Effect of Concentric Isokinetic Knee Strength Training on Gait, Balance and Quality of Life in Chronic Stroke Patients

OBJECTIVE: To determine the effects of concentric isokinetic knee strength training on gait, balance and health related quality of life in chronic stroke patients. METHOD: Fifteen patients with chronic stroke participated in this study. All subjects were community ambulators and trained using Biodex System 3 isokinetic dynamometer three times a week for 6 weeks. The training program consisted of concentric isokinetic strengthening of both knee extensors and flexors. Peak torque of knee extensors and flexors, walking performance (temporospatial parameter of gait and stair climbing time), balance (overall balance index, anterior/ posterior index and medial/lateral index) and health-related quality of life measure (36-item short form health survey, SF-36) were evaluated before and after training period. RESULTS: Muscle strength improved significantly after training. Walking speed, stride length and stair climbing time improved significantly after training. Balance indices and SF-36 score also improved significantly after training. CONCLUSION: Gain in muscle strength appeared to be transferred to functional improvement. Therefore, isokinetic resistance training program would be one of the effective rehabilitation programs for chronic stroke survivors. Further investigations are required for long-term effect and development of strength-specific resistance training program.

Interactions between Estradiol-17beta-BSA and Calcitropic Hormones in Ca2+ Uptake in Renal Proximal Tubule Cells

The aim of the present study was to investigate the interaction of estradiol-17beta-bovine serum albumin (E2-BSA) and calcitropic hormones, such as parathyroid hormone, calcitonin, and vitamin D, in regulation of Ca2+ uptake in primary cultured renal proximal tubule cells. Statistically significant increase in Ca2+ uptake was found from 2 hours after E2-BSA (10(-9) M) treatment, while estradiol-17beta (10(-9) M) did not affect. Treatment of the cells with E2-BSA (10(-9) M) together with parathyroid hormone (PTH) (10(-8) M), vitamin D (10(-8) M), or calcitonin (10(-8) M) significantly stimulated Ca2+ uptake by 32.50%, 29.30%, or 27.75%, respectively, compared with the control. However, calcitropic hormones did not exhibit any synergistic effect on the E2-BSA-induced stimulation. E2-BSA significantly increased cAMP generation and PKC activity. The stimulatory effect of cotreatment of E2-BSA and PTH or vitamin D was blocked by SQ22536 (an adenylate cyclase inhibitor) and staurosporine (a PKC inhibitor), but the effect of cotreatment of E2-BSA and calcitonin was not blocked. Furthermore, 8-Br-cAMP and TPA (an artificial PKC promoter) increased Ca2+ uptake by 25.51% and 16.47%, respectively, compared with the control. In conclusion, E2-BSA combined with calcitropic hormones regulated Ca2+ uptake partially via cAMP and PKC-dependent mechanisms in renal proximal tubule cells.

Ultrasonographic study on the masseter muscle thickness of adult Korean / 대한치과교정학회지

It is widely accepted that the shape and structure of bone are closely related to the activity of attached muscle. Numerous clinical and animal experimental studies indicated the significant effects of masticatory muscle function on maxillofacial morphology. Recently, the development of ultrasonography has spread throughout different fields of medicine. In the clinical examinations, ultrasonography is a convenient, inexpensive technique to apply with accurate and reliable results. The aim of this study is to assess the thickness of the masseter muscle and its correlation to maxillofacial skeleton by examining 35 male and 15 female dental students at Kangnung National University. The masseter muscle thickness of the subjects were measured by ultrasonographic scanning with a 7.5MHz linear probe, and their maxillofacial morphology were investigated by lateral cephalometric radiographs. The relationship between the masseter muscle thickness and maxillofacial morphology of normal adult was statistically analyzed, and the following results were obtained. 1. The average thickness of male masseter muscle was 13.8+/-1.71mm in the relaxed state and 14.8+/-1.77mm at maximal clenching state, while that of female was 11.6+/-1.58mm and 12.4+/-1.47mm, respectively. Ethnic difference in thickness of the masseter muscle and maxillofacial skeleton was found when the results of many researchers were compared with those of this study. 2. The thickness of the masseter muscle in both sexes increased significantly at maximal clenching state than in relaxed state(P<0.05). 3. The masseter muscle thickness of male was greater than that of female both in the relaxed state and maximal clenching states(P<0.05). 4. In males, the thickness of the masseter muscle was negatively correlated with the mandibular plane angle and positively correlated with the mandibular ramus height and anterior cranial base length(P<0.05). It may suggest that the male with thicker masseter muscle has smaller facial divergence. 5. No significant correlation was found between the masseter muscle thickness and maxillofacial morphology in females(P<0.05).

The roles of arachidonic acid and calcium in the angiotensin II-induced inhibition of Na+ uptake in renal proximal tubule cells

Angiotensin II (ANG II) has a biphasic effect on Na+ transport in proximal tubule: low doses of ANG II increase the Na+ transport, whereas high doses of ANG II inhibit it. However, the mechanisms of high dose ANG II-induced inhibition on Na+ uptake are poorly understood. Thus the aim of the present study was to investigate signal transduction pathways involved in the ANG II-induced inhibition of Na+ uptake in the primary cultured rabbit renal proximal tubule cells (PTCs) in hormonally defined serum-free medium. ANG II (10-9 M)-induced inhibition of Na+ uptake was blocked by losartan (10-8 M, AT1 antagonist), but not by PD123319 (10-8 M, AT2 antagonist) (P < 0.05). ANG II-induced inhibition of Na+ uptake was also completely abolished by neomycin (10-4 M, PLC inhibitor), W-7 (10-4 M, calmodulin antagonist), and AACOCF3 (10-6 M, PLA2 inhibitor) (P < 0.05). ANG II significantly increased (3H)arachidonic acid (AA) release compared to control. The ANG II-induced (3H)AA release was blocked by losartan, AACOCF3, neomycin, and W-7, but not by PD123319. ANG II-induced (3H)AA release in the presence of extracellular Ca2+ was greater than in Ca2+-free medium, and it was partially blocked by TMB-8 (10-4 M, intracelluar Ca2+ mobilization blocker). However, in the absence of extracellular Ca2+, it was completely blocked by TMB-8. In addition, econazole (10-6 M, cytochrome P-450 monooxygenase inhibitor) and indomethacin (10-6 M, cyclooxygenase inhibitor) blocked ANG II-induced inhibition of Na+ uptake, but NGDA (10-6 M, lipoxygenase inhibitor) did not affect it. In conclusion, PLA2-mediated AA release is involved in ANG II-induced inhibition of Na+ uptake and is modulated by (Ca2+)i in the PTCs.

Interaction of 17beta-estradiol with EGF and IGF-I on proliferation and Pi uptake in primary cultured rabbit renal proximal tubular cells

The most significant direct role of estrogen in vivo is its ability to elicit receptor-mediated cellular proliferation in mammalian target tissues. However, the mechanism by which exogenously added estrogen causes the neoplastic transformation of renal cortical cells is yet to be uncovered. The present study was designed to evaluate interaction of 17beta-estradiol (E2) with epidermal growth factor (EGF) and insulin-like growth factor-I (IGF-I) on proliferation and Pi uptake in primary cultured rabbit renal proximal tubular cells in phenol red-free, hormonally defined-medium. (3H)-thymidine incorporation increased markedly by about 133% and 141% more in the presence of 10-9 and 10-6 M E2, respectively, than that of control. Cell count was 162% and 143% greater in the presence of 10-9 and 10-6 M E2, respectively, compared with control. Among all time points examined, there was an increase in (3H)-thymidine incorporation in the presence of 10-9 M E2 at day 9 or 13, respectively. However, E2 (10-9 M) significantly drove up cell count to 160% of that of control at day 13, while it had a slight but statistically insignificant effect at day 9. E2-induced stimulation of (3H)-thymidine incorporation was completely reversed by E2 antagonists (progesterone or tamoxifen). E2 (10-9 M) or EGF (10-8 M) significantly stimulated (3H)-thymidine incorporation by 144% and 154% of control. E2 plus EGF was synergistic on (3H)-thymidine incorporation (204% of control), while E2 plus IGF-I showed a slight but no significant synergistic effect. Cell number also displayed similar pattern. E2 (10-9 M) significantly stimulated Pi uptake to 134% of control. E2-induced stimulation of Pi uptake was partially reversed by E2 antagonists. EGF or IGF-I (10-8 M) significantly also increased Pi uptake to 132% or 129% of control. E2 plus EGF had synergistic effect on Pi uptake, while E2 plus IGF-I did not. In conclusion, E2 may act not only directly interaction with its receptors but also indirectly as a modulator of EGF in proliferation and Pi uptake of primary cultured rabbit renal proximal tubular cells.