Effects of Upper Body Eccentric versus Concentric Strength Training and Detraining on Maximal Force,Muscle Activation,Hypertrophy and Serum Hormones in Women

Effects of eccentric (ECC) versus concentric (CON) strength training of the upper body performed twice a week for 10 weeks followed by detraining for five weeks on maximal force, muscle activation, muscle mass and serum hormone concentrations were investigated in young women (n = 11 and n = 12). One-repetition bench press (1RM), maximal isometric force and surface electromyography (EMG) of triceps brachii (TB), anterior deltoid (AD) and pectoralis major (PM), cross-sectional area (CSA) of TB (Long (LoH) and Lateral Head (LaH)) and thickness of PM, as well as serum concentrations of free testosterone, cortisol, follicle-stimulating hormone, estradiol and sex hormone-binding globulin were measured. ECC and CON training led to increases of 17.2 ± 11.3% (p < 0.001) and 13.1 ± 5.7% (p < 0.001) in 1RM followed by decreases of -6.6 ± 3.6% (p < 0.01) and -8.0 ± 4.5% (p < 0.001) during detraining, respectively. Isometric force increased in ECC by 11.4 ± 9.6 % (p < 0.05) from week 5 to 10, while the change in CON by 3.9±6.8% was not significant and a between group difference was noted (p < 0.05). Maximal total integrated EMG of trained muscles increased only in the whole subject group (p < 0.05). CSA of TB (LoH) increased in ECC by 8.7 ± 8.0% (p < 0.001) and in CON by 3.4 ± 1.6% (p < 0.01) and differed between groups (p < 0.05), and CSA of TB (LaH) in ECC by 15.7 ± 8.0% (p < 0.001) and CON by 9.7 ± 6.6% (p < 0.001). PM thickness increased in ECC by 17.7 ± 10.9% (p < 0.001) and CON by 14.0 ± 5.9% (p < 0.001). Total muscle sum value (LoH + LaH + PM) increased in ECC by 12.4 ± 6.9% (p < 0.001) and in CON by 7.1 ± 2.9% (p < 0.001) differing between groups (p < 0.05) and decreased during detraining in ECC by -6.5 ± 4.3% (p < 0.001) and CON by -6.1 ± 2.8% (p < 0.001). The post detraining combined sum value of CSA and thickness was in ECC higher (p < 0.05) than at pre training. No changes were detected in serum hormone concentrations, but baseline free testosterone levels in the ECC and CON group combined correlated with changes in 1RM (r = 0.520, p < 0.016) during training. Large neuromuscular adaptations of the upper body occurred in women during ECC, and CON training in 10 weeks. Isometric force increased only in response to ECC, and total muscle sum value increased more during ECC than CON training. However, no changes occurred in serum hormones, but individual serum-free testosterone baseline concentrations correlated with changes in 1RM during strength training in the entire group. Both groups showed significant decreases in neuromuscular performance and muscle mass during detraining, while post detraining muscle sum value was only in ECC significantly higher than at pre training. Key points

• Maximal eccentric and concentric strength training in women for 10 weeks (only twice a week) led to great gains in dynamic strength of upper body.
• Upper body muscle mass increased more after eccentric than concentric strength training.
• During detraining for 5 weeks both groups showed decreases in strength and muscle mass.
• However, post-detraining combined sum muscle mass value was only in ECC higher than at pre-training.

Key words: Muscle force, training, EMG, mass, females, testosterone     

选择性头部降温对胎羊缺血性脑损伤纹状体神经元凋亡和星形胶质细胞增殖的影响

目的研究选择性头部降温对缺血性脑损伤胎羊纹状体神经元凋亡和星形胶质细胞增殖的影响。方法胎羊于妊娠117~124d时通过双侧颈动脉阻塞30min造成双侧脑缺血损伤,损伤后将胎羊随机分为:损伤组(n=10)、2h低温组(损伤后2h开始亚低温治疗,n=7)和6h低温组(损伤后6h开始亚低温治疗,n=8),另设正常对照组(n=5)。通过冷循环水进行选择性头部降温,取脑组织用免疫组化法检测胎羊纹状体caspase-3(半胱天冬氨酸酶-3),GFAP(胶质纤维酸性蛋白)和PCNA(增殖细胞核抗原)的表达。结果①纹状体神经元凋亡:正常对照组中,caspase-3表达极少(11.00±13.77),损伤组caspase-3免疫阳性细胞为177.70±48.69,明显增加(P=0.000),损伤后2h治疗组(54.14±39.44,P=0.000)和损伤后6h治疗组(122.43±52.36,P=0.017)均能减少caspase-3免疫阳性细胞。②纹状体星形胶质细胞增殖:与正常对照组(163.40±21.98)相比,缺血性脑损伤组的GFAP免疫阳性细胞明显增多(433.25±66.69,P=0.000),损伤后2h开始亚低温治疗(219.50±35.31,P=0.000)和损伤后6h开始亚低温治疗(272.50±86.20,P=0.000)均能减少GFAP免疫阳性细胞。③纹状体PCNA阳性细胞的表达:在正常对照组中,PCNA免疫阳性细胞较少,为153.40±12.46,缺血性脑损伤组的PCNA免疫阳性细胞明显增多(353.70±45.60,P=0.000),损伤后2h开始亚低温治疗(187.14±26.26,P=0.000)和损伤后6h开始亚低温治疗(230.25±67.46,P=0.000)均能减少PCNA免疫阳性细胞。结论亚低温可以抑制纹状体神经元的凋亡和星形胶质细胞的增殖,该作用可能为选择性头部降温的脑保护作用机制之一。     

Minactivin expression in human monocyte and macrophage populations

Adherent monolayer cultures of human blood monocytes, peritoneal macrophages, bone marrow macrophages, and colonic mucosa macrophages were examined for their ability to produce and secrete minactivin, a specific inactivator of urokinase-type plasminogen activator. All except colonic mucosa macrophages produced and secreted appreciable amounts of minactivin, but only blood monocytes were stimulated by muramyl dipeptide (adjuvant peptide) to increase production. The minactivin from each of these populations could be shown to preferentially inhibit urokinase-type plasminogen activator and not trypsin, plasmin, or "tissue"-type plasminogen activator (HPA66). A plasminogen-activating enzyme present in monocyte cultures appeared unaffected by the presence of minactivin and could be shown to be regulated independently by dexamethasone.     

恶性肿瘤靶向给药的临床应用

恶性肿瘤靶向给药是指利用具有一定肿瘤靶向性的导向分子（载体）携带治疗肿瘤的药物,在肿瘤局部选择性杀伤肿瘤细胞（及转移的肿瘤细胞）,以避免药物的全身毒副作用,提高疗效的一种治疗方法．由于抗癌药物在杀伤肿瘤细胞的同时也杀伤正常细胞,增加了全身的毒副作用．因此,近几年来,对恶性肿瘤靶向治疗的研究突飞猛进,发展了人源性抗HER-2mAb、依西美坦、放射性核素、     

"Stem cell" origin of the hematopoietic defect in dyskeratosis congenita

We have used the long-term bone marrow culture (LTBMC) system to analyze hematopoiesis in three patients with dyskeratosis congenita (DC), two of whom had aplastic anemia, and the third had a normal blood count (apart from mild macrocytosis) and normal BM cellularity. Hematopoiesis was severely defective in all three patients, as measured by a low incidence of colony-forming cells and a low level of hematopoiesis in LTBMC. The function of the marrow stroma was normal in its ability to support the growth of hematopoietic progenitors from normal marrows seeded onto them in all three cases, but the generation of hematopoietic progenitors from patients marrow cells inoculated onto normal stromas was reduced, thus suggesting the defect to be of stem cell origin. The parents and unaffected brother of one of the families have also been studied in LTBMC and all showed normal hematopoietic and stromal cell function. From this study we speculate that there are some similarities between DC and the defect in the W/Wv mouse.     

Effectiveness of diclofenac versus paracetamol in knee osteoarthritis: a randomised controlled trial in primary care

Background

The effectiveness of diclofenac versus paracetamol in primary care patients with pain caused by knee osteoarthritis is unclear.

Aim

To assess the effectiveness of diclofenac compared with paracetamol over a period of 2, 4, and 12 weeks in patients with knee osteoarthritis.

Design and setting

Randomised controlled trial in general practice.

Method

There were 104 patients included in the study, they were aged ≥45 years consulting their GP with knee pain caused by knee osteoarthritis. Patients were randomly allocated to diclofenac (n = 52) or paracetamol (n = 52) for at least 2 weeks. Primary outcomes were daily knee pain severity, and knee pain and function measured with the Knee Injury and Osteoarthritis Outcome Score (KOOS).

Results

Over a period of 2- and 4-weeks follow-up, no significant difference in daily knee pain was found between the patient groups: estimated differences of 0.5 (95% CI = −0.2 to 1.3) and −0.2 (95% CI = −1.0 to 0.7), respectively. Over the 12-weeks follow-up, no significant differences were found between both groups for KOOS pain: estimated difference of −2.8 (95% CI = −10.7 to 5.1) and KOOS function of −2.7 (−10.6 to 5.0).

Conclusion

Over a period of 2- and 4-weeks follow-up no significant difference in daily measured knee pain severity was found between primary care patients with knee osteoarthritis taking paracetamol or diclofenac. Also, over a period of 12-weeks follow-up no significant differences were found regarding KOOS pain and KOOS function between both groups. Patients more frequently reported minor adverse events after taking diclofenac (64%) than paracetamol (46%).     

Age-dependent neurological phenotypes in a mouse model of PRRT2-related diseases

Paroxysmal kinesigenic dyskinesia is an episodic movement disorder caused by dominant mutations in the proline-rich transmembrane protein PRRT2, with onset in childhood and typically with improvement or resolution by middle age. Mutations in the same gene may also cause benign infantile seizures, which begin in the first year of life and typically remit by the age of 2 years. Many details of PRRT2 function at the synapse, and the effects of mutations on neuronal excitability in the pathophysiology of epilepsy and dyskinesia, have emerged through the work of several groups over the last decade. However, the age dependence of the phenotypes has not been explored in detail in transgenic models. Here, we report our findings in heterozygous and homozygous Prrt2 knockout mice that recapitulate the age dependence of dyskinesia seen in the human disease. We show that Prrt2 deletion reduces the levels of synaptic proteins in a dose-dependent manner that is most pronounced at postnatal day 5 (P5), attenuates at P60, and disappears by P180. In a test for foot slippage while crossing a balance beam, transient loss of coordination was most pronounced at P60 and less prominent at age extremes. Slower traverse time was noted in homozygous knockout mice only, consistent with the ataxia seen in rare individuals with biallelic loss of function mutations in Prrt2. We thus identify three age-dependent phenotypic windows in the mouse model, which recapitulate the pattern seen in humans with PRRT2-related diseases.