Prevotella copri and its related taxa are widely detected in mammalian gut microbiomes and have been linked with an enterotype in humans.However,their microevolution and macroevolution among hosts are poorly characterized.In this study,extensively collected marker genes and genomes were analyzed to trace their evolutionary history,host specificity,and biogeographic distribution.Investigations based on marker genes and genomes suggest that a P.copri-containing lineage(PCL)harbors diverse species in higher primates.Firstly,P.copri in the human gut consisted of multiple groups exhibiting high genomic divergence and conspicuous but non-strict biogeographic patterns.Most African strains with high genomic divergence from other strains were phylogenetically located at the root of the species,indicating the co-evolutionary his-tory of P.copri and Homo sapiens.Secondly,although long-term co-evolution between PCL and higher primates was revealed,sporadic signals of co-speciation and extensive host jumping of PCL members were suggested among higher primates.Metagenomic and phylogenetic analyses indicated that P.copri and other PCL species found in domesticated mammals had been recently transmitted from humans.Thirdly,strong evidence was found on the extensively horizontal transfer of genes(e.g.,genes encoding carbohydrate-active enzymes)among sympatric P.copri groups and PCL species in the same primate host.Our study provides panoramic insights into the combined effects of vertical and horizontal transmission,as well as potential niche adaptation,on the microevolutionary and macroevolutionary history for an enterotype-representative lineage.

OBJECTIVETo evaluate the causes of alanine aminotransferase (ALT) level elevation in HBsAg-positive chronic hepatitis B (CHB) patients with low HBV DNA loads.

METHODSOne hundred nineteen HBsAg positive CHB patients with both serum HBV DNA loads less than 1000 copies/ml and ALT more than 1.25 upper limits of normal (ULN) lasting for at least 6 months were enrolled in this study. Patients co-infected with hepatitis C virus or HIV or suffering from other liver diseases were not included. HBV DNA loads were assayed by PCR. Serological biochemistry and liver biopsy histopathological changes and clinical characteristics of the patients were analyzed.

RESULTSOf the 119 patients 102 were males and 17 were females. The mean age of the patients was (33.9+/-9.7) years and their body mass index (BMI) was (23.4+/-3.7) kg/m2. Mean ALT levels were (150.0+/-166.6) U/L and AST levels were (102.4+/-193.2) U/L. Liver biopsies showed hepatic steatosis in 26.9 % (32/119) of the cases, chronic hepatitis in 53.8% (64/119), non-specific changes in 12.6% (15/119), and 1 without any change. However, hepatic steatosis was more frequently seen in patients taking nucleoside analogs (56.7%), x2=10.394, Probability value less than 0.01. BMI, apolipoprotein B (APO-B), triglyceride, cholesterol and uric acid were all significantly higher in patients with hepatic steatosis than those without (t values were 5.369, 4.276, 3.216, 4.223 and 2.438 respectively, all P less than 0.05) while ALT, AST and apolipoprotein A were much lower in those with steatosis than those without (t values were -2.234, -3.877 and -2.956 respectively, all P less than 0.05). Obesity, dyslipidemia and hyperuricemia were more frequently seen in patients with steatosis than in patients without it (x2 value 3.829, 7.659, 13.389, 0.549, all P less than 0.05). The severity of inflammation and fibrosis were also more significant in patients with steatosis (x2 value 20.978, 17.550, all P less than 0.05). As compared to those patients without specific changes, serum levels of ALT, AST, GGT in patients with chronic hepatitis were obviously higher, all P less than 0.05. In contrast, there were no significant differences in mean age, BMI, male preference, obesity, diabetes, dyslipidemia or hyperuricemia, and the levels of triglyceride, cholesterol, and fasting plasma glucose between the two groups.

CONCLUSIONOur data indicate that hepatic steatosis might be a factor associated with elevated ALT levels in HBsAg-positive CHB patients with low HBV DNA loads, especially in patients treated with nucleoside analogs.

Adult ; Alanine Transaminase ; blood ; Carrier State ; Fatty Liver ; physiopathology ; virology ; Female ; Hepatitis B Surface Antigens ; blood ; Hepatitis B virus ; Hepatitis B, Chronic ; blood ; virology ; Hepatocytes ; pathology ; Humans ; Male ; Viral Load ; Young Adult

OBJECTIVETo investigate the diagnosis and treatment of patients with Crohn disease (CD) complicated with gastrointestinal fistulae.

METHODSClinical data of sixty-two cases with CD complicated with gastrointestinal fistula e from 1978 to 2004 were analyzed.

RESULTSThese were 68 external fistulae in 6 2 patients including recurrent fistulae in 6 cases, internal fistulae in 8 cases . Twenty- seven fistulae were located in the terminal ileum and 21 fistulae wer e located in ileocolic anastomosis site. The main surgery included 14 ileocecal resections with primary anastomosis and 26 resections of original ileocolic anastomosis with fistula and re-anastomosis. The incidence of recurrence was lower (15.4% ) in patients with postoperative medication including sulfasalazine and immunomodulator than that (34.8% ) in patients without postoperative immunomodulator,but the recurrence time was longer [(40+/- 17) months] in patients with postoperative medication than that [(8+/- 3)months] in the patients without postoperative specific medication.

CONCLUSIONSMost CD fistulae are external fistulae,most of the external fistulae are treated by resection of the fistula and anastomosis. Specific medication including sulfasalazine,mesalamine and immunomodulators should be used to prevent postoperative complications and CD recurrence.

Adult ; Crohn Disease ; complications ; diagnosis ; surgery ; Female ; Humans ; Intestinal Fistula ; complications ; diagnosis ; surgery ; Male ; Middle Aged

OBJECTIVETo identify the mutation of ENG and ALK1 genes in a hereditary hemorrhagic telangiectasia pedigree.

METHODS14 exons of ENG gene and 9 exons of ALK1 gene in 11 menbers of this pedigree 4 generation were amplified by reverse transcription-polymerase chain reaction (RT-PCR), the PCR products were screened by direct sequencing.

RESULTSA nonsense mutation c.447G > A was found in exon 4 of ENG gen of the pedigreee, resulting in change of Trp 149 into Stop, while no gene mutation was found in ALK1 gene.

CONCLUSIONThe hereditary hemorrhagic telangiectasia in this pedigree is caused by the nonsense mutation c.447G > A in ENG gene.

Codon, Nonsense ; Exons ; Humans ; Mutation ; Pedigree ; Polymerase Chain Reaction ; Telangiectasia, Hereditary Hemorrhagic