Objective To study the effect of the compatibility on treating Ⅱ toⅢphase pressure sore of senior citizen by auricularia in-depth fermentation extracts and the dimethyl acrylyl hydropathic compress.Methods A total of 60 patients with Ⅱto Ⅲ phase pressure sore were divided randomly into the expedmental group and the control group with 30 cases in each group.The experimental group(30 cases.50 pressure sores)were treated with the auricularia in--depth fermentation extracts and the dimethyl acrylyl hydropathic compress.The control group(30 case8,46 pressure sores)were treated with conventional methods of dressing change,0.5% iodine to disinfect the wound surface.then bounded it up with the aseptic vaseline yarn and the sursical dressing.The curative effect Was compared by observing the effect indicators.Results The response rate of the experimental group was 100.0%.with an average healing time of 10.33 d.For the control group.the response rate was 78.3%,the average healing time Was 24.27 d.There Was significant difference on efficiency and the average healing time between the two groups,P<0.01.Conclusions Auricularia in-depth fermentation extracts and the dimethyl acrylyl hydropathic compress to treat the senior citizen Ⅱ toⅢphase pressure gore with a view to easy.safe and economical characteris tic.has a significant effect on the new agricultural co-medical health care and community groups.

Objective To investigate the influence of Let-7f regulation on MMP-11 in migration and in-vasion of pancreatic cancer. Methods RT-qPCR was performed to assay the expression of Let7 and MMP-11 ex-pression in pancreatic cancer cells and normal pancreatic cells. Let-7f mimic and inhibitor were transfected to PANC-1 and Bx-PC3, respectively. The influence of Let-7f expression on migration and invasion of pancreatic cancer cells was analyzed by transwell. The influence of Let-7f intervention on MMP-11 expression was observed by RT-qPCR. Results Let-7f expression decreased in PANC-1 and Bx-PC3, compared to HPDE6c7, while MMP-11 expression up-regulated in PANC-1 and Bx-PC3 , compared to HPDE6c7 cells. Let-7f overexpression in-hibited the expression of MMP-11. Up-regulated Let-7f could significantly inhibit migration and invasion of PANC-1 and Bx-PC3 and Let-7f inhibitor enhanced MMP-11 expression. However , down-expression of Let-7f could not significantly promote migration and invasion abilities of PANC-1 and Bx-PC3cells. Conclusions Let-7f may affect migration and invasion by regulating MMP-11 expression in pancreatic cancer , suggesting that Let-7f might be a potential target for gene therapy in human pancreatic cancer.

Objective To evaluate the effect of comprehensive schistosomiasis control measures based on infection source control in plateau mountain areas of Yunnan Province. Methods From 2006 to 2004,four administrative villages were selected as test areas from plateau canyon and plateau basin endemic areas in Jindun Town,Heqing County,two villages each type,and the comprehensive control measures were implemented,including the examination and treatment of schistosomiasis,Oncomela?nia hupensis snail survey and control,health education,improving drinking water and lavatories,banning grazing,constructing sanitary pen of livestock,replacing cattle with machine,etc. The schistosome infection state and snail status in 2006 were treat?ed as the baseline information,and the effect of the comprehensive measures were evaluated. Results The infection rate of hu?man in plateau canyon areas decreased from 4.94%in 2006 to 0.06%in 2014,and that of livestock decreased from 1.11%to 0. In plateau basin areas,there was only 1 case of schistosomiasis found in Xiaolian Village in 2007,and no any other cases found in the other years,the infection rates of livestock dropped from 7.38%to 0. Compared with 2006,the snail areas in the two type areas decreased by 74.89%and 75.30%,respectively,meanwhile,the percentage of snail area,the occurrence rate of frames with snails,as well as the average density of living snails also decreased,and no infected snails were found since 2008. Xidian and Xinzhuang villages in plateau canyon area reached the criteria of schistosomiasis transmission controlled in 2009,and Xiao?lian and Kangfu villages in plateau basin reached the criteria of transmission interrupted in 2014. Conclusions The comprehen?sive schistosomiasis control measures based on infection source control can effectively control the endemic situation of schistoso? miasis in plateau areas of Yunnan Province. In the future,we should pay an equal attention to the infection sources control and snail control to consolidate and amplify the achievement of schistosomiasis control.

Objective:To explore the effect of kangaroo mother care (KMC) on lactation, uterine involution of parturients and neonatal pain.Methods:A total of 200 parturients who gave birth at full term in our hospital from January 2019 to June 2019 and their newborns were selected as the research objects, they were randomly divided into control group and observation group of 100 pairs each. The control group received routine obstetric postpartum care and the observation group received KMC. The KMC cognition, postpartum lactation and uterine involution, neonatal pain during neonatal heel blood collection were compared between the two groups.Results:The cognition of KMC in the observation group was significantly better than that in the control group, and the difference was statistically significant ( χ 2 value was 24.700, P<0.01). The first lactation time of parturients in the observation group was (41.25±3.20) hours after birth, which was earlier than (54.17±2.20) hours in the control group, there was significant difference between the two groups ( t value was 2.378, P value was 0.019). The breast pain Ⅰ degree (20 cases), Ⅱ degree (56 cases), Ⅲ degree (24 cases) in observation group were significantly lighter than those in control group (62, 27, 11 cases respectively) 72h after delivery, the differences were statistically significant ( t value was 12.166, P value was 0.011). The parturients of sufficient lactation in the observation group (73 cases) were more than those in the control group (34 case),the differences was statistically significant ( χ 2 value was 30.570, P value was 0.000). The uterine fundus of the observation group decreased by (3.06±1.26) cm and (1.67 ±0.43) cm at 24h and 48h postnatally, which were better than those of the control group (1.97±0.92) cm and (1.23±0.18) cm,the differences were statistically significant ( t value was 3.162, P value was 0.002; t value was 2.689, P value was 0.009). In the process of heel blood collection after 72h of delivery in both groups, the pain scores of the observation group during and after blood collection were 4.92±0.33 and 2.37±1.27 respectively, which were lower than those of the control group (5.57±1.37 and 5.01±1.09), and the differences were statistically significant ( t value was 2.035, P value was 0.046; t value was 2.579, P value was 0.011). The heart rates of the observation group during and after blood collection were (121.36±22.13) and (142.55±23.91) beats/min, respectively, which were lower than (152.64±18.21) and (156.79±17.37) beats/min of the control group, the difference were statistically significant ( t value was 2.375, P value was 0.018; t value was 2.126, P value was 0.037). The blood oxygen saturation of the observation group during and after blood collection were 0.967 2±0.013 7 and 0.985 5 ±0.022 4 respectively, which were significantly higher than 0.891 7±0.116 5 and 0.914 5±0.137 8 of the control group ( t value was 2.036, P value was 0.046; t value was 2.017, P value was 0.047). Conclusions:The implementation of KMC can promote lactation, accelerate uterine involution, and relieve the pain of neonats during neonatal heel blood collection; Strengthening the health education of KMC can improve the cognition of parturients and their families about KMC, which has positive significance in promoting maternal and infant health and is worthy of clinical application.

Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment landscape for chronic myeloid leukemia (CML). However, TKI resistance poses a significant challenge, leading to treatment failure and disease progression. Resistance mechanisms include both BCR::ABL1-dependent and BCR::ABL1-independent pathways. The mechanisms underlying BCR::ABL1 independence remain incompletely understood, with CML cells potentially activating alternative signaling pathways, including the AKT/mTOR and JAK2/STAT5 pathways, to compensate for the loss of BCR::ABL1 kinase activity. This study explored tumoral VISTA (encoded by VSIR) as a contributing factor to TKI resistance in CML patients and identified elevated tumoral VISTA levels as a marker of resistance and poor survival. Through in vitro and in vivo analyses, we demonstrated that VSIR knockdown and the application of NSC-622608, a novel VISTA inhibitor, significantly impeded CML cell proliferation and induced apoptosis by attenuating the AKT/ mTOR and JAK2/STAT5 pathways, which are crucial for CML cell survival independent of BCR::ABL1 kinase activity. Moreover, VSIR overexpression promoted TKI resistance in CML cells. Importantly, the synergistic effect of NSC-622608 with TKIs offers a potent therapeutic avenue against both imatinib-sensitive and imatinib-resistant CML cells, including those harboring the challenging T315I mutation. Our findings highlight the role of tumoral VISTA in mediating TKI resistance in CML, suggesting that inhibition of VISTA, particularly in combination with TKIs, is an innovative approach to enhancing treatment outcomes in CML patients, irrespective of BCR::ABL1 mutation status. This study not only identified a new pathway contributing to TKI resistance but also revealed the possibility of targeting tumoral VISTA as a means of overcoming this significant clinical challenge.

Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment landscape for chronic myeloid leukemia (CML). However, TKI resistance poses a significant challenge, leading to treatment failure and disease progression. Resistance mechanisms include both BCR::ABL1-dependent and BCR::ABL1-independent pathways. The mechanisms underlying BCR::ABL1 independence remain incompletely understood, with CML cells potentially activating alternative signaling pathways, including the AKT/mTOR and JAK2/STAT5 pathways, to compensate for the loss of BCR::ABL1 kinase activity. This study explored tumoral VISTA (encoded by VSIR) as a contributing factor to TKI resistance in CML patients and identified elevated tumoral VISTA levels as a marker of resistance and poor survival. Through in vitro and in vivo analyses, we demonstrated that VSIR knockdown and the application of NSC-622608, a novel VISTA inhibitor, significantly impeded CML cell proliferation and induced apoptosis by attenuating the AKT/ mTOR and JAK2/STAT5 pathways, which are crucial for CML cell survival independent of BCR::ABL1 kinase activity. Moreover, VSIR overexpression promoted TKI resistance in CML cells. Importantly, the synergistic effect of NSC-622608 with TKIs offers a potent therapeutic avenue against both imatinib-sensitive and imatinib-resistant CML cells, including those harboring the challenging T315I mutation. Our findings highlight the role of tumoral VISTA in mediating TKI resistance in CML, suggesting that inhibition of VISTA, particularly in combination with TKIs, is an innovative approach to enhancing treatment outcomes in CML patients, irrespective of BCR::ABL1 mutation status. This study not only identified a new pathway contributing to TKI resistance but also revealed the possibility of targeting tumoral VISTA as a means of overcoming this significant clinical challenge.

Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment landscape for chronic myeloid leukemia (CML). However, TKI resistance poses a significant challenge, leading to treatment failure and disease progression. Resistance mechanisms include both BCR::ABL1-dependent and BCR::ABL1-independent pathways. The mechanisms underlying BCR::ABL1 independence remain incompletely understood, with CML cells potentially activating alternative signaling pathways, including the AKT/mTOR and JAK2/STAT5 pathways, to compensate for the loss of BCR::ABL1 kinase activity. This study explored tumoral VISTA (encoded by VSIR) as a contributing factor to TKI resistance in CML patients and identified elevated tumoral VISTA levels as a marker of resistance and poor survival. Through in vitro and in vivo analyses, we demonstrated that VSIR knockdown and the application of NSC-622608, a novel VISTA inhibitor, significantly impeded CML cell proliferation and induced apoptosis by attenuating the AKT/ mTOR and JAK2/STAT5 pathways, which are crucial for CML cell survival independent of BCR::ABL1 kinase activity. Moreover, VSIR overexpression promoted TKI resistance in CML cells. Importantly, the synergistic effect of NSC-622608 with TKIs offers a potent therapeutic avenue against both imatinib-sensitive and imatinib-resistant CML cells, including those harboring the challenging T315I mutation. Our findings highlight the role of tumoral VISTA in mediating TKI resistance in CML, suggesting that inhibition of VISTA, particularly in combination with TKIs, is an innovative approach to enhancing treatment outcomes in CML patients, irrespective of BCR::ABL1 mutation status. This study not only identified a new pathway contributing to TKI resistance but also revealed the possibility of targeting tumoral VISTA as a means of overcoming this significant clinical challenge.

Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment landscape for chronic myeloid leukemia (CML). However, TKI resistance poses a significant challenge, leading to treatment failure and disease progression. Resistance mechanisms include both BCR::ABL1-dependent and BCR::ABL1-independent pathways. The mechanisms underlying BCR::ABL1 independence remain incompletely understood, with CML cells potentially activating alternative signaling pathways, including the AKT/mTOR and JAK2/STAT5 pathways, to compensate for the loss of BCR::ABL1 kinase activity. This study explored tumoral VISTA (encoded by VSIR) as a contributing factor to TKI resistance in CML patients and identified elevated tumoral VISTA levels as a marker of resistance and poor survival. Through in vitro and in vivo analyses, we demonstrated that VSIR knockdown and the application of NSC-622608, a novel VISTA inhibitor, significantly impeded CML cell proliferation and induced apoptosis by attenuating the AKT/ mTOR and JAK2/STAT5 pathways, which are crucial for CML cell survival independent of BCR::ABL1 kinase activity. Moreover, VSIR overexpression promoted TKI resistance in CML cells. Importantly, the synergistic effect of NSC-622608 with TKIs offers a potent therapeutic avenue against both imatinib-sensitive and imatinib-resistant CML cells, including those harboring the challenging T315I mutation. Our findings highlight the role of tumoral VISTA in mediating TKI resistance in CML, suggesting that inhibition of VISTA, particularly in combination with TKIs, is an innovative approach to enhancing treatment outcomes in CML patients, irrespective of BCR::ABL1 mutation status. This study not only identified a new pathway contributing to TKI resistance but also revealed the possibility of targeting tumoral VISTA as a means of overcoming this significant clinical challenge.

Objective　To determine the prevalence of human herpesvirus 8 (HHV-8) DNA in acute leukemia (AL) patients. Methods　The presence of HHV-8 DNA sequences in peripheral blood mononuclear cells (PBMC) and bone marrow mononuclear cells (BMMC) from 50 AL patients was examined using polymerase chain reaction (PCR). Nine human hematopoietic cell lines and PBMC from 30 normal donors were also included. Results　HHV-8 DNA sequences were detected in one case of acute myelogenous leukemia (AML). The specimens from the bone marrow aspirate, peripheral blood and serum of this patient were all positive. None of the normal donors and human hematopoietic cell lines showed evidence of HHV-8 DNA. Conclusion　The results suggest that the prevalence of HHV-8 is low in AL in China.