Objective To explore the correlation between intestinal mucosal immune barrier and pathogenesis of pigment gallstone and its possible mechanism.Methods Eighty guinea pigs were randomly divided into control group(group CON),pigment gallstone group(group PS),and intestinal mucosal protection group(group GLN).The guinea pigs were fed with normal diet in group CON,pigment gallstonein during diet in group PS,and glutamine-supplemented diet in group GLN for 8 weeks.The guinea pig model of pigment gallstone was established.The incidence of pigment gallstone was detected.The morphology of intestinal mucosa was observed,and the numbers of CD3~+T cell,CD40~+B cell,and IgA~+ plasma cell were counted.Results The incidence of pigment gallstone was significantly higher in group PS than in groups GLN and CON(P＜0.05).Compared with group CON,the intestinal wall was significant thinner and represented obvious signs of inflammation in group PS,and the numbers of CD3~+ T cell,CD40~+ B cell,and IgA~+ plasma cell significantly decreased(CD3~+ T cell,21.8±2.5 vs 11.1±3.4,P＜0.01;CD 40~+B cell,12.9±2.0 vs 10.7±3.6,P＜0.01;IgA~+ plasma cell,12.4±3.4 vs 10.7±3.5,P＜0.01).The signs of inflammation were less severe in group GLN than in group PS.There were significant differences in the numbers of CD3~+ T cell,CD40~+ B cell,and IgA~+plasma cell between groups GLN and PS.Conclusion Intestinal barrier dysfunction,including mechanical barrier and immune barrier,is involved in the formation of pigment gallstone.Glutamine has proved to improve the function of intestinal mucosal barrier and decrease the incidence of pigment gallstone.

More and more studies have found that intestinal flora is associated with connective tissue diseases. This review summarizes characteristics of intestinal flora and its mechanism of action in connective tissue diseases, and mainly elaborates correlations between intestinal flora imbalance and 3 common connective tissue diseases (lupus erythematosus, systemic scleroderma and Sjogren′s syndrome) , its possible mechanism of action and related hypothesis. Probiotics can regulate the intestinal flora imbalance, and serve as one of treatments for these common connective tissue diseases.

Colorectal cancer (CRC) is one of the leading causes of death worldwide. Thus, the development of new therapeutic targets for CRC treatment is urgently needed. SGK1 is involved in various cellular activities, and its dysregulation can result in multiple cancers. However, little is known about its roles and associated molecular mechanisms in CRC. In present study, we found that SGK1 was highly expressed in tumor tissues compared with peri-tumor samples from CRC patients. In vitro experiments revealed that SGK1 overexpression promoted colonic tumor cell proliferation and migration and inhibited cell apoptosis induced by 5-fluorouracil (5-FU), while SGK1 shRNA and inhibitors showed the inverse effects. Using CRC xenograft mice models, we demonstrated that knockdown or therapeutic inhibition of SGK1 repressed tumor cell proliferation and tumor growth. Moreover, SGK1 inhibitors increased p27 expression and promoted p27 nuclear accumulation in colorectal cancer cells, and p27 siRNAs could attenuate the repression of CRC cell proliferation induced by SGK1 inhibitors. Collectively, SGK1 promotes colorectal cancer development via regulation of CRC cell proliferation, migration and survival. Inhibition of SGK1 represents a novel strategy for the treatment of CRC.
Animals ; Apoptosis ; Cause of Death ; Cell Proliferation ; Colon ; Colorectal Neoplasms* ; Fluorouracil ; Heterografts ; Humans ; In Vitro Techniques ; Mice ; Repression, Psychology ; RNA, Small Interfering

Objective To analyze the clinical characteristics of patients with presbycusis by using disyllabic mandarin speech test materials (MSTMs).Methods A total of 59 subjects (23 men and 36 women) with presbycusis,from 61 to 84 years old with the average as 71.3±6.7.They were divided into three groups:the mild group (10 subjects),the moderate group (35 subjects)and the severe group (14 subjects)according to the pure tone average (PTA) thresholds at 0.5,1,2 and 4 kHz from the better ear.In addition,11 subjects of elderly persons with normal hearing were used as the control group.All the subjects enrolled in this study could speak Mandarin well in their daily lives.Nine lists of disyllabic mandarin speech test materials were utilized to test speech recognition threshold (SRT) and P-I function for these groups respectively.Results The PTA(51.65±11.98)and SRT (50.98±16.05)from presbycusis group were much higher than the control group(PTA 19.55± 4.55,SRT 18.79± 7.45),while the average slope of the P-I function 2.63％/dB from the presbycusis group was lower than the control group 4.65％/dB (P＜0.01).The SRT of male patients (56.54±17.23) was higher than the females(47.99± 15.63) (P＜0.05).The PTA and SRT in these three groups divided by degrees of hearing loss were higher than the control group obviously.The PTA and SRT had significantly increased as the degree of hearing loss increased.The differences among these groups were significant (P＜0.01).The average slope of P-I function of these three groups divided by degrees of hearing loss (mild group:2.47％/dB,moderate group:2.76％/dB,severe group:2.42％/dB) was smaller than the slopes in the control group which was 4.65 ％/dB (P＜0.01).The average slope of P-I function among these groups had no significant difference (P＞0.05).Conclusion The SRT of patients with presbycusis increased and the SRT of male was higher than the females.The average slope of P-I function decreased and the curve moved to right side and became a gradual curve.As hearing loss became more severe,the SRT rose more apparently.

OBJECTIVE: To analyze the clinical features and pathogenesis of a fetus with holoprosencephaly. METHODS: The findings of prenatal ultrasonography was reviewed. Following elective abortion, whole exome sequencing (WES) was carried out to identify potential pathogenic variant. Copy number variants (CNVs) of the abortus and its parents were detected by low-depth high-throughput sequencing. The parents were also analyzed by chromosomal karyotyping. RESULTS: Prenatal ultrasound suggested that the fetus had holoprosencephaly. WES revealed that it had approximately 33 Mb deletion at chromosome 13 involving ZIC2, a haploid dose sensitive gene. The results of low-depth high-throughput sequencing confirmed that the fetus carried a de novo 32.32 Mb deletion at 13q31.1-34. Karyotyping analysis has excluded gross chromosomal aberration in both parents. CONCLUSION The fetus was diagnosed with holoprosencephaly, which may be attributable to the 13q31.1-34 deletion involving the ZIC2 gene.
Adult ; Chromosomes, Human, Pair 13 ; genetics ; Female ; Fetus ; Genetic Testing ; Holoprosencephaly ; diagnostic imaging ; genetics ; pathology ; Humans ; Karyotyping ; Male ; Nuclear Proteins ; genetics ; Pregnancy ; Prenatal Diagnosis ; Sequence Deletion ; Transcription Factors ; genetics ; Ultrasonography, Prenatal ; Whole Exome Sequencing