For the nonunion of humeral shaft, there have been many methods of treatment. We are aimed to analyse the causes of nonunion of humeral shaft fracture and present the direction of treatment. We reviewed total 21 cases which were diagnosed as delayed or nonunion of humeral shaft and analysed the causes. l. Initial method of treatment was surgical in 19 out of 21 cases. Among these 19 cases, 14 cases were operated with internal fixation with plate and screw. 2. The most common cause of nonunion was inadequate internal fixation in 26 cases(81%) in which were unstable fixation in 13 cases, choice of inadequate internal fixator in 11 cases, and failure of operative technique in 2 cases. Other causes were distraction between fracture fragments in 4 cases(13%) and open comminuted fracture in 2 cases. 3. Eighteen cases of established nonunion due to inadequate internal fixation were treated by rigid fixation with longer and broader plate and bone graft, and 1 case interlocking IM nailing, 1 case Ender nailing and 1 case bone graft only. 4. Union was obtained in all cases at least in 5 months. And there were no specific complications. In conclusion, surgeons should contemplate the operative indication and principles in primary treatment. In treatment of nonunion, surgeons should treat by more longer and broder internal fixator and additional bone graft.
Fractures, Comminuted ; Humerus ; Internal Fixators ; Methods ; Surgeons ; Transplants

No abstract available.
Cardiomyopathy, Dilated* ; Child* ; Humans

No abstract available.
Actinomycosis*

No abstract available.

Kawasaki disease is an acute febrile vasculitis that occurs predominantly in young children under 5- years-old. The patients present generally with a high spiking fever that is unresponsive to antibiotics and lasts for more than five days at least. Prolonged fever has been shown to be a risk factor in the development of coronary artery disease. It seems to be certain that infectious agents are associated with the pathogenesis of Kawasaki disease. The differential diagnosis of Kawasaki disease must rule out infectious diseases including scarlet fever, toxic shock syndrome, measles, and so on. This is very important for adequate treatment and prevention of cardiac complications of Kawasaki disease. We experienced a 25-month-old boy who had high fever and pneumonic consolidation in the right middle and lower lobe of the lung that was considered as mycoplasma pneumonia on admission and developed coronary artery aneurysmal dilatation during treatment with roxythromycin.
Aneurysm ; Anti-Bacterial Agents ; Child ; Child, Preschool ; Communicable Diseases ; Coronary Artery Disease ; Coronary Vessels ; Diagnosis, Differential ; Dilatation ; Fever ; Humans ; Lung ; Male ; Measles ; Mucocutaneous Lymph Node Syndrome* ; Mycoplasma* ; Pneumonia, Mycoplasma* ; Risk Factors ; Scarlet Fever ; Shock, Septic ; Vasculitis

Leukemic infiltration of the testes has been relatively rare disease. But increased survival due to advance in the treatment of childhood leukemia has been associated with an increase in incidence of leukemic infiltration of the tests. Six of 66 male children with acute lymphocytic leukemia and 2 of 2 male children with leukemic transformation on non-Hodgkin's lymphoma, who have been admitted to our pediatric department during past 7.5 years period, from January, 1974 to June, 1981 developed testicular leukemia. This represents an incidence of 11.8% and the median age was 6.6 years(9 mo. to 14 yrs). All patients were symptom free despite testicular enlargement. Testicular enlargement was initial presenting manifestation in two patients. The enlargement was unilateral in 5 and bilateral in 3. Initial white blood cell count was greater than 100,000/mm3 in five patients and was less than 10,000/3 in other three. Microscopic findings on specimens were leukemic infiltration mainly in the interstitial spaces and atrophy of spermatogenic cells. Four patients developed testicular relapse during bone marrow remission. Hepatosplenomegaly and lymphadenopathy were present in 5 and 6, and these appeared to imply an increased risk of testicular relapse. The median duration from diagnosis to testicular relapse was 33.5 months(2 mo. to 93 mo.). Three patients developed subsequent relapses(CNS; 2, BM; 1) 1.5 to 26 months after the testicular relapse, the median interval being 14.5 months. Radiotherapy with chemotherapy has resulted clinical improvement, but only one patient showed long survival without relapse.
Atrophy ; Bone Marrow ; Child ; Diagnosis ; Drug Therapy ; Humans ; Incidence ; Leukemia* ; Leukemic Infiltration ; Leukocyte Count ; Lymphatic Diseases ; Lymphoma, Non-Hodgkin ; Male ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; Radiotherapy ; Rare Diseases ; Recurrence ; Testis

Apert syndrome is an uncommon congenital disorder characterized by malformation of the skull, most often acrocephaly or oxycephaly, in association with symmetrical syndactyly of both hands and feet. It is due to a disturbance in the growth of bone and soft tissue, affecting principally the head, hands, and feet. Recently we experienced a typical Apert syndrome expressed only in one neonate of dizygotic twin.
Acrocephalosyndactylia* ; Congenital, Hereditary, and Neonatal Diseases and Abnormalities ; Craniosynostoses ; Foot ; Hand ; Head ; Humans ; Infant, Newborn* ; Skull ; Syndactyly ; Twins, Dizygotic*

Sixty two properly treated acute lymphocytic leukemia cases who were diagnosed at SNUH, from 1958 to July, 1981 were studied. Among them, 20 cases had survived more than 3 years and 42 cases survived less than 3 years. The 11 cases of 20 are now alive and off theray and the remainder 9 cases were expired after survival for more than three years. The clinical features of the 11 currently living cases are as follows. The survival time of 11 cases are 3 years and 1 month - 16 years and 1 month. Except one case, first remission have continued till now. Average leukocyte count and liver size are 7,710/mm3 and 1.5 fingerbreadth respectively. The proportion of cases who showed splenomegaly, lymph node enlargement and hemorrhagic phenomena is 18.2%, 9.1% and 36.4% respectively. The clinical features of the 9 expired cases are as follows. Average leukocyte count is 7,780/mm3 and average liver size is 2.4 finger-breadth and average spleen size is 2.8 fingerbreadth. The proportion of cases who showed lymph node enlargement and hemorrhagic phenomean in 50.0% and 37.5% respectively. The clinical features of 29 cases who attained initial remission but survived less than 3 years are as follows. Average leukocyte count, liver size and spleen size 72,910/mm3, 2.8 finger-breadth and 2.0 finger-breadth respectively. The proportion of cases who showed lymph node enlargement and hemorrhagic phenomean is 52% and 75.9% respectively. The clinical features of 13 cases who died before initial remission are as follows. Average leukocyte count, liver size and spleen size are 244,570/mm3, 2.4 finger-breadth and 2.0 finger-breadth respectively. The proportion of cases who showed lymph node enlargement and hemorrhagic phenomena is 53.8% and 90.9% respectively. Various prognostic factors were related to duration of survival. The proportion of cases who were over 10 years of age at diagnosis and male to female ratio are higher in cases who survived less than 3 years. The leukocyte count, liver size, proportion of lymph node enlargement and proportion of hemorrhagic phenomeana are significantly lower in long survivors. In long survivors, spleen size in smaller but statistically not significant.
Diagnosis ; Female ; Humans ; Leukocyte Count ; Liver ; Lymph Nodes ; Male ; Precursor Cell Lymphoblastic Leukemia-Lymphoma* ; Prognosis ; Spleen ; Splenomegaly ; Survivors

Aspergillus funigatus and other pathogenic fungi synthesize a toxic epidithi- odiopiperzine (ETP) metabolite called gliotoxin. Gliotoxin is an epidithiodiopiperzine compound which can both react with sulfhydryl groups and form hydrogen peroxide. The fungal toxin gliotoxin induces apoptotic cell death in a variety of cells. Apoptosis induced by gliotoxin need calcium but effect of calcium preconditioning is unknown by gliotoxin. We studied the effect of protein kinase C and calcium preconditioning on gliotoxin-induced apoptosis in H9c2 cell. PKC and calcium preconditiong inhibited DNA fragmentation by gliotoxin. From this above results suggest that gliotoxin induce apoptosis via caspase-3 activation, because caspase-3 inhibitor (DEVD-CHO) didn't induce apoptosis in gliotoxin treated H9c2 clls. Calcium and PKC preconditioning inhibit caspase-3 activation by gliotoxin. These data means that PKC preconditioning is related with caspase-3 regulate in gliotoxin-induced apoptosis.
Apoptosis* ; Aspergillus ; Calcium ; Caspase 3 ; Cell Death ; DNA Fragmentation ; Fungi ; Gliotoxin* ; Hydrogen Peroxide ; Protein Kinase C* ; Protein Kinases*

Nitric oxide (NO) is mainly involved in brain ischemic damage to elucidate the protective mechanism of NO pretreatment on ischemic-induced cytotoxicity. This study was investigated whether NO pretreatment inhibits the increase of iNOS expression by lipopolysaccharide (LPS) combined phorbol 12-myristate 13-acetate (PMA) via regulating NF-kB activation in C6 glial cells. C6 glial cells with LPS and PMA for 72 hours markedly induced NO, but sodium nitroprusside (SNP) (100 nM) pretreatment before exposure of LPS and PMA significantly supressed NO production, iNOS expression and NF-kB activation by LPS and PMA. In addition, LPS and PMA treatment for 72 hours induced severely cell death and LDH release from cell into media in C6 glial cells. However SNP pretreatment before treatment of LPS and PMA significantly protected LPS and PMA induced cytotoxicity. Treatment with LPS and PMA induced caspase 3 activation follewed by chromosomal condensation, and fragmentation of nuclei in C6 glial cells. SNP pretreatment before exposure to LPS and PMA supressed caspase 3 activation and inhibited chromosomal condensation and fragmentation of nuclei. From these above results, it is suggest that the protective effects of SNP pretreatment against LPS and PMA induced cytotoxicity may be mediated by inhibiting the expression of iNOS via regulating NF-kB activation.
Brain ; Caspase 3 ; Cell Death ; Neuroglia ; NF-kappa B ; Nitric Oxide* ; Nitroprusside