The molecular mechanism of carcinogenesis is a multistep process that is characterized by both activation of oncogenes and inactivation of tumor suppressor genes. In the present study, mutations of N-ras, p53 and FMS-like tyrosine kinase 3 (FLT-3) genes and loss of expression of the deleted in colorectal carcinoma (DCC) gene were analyzed in 59 patients with myelodysplastic syndromes (MDS). Mutations of N-ras, p53, and FLT-3 genes were detected in 7, 7, 1 of the 59 patients with MDS, respectively. Loss of DCC expression was detected in 16 patients. Type of MDS patients with N-ras mutation were all refractory anemia with excess of blasts in transformation (RAEB-T). Abnormalities of p53 and DCC genes were significantly associated with survival time (p< 0.02, p< 0.004, respectively).

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Thirty ununited tibial fractures with a median time since injury of 18±9 months were treated by electrical stimulation using pulsing electromagnetic field therapy. Union was achieved in 25 cases (83.3%) in a median interval of 8.6±3.2 months. Patient age and gender, the presence of surgical hardware, length of disability, and the number of surgical procedures did not affect the outcome. Ununited fractures that appeared to be hypertrophic or sclerotic type radiographically, indicating a good blood supply to the bone ends, all healed. Treatment failures occurred only among lesions with a poor blood supply, and in necrotic or defective radiopraphic types. Pulsing electromagnetic field therapy is an effective treatment for ununited tibial fractures with good blood supply to the bone ends.

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To examine the protective effects of hepatocyte growth-promoting factor (pHGF) against carbon tetrachloride (CCl₄) -induced acute liver injury in rats, the pathological changes were observed by light and electron microcopy, and the serum GOT and GPT levels were measured. Acute liver injury was produced by the injection of CCl₄(2ml/kg BW) in two groups of animals, of which one received pHGF (300μg/kg BW) via the tail vein after 4 hrs. In the group treated with CCl₄ alone, serum GOT and GPT were significantly elevated (1280±228 and 187±73 IU/l, respectively) 6 hrs after injection, indicating the induction of liver injury by CCl₄. They reached a peak (3836±654 and 1022±230 IU/l, respectively) at 48 hrs and declined thereafter, but did not completely recover after 72 hrs. PAS-negative cells were observed around the central veins after 6 hrs and most of the hepatocytes were PAS-negative at 12 hrs. PAS-positive cells began to appear and increased in number after 24 hrs. There were scarcely any PAS-negative cells remaining in the lobules after 72 hrs. In the group treated with CCl₄ followed by pHGF, serum GOT and GPT levels were significantly lower than in the CCl₄-treated group, and abundant PAS-positive hepatocytes were observed. Also, all hepatocytes were PAS-positive (as in normal liver) after 72 hrs. Administration of pHGF resulted in a decrease in the ultrastructural changes in rats with CCl₄-induced liver injury such as vacuolation, cisternae formation and dilatation of the rough endoplasmic reticulum. These results suggest that pHGF acts to stabilize cell membranes, thereby providing protection against CCl₄-induced hepatic injury.

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We measured serum and synovial fluid levels of chondroitin sulfate (CS) in patients with osteoarthritis (OA) of the knee joint to clarify whether CS levels differ in various stages of OA, and whether measurement of CS levels is useful in evaluating the pathology of OA. The study population was 117 OA patients and 23 healthy young volunteers. Synovial fluid was obtained from 69 of 117 OA patients. The mean serum level of C4S in all of the OA patients was significantly higher than that in the controls (p< 0.05). However, there was little difference between respective OA stages. A small amount of serum C6S (0.2 to 0.6 nmol/ml) was detected in 31.6% of the OA patients and in 26.1%of the control subjects. The mean serum C0S level in all OA patients was significantly higher than that in the controls (p< 0.01). However no significant difference was found between respective OA stages. As for synovial fluid CS, the C4S level in the early stage of OA tended to be higher than that in the advanced stage. C6S levels showed a markedly decreasing trend with advancing OA stage. C0S was not detected in synovial fluid. The present study demonstrated that serum levels of C4S and C0S in OA patients are elevated compared with normal subjects, and that synovial fluid levels of C4S and C6S may provide useful in assessing the pathology of OA.

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The incidence and the distribution of blood vessels were examined in normal and abnormal mitral valve leaflets. Materials and methods: Normal valves were obtained from 12 autopsy cases without cardiovascular disease (8 men, 4 women, 33 to 93 years of age). Twenty-one abnormal valves were obtained at the time of mitral valve replacement (12 men, 9 women, 16 to 78 years of age). Clinical and pathological diagnoses were rheumatic valvular disease (RVD: n=8), floppy mitral valve (FMV: n=9), and healed infective endocarditis (HIE: n=4, 1 with RVD, 3 with FMV). The number of vessels was counted at the surgical excision line of the valvular rings by immunohistochemical study using Factor VIII related antigen and CD34. Histologic studies were also made at the 5 mm distal line from the ring in normal valves, and at the vertical line to the ring in abnormal valves.
Results: In normal valves, the number of vessels at the ring area, except in myocardial tissues that extended from the left atrium to the auricularis, ranged from 3 to 184. Vessels were also found at the 5 mm distal area from the ring in 6 valves out of 12. Vessels were mainly distributed near the commissure areas of the auricularis and/or the spongiosa and were extended with myocardial tissues. There was no difference in the number of vessels related to age or sex. In RVD, the number of vessels at the ring area ranged from 22 to 517 in 8 anterior leaflets (AML) and 2 to 151 in 5 posterior leaflets (PML). Many vessels also appeared in the distal spongiosa of the leaflets, and arterioles were frequently found in these areas. In FMV, a few (3 and 6) vessels were found in 2 leaflets (AML: 2/8, PML: 0/4). In HIE, the number of vessels was 216 in the case with RVD, and 3 to 110 in cases with FMV.
Conclusion: At the ring area, normal mitral valve leaflets were supplied with nutrition from blood vessels that mainly extended from the left atrium with myocardial tissues. In RVD, the vessels branchd from previously existing capillaries, extending to the distal area, and increased in number. Mechanical stress during opening and closing of the leaflets contributes to the arterialization of these vessels. In FMV, the number of capillaries, which is smaller than innormal valves, might be related to the progression of this disorder. In HIE with valvular disease, the number of vessels is related to the preexisting disease.

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We evaluated the short-term efficacy of terazosin for treating symptomatic benign prostatic hyperplasia (BPH). Thirty men, aged 52 to 83 years (mean: 69.2 years) complaining of obstructive urinary symptoms due to BPH who had not received any prior treatment for their symptoms were orally administered 2 mg/day of terazosin. Symptoms (the total IPSS and the obstructive and irritative symptom scores) and objective parameters (peak flow rate [Qmax] and prostatic volume) were evaluated before treatment and after 1, 2, and 4 weeks of treatment. The mean total IPSS and the mean symptom scores for weak stream and nocturia were significantly decreased after only 1 week of treatment, while the mean scores for emptying, frequency, and urgency were significantly decreased after 2 weeks of treatment. However, the mean scores for intermittency and hesitancy did not decrease significantly at any time during treatment. Regarding objective parameters, the mean Qmax was significantly improved after 1 week of treatment, but the mean prostatic volume remained almost unchanged after 4 weeks. In conclusion, short-term terazosin therapy not only improved Qmax but also alleviated symptoms including irritative symptoms.

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Spondyloepiphyseal dysplasia congenita (SED) is a rare form of skeletal systemic disease, characterized by congenital dwarfism with a short trunk and epiphysial dysplasia in the long bones and vertebral bodies. Patients also frequently saffer from atlanto-axial instability due to os odontoideum. Compression of the spinal cord caused by atlanto-axial instability is a common, serious complication in SED patients, and causes severe spinal cord symptoms or occasionally sudden death. We present an SED patient who underwent a posterior fusion of the occiput to the cervical spine for severe spinal cord symptoms due to atlanto-axial instability.

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