Clinical effect of laparoscopic radical resection of colorectal cancer based on propensity score matching

BACKGROUND The incidence of colorectal cancer(CRC)is increasing annually.Laparoscopic radical resection of CRC is a minimally invasive procedure preferred in clinical practice.AIM To investigate the clinical effect of laparoscopic radical resection of CRC on the basis of propensity score matching(PSM).METHODS The clinical data of 100 patients who received inpatient treatment for CRC at Changde Hospital,Xiangya School of Medicine,Central South University(The First People’s Hospital of Changde City)were analyzed retrospectively.The control group included patients who underwent open surgery(n=43),and those who underwent laparoscopic surgery formed the observation group(n=57).The baseline information of both groups was equipoised using 1×1 PSM.Differences in the perioperative parameters,inflammatory response,immune function,degree of pain,and physical status between the groups were analyzed.RESULTS Thirty patients from both groups were successfully matched.After PSM,baseline data showed no statistically significant differences between the groups:(1)Periop-erative parameters:The observation group had a longer surgery time,less intra-operative blood loss,earlier first ambulation and first anal exhaust times,and shorter gastric tube indwelling time than the control group;(2)Inflammatory response:24 h after surgery,the levels of interleukin-6(IL-6),C-reactive protein(CRP),and tumor necrosis factor-α(TNF-α)between groups were higher than preoperatively.IL-6,CRP,and TNF-αlevels in the observation group were lower than in the control group;(3)Immune function:At 24 h after surgery,counts of CD4-positive T-lymphocytes(CD4+)and CD4+/CD8-positive T-lymphocytes(CD8+)in both groups were lower than those before surgery,whereas CD8+was higher than that before surgery.At 24 h after surgery,both CD4+counts and CD4+/CD8+in the observation group were higher than those in the control group,whereas CD8+counts were lower;(4)Degree of pain:The visual analog scale scores in the observation group were lower than those in the control group at 24 and 72 h after surgery;and(5)Physical status:One month after surgery,the Karnofsky performance score in the observation group was higher than that in the control group.CONCLUSION Laparoscopic radical resection of CRC has significant benefits,such as reducing postoperative pain and postoperative inflammatory response,avoiding excessive immune inhibition,and contributing to postoperative recovery.

Stem cell therapies in tendon-bone healing

Tendon-bone insertion injuries such as rotator cuff and anterior cruciate ligament injuries are currently highly common and severe.The key method of treating this kind of injury is the reconstruction operation.The success of this reconstructive process depends on the ability of the graft to incorporate into the bone.Recently,there has been substantial discussion about how to enhance the integration of tendon and bone through biological methods.Stem cells like bone marrow mesenchymal stem cells(MSCs),tendon stem/progenitor cells,synovium-derived MSCs,adipose-derived stem cells,or periosteum-derived periosteal stem cells can self-regenerate and potentially differentiate into different cell types,which have been widely used in tissue repair and regeneration.Thus,we concentrate in this review on the current circumstances of tendon-bone healing using stem cell therapy.

Resuscitative endovascular balloon occlusion of the aorta in the treatment of severe hemorrhagic shock caused by upper gastrointestinal bleeding

Hemorrhagic shock is a life-threatening disease often encountered in emergency departments(EDs).Hemorrhagic shock caused by extensive bleeding from multiple sites is often associated with high mortality and morbidity.In recent years,resuscitative endovascular balloon occlusion of the aorta(REBOA)has been widely used in traumatic hemorrhagic shock and is considered to be an effective resuscitation measure.[1]Some studies reported that REBOA was also effective for non-traumatic hemorrhage.[2,3]In this study,we report a case of hemorrhagic shock caused by acute upper gastrointestinal bleeding that was successfully treated and received REBOA to obtain a transition time.This report may provide feasible options for emergency physicians,gastroenterologists,or surgeons to more actively treat refractory gastrointestinal bleeding.

Macrophage CARD9 mediates cardiac injury following myocardial infarction through regulation of lipocalin 2 expression

Immune cell infiltration in response to myocyte death regulates extracellular matrix remodeling and scar formation after myocardial infarction(MI).Caspase-recruitment domain family member 9(CARD9)acts as an adapter that mediates the transduction of pro-inflammatory signaling cascades in innate immunity;however,its role in cardiac injury and repair post-MI remains unclear.We found that Card9 was one of the most upregulated Card genes in the ischemic myocardium of mice.CARD9 expression increased considerably 1 day post-MI and declined by day 7 post-MI.Moreover,CARD9 was mainly expressed in F4/80-positive macrophages.Card9 knockout(KO)led to left ventricular function improvement and infarct scar size reduction in mice 28 days post-MI.Additionally,Card9 KO suppressed cardiomyocyte apoptosis in the border region and attenuated matrix metalloproteinase(MMP)expression.RNA sequencing revealed that Card9 KO significantly suppressed lipocalin 2(Lcn2)expression post-MI.Both LCN2 and the receptor solute carrier family 22 member 17(SL22A17)were detected in macrophages.Subsequently,we demonstrated that Card9 overexpression increased LCN2 expression,while Card9 KO inhibited necrotic cell-induced LCN2 upregulation in macrophages,likely through NF-κB.Lcn2 KO showed beneficial effects post-MI,and recombinant LCN2 diminished the protective effects of Card9 KO in vivo.Lcn2 KO reduced MMP9 post-MI,and Lcn2 overexpression increased Mmp9 expression in macrophages.Slc22a17 knockdown in macrophages reduced MMP9 release with recombinant LCN2 treatment.In conclusion,our results demonstrate that macrophage CARD9 mediates the deterioration of cardiac function and adverse remodeling post-MI via LCN2.

Role of 5-azacytidine in differentiation of human mesenchymal stem cell sinto cardiomyocytes in vitro

Objective 5-azacytidine could induce the differentiation of stem cells into cardiomyocytes （CMs）. The aim of this study was to screen the optimal condition for 5-azacytidine inducing differentiation of human mesenchumal stem cells （hMSCs） into CMs, and the effect of 5-azacytidine on adherence, cell vigor and chromosome karyotype of hMSCs. Methods hMSCs were isolated from human bone marrow and cultured in vitro. The phenotypes ofhMSCs were identified by flow cytometric analyses. MTT test was used to investigate the effect of different concentrations of 5-azacytidine on proliferation ofhMSCs. Four weeks after 5-azacytidine induction, semi-quantitative RT-PCR, transmission electron microscopy （TEM）, single-cell action potentials, detection of cardio-enzyme AST and LDH, cell adherence, cell viability and chromosome karyotype test were performed. Results The typical morphological features of hMSCs were fibroblast-like in shape, hMSCs expressed CD44 and CD105,and did not express CD34, CD45 and CD31. The optimal concentration of 5-azacytidine was 10μ mol/L. The shape of hMSCs treated with 5-Azacytidine changed from fusiform to polygon or astrocyte gradually, and passaged cells were evenly arranged as polarity structure. Indueed-hMSCs connected with neighbouring cells, fbrming myotube-like structures 4 weeks later. It was confirmed that induced hMSCs shaped myotubule-like structure and had some of micro-histologic structures of CMs by TEM. RT-PCR showed that induced hMSCs expressed cardiac specific product BNNP and early cardio-myogenesis specific transcription factor NKX2.5mRNA. Besides, induced-MSCs led to the weak action potential and secreted cardio-enzyme AST and LDH. There was no significant difference in cell adherence and viability before and after induction. Both hMSCs and induced-hNSCs kept stable normal diploid nucleus. Conclusion The optimal condition for inducing effect of 5-azacytidine is 10 la mol/L and 24-hour incubation; and under this condition, the adherence, vigor and chromosome karyotype ofhMSCs would not be affected （J Geriatr Cardio12009; 6：182-188）.

Cardiac Fibroblast-Specific Activating Transcription Factor 3 Promotes Myocardial Repair after Myocardial Infarction

Background：Myocardial ischemia injury is one of the leading causes of death and disability worldwide.Cardiac fibroblasts （CFs） have central roles in modulating cardiac function under pathophysiological conditions.Activating transcription factor 3 （ATF3） plays a self-protective role in counteracting CF dysfunction.However,the precise function of CF-specific ATF3 during myocardial infarction （MI） injury/repair remains incompletely understood.The aim of this study was to determine whether CF-specific ATF3 affected cardiac repair after MI.Methods：Fifteen male C57BL/6 wild-type mice were performed with MI operation to observe the expression of ATF3 at 0,0.5,1.0,3.0,and 7.0 days postoperation.Model for MI was constructed in ATF3TGfl/flColla2-Cre＋ （CF-specific ATF3 overexpression group,n =5） and ATF3TGfl/flColla2-Cre-male mice （without CF-specific ATF3 overexpression group,n =5）.In addition,five mice of ATF3TGfl/flCol1a2-Cre＋ and ATF3TGfl/flCol 1 a2-Cre-were subjected to sham MI operation.Heart function was detected by ultrasound and left ventricular remodeling was observed by Masson staining （myocardial fibrosis area was detected by blue collagen deposition area） at the 28th day after MI surgery in ATF3TGfl/flColla2-Cre＋ and ATF3TGfl/flColla2-Cre-mice received sham or MI operation.Quantitative real-time polymerase chain reaction （qRT-PCR） was used to detect cell proliferation/cell cycle-related gene expression in cardiac tissue.BrdU staining was used to detect fibroblast proliferation.Results：After establishment of an MI model,we found that ATF3 proteins were increased in the heart of mice after MI surgery and dominantly expressed in CFs.Genetic overexpression of ATF3 in CFs （ATF3TGfl/flCol1a2-Cre＋ group） resulted in an improvement in the heart function as indicated by increased cardiac ejection fraction （41.0% vs.30.5%,t =8.610,P =0.001） and increased fractional shortening （26.8% vs.18.1%,t =7.173,P =0.002）,which was accompanied by a decrease in cardiac scar area （23.1% vs.11.0%,t =8.610,P =0.001）.qRT-PCR analysis of CFs isolated from ATF3TGfl/flCol1a2-Cre＋ and ATF3TGfl/flCol1a2-Cre-ischemic hearts revealed a distinct transcriptional profile in ATF3-overexpressing CFs,displaying pro-proliferation properties.BrdU-positive cells significantly increased in ATF3-overexpressing CFs than control CFs under angiotensin Ⅱ stimuli （11.5% vs.6.8%,t =31.599,P =0.001） or serum stimuli （31.6% vs.20.1%,t =31.599,P =0.001）.The 5（6）-carboxyfluorescein N-hydroxysuccinimidyl ester assay showed that the cell numbers of the P2 and P3 generations were higher in the ATF3-overexpressing CFs at 24 h （P2：91.6% vs.71.8%,t =8.465,P=0.015） and 48 h （P3：81.6% vs.51.1%,t =9.029,P =0.012） after semm stimulation.Notably,ATF3 overexpression-induced CF proliferation was clearly increased in the heart after MI injury.Conclusions：We identify that CF-specific ATF3 might contribute to be MI repair through upregulating the expression of cell cycle/proliferation-related genes and enhancing cell proliferation.