Arteriotomy patching by means of intraluminal pressure sealing venous autografts. A preliminary technical report.
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Animals↗
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Development of a computerized microstereotaxic method for localization and removal of minute CNS lesions under direct 3-D vision. Technical report.
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Brain Neoplasms↗
Role of computer-assisted analysis of the corneal endothelium in vitreoretinal surgery with intraocular silicone oil injection: a technical report.
The innermost lining of the cornea consists of a single layer of cells called the endothelium. Despite its name, the endothelium of the cornea differs considerably from the vascular endothelium, both functionally and morphologically. The corneal endothelium plays a fundamental role in maintaining the transparency of the corneal membrane, as the result of both its function as a barrier against penetration of the aqueous humor in the parenchyma and its ability to remove water from the stroma (usually referred to as the endothelial "pump" function). Any abnormality in the corneal endothelium causes, first, the impairment of its function as a barrier and pump due to the loss of stromal anti-turgor mechanisms, followed by edema and possible development into keratopathy. The specular microscope is an instrument which makes it possible to see the endothelial "mosaic" in the reflected image of the posterior corneal surface. A large variety of clinical specular microscopes is presently available, both contact and non-contact, which allow, for easy and rapid photography of the corneal endothelium "in vivo". In the present case, we used a non-contact computerized specular microscope to analyze the corneal endothelium in a group of patients affected by retinal detachment who needed to undergo vitreoretinal surgery with immission of silicone oil into the vitreal chamber.
Adult↗
Role of audiologists in vestibular and balance rehabilitation: position statement, guidelines, and technical report. ASHA Ad Hoc Committee on Vestibular Rehabilitation.
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Audiology↗
Technical report of the International Working Group on Breast MRI.
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Biopsy↗
Assessment of the diabetic foot using spiral computed tomography imaging and plantar pressure measurements: a technical report.
Persons with diabetes mellitus (DM) and peripheral neuropathy are at high risk for skin breakdown due to unnoticed excessive pressures to the plantar foot during walking. We developed methods that combined spiral x-ray computed tomography (SXCT) imaging and plantar pressure analysis to quantify internal foot structure and external pressure during plantar loading. Methods were tested using a subject with DM who had a plantar ulcer, and a healthy control. SXCT measurements were within 2 mm of truth and SXCT plantar recordings were within 6.5% of walking trials. Hammer toe deformity (second toe), severe atrophy of the intrinsic muscles and less contact area during plantar loading, and a peak plantar pressure three times greater at the site of the ulcer were measured in the diabetic foot as compared with the healthy control. This preliminary investigation suggests that these methods are accurate for structural and pressure measurements of diabetic and healthy feet.
Adult↗
Vertebroplasty in patients with severe vertebral compression fractures: a technical report.
Vertebroplasty is a procedure in which polymethlymethacrylate (PMMA) is injected into a vertebral body compression fracture. It has been suggested that fractues greater than 65% to 70% of the original vertebral body height are too compressed to be treated successfully with this procedure. We describe six patients with severe compression fractures that were successfully treated with vertebroplasty in which the trocar was inserted in the far lateral aspect of the vertebral body, because of the typical morphology of severe compression fractures.
Aged↗
Technical report: congenital adrenal hyperplasia. Section on Endocrinology and Committee on Genetics.
The Section on Endocrinology and the Committee on Genetics of the American Academy of Pediatrics, in collaboration with experts from the fields of pediatric endocrinology and genetics, developed this policy statement as a means of providing up-to-date information for the practicing pediatrician about current practice and controversial issues in congenital adrenal hyperplasia (CAH), including the current status of prenatal diagnosis and treatment, the benefits and problem areas of neonatal screening programs, and the management of children with nonclassic CAH. The reference list is designed to allow physicians who wish more information to research the topic more thoroughly.
Adrenal Hyperplasia, Congenital↗
Technical report: a technique of rapidly re-establishing a pneumoperitoneum with use of a wound protector during laparoscopic-assisted surgery.
The authors described a technique of rapidly reestablishing a pneumoperitoneum after laparoscopically assisted surgery by pulling up and clamping the edge of the wound protector. Our laparoscopic assisted surgical technique for the digestive tract is useful and easy to perform without using special devices.
Bedding and Linens↗
AAP technical report on the prevention of pneumococcal infections. American Academy of Pediatrics.
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Adult↗
[Vascular access for intermittent haemodialysis. Use of a Sparks obturator. Preliminary technical report (author's transl)].
It appears possible to envisage, and especially in patients where the vascular and in particular, venous system is defective, the insertion of a Sparks obturator as soon as the indication for haemodialysis is considered and before is indispensable. In the case of urgent haemodialysis, in most instances the nephrologist himself inserts a Scribner shunt in order to be able to dialyse his patient as rapidly as possible. There is no contraindication to the insertion, either at the same time or during the next few days, of an obturator which may be anastomosed to the vessels much later. All arterio-venous fistulae, all systems which may alter, should, in our opinion, be equipped in this way, so that as soon as maturation of the obturator has occurred immediate availability of an excellent means of access exists.
Arteriovenous Shunt, Surgical↗
NTP technical report on the toxicity studies of benzophenone (CAS No. 119-61-9). Administered in feed to F344/N rats and B6C3F mice.
Benzophenone is used as a photoinitiator, a fragrance enhancer, an ultraviolet curing agent, and, occasionally, as a flavor ingredient; it is also used in the manufacture of insecticides, agricultural chemicals, and pharmaceuticals and is an additive for plastics, coatings, and adhesives. In 14-week studies conducted to determine the toxicity of benzophenone, groups of 10 male and 10 female F344/N rats and B6C3F1 mice were given 0, 1,250, 2,500, 5,000, 10,000, or 20,000 ppm benzophenone in feed. These exposure concentrations resulted in the following average daily doses: 75, 150, 300, 700, or 850 mg benzophenone per kilogram body weight for male rats; 80, 160, 300, 700, or 1,000 mg/kg for female rats; 200, 400, 800, 1,600, or 3,300 mg/kg for male mice; and 270, 540, 1,000, 1,900, or 4,200 mg/kg for female mice. Animals were evaluated for clinical pathology, reproductive system effects, liver cytochrome P450 effects, and histopathology. Genetic toxicity studies were conducted in Salmonella typhimurium and mouse bone marrow polychromatic erythrocytes. Benzophenone was unpalatable at 20,000 ppm. All 20,000 ppm rats had significant body weight loss and were terminated for humane reasons before the end of studies. All male mice and four female mice in the 20,000 ppm group died. There was no exposure-related mortality in the remaining groups. Significantly decreased body weights relative to the controls were observed in all exposed groups of female rats and all exposed groups of male rats except the 1,250 ppm group. Lower body weights were apparent in 10,000 ppm male mice and in 5,000 ppm or greater female mice. In rats, the liver and kidney were identified as target organs of benzophenone toxicity. Treatment-related increases in liver weights were attributed to hypertrophy and/or cytoplasmic vacuolization of hepatocytes. Increased kidney weights were associated with a spectrum of renal changes in exposed males and females. Unique lesions observed in animals that died early as well as in survivors were well demarcated, wedge-shaped areas of prominent tubule dilatation. The lesion occurred in 2,500 ppm or greater males and in 10,000 and 20,000 ppm females. Foci of tubule regeneration were increased relative to the controls in exposed males and females. In exposed mice, significant microscopic findings were limited to centrilobular hypertrophy in the liver that corresponded to increased liver weights. The severity of hepatocyte hypertrophy was exposure-concentration dependent, with marked severity in all 20,000 ppm animals. Clinical chemistry analyses confirmed liver toxicity. In rats, increases in serum bile salt concentrations indicated cholestatic liver disease. On day 22, a 15-fold increase was evident in the 20,000 ppm groups, and at week 14, a twofold increase was seen in the 10,000 ppm groups. Increases in alanine aminotransferase and sorbitol dehydrogenase activities were mild in mice; however, more convincing of liver damage were increased alkaline phosphatase activities and serum bile salt concentrations, especially in 20,000 ppm females. Biochemical data indicated that benzophenone was a relatively potent inducer of the phenobarbital-type (2B) cytochrome P450 enzymes. Overall, induction was greater in rats than in mice. The gross (increased organ weights) and microscopic (hepatocellular hypertrophy) liver changes associated with benzophenone administration in rats and mice accompanied benzophenone-induced increases in pentoxyresorufin dealkylase activity. Benzophenone was not mutagenic in S. typhimurium strain TA98, TA100, TA1535, or TA1537, with or without S9 activation, and it did not induce micronuclei in bone marrow erythrocytes of male mice administered benzophenone by intraperitoneal injection. In conclusion, the liver is the primary target organ of benzophenone toxicity in rats and mice based on increases in liver weights, hepatocellular hypertrophy, clinical chemistry changes, and induction of liver microsomal cytochrome P450 2B isomer. The kidney was also identified as a target organ of benzophenone toxicity in rats only, based on exposure concentration-related increases in kidney weights and microscopic changes. The no-observed-adverse-effect level for benzophenone was not achieved in these studies.
Animals↗
NTP technical report on the toxicity and metabolism studies of chloral hydrate (CAS No. 302-17-0). Administered by gavage to F344/N rats and B6C3F1 mice.
Chloral hydrate is widely used as a sedative and a hypnotic in pediatric medicine. It is also a byproduct of water chlorination. Chloral hydrate has been shown to be genotoxic in numerous prokaryotic and eukaryotic assay systems including human lymphocytes in vitro. One of its metabolites, trichloroacetic acid, has demonstrated hepatocarcinogenic activity in mice. Trichloroethylene and perchloroethylene, both of which are metabolized to chloral hydrate, have been shown to be carcinogenic in rats and/or mice. Because of this evidence of carcinogenicity and because of the wide-spread use of chloral hydrate, 16- or 17-day range-finding toxicity studies and separate 16- or 17-day metabolism studies were performed in F344/N rats and B6C3F1 mice in preparation for further long-term rodent studies. In addition, in vitro studies of the metabolism and DNA-binding capacity of chloral hydrate and its metabolites were performed. Genetic toxicity studies were conducted in Salmonella typhimurium, cultured Chinese hamster ovary cells, Drosophila melanogaster, and mouse bone marrow cells. For the range-finding studies, groups of eight male and eight female F344/N Nctr BR rats and B6C3F1/Nctr BR (C57BL/6N x C3H/HeN MTV-) mice were administered 0, 50, 100, 200, 400, or 800 mg chloral hydrate per kg body weight in water by gavage 5 days per week for 17 days (rats) or 16 days (mice) for a total of 12 doses. One male rat receiving 800 mg/kg died after five doses. Two 800 mg/kg female rats died after dosing ended but before study termination. One male mouse in each group except the 400 mg/kg group died before the end of the study. Two 800 mg/kg female mice also died before the end of the study. The final mean body weight of 800 mg/kg male rats and the mean body weight gains of 400 and 800 mg/kg males were significantly less than those of the vehicle controls. The mean body weight gains of all groups of dosed male mice were significantly greater than that of the vehicle control group. The only clinical finding in rats and mice attributed to chloral hydrate treatment was light sedation in the 400 mg/kg groups and heavy sedation in the 800 mg/kg groups; sedation subsided within 30 minutes or 3 hours, respectively. The liver weights of 400 mg/kg male mice and 800 mg/kg male and female mice were significantly greater than those of the vehicle control groups. No chemical-related lesions were observed in rats or mice. Male and female rats and mice were administered a single dose of 50 or 200 mg chloral hydrate per kg body weight in water by gavage, or 12 doses of 50 or 200 mg/kg over 17 days (rats) or 16 days (mice). Plasma concentrations of chloral hydrate and its metabolites were determined 15 minutes, 1, 3, 6, and 24 hours, and 2, 4, 8, and 16 days after receiving 1 or 12 doses. Maximum concentrations of chloral hydrate were observed at the initial sampling point of 15 minutes. By 1 hour, the concentrations had dropped substantially, and by 3 hours, chloral hydrate could not be detected in rats or mice. Trichloroacetic acid was the major metabolite detected in the plasma. In rats, the concentrations rose slowly, with the peaks occurring between 1 and 6 hours after treatment. In mice, the peak concentrations were found 1 hour after dosing. The concentrations then slowly decreased such that by 2 days the metabolite could no longer be detected in rats or mice. Trichloroethanol was assayed both as the free alcohol and its glucuronide. In rats, the maximum concentrations of free trichloroethanol occurred at 15 minutes, while the peak concentrations of trichloroethanol glucuronide were found at 1 hour; by 3 hours, concentrations of both metabolites approached background levels. In mice, the maximum concentrations of both metabolites occurred at 15 minutes, and by 1 to 3 hours concentrations approached background levels. The plasma concentrations of chloral hydrate and its metabolites were dose dependent in rats and mice. In mice, plasma concentrations of trichloroacetic acid were significantly higher after a single dose than after 12 doses. None of the metabolic parameters appears to account for species differences that may exist in hepatocarcinogenicity. The data from the study of metabolism and DNA adduct formation indicated that in vitro metabolism of 200 microM to 5 mM chloral hydrate by male B6C3F1 mouse liver microsomes (control microsomes) generated free radical intermediates that resulted in endogenous lipid peroxidation, forming malondialdehyde, formaldehyde, acetaldehyde, acetone, and propionaldehyde. Similar concentrations of trichloroacetic acid and trichloroethanol, the primary metabolites of chloral hydrate, also generated free radicals and induced lipid peroxidation. Lipid peroxidation induced by trichloroacetic acid nearly equaled that induced by chloral hydrate, while that from trichloroethanol was three- to fourfold less. Metabolism of 200 microM to 5 mM chloral hydrate, trichloroacetic acid, and trichloroethanol by liver microsomes of B6C3F1 mice pretreated with pyrazole (pyrazole-induced microsomes) yielded lipid peroxidation products at concentrations two- to threefold greater than those from liver microsomes of untreated mice. Additionally, chloral hydrate-induced lipid peroxidation catalyzed by control and pyrazole-induced microsomes was reduced significantly by 2,4-dichloro-6-phenylphenoxyethylamine, a general cytochrome P450 inhibitor. Human lymphoblastoid transgenic cells expressing cytochrome P(450)2E1 metabolized 200 to 5,000 micrograms/mL chloral hydrate to reactants inducing mutations, whereas the parental cell line was inactive. The malondialdehyde-modified DNA adduct, 3-(2-deoxy-beta-D-erythro-pentofuranosyl)pyrimido[1,2 alpha]purin-10(3H)-one (MDA-MG-1), formed from the metabolism of 1 mM chloral hydrate, trichloroacetic acid, and trichloroethanol by control B6C3F1 mouse liver microsomes, mouse pyrazole-induced microsomes, male F344/N rat liver microsomes, and human liver microsomes in the presence and absence of calf thymus DNA was also determined. When incubated in the absence of calf thymus DNA, the amount of malondialdehyde formed from metabolism by pyrazole-induced mouse microsomes was twice that from rat or human liver microsomes. Amounts of chloral hydrate-induced and trichloroacetic acid-induced lipid peroxidation products formed from metabolism by rat and human liver microsomes were similar, and these quantities were about twice those formed from the metabolism of trichloroethanol. The quantity of MDA-MG-1 formed from the metabolism of chloral hydrate, trichloroacetic acid, and trichloroethanol by mouse, rat, and human liver microsomes exhibited a linear correlation with the quantity of malondialdehyde formed under incubation conditions in the absence of calf thymus DNA. Chloral hydrate was shown to be mutagenic in vitro and in vivo. At doses from 1,000 to 10,000 micrograms/plate, it induced mutations in S. typhimurium strain TA100, with and without S9 activation; an equivocal response was obtained in S. typhimurium strain TA98 in the absence of S9, and no mutagenicity was detected with strain TA1535 or TA1537. Chloral hydrate at doses from 1,700 to 5,000 micrograms/mL induced sister chromatid exchanges; at doses from 1,000 to 3,000 micrograms/mL, chromosomal aberrations were induced in cultured Chinese hamster ovary cells, with and without S9. Results of a sex-linked recessive lethal test in D. melanogaster were unclear; administration of chloral hydrate by feeding produced an inconclusive increase in recessive lethal mutations, results of the injection experiment were negative. An in vivo mouse bone marrow micronucleus test with chloral hydrate at doses from 125 to 500 mg/kg gave a positive dose trend. In summary, due to the absence of chloral hydrate-induced histopathologic lesions in rats and mice, no-observed-adverse-effect levels (NOAELs) were based on body weights of rats and liver weights of mice. The NOAELs for rats and mice were 200 mg/kg. Chloral hydrate was rapidly metabolized by rats and mice, with trichloroacetic acid occurring as the major metabolite. Peak concentrations of trichloroacetic acid occurred more quickly in mice. Plasma concentrations of chloral hydrate were dose dependent, but metabolic rates were unaffected by dose or sex. Chloral hydrate was mutagenic in vitro and in vivo. Metabolism of chloral hydrate and its metabolites produced free radicals that resulted in lipid peroxidation in liver microsomes of mice, rats, and humans. Induction of cytochrome P(450)2E1 by pyrazole increased the concentrations of lipid peroxidation products; inhibition of cytochrome P(450)2E1 by 2,4-dinitrophenylhydrazine reduced these concentrations. Metabolism of chloral hydrate and its metabolites by mouse, rat, and human liver microsomes formed malondialdehyde, and in the presence of calf thymus DNA formed the DNA adduct MDA-MG-1.
Animals↗