[Penicillin V and not amoxicillin is the first choice preparation in acute otitis].
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Biomedical subjects
Publications and source records attributed to K Lundgren.
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A biosurvey in the Danish metal industry measured the genotoxic exposure from stainless steel welding. The study comprised measurements of chromosomal aberrations (CA), sister-chromatid exchanges (SCE), unscheduled DNA synthesis (UDS) in peripheral lymphocytes and serum immunoglobulin G. Environmental monitoring of welding fumes and selected metal oxides, biomonitoring of chromium and nickel in serum and urine and mutagenic activity in urine, and evaluation of semen quality were also done. Manual metal arc (MMA) welding and tungsten inert gas (TIG) welding were the dominant welding processes. A higher frequency of chromosomal aberrations, classified as translocations, double minutes, exchanges and rings, was observed in stainless steel welders than in non-welders. SCE was lower in welders working with both MMA and TIG welding than in reference persons. N-Acetoxy-N-acetylaminofluorene (NA-AAF)-induced UDS was lower in 23 never-smoking welders than in 19 unexposed never-smokers. Smoking was a confounding factor resulting in significantly higher CA, SCE, NA-AAF binding to DNA and mutagenic activity in urine. Age was also a confounder: CA, SCE, NA-AAF binding to DNA and UDS increased significantly with age. No significant correlation between SCE and CA or between CA and UDS was found. UDS decreased significantly with increasing lymphocyte count and a higher lymphocyte count was seen in MMA welders than in reference persons and in smokers than in non-smokers. Differences in the composition among lymphocytes in exposed persons compared with non-exposed are suggested. MMA welding gave the highest exposure to chromium, an increased number of chromosomal aberrations and a decrease in SCE when compared with TIG welding. Consequently improvements in the occupational practice of stainless steel welding with MMA is recommended.
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The carcinogenic effect of three UVA tanning sources was studied in lightly pigmented hairless mice. The three tanning sources (Bellarium-S SA-1-12, Philips TL 09R and Philips TL 10R) have different emission spectra, and emit different amounts of UVB. Radiation from the tanning sources was administered for 20 min/day, 5 day/week in daily doses equivalent to those used in suntan salons. The radiation was given alone or after 12 weeks of exposure to solar-simulated UV radiation (SOLAR UV) (10 min/day, 4 day/week; daily dose, 19.5 kJ/m2 UVA and 3.9 kJ/m2 UVB). Irradiation with Bellarium-S SA-1-12 for 47 weeks and Philips TL 09R for 74 weeks induced skin tumours in 20/20 and 13/20 of the animals, respectively. When irradiation with Bellarium-S SA-1-12 and PHilips TL 09R was administered after 12 weeks of SOLAR-UV exposure, a strong enhancement of SOLAR-UV-induced photocarcinogenesis was observed (p < 0.001). Irradiation with Philips TL 10R was only slightly carcinogenic, and during 85 weeks of irradiation only one skin tumor appeared in a group of 20 mice. However, when irradiation with Philips TL 10R was administered after 12 weeks of exposure to SOLAR UV, an enhancement of SOLAR-UV-induced carcinogenesis was observed (p < 0.001). Our results suggest that the hazards of exposure to commercial tanning devices are increased when they are used after a period of natural sun exposure. Even tanning sources with a low carcinogenic potential are able to increase SOLAR-UV-induced carcinogenesis significantly.
wee1 acts antagonistically to cdc25 in the tyrosine dephosphorylation and activation of cdc2, yet biochemical evidence suggests that wee1 is not required for tyrosine phosphorylation and its role is obscure. We show here that a related 66 kd kinase, called mik1, acts redundantly with wee1 in the negative regulation of cdc2 in S. pombe. A null allele of mik1 has no discernible phenotype, but a mik1 wee1 double mutant is hypermitotically lethal: all normal M phase checkpoints are bypassed, including the requirement for initiation of cell cycle "start," completion of S phase, and function of the cdc25+ mitotic activator. In the absence of mik1 and wee1 activity, cdc2 rapidly loses phosphate on tyrosine, both in strains undergoing mitotic lethality and in those that are viable owing to a compensating mutation within cdc2. The data suggest that mik1 and wee1 act cooperatively on cdc2, either directly as the inhibitory tyrosine kinase or as essential activators of that kinase.
Immunocytochemistry was used to examine MAP5 immunoreactivity in the hippocampal formation obtained postmortem from five elderly, normal individuals, six individuals with Alzheimer's disease (AD), and two "transition" cases that did not have a history of dementia but did exhibit significant AD pathology. In all of the cases examined, axonal staining was restricted to the mossy fibers and their terminal field in CA3 stratum lucidum. In control cases, MAP5 immunoreactivity was observed in the neuronal cytoplasm and the proximal portion of the apical dendrites of pyramidal and granule cells. In both AD and transition cases, increased intensity of immunostaining was observed in CA3 pyramidal, subicular, and dentate gyrus granule cell neurons. Within individual neurons, immunoreactivity filled the neuronal perikarya, including the nuclear region, and the apical dendrite. Punctate staining was observed in neuritic plaques, but neurofibrillary tangles and neuropil threads were not immunostained. The increase and altered distribution of MAP5 immunoreactivity in both vulnerable and nonvulnerable neurons in AD may reflect an aberrant sprouting response. The increased expression of early cytoskeletal proteins may be tolerated in some regions such as CA3, but not in others including CA1 where the increased expression appear to precede aberrant phosphorylation, proteolysis, and incorporation of cytoskeletal proteins into AD pathology. Alternatively, the results could reflect sprouting in response to the neuronal loss and degeneration.
The effect of cisapride on duration of post-operative ileus after surgery was investigated in a randomized, double-blind, placebo-controlled study. Patients undergoing elective upper gastrointestinal (n = 47) or colonic (n = 22) surgery were pre-operatively randomly allocated to treatment with either cisapride 30 mg t.d.s., by rectal administration, or placebo. Treatment started exactly 48 h after surgery if the patient at this time had not passed stool. Time to passage of first stool after surgery was estimated. Mean time to passage of stool was 85 (32) h (s.d.) for cisapride-treated and 91 (43) h for placebo-treated patients. No difference between the treatment groups was noted. Treatment with cisapride did not shorten the duration of postoperative ileus after either upper gastrointestinal or colonic surgery.
A total of 102 children with recurrent otitis media or therapeutic failure after treatment with phenoxymethyl penicillin were entered into a double-blind study with parallel groups, comparing treatment with amoxycillin/clavulanate suspension (Spektramox) for 7 days with amoxycillin suspension (Imacillin) for 10 days. Bacterial and clinical investigations were performed. A total of 91 patients were evaluated for efficacy at the first follow-up visit (10-12 days after start of treatment). Amoxycillin/clavulanate and amoxycillin showed equally high, satisfactory treatment results, i.e. more than a 90% response. Similarly, there was no statistically significant difference between the treatment groups at the second follow-up visit (about 30 days after start of treatment). Bacteriological cultures from the nasopharynx showed equal distribution of Haemophilus influenzae, Branhamella catarrhalis and Streptococcus pneumoniae between the study groups. Elimination of the initially occurring pathogens was equal in the two study groups with the exception of B. catarrhalis which was eliminated to a significantly higher extent with amoxycillin/clavulanate. Both drugs were well tolerated. In patients with recurrent otitis media or therapeutic failure, treatment with amoxycillin/clavulanate for 7 days results in high, satisfactory clinical effects and is comparable to treatment with amoxycillin for 10 days.
The carcinogenic effect of 3 commercially available ultraviolet A (UVA) tanning sources was studied in lightly pigmented hairless mice. The tanning sources (Bellarium-S SA-1-12 and Philips TL 09R and TL 10R) have different emission spectra and emit different quantities of UVB. The tanning sources were administered either alone, or before irradiation with solar-simulated UV (solar UV). All 3 UVA tanning sources were able to induce skin tumors when administered in daily doses resembling those used in tanning salons (20 min/d, 5 d/week). Irradiation with Bellarium-S during 32 weeks induced skin tumors in all mice; a similar response was seen after 66 weeks of irradiation with Philips TL 09R. Irradiation with Philips TL 10R during 98 weeks induced tumors in 6 of 20 mice. Nine groups of 20 mice were pretreated 20 min/d, 5 d/week during 13 weeks with one of the UVA tanning sources. Three groups were irradiated with Bellarium-S, 3 groups with Philips TL 09R and 3 groups with Philips TL 10R in daily doses ranging from 0.2 to 1.8 minimum erythema doses (MED). The highest daily doses were equivalent to the doses received during one session in a commercial solarium. Subsequently all 9 groups were irradiated with 3.1 MED/d solar UV 10 min/d, 4 d/week until all mice had died. Time to first tumor was compared. All groups pretreated with Bellarium-S and Philips TL 09R showed an enhanced tumor development compared with a group irradiated with solar UV only. Pretreatment with Philips TL 10R did not enhance the carcinogenic effect of solar UV.
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At the ENT clinic in Luanda, Angola, 110 consecutive cases of children with chronic otitis media (COM) were studied to find out some clinical characteristics regarding age of onset and duration of otorrhea as well as the general state of health of the children. Eighty-five percent of the children had had longstanding otorrhea. In 75% of all the cases ear discharge had started during early childhood. It was possible to institute a simple conservative treatment of COM. Fifty percent returned to the clinic for a follow-up. The majority of the children came from families who lived under fairly good social conditions. One-hundred and five children with sensorineural hearing loss consulted the clinic. Many of them had had their hearing loss for several years before coming to the clinic. The etiology was in 39 cases infectious disease, meningitis being the most common one. Seventy-two percent had severe to profound hearing loss. Children with slight to moderate hearing loss rarely appeared at the clinic. Some of the hearing-handicapped children could be sent to a special school for rehabilitation.
Forty-seven patients in psychogeriatric day centre were analysed regarding use of resources, costs and well-being. The level of well-being was based on interviews with staff and relatives and related to the economic outcome--a cost utility analysis. A 6 month period prior to day care was compared with the first 6 months in such care. The use of resources at home increased by 20% while the use of institutional care was reduced by 22%. Fifty-three percent of the patients improved in their well-being after participation in day care. When the cost of utility analysis was applied, the cost for a well-year was 4293 pounds.
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Nucleic acid sequences can be localized on chromosomes in the electron microscope after hybridization with a biotinylated DNA probe followed by detection with a primary antibiotin antibody and a secondary antibody coupled to colloidal gold. Hybridization probes can also be labelled with alternative ligands such as N-acetoxy-2-acetylaminofluorene (AAF), Dinitrophenyl-dUTP and Digoxigenin-dUTP. Multiple labelling is possible if these differently modified DNA probes are used in conjunction with colloidal gold preparations of varying particle sizes. A substantial signal amplification can be achieved by incubating preparations with successive cycles of primary antibiotin antibody followed by a biotinylated secondary antibody. Detection is with Streptavidin-gold, and in the case of highly and moderately repeated sequences, the signal is visible in the light microscope. Detailed protocols are given for EM in-situ hybridization to whole mount metaphase chromosomes and include instructions necessary to perform multiple sequence localization and signal amplification.
More potent narrow-band UV sources need to be developed to determine the in vivo action spectra of long-term UV effects, such as photocarcinogenesis. This article describes the development of a potent, narrow-band UVB source, an Oriel solar simulator modified by the use of newly developed all-dielectric interference (ADI) filters. The sharp cut-off edges and high levels of transmission are unique features of these filters. Further, they can be produced as long-wave-pass or short-wave-pass filters with maximum transmittance at any given wavelength. The simulator is equipped with up to 4 ADI filters and potentially emits narrow UV bands. The filter combinations for narrow bands allow transmission of up to 80% of the incoming radiation. There was a homogeneous intensity area of 25 X 25 cm at a distance of 150 cm from the source in the centre of the irradiation field. The average intensity of UV available in narrow bands of UV (with a minimum half-band width of 11 nm) was 140 mW/m2. These values are sufficient to determine action spectra in groups of live animals (mice).