Width and depth of resection for small colorectal polyps: hot versus cold snare polypectomy

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Repair of potentially lethal damage by total and quiescent cells in solid tumors following a neutron capture reaction

Purpose: We analyzed the time-course of changes in the sensitivity of total (proliferating + quiescent and quiescent (Q) cell populations within solid tumors in situ following a neutron capture reaction and compared it with that after γ-ray irradiation. Methods: After continuous labeling of proliferating cells with BrdU for 5 days, mice bearing SCC VII tumors received thermal neutron irradiation with or without a ¹⁰B-labeled compound (sodium [¹⁰B]borocaptate, BSH, or dl-p-[¹⁰B]boronophenylalanine, BPA), or γ-ray irradiation. From 5 min to 72 h after treatment, tumors were excised, minced, and trypsinized. Cell suspensions were incubated for 48 h with the cytokinesis blocker cytochalasin-B. The micronucleus frequency for BrdU-unlabeled cells, Q cells at treatment, was then determined by immunofluorescence staining for BrdU. The micronucleus frequency for total cells was obtained from tumors that had not been pretreated with BrdU labeling. The sensitivity was evaluated in terms of the frequency of induced micronuclei in binuclear tumor cells (micronucleus frequency). Results: Overall, Q cells showed greater repair capacities than total cells. γ-Ray irradiation and neutron irradiation with BPA induced larger repair capacities in each cell population. In contrast, thermal neutron irradiation without a ¹⁰B-labeled compound induced the smallest repair capacity in both cell populations. The use of a ¹⁰B-labeled compound, especially BPA, widened the difference in sensitivity between total and Q cells, resulted in an increase in repair capacity in both cell populations, and made the repair patterns of the two cell populations look like those induced by γ-ray irradiation. Conclusion: Differences in sensitivity and repair patterns following the neutron capture reaction were thought to depend on differences in the distribution of the ¹⁰B-labeled compound between the proliferating and Q cell populations. Received: 18 February 1999 / Accepted: 4 June 1999     

Inhaled Rho kinase inhibitors are potent and selective vasodilators in rat pulmonary hypertension

We have found in chronically hypoxic rats that acute intravenous administration of the Rho kinase inhibitor Y-27632 nearly normalizes the pulmonary hypertension (PH) but has no pulmonary vascular selectivity. In this study, we tested if oral or inhaled Y-27632 would be an effective and selective pulmonary vasodilator in hypoxic PH. Although acute oral Y-27632 caused a marked and sustained decrease in mean pulmonary arterial pressure (MPAP), it also decreased mean systemic arterial pressure (MSAP). In contrast, 5 minutes of inhaled Y-27632 decreased MPAP without reducing MSAP. The hypotensive effect of inhaled Y-27632 on hypoxic PH was greater than that of inhaled nitric oxide, and the effect lasted for at least 5 hours. Inhaled fasudil, another Rho kinase inhibitor, caused selective MPAP reductions in monocrotaline-induced PH and in spontaneous PH in fawn-hooded rats, as well as in chronically hypoxic rats. These results suggested that inhaled Y-27632 was more effective than inhaled nitric oxide as a selective pulmonary vasodilator in hypoxic PH, and that Rho kinase-mediated vasoconstriction was also involved in the other models of PH. Inhaled Rho kinase inhibitors might be useful for acute vasodilator testing in patients with PH, and future work should evaluate their efficacy in the long-term treatment of PH.     

Pathological fractures due to intraosseous fat necrosis associated with pancreatitis

SIR, Necrosis of fatty bone marrow is an unusual complicationof severe pancreatic disorders. We describe a patient presentingwith multiple pathological fractures associated with alcoholicpancreatitis. A 76-yr-old man was admitted to our hospital in May 2000 forpain and swelling of the right hand, both feet and     

Detection and monitoring of methotrexate-associated lung injury using serum markers KL-6 and SP-D in rheumatoid arthritis

The applicability of monitoring concentrations of serum KL-6 and serum surfactant protein-D (SP-D) in the detection of methotrexate-associated lung injury (MTX pneumonitis) in patients with rheumatoid arthritis (RA) was investigated. The concentrations of these markers, sequentially measured in two patients with RA complicated with MTX pneumonitis, were increased in accordance with the severity of MTX pneumonitis. Conversely, the concentrations of these markers were decreased with the improvement of MTX pneumonitis, suggesting that the monitoring of these markers could be applicable not only for detecting the onset of MTX pneumonitis, but also for detecting the therapeutic response of MTX pneumonitis.     

Balloon catheter with check valves for experimental relief of acute aortic regurgitation.

To evaluate the ability of a newly designed balloon catheter with check valves to temporarily relieve hemodynamic deterioration in acute aortic regurgitation, we produced an experimental model of acute aortic regurgitation in closed-chest dogs using endomyocardial biopsy forceps. Aortic regurgitation was produced until an increase in aortic pulse pressure of over 50% was achieved. Left ventricular end-diastolic pressure rapidly increased after the production of aortic regurgitation. Immediately after the catheter began functioning, pulse pressure decreased from 133 +/- 1 to 78 +/- 5 mm Hg (mean +/- SEM) and left ventricular end-diastolic pressure also decreased from 26 +/- 1 to 13 +/- 1 mm Hg. These effects lasted as long as the catheter functioned. Although a mild (21 +/- 8 mm Hg) pressure gradient between the left ventricular peak systolic pressure and the aortic peak systolic pressure was observed when this catheter was used, forward stroke volume was no less than in the group in which the catheter had not been used. These findings suggest that the balloon catheter with check valves may effectively reduce aortic regurgitation.     

Identification of a point mutation in the catalytic domain of the protooncogene c-kit in peripheral blood mononuclear cells of patients who have mastocytosis with an associated hematologic disorder.

Both stem cells and mast cells express c-kit and proliferate after exposure to c-kit ligand. Mutations in c-kit may enhance or interfere with the ability of c-kit receptor to initiate the intracellular pathways resulting in cell proliferation. These observations suggested to us that mastocytosis might in some patients result from mutations in c-kit. cDNA synthesized from peripheral blood mononuclear cells of patients with indolent mastocytosis, mastocytosis with an associated hematologic disorder, aggressive mastocytosis, solitary mastocytoma, and chronic myelomonocytic leukemia unassociated with mastocytosis was thus screened for a mutation of c-kit. This analysis revealed that four of four mastocytosis patients with an associated hematologic disorder with predominantly myelodysplastic features had an A-->T substitution at nt 2468 of c-kit mRNA that causes an Asp-816-->Val substitution. One of one patient examined who had mastocytosis with an associated hematologic disorder had the corresponding mutation in genomic DNA. Identical or similar amino acid substitutions in mast cell lines result in ligand-independent autophosphorylation of the c-kit receptor. This mutation was not identified in the patients within the other disease categories or in 67 of 67 controls. The identification of the point mutation Asp816Val in c-kit in patients with mastocytosis with an associated hematologic disorder provides insight not only into the pathogenesis of this form of mastocytosis but also into how hematopoiesis may become dysregulated and may serve to provide a means of confirming the diagnosis, assessing prognosis, and developing intervention strategies.