA2.7 was removed during infection.A145 nt-in-length motif within RNA2.7 was identified to inhibit the phosphorylation of PolⅡSerine-2(PolⅡS2)by reducing the interaction between PolⅡand phosphorylated cyclin-dependent kinase 9(pCDK9).Due to the loss of PolⅡS2 phosphorylation,cellular DNA pre-replication complex(pre-RC)factors,including Cdt1 and Cdc6,were significantly decreased,which prevented more cells from entering into S phase and facilitated viral DNA replication.Our results provide new insights of HCMV RNA2.7 functions in regulation of host cellular transcription.展开更多
基金co-funded by the Key Project of the National Natural Science Foundation of China [grant number 42230609 and 41630425]the National Key Research and Development Plan projects [grant number 2022YFC3004101]
基金the grants from Shandong Medical Academy, No. 2004-023
文摘BACKGROUND： The pathways induced/activated by mercury poisoning that lead to muscle pain remain unclear. The present study addressed the structural changes observed in the peripheral nerve following mercury poisoning. OBJECTIVE： To establish the mercury poison rat model, rats were intragastrically administered mercury, The correlation between post-mercury poison-induced muscular pain and tibial nerve morphological changes were observed. DESIGN： Observational contrast animal study. SETTING： Shangdong Academy of Occupational Health and Occupational Medicine. MATERIALS： Thirty adult Sprague Dawley rats of equal gender. Mercury chloride （HgCl2, analytical grade： 99.99%; batch number： 990402） was provided by Shanghai Chemical Reagent Factory, and sodium dimercaptopropanesulfonate （DMPS） injection by Shanghai Harvest Pharmaceutical Co., Ltd. （batch number： 0309011）. METHODS： This study was performed at the Animal Experimental Center of Shangdong Academy of Occupational Health and Occupational Medicine from December 2005 to January 2006. Rats were randomly divided into high-dose mercury, low-dose mercury, and control groups, with 10 rats in each group. Rats in the two mercury groups were intragastrically administered 17 mg/kg and 8.5 mg/kg HgCl2 solution, respectively, once a day to establish a rat model of subacute mercury poisoning. Rats in the control group were intragastrically administered 2 mL saline, once a day. Intragastric administration in the three groups lasted for （20± 2） days. After model establishment, rats in the two mercury groups were injected DMPS once a day to remove mercury. The injection lasted for 3 days after every 4-day interval. Seven days was regarded as one treatment cycle, and there were two treatment cycles in total. MAIN OUTCOME MEASURES： Mercury-induced muscular pain status; ultrastructural changes of the right tibial nerve following model establishment and mercury removal under transmission electron microscope. RESULTS： Thirty rats were included in the final analysis. Muscular pain status： one rat exhibited mercury-induced muscular pain. Red swelling of the skin was observed on the posterior claws, lower limbs, and tail. The rat incessantly licked and scratched the red swelling of the skin, turned over, and occasionally hissed. The axon myelin sheath of the tibial nerve was intact, clear, and dense. The mitochondrial membrane was intact and smooth, and the cristallin was clear. Microfilaments and microtubules were tightly arranged. Axon pathological changes and demyelination lesion occurred in the right tibial nerve in the two mercury groups. However, mercury removal with DMPS for two treatment cycles did not inhibit the peripheral nerve lesion. In the pain model rats, the myelin sheath of the tibial nerve was mottled. Mitochondria in the axoplasm were swollen, the structure was unclear, numbers were decreased, and cristallin disappeared. The mitochondrial membrane was broken, and the microfilament was reduced and unorganized. After two treatment cycles of mercury removal with DMPS, nerve demyelination lesion was aggravated, and the myelin sheath was increasingly mottled. Both rarefaction degeneration and vacuolar transformation were observed in most of the axon myelin sheath. The axonal membrane was damaged to a certain degree. CONCLUSION： Subacute HgCl2 poisoning might result in tibial nerve injury. The myelin sheath of the tibial nerve was mottled in mercury poisoned rats without muscular pain. Nevertheless, the correlation between mercury poisoning and pain remains unclear. The injured tibial nerve of the rats was not repaired after dimercaptopropanesulfonate treatment.
基金supported by the National Natural Science Foundation of China(82071664)。
文摘Human cytomegalovirus(HCMV)is a ubiquitous pathogen belongs to betaherpesvirus subfamily.RNA2.7 is a highly conserved long non-coding RNA accounting for more than 20%of total viral transcripts.In our study,functions of HCMV RNA2.7 were investigated by comparison of host cellular transcriptomes between cells infected with HCMV clinical strain and RNA2.7 deleted mutant.It was demonstrated that RNA polymeraseⅡ(PolⅡ)-dependent host gene transcriptions were significantly activated when RNA2.7 was removed during infection.A145 nt-in-length motif within RNA2.7 was identified to inhibit the phosphorylation of PolⅡSerine-2(PolⅡS2)by reducing the interaction between PolⅡand phosphorylated cyclin-dependent kinase 9(pCDK9).Due to the loss of PolⅡS2 phosphorylation,cellular DNA pre-replication complex(pre-RC)factors,including Cdt1 and Cdc6,were significantly decreased,which prevented more cells from entering into S phase and facilitated viral DNA replication.Our results provide new insights of HCMV RNA2.7 functions in regulation of host cellular transcription.
