[Vaccinations--primary prevention with problems].
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Biomedical subjects
Publications and source records attributed to Anders Lindberg.
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This in vitro study evaluated curing depths of a universal hybrid resin composite with two viscosities (Tetric Ceram and Tetric Flow) after curing with 6 different quartz tungsten halogen and light-emitting diode curing units. Irradiance (light intensity) of the curing units varied between 200 and 700 mW/cm2. The curing units were used for standard, soft-start, or pulse curing. Curing times were 20 and 40 s for standard curing, 3 + 10 s and 3 + 30 s for pulse curing, and 40 s for soft-start. Resin composite specimens, 5 in each group, with a diameter of 4 mm and a height of 6 mm, were made in brass molds and cured from one side at a distance of 6 mm. After 2 weeks, the specimens were ground longitudinally half through the specimen. Curing depth was then determined by measurement of Wallace hardness for each half millimeter starting at 0.5 mm from the top surface. For all curing units and for both resin composites an increased curing time led to statistically significantly higher depth of cure (P < 0.0005). Tetric Flow showed a statistically significantly higher depth of cure than Tetric Ceram (P < 0.0005). All curing units cured more than 2.0 mm of both composites from a distance of 6 mm at 20 s curing time. The value for 40 s was 3.0 mm. The composite closer to the surface than the depth of cure value was equally well cured with all curing units investigated. There was a significant linear correlation between the determined irradiance of the curing units and the depths of cure obtained (20s: r = 0.89, P < 0.025; 40 s: r = 0.91, P < 0.01).
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The introduction of the 2 neuraminidase inhibitors (NAIs) zanamivir and oseltamivir has offered new options for the prevention and treatment of influenza. This article summarizes a Swedish consensus guidance document on the rational use of antiviral drugs in the management of influenza virus infections. Vaccination remains the cornerstone for influenza prophylaxis. Target groups for the annual vaccination programme are the 'at-risk' individuals, i.e. elderly patients ( > or = 65 y) and patients with chronic pulmonary disease or cardiovascular disease or other chronic diseases predisposing for a complicated course of influenza. Antiviral drugs are not a substitute for influenza vaccination, but could be used as adjuncts. Currently, 3 drugs have been approved for the treatment of influenza, including zanamivir and oseltamivir and the M2 inhibitor amantadin. Amantadin has come to very limited use, has recently been withdrawn from the Swedish market and is available only on a named patient basis. Compared with amantadin, the NAIs have clear advantages because of their broader anti-influenza activity against both type A and B, improved safety profiles and low potential for inducing drug resistance. The NAls are therefore recommended as first options in the treatment of influenza. Oseltamivir can be taken orally, whereas zanamivir is for oral inhalation. Limited in vitro and in vivo data suggest that oseltamivir is less potent against influenza B, whereas zanamivir seems equally effective against influenza A and B. In influenza-positive healthy adults and children, treated within 48 h after symptom onset, the NAIs shorten the duration of illness by about 1 d. No significant effect on the duration of symptoms has been documented in treated at-risk patients with influenza. Owing to their limited therapeutic benefit, general use of the NAIs in the treatment of influenza is not recommended, but they can be advocated on an individualized basis for patients with severe influenza who can start therapy within 48 h of the onset of symptoms. Zanamivir is the preferred choice in a confirmed influenza B epidemic. For prevention of influenza, 2 drugs are approved, oseltamivir in adults above 12 y old and amantadin in people above 10 y old. The 70-90% protective efficacy of oseltamivir for household postexposure prophylaxis and for seasonal prophylaxis is comparable to that reported for amantadin. Oseltamivir is the preferred drug for prophylactic use. Chemoprophylaxis is targeted at high-risk groups and should be considered on a case-by-case basis depending on the circumstances and the population requiring protection. A broader preventive use of oseltamivir can be advocated in at-risk groups during seasons when there is a poor antigenic match between the epidemic strains and the vaccine strains. Oseltamivir prophylaxis is otherwise recommended for patients unable to be vaccinated and for families exposed to influenza which include a member of the at-risk groups. In high-risk hospital units and in institutions caring for the elderly, oseltamivir prophylaxis, in combination with vaccination, can be recommended as measures to control an influenza outbreak.
Growth hormone (GH) deficiency is normally diagnosed when the affected child is between 6 and 8 years of age and a lack of normal growth first becomes noticeable. Some patients, however, are diagnosed as being GH deficient at a relatively young age (<2 years). These patients differ from the later-diagnosed patients in terms of their background, their characteristics of GH deficiency (GHD) and their response to GH replacement therapy. The analysis described in this article examined the similarities and differences between children in these categories identified from KIGS (Pharmacia International Growth Database). The results showed that although early-diagnosed patients had more severe GHD, they were much more responsive to GH therapy. Thus, it is suggested that early diagnosis and initiation of treatment in GH-deficient patients is strongly needed to achieve the maximum effects from therapy.
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Although recombinant techniques have enabled the production of limitless amounts of human growth hormone (GH), and clinical methods for diagnosis and treatment have been greatly enhanced, the mean final heights of children with idiopathic GH deficiency (IGHD) treated with GH remain in the range of -1.3 standard deviation scores (SDS) below normal height. One of the methods used to increase height outcomes is to delay the onset and progression of puberty to allow for a longer 'pre-pubertal' growth phase. We reviewed the KIGS (Pharmacia International Growth Database) data of patients with IGHD who had been treated with gonadotropin-releasing hormone agonists (GnRHa) in order to see if a greater gain in height could be achieved by altering the tempo of pubertal maturation. Near-final height data were analysed in 39 adolescents (out of a total of 249) who had received GH + GnRHa therapy and were compared with similar data from 1,893 patients with IGHD treated with GH alone. The total change in height SDS in boys who received GH alone was +1.6, in contrast to +1.1 in GH + GnRHa-treated boys; the total change in height SDS in girls who received GH alone was +1.4 in contrast to +1.1 in girls treated with GH + GnRHa. The near final height SDS in girls treated with GH + GnRHa was 1.0 below the mid-parental target height (MPH), whereas there was only a -0.5 SDS difference in girls treated with GH. Approximation to the MPH did not differ in boys between the two treatment groups. These data suggest that the attainment of a substantial height SDS by manipulating the tempo of puberty is limited, but that optimizing growth during the pre-pubertal phase is a more important factor.
A model was developed that allows physicians to individualize GH treatment in children born short for gestational age (SGA) who fail to show spontaneous catch-up growth. Data from children (n = 613) in a large pharmacoepidemiological survey, the KIGS (Pharmacia International Growth Database), or who had participated in clinical trials were used to develop the model. Another group of similar children (n = 68) from KIGS was used for validation. In the first year of GH treatment, the growth response correlated positively with GH dose, weight at the start of GH treatment, and midparental height SD score and negatively with age at treatment start. Using this model, 52% of the variability of the growth response could be explained, with a mean error SD of 1.3 cm. GH dose was the most important response predictor (35% of variability), followed by age at treatment start. The second year growth response was best predicted by a three-parameter model (height velocity in yr 1 of treatment, age at start of treatment, and GH dose), which accounted for 34% of the variability, with an error SD of 1.1 cm. The first year response to GH treatment was the most important predictor of the second year response, accounting for 29% of the variability. No statistically significant differences between the predicted and observed growth responses were found when the models were applied to the validation groups. In conclusion, using simple variables, we have developed a model that can be used in clinical practice to adjust the GH dose to achieve the desired growth response in patients born SGA. Furthermore, this model can be used to provide patients with a realistic expectation of treatment and may help to identify compliance problems or other underlying causes of treatment failure.
The role of GH treatment during total pubertal growth (TPG) is still unclear. We developed a prediction model for TPG (centimeters) through a multiple regression analysis of various prepubertal parameters in 303 adolescents with idiopathic GH deficiency from the KIGS database. Prepubertal catch-up growth and near-adult height were achieved, and GH dose was kept constant at approximately 30 micro g/kg.d. The model was validated on a cohort of 36 patients from one center. Four TPG predictors explained 70% of the variability with an error SD of 4.2 cm: gender (TPG in males was >11.3 cm vs. that in females), age at onset of puberty (negative), height SD score minus midparental height SD score at puberty onset (negative), and mean GH dose during puberty (positive). Our analysis suggests that TPG in idiopathic GH deficiency is only moderately dependent on GH dose. The use of a higher GH dosage at the onset of puberty should thus depend on the individual's height development. The TPG model aids in the planning of individually optimized and cost-effective GH treatment.
PURPOSE: To evaluate the durability of a new open sandwich restoration with, as shown in a previous scanning electron microscope study, improved interfacial adaptation. A polyacid-modified resin-based composite (PMRC; compomer) was placed as an intermediate layer and covered with resin composite (RC). A direct RC restoration was used as control. MATERIALS AND METHODS: Of 57 patients, each received at least one pair of Class II restorations, one PMRC/RC open sandwich and one RC control. In total, 75 pairs of Class II restorations, 68 premolars and 82 molars, all in occlusion, were placed by two dentists. Most of the cavities were surrounded by enamel. The restorations were evaluated at baseline, 6, 12, 24 and 36 months by a slightly modified USPHS criteria. RESULTS: Five of 148 restorations evaluated during 3 years were rated as unacceptable. Two, one in each group, because of endodontic treatment and one RC restoration was replaced because of tooth fracture. Secondary caries was observed contiguous to one restoration in each group at the 36-month recall. Except for the two patients with pulpitis, none of the others reported postoperative sensitivity. No significant differences were seen between the restoration techniques. For marginal adaptation a significant change occurred between baseline and 6 months in both groups. For marginal discoloration, a significant change was observed at 6 months in the sandwich group and at 36 months in the RC group. Color match of the resin composite material changed significantly in both groups at 36 months. It was concluded that both techniques showed good durability during the 3-year follow up.
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