Objective To investigate the value of ultrasonic two‐dimensional speckle tracking imaging ( 2D‐ST I) layer‐specific strain and transmural gradient in evaluating the changes of hypertensive patients′left ventricular three layers myocardial function . Methods Thirty‐five hypertensive patients without renal insufficiency were selected as group A ,and 25 hypertensive patients with renal insufficiency as group B .For comparison ,40 healthy volunteers were gathered as control group . T hen ,the systolic peak longitudinal strain of the left ventricle( LPS) ,endocardium( LPS Endo ) ,mid‐cardium ( LPSMid ) and epicardium ( LPSEpi ) were collected .After that ,features of transmural gradient ( ΔLS ) and its percentage ( ΔLS% ) were analyzed . Results For each group ,gradient features exist in each layer of left ventricular myocardium :LPS Endo ＞LPSMid＞LPSEpi . For each group ,the differences between LPSEndo and LPSMid ,and that between LPSEndo and LPSEpi were both statistically significant( P ＜0 .05) . When it came to the differences between LPS Mid and LPSEpi ,those of group A and control group were both statistically significant ( P ＜0 .05 ) . Compared with control group ,the LPSEndo of group A ,and LPSEndo ,LPSMid and LPSEpi of group B declined ,all the differences were statistically significant ( P ＜0 .05 ) . Compared with group A ,LPS Endo ,LPSMid and LPSEpi of group B declined ,the differences were statistically significant ( all P ＜0 .05) . For ΔLS′s differences among all three groups ,there was no statistical significance( P ＞0 .05) . Compared with control group ,the ΔLS% Endo‐Mid of group A rised , and the ΔLS% Endo‐Mid , ΔLS% Mid‐Epi of group B rised , the differences were statistically siginificant ( all P ＜ 0 .05 ) . Compared with group A ,the ΔLS% Endo‐Mid ,ΔLS% Mid‐Epi of group B rised ,the differences were statistically siginificant( all P ＜0 .05) . Conclusions T he layer‐specific strain technique can quantitatively evaluate the changes of systolic function of the left ventricular myocardium in hypertensive patients . ΔLS% may have better sensitivity than ΔLS in dection of systolic function damage of the left ventricular myocardium and can provide more reference for the evaluation of left ventricular systolic function .

Fanconi anemia (FA) is an inheritable disorder that presents with bone marrow failure, developmental anomalies, and an increased susceptibility to cancer. The etiology of this condition stems from a genetic mutation that disrupts the proper repair of interstrand DNA cross-links (ICLs). The resultant dysregulation of the DNA damage response mechanism can induce genomic instability, thereby elevating the mutation rates and the likelihood of developing cancer. The FA pathway assumes a pivotal role in safeguarding genome stability through its involvement in the repair of DNA cross-links and the maintenance of overall genomic integrity. A mutation in the germ line of any of the genes responsible for encoding the FA protein results in the development of FA. The prevalence of aberrant FA gene expression in somatic cancer, coupled with the identification of a connection between FA pathway activation and resistance to chemotherapy, has solidified the correlation between the FA pathway and cancer. Consequently, targeted therapies that exploit FA pathway gene abnormalities are being progressively developed and implemented. This review critically examines the involvement of the FA protein in the repair of ICLs, the regulation of the FA signaling network, and its implications in cancer pathogenesis and prognosis. Additionally, it explores the potential utility of small-molecule inhibitors that target the FA pathway.