Neonatal necrotizing enterocolitis is a common gastrointestinal disease in neonate.Recently,with the establishment of the NICU and the all-round development of perinatal medicine and pediatrics,survival rate of premature especially very low birth weight neonates have obviously increased and the incidence of the disease is rising year by year.It is generally considered that multiple risk factors such as premature birth,low birth weight,infections,asphyxia,irrational use of drugs and so on,acting on the immature intestine,but the pathogenesis is still unknown.Therefore,it is significant to clearify the pathogenesis of the risk factors of NEC for studying the pathogenesis of the disease and providing prevention and control strategy.

Objective To determine the influencing factors on prognosis of neonatal necrotizing enterocolitis (NEC) in premature infants with a gestational age of 28-32 weeks.Methods Forty-six cases of NEC (Bell stage Ⅱ or Ⅲ) with a gestational age of 28-32 weeks admitted to Bayi Children's Hospital from January,2009 to January,2013 were analyzed retrospectively.Twenty-nine cases were assigned to the cured group and 17 cases were assigned to the poor prognosis group according to prognosis.General conditions,laboratory results,treatment and complications in the two groups were analyzed.The Chi-square test,Fisher's exact test and univariate analysis of variance were used for statistical analysis.Results There were no statistically significant differences regarding gender,average birth weight and mean age of onset between the two groups [average birth weight (1 410.52±281.59) g vs (1 266.47±280.32) g and mean age of onset:(20.79± 10.61) d vs (16.71 ±9.41) d for the cured group versus the poor prognosis group,respectively].There were no difference in changes in white blood cells and platelets between the two groups.There were six cases of positive blood culture in the poor prognosis group and none in the cured group.There were no differences in procedures such as blood transfusion and ibuprofen administration [41.4％ (12/29) vs 11/17 and 6.9％ (2/29) vs 5/17,both P＞0.05,in the cured group versus the poor prognosis group,respectively].There were significant differences in the use of Bifidobacterium between the two groups [69.0％ (20/29) vs 5/17,x2=6.758,P=0.009].Fourteen cases in the cured group and 10 cases in the poor prognosis group underwent surgery,and all 10 cases in the poor prognosis group died.Seven cases underwent repeated surgery,one infant in the cured group and six infants in the poor prognosis group and a significant difference was observed (Fisher's exact,P=0.007).A statistically significant difference in granulocyte colony-stimulating factor (G-CSF) treatment was observed between the two groups,where 15 cases in the cured group and three cases in the poor prognosis group were treated with G-CSF (x2=5.225,P＜0.05).Statistically significant differences in septicemia,patent ductus arteriosus,gastrointestinal perforation,multiple organ failure (MOF),disseminated intravascular coagulopathy (DIC) and septic shock were observed between the two groups [septicemia:44.8％ (13/29) vs 15/17,x2=8.478; patent ductus arteriosus:17.2％ (5/29) vs 9/17,x2=6.451; gastrointestinal perforation:3.4％ (1/29) vs 6/17; MOF:0.0％ (0/29) vs 5/17; DIC:0.0％ (0/29) vs 3/17; septic shock:3.4％ (1/29) vs 6/17,all P＜0.05 in the cured group versus the poor prognosis group,respectively).Conclusions Oral intestinal microbial preparations before the onset of NEC and G-CSF therapy after the onset of NEC may be protective factors in improving the prognosis of NEC,while patent ductus arteriosus,septicemia,gastrointestinal perforation,MOF,DIC and septic shock are risk factors.Emphasis should be placed on the administration of intestinal microbial agents,prevention of infection and treatment of complications.

This study is to investigate the binding capability of lidamycin apoprotein (LDP), an enediyne-associated apoprotein of the chromoprotein antitumor antibiotic family, to human breast cancer and normal tissues, the correlation of LDP binding capability to human breast cancer tissues and the expression of tumor therapeutic targets such as VEGF and HER2. In this study, the binding capability of LDP to human breast cancer tissues was detected with tissue microarray. The correlation study of LDP binding capability to human breast tumor tissues and relevant therapeutic targets was performed on breast cancer tissue microarrays. Immunocytochemical examination was used to detect the binding capability of LDP to human breast carcinoma MCF-7 cells. As a result, tissue microarray showed that LDP staining of 73.2% (30/41) of breast cancer tissues was positive, whereas that of 48.3% (15/31) of the adjacent normal breast specimens was positive. The difference between the tumor and normal samples was significant (Chi2 = 4.63, P < 0.05). LDP immunoreactivity in breast cancer correlated significantly with the overexpression of VEGF and HER2 (P < 0.001 and < 0.01, r = 0.389 and 0.287, respectively). Determined with confocal immunofluorescent analysis, LDP showed the binding capability to mammary carcinoma MCF-7 cells. It is demonstrated that LDP can bind to human breast cancer tissues and there is significant difference between the breast cancer tissues and the corresponding normal tissues. Notably, the binding reactivity shows positive correlation with the expression of VEGF and HER2 in breast carcinoma tissues. The results imply that LDP may have a potential use as targeting drug carrier in the research and development of new anticancer therapeutics. This study may provide reference for drug combination of LDM and other therapeutic agents.

BACKGROUND: Interleukin-1 is an important pro-inflammatory cytokine that has been documented in the regulation of bone inflammation and bone remodeling. A previous study has demonstrated that interleukin-1α can induce apoptosis while inhibiting osteoblast differentiation in MC3T3-E1 cells. OBJECTIVE: To investigate the role and mechanism of interleukin-1α on osteoclast activation and bone loss in mice. METHODS: (1) Cell test: RAW264.7 cells were either treated with interleukin-1α alone or with receptor activator of nuclear factor-κB ligand (RANKL) for 1 and 4 days. Cell viability was tested by cell counting kit-8 assay. The number of multinuclear osteoclasts was detected by tartrate resistant acid phosphatase assay. The mRNA and protein levels of osteoclast-specific genes and genes related to nuclear factor-κB pathway and Wnt/β-catenin pathway were tested by real-time fluorescence quantitative PCR, immunofluorescence staining or western blot. Bone marrow-derived macrophages were either treated with interleukin-1α alone or with RANKL and macrophage colony-stimulating factor for 7 days. The number of multinuclear osteoclasts was detected by tartrate resistant acid phosphatase assay. The protein levels of osteoclast-specific genes were tested by western blot. (2) Animal test: Twenty-four male C57BL/6J mice (6-8 weeks old) were assigned into two groups at random: control group and test group. Mice were subsequently treated with interleukin-1α solution or PBS by intraperitoneal injection twice a week for 5 weeks. Bone tissues from the femurs were performed with micro-computed tomography analysis and hematoxylin-eosin staining, tartrate resistant acid phosphatase, and immunofluorescence analysis. RESULTS AND CONCLUSION: Cell test: Interleukin-1α alone significantly increased RAW264.7 cell proliferation, but stimulated cell differentiation into osteoclasts in combination with RANKL (P < 0.05). Interleukin-1α significantly increased the expression of osteoclast-related markers and the number of tartrate resistant acid phosphatase-positive multinuclear cells in RAW264.7 cells and bone marrow-derived macrophages in the existence of RANKL or RANKL+macrophage colony-stimulating factor (both P < 0.05). Interleukin-1α was found to significantly enhance the nuclear factor-κB and Wnt/beta-catenin signaling in RAW264.7 cells (P < 0.05). Blocking of nuclear factor-κB or Wnt3 signaling not only reversed the activation of nuclear factor-κB and Wnt3 signaling but also weakened the enhanced expression of osteoclast-specific genes induced by interleukin-1α in RAW264.7 cells (P < 0.05). Animal test: interleukin-1α induced bone loss in mice while also upregulating the expression of osteoclast-specific markers, RANK, TRAF6 and p65, and Wnt3 in vivo (P < 0.05). The findings indicate that interleukin-1α can induce osteoclast activation and bone loss by promoting the nuclear factor-κB and Wnt signaling pathways.

As one of the pathogenic mechanisms contained in The Inner Canon of Yellow Emperor （《黄帝内经》）， “disease with latent pathogen induced by a new pathogen” means that the induced new pathogen resulted to a combination of the latent previous pathogen and the new pathogen， which caused the disease. Based on this， it is believed that the change of “nodule-cancer transformation” of pulmonary nodules is actually based on the deficiency of original qi， and the new pathogen induces the latent pathogens like phlegm coagulation， qi stagnation， blood stasis， toxicity， so healthy qi can not drive the pathogens out， and the long-time detention generated into cancerous turbidity， and deve-loped into cancerous tumour at the end. Therefore， based on the three-stage treatment of unformed cancer， dense cancerous toxin， and developed cancer， the clinical practice applied six methods of clearing， expelling， dissipating， tonifying， harmonizing， and transforming， taking into account both the manifestation and root cause， moving the treatment window of pulmonary nodules forward， attacking the pathogens when the toxin was not yet overbearing， supporting the healthy qi before declining， delaying the process of nodules-cancer transformation， and providing ideas for the prevention and treatment of pulmonary nodules “nodule-cancer transformation” in traditional Chinese medicine.

【Objective】 To evaluate the detection and distribution characteristics of anti-P1 in tumor patients, so as to aid in blood screening and transfusion safety. 【Methods】 The clinical data of 112 658 tumor patients who underwent blood preparation and transfusion in our hospital from January 2014 to December 2021 were retrospectively analyzed, and column agglutination technique was used to perform transfusion compatibility test. 【Results】 A total of 1 079 (0.96%, 1 079/112 658) cases were detected with unexpected antibodies, of which 71 (6.58%, 71/1 079) were identified as anti-P1. In anti-P1 cases, 59.15% (42/71) were males; 60.56% had no pregnancy history (P<0.01); 29.58% (21/71), 52.11%(37/71), 12.68%(9/71) and 5.63%(4/71) of anti-P1 patients were with type A, B, O and AB, respectively. 57 cases of anti-P1 patients (80.28%) had difficulty in ABO blood group identification. The incidence of interfering in patients with type B was higher than that of other blood types (P<0.05), as the frequency of w+ in reverse blood typing was higher than other reactive patterns (P<0.05). The incidence of gastric tumor and brain space-occupying lesion in patients with anti-P1 was higher than that in patients with other alloantibodies, while the incidence of gynecological tumors was lower (P<0.05). 【Conclusion】 Anti-P1 affects the ABO blood group identification of tumor patients, and most of them had difficulty in ABO blood group identification. Compared with patients with other alloantibodies, patients with anti-P1 are more likely to be male and suffer from gastric and brain tumors, but less likely from gynecological tumors.

【Objective】 To analyze the clinical manifestations of delayed serological transfusion reactions (DSTR) after platelet transfusion in tumor patients, and to explore the transfusion strategy. 【Methods】 Clinical data and laboratory test results of patients with positive antibody screening were analyzed after platelet transfusion in our hospital from January 1, 2015 to June 30, 2023, and the incidence rate, clinical characteristics and transfusion strategy of patients with DSTR were analyzed. 【Results】 A total of 2 553 patients with 6 057 platelet transfusions were reviewed. Eight patients developed DSTR and received a total of 21 therapeutic amounts of platelets, and 5 patients were subsequently transfused with red blood cells. Rh system antibodies were detected in 7 cases (4 anti-E, 1 anti-c/E, 1 anti-C and 1 anti-c) and Kell system antibodies in 1 case. 【Conclusion】 Tumor patients may also develop DSTR after platelet transfusion. It is necessary to pay close attention to the antibody situation and perform matched transfusion when transfusing blood again.