Objective To reveal the effect of fasting insuline(FINS) and insuline resistance(IR) in the process of benign prostatic hyperplasia(BPH). Methods One hundred and seventeen outpatients( ≥60 ys)with BPH from geriatric department were enrolled into the study. The patients were divided into groups according to their FINS and insulin resistance index (HOMA-IR). The indices of BPH, including volume of prostate ( PV ),prostate specific antigen( PSA ), international prostate symptom score (IPSS), course of BPH were analyzed in both groups. Results The PV ( [ 56. 46 ± 26. 88 ] ml vs [ 44. 84 ± 17.66 ] ml, P = 0. 017 ) and the course ( [ 18. 00 ± 6. 91 ] years vs [ 13.93 ± 7. 74 ] years, P = 0. 031 ) were significantly greater in BPH combined hyperinsulinemias(HINS) group than the BPH with normal FINS group;but we found no significant differences in the comparisons of serum PSA level or IPSS between two groups. The PV( [54. 17 ± 25.38 ] ml vs [42. 26 ±14. 15]ml,P =0. 004)and the course([ 16.58 ±7. 65] years vs [13.49 ±7. 59] years,P = 0. 036) were also significantly greater in BPH combined insuline resistance gruop than the insulin sensitivity group, again we found no significant differences in the comparisons of serum PSA level or IPSS between two groups. Conclusion FINS and IR are risk factors of progressed BPH and can promote the progress of BPH.

Even though mutations in LMNA have been reported in patients with typical dilated cardiomyopathy (DCM) and atrioventricular block (AVB) previously, the purpose of this study was to disclose this novel genetic abnormality in one Chinese family with the atypical phenotype of progressive AVB followed by DCM with normal QRS interval. Genome-wide linkage analysis mapped the AVB gene in this family to a marker at chromosome 1q21.2, where the LMNA gene was located. Direct DNA sequence analysis revealed a heterozygous G to A transition at nucleotide 244 in exon 1 of LMNA, which resulted in an E82K mutation. The E82K mutation co-segregated with all affected individuals in the family, and was not present in 200 normal controls. Further clinical evaluation of mutation carriers showed that 5 of 6 AVB patients exhibited mild DCM with a late onset of age in the fourth and fifth decades. Ejection fractions were documented in 5 patients with DCM, but 4 showed a normal value of [Symbol: see text]50%. Echocardiography showed that atrial dilatation occurred earlier than ventricular dilatation in the patients. This study suggests that progressive AVB with normal QRS interval and accompanying DCM at later stages may represent a distinct type of DCM. The molecular mechanism by which the E82K mutation causes AVB as the prominent phenotype in DCM may be a focus of future studies.

Even though mutations in LMNA have been reported in patients with typical dilated cardio-myopathy(DCM)and atrioventricular block(AVB)previously,the purpose of this study was to disclose this novel genetic abnormality in one Chinese family with the atypical phenotype of progressive AVB followed by DCM with normal QRS interval.Genome-wide linkage analysis mapped the AVB gene in this family to a marker at chromosome 1q21.2,where the LMNA gene was located.Direct DNA sequence analysis revealed a heterozygous G to A transition at nucleotide 244 in exon 1 of LMNA,which resulted in an E82K mutation.The E82K mutation co-segregated with all affected individuals in the family,and was not present in 200 normal controls.Further clinical evaluation of mutation carriers showed that 5 of 6 AVB patients exhibited mild DCM with a late onset of age in the fourth and fifth decades.Ejection fractions were documented in 5 patients with DCM,but 4 showed a normal value of ≥50%.Echocardiography showed that atrial dilatation occurred earlier than ventricular dilatation in the patients.This study suggests that progressive AVB with normal QRS interval and accompanying DCM at later stages may represent a distinct type of DCM.The molecular mechanism by which the E82K mutation causes AVB as the prominent phenotype in DCM may be a focus of future studies.

Intestinal injury is a common adverse reaction of clinical chemotherapy drugs, which limits the further application of chemotherapy drugs and causes serious physical and mental burden to patients. At present, the mechanism of chemotherapy-induced intestinal injury is complex, and traditional Chinese medicine has an excellent preventive effect. This article reviews the related mechanisms of intestinal flora imbalance, oxidative stress, inflammatory response, cell apoptosis, and immune damage caused by chemotherapy, and summarizes the role of traditional Chinese medicine in prevention and treatment of oxidative stress, inflammatory response, cell apoptosis, and immune damage.