OBJECTIVE: Invastigation of macrolides in the treatment of drug effects in chronic rhinosinusit. METHOD: The 165 patients with chronic rhinosinusit were randomly divided into 80 cases of macrolides drug group and 85 cases of cephalosporins group, and therapeutic effect was observed. The therapeutic effect of macrolides was also observed in refractory chronic rhinosinusit. RESULT: Comparing macrolides group and cephalosporins group,there is not statistically significant (P > 0.05). Treatment with macrolides cefixime tablet ineffective treatment of patients for 3 months, compared before and after treatment was statistically significant (P < 0.01). Treatment with cefixime tablet macrolides ineffective treatment of patients for 3 months, compared before and after treatment was not statistically significant (P > 0.05). CONCLUSION Long-term low-dose applications of macrolides have a good effect in patients with chronic rhinosinusit, particularly for refractory chronic rhinosinusit have a significant effect.
Anti-Bacterial Agents ; therapeutic use ; Cephalosporins ; therapeutic use ; Chronic Disease ; Humans ; Macrolides ; therapeutic use ; Rhinitis ; drug therapy ; Sinusitis ; drug therapy ; Treatment Outcome

Mitochondrial diseases are maternally inherited heterogeneous disorders that are primarily caused by mitochondrial DNA (mtDNA) mutations. Depending on the ratio of mutant to wild-type mtDNA, known as heteroplasmy, mitochondrial defects can result in a wide spectrum of clinical manifestations. Mitochondria-targeted endonucleases provide an alternative avenue for treating mitochondrial disorders via targeted destruction of the mutant mtDNA and induction of heteroplasmic shifting. Here, we generated mitochondrial disease patient-specific induced pluripotent stem cells (MiPSCs) that harbored a high proportion of m.3243A>G mtDNA mutations and caused mitochondrial encephalomyopathy and stroke-like episodes (MELAS). We engineered mitochondrial-targeted transcription activator-like effector nucleases (mitoTALENs) and successfully eliminated the m.3243A>G mutation in MiPSCs. Off-target mutagenesis was not detected in the targeted MiPSC clones. Utilizing a dual fluorescence iPSC reporter cell line expressing a 3243G mutant mtDNA sequence in the nuclear genome, mitoTALENs displayed a significantly limited ability to target the nuclear genome compared with nuclear-localized TALENs. Moreover, genetically rescued MiPSCs displayed normal mitochondrial respiration and energy production. Moreover, neuronal progenitor cells differentiated from the rescued MiPSCs also demonstrated normal metabolic profiles. Furthermore, we successfully achieved reduction in the human m.3243A>G mtDNA mutation in porcine oocytes via injection of mitoTALEN mRNA. Our study shows the great potential for using mitoTALENs for specific targeting of mutant mtDNA both in iPSCs and mammalian oocytes, which not only provides a new avenue for studying mitochondrial biology and disease but also suggests a potential therapeutic approach for the treatment of mitochondrial disease, as well as the prevention of germline transmission of mutant mtDNA.
Animals ; DNA, Mitochondrial ; genetics ; Humans ; Induced Pluripotent Stem Cells ; cytology ; metabolism ; MELAS Syndrome ; genetics ; Male ; Mice ; Microsatellite Repeats ; genetics ; Mitochondria ; genetics ; metabolism ; Mutation ; genetics