OBJECTIVE: To evaluate the effect of biodegradable magnesium alloy materials in promoting tendon-bone healing during rotator cuff tear repair and to investigate their potential underlying biological mechanisms. METHODS: Forty-eight 8-week-old Sprague Dawley rats were taken and randomly divided into groups A, B, and C. Rotator cuff tear models were created and repaired using magnesium alloy sutures in group A and Vicryl Plus 4-0 absorbable sutures in group B, while only subcutaneous incisions and sutures were performed in group C. Organ samples of groups A and B were taken for HE staining at 1 and 2 weeks after operation to evaluate the safety of magnesium alloy, and specimens from the supraspinatus tendon and proximal humerus were harvested at 2, 4, 8, and 12 weeks after operation. The specimens were observed macroscopically at 4 and 12 weeks after operation. Biomechanical tests were performed at 4, 8, and 12 weeks to test the ultimate load and stiffness of the healing sites in groups A and B. At 2, 4, and 12 weeks, the specimens were subjected to the following tests: Micro-CT to evaluate the formation of bone tunnels in groups A and B, HE staining and Masson staining to observe the regeneration of fibrocartilage at the tendon-bone interface after decalcification and sectioning, and Goldner trichrome staining to evaluate the calcification. Immunohistochemical staining was performed to detect the expressions of angiogenic factors, including vascular endothelial growth factor (VEGF) and bone morphogenetic protein 2 (BMP-2), as well as osteogenic factors at the tendon-bone interface. Additionally, immunofluorescence staining was used to examine the expressions of Arginase 1 and Integrin beta-2 to assess M1 and M2 macrophage polarization at the tendon-bone interface. The role of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway in tendon-bone healing was further analyzed using real-time fluorescence quantitative PCR. RESULTS: Analysis of visceral sections revealed that magnesium ions released during the degradation of magnesium alloys did not cause significant toxic effects on organs such as the heart, liver, spleen, lungs, and kidneys, indicating good biosafety. Histological analysis further demonstrated that fibrocartilage regeneration at the tendon-bone interface in group A occurred earlier, and the amount of fibrocartilage was significantly greater compared to group B, suggesting a positive effect of magnesium alloy material on tendon-bone interface repair. Additionally, Micro-CT analysis results revealed that bone tunnel formation occurred more rapidly in group A compared to group B, further supporting the beneficial effect of magnesium alloy on bone healing. Biomechanical testing showed that the ultimate load in group A was consistently higher than in group B, and the stiffness of group A was also greater than that of group B at 4 weeks, indicating stronger tissue-carrying capacity following tendon-bone interface repair and highlighting the potential of magnesium alloy in enhancing tendon-bone healing. Immunohistochemical staining results indicated that the expressions of VEGF and BMP-2 were significantly upregulated during the early stages of healing, suggesting that magnesium alloy effectively promoted angiogenesis and bone formation, thereby accelerating the tendon-bone healing process. Immunofluorescence staining further revealed that magnesium ions exerted significant anti-inflammatory effects by regulating macrophage polarization, promoting their shift toward the M2 phenotype. Real-time fluorescence quantitative PCR results demonstrated that magnesium ions could facilitate tendon-bone healing by modulating the PI3K/AKT signaling pathway. CONCLUSION Biodegradable magnesium alloy material accelerated fibrocartilage regeneration and calcification at the tendon-bone interface in rat rotator cuff tear repair by regulating the PI3K/AKT signaling pathway, thereby significantly enhancing tendon-bone healing.
Animals ; Rotator Cuff Injuries/metabolism* ; Rats, Sprague-Dawley ; Signal Transduction ; Wound Healing/drug effects* ; Alloys/pharmacology* ; Rats ; Proto-Oncogene Proteins c-akt/metabolism* ; Rotator Cuff/metabolism* ; Macrophages/metabolism* ; Magnesium/pharmacology* ; Phosphatidylinositol 3-Kinases/metabolism* ; Vascular Endothelial Growth Factor A/metabolism* ; Male ; Biocompatible Materials ; Bone Morphogenetic Protein 2/metabolism*

Objective:To understand the clinical manifestations, diagnosis, treatment, and prognosis of children with hereditary thrombocytopenia (HT).Methods:The clinical data of 5 patients with HT in the Hematology and Oncology Department of Children′s Hospital of Chongqing Medical University from August 2015 to October 2017 were retrospectively analyzed. The clinical and laboratory characteristics, treatment, and prognosis of HT were discussed by reviewing relevant literatures.Results:Five patients included 3 boys and 2 girls.The median age at onset of 4 years and 2 months old and the median age at diagnose was 4 years and 4 months old.All patients presented with the thrombocytopenia, among which 4 cases were macrothrombocytopenia and 1 case was normothrombocytopenia.The main clinical presentations of 5 patients were skin petechiae and ecchymoses.Four cases were initially misdiagnosed as immune thrombocytopenia (ITP) and received the glucocorticoid and immunoglobulin, while the therapeutic effect was not satisfactory.The gene sequencing confirmed MYH9 gene mutation(c.3493C>T), MYH9 gene mutation(c.5878G>A), NBEAL2 gene compound heterozygous mutation(c.295C>T; c.4169C>T), GP1BA gene mutation(c.1761A>C), and ANKRD26 gene mutation(c.5123A>G), in 5 patients respectively. Conclusions:HT should be suspected among those with recurrent isolated thrombocytopenia and no response to the ITP regimen, and the early gene screening is of great significance to the patients′ treatment and prognosis.

Objective: To explore the recovery time and risk factors of coagulopathy caused by rodenticide poisoning through analyzing and following up the confirmed cases, and to provide more useful guidance information for the clinic practice. Methods: A total of 96 cases with coagulation dysfunction caused by anticoagulant rodenticide poiso-ning in Children′s Hospital, Chongqing Medical University from January 2014 to December 2016, were analyzed retrospectively.The recovery time of coagulation function and the relationship between recovery time and drug involved way, dysfunction organs and poison concentration were studied respectively. Results: (1) A total of 96 patients were hospitalized because of severe coagulopathy caused by the poisoning of second generation anticoagulant rodenticide.Brodifacoum was detected from 33 blood samples and the median concentration was 364 μg/L (55-4 654 μg/L). Bromadiolone was detected from 7 blood samples and the median concentration was 130 μg/L (18-652 μg/L). Brodifacoum and Bromadiolone were both detected from 8 cases and the median concentration was 741 μg/L (63-6 000 μg/L) and 11 μg/L (3-3 694 μg/L), respectively.(2) A total of 57 cases of the patients were successfully followed up.A total of 18 cases were confirmed with oral poisoning, 16 cases with dermal poisoning, while 23 cases denied any involved ways of poisoning, and 7 cases had organs dysfunction.The follow-up time was 12-54 months.All the hospitalized patients were given specific antidote Vitamin K treatment and recovered successfully without any sequelae.(3) The median recovery time of coagulopathy caused by rodenticide poisoning was 2.5 months.(4) The recovery time of coagulation function was positively correlated with the plasma concentration of Brodifacoum(r=0.619, P<0.01). (5) There was no significant correlation between recovery time and organ dysfunction or drug involved ways of poisoning involvement (all P>0.05). Conclusions The recovery time of coagulation dysfunction caused by anticoagulant rodenticide in children is much longer.The higher the concentration of Brodifacoum poison is, the longer the recovery time.Enough supplementation course of Vitamin K should be given according to the follow-up of coagulation function.

Objective To investigate the clinical features and prognosis of central nervous system(CNS)in-volvement in Epstein-Barr virus(EBV)associated hemophagocytic lymphohistiocytosis(HLH).Methods A total of 89 patients with EBV-HLH diagnosed in Children's Hospital of Chongqing Medical University from June 2006 to Octo-ber 2015 were divided into involved CNS group and non-involved group according to whether there was CNS involve-ment. The clinical manifestations,laboratory examinations and outcomes of these two groups were analyzed. Results Among these 89 patients with EBV-HLH,39 patients developed CNS disease,19 cases of them had neuro-logical symptoms or signs,including convulsions,unconsciousness,facial palsy,dysarthria,dysphagia,irritability,neck stiffness,Babinski sign positive,opisthotonus;9 cases of them had abnormal cerebrospinal fluid(CSF),with elevated white blood cell count and protein level;26 patients had abnormal brain images,including deepen or widening cortical sulci,atrophy,hemorrhage,high T2 signal in magnetic resonance imaging(MRI).The 3-year survival rate in involved CNS group was lower than those of non-involved group(66.7% vs.86.0%),and there was statistical significance (χ2=4.267,P=0.039).The involved CNS group had higher ferritin(χ2=5.092,3.921;P=0.024,0.048)and lower platelets(Z= -2.643,P=0.008)than those of non-involved group,and there were statistical significances.COX mul-tivariate analysis showed that neurological symptom and abnormal CSF were independent prognostic factors(RR=3.134, 3.339,all P<0.05).Conclusion CNS involvement is frequent in EBV-HLH.The prognosis of children with involved CNS group is worse than those of non-involved group.Neurological symptoms and abnormal CSF are related to poor prognosis.

Objective To investigate the relationship between EVI1 gene expression and clinical features and prognosis of children with acute myeloid leukemia (AML). Methods EVI1 gene was detected in AML children, correlation of clinical and lab features, prognosis of AML children with EVI1 gene were analyzed. Results EVI1 expression is positive in 38 of 145 children with AML. There were no significant differences in age, gender, hemoglobin concentration, leukocytes and platelet count, subtype of morphology, ratio of chromosomal anomaly and complex karyotypes between EVI1 positive and EVI1 negative group (P>0.05); coexist genes were detected in 9 cases (23.68%) of EVI1 positive group. Rate of complete remission (CR) was 91.67% in 24 cases of EVI1 positive patients received chemotherapy. Relapse rate was 64.29% and 14.29% in EVI1 positive patients who received chemotherapy and allo-hematopoietic stem cell transplantation (allo-HSCT), retrospectively and significant differences were found (P<0.05). There was no significant difference in CR but significant difference was found in event free survival (P<0.05) for EVI1 positive and EVI1 negative patients who received chemotherapy. EVI1 gene kept negative when bone marrow relapse occurred in two patients with EVI1 positive at diagnosis. Conclusion EVI1 gene may play adverse role in pediatric AML; prognosis of EVI1 positive AML patients can be improved by allo-HSCT; follow-up of EVI1 transcript levels is insufficient to monitoring of minimal residual disease.

Objective: To investigate the characteristics and prognostic factor of central nervous system (CNS) involvement in patients with hemophagocytic lymphohistiocytosis (HLH) . Methods: From January 2006 to October 2015, 152 patients with HLH, 88 patients had CNS involvement, their clinical data were collected, and survival was analyzed using the Kaplan-Meier life table method, univariate and multivariate Cox regression model analyses were applied to identify the risk factors of prognosis. Results: ①57.9% patients complicated with neurological symptoms, cerebrospinal fluid abnormalities were observed in 37.0% patients, 57.5% patients had abnormal neuroradiology. ②36 patients survived well, 3 patients lost to follow-up, 49 dead, 1 survival patient had epilepsy. ③The 3-year overall survival rate of 88 patients was 44%. ④abnormal CSF and unreceived IT bore a significant, independent adverse prognostic value (P<0.05) . Conclusion CNS involvement in HLH has a high frequency and poor prognosis, few patients remained neurologic sequelae; abnormal CSF related to poor prognosis, positive intrathecal injections could improve the prognosis.

OBJECTIVETo explore the clinical features, laboratory findings and treatment of infant leukemia.

METHODSA retrospective analysis of the clinical data was performed of the cases with the diagnosis of infant acute leukemia from August 1993 to October 2014 in our hospital.

RESULTSA total of 144 cases of infant leukemia were diagnosed in the defined period, including 83 cases of acute lymphoblastic leukemia, 55 myeloid leukemia, 1 hybrid acute leukaemia and 5 with incompatible cytological and immunophenotyping findings. The patients at the age of 9 to 12 months accounted for the largest proportion (38.2%), and 87.5% of the patients had hepatosplenomegaly; Six patients below 6 months old had skin infiltration. In about 1/3 of the patients, the white blood cells count was no greater than 100 × 10⁹ /L. Ninety-five patients had chromosome examinations, which identified chromosome abnormalities in 67 patients, including 18 positive for t(4;11)or t(9;11)or t(11;19), and younger patients were more likely to have chromosome abnormalities. Thirty-seven patients underwent MLL gene detection and 11 of them had positive results; the positive patients had higher rate of chromosome 11 abnormalities than the negative patients. Most of the patients gave up treatments after diagnosis and only 6 patients older than 6 months completed regular chemotherapeutic treatments and were now in complete remission.

CONCLUSIONInfant leukemia is a rare type of leukemia with different clinical features from other types of leukemia. The patients often present with hepatosplenomegaly, high white blood cell counts, MLL gene fusion, and chromosome 11 abnormalities. The prognosis of infant leukemia is not favorable, and the current treatment still relies on chemotherapy.

Acute Disease ; Chromosome Aberrations ; Chromosome Disorders ; Chromosomes, Human, Pair 11 ; Humans ; Immunophenotyping ; Infant ; Leukemia, Myeloid ; pathology ; Leukocyte Count ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; pathology ; Prognosis ; Retrospective Studies

Objective To evaluate the treatment of current status and prognosis in childhood APL with APL2008 ,which was administrated since 2008 in our center .Methods A total of 43 children with newly diagnosed APL between 2008 to 2014 were studied retrospectively .Treatment options and current status were summarized from 28 patients who received APL2008 therapy . Results Studied 43 patients were at median age of 8 years and 4 months ,with 28 boys and 15 girls .The main clinical manifestations were infection ,anemia ,bleeding ,fever ,hepatomegaly ,splenomegaly and lymphadenopathy .The proportions of low ,intermediate and high risk groups were 27 .9% ,48 .8% and 23 .3% ,respectively .Eleven cases could be diagnosed as DIC .Bone marrow morphology showed abnormal elevation of promyelocyte .37 patients had distinctive immunophenotype such as frequent expression of CD33 , CD117 and MPO .PML/RARαfusion gene positive rate was 100% in 43 children and cytogenetic analysis were positive in 37 cases , of which specific genetic lesion in APL cells with t (15 ;17)(q22 ;q12) was found in 28 cases ,and karyotypes was found in 9 cases as infrequent chromosomal abnormalities .In 43 patients ,4 cases were early dead from intracranial hemorrhage at early stage ,and 11 cases were given up early .There were only 2 cases dead ,2 cases relapsed and 1 case lost among 28 APL children ,which enabled ef‐ficacy analysis possible .96 .4% of these 28 cases achieved HCR .The 2 year Kaplan Meier estimates of OS and EFS were 85 .9% ± 7 .6% and 80 .4% ± 8 .8% .But OS and EFS would be 94 .7% ± 5 .1% and 88 .9% ± 7 .4% if 3 patients who had non standard treat‐ment were excluded .Conclusion Childhood APL were characterized by anemia ,bleeding ,fever and infiltration .APL′s coincidence rate between PML/RARa fusion gene and morphology ,immunology and cytogenetics were 95 .3% ,90 .2% and 86 .5% ,respective‐ly .APL2008 significantly improved the prognosis of APL .

Objective To explore the clinical features, laboratory findings and treatment of infant leukemia. Methods A retrospective analysis of the clinical data was performed of the cases with the diagnosis of infant acute leukemia from August 1993 to October 2014 in our hospital. Results A total of 144 cases of infant leukemia were diagnosed in the defined period, including 83 cases of acute lymphoblastic leukemia, 55 myeloid leukemia, 1 hybrid acute leukaemia and 5 with incompatible cytological and immunophenotyping findings. The patients at the age of 9 to 12 months accounted for the largest proportion (38.2%), and 87.5%of the patients had hepatosplenomegaly;Six patients below 6 months old had skin infiltration. In about 1/3 of the patients, the white blood cells count was no greater than 100×109/L. Ninety-five patients had chromosome examinations, which identified chromosome abnormalities in 67 patients, including 18 positive for t(4;11)or t(9;11)or t(11;19), and younger patients were more likely to have chromosome abnormalities. Thirty-seven patients underwent MLL gene detection and 11 of them had positive results; the positive patients had higher rate of chromosome 11 abnormalities than the negative patients. Most of the patients gave up treatments after diagnosis and only 6 patients older than 6 months completed regular chemotherapeutic treatments and were now in complete remission. Conclusion Infant leukemia is a rare type of leukemia with different clinical features from other types of leukemia. The patients often present with hepatosplenomegaly, high white blood cell counts, MLL gene fusion, and chromosome 11 abnormalities. The prognosis of infant leukemia is not favorable, and the current treatment still relies on chemotherapy.

Objective To explore the clinical features, laboratory findings and treatment of infant leukemia. Methods A retrospective analysis of the clinical data was performed of the cases with the diagnosis of infant acute leukemia from August 1993 to October 2014 in our hospital. Results A total of 144 cases of infant leukemia were diagnosed in the defined period, including 83 cases of acute lymphoblastic leukemia, 55 myeloid leukemia, 1 hybrid acute leukaemia and 5 with incompatible cytological and immunophenotyping findings. The patients at the age of 9 to 12 months accounted for the largest proportion (38.2%), and 87.5%of the patients had hepatosplenomegaly;Six patients below 6 months old had skin infiltration. In about 1/3 of the patients, the white blood cells count was no greater than 100×109/L. Ninety-five patients had chromosome examinations, which identified chromosome abnormalities in 67 patients, including 18 positive for t(4;11)or t(9;11)or t(11;19), and younger patients were more likely to have chromosome abnormalities. Thirty-seven patients underwent MLL gene detection and 11 of them had positive results; the positive patients had higher rate of chromosome 11 abnormalities than the negative patients. Most of the patients gave up treatments after diagnosis and only 6 patients older than 6 months completed regular chemotherapeutic treatments and were now in complete remission. Conclusion Infant leukemia is a rare type of leukemia with different clinical features from other types of leukemia. The patients often present with hepatosplenomegaly, high white blood cell counts, MLL gene fusion, and chromosome 11 abnormalities. The prognosis of infant leukemia is not favorable, and the current treatment still relies on chemotherapy.