INH is the core anti-TB drug, and inhA and katG mutations are the primary molecular mechanism of INH resistance. It has been reported that 8%-43% and 5-%-95% of the resistant isolates have inhA and katG mutations [20]. Detection of these two genes in clinical samples has been used for the diagnosis of INH resistance in most MTB isolates. inhA mutation is the molecular basis for ETH/PTH resistance and cross-resistance to INH. Therefore, inhA genotyping can assist the diagnosis of ETH resistance. Fluorescent PCR andmelting curve technology has been used in the rapid detection of drug susceptibility of MTB isolates. The common INH resistance-associated mutation sites under detection include inhA promoter (-17~-8), inhA 94 and katG codon 315, in addition to RIF resistance-associated mutations in rpoB codon 507-533. Genotyping at these sites is used for rapid prediction of INH and RFP resistance[7]. The present study involved genotyping of inhA and katG genes and the phenotypic susceptibility testing of clinicalMTB isolates. Of the 118 INH-resistant isolates analyzed, 56.7% (67/118) of the isolates had katG mutation, and 24.5% (29/118) had inhA mutation; of 28 isolates with ETH phenotypic resistance, 42.9% of the isolates (12/28) had inhA mutation, and these results agreed with the previous reports [20][10]. However, only 35.3% (12/34) of the 34 isolates with inhA mutation were resistant to ETH; of all ETH-resistant isolates, only 42.9% had inhA mutation.

                                                                                                                       
                                                                             英译中

Many studies at home and abroad have shown that the intestinal flora is different in PD patients, simple chronic constipationpatients and healthy controls. Changes of intestinal flora in some PD patients are similar to those in simple chronic constipation patients^{[8，15，16,17,18，23]}. Notably, the prevalence of constipation increases in PD patients^[9],but there is still a lack of studies on the influence of constipation on intestinal flora in PD. Much misunderstanding still exists as to the realchanges in intestinal flora in PD: 1. If constipation in PD patients is caused by accumulation of Lewy-body inclusions in the presence of certain intestinalbacteria, the induced constipation symptoms will cause further changes in intestinal bacteria over time, intervening identification of the initial bacteria; 2. Intestinal bacteria may activate microglial cells via parenteral pathway such as short chain fatty acids to induce PD. At this stage, constipation in PD patients may be related to lack of mobility and medication, but not to the course of PD itself. Therefore, it is necessary to conduct a subgroup analysis for PD patients with or without constipation.

国内外多项研究先后揭示PD患者、单纯慢性便秘患者肠道菌群与健康人群不同，且部分PD患者菌群改变与单纯慢性便秘患者肠道菌群改变相似^{[8，15，16,17,18，23]}。值得注意的是，PD患者便秘发生率较高^[9]，但是便秘对PD肠道菌群影响的研究依然缺乏，这对揭示PD真实肠道菌群改变会造成较大的偏差：1.如果PD便秘是某些肠道菌群导致路易小体聚集引起，那么诱导的PD便秘症状随着时间发展会导致肠道菌群进一步变化，因而干扰甄别最初发生改变的菌群；2.肠道菌群可能通过肠外途径如短链脂肪酸引起小胶质细胞激活而导致PD发病，此时帕金森病患者的便秘产生可能与运动少、药物等因素有关，而与PD病程无关。因而，有必要按有无便秘对PD患者进行分组研究。