Objective: To investigate whether the cyclic adenosine monophosphate (cAMP) / exchange proteins directly activated by cAMP (Epac) / ras-related protein 1 ( Rap1 ) signalling pathway is involved in the intervening mechanisms of interleukin-1 β (IL-1 β) ，tumor necrosis factor-α (TNF-α) ，brain-derived neurotrophic factor (BDNF) and Jujuboside A(JuA) secretion by NG2 cells． Methods: NG2 cells were cultured in vitro and the experiment was divided into control group ，pertussis toxin ( PTX) group ，ESI-09 group，JuA group and positive drug group．The effect of different concentrations of JuA on the survival rate of NG2 cells was detected by CCK-8 method，and the expression of IL-1 β , TNF-α , BDNF，cAMP，Epac，Rap1 mRNA and protein in each group was detected by RT-PCR and Western blot. Results: Compared with the control group，the PTX group decreased the expression of IL-1 β and TNF-α mRNA and protein (P＜0. 01) and increased the expression of cAMP and BDNF mRNA and protein (P＜0. 01) ; the ESI-09 group increased the expression of IL-1 β and TNF-α mRNA and protein (P < 0. 05) and decreased the expression of BDNF，Epac and Rap1 mRNA and protein expression (P＜0. 01) ; the JuA group and positive drug group increased IL-1 β , TNF-α , BDNF，cAMP，Epac，Rap1 mRNA and protein expression (P＜0. 01) ． Conclusion The cAMP / Epac / Rap1 signaling pathway is involved in the secretion of IL-1 β , TNF- α , and BDNF by NG2 cells．JuA may act on cAMP / Epac / Rap1 signaling pathway to affect the secretion of BDNF by NG2 cells.

Laparoscopic inguinal hernia repair (LIHR) has been widely used in clinical practice and has become the main surgical method for inguinal hernia repair. Although hematoma after LIHR is less common than seroma, it may lead to more serious complications and should be paid enough attention. Currently, the prevention and treatment strategies for hematoma after LIHR are still lacking in sorting and summary. The authors elaborate on the prevention and treatment of hematoma after LIHR, aiming at providing references for clinical surgeons to ensure the life safety of patients and promote rapid recovery after surgery.

ObjectiveTo investigate the effect of Bufeitang on intestinal flora of rats with lung Qi-deficiency syndrome of chronic obstructive pulmonary disease（COPD）， and to explore the mechanism of traditional Chinese medicine in regulating intestinal flora and thus restoring the balance of lung-gut axis. MethodA total of 84 rats were randomly divided into 7 groups， including blank group， model group， fecal bacterial transplantation（FMT） group， dexamethasone group and low， medium and high dose groups of Bufeitang， 12 rats in each group. Except for the blank group， cigarette and sawdust fumigation combined with intratracheal instillation of lipopolysaccharide（LPS） were used to establish the COPD rat model with lung Qi-deficiency syndrome in all other groups. The low， medium and high dose groups of Bufeitang were intragastric administrated with Bufeitang（3.645， 7.29， 14.58 g·kg^-1）， the FMT group was given fecal bacteria liquid enema（10 mL·kg^-1）， dexamethasone group was given dexamethasone acetate tablet suspension by gavage（0.135 mg·kg^-1）， the blank group and model group were given equal amount of distilled water. Fresh feces were collected after 28 d of continuous intervention for 16S rRNA gene sequencing. Lung and colon tissues were stained with hematoxylin-eosin（HE） for pathomorphological observation， and enzyme-linked immunosorbent assay （ELISA） was performed to detect the contents of tumor necrosis factor-α（TNF-α） and interleukin-8（IL-8） in lung tissues. ResultCompared with the blank group， the model group showed severe abnormal lung tissue structure with alveolar atrophy and collapse accompanied by severe inflammatory cell infiltration. Compared with the model group， the extent of injury was significantly improved， and inflammatory cell infiltration was reduced with basically normal alveolar structure in the high dose group of Bufeitang. Compared with the blank group， the model group had severely abnormal colonic tissue structure， the epithelial cells in the mucosal layer were eroded and shed， the number of inflammatory cells increased， the submucosal layer was edematous and the gap was enlarged. Compared with the model group， the extent of damage was significantly improved in the medium and high dose groups of Bufeitang， the epithelial cells in the mucosal layer were neatly and closely arranged， with only a small amount of inflammatory cell infiltration and no significant degeneration. Compared with the blank group， the TNF-α and IL-8 levels of lung tissue in the model group were significantly increased（P<0.01）. Compared with the model group， the TNF-α and IL-8 levels of lung tissues in the low， medium and high dose groups of Bufeitang were significantly decreased（P<0.01）. Bufeitang significantly modulated the number of bacteria species as well as alpha and beta diversity of model rats， corrected the return of intestinal flora to normal abundance and diversity， and positively regulated 4 differential phyla（such as Firmicutes， Proteobacteria） and 13 differential genera（such as Turicibacter， Lactobacillus， Anaerobiospirillum， Intestinimonas） in COPD model rats with lung Qi-deficiency syndrome， and down-regulated 2 carbohydrate metabolic pathway functions， including the pentose phosphate pathway（non-oxidative branch） Ⅰ and the Calvin-Benson-Bassham cycle. ConclusionBufeitang can modulate the abundance and diversity of intestinal flora species， affect the function of metabolic pathways， repair the structure of lung and colon tissues， regulate the level of inflammatory factors， and thus improve COPD with lung Qi-deficiency syndrome. The mechanism may be related to its regulation of inflammation-related intestinal flora to restore the balance of lung-gut axis in COPD with lung Qi-deficiency syndrome.

Elevated blood pressure is one of the major contributors to cardiovascular disease and premature death. The exposure to ambient fine particulate matter (PM_2.5) is closely associated with changes in blood pressure, and even short-term exposure to PM_2.5 can lead to an increase in blood pressure. PM_2.5 is a complex mixture that exerts different toxicities and triggers increased blood pressure through various mechanisms. Therefore, in this article, we provided a comprehensive review of published studies on the effects of short-term exposure to PM_2.5 and its components on blood pressure, and elaborated potential mechanisms from four aspects, including oxidative stress and inflammatory response, endothelial dysfunction, autonomic nervous system disorders and hypothalamus-pituitary-adrenal axis activation, and epigenome alteration. Given the limitations of existing research, future prospective studies can be conducted on diverse populations, using more precise exposure measurement methods and multi-omics approaches, to further elucidate the mechanisms underlying the effects of PM_2.5 and its various components on blood pressure. The findings would provide a theoretical foundation for effective protection of public health, particularly vulnerable groups.

The use of two inhibitors of Mek1/2 and Gsk3β (2i) promotes the generation of mouse diploid and haploid embryonic stem cells (ESCs) from the inner cell mass of biparental and uniparental blastocysts, respectively. However, a system enabling long-term maintenance of imprints in ESCs has proven challenging. Here, we report that the use of a two-step a2i (alternative two inhibitors of Src and Gsk3β, TSa2i) derivation/culture protocol results in the establishment of androgenetic haploid ESCs (AG-haESCs) with stable DNA methylation at paternal DMRs (differentially DNA methylated regions) up to passage 60 that can efficiently support generating mice upon oocyte injection. We also show coexistence of H3K9me3 marks and ZFP57 bindings with intact DMR methylations. Furthermore, we demonstrate that TSa2i-treated AG-haESCs are a heterogeneous cell population regarding paternal DMR methylation. Strikingly, AG-haESCs with late passages display increased paternal-DMR methylations and improved developmental potential compared to early-passage cells, in part through the enhanced proliferation of H19-DMR hypermethylated cells. Together, we establish AG-haESCs that can long-term maintain paternal imprints.

Objective To investigate the clinical characteristics,early diagnosis,and rational treatments of traumatic renal artery thrombosis or other traumatic emboli.Methods We summarized the clinical data of 10 patients with traumatic renal artery thrombosis or other traumatic emboli.Results Six of ten patients had left renal artery thrombosis,while four of the ten patients had right renal artery thrombosis.Ultrasonography reported a reduced blood flow signal in one patient,and then renal artery embolism was confirmed by enhanced CT.The other nine patients were directly definitely diagnosed as renal artery embolism by enhanced CT.Four patients were treated with low molecular weight heparin calcium,in whom the CT follow-up showed no obvious blood reperfusion in injured kidneys,but the renal function was in normal range.Renal hypertension occurred in two patients,and one of them received nephrectomy because of poorly controlled hypertension with medication.Conclusions Clinical symptoms,signs and laboratory examinations show no specific findings for diagnosis of traumatic renal artery thrombosis.The color Doppler ultrasound is a preliminary screening method for,and an enhanced CT scan is an effective method for,diagnosis of renal artery thrombosis.The early recovery of renal blood circulation is an evidence of effective treatment.Major concerns are supposed to focus on renal function and blood pressure during followup.

Deep vein thrombosis (DVT) refers to a venous reflux disorder caused by abnormal condensation of blood in deep veins,It is detected in cardinal veins of the whole body and often occurred in the lower extremities.Desquamation of thrombus may cause pulmonary embolism (PE).PE and DVT are two clinical manifestations of different stages of the same disease,which are collectively referred to as venous thromboembolism (VTE).Five famous experts in hernia and abdominal wall surgery explored the prevention and treatment of DVT during perioperative period in patients undergoing abdominal wall hernia surgery from different angles based on clinical experiences.Professor Liu Ziwen introduced the epidemiology of DVT during perioperative period in patients undergoing abdominal wall hernia surgery,emphasized its risks,analyzed systematically its mechanisms including slow venous blood flow,vein injury,high blood coagulation state,underlying diseases and specific factors of abdominal wall hernia surgery,focused on mechanisms of inflammation caused by meshes inducing DVT.Professor Zhang Guangyong introduced informatively its diagnosis with clear and careful thinking,from the clinical manifestations to assistant examinations and moreover to Wells quantitative scoring,from general to specific and from qualitative to quantitative,striving to achieve early and precise diagnosis in order to prevent misseddiagnosis or ignoration of its danger level.Professor Li Hangyu emphasized appropriate preventive and treatment measures according to different stages and risk levels by evaluating the risk factors of preoperative,intraoperative and postoperative DVT.Professor Shen Yingmo analyzed special factors of laparoscopic abdominal wall hernia inducing DVT during the perioperative period,and indicated that surgeons should select surgical methods individually after comprehensive evaluation and consideration because of uncertainty of risk degree in laparoscopic and open surgery inducing DVT during perioperative period based on exis-ting evidence-based medicine and related guidelines.Professor Lu Chaoyang introduced three categories of main treatments including anticoagulation therapy,thrombolytic therapy and surgical therapy,and specific drugs,indications,advantages and disadvantages,opportunities,recommended clinicians to select individually and rationally.

Objective To identify Mobiluncus species with matrix-assisted laser desorption/ioniza-tion time-of-flight mass spectrometry (MALDI-TOF MS) and 16S rRNA gene sequencing and to analyze anti-biotic resistance genes and phylogenetic relationships among Mobiluncus species with whole genome sequen-cing. Methods Twenty-five Mobiluncus strains were isolated after anaerobic culture of 65 vaginal secretion samples of patients with bacterial vaginosis (BV) and identified to species level by MALDI-TOF MS and 16S rRNA gene sequencing. The whole genome DNA of each strain was extracted for next-generation sequencing. SPAdes was used to assembly genomes. Resistance genes were searched in ARGD database. The core ge-nome of all isolates was analyzed by Harvest to construct phylogenetic tree. Results MALDI-TOF MS could only identify Mobiluncus curtisii, while 16S rRNA gene sequencing could identify both Mobiluncus mulieris and Mobiluncus curtisii. Results of the whole genome sequencing showed that tetracycline resistance gene tet ( o) and macrolides resistance gene erm(x) were the two predominant acquired resistance genes of Mobilun-cus with a positive rate of 84. 7% and 61. 5% respectively. Intra-species relationships of the two Mobiluncus species were close, but a distant phylogenetic relationship was found between the two species. Conclusion This study shows that MALDI-TOF MS can't be used to identify Mobiluncus mulieris at present. Mobiluncus strains have potential resistance to tetracycline and macrolides. Intra-species evolution of Mobiluncus is slow, which indicates that there is no growing trend towards new species for the time being.

OBJECTIVETo study the reasons for the discrepancies in pathologic diagnosis of gastric dysplasia/early cancer in endoscopic submucosal dissection (ESD) specimens, and how to cope with the discrepancies.

METHODSThe pathologic diagnoses in 60 cases of ESD specimens according to the three currently used classification systems (namely Western criteria, Japanese criteria and Vienna classification) were compared. The diagnostic discrepancies were analyzed.

RESULTSFifteen of the 17 cases diagnosed as low-grade intraepithelial neoplasia according to the Western criteria were revised as adenoma by the Japanese criteria. Amongst the 43 cases of gastric intramucosal adenocarcinoma diagnosed according to the Japanese criteria, 23 cases had concordant diagnosis by the Western criteria. While the diagnosis of low-grade intraepithelial neoplasia/adenoma was basically similar irrespective of classification system used, there were significant differences in the interpretation of gastric early cancer.

CONCLUSIONSThe diagnostic discrepancies in the gastric dysplasia/early cancer are mainly related to the morphologic criteria applied in different classifications. In order to facilitate clinical and pathologic communication, a consensus using Vienna/WHO classifications, supplemented with Japanese system, is desirable.

Adenoma ; pathology ; Carcinoma in Situ ; pathology ; Dissection ; methods ; Gastroscopy ; Humans ; Hyperplasia ; pathology ; Stomach ; pathology ; Stomach Neoplasms ; pathology

OBJECTIVETo investigate the protective effect of Apelin-13 on focal cerebral ischemia-reperfusion injury in rats.

METHODSFocal transient cerebral ischemia-reperfusion injury was induced in male SD rats using modified suture occlusion technique. The rats were randomly divided into 5 groups: Sham group, Model group, Apelin-low dose (A) group, Apelin-middle dose (B) group and Apelin-high dose (C) group. Apelin-13 was injected into lateral cerebral ventricle, and the neurological function score, brain edema, infarct volume, apoptosis, malondialdehyde (MDA), superoxide dismutase (SOD) and extracellular regulated kinase1/2 (ERK1/2) protein were measured.

RESULTSNeurological function scores, percentage of brain water content, infarct volumes and TUNEL-positive cells in B and C groups were lower than those in Model group (P<0.05). The level of MDA in the tissue bomogenate of brain tissue in the surrounding area of ischemia of B and C groups was lower than that of Model group, while the activity of SOD was higher (P<0.05). There was no significant difference in ERK1/2 protein expression among the groups (P>0.05). P-ERK1/2 increased in Model group and A, B, and C groups compared with Sham group (P<0.05), and that of A, B, and C group was higher than that of Model group (P<0.05).

CONCLUSIONApelin-13 may play an important role by inhibiting oxidative stress to protect against focal cerebral ischemia-reperfusion injury; ERK1/2 signaling pathway may be involved in the protective mechanism of Apelin-13.

Animals ; Apoptosis ; Brain Edema ; Brain Ischemia ; drug therapy ; Intercellular Signaling Peptides and Proteins ; pharmacology ; Male ; Malondialdehyde ; metabolism ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; drug therapy ; Signal Transduction ; Superoxide Dismutase ; metabolism