中频交变磁场照射后小鼠的行为学变化

目的:目前电磁辐射对生物体行为学方面的研究还很薄弱,设立不同磁场的强度和不同照射的周期,观察中频领域磁场照射对小鼠的自主活动和学习记忆的影响。方法:实验于2007-05-10/06-15在清华大学医学院和中国医学科学院药用植物研究所完成。①实验材料:磁场发生装置:中频交变磁场发生装置由清华大学工程物理系医学物理与工程研究所自主研发,可产生频率为40kHz,场强为28.8A/m,28.8kA/m的中频交变磁场。自主活动测试箱:中国医学科学院药用植物研究所提供,为一可封闭的金属箱,内置摄像头。4只黑色塑料测试桶分别置于箱子四角。水迷宫测试箱:中国医学科学院药用植物研究所提供。②实验动物及方法:将80只小鼠随机分为不同场强照射组和对照组。强磁场照射1组:11.6kA/m/40kHz,1h/d,连续照射7d。强磁场照射2组:11.6kA/m/40kHz,2h/d,连续照射7d。强磁场照射3组:11.6kA/m/40kHz,2h/d连续照射15d。弱磁场照射组:28.8kA/m/40kHz,2h/d,连续照射7d。对照组除了未放入磁场照射,其他条件与照射组一致。实验过程中对动物处置符合动物伦理学要求。③实验评估:观察其一般活动的改变,并采用自主活动测试箱和水迷宫测试箱进行测试,观察各组小鼠的自主活动和学习记忆的改变。结果:①一般行为观察:与对照组小鼠对比,经过中频交变磁场照射过的各组小鼠活跃度减低,毛色较差。强磁场照射3组(145G,2h/d,连续15d)于第11天和13天分别死亡1只。②自主活动检测结果:强磁场照射2,3组小鼠的运动路程、运动速度、运动时间明显低于对照组(P<0.05)。③水迷宫测试结果:在学习记忆检测阶段撤掉平台,发现各组动物2min内穿越平台原来所在象限的次数没有明显差别(P>0.05)。结论:中频交变磁场照射会给小鼠的自发活动造成一定影响,对学习记忆没有影响。     

Titanium elastic nailing in femoral diaphyseal fractures of children in 6-16 years of age

Background:

Management of femoral diaphyseal fractures in the age group of 6-16 years is controversial. There has been a resurgence worldwide for operative fixation.

Materials and Methods:

Twenty-two children (18 boys, 4 girls) aged 6-16 years with recent (> 3 days) femoral diaphyseal fractures (20 closed, 2 open) were stabilized with Titanium Elastic Nail (TEN). These fractures were in proximal third (n=3), middle third (n=15) and in the distal third (n=4) 17 patients underwent surgery within seven days of their injury. The results were evaluated using Flynn''s scoring criteria. Statistical analysis was done using Fischer''s exact test.

Results:

All 22 patients were available for evaluation after a mean of 26 months (14-36 months) of followup. Radiological union in all cases were achieved in a mean time of 8.7 weeks. Full weight bearing was possible in a mean time of 8.8 weeks. Mean duration of hospital stay was 9.8 days. The results were excellent in 13 patients (59.0%), successful in six (27.2%) and poor in three patients (13.6%). All patients had early return to school.

Conclusion:

Intramedullary fixation titanium elastic nailing is an effective treatment of diaphyseal fractures of the femur in properly selected patients of the 6-16 years age group.     

Anterior compartment pressure measurement in closed fractures of leg

Background:

Compartment syndrome is a potentially devastating condition. Increased intracompartmental pressure has been incriminated as the primary pathogenic factor in compartment syndrome. The purpose of this prospective study was to monitor the anterior compartmental pressure and differential pressure to minimize the incidence of acute compartment syndrome.

Materials and Methods:

Seventy-five consecutive cases of closed fractures of leg presenting within six hours of injury were taken for measurement of anterior compartment pressure at the level of fracture and at 5 cm and 10 cm away from the fracture site, using the Whitesides'' infusion technique. A differential pressure of less than 30 mm Hg was taken as the criterion for diagnosis of compartment syndrome.

Results:

Two patients (2.67%) developed acute compartment syndrome. The mean anterior compartment pressures were highest at the level of the fracture and went on decreasing as we went away from the fracture site, which was found to be statistically significant (P < 0.001).

Conclusion:

Compartment pressure measurement is the most reliable and objective method for early diagnosis of compartment syndrome. Whitesides'' infusion technique is a relatively easy and inexpensive method to come to a diagnosis of compartment syndrome in a developing country like India. Differential pressure is more reliable than absolute pressure in predicting the development of an impending compartment syndrome.     

Effects of gene delivery on collateral development in chronic hypoperfusion: diverse effects of angiopoietin-1 versus vascular endothelial growth factor

OBJECTIVES: The aim of this research was to test the effects of vascular endothelial growth factor (VEGF)/angiopoietin-1 (Ang-1) on adult hypoperfused tissues. BACKGROUND: Angiopoietin-1 and VEGF act separately and synergistically in vascular development during embryogenesis. However, little is known regarding their relative roles in collateral development after chronic arterial obstruction and tissue ischemia in the adult. METHODS: Central and caudal ear arteries of 32 rabbits were ligated to induce ischemia. At two months, when flow was about 65% of pre-ligation values, we injected intradermally 10(9) plaque-forming unit adenovirus with the following transgenes: Ang-1, VEGF, or a combination of both. Ear perfusion was followed up for four weeks, and vessel leakage was assessed by Evens Blue test. RESULTS: Before injection, flow was 65% of baseline, and endogenous VEGF levels in ischemic tissue were increased. Adenovirus-encoding VEGF gene (Ad.VEGF) at one week caused a visible inflammatory response associated with a 24% flow increase (p = 0.018). Adenovirus-encoding Ang-1 gene (Ad.Ang-1) increased flow 22% (p = 0.004) with no visible inflammation; Ad.VEGF caused three times as much vessel leakage as Ad.Ang-1 (142.5 +/- 38 vs. 49.5 +/- 9.8 ng Evens Blue/mg tissue; p < 0.001). However, at four weeks, compared with baseline, VEGF decreased flow 18% (p = 0.004), whereas Ang-1 increased tissue perfusion 26% (p < 0.001). This effect was abolished when Ad.Ang-1 was injected with soluble VEGF receptor [Ad.Flt(1-3)-Fc], which blocks VEGF-dependent signaling. Exogenous Ang-1 did not increase perfusion in a normally perfused ear, in which endogenous VEGF is not expressed. CONCLUSIONS: Exogenous Ang-1 enhances perfusion in hypoperfused tissues only in the presence of increased levels of endogenous VEGF. Overexpression of VEGF, however, after causing an inflammatory response, does not improve collateral blood flow.     

Targeting the A2A adenosine receptor counteracts immunosuppression in vivo in a mouse model of chronic lymphocytic leukemia

Tumor immunosuppression is a major cause of treatment failure and disease relapse, both in solid tumors and leukemia. Local hypoxia is among the conditions that cause immunosuppression, acting at least in part through the upregulation of extracellular adenosine levels, which potently suppress T-cell responses and skew macrophages towards an M2 phenotype. Hence, there is intense investigation to identify drugs that target this axis. By using the TCL1 adoptive transfer chronic lymphocytic leukemia mouse model, we show that adenosine production and signaling are upregulated in the hypoxic lymphoid niches, where intense colonization of leukemic cells occurs. This leads to a progressive remodeling of the immune system towards tolerance, with expansion of T regulatory cells (Treg), loss of CD8⁺ T-cell cytotoxicity and differentiation of murine macrophages towards the patrolling (M2-like) subset. In vivo administration of {"type":"entrez-protein","attrs":{"text":"SCH58261","term_id":"1052882304"}}SCH58261, an inhibitor of the A2A adenosine receptor, re-awakens T-cell responses, while limiting Treg expansion, and re-polarizes monocytes towards the inflammatory (M1-like) phenotype. These results show for the first time the in vivo contribution of adenosine signaling to immune tolerance in chronic lymphocytic leukemia, and the translational implication of drugs interrupting this pathway. Although the effects of {"type":"entrez-protein","attrs":{"text":"SCH58261","term_id":"1052882304"}}SCH58261 on leukemic cells are limited, interfering with adenosine signaling may represent an appealing strategy for combination-based therapeutic approaches.     

Do empowerment strategies facilitate knowledge and behavioral change? The impact of family health advocacy on health outcomes

This study evaluates the impact of a Family Health Advocacy (FHA) intervention on 46 African American women ages 13 to 35 living in a rural southern community. FHA utilizes empowerment strategies to provide education and social support to reduce risk factors for poor pregnancy outcomes. Use of a paired t test demonstrated a statistically significant difference between pretest and posttest scores in the acquisition of knowledge of safer sex practices, alcohol consumption, early prenatal care, maternal infection, and nutrition. Behavioral change was not realized in the areas of nutrition or behaviors that cause risk of maternal infection. Social workers can influence behavioral change for at-risk populations by addressing microlevel barriers such as education and resources and macrolevel barriers such as advocacy for expanded health and social services.     

Cell therapy in myocardial infarction.

Heart failure is associated with a high rate of morbidity and mortality. In some patients, current treatment modalities may not be adequate to prevent myocardial remodeling, which leads to exacerbation of the disease. Cell therapy is based on the premise of replacing damaged myocardium with functional tissues. Multiple forms of stem cells, including bone marrow-derived stem cells and skeletal myoblasts, have been investigated using several delivery routes of administration. Different mechanisms have been proposed to explain the beneficial effects of cell-based therapy. These include cell transdifferentiation, cell fusion, and release of paracrine growth factors. The beneficial effects of cell therapy may involve multiple mechanisms. The encouraging results of early clinical cell therapy studies have not been sustained by subsequent robust studies. These findings suggest that many unanswered questions need to be addressed before cell therapy becomes an acceptable adjunctive treatment for heart failure.     

Differential effect of phorbol esters and interleukin-3 on protein kinase C isoform content and kinase activity in the FDC-P1 cell line

FD/PMA is a subclone of the interleukin-3 (IL-3)-dependent, FDC-P1 cell line, which proliferates in response to either 12-O- tetradecanoylphorbol-13 acetate (PMA) or IL-3. While several endogenous substrates were phosphorylated in response to protein kinase C (PKC) activation in FDC-P1, phospholipid-dependent phosphorylation in the FD/PMA grown in PMA was not observed. Basal, phosphatidylserine- independent, and diolein-independent phosphorylation of cytosolic substrates with molecular weights of 17, 52, 57, and 105 Kd were enhanced in FD/PMA cells grown in PMA as compared with FDC-P1 cells cultured in IL-3. Phosphorylation of a 105-Kd substrate was enhanced in the particulate fraction of FD/PMA cells maintained in PMA. The 17-Kd substrate in FD/PMA cells comigrated with a substrate phosphorylated in a PKC-dependent manner in FDC-P1 cells. Phosphorylation of the 52- and 57-Kd substrates, but not of the 17-Kd substrate, was inhibited by H-7 and staurosporine. A portion of the PMA-induced cytosolic kinase activity coeluted with PKC on diethyl aminoethyl chromatography. While FD/PMA cells cultured in PMA contained negligible PKC-dependent phosphorylation of endogenous substrates or histone, alpha and epsilon PKC isoforms were detected by Western blot analysis. PKC phosphotransferase activity was observed in FD/PMA cells grown in PMA when peptides corresponding to residues 720 to 737 of PKC-epsilon or residues 4 to 14 of myelin basic protein were used as substrates. These data indicate that maintenance of FD/PMA cells in PMA stimulates proliferation and markedly alters PKC substrate specificity. Generation of at least two phospholipid-independent kinases occurs in PMA-treated cells.