Objective To investigate the effectiveness of percutaneous intracystic steroid injection using two needles in the treatment of solitary bone cysts in children. Methods A total of 28 children with solitary bone cyst underwent steroid injection from January 1996 to January 2004. Under fluoroscopy, two fine needles (either bone marrow biopsy needle or lumbar puncture needle) pierced the bone cyst by way of the top and the bottom of the cyst, respectively. The intracystic fluid was drawn off, the cyst cavity irrigated and the steroid injected into. Results Follow-up checkups for 10~62 months (mean, 28 months) in 27 children found no complications. According to the Chigira classification on the new bone formation, 20 cases were classified as grade Ⅳ, 5 case grade Ⅲ, 1 case grade Ⅱ and 1 case grade Ⅰ, the cure rate being 92 6% (25/27). The time for bone cysts to grow together again in the 25 children was 3~10 months (mean, 4 5 months). Conclusions Percutaneous intracystic steroid injection using two needles for solitary bone cysts in children is simple, safe and effective.

OBJECTIVETo investigate the mechanism of refractoriness of acute myeloid leukemia (AML) by studying the changes of gene mRNA expression from primary diagnosis to relapsed disease in AML.

METHODSDifferences in gene expression profile of bone marrow mononuclear cells were compared between primary diagnosis and relapsed/refractory disease in 3 patients with M(2a) subtype of AML using Agilent human 1B 60mer oligonucleotide microarray.

RESULTSCommon alterations were found in 10 genes among the 20173 genes tested at relapsed/refractory disease as compared with that at primary diagnosis in 3 patients. Of these 10 genes, 7 were up-regulated while 3 down-regulated at relapse in all the 3 patients.

CONCLUSIONDevelopment of relapsed/refractory disease in AML-M(2a) might be associated with the mRNA expression changes in the 10 genes tested including DAPK1. The alteration of these genes may be indications for the early diagnosis of refractoriness of AML, and these genes might provide new therapeutic targets for the treatment of refractory AML.

Adult ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Leukemic ; Humans ; Leukemia, Myeloid, Acute ; genetics ; Male ; Middle Aged ; Oligonucleotide Array Sequence Analysis

OBJECTIVEIt has been known that the intrahepatic renin-angiotensin-aldosterone system (RAAS) plays a key role in the fibrogenesis in livers. Aldosterone (Aldo), the principal effector molecule of the RAAS, exerts local effects on cell growth and fibrogenesis. However, the signal transduction mechanisms underlying the effects of Aldo on hepatic fibrogenesis remain to be fully elucidated. The present study aims to investigate the signal transduction mechanism underlying the effects of Aldo on the signal passageway of active protein-1 (AP-1).

METHODSIn vitro, HSCs-T6 cell line was treated with Aldo for 10 min, 30 min, 60 min, 120 min and 180 min, and protein expression of Phospho-P42/44 was detected by Western blot. In addition, HSCs-T6 cell line was preincubated for 60 min or not with U0126 (an inhibitor of the MAPK/ERK kinase), and also with antioxidant-N-acetylcysteine (NAC) prior to exposure to Aldo for the indicated times. Protein expression of Phospho-P42/44 was measured by Western blot. DNA biding activity of AP-1 was analyzed by electrophoretic gel mobility shift assay (EMSA). By means of RT-PCR, expression of alpha1(1) procollagen mRNA was detected.

RESULTSAldo stimulated HSC via extracellular signal-regulated kinase (ERK1/2) pathway. Time course experiments showed that Aldo induced Phospho-P42/44 expression, which was abrogated by U0126, reaching a maximum at 10 minutes, and then declined progressively. NAC inhibited the Phospho-P42/44 expression. EMSA showed that stimulation of HSC by Aldo markedly increased AP-1 DNA binding activity. U0126 markedly reduced AP-1 DNA binding activity induced by Aldo; NAC partly decreased AP-1 activity induced by Aldo. Aldo up-regulated expression of alpha1(1) procollagen mRNA, which was attenuated by U0126 and NAC.

CONCLUSIONStimulation of HSC by Aldo results in activation of AP-1 via ERK1/2 pathway, leading to up-regulation of AP-1 target gene alpha1(1) procollagen mRNA expression.

Aldosterone ; pharmacology ; Cell Line ; Collagen Type I ; biosynthesis ; genetics ; Hepatocytes ; cytology ; metabolism ; Humans ; Mitogen-Activated Protein Kinase 3 ; metabolism ; RNA, Messenger ; biosynthesis ; genetics ; Transcription Factor AP-1 ; metabolism

OBJECTIVEIt is known that intrahepatic renin-angiotensin-aldosterone system (RAAS) plays a key role in liver fibrogenesis. Aldosterone (Aldo), the principal effector molecule of the RAAS, exerts local effects on cell growth and fibrogenesis. However, the signal transduction mechanisms underlying the effects of Aldo on hepatic fibrogenesis remain to be fully elucidated. The present study aims to investigate the signal transduction mechanism underlying the effects of Aldo on extracellular signal-regulated kinase 1/2 (ERK1/2), early growth response-1 (EGR-1) and on the platelet-derived growth factor-B (PDGF-B).

METHODSIn vitro, hepatic stellate cell (HSC)-T6 cell line was treated with Aldo for 10 min, 0.5 h, 1 h, 2 h and 3 h. Protein expression of phospho-p42/44 was detected by Western blot. In addition, HSC-T6 were preincubated for 1 h or not at all with U0126 (an inhibitor of the MAPK/ERK kinase), and antioxidant-N-acetylcysteine (NAC) prior to exposure to Aldo for the indicated times. Protein expressions of phospho-p42/44 and PDGF-B were measured by Western blot. DNA biding activity of EGR-1 was analyzed by electrophoretic gel mobility shift assay (EMSA). By means of immunohistochemistry, expression of PDGF-B was detected.

RESULTSAldo induced phospho-p42/44 expression could be abrogated by U0126; NAC did not inhibit phospho-p42/44 expression. Gel shift study showed that stimulation of HSC by Aldo markedly increased the EGR-1 DNA binding activity, which was abrogated by U0126, reaching a maximum at 60 minutes, and then declined progressively. NAC did not reduce the EGR-1 activity. Aldo increased the PDGF-B protein level in HSC, which was not attenuated by NAC and U0126.

CONCLUSIONSStimulation of HSC by Aldo results in activation of EGR-1 via ERK1/2 pathway, leading to up-regulation of PDGF-B expression.

Aldosterone ; pharmacology ; Cell Line ; Early Growth Response Protein 1 ; biosynthesis ; genetics ; Hepatocytes ; cytology ; metabolism ; Humans ; Mitogen-Activated Protein Kinase 3 ; biosynthesis ; genetics ; Proto-Oncogene Proteins c-sis ; biosynthesis ; genetics ; Signal Transduction

Angiotensin II ; pharmacology ; Animals ; Cells, Cultured ; Cyclooxygenase 2 ; biosynthesis ; genetics ; Kupffer Cells ; cytology ; metabolism ; NF-kappa B ; metabolism ; Platelet-Derived Growth Factor ; biosynthesis ; genetics ; Proto-Oncogene Proteins c-sis ; Rats ; Rats, Wistar ; Receptors, Angiotensin ; biosynthesis ; genetics ; Transforming Growth Factor beta ; biosynthesis ; genetics

Tubal pregnancy is common and is in lackof detailed clinical research.It seems to be simple todiagnose and easy to handle,but once it is ignored,itcan lead to serious consequences and even death.Withthe changes in today′s social environment and people′sconcept,and with the widespread use of IVF and othertechnologies,new cases have emerged in tubal preg-nancy.We should re-emphasize the diagnosis andtreatment of tubal pregnancy.

Objective:To investigate the knowledgement and clinical application of neurogenic bladder and intermittent catheterization among nurses in Guangdong. Methods:From December, 2020 to January, 2021, 241 nurses in Guangdong were investigated with a questionnaire designed by ourselves. Results:The score was low in understanding the neurogenic bladder rehabilitation nursing management and intermittent catheterization through self-assessment. The awareness was deficient in the complication and risk management of neurogenic bladder. Although there were a lot of patients with dysuria in clinical practice, 67.2% of nurses still used indwelling catheter, and only 24.1% used intermittent catheterization. Only 9.9% nurses thought that patients with dysuria were treated positively by doctors. Most of nurses would like to participate in the training and nursing alliance in neurogenic bladder rehabilitation nursing management and intermittent catheterization, and manage patients with neurogenic bladder after discharge. Conclusion:The knowledge of guidelines related with neurogenic bladder and intermittent catheterization among nurses is insufficient, and is not applied in clinical practice. More work should be done to improve the knowledge and standardization of management of neurogenic bladder.

BACKGROUNDTo evaluate the effect of ⁸⁹SrCl₂ and/or Bonefos in the treatment of bone metastasis from pulmonary carcinoma.

METHODSA total of sixty-seven lung cancer patients with bone metastasis were enrolled in this study, who were divided into three groups: nineteen cases were treated with ⁸⁹SrCl₂; twenty-eight cases with Bonefos; and twenty cases combined ⁸⁹SrCl₂ with Bonefos.

RESULTSThe total relief rate of the bone pain: the ⁸⁹SrCl₂ group was 84.2%, and the Bonefos group was 80.4%, the combination group was 90.0%. There was no statistical difference among three groups (P > 0.05). The effective rate of the bone metastasis: the ⁸⁹SrCl₂ group was 15.7%, the Bonefos group was 10.7%, and the combination group was 45.0%. The combination group had significantly higher effective rate than that of the ⁸⁹SrCl₂ group or the Bonefos group alone (P < 0.05). The rate of improvement of quality of life: the ⁸⁹SrCl₂ group was 47.3%, the Bonefos group was 42.8%, and the combination group was 80.0%. The combination group had significantly higher effective rate than that of the ⁸⁹SrCl₂ group or the Bonefos group alone (P < 0.05). The side effects of three groups were minimal.

CONCLUSIONS⁸⁹SrCl₂ and Bonefos are two effective and safe drugs on relief of pain. Combined ⁸⁹SrCl₂ and Bonefos might be a better therapy for bone metastasis and improvement of quality of life than the single one, and the side effect is slight and tolerable.

OBJECTIVETo evaluate the effects of angiotensin-converting enzyme inhibitor (ACEI) and angiotensin II type 1 receptor (AT-1 receptor) blocker on the progression of rat pulmonary fibrosis induced by bleomycin A5.

METHODSTwenty-four male Wistar rats were randomized into pulmonary fibrosis model, perindopril treatment, losartan treatment and control groups. In the former 3 groups, pulmonary fibrosis was induced via intratracheal injection of bleomycin A5 (5 mg/kg), after which the rats in the perindopril and losartan groups received intragastric administration of the corresponding agents at the daily dose of 2 mg/kg and 10 m/kg, respectively. The rats in the control group had intratracheal injection of normal saline only. In the 4th week, the histological changes of the lung tissues were examined microscopically with Masson staining. Hydroxyproline content in the lungs was measured, and the protein expressions of AT-1 receptor, TGF-beta1 and IkappaBalpha were examined using Western blotting. DNA binding activity of NF-kappaB was analyzed with electrophoretic gel mobility shift assay (EMSA), and zymography was used to assess the activity of matrix metalloproteinase-2 and 9 (MMP-2, 9).

RESULTSBoth perindopril and losartan treatment significantly reduced the pulmonary fibrosis score, content of hydroxyproline, protein expression of TGF-beta1, DNA binding activity of NF-kappaB and MMP-2, 9 activity, and increased cytoplasmic protein expression of IkappaBalpha. Perindopril treatment lowered the protein level of AT-1 receptor.

CONCLUSIONPerindopril and losartan may inhibit bleomycin A5-induced pulmonary fibrosis in rats by reducing the protein expression of TGF-beta1 and suppressing the DNA binding activity of NF-kappaB and MMP-2, 9 activity.

Angiotensin II Type 1 Receptor Blockers ; therapeutic use ; Angiotensin-Converting Enzyme Inhibitors ; therapeutic use ; Animals ; Bleomycin ; analogs & derivatives ; Blotting, Western ; Losartan ; therapeutic use ; Male ; NF-kappa B ; metabolism ; Perindopril ; therapeutic use ; Pulmonary Fibrosis ; chemically induced ; drug therapy ; metabolism ; Random Allocation ; Rats ; Rats, Wistar ; Receptor, Angiotensin, Type 1 ; metabolism ; Transforming Growth Factor beta1 ; metabolism

OBJECTIVE: To investigate the clinical characteristics of lower extremity arterial disease (LEAD) and its risk factors in patients with diabetic foot ulcer (DFU). METHODS: We retrospectively collected the clinical and follow-up data of 650 patients with DFU treated in the Department of Endocrinology and Metabolism of Nanfang Hospital between January, 2017 and December, 2019. We compared the data between patients who had LEAD and those without LEAD and used a multivariate logistic regression model to analyze the risk factors of LEAD in DFU patients. RESULTS: Among the 650 DFU patients, 470 (72.4%) had LEAD. The patients were followed up for a mean of 3.5 months, and the mean healing time of DFU was 2.55 months; healing of DFU occurred in 453 patients and 183 patients received amputation. The patients with LEAD and those without LEAD differed significantly in age, hospitalization costs, diastolic blood pressure (DBP), glycated hemoglobin, blood lipid levels, disease course, ankle brachial index, healing time, smoking history, clinical outcomes, Wagner grade and imaging results (P < 0.05). Multivariate logistic regression analysis identified age (OR=1.070, 95% CI: 1.049-1.091), smoking history (OR= 2.013, 95% CI: 1.268-3.195), and a decreased DBP (OR=0.980, 95% CI: 0.963-0.997) as independent risk factors for LEAD in DFU patients. A prolonged healing time was a prominent clinical feature of DFU complicated by LEAD. CONCLUSION DFU patients have a high incidence of LEAD, which leads to high rates of disability and mortality and is associated with an advanced age, high smoking rate and longer healing time. A decreased DBP is also a risk factor for LEAD in DFU patients.
Amputation ; Diabetes Mellitus ; Diabetic Foot/epidemiology* ; Humans ; Lower Extremity ; Retrospective Studies ; Risk Factors