Patients with severe trauma require an extremely timely treatment and transfusion plays an irreplaceable role in the emergency treatment of such patients. An increasing number of evidence-based medicinal evidences and clinical practices suggest that patients with severe traumatic bleeding benefit from early transfusion of low-titer group O whole blood or hemostatic resuscitation with red blood cells, plasma and platelet of a balanced ratio. However, the current domestic mode of blood supply cannot fully meet the requirements of timely and effective blood transfusion for emergency treatment of patients with severe trauma in clinical practice. In order to solve the key problems in blood supply and blood transfusion strategies for emergency treatment of severe trauma, Branch of Clinical Transfusion Medicine of Chinese Medical Association, Group for Trauma Emergency Care and Multiple Injuries of Trauma Branch of Chinese Medical Association, Young Scholar Group of Disaster Medicine Branch of Chinese Medical Association organized domestic experts of blood transfusion medicine and trauma treatment to jointly formulate Chinese expert consensus on blood support mode and blood transfusion strategies for emergency treatment of severe trauma patients ( version 2024). Based on the evidence-based medical evidence and Delphi method of expert consultation and voting, 10 recommendations were put forward from two aspects of blood support mode and transfusion strategies, aiming to provide a reference for transfusion resuscitation in the emergency treatment of severe trauma and further improve the success rate of treatment of patients with severe trauma.

Objective:To analyze and summarize adverse reactions such as hypoglycemia, lactic acidosis and pancytopenia caused by Linezolid in elderly patients, in order to enhance clinicians' awareness of adverse reactions of Linezolid.Methods:One case with Linezolid-induced lactic acidosis, pancytopenia and hypoglycemia was reported in a patient receiving long-term and repeated use of Linezolid for recurrent urinary tract infections(RUTI)in Beijing Hospital.National and international literature on the three severe and rare adverse reactions caused by Linezolid before December 2018 was reviewed, and the risk factors, clinical characteristics and prognosis of the three severe adverse reactions caused by Linezolid were summarized and analyzed.Results:A total of 86 cases with Linezolid-induced adverse reactions such as hypoglycemia, lactic acidosis and pancytopenia were analyzed.Among them, the ratio of males to females was 1.8∶1.0, the median age was 64.5 years, and 44 cases were over 65 years, accounting for 51.2%.Among the 57 patients with lactic acidosis, 25 lactic acidosis cases were combined with liver and kidney diseases, which were the most commonly involved organs(43.9%, 25/57). The time of onset for lactic acidosis was 4 h-109 d, with a median value of 32 d, and the peak values of blood lactate were 2.6-38.1 mmol/L, with a median value of 13.3 mol/L.Pancytopenia occurred 4 h-120 days after the treatment, and the median value was 21 days.The time of onset for hypoglycemia was 8 h-26, and the median time was 10.3 days.The lowest value of blood glucose was 0.2 mmol/L.Of the 86 cases, 61(70.9%)patients improved, and 12 cases of 51 patients with lactic acidosis died, with a mortality rate of 23.5%.Conclusions:Clinicians should be aware of serious adverse reactions including hypoglycemia, lactic acidosis and pancytopenia during Linezolid treatment in elderly patients.It is recommended to monitor changes in blood glucose, blood lactate and blood cell count during Linezolid treatment, and to avoid long-term use of Linezolid, so as to maximize the benefits for patients.

Objective To investigate the expression and prognostic significance of DEAH-box helicase (DHX16) by pan-cancer analysis. Methods The expression and prognostic significance of DHX16 were analyzed using the UALCAN web-portal. Gene ontology and kyoto encyclopedia of genes and genomes analyses of proteins interacting with DHX16 were performed using DAVID 6.8 functional annotation software. Results DHX16 was highly expressed in bladder urothelial carcinoma, head and neck squamous cell carcinoma, esophageal carcinoma, liver hepatocellular carcinoma, and cholangiocarcinoma (all P ＜ 0.001). Proteins interacting with DHX16 were located mainly in catalytic step 2 spliceosome, nucleoplasm, and cell membrane, and participated in mRNA splicing and processing, binding to poly (A) RNA and nucleic acids, and RNA helicase activity. Spliceosome, mRNA surveillance, RNA degradation, and transport pathways were implicated. Conclusion The high expression of DHX16 is helpful for the prognosis of bladder urothelial carcinoma prognosis, and unfavorable for prognoses of adrenocortical carcinoma, sarcoma, brain lower grade glioma, liver hepatocellular carcinoma, and acute myeloid leukemia. Thus, DHX16 may have value as a prognostic marker.

Acute ischemic stroke (AIS), as the third leading cause of death worldwide, is characterized by its high incidence, mortality rate, high incurred disability rate, and frequent reoccurrence. The neuroprotective effects of Ginkgo biloba extract (GBE) against several cerebral diseases have been reported in previous studies, but the underlying mechanisms of action are still unclear. Using a novel in vitro rat cortical capillary endothelial cell-astrocyte-neuron network model, we investigated the neuroprotective effects of GBE and one of its important constituents, Ginkgolide B (GB), against oxygen-glucose deprivation/reoxygenation and glucose (OGD/R) injury. In this model, rat cortical capillary endothelial cells, astrocytes, and neurons were cocultured so that they could be synchronously observed in the same system. Pretreatment with GBE or GB increased the neuron cell viability, ameliorated cell injury, and inhibited the cell apoptotic rate through Bax and Bcl-2 expression regulation after OGD/R injury. Furthermore, GBE or GB pretreatment enhanced the transendothelial electrical resistance of capillary endothelial monolayers, reduced the endothelial permeability coefficients for sodium fluorescein (Na-F), and increased the expression levels of tight junction proteins, namely, ZO-1 and occludin, in endothelial cells. Results demonstrated the preventive effects of GBE on neuronal cell death and enhancement of the function of brain capillary endothelial monolayers after OGD/R injury in vitro; thus, GBE could be used as an effective neuroprotective agent for AIS/reperfusion, with GB as one of its significant constituents.
Animals ; Apoptosis ; drug effects ; Brain Ischemia ; drug therapy ; Cell Survival ; Cells, Cultured ; Disease Models, Animal ; Endothelial Cells ; drug effects ; Ginkgolides ; pharmacology ; Glucose ; Lactones ; pharmacology ; Neurons ; drug effects ; Neuroprotective Agents ; pharmacology ; Oxygen ; Plant Extracts ; pharmacology ; Rats ; Stroke ; drug therapy

The sodium hydrogen exchanger 1 (NHE1), which functions in maintaining the ratio of Na+ and H+ ions, is widely distributed in cell plasma membranes. It plays a prominent role in pH balancing, cell proliferation, differentiation, adhesion, and migration. However, its exact subcellular location and biological functions in Toxoplasma gondii are largely unclear. In this study, we cloned the C-terminal sequence of T. gondii NHE1 (TgNHE1) incorporating the C-terminal peptide of NHE1 (C-NHE1) into the pGEX4T-1 expression plasmid. The peptide sequence was predicted to have good antigenicity based on the information obtained from an immune epitope database. After induction of heterologous gene expression with isopropyl-b-D-thiogalactoside, the recombinant C-NHE1 protein successfully expressed in a soluble form was purified by glutathione sepharose beads as an immunogen for production of a rabbit polyclonal antiserum. The specificity of this antiserum was confirmed by western blotting and immunofluorescence. The antiserum could reduce T. gondii invasion into host cells, indicated by the decreased TgNHE1 expression in T. gondii parasites that were pre-incubated with antiserum in the process of cell entry. Furthermore, the antiserum reduced the virulence of T. gondii parasites to host cells in vitro, possibly by blocking the release of Ca2+. In this regard, this antiserum has potential to be a valuable tool for further studies of TgNHE1.
Animals ; Cell Line ; Immune Sera/genetics/immunology/*metabolism ; Male ; Mice ; Protozoan Proteins/genetics/*metabolism ; Rabbits ; Recombinant Proteins/immunology ; Sheep ; Sodium-Hydrogen Antiporter/genetics/immunology/*metabolism ; Toxoplasma/genetics/immunology/*metabolism ; Toxoplasmosis/parasitology/prevention & control

Objective To investigate the effects of four interior-warming drugs( galangal,cinnamon,evodia rutaecarpa,and dried ginger)on the tension of ileum smooth muscle and Ca2+-ATPase on the cell membrane in rabbits. Methods The effects of galangal,cinnamon,evodia rutaecarpa,and dried ginger were examined on normal ileum smooth muscle,in vitro intestinal muscle contraction caused by acetylcholine(ACh),barium chloride(BaCl2 )and histamine(His), and ACh-induced calcium release by using BL-420E+ biological signal collection and processing system.The average tension was measured within 1 min before delivery and within 3 minutes after the treatment,and the inhibition rate was calculated according to the average tension value.The effects of sera containing galangal,cinnamon,evodia rutaecarpa,and dried ginger on Ca2+-ATPase activity on the cell membrane of the intestinal smooth muscle were examined by phosphorus method. Results Galangal,cinnamon,evodia rutaecarpa,and dried ginger at high concentrations could restrain in vitro intestinal contraction in normal circumstances(P<0.05 or P<0.01).Significant inhibitory effects on intestinal contraction caused by ACh,His and BaCl2 were found in low,medium and high concentration groups(P<0.01).There was a dose-effectiveness relationship between the inhibition rate and final drug concentrations.The ACh-induced intracellular and extracellular calcium dependent contraction were significantly inhibited by the four interior-warming drugs( P < 0. 05 or P < 0. 01). The Ca2+-ATPase activities were( 0. 384 ± 0.070),(0.302±0.016),(0.307±0.016),(0.296±0.016),(0.313±0.003)U·mg-1 ,respectively,in intestinal smooth muscle in normal control group and high concentration groups of galangal,cinnamon,evodia rutaecarpa,and dried ginger(P<0.01). Conclusion Interior-warming drugs may relax intestinal smooth muscle by reducing the intracellular calcium release and the extracellular calcium inflow via receptor-controlled calcium channels,and inhibiting the Ca2+-ATPase activity in smooth muscle.

Adult ; Aged ; Carcinoma, Hepatocellular ; epidemiology ; Female ; Hepatitis B, Chronic ; drug therapy ; Humans ; Liver Neoplasms ; epidemiology ; Male ; Middle Aged ; Nucleosides ; administration & dosage ; therapeutic use

Objective Motility is an important physiological characteristic of a mature sperm.Nerve growth factor(NGF) is a protein essential for the development,maintenance and survival of the peripheral and central nervous systems.NGF and its receptors TrkA and p75 are widely expressed in the testis,accessory reproductive organ,and the epididymal sperms.In the present study,we investigated the role of NGF on human sperm motility.Methods Use 0.1,1 and 10 μmol/L concentrations of NGF,on sperm motility study to investigate the optimal concentration.Use CASA to detect Sperm motility changes every 10 minutes in an hour after 10 μmol/L NGF was added to the semen.Results The parameters of sperm motility increased after NGF incubation had significant difference, in particular,VAP,VSL,VCL,BCF and LIN mean were significantly increased more than 32%.MAD,STR,ALH and WOB mean had no notable difference.Furthermore,NGF promotes the sperm motility in a time- and dose- dependent manner.In addition,the enhancement of NGF on sperm motility was more stronger than those of sperm culture medium.Conclusion Our findings suggest that NGF plays a promoted role in human sperm motility.

BACKGROUND AND OBJECTIVEThe expression of TSLC1 is downregulated or abrogated in many kinds of tumors, and its downregulation is highly associated with DNA hypermethlyation. The aim of this study is to explore the relationship between TSLC1 silencing and DNA methylation of its promoter region in lung cancer cells.

METHODSWe detected the expression pattern of TSLC1 in human normal lung tissue and three lung cancer cell lines (A549, NCI-H446 and Calu-3) by semi-quantitative RT-PCR and Real-time PCR. Then we detected the status of DNA methylation in TSLC1 promoter region with bisulfite sequencing in above normal lung tissue and lung cancer cell lines. After treatment of above cell lines with the inhibitor of DNA methyltransferase 5-Aza-2-deoxycytidine (5-Aza-dC), we detected the expression change of TSLC1 by Real-time PCR before and after the treatment of 5-Aza-dC.

RESULTSThere was no methylation in TSLC1 promoter region in normal lung tissue and A549 cell line in which TSLC1 expressed; while there was DNA hypermethylation in TSLC1 promoter region in NCI-H446 and Calu-3 cell lines in which TSLC1 was abrogated, also the expression of TSLC1 in NCI-H446 and Calu-3 cell lines could be restored after treatment of 5-Aza-dC.

CONCLUSIONThe silencing of TSLC1 in lung cancer cells is due to the hypermethylation of its promoter region.

Azacitidine ; analogs & derivatives ; pharmacology ; Cell Adhesion Molecule-1 ; Cell Adhesion Molecules ; antagonists & inhibitors ; genetics ; Cell Line, Tumor ; DNA Methylation ; Gene Silencing ; Humans ; Immunoglobulins ; genetics ; Lung Neoplasms ; genetics ; pathology ; Promoter Regions, Genetic ; Tumor Suppressor Proteins ; antagonists & inhibitors ; genetics

Objective To clone and to identify the core promoter of human TSLCI used for exploring of transcrip-tion regulatory mechanism.Methods A series of different fragments located in the upstream of translation start site of TSLC1 were amplified from human genomic DNA by PCR,and then constructed into pGL3-Basic luciferase re-porter vector.The activity of different fragments in A549 and NCI-H446 cells was examined by a dual-luciferase as-say after transient transfection,and then the core promoter of TSLC1 was identified.Results Among the different constructs,the fragment of -68 ～ -329 bp located in the upstream of ATG showed the strong activity both in A549 cells and NCI-H446 cells,which played an important role in the transcription of TSLC1.Conclusion The fragment of -68 ～ -329 bp located in the upstream of translation start site of TSLC1 might be the core promoter region.