Position of the superficial femoral artery in closed hip nailing

Introduction Adduction of the ipsilateral hip joint is necessary to facilitate closed hip nailing for trochanteric fracture. Even though positioning the patient supine with the perineal post against the ipsilateral medial thigh can change the course of the neurovascular structure in the proximal thigh, there have been no reports regarding the position of the femoral artery in the hip nailing position.Materials and methods We studied the position of the superficial femoral artery in 59 thighs using color-flow duplex scanning method in three hip nailing positions.Results The mean of the distance between the superficial femoral artery and the femur in 48 normal limbs was 20.28 mm in neutral position (D1), 11.85 mm in 20^o adduction (D2), and 9.53 mm in 20^o adduction plus 20^o internal rotation of the foot plate (D3). The distances D2 and D3 were always shorter than D1 (p<0.001). D3 was less than 10 mm in 30 of the normal limbs (62.5%) and less than 5 mm in 4 (8%). In 11 patients who sustained a trochanteric fracture, the mean of D1, D2, and D3 in the injured limbs was 25.28 mm, 17.98 mm, and 14.38 mm, respectively. The mid-thigh circumference and D3 of the injured limbs were always greater than those of the normal limbs (p<0.001). However, D3 of both sides was less than 10 mm in 3 patients.Conclusion To lessen the vascular injury during hip nailing, we recommend that the limb be placed in neutral position during preparation of the interlocking holes.     

Solitary fibrous tumor arising in gastric serosa

The solitary fibrous tumor (SFT) of peritoneum, especially arising in gastric serosa, is extremely rare. A case of SFT arising in gastric serosa of a 70-year-old man is reported. On abdominal computed tomography scan, an approximate 8.0 × 5.3 cm-sized solid mass with multiple nodular calcifications was noted in the omentomesentery of right upper abdomen, which was abutting to the gastric antral wall. At laparotomy the tumor was tightly attached to the gastric serosa and was completely excised by wedge resection of the stomach. The cut surfaces of the tumor were pale brown to pale yellow, firm, with multifocal yellowish, gritty, stony-hard nodules and cystic changes. Microscopically, the tumor was composed of mildly cellular benign-appearing spindle-shaped cells and bands of hyalinized collagen in varying proportions. The tumor revealed predominantly sclerosing pattern with extensive hyalinized fibrosis and multifocal dystrophic calcifications. The tumor was mainly located at the gastric serosa and subserosa, and its growth pattern was expansile with entrapping of muscularis propria and submucosa in the periphery of the tumor. By immunohistochemistry, the tumor cells were diffusely positive for CD34 and vimentin but negative for cytokeratin, desmin, smooth muscle actin, CD99 and c-kit. Although its occurrence is rare, SFT should be considered in the differential diagnosis of mesenchymal tumors of the stomach.     

Immobilization of cell adhesive RGD peptide onto the surface of highly porous biodegradable polymer scaffolds fabricated by a gas foaming/salt leaching method

A cell adhesive peptide moiety, Gly-Arg-Gly-Asp-Tyr (GRGDY), was immobilized onto the surface of highly porous biodegradable polymer scaffolds for enhancing cell adhesion and function. A carboxyl terminal end of poly(D,L-lactic-co-glycolic acid) (PLGA) was functionalized with a primary amine group by conjugating hexaethylene glycol-diamine. The PLGA-NH2 was blended with PLGA in varying ratios to prepare films by solvent casting or to fabricate porous scaffolds by a gas foaming/salt leaching method. Under hydrating conditions, the activated GRGDY could be directly immobilized to the surface exposed amine groups of the PLGA-NH2 blend films or scaffolds. For the PLGA blend films, the surface density of GRGDY, surface wettability change, and cell adhesion behaviors were characterized. The extent of cell adhesion was substantially enhanced by increasing the blend ratio of PLGA-NH2 to PLGA. The level of an alkaline phosphatase activity, measured as a degree of cell differentiation, was also enhanced as a result of the introduction of cell adhesive peptides.     

Clinical manifestations and diagnosis of extrapulmonary tuberculosis

Since the diagnosis of extrapulmonary tuberculosis (EPT) is largely depended on the physician's suspicion in respect of the disease, we believed that it would be worthwhile to scrutinize the clinical characteristics of EPT. Thus, here we present retrospectively evaluated clinical manifestations of patients who were diagnosed as EPT cases in a tertiary referral care hospital. Medical records of 312 patients, diagnosed as having EPT at Yongdong Severance hospital from January 1997 to December 1999, were reviewed retrospectively. In total 312 patients, 149 (47.8%) males and 163 (52.2%) females aged from 13 years to 87 years, were included into this study. The most common site of the involvement was pleura (35.6%). The patients complained of localized symptoms (72.4%) more frequently than systemic symptoms (52.2%). The most common symptom was pain at the infected site (48.1%). Leukocytosis, anemia, and elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were found in 12.8%, 50.3%, 79.3% and 63.1% of the patients, respectively. Twenty-four percent of the patients had underlying medical illnesses such as, diabetes mellitus or liver cirrhosis, or were over 60 years old. In 67.3% of patients, tuberculosis was suspected at the initial visit. However, tuberculosis was microbiologically proven in only 23.7% of the patients. The time interval from the symptom onset to the diagnosis varied, with the mean duration of the period 96 days. Pulmonary parenchymal abnormal lesions were found in 133 patients (42.6%) on chest radiographs. EPT has a wide spectrum of clinical manifestations, so it is difficult to diagnose it. Based on our studies, only 11.2% of the patients were confirmed as EPT. So it is important that the physician who first examines the patient should have a high degree of suspicion based on the chest radiography, localized or systemic symptoms and several laboratory parameters reviewed in this study.     

Burkitt's lymphoma representing periportal infiltrating mass on CT

Imaging findings of secondary hepatic lymphoma have been reported as variable, ranging from single or multiple small nodules to diffuse infiltrative tumor patterns. We hear present a rare case report concerning aggressive B cells, secondary Burkitt's lymphoma in non-AIDS demonstrating a surprising periportal lymphoma infiltration, without upper abdominal lymphadenopathy or splenomegaly on the sonography and CT scans. Clinically, the case was characterized by atypical and highly aggressive course, with the patient presenting an abruptly developed obstructive jaundice with rapidly deteriorating hepatic function that could be indicative of cholestatic hepatitis, which differs in its clinical manifestations from hepatic lymphoma without functional deterioration in respect of its non-tissue destructive growth pattern. We suggest that hepatic lymphoma can sometimes be consistent with periportal infiltrating homogeneous mass, with no lymphadenopathy or splenomegaly on the imaging examination, with a predictable aggressive clinical course of the disease and poor prognosis.     

Association of Angiotensin-converting enzyme and angiotensinogen gene polymorphisms with preeclampsia

We tested the hypothesis that angiotensin-converting enzyme (ACE) and angiotensinogen gene polymorphism influence the incidence, development and outcome of preeclampsia. Subjects were recruited from 90 Korean patients with preeclampsia during pregnancy and 98 age-matched controls. After isolation of DNA, polymerase chain reactions (PCR) were carried out to detect polymorphism of the ACE and angiotensinogen. M235T and T174M genotypes of angiotensinogen were determined by digestion with restriction enzyme endonuclease Tth 111-I and NCo I, respectively. The frequency of DD genotype was significantly greater in preeclampsia (0.36) than in controls (0.14) (p<0.05). The frequency of D allele was 0.55 in preeclampsia and 0.40 in controls (p<0.05). There were no differences in the onset of preeclampsia and pregnancy outcomes according to the ACE genotypes. There was no difference in the frequency of a allele of angiotensinogen M235T between the groups (0.79:0.78 in preeclampsia : controls). The frequency of T allele of angiotensinogen T174M gene was slightly increased, but not significantly, in preeclampsia (0.11) than in controls (0.07). In a multivariate analysis, only ACE genotype was associated with the development of preeclampsia (beta=0.27, p=0.05). In conclusion, a molecular variant of ACE, but not angiotensinogen, gene is associated with preeclampsia in Korean women.     

A case of focal segmental glomerulosclerosis associated with aplastic anemia

The pathogenic mechanism of focal segmental glomerulosclerosis (FSGS) and aplastic anemia are associated with immunologic events which lead to glomerular cell injury or hematopoietic cell destruction. We present an extremely rare case of FSGS with aplastic anemia in a 30-yr-old woman. The laboratory examination showed hemoglobin 7.2 g/dL, white blood count of 4,200/ microL, platelet count 70,900/microL. Proteinuria (2+, 3.6 g/day) and microscopic hematuria were detected in urinalysis. The diagnosis of FSGS and aplastic anemia were confirmed by renal and bone marrow biopsy. She was treated with immunosuppressive therapy of prednisone 60 mg/day orally for 8 weeks and cyclosporine A 15 mg/kg/day orally. She responded with gradually improving her clinical manifestation and increasing peripheral blood cell counts. Prednisone was maintained at the adequate doses with tapering after 8 weeks and cyclosporine was given to achieve trough serum levels of 100-200 ng/mL. At review ten month after diagnosis and initial therapy, the patient was feeling well and her blood cell counts increased to near normal (Hb 9.5 g/dL, Hct 32%, WBC 8,300/microL, platelet 123,000/microL) and renal function maintains stable with normal range proteinuria (0.25 g/day).     

Prologation of c-Jun N-terminal kinase is associated with cell death induced by tumor necrosis factor alpha in human chondrocytes

The aim of this study was to elucidate the role of JNK signaling pathway involved in tumor necrosis factor-alpha (TNF-alpha)-induced death of chondrocytes. Primary chondrocyte cultures were obtained from human knee osteoarthritis cartilages. First passage chondrocytes were treated with TNF-alpha and various potentiators, and cell death was measured with MTT assay. C-Jun N terminal kinase (JNK) activation was investigated with the solid phase kinase assay. Expression of apoptosis-related molecule was assayed with Western blot. Chondrocytes were resistant to TNF-alpha-induced cell death. In contrast, pretreatment with actinomycin D, the phosphatase inhibitor vanadate or MAP kinase phosphatase-1 (MKP-1) inhibitor Ro318220 invariably led to chondrocyte death. While TNF-alpha alone stimulated a single, brief JNK activity, a second JNK peak was observed when the cells were pretreated with actinomycin D. When the cells were pretreated with vanadate or Ro318220, TNF-alpha-induced JNK activation was greatly prolonged, which was associated with the induction of cell death. The expression of Bcl-2 and Mcl-1 decreased significantly in conditions of cell death. In conclusions, our data suggest that chondrocyte death induced by TNF-alpha is associated with sustained JNK activation. This effect may be due to downregulation of TNF-alpha induced phosphatase that inactivates JNK and of Bcl-2 family proteins.