No abstract available.

BACKGROUND: Cadmium, an environmental pollutant, has implicated in the pathogenesis of cardiovascular diseases. Biochemical and pathophysiological changes characterized by arterial hypertension, accelerated cholesterol plaque formation on arterial walls, cardiac conduction abnormalities, and reduction in myocardial contractility have been reported in experimental animals chronically exposed to low concentration of cadmium. This study was undertaken to evaluate the ultrastructural changes of the cardiac muscle in rats exposed to cadmium chloride and to ascertain whether these changes are modified after discontinuation of cadmium feeding. METHOD: Wistar strain rats(body weight 200~250gram) were injected intraperitoneally once weekly with 3.75mg/kg of cadmium chloride for 10 weeks and were sacrificed at 1 day, 1 week and 2 weeks after discontinuation of cadmium administration. RESULT: Ultrastructure if rat cardiac muscle fibers after cadmium administration revealed that mitochondria were increased in number and their cristae were severely damaged. Cardiac myofibrils and myofilaments were reduced. Z-disc were partly dislocated and A-bands and I-bands were not clearly defined. Irregularly arranged intercalated disc and disrupted sarcolemma were also found. These structural alterations resulting from cadmium feeding were partly reduced after removal of cadmium exposure for 2 weeks. These structural alterations resulting from cadmium feeding were partly reduced after removal of cadmium exposure for 2 weeks. CONCLUSIONS: It is suggested that exposure to cadmium chloride was associated with cardiac ultrastructural changes which might be responsible for physiologic abnormalities and these alterations may be partly reversible after discontinuation of cadmium administration.
Animals ; Cadmium Chloride* ; Cadmium* ; Cardiovascular Diseases ; Cholesterol ; Hypertension ; Mitochondria ; Myocardium* ; Myofibrils ; Rats* ; Sarcolemma

Clinical findings, electrocardiographic voltage and left ventricular function were evaluated in 104 patients with percardial effusion. Patients were classified into three groups by the amounts of pericardial effusion measured by two-dimensional echocardiography. 49 patients had small pericardial effusion, 31 moderate effusion and 24 large effusion. In 47 patients the effusions were clinically unsuspected prior to echocardiographic examination. Pericardial friction rub was noted in 14 patients, two-thirds of whom had moderate to large effusions. There was no relationship between the size of effusion and the presence of friction rub. Total QRS amplitudes were lower in patients with moderate to large effusions than those in control group. Maximum diastolic endocardial velocity(DEVM) and E-F slope of the anterior mitral leaflet were decreased significantly in patients with moderate to large effusions as compared with those with small effusions. As a result, authors concluded that reduction in the QRS voltages in serial ECGs may suggest the presence and the amount of pericardial effusion and also DEVM and E-F slope of the anterior mitral leaflet can be sensitive measures of left ventricular relaxation in patients with pericardial effusion.
Echocardiography* ; Electrocardiography* ; Friction ; Humans ; Pericardial Effusion* ; Relaxation ; Ventricular Function, Left*

Left ventricular hypertrophy(LVH) is one of common cardiovascular complications in hypertensive patients and it is well known that hypertensive cardiac disease accompained by LVH is still common cause of congestive heart failure in spite of treatment of hypertension. The authors assessed the prevalence of anatomical and functional abnormalities of left ventricle by EKG, chest X-ray and echocardiography in 45 essential hypertensive patients and also in 20 normal controls. Average values of left ventricular posterior wall thickness(LVPWd), interventricular septal thickness(IVSd), left ventricular mass(LVM), and left ventricular mass index(LVM/BSA) by echocardiography in hypertensive groups with LVH by EKG or chest X-ray were significantly higher than those of hypertensive groups without LVH by EKG or chest X-ray(P<0.005). Among 27 hypertensive patients with LVH by EKG and chest X-ray increased LVPWd was found in 24 patients(18%) and increased LVH in 26 patients(19%). Increased LVPWd and LVM were found in 3 patients(23%) among 13 hypertensives without LVH by EKG and chest X-ray. Hypertensive patients with increased LVH showed LVH by EKG and chest X-ray more frequently than those with increased LVPWd. Also, hypertensive patients without increased LVM showed MVH by EKG and chest X-ray less frequently than those without increased LVPWd. Therefore, echocardiography appears to be superior to routine chest X-ray and EKG for defecting LVH in hypertensive patients, especially without LVH by these tests. In conclusion, even though estimation of LVM by echocardiography seems to be a better method than single measurement of LVPWd, it seems thant estimation of LVM together with LVPWd will be more valuable in diagnosis of LVH in hypertensive patients.
Diagnosis ; Echocardiography* ; Electrocardiography ; Heart Diseases ; Heart Failure ; Heart Ventricles ; Humans ; Hypertension* ; Hypertrophy, Left Ventricular* ; Prevalence ; Thorax

This is a case report of the familial olivo-ponto-cerebellar atrophy (Menzel type OPCA, OPCA III with retinal degeneration). The patient is a 37 year-old male with 5 years history of slowly progressive cerebellar ataxia, dysarthria, visual change, horizontal nystagmus and signs of pyramidal dysfunction. The CT brain scan shows significant atrophy of brain stem and cerebellum with dilatation of cisterns. His younger sister, also, has similar clinical manifestations and radiological abnormalities, but mild. By history, his mother who died at 47 years of her age looked like to have same kind of chronic disease.
Adult ; Atrophy ; Brain ; Brain Stem ; Cerebellar Ataxia ; Cerebellum ; Chronic Disease ; Dilatation ; Dysarthria ; Humans ; Male ; Mothers ; Nystagmus, Pathologic ; Olivopontocerebellar Atrophies* ; Retinaldehyde* ; Siblings

No abstract available.

No abstract available.
Genes, ras* ; Humans

No abstract available.

OBJECTIVE: The importance of traumatic dural venous sinus injury lies in the probability of massive blood loss at the time of trauma or emergency operation resulting in a high mortality rate during the perioperative period. We considered the appropriate methods of treatment that are most essential in the overall management of traumatic dural venous sinus injuries. METHODS: We conducted a retrospective review of all cases involving patients with dural venous sinus injury who presented to our hospital between January 1999 and December 2014. RESULTS: Between January 1999 and December 2014, 20 patients with a dural venous sinus injury out of the 1,200 patients with severe head injuries who had been operated upon in our clinic were reviewed retrospectively. There were 17 male and 3 female patients. In 11 out of the 13 patients with a linear skull fracture crossing the dural venous sinus, massive blood loss from the injured sinus wall could be controlled by simple digital pressure using Gelfoam. All 5 patients with a linear skull fracture parallel to the sinus over the venous sinus developed massive sinus bleeding that could not be controlled by simple digital pressure. CONCLUSION: When there is a linear skull fracture parallel to the sinus over the dural venous sinus or a depressed skull fracture penetrating the sinus, the surgeon should be prepared for the possibility of potentially fatal venous sinus injury, even in the absence of a hematoma.
Craniocerebral Trauma ; Emergencies ; Female ; Gelatin Sponge, Absorbable ; Hematoma ; Hemorrhage ; Humans ; Male ; Mortality ; Perioperative Period ; Retrospective Studies ; Skull Fracture, Depressed ; Skull Fractures ; Superior Sagittal Sinus

The blood sugar control has been a significant problem after transplantation. Cyclosporine is partly responsible for post-transplantation diabetes mellitus (PTDM), but steroid has been well known to have diabetogenic effect and mainly responsible for glucose intolerance after transplantation. Deflazacort, a new steroid, has been introduced as a substitute of conventional steroid to prevent glucose intolerance after transplantation. We performed prospective study of deflazacort conversion from conventional steroid in kidney transplant patients with pre-transplantation diabetes mellitus(pre-Tx DM) or PTDM. A total of 82 kidney transplant patients was included for this study. Forty two patients were converted to deflazacort as a conversion group and 40 patients were remained on conventional steroid as a control group. In conversion group, the patients were converted from steroid to deflazacort with ratio of 5:6 in dosage. Nine patients developed severe anorexia with nausea/vomiting and three patients among them went back on steroid within 3 months after conversion(conversion failure 7.1%). After minimal 6 months of follow-up, there was neither episodes of graft dysfunction nor rejection. There was a significant improvement of glucose control in conversion group. In 12 patients(30.8%), more than 50% dose reduction of insulin or oral hypoglycemics requirement was possible. In control group, however, only 2 patients showed greater than 50% of insulin or oral hypoglycemics dose reduction. We could find that deflazacort conversion had a significant impact on blood sugar control in PTDM patients(11/26) but not in pre-Tx DM patients(1/13). In conclusion, conversion to deflazacort in PTDM patients with stable graft function was safe and blood sugar control was readily possible without an increment of risks of rejection and infection. We propose to use deflazacort as a substitute for prednisone in PTDM patients with stable graft function.
Anorexia ; Blood Glucose ; Cyclosporine ; Diabetes Mellitus ; Follow-Up Studies ; Glucose ; Glucose Intolerance ; Humans ; Hypoglycemic Agents ; Insulin ; Kidney* ; Prednisone* ; Prospective Studies ; Transplants