OBJECTIVE:To study protective effects of glutamine (Gln) on cardiac muscle cell in septic model rats. METH-ODS:Rats were randomly divided into sham operation group (normal saline),model group (normal saline) and Gln low-dose, medium-dose and high-dose groups(0.5,0.75,1.0 g/kg)with 10 rats in each group. In these groups,septic rat model was induced by cecal ligation and puncture except sham operation group received sham operation. They were given relevant medicine intrave-nously 10 min after operation,and the characteristics and apoptosis of cardiac muscle cell were observed 12 h after operation. The serum contents of CK,LDH and TnⅠ,and the expression of Bcl-2 and p53 mRNA were all detected. RESULTS:Compared with sham operation group,myocardial necrosis of model group was found,and the serum content of CK,LDH and TnⅠ and apoptotic index increased,and mRNA expression of Bcl-2 in cardiac muscle cell decreased while that of p53 increased,with statistical signifi-cance(P<0.05). Compared with model group,myocardial injury relieved significantly in Gln high-dose and medium-dose groups, and serum contents of CK,LDH and TnⅠ and apoptotic index decreased;mRNA expression of Bcl-2 increased in cardiac muscle cell while that of p53 decreased,with statistical significance (P<0.05). CONCLUSIONS:Gln can improve myocardial injury of septic model rats significantly,by a possible mechanism of down-regulating the expression of p53 gene and up-regulating the ex-pression of Bcl-2 gene.

Bow hunter′s syndrome, also known as vertebral basilar artery insufficiency, is a rare disease characterized by post?circulation blood supply insufficiency caused by mechanical or stenosis of the vertebral artery when the head and neck rotate or over?extend. To date, few cases regarding the bilateral hunter′s bow syndrome concurrent with epilepsy have been reported. A 29?year?old man was admitted to the First Hospital of Jilin University due to seizures. Results from transcranial Doppler ultrasound and carotid ultrasound showed that the patient had bilateral hunter′s bow syndrome. Further imaging examination showed that the syndrome was caused by congenital bone fusion which resulted in mechanical occlusion of C1-C2 vertebral artery. This case indicates that seizures are closely related to hunter′s bow syndrome.

Spinocerebellar ataxias (SCAs), formerly known as autosomal dominant cerebellar ataxia, are a group of hereditary heterogeneous neurodegenerative disease that contains many subtypes. Spinocerebellar ataxia type 23 (SCA23), one type of SCAs, is caused by mutant prodynorphin (PDYN) gene. A 22-year-old patient was diagnosed with sporadic SCA23 due to gene detection, with a novel identified mutation, PDYN c.647C>T (p.P216L). Located in the dynorphin A-coding-region of PDYN gene, the pathogenic mechanism of the mutation may be relevant to the pathological changes caused by the variant including neurological dysfunction and death of cells. Mild improvement with the patient has been witnessed after active balance and speaking exercise.

Bow hunter′s syndrome, also known as vertebral basilar artery insufficiency, is a rare disease characterized by post-circulation blood supply insufficiency caused by mechanical or stenosis of the vertebral artery when the head and neck rotate or over-extend. To date, few cases regarding the bilateral hunter′s bow syndrome concurrent with epilepsy have been reported. A 29-year-old man was admitted to the First Hospital of Jilin University due to seizures. Results from transcranial Doppler ultrasound and carotid ultrasound showed that the patient had bilateral hunter′s bow syndrome. Further imaging examination showed that the syndrome was caused by congenital bone fusion which resulted in mechanical occlusion of C₁-C₂ vertebral artery. This case indicates that seizures are closely related to hunter′s bow syndrome.

BACKGROUNDThere are limited eligible clinical markers at present to monitor the progress of chronic myeloid leukemia (CML). Heme oxygenase-1 (HO-1), as one of the most important oxidation-regulating enzymes in vivo, suggests the onset and progression of cancer when highly expressed. Furthermore, HO-1 level is related with the occurrence and development of hematological diseases. But the relationship between HO-1 expression and progression/relapse of CML has seldom been studied hitherto. This study aimed to investigate the relationship between them to find out a new molecular marker for prediction.

METHODSA total of 60 peripheral blood and bone marrow (BM) samples from 25 CML patients in different phases were collected respectively to detect the expressions of HO-1 and bcr/abl using real-time PCR. Routine blood test was performed to detect the changes of leukocyte and platelet counts. The proportion of primitive cells in BM was detected by flow cytometry. The relationship between high HO-1 expression and CML progression and relapse was explored by the analysis of variance by Wilcoxon test and linear regression analysis. The diagnostic accuracy and cutoff values were determined by receiver operating characteristic curve.

RESULTSRelative expression of HO-1 mRNA in CML patients peripheral blood was significantly higher than that of donors (P < 0.0001), which were 0.57±3.78 and (1.417±1.125)×10(-6), respectively. HO-1 expression level in CML patients was 0.061 5±0.062 4, which decreased to 0.009 4±0.006 7 upon CMoR, and remained remarkably higher 0.016 3±0.017 5 than that of normal donors (1.417±1.125)×10(-6), P < 0.001. When relapse occurred, HO-1 expression significantly increased from 0.020 6±0.021 0 to 3.852±10.285 in CMoR stage and undergoing relapse. According to progression of CML, HO-1 expression level in CML patients increased from CP (0.009 5±0.017 6) to AP (0.028 0±0.055 7) and then to BP (0.276 7 ± 0.447 0). And there was a linear correlation between HO-1 expression and proportion of primitive CML cells. The diagnostic accuracies and cutoff values of HO-1 expression for CML-CP, CML-AP, and CML-BP were 1.0, 0.748, and 0.965, respectively, as well as 0.000 070, 0.001 917, and 0.020 696, respectively.

CONCLUSIONHO-1 may be a potential molecular indicator for the progression and relapse of CML.

Bone Marrow ; metabolism ; Female ; Flow Cytometry ; Gene Expression ; Heme Oxygenase-1 ; blood ; genetics ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; diagnosis ; enzymology ; pathology ; Male ; Predictive Value of Tests ; Real-Time Polymerase Chain Reaction