Correlation between clinical features and total maturation score by magnetic resonance imaging in very low birth weight premature infants with brain injury.

BACKGROUND: Brain injury in premature infants (BIPI) seriously affects the growth and development of preterm infants. Magnetic resonance imaging (MRI) has become an important method of assessing brain development. The aim of this study was to explore the correlation between clinical features and total maturation score (TMS) by MRI in very low birth weight (VLBW) preterm infants with brain injury at term postmenstrual age (PMA). METHODS: A retrospective cohort of 65 cases of BIPI with VLBW and 40 normal control cases were included, and all cases underwent MRI examination. The 2 groups were assessed in terms of TMS and sub-parameters (myelination, cortical infolding, germinal matrix, bands of migrating glial cells), and the correlation between TMS and term PMA was also analyzed. RESULTS: The TMS of the BIPI group was lower than that of the control group (P<0.01). The differences in myelination and cortical infolding were statistically significant (P<0.01). No significant differences in the germinal matrix and bands of migrating glial cells were found. The linear regression equation showing a positive correlation between TMS and term PMA in normal preterm infants was y=1.164x-28.888 (t=9.478, P=0.000). CONCLUSIONS: TMS by conventional cranial MRI can objectively reflect the brain maturity and brain damage of premature infants, and is related to the term PMA.

Protective Effects of Allicin on ISO-Induced Rat Model of Myocardial Infarction via JNK Signaling Pathway.

OBJECTIVE: This research was aimed to explore protective effects of allicin on rat model of myocardial infarction via JNK signaling pathway. METHODS: Rat myocardial ischemia model was established with subcutaneous injection of isoproterenol (ISO). Seventy-five rats were randomly divided into 5 groups (n = 15): sham group, ISO group, low-dose group (1.2 mg/kg/days for 7 days), medium-dose group (1.8 mg/kg/days for 7 days), and high-dose group (3.6 mg/kg/days for 7 days). Routine HE staining and Masson staining were performed to observe myocardial histopathology. The expression of oxidative stress-related indicators, heart tissue apoptosis-related proteins, and JNK and p-JNK proteins were measured for different groups. RESULTS: Compared with the sham group, the T wave value of the ISO group was significantly increased (p < 0.01). When allicin was administered, the T wave values at different time points in all groups were all decreased. Compared with the sham group, the ratio of eNOS, Bcl-2/Bax was significantly decreased, and p-eNOS, iNOS, caspase-3, caspase-9, and Cyt-c were significantly elevated in the ISO group (p < 0.05). After allicin was administered, significant changes in these proteins were observed in the medium- and high-dose groups. There was no significant change in the expression of JNK protein in the ISO group compared with the sham group; however, the expression of eNOS and p-JNK protein were significantly upregulated (p < 0.01) and the expression of p-eNOS and iNOS were significantly downregulated (p < 0.01). When allicin was administered, expression of p-JNK protein was significantly downregulated. CONCLUSION: Allicin can reduce oxidative stress damage and cardiomyocyte apoptosis in rat model of myocardial infarction and can significantly regulate JNK signaling pathway.

Correlations between EGFR gene polymorphisms and pleural metastasis of lung adenocarcinoma.

Proliferation, growth, and differentiation of cells are strictly controlled by the signal system of epidermal growth factor receptor (EGFR). If any link of the EGFR signals system is interfered with or damaged, the proliferation, growth, and differentiation of cells would become uncontrolled. EGFR is overexpressed in a variety of malignant tumors, such as non-small-cell lung cancer, colorectal cancer and breast cancer. Results of the study have proved that EGFR overexpression is closely associated with mutations and variants of the EGFR genes, whose mutations and variants are associated with occurrence, metastasis, and prognosis of different types of tumors, including lung cancer. This study is aimed at investigating whether the polymorphisms of CA simple sequence repeat in intron 1 (CA-SSR1), -216G/T, and R497K in the EGFR are able to induce EGFR activation and whether overexpression is associated with pleural metastasis of lung adenocarcinoma. A total of 432 lung adenocarcinoma patients with pleural metastasis (metastasis group) and 424 patients with lung adenocarcinoma but without pleural metastasis (nonmetastasis group) were enrolled in this study. For all patients, the CA-SSR1 genotypes were determined by capillary electrophoresis, polymerase chain reaction amplification, and direct DNA sequencing, and the R497K and -216G/T genotypes were determined by polymerase chain reaction amplification and direct DNA sequencing. EGFR expression was evaluated by immunohistochemical staining in primary tumor tissues with different -216G/T, R497K, and CA-SSR1 genotypes. Our results showed significant differences between pleural metastasis and nonmetastasis groups in the genotype and allele distribution of -216G/T, R497K, and CA-SSR1 polymorphisms of the EGFR gene. The -216T allele, Arg allele, and shorter CA-SSR1 (<17) had significantly increased risks of pleural metastasis compared with the -216G allele, Lys allele, and longer CA-SSR1 (≥17), respectively. The expression of EGFR was higher in patients with genotypes of -216T/T or -216G/T, Arg/Arg or Arg/Lys, and shorter CA-SSR1 (<17) than that in patients with genotypes of -216G/G, Lys/Lys, and longer CA-SSR1 (≥17), respectively. These results indicate that -216G/T, R497K, and CA-SSR1 polymorphisms are associated with the risk of pleural metastasis of lung adenocarcinoma, which may be related to the overexpression of EGFR protein induced by -216G/T, R497K, and CA-SSR1 polymorphisms.

[The short-term outcomes of patients with acute leukemia treated by thalidomide].

OBJECTIVE: To study the efficacy of thalidomide for treating acute leukemia (AL). METHODS: 38 cases of AL were studied. 27 of the 38 cases receiving initial treatment were randomly divided into two groups, one treated with routine chemotherapy plus thalidomide (A) and the other with routine chemotherapy alone (B). 11 of the 38 were relapsing cases and all treated with routine chemotherapy plus thalidomide (C). Marrow microvascular density (MVD) and vascular endothelial growth factor (VEGF) were examined with factor-VIII related antigen/CD(34) immunohistological stain and ELISA respectively before and after the treatment. The initial dose of thalidomide was 200 mg/d and increased to 400 - 500 mg/d by increasing 50 mg/d weekly for 4 to 6 months. RESULTS: The complete remission (CR) rate and efficacy rate were 57.1%, 53.8% and 78.6%, 76.9% in the two groups respectively with no statistical difference. The CR rate and efficacy rate in the relapsing group were 27.3%, 54.5%. The relapsing rate 6 months after the treatment was low in the thalidomide group. MVD and VEGF were significantly different before and after the treatment (P < 0.001). There was a negative correlation between the MVD, VEGF and efficacy. The relapsing rate was low in cases with low MVD, VEGF. No particular side effects were observed in thalidomide group. CONCLUSION: Anti-angiogenesis may decrease relapse and maintain recovery state of AL patients. There are no severe side effects in the thalidomide group.

[Therapeutic effectiveness of thalidomide to multiple myeloma and its mechanism].

OBJECTIVE: To observe the effective mechanism and side effects of thalidomide to multiple myeloma (MM). METHODS: Ten cases of MM were studied, of which 3 were previously untreated and 7 refractory or relapsed. Bone marrow microvascular density (MVD) was detected by factor-VIII related antigen and CD(34) immunohistological staining and serum concentration of vascular endothelial growth factor (VEGF) before and after treatment was determined by ELISA. The initial dosage of thalidomide was 100 approximately 200 mg/d with a weekly escalation of 50 mg/d to 450 approximately 650 mg/d. The therapeutic effectiveness is classified into partial remission, improvement and uneffective according to the decrease of serum M protein and bone marrow myeloma cells. Anemia, renal function and blood electrolytes were also observed. RESULTS: Before treatment, MVD was 73.32 +/- 28.80 and 32.30 +/- 12.50 in MM and control group, respectively, (P < 0.01). MVD in MM group decreased to 56.12 +/- 19.34 after treatment, and was of significant difference (P < 0.05) as compared to the pretreatment value. However, there was still a significant difference as compared to control (56.12 +/- 19.34 vs 32.30 +/- 12.50, P < 0.01). The concentration of VEGF significantly decreased after treatment [from (178.23 +/- 26.56) ng/L to (78.48 +/- 19.98) ng/L, P < 0.01)]. The total effective rate was 70%. There were no serious side effects. CONCLUSION: MVD and VEGF concentration were decreased obviously by thalidomide treatment. The dosage of 450 approximately 650 mg/d might be effective in refractory or initial MM.