Changes in arthroscopic findings before and after acetabular labrum resection for osteoarthritis of the hip were studied. Acetabular labrum resection for osteoarthritis of the hip was performed on 27 hips in this study. Before acetabular labrum resection, detachment of the acetabular labrum was observed in 26 hips and inversion was observed in 1 hip. These labrums were always interposed between the femoral head and the acetabulum. Marked damage of the articular cartilage in 19 hips was seen in the area corresponding to the acetabular labrum. A second arthroscope (1-1.5 years later), demonstrated improvement of the articular cartilage in 11 hips, but, the degree of fibrillation and irregularity on the articular cartilage was increased in 6 hips. We conclude that the interposed acetabular labrum may be the cause of the cartilage damage and that acetabular labrum resection should be carried out in such cases.

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The purpose of this study was to investigate the etiologic relationship between cytokines and the onset and progression of acute pancreatitis. Acute pancreatitis was induced in BALB / c mice by administering six intraperitoneal injections of caerulein, each 1 hour apart. Measurements of pancreatic weight, plasma amylase, histopathologic scores, pancreatic myeloperoxidase (MPO), DNA, and protein were determined at 6, 12, 18, 24, 72, and 120 h after the first injection, and the levels of pancreatic tumor necrosis factor ( TNF) - α and interleukin (IL) -1β were measured at 6, 12, and 18 h. Some mice were treated with FR167653, a potent suppressant of TNF- α and IL-1 β production, and measurements were taken 18 h after the first injection of caerulein to see if this drug could affect the progression of acute pancreatitis. Plasma amylase concentration was highest at 12 h. The histologic severity . and pancreatic MPO activity were highest at 18 h. Pancreatic TNF- α was highest at 6 h, and IL-1β was highest at 12 h. Pancreatic weight, relative to DNA content, was significantly increased at 24 h. Pancreatic protein levels, relative to DNA content, were significantly increased at 12 and 18 h. The plasma amylase concentration, pancreatic MPO activity, pancreatic histologic scores, and the protein levels relative to DNA content, were significantly lower at 18 h, in mice treated with FR167653. Preventive administration of FR167653 ameliorated the caerulein-induced acute pancreatitis. TNF- α and IL-1β seem to be crucial factors in the onset and progression of acute pancreatitis, and blockade of these cytokines may attenuate the severity of acute pancreatitis.

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We examined the effectiveness of QT interval behavior in evaluating the viability of reperfused infarct-related myocardium in patients with myocardial infarction. Exercise thallium-201 single photon emission computed tomography was performed six months following successful direct angioplasty on 67 patients (60.6 ± 11.5 years) with myocardial infarction. QTc interval and QT dispersion from 12 lead electrocardiography and the number of perfusion defect areas from SPECT images were measured at rest and during exercise. Sixty-two patients with a resting perfusion defect were divided into 3 groups based on the SPECT image patterns. Group A consisted of 11 patients with partial redistribution, Group B consisted of 18 patients with reverse redistribution, and Group C consisted of 32 patients with fixed defect. The change in the number of defect areas from rest to exercise was related to the change in maximal QTc interval (y =15.4-3.31X, r = 0.298, p = 0.0138) . The maximal QTc interval was longer in all groups with myocardial infarction compared with 12 normal volunteers at rest (p<0.05), and increased during exercise in group B (465.8 ± 46.6 to 487.8 ± 27.2, p = 0.0193) and group C (458.7±25.4 to 479.5±31.1, p<0.0001), but not in group A (458.9± 26.4 to 462.1 ± 25.8, p = not significance) . QT dispersion decreased during exercise in the former 2 groups (62.9 ± 30.3 to 42.3 ± 14.7, in group B, p = 0.0 102, 53.8 ±20.3 to 41.7± 18.7, in group C, p=0.0002), but not group A (45.6±22.3 to 32.8±9, in the group A, p = no significance) . QT interval behavior is an effective predictor of scarred myocardial viability following reperfusion.

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The initial treatment of T 1 esophageal squamous cell carcinoma ( SCC) is partly controversial due to the difficulties in accurate detection of metastatic lymph nodes by imaging and evaluation of treatment results. In this retrospective analysis, we investigated the efficacy and feasibility of chemoradiotherapy for T1N0-1M0 esophageal SCC. Concurrent chemoradiotherapy was applied to 12 patients with T 1 disease (T 1 N0-1 M0) evaluated according to UICC-TNM classification. Chemotherapy consisted of infusion of 5-fluorpuracil at 400 mg/m²/day on days 1 to 5 and 8 to 12, combined with 2-hour infusion of 40 mg/m² cisplatin on days 1 and 8. Radiation dose of 30 Gy in 15 fractions of the mediastinum was applied during chemotherapy. A course schedule with 3 weeks of treatment and 2 weeks of break was applied twice, with a total radiation dose of 60 Gy. Based on CT scan, 3 patients had regional lymph node metastasis and 9 had no such metastasis. All 12 patients achieved complete response and the 3-year survival rate was 92%. Major toxicities were leukocytopenia (25%) and esophagitis (33%) . Minute local recurrence was found in 2 (17%) patients who subsequently underwent EMR, and no recurrence was noted more than two years after EMR. No patient underwent esophagectomy for local recurrence or lymph node metastasis. All patients had good performance status before and after chemoirradiation. Concurrent chemoradiotherapy is potentially curative for T1 esophageal SCC including N1 disease.

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Nitric oxide (NO _??_), a paramagnetic molecule, has a very short half-life of less than five seconds. The direct measurement of NO _??_ is therefore difficult and is not commonly performed. The liver is one of the organs in the body that is clearly influenced by NO _??_ which is generated in response to septic shock, portal hypertension and liver surgery such as, in the case presented here, partial hepatectomy. To detect time-dependent changes in NO _??_ after hepatectomy and regeneration of the liver, we used ex vivo electron spin resonance (ESR) spectroscopy by injection of an N-methyl-D-glucamine dithiocarbamate (MGD) and Fe²⁺ complex ( [ (MGD) ₂Fe] ) . After injection of this complex, NO _??_ signals were detected by ESR in both regenerating and sham-operated livers. NO _??_ generation had increased significantly at 36 h and peaked at 72 h after partial hepatectomy. The expression of inducible nitric oxide (iNOS) mRNA was analyzed by real-time PCR and its maximum level was detected at 72 h after partial hepatectomy. These results indicate that NO _??_ may play an important role in regulating liver regeneration after partial hepatectomy.

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This study aimed to investigate the direct effects of Triton WR-1339 on the production of fibrinogen in cells grown in vitro. HepG2 cells were incubated in Dulbecco's modified Eagle's medium (DMEM) for 6, 12 and 24 hr in the absence and presence of Triton WR-1339, used at four dose concentrations (0.12, 1.2, 12 and 120 μg/ml) . The high dose Triton WR-1339 treatment (120 μg/ml) for 24 hr induced significant cell toxicity as determined by the leakage of alanine aminotransferase (ALT) to the medium and by the cell viability using 3- (4, 5-dimethylthiazol-2-yl) -2, 5-diphenyl tetrazolium bromide (MTT) assay. Fibrinogen released into the medium from the HepG2 cells was measured by ELISA at 6, 12 and 24 hr. The low dose Triton WR-1339 treatments (0.12 and 1.2 μg/ ml) for 24 hr resulted in significantly increased fibrinogen secretion compared with the non-treated cells. Expression of α -, β - and γ -chains of fibrinogen at the mRNA level was determined by RT-PCR. After a 6 hr incubation with 0.12 and 12 μg / ml of Triton WR-1339, mRNA levels of γ -chain fibrinogen increased significantly. After 24 hr in the same treatment conditions, the fibrinogen β - and γ -chain mRNA levels were significantly increased, whereas the α - chain levels were unchanged as compared with non-treated controls. These results indicate that Triton WR-1339 induces the synthesis of fibrinogen by increasing the transcription of the β- and γ -chains of fibrinogen in HepG2 cells.

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Most studies on the effect of phosphorous on parathyroid cell proliferation were performed only on short duration and long-term observation has not been reported. Therefore, the present study was undertaken to assess the long-term effect of high phosphorous intake on cell proliferation in the parathyroid gland of chronic renal failure rats. Rats were made uremic by the procedure of 5/6 Nephrectomy and then were divided into two groups : group 1 received a high phosphorus diet containing 1.2% phosphorous and 1.2% calcium, and group 2 received a normal phosphorus diet containing 0.5% phosphorous and 0.6% calcium. The control group comprised normal rats receiving a normal level of phosphorous in their diets, and was denoted group 3. Six, 9 and 16 weeks after the partial nephrectomy, 5 rats from each group were sacrificed and samples of blood, 24-hour urine, and parathyroid tissue were taken. Sections of parathyroid gland were immunostained for proliferative cell nuclear antigen (PCNA) to assess parathyroid cell proliferation. A diet high in phosphorous was shown to significantly accelerate parathyroid cell proliferation in CRF rats (P< 0.05) at each time point studied, and serum intact parathyroid hormone significantly increased in parallel with parathyroid cell proliferation (P< 0.05) . This study demonstrates that a long-term intake of high phosphorous levels may mediate the development of continuous cell proliferation of the parathyroid gland with the subsequent development of secondary hyperparathyroidism.

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The hydrophilic bile salt tauroursodeoxycholic acid (TUDCA) is a potent inhibitor of apoptosis. The aim of this study was to determine the mechanism of the protective effect of TUDCA against the apoptosis induced by glycochenodeoxycholic acid (GCDCA) in rat hepatocytes (RLN-8 cells) . RLN-8 cells were treated with GCDCA and TUDCA. Expression of Fas, Bax α and Bcl-2 genes was detected by RT-PCR. The level of mitochondrial cytochrome C released into the cytosol, and the degree of caspase activity (caspase-3, -8 and -9) was determined. GCDCA increased the expression of mitochondrial-associated Bax α and caused release of cytochrome C, subsequently inducing apoptosis. Co-treatment with TUDCA significantly increased the viability of cells, compared with GCDCA alone. Co-incubation of TUDCA with GCDCA increased the expression of Bcl-2 and significantly inhibited the release of cytochrome C from mitochondria into the cytosol. TUDCA also inhibited activation of caspase-9 and caspase-3 in GCDCA-induced apoptotic cells. These results suggest that the effects of TUDCA are due to the increase in the mRNA levels of Bcl-2 which acts as an anti-apoptotic factor that sequentially prevents the release of cytochrome C from mitochondria and inhibits the activation of caspase-9 and caspase-3.

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We report a case of a 4-year-old boy with difficult asthma who responds poorly to the recommended therapy. On addition of suplatast tosilate to his maintenance regimen, a remarkable improvement was observed in his asthma and in the atopic dermatitis that he also suffered. Suplatast tosilate is therefore a potential add-on medication for the treatment of difficult asthma and atopic dermatitis, although further investigation is warranted.

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A 56-year-old woman presented with a sudden occipitalgia that occurred while swimming. No obvious abnormality was detected on the first CT scan. Thirty-five hours after the onset of occipitalgia, a second CT scan demonstrated a diffuse subarachnoid hemorrhage. Cerebral angiography revealed a pearl string sign on the left vertebral artery, suggesting a dissecting aneurysm. Proximal clipping of the left vertebral artery was successfully performed. The relationship between occipitalgia and the subsequent subarachnoid hemorrhage is discussed.

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