Cuff bulk of tracheal tubes in adolescence

Purpose

To investigate cuff types for potential use in late childhood and early adolescence for appropriate fit.

Method

Formulae suggest the use of a tracheal tube having a 6.5 mm internal diameter at ages 8 to 10 years, so a model system was used to test the passage of cuffed and uncuffed tracheal tubes of 6.5 mm internal diameter through calibrated holes 8.1–16.6 mm diameter, in plastic plates.

Results

Uncuffed tracheal tubes passed through 9.0 mm diameter holes. “High pressure” cuffed tubes passed through 10.5 to 11.3 mm holes. “Low pressure” cuffed tubes passed through 12.3 to16.4 mm.

Conclusion

Patients aged 8 to 10 yr have a limiting internal diameter at the cricoid of 8 to 10 mm. Their unstretched tracheal diameter below the cricoid is only about 11 mm. The actual outside diameters of “low pressure” cuffs chosen by commonly used formulae considerably exceed the limiting diameters of eight to ten year old patients, even considering recommended compensation factors. Analysis of background data indicates that these problems are especially aggravated at this age by non-linear growth of the cricoid.     

An acute fatal occupational cadmium poisoning by inhalation

Summary A 43-year-old male smelter was admitted to a hospital on account of severe dyspnea about 2 days after exposure to brownish-yellow smoke produced by melting of copper scrap. On admission pronounced hypoxemia was revealed, and an oxygen-enriched gas was administered after intubation. Although inspired oxygen concentration was gradually increased, hypoxemia progressed and he died on day 11 in hospital.The principal autopsy finding was chiefly confined to the lungs. Both lungs were heavy (the left weighing 1,470 g; the right 1,710 g) and firm to the touch. Histologically, no normal alveoli were found throughout the entire lung. Some alveolar spaces were occupied by pneumocytes, others by organized exudate with fibrosis. Interstitial fibrosis was present. Patchy areas of inflammatory cell infiltrations as well as intra-alveolar hemorrhages were observed. On the basis of the above findings a diagnosis of diffuse alveolar damage was made.Based on the available evidence (presence of cadmium in the copper scrap, feature of the smoke, clinical signs with latent time, and high cadmium concentration of the lung), the diffuse alveolar damage was considered to have been caused by inhaled cadmium. The pulmonary change of the present case was more advanced in pathologic stage in comparison with those reported in the literature.     

Delirious episodes induced by intravenous administration of clomipramine associated with an acute increase in its plasma concentrations

The aim of this paper is to describe two cases of clomipramine-induced delirium. One 61-year-old and one 67-year-old female depressive patients became delirious after beginning intravenous clomipramine injections in addition to their oral clomipramine administrations. Their plasma levels of both clomipramine and its metabolite, desmethylclomipramine, were acutely increased about twofold during delirium. The intravenous clomipramine administrations were discontinued. Their delirious state was gradually improved after stopping the intravenous clomipramine administrations. These findings suggest that acute increases of plasma levels of clomipramine and desmethylclomipramine after intravenous clomipramine injections might be related to the appearance of the delirious episodes.     

In vitro metabolism of fenthion and fenthion sulfoxide by liver preparations of sea bream, goldfish, and rats.

The in vitro metabolism of fenthion and its sulfoxide (fenthion sulfoxide) in sea bream (Pagrus major) and goldfish (Carassius auratus) was investigated and compared with that in rats. Fenthion was oxidized to fenthion sulfoxide and the oxon derivative, but not to its sulfone, in the presence of NADPH by liver microsomes of sea bream, goldfish, and rats. These liver microsomal activities of the fish were lower than those of rats but were of the same order of magnitude. The NADPH-linked oxon- and sulfoxide-forming activities of liver microsomes of the fish and rats were inhibited by SKF 525-A, metyrapone, alpha-naphthoflavone, and carbon monoxide. The oxidizing activity to fenthion sulfoxide was also inhibited by alpha-naphthylthiourea. Several cytochrome P450 isoforms and flavin-containing monooxygenase 1 exhibited these oxidase activities. Fenthion sulfoxide was reduced to fenthion with liver cytosol of the fish and rats upon addition of 2-hydroxypyrimidine, N(1)-methylnicotinamide, or butyraldehyde, each of which is an electron donor of aldehyde oxidase, under anaerobic conditions. The activity was inhibited by menadione, beta-estradiol, and chlorpromazine, which are inhibitors of aldehyde oxidase. The activities in the fish livers were similar to those of rat liver. Aldehyde oxidase purified from the livers of sea bream and rats exhibited the reducing activity. Thus, fenthion and fenthion sulfoxide are interconvertible in fish and rats through the activities of cytochrome P450, flavin-containing monooxygenase, and aldehyde oxidase.     

Possible dominant-negative mutation of the SHIP gene in acute myeloid leukemia.

The SH2 domain-containing inositol 5'-phosphatase (SHIP) is crucial in hematopoietic development. To evaluate the possible tumor suppressor role of the SHIP gene in myeloid leukemogenesis, we examined primary leukemia cells from 30 acute myeloid leukemia (AML) patients, together with eight myeloid leukemia cell lines. A somatic mutation at codon 684, replacing Val with Glu, was detected in one patient, lying within the signature motif 2, which is the phosphatase active site. The results of an in vitro inositol 5'-phosphatase assay revealed that the mutation reduced catalytic activity of SHIP. Leukemia cells with the mutation showed enhanced Akt phosphorylation following IL-3 stimulation. K562 cells transfected with the mutated SHIP-V684E cDNA showed a growth advantage even at lower serum concentrations and resistance to apoptosis induced by serum deprivation and exposure to etoposide. These results suggest a possible role of the mutated SHIP gene in the development of acute leukemia and chemotherapy resistance through the deregulation of the phosphatidylinositol-3,4,5-triphosphate (PI(3,4,5)P3)/Akt signaling pathway. This is the first report of a mutation in the SHIP gene in any given human cancer, and indicates the need for more attention to be paid to this gene with respect to cancer pathogenesis.     

Macrophage-derived transforming growth factor-beta1 induces hepatocellular injury via apoptosis in rat severe acute pancreatitis

BACKGROUND: The mechanism of acute pancreatitis-induced hepatocellular injury is unclear. We have observed hepatocyte apoptosis in rat acute necrotizing pancreatitis. These studies were designed to determine the mediator(s) responsible for hepatocyte apoptosis and to clarify the significance of macrophages as its source. METHODS: A rat sodium deoxycholate-induced pancreatitis model was used. Immunohistochemical studies for apoptosis-inducing mediators on hepatocytes were examined in the liver and on the peritoneal macrophages. The levels of transforming growth factor-beta1 (TGF-beta1) were also evaluated quantitatively with an enzyme-linked immunosorbent assay. Induction of apoptosis on the hepatocytes was evaluated by in situ nick-end labeling and tissue DNA fragmentation enzyme-linked immunosorbent assay. Finally, the effects of TGF-beta1 neutralization and macrophage depletion were examined. RESULTS: In the liver and the peritoneal macrophages, strong expression of TGF-beta1 was detected early in the course of pancreatitis. In sodium deoxycholate-induced pancreatitis, the levels of TGF-beta1 were also elevated in the plasma (9.2 +/- 0.8 ng/mL), in the pancreatitis-associated ascitic fluid (11.5 +/- 0.6 ng/mL), and in the liver homogenate (2.8 +/- 0.3 ng/g of liver tissue). Moreover, the amount of fragmented DNA of the liver with pancreatitis was 290% +/- 20% of that with a sham operation and serum alanine aminotransferase levels elevated to 248.2 +/- 67.0 IU/L. TGF-beta1 neutralization partly blocked the positive labeling on the nuclei of the hepatocytes, the elevation of the amounts of fragmented DNA (205% +/- 10% of sham operation), and the serum alanine aminotransferase level (144.2 +/- 14.9 IU/L). On the other hand, the macrophage depletion caused a marked decrease in the TGF-beta1 protein level in the plasma (4.8 +/- 1.2 ng/mL) or in the pancreatitis-associated ascitic fluid (8.0 +/- 1.0 ng/mL). Moreover, the macrophage depletion completely inhibited the elevation of the TGF-beta1 protein level in the liver homogenate (1.5 +/- 0.4 ng/g of liver tissue), and thereafter decreased the amounts of the positive labeling on the nuclei of the hepatocytes and decreased the amount of fragmented DNA (120% +/- 18% of sham operation) and the serum alanine aminotransferase elevation (119.2 +/- 24.2 IU/L). CONCLUSIONS: In a model of sodium deoxycholate-induced pancreatitis, macrophages are responsible for pancreatitis-induced hepatocellular injury by means of apoptosis, and macrophage-derived TGF-beta1 is one of the major factors inducing the hepatocyte apoptosis.     

Sulfatide elongates dorsal skin flap survival in rats

Monoclonal antibodies to adhesive molecules have been used in many trials to decrease ischemia-reperfusion injury, which is considered to occur in areas such as the distal region of the random pattern flap. The monoclonal antibody to the primary neutrophil adherence-mediating glycoprotein CD18 improves the survival length of the random pattern flap. Sulfatide binds strongly with L- and P-selectin. We found that sulfatide has a protective effect against ischemia-reperfusion injury. The purpose of this study was to evaluate the effect of sulfatide on the survival length of the random pattern flap in rats. Sulfatide was administered intravenously just before elevation of the cranially based dorsal skin flap. Administration of sulfatide significantly augmented flap survival length (49.5 +/- 1.7 mm vs control 41.5 +/- 2.1 mm, P = 0. 01). Flap survival length was significantly longer than dye distance (49.1 +/- 2.0 mm vs 39.7 +/- 1.1 mm, P = 0.01). In the control flap, no significant difference between survival length and dye distance was detected. Histological examination 48 h after flap elevation showed leukocyte invasion in the dermal layer of control flaps, whereas little leukocyte invasion was observed in the flaps of rats administered sulfatide.