A survey of the literature on the treatment of ruptures of deltoid ligament associated with fracture of distal part of fibula is controversial. Some authors advocated surgical repair of the ruptured deltoid ligament based on the theoretical consideration, while others advocated non-operative treatment based on the clinical consideration. We studied the results in forty-five patients who were treated for disruption of the deltoid ligament and a distal fibular fracture. The length of follow-up in our series was twelve to twenty-four months, with an average of fifteen months. When the fibular fracture was adequately reduced and medial clear space was returned to its normal width, the 91 percents both of patients of being treated with repair of deltoid ligament and patients of being treated without repair had a good or excellent results.
Clinical Study ; Fibula ; Follow-Up Studies ; Humans ; Ligaments ; Rupture

Angiotensin II (Ang II) induces the pathological process of vascular structures, including renal glomeruli by hemodynamic and nonhemodynamic direct effects. In kidneys, Ang II plays an important role in the development of proteinuria by the modification of podocyte molecules. We have previously found that Ang II suppressed podocyte AMP-activated protein kinase (AMPK) via Ang II type 1 receptor and MAPK signaling pathway. In the present study, we investigated the roles of AMPK on the changes of p130Cas of podocyte by Ang II. We cultured mouse podocytes and treated them with various concentrations of Ang II and AMPK-modulating agents and analyzed the changes of p130Cas by confocal imaging and western blotting. In immunofluorescence study, Ang II decreased the intensity of p130Cas and changed its localization from peripheral cytoplasm into peri-nuclear areas in a concentrated pattern in podocytes. Ang II also reduced the amount of p130Cas in time and dose-sensitive manners. AMPK activators, metformin and AICAR, restored the suppressed and mal-localized p130Cas significantly, whereas, compound C, an AMPK inhibitor, further aggravated the changes of p130Cas. Losartan, an Ang II type 1 receptor antagonist, recovered the abnormal changes of p130Cas suppressed by Ang II. These results suggest that Ang II induces the relocalization and suppression of podocyte p130Cas by the suppression of AMPK via Ang II type 1 receptor, which would contribute to Ang II-induced podocyte injury.
AMP-Activated Protein Kinases/antagonists & inhibitors/chemistry/*metabolism ; Aminoimidazole Carboxamide/analogs & derivatives/pharmacology ; Angiotensin II/*pharmacology ; Angiotensin II Type 1 Receptor Blockers/pharmacology ; Animals ; Blotting, Western ; Cell Line ; Cell Nucleus/metabolism ; Crk-Associated Substrate Protein/*metabolism ; Cytoplasm/metabolism ; Focal Adhesion Kinase 1/metabolism ; Losartan/pharmacology ; Metformin/pharmacology ; Mice ; Microscopy, Confocal ; Podocytes/cytology/drug effects/metabolism ; Protein Kinase Inhibitors/*pharmacology ; Ribonucleotides/pharmacology ; Signal Transduction/*drug effects

Pressure overload diseases, such as valvular stenosis and systemic hypertension, manifest morphologically in patients as cardiac concentric hypertrophy. Prevention of cardiac remodeling due to increased pressure overload is important to reduce morbidity and mortality. Epigallocatechin-3 gallate (EGCG) is a major bioactive polyphenol present in green tea which has been found to be a nitric oxide-mediated vasorelaxant and to be cardioprotective in myocardial ischemia-reperfusion injury. Therefore, we investigated whether EGCG supplementation could reduce in vivo pressure overloadmediated cardiac hypertrophy. Cardiac hypertrophy was induced by suprarenal transverse abdominal aortic constriction (AC) in rats. Three weeks after AC surgery, heart to body weight ratio increased in the AC group by 34% compared to the sham group. EGCG administration suppressed the load-induced increase in heart weight by 69%. Attenuation of cardiac hypertrophy by EGCG was associated with attenuation of the increase in myocyte cell size and fibrosis induced by aortic constriction. Despite abolition of hypertrophy by EGCG, transstenotic pressure gradients did not change. Echocardiogram revealed that increased left ventricular systolic dimensions and deteriorated systolic function were relieved by EGCG. These results suggest that EGCG prevents the development of left ventricular concentric hypertrophy by pressure overload and may be a useful therapeutic modality to prevent cardiac remodeling in patients with pressure overload myocardial diseases.
Animals ; Blood Pressure/drug effects ; Cardiomegaly/pathology/*prevention & control ; Catechin/*analogs & derivatives/pharmacology ; Echocardiography ; Heart Rate/drug effects ; Histocytochemistry ; Male ; Organ Size/drug effects ; Rats ; Rats, Sprague-Dawley

OBJECTIVE: The lateral extracavitary approach(LECA) to the thoracolumbar spine is known as one of procedure which allows not only direct vision of pathologic lesion, but also ventral decompression, and dorsal fixation of the spine through the same incision. However, some drawbacks of LECA, including the technically- demanding, time-consuming, unfamiliar surgical anatomy and excessive blood loss, make surgeons to hesitate to use this approach. This study is to provide the surgical anatomy of LECA using cadavers, for detailed informations when LECA is considered for the surgery. METHODS: We performed the 10 cadaveric studies, 7 male and 3 female, and careful dissection was carried out on right side of thoracolumbar region, except one for thoracic region. The photographs with micro-lens were taken to depict the close-up findings and for demonstrating detailed anatomy. RESULTS: The photographs and hand-drawings demonstrated the relationships among the musculature, segmental vessels and nerve roots seen during each dissection plane. The lateral branches of dorsal rami of spinal nerve and the transverse process were confirmed to be the most important landmark of this approach. CONCLUSION: We concluded that detailed anatomical findings for LECA through this step-by-step dissection would be useful during operative intervention to reduce the intraoperative complications in LECA.
Cadaver* ; Decompression ; Female ; Humans ; Intraoperative Complications ; Male ; Spinal Nerves ; Spine*

BACKGROUND: It is important for the health care provider, particularly primary care physicians as gatekeepers of health care, to understand the social interests and needs toward health care. This study was done to find ways to deal with public opinion by analyzing the contributions of health care in the newspapers. METHODS: Two hundred twenty four contributions about health care were sorted out in the three national newspapers during one calendar year from January to December, 1996. These contributions were coded by themes and subjects according the content analysis and qualitative text interpretation. RESULTS: The contributions were classified into three categories, medical insurance, and hospital services, and health care policies. Forty four contributions of medical insurance category were coded into 5 themes and 18 subject. Fifty eight contributions of hospital services category were coded into 3 themes and 31 subjects. One hundred twenty two contributions of medical insurance category were coded into 8 themes and 32 subjects. The themes and subjects were listed and findings were described qualitatively. The characteristics of public opinions about health care were diversity, conflicting interests, plentifulness of complaints and discontent, and finally, infrequency of alternative proposals for problem solving. How to deal with public opinions were discussed. CONCLUSIONS: We can recognize the public attitude of health care and complaints of patients and consumers of health care by analyzing the contributions in the newspapers. These data can be used to develop ways of primary care physicians to deal with patients' needs.
Delivery of Health Care* ; Health Personnel ; Humans ; Insurance ; Periodicals* ; Patient Education as Topic ; Physicians, Primary Care ; Problem Solving ; Public Opinion

An early feature of diabetic nephropathy is the alteration of the glomerular basement membrane (GBM), which may result in microalbuminuria, subsequent macroproteinuria, and eventual chronic renal failure. Although type IV collagen is the main component of thickened GBM in diabetic nephropathy, cellular metabolism of each alpha chains of type IV collagen has not been well studied. To investigate the regulation of alpha(IV) chains in diabetic conditions, we examined whether glucose and advanced glycosylation endproduct (AGE) regulate the metabolism of each alpha(IV) chains in the diabetic tissue and glomerular epithelial cells (GEpC). Glomerular collagen alpha3(IV) and alpha5(IV) chains protein were higher and more intense in immunofluorescence staining according to diabetic durations compared to controls. In vitro, mainly high glucose and partly AGE usually increased total collagen protein of GEpC by [3H]-proline incorporation assay and each alpha(IV) chain proteins including alpha1(IV), alpha3(IV), and alpha5(IV) in time-dependent and subchain-specific manners. However, the changes of each alpha(IV) chains mRNA expression was not well correlated to the those of each chain proteins. The present findings suggest that the metabolism of individual alpha(IV) chains of GBM is differentially regulated in diabetic conditions and those changes might be induced not only by transcriptional level but also by post-translational modifications.
Animals ; Cells, Cultured ; Collagen Type IV/genetics/*metabolism/physiology ; Diabetic Nephropathies/*metabolism ; Epithelial Cells/*metabolism ; Glomerular Basement Membrane/metabolism ; Glucose/metabolism ; Glycosylation End Products, Advanced/metabolism ; Male ; Podocytes/*metabolism ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley

AMP-activated protein kinase (AMPK) protects various tissues and cells from ischemic insults and is activated by many stimuli including mechanical stretch. Therefore, this study investigated if the activation of AMPK is involved in stretch-induced cardioprotection (SIC). Intraventricular balloon and aorto-caval shunt (ACS) were used to stretch rat hearts ex vivo and in vivo, respectively. Stretch preconditioning reduced myocardial infarct induced by ischemia-reperfusion (I/R) and improved post-ischemic functional recovery. Phosphorylation of AMPK and its downstream substrate, acetyl-CoA carboxylase (ACC) were increased by mechanical stretch and ACC phosphorylation was completely blocked by the AMPK inhibitor, Compound C. AMPK activator (AICAR) mimicked SIC. Gadolinium, a blocker of stretch-activated ion channels (SACs), inhibited the stretch-induced phosphorylation of AMPK and ACC, whereas diltiazem, a specific L-type calcium channel blocker, did not affect AMPK activation. Furthermore, SIC was abrogated by Compound C and gadolinium. The in vivo stretch induced by ACS increased AMPK activation and reduced myocardial infarct. These findings indicate that stretch preconditioning can induce the cardioprotection against I/R injury, and activation of AMPK plays an important role in SIC, which might be mediated by SACs.
Acetyl-CoA Carboxylase ; AMP-Activated Protein Kinases ; Animals ; Calcium Channels, L-Type ; Diltiazem ; Gadolinium ; Heart ; Ion Channels ; Myocardial Infarction ; Phosphorylation ; Rats ; Reperfusion Injury

Vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), P- and E-selectin play a pivotal role for initiation of atherosclerosis. Ginsenoside, a class of steroid glycosides, is abundant in Panax ginseng root, which has been used for prevention of illness in Korea. In this study, we investigated the mechanism(s) by which ginsenoside Rg2 may inhibit VCAM-1 and ICAM-1 expressions stimulated with lipopolysaccharide (LPS) in human umbilical vein endothelial cell (HUVEC). LPS increased VCAM-1 and ICAM-1 expression. Ginsenoside Rg2 prevented LPS-mediated increase of VCAM-1 and ICAM-1 expression. On the other hand, JSH, a nuclear factor kappa B (NF-kappaB) inhibitor, reduced both VCAM-1 and ICAM-1 expression stimulated with LPS. SB202190, inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), and wortmannin, phosphatidylinositol 3-kinase (PI3-kinase) inhibitor, reduced LPS-mediated VCAM-1 but not ICAM-1 expression. PD98059, inhibitor of mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK) did not affect VCAM-1 and ICAM-1 expression stimulated with LPS. SP600125, inhibitor of c-Jun N-terminal kinase (JNK), reduced LPS-mediated ICAM-1 but not VCAM-1 expression. LPS reduced IkappaBalpha (IkappaBalpha) expression, in a time-dependent manner within 1 hr. Ginsenoside Rg2 prevented the decrease of IkappaBalpha expression stimulated with LPS. Moreover, ginsenoside Rg2 reduced LPS-mediated THP-1 monocyte adhesion to HUVEC, in a concentration-dependent manner. These data provide a novel mechanism where the ginsenoside Rg2 may provide direct vascular benefits with inhibition of leukocyte adhesion into vascular wall thereby providing protection against vascular inflammatory disease.
Androstadienes ; Anthracenes ; Atherosclerosis ; E-Selectin ; Endothelial Cells ; Flavonoids ; Ginsenosides ; Glycosides ; Hand ; Humans ; I-kappa B Proteins ; Imidazoles ; Intercellular Adhesion Molecule-1 ; JNK Mitogen-Activated Protein Kinases ; Korea ; Leukocytes ; Monocytes ; NF-kappa B ; Panax ; Phosphatidylinositol 3-Kinase ; Phosphotransferases ; Protein Kinases ; Pyridines ; Umbilical Veins ; Vascular Cell Adhesion Molecule-1

Calcium (Ca) is an essential element to maintain body homeostasis. However, many factors disturb calcium absorption. Aspartic acid chelated calcium (AAC) was synthesized by new methods using calcium carbonate and aspartic acid. This study was carried out to investigate the bioavailability of AAC in Ca-deficient rats. The experimental groups were as follows: NC; normal diet control group, CD-C; untreated control group of Ca-deficient (CD) rats, CD-CaCO3; CaCO3 treated group of CD rats, CD-AAC; AAC treated group of CD rats, and CD-SWC; and seaweed-derived Ca treated group of CD rats. The Ca content of various types of Ca was held constant at 32 mg/day, and the four CD groups were fed for 7 days after randomized grouping. Ca content in serum, urine, and feces within feeding periods were analyzed to confirm Ca absorption. Serum Ca content was significantly higher in the CD-AAC (11.24 mg/dL) and CD-SWC (10.12 mg/dL) groups than that in the CD-C (8.6 mg/dL) group 2 hours following the first administration. The Ca content in feces was significantly lower in the CD-AAC (35.4 mg/3 days) and CD-SWC (71.1 mg/3 day) groups than that in the CD-CaCO3 (98.7 mg/3 days) group (p > 0.05). AAC had a 2.3-fold higher absorption rate of Ca than that of SWC. No differences in fibula length were observed in the NC and CD groups. The fibula weights of the CD-AAC (0.33 g) and CD-SWC (0.33 g) groups increased compared to those in the CD-C (0.27 g) group; however, no significant difference was observed between the CD groups. We conclude that bioavailability of AAC is higher than that of seaweed-derived Ca or inorganic Ca. Thus, these findings suggest the AAC has potential as a functional food material related to Ca metabolism.
Absorption ; Adsorption ; Animals ; Aspartic Acid ; Biological Availability ; Calcium ; Calcium Carbonate ; Diet ; Feces ; Fibula ; Functional Food ; Homeostasis ; Rats ; Weights and Measures

Vascular NADPH oxidase plays a pivotal role in producing superoxide in endothelial cells and thus acts in the initiation and development of inflammatory cardiovascular diseases such as atherosclerosis. Epigallocatechin-3-gallate (EGCG), the major catechin derived from green tea, has multiple beneficial effects for treating cardiovascular disease but the effect of EGCG on the expression of vascular NADPH oxidase remains unknown. In this study, we investigated the mechanism(s) by which EGCG might inhibit the expression of subunits of NADPH oxidase, namely p47(phox), p67(phox) and p22(phox), induced by angiotensin II (Ang II) in human umbilical vein endothelial cells. Ang II increased the expression levels of p47(phox), p67(phox), and p22(phox), but EGCG counteracted this effect on p47(phox). Moreover, EGCG did not affect the production of reactive oxygen species induced by Ang II. These data suggest a novel mechanism whereby EGCG might provide direct vascular benefits for treating inflammatory cardiovascular diseases.
Angiotensin II ; Atherosclerosis ; Cardiovascular Diseases ; Catechin ; Endothelial Cells ; Human Umbilical Vein Endothelial Cells ; Humans ; NADP ; NADPH Oxidase ; Reactive Oxygen Species ; Superoxides ; Tea