Approach through the temporal horn of the lateral ventricle for clipping of large dorsal type basilar bifurcation aneurysms

Summary The authors describe an approach through the temporal horn of the lateral ventricle which proved to be useful for clipping of a large dorsal type basilar bifurcation aneurysms. It facilitates the preservation of the perforating arteries behind the aneurysm, because it gives sufficient working space to move the aneurysm dome. Furthermore this approach avoids many of the disadvantages of other approaches, especially the risk of iatrogenic injuries of the Sylvian or Labe's vein.     

HTLV-I, HIV-I, and Hepatitis B and C Viruses in Western Province, Papua New Guinea: A Serological Survey

Seven hundred and twenty-three serum samples from individuals in 13 Gidra-speaking villages in Western Province, Papua New Guinea were tested for evidence of infection with human T- lymphotropic virus type I (HTLV-I), human immunodeficiency virus type I (HIV-I), hepatitis B virus (HBV) and hepatitis C virus (HCV). No samples were positive for antibodies to HIV-I. Antibodies to HTLV-I were found in 13 samples (1.8%), HBV surface antigens (HBsAg) were found in 86 samples (11.9%), and antibodies to HCV were found in 30 samples (4.1%). Six (46.2%) of 13 HTLV-I positive samples were positive for HCV or HBsAg. The seropositive rate varied in different villages and the incidence of HTLV-I and HCV was higher in coastal and riverine areas than inland.     

Characterization of certain hepatocyte-proliferating and/or protective factors induced by the sensitization of freezing-thawing hepatic tissue

Although tumor cryosurgery would be expected to produce beneficial immunological effects from the enhancement of anti-tumor activity, under certain conditions the tumor may become enlarged and metastases promoted due to increased immunosuppressive activity and a high zone tolerance. In the present study, we examined whether hepatocyteproliferating factors were produced by the inoculation of freezing-thawing hepatic tissue (FTHT). Serum obtained from rats inoculated with FTHT increased DNA synthesis, according to measurement by [³H]thymidine incorporation in primary cultured rat hepatocytes. This increase was dependent on the serum concentration, with serum obtained on day 14 after the inoculation being the most potent for hepatocyte proliferation. The sensitized serum promoted DNA synthesis nearly as much as serum obtained from a 70% hepatectomized rat, but slightly less than 10ng/ml hepatocyte growth factor. The sensitized serum also protected hepatocytes from carbon tetrachloride (CCI₄)-induced hepatotoxicity. Optical density measured by the 3-(4,5-dimethyl-thiazole-2-yl)-2,5-diphenyl tetrozolium bromide (MTT) cytotoxicity assay was increased, and the release of aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase in medium was decreased by treating hepatocytes damaged by CCI₄ with the sensitized serum. These results suggest that certain hepatocyte-proliferating and protective factors are induced in serum by the inoculation of freezing-thawing hepatic tissue, and that the sensitized serum may be useful in the treatment of liver failure.     

EFFECTS OF SARAFOTOXIN S6c ON RENAL HAEMODYNAMICS AND URINE FORMATION IN ANAESTHETIZED DOGS

1. The effects of sarafotoxin S6c (S6c), a selective endothelin ETB receptor agonist, on renal haemodynamics and urine formation were examined in anaesthetized dogs. 2. Intrarenal arterial infusion of S6c at a rate of 1 or 5 ng/kg per min produced a transient increase in renal blood flow (RBF), with no change in systemic blood pressure and heart rate; RBF then decreased gradually to below the basal value. There were significant and dose-dependent increases in urine flow and free water clearance and decreases in urine osmolality during S6c infusion, whereas urinary excretion of sodium and glomerular filtration rate (GFR) remained unchanged. Simultaneously, S6c administration elicited a marked increase in urinary excretion of nitric oxide (NO) metabolites, N0₂^? and N0₃^? (UNO*V). 3. In dogs simultaneously administered S6c (5 ng/kg per min) and iV^G-nitro-L-arginine (NOARG; 40 (jig/kg per min), a NO synthase inhibitor, the renal vasodilator effect of S6c was abolished and marked reductions in RBF and GFR were observed. The S6c-induced diuretic action was not affected by NOARG. In the presence of NOARG, there was a small amount of UNO_xV at the basal level and the administration of S6c did not increase UNOxV. 4. These results suggest that an intrarenal arterial infusion of S6c enhances the production of NO in the kidney and that this enhancement contributes to the peptide-induced renal vasodilation. In contrast, it is unlikely that S6c-induced water diuresis is related to NO production stimulated by this peptide.     

The localization of CD44 and moesin in osteoclasts after calcitonin administration in mouse tibiae

We investigated the immunohistochemical localization of CD44, hyaluronate receptor, and moesin, of the ezrinradixin-moesin (ERM) family, in osteoclasts after calcitonin adminstration using confocal laser scanning microscopy and transmission electron microscopy to clarify the role of CD44 and moesin in their cytoskeletal organization and cell polarity. We also elucidated the localization of osteopontin (OPN) to confirm its possible role in cell-matrix recognition via CD44. In untreated mice, intense immunoreactivities for CD44 and moesin were detected on the basolateral plasma membrane of osteoclasts. Rhodamine-phalloidin reactivity was seen in a bandlike pattern on the region of contact between osteoclasts and bone and was also detected moderately along their basolateral plasma membrane. At 30 min after calcitonin administration, osteoclasts did not show either clear zones or ruffled borders. The bandlike reactivity of rhodamine-phalloidin in the contact region was diminished, although labeling was seen along osteoclasts. CD44 and moesin were colocalized along their plasma membranes, including the region facing the bone surface. Electron microscopic observation revealed that the microvillus processes in the contacting region with bone surface, as well as the basolateral plasma membrane, showed immunoreactivities to CD44 and moesin. At 60 min, some osteoclasts attached to bone and showed a bandlike pattern of rhodamine-phalloidin. On the other hand, OPN was localized under CD44-positive cytoplasmic processes and the clear zone of osteoclasts. These findings suggest that calcitonin effects on the cell polarity of osteoclasts and the CD44-moesin-actin filament system in osteoclasts plays an imporant role in cell polarity and cell-matrix recognition.     

Screening of H-ras Gene Point Mutations in 50 Cases of Bladder Carcinoma

Background Mutation converts the H-ras gene into an activated oncogene in about 10% of human bladder cancers. Codons 12 and 61 are the major "hot spots" for activation. A simple and accurate method to detect point mutations in these codons may be clinically useful for early diagnosis of bladder cancer.
Methods Bladder cancer samples from 50 patients, plus 10 samples of normal bladder mucosa, were analyzed for possible point mutation of the H-ras gene at either codon 12 or codon 61. The H-ras gene DNA segments that include these 2 codons were amplified by PCR methods, then the possible presence of a point mutation was evaluated at each codon by susceptibility of the respective DNA segments to digestion with the restriction enzyme and by dot blot hybridization assay. A bladder cancer patient who had an H-ras gene mutation was examined to see whether the mutation was also detectable in the cells released in the urine.
Results Definite or possible point mutations were found in 6 (1 2%) out of 50 bladder cancer patients, while no mutation was detected in normal mucosa. A point mutation could also be detected in cells isolated from the patient's urine sample.
Conclusion The prevalence of point mutations at codon 1 2 or codon 61 of the H-ras gene found in this study was similar to that previously estimated for human bladder cancer by DNA transfection assay. The method we have used for detecting point mutations of the H-ras gene provides a simple and highly accurate way to detect mutated cancer cells even in the urine. It may be clinically usable for early diagnosis of bladder cancer.     

Ross procedure in an infant weighing 4.5 kg

A 6 month-old male infant (weight: 4.5 kg) with congenital aortic stenosis underwent aortic valve replacement with a pulmonary autograft (Ross procedure). The right ventricular outflow tract (RVOT) was reconstructed with a polytetrafluoroethylene (PTFE)-valved equine pericardial conduit. At the age of 5, re-RVOT reconstruction with an equine pericardial patch bearing a PTFE monocusp was required because of severe pulmonary stenosis resistant to 2 attempts of percutaneous transluminal pulmonary valvotomy. Currently, at the age of 8, the degree of aortic regurgitation is trivial and the pulmonary autograft is free of functional deterioration despite somatic growth.     

Inhibitory effects of nisoldipine and saralasin on angiotensin II-induced antidiuresis in anesthetized dogs

Inhibitory effects of the calcium channel blocker nisoldipine on angiotensin II-induced antidiuresis were investigated in anesthetized dogs, and the findings were compared with those of saralasin. Intrarenal arterial infusion of 10 ng/kg/min angiotensin II resulted in marked decreases in renal blood flow (RBF) and urine formation, with a relatively moderate decrease in glomerular filtration rate. There were marked reductions in the fractional excretion of lithium, which is used as an index of the fractional proximal excretion of sodium, and the fractional distal excretion of sodium. Nisoldipine (50 ng/kg/min) administered intrarenally produced a partial inhibition on the decreased response of RBF to angiotensin II. The peptide-induced decreases in urine flow, urinary excretion of electrolytes and fractional excretion of electrolytes were abolished by nisoldipine. In contrast, when saralasin was administered intrarenally at 10 ng/kg/min, a dose which could partially inhibit the angiotensin II-induced decrease in RBF to the same extent as seen with nisoldipine, the antagonist attenuated, but did not abolish, the antidiuretic action of angiotensin II. Significant decreases in urine formation by angiotensin II were observed, even in the presence of saralasin. These results suggest that nisoldipine, unlike saralasin, preferentially interferes with the stimulatory effect of angiotensin II, as related to the renal tubular reabsorption of sodium and water.