Social status qualifiers: dimensions and determinants of factors shaping social status for women and men in Sweden.

This study contributes to our understanding of what lifestyle factors affect the social status of women and men in contemporary postmaterialist societies. We examine the dimensions and determinants of social status qualifiers among Swedish people using a survey of 1,650 Swedish respondents who ranked the importance of 14 qualifiers for the social status of a woman and a man. The analysis showed surprisingly strong similarities in what factors affect the social status of women and men - both in the importance of individual status qualifiers and in the three underlying status dimensions: The highest-ranked dimension included status qualifiers related to external material resources and properties. The second most important dimension comprised interactional resources such as manners, looks, being married and having children. The third dimension concerned the importance of interest and engagement in politics, the environment, and fine art, which were of the least importance for social status. The few significant differences in ascriptions of status for a woman or a man were rather gender stereotypical. In addition, the analysis revealed some significant differences in status perceptions among the respondents: Gender, class, educational background, and country of birth were among the main determinants of such differences.

Oral neuromuscular training in patients with dysphagia after stroke: a prospective, randomized, open-label study with blinded evaluators.

BACKGROUND: Oral and pharyngeal swallowing dysfunction are common complications in acute stroke patients. This primary aim of this study was to determine whether oral neuromuscular training improves swallowing function in participants with swallowing dysfunction after stroke. A secondary aim was to assess how well results of the timed water-swallow test (TWST) correspond with swallowing dysfunction diagnosed by videofluoroscopy (VFS). METHODS: This was an intention-to-treat two-centre prospective randomized open-label study with blinded-evaluators (PROBE) design. At 4 weeks after stroke onset, participants with swallowing dysfunction were randomized to 5 weeks of continued orofacial sensory-vibration stimulation with an electric toothbrush or additional oral neuromuscular training with an oral device (Muppy®). Participants were examined with TWST, a lip-force test, and VFS before (baseline), after 5 weeks' treatment (the end-of-treatment), and 12 months after treatment (follow-up). The baseline VFS results were compared with the TWST results. The primary endpoint was changes in swallowing rate assessed using TWST, from baseline to the end of training and from baseline to follow-up based on intention-to-treat analyses. The secondary endpoint was the corresponding changes in lip-force between baseline, the end of treatment, and follow-up. RESULTS: The participants were randomly assigned as controls (n = 20) or for intervention with oral neuromuscular training (n = 20). After treatment, both groups had improved significantly (intervention, P < 0.001; controls, P = 0.001) in TWST but there was no significant between-group difference in swallowing rate. At the 12-month follow-up, the intervention group had improved further whereas the controls had deteriorated, and there were significant between-group differences in swallowing rate (P = 0.032) and lip force (P = 0.001). A TWST < 10 mL/sec at baseline corresponded to VFS-verified swallowing dysfunction in all assessed participants. CONCLUSION: The 5-week oral neuromuscular training improved swallowing function in participants with post-stroke dysphagia compared with the controls 12 months after intervention, but there was no between-group difference in improvement immediately after treatment. TWST results corresponded with VFS results, making TWST a feasible method for identifying persons with swallowing dysfunction after stroke. Larger randomized controlled trials are required to confirm our preliminary positive long-term results. TRIAL REGISTRATION: Retrospectively registered at ClinicalTrials.gov : NCT04164420 . Registered on 15 November 2019.

Quantification and reliability of [11C]VC - 002 binding to muscarinic acetylcholine receptors in the human lung - a test-retest PET study in control subjects.

BACKGROUND: The radioligand [11C]VC-002 was introduced in a small initial study long ago for imaging of muscarinic acetylcholine receptors (mAChRs) in human lungs using positron emission tomography (PET). The objectives of the present study in control subjects were to advance the methodology for quantification of [11C]VC-002 binding in lung and to examine the reliability using a test-retest paradigm. This work constituted a self-standing preparatory step in a larger clinical trial aiming at estimating mAChR occupancy in the human lungs following inhalation of mAChR antagonists. METHODS: PET measurements using [11C]VC-002 and the GE Discovery 710 PET/CT system were performed in seven control subjects at two separate occasions, 2-19 days apart. One subject discontinued the study after the first measurement. Radioligand binding to mAChRs in lung was quantified using an image-derived arterial input function. The total distribution volume (VT) values were obtained on a regional and voxel-by-voxel basis. Kinetic one-tissue and two-tissue compartment models (1TCM, 2TCM), analysis based on linearization of the compartment models (multilinear Logan) and image analysis by data-driven estimation of parametric images based on compartmental theory (DEPICT) were applied. The test-retest repeatability of VT estimates was evaluated by absolute variability (VAR) and intraclass correlation coefficients (ICCs). RESULTS: The 1TCM was the statistically preferred model for description of [11C]VC-002 binding in the lungs. Low VAR (< 10%) across analysis methods indicated good reliability of the PET measurements. The VT estimates were stable after 60 min. CONCLUSIONS: The kinetic behaviour and good repeatability of [11C]VC-002 as well as the novel lung image analysis methodology support its application in applied studies on drug-induced mAChR receptor occupancy and the pathophysiology of pulmonary disorders. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT03097380, registered: 31 March 2017.

Pharmacokinetics of the Oral Selective CXCR2 Antagonist AZD5069: A Summary of Eight Phase I Studies in Healthy Volunteers.

OBJECTIVE: The aim of this study was to summarise the pharmacokinetic findings from eight phase I studies in healthy volunteers given oral AZD5069, a selective small-molecule CXCR2 antagonist. METHODS: 240 healthy volunteers across eight phase I studies received single (0.1-200 mg) or multiple once- or twice-daily (10-120 mg) oral AZD5069 as solution, suspension, capsules or tablets. Pharmacokinetics were evaluated using non-compartmental analysis methods. RESULTS: AZD5069 was rapidly absorbed (time to maximum concentration ~ 2 h) under fasting conditions. A high-fat, high-calorie meal delayed and reduced the peak plasma AZD5069 concentration (Cmax) by 50%, but total exposure (AUC) was unchanged (fed:fasting geometric mean ratio 90% confidence interval within 0.80-1.25). The plasma concentration of AZD5069 declined with an initial half-life of 4 h and terminal half-life of 11 h. Steady-state plasma concentrations were achieved within 2-3 days and accumulation was ~ 1.1-fold with twice-daily dosing. Systemic exposure was approximately proportional to dose. Intra- and inter-subject variability in AUC was 3-11 and 29-64%, respectively. Less than 5% of the AZD5069 dose was excreted as parent drug in the urine. Elderly subjects had 39% higher AZD5069 AUC and 21% higher Cmax than younger adults. Japanese subjects had similar or slightly higher exposure to AZD5069 than Caucasian subjects. Co-administration with ketoconazole resulted in 2.1-fold higher AUC and 1.6-fold higher Cmax. All formulations had similar bioavailability. CONCLUSIONS: AZD5069 demonstrated predictive linear pharmacokinetics with low intra- and moderate inter-subject variability and no major influences from ethnicity, age, food or formulation. Half-life data indicated suitability for twice-daily dosing. CLINICALTRIALS. GOV IDENTIFIERS: NCT00953888, NCT01051505, NCT01083238, NCT01100047, NCT01332903, NCT01480739, NCT01735240, NCT01989520.

Dipeptidyl Peptidase 1 Inhibitor AZD7986 Induces a Sustained, Exposure-Dependent Reduction in Neutrophil Elastase Activity in Healthy Subjects.

Neutrophil serine proteases (NSPs), such as neutrophil elastase (NE), are activated by dipeptidyl peptidase 1 (DPP1) during neutrophil maturation. High NSP levels can be detrimental, particularly in lung tissue, and inhibition of NSPs is therefore an interesting therapeutic opportunity in multiple lung diseases, including chronic obstructive pulmonary disease (COPD) and bronchiectasis. We conducted a randomized, placebo-controlled, first-in-human study to assess the safety, tolerability, pharmacokinetics, and pharmacodynamics of single and multiple oral doses of the DPP1 inhibitor AZD7986 in healthy subjects. Pharmacokinetic and pharmacodynamic data were analyzed using nonlinear mixed effects modeling and showed that AZD7986 inhibits whole blood NE activity in an exposure-dependent, indirect manner-consistent with in vitro and preclinical predictions. Several dose-dependent, possibly DPP1-related, nonserious skin findings were observed, but these were not considered to prevent further clinical development. Overall, the study results provided confidence to progress AZD7986 to phase II and supported selection of a clinically relevant dose.

Efficacy and safety of a CXCR2 antagonist, AZD5069, in patients with uncontrolled persistent asthma: a randomised, double-blind, placebo-controlled trial.

BACKGROUND: Airway neutrophilic inflammation is a pathological feature in some patients with severe asthma. Stimulation of the chemokine receptor CXCR2 mediates neutrophil migration into the airways. We investigated the safety and efficacy of AZD5069, a CXCR2 antagonist, as an add-on therapy in patients with uncontrolled severe asthma. METHODS: In this multicentre, randomised, double-blind, placebo-controlled, dose-finding trial, we enrolled patients aged 18 years or older with uncontrolled asthma despite combination therapy with long-acting ß2 agonists and medium-dose or high-dose inhaled corticosteroids. Patients were randomised in a 1:1:1:1 ratio via an interactive voice-response or web-response system to receive 5, 15, or 45 mg oral AZD5069 twice daily or matched placebo. The primary endpoint was the number of severe asthma exacerbations in 6 months. Safety was assessed in the 6-month treatment period and an optional 6-month safety extension. This trial is registered with ClinicalTrials.gov, number NCT01704495. FINDINGS: 640 patients with a mean age of 52 (SD 11·8) years were randomised, 478 to receive AZD5069 (5 mg n=160, 15 mg n=156, and 45 mg n=162) and 162 placebo. No dose of AZD5069 reduced the rate of severe exacerbations compared with placebo (rate ratio for 5 mg 1·29, 90% CI 0·79-2·11; for 15 mg 1·53, 0·95-2·46; and for 45 mg 1·56, 0·98-2·49). Treatment with AZD5069 was generally well tolerated. The most commonly reported adverse event overall was nasopharyngitis, seen in 18 (11·5%) receiving 5 mg, 13 (8·5%) receiving 15 mg, and 18 (11·2%) receiving 45 mg AZD5069, and 31 (19·5%) of those receiving placebo. INTERPRETATION: Treatment with this selective CXCR2 antagonist did not reduce the frequency of severe exacerbations in patients with uncontrolled severe asthma. These findings bring into question the role of CXCR2-mediated neutrophil recruitment in the pathobiology of exacerbations in severe refractory asthma. FUNDING: AstraZeneca.

A randomised, placebo-controlled study of the CXCR2 antagonist AZD5069 in bronchiectasis.

This randomised double-blind placebo-controlled parallel-group multicentre phase IIa study evaluated the effect of the CXCR2 antagonist AZD5069 on sputum neutrophil counts in adults with bronchiectasis.Patients were randomised 1:1 to receive AZD5069 80 mg or placebo orally twice daily for 28 days. Assessments included blood cell counts, inflammatory markers in blood, morning spontaneous sputum, lung function, safety and tolerability and patients completed daily BronkoTest diary cards. The primary outcome measure was the change in absolute sputum neutrophil count.Of 52 randomised patients, 45 completed treatment, 20 (76.9%) out of 26 receiving AZD5069 and 25 (96.2%) out of 26 receiving placebo. AZD5069 reduced the absolute neutrophil cell count in morning sputum by 69% versus placebo (p=0.004); percentage sputum neutrophil count was reduced by 36% (p=0.008). The number of infections/exacerbations was similar with AZD5069 and placebo (nine versus eight), but these led to more study discontinuations with AZD5069 (four versus zero). Sputum interleukin (IL)-6 and growth-regulated oncogene (GRO)-α and serum GRO-α, IL-1ß and IL-8 levels increased with AZD5069 versus placebo (all p<0.001), while serum high-sensitivity C-reactive protein levels did not change. AZD5069 was well tolerated.AZD5069 markedly reduced absolute sputum neutrophil counts in bronchiectasis patients, although this was not associated with improvements in clinical outcomes in this exploratory study.

The effect of a selective CXCR2 antagonist (AZD5069) on human blood neutrophil count and innate immune functions.

AIMS: The aim of the present study was to investigate whether selective antagonism of the cysteine-X-cysteine chemokine receptor-2 (CXCR2) receptor has any adverse effects on the key innate effector functions of human neutrophils for defence against microbial pathogens. METHODS: In a double-blind, crossover study, 30 healthy volunteers were randomized to treatment with the CXCR2 antagonist AZD5069 (100 mg) or placebo, twice daily orally for 6 days. The peripheral blood neutrophil count was assessed at baseline, daily during treatment and in response to exercise challenge and subcutaneous injection of granulocyte-colony stimulating factor (G-CSF). Neutrophil function was evaluated by phagocytosis of Escherichia coli and by the oxidative burst response to E. coli. RESULTS: AZD5069 treatment reversibly reduced circulating neutrophil count from baseline by a mean [standard deviation (SD)] of -1.67 (0.67) ×10(9) l(-1) vs. 0.19 (0.78) ×10(9) l(-1) for placebo on day 2, returning to baseline by day 7 after the last dose. Despite low counts on day 4, a 10-min exercise challenge increased absolute blood neutrophil count, but the effect with AZD5069 was smaller and not sustained, compared with placebo treatment. Subcutaneous G-CSF on day 5 caused a substantial increase in blood neutrophil count in both placebo- and AZD5069-treated subjects. Superoxide anion production in E. coli-stimulated neutrophils and phagocytosis of E. coli were unaffected by AZD5069 (P = 0.375, P = 0.721, respectively vs. baseline, Day 4). AZD5069 was well tolerated. CONCLUSIONS: CXCR2 antagonism did not appear adversely to affect the mobilization of neutrophils from bone marrow into the peripheral circulation, phagocytosis or the oxidative burst response to bacterial pathogens. This supports the potential of CXCR2 antagonists as a treatment option for diseases in which neutrophils play a pathological role.

Inhalation of LPS induces inflammatory airway responses mimicking characteristics of chronic obstructive pulmonary disease.

AIM: Inhalation of lipopolysaccharide (LPS) produces both systemic and pulmonary inflammatory responses. The aim of this study was to further characterize the response to LPS in order to develop a human model suitable for early testing of drug candidates developed for the treatment for chronic obstructive pulmonary disease (COPD). MATERIALS: Blood and induced sputum were obtained 4, 24 and 48 h following inhalation of saline and LPS (5 and 50 µg). Blood was analysed for C-reactive protein (CRP), α(1)-antitrypsin and neutrophils/leucocytes, and sputum was analysed for biomarkers of neutrophil inflammation and remodelling activities, i.e. neutrophil elastase (NE) protein/activity and α(1)-antitrypsin. Levels of tumour necrosis factor-α (TNFα) were measured in both blood and sputum. Urine was collected 0-24 and 24-48 h postchallenge, and desmosine, a biomarker of elastin degradation, was measured. RESULTS: Lipopolysaccharide inhalation induced dose-dependent flu-like symptoms and increases in plasma CRP and α(1)-antitrypsin as well as increases in blood neutrophil/leucocyte numbers. Furthermore, LPS produced increases in sputum TNFα and sputum NE activity. Urine levels of desmosine were unaffected by the LPS challenge. All subjects recovered 48 h postchallenge, and indices of inflammatory activity were significantly lower at this observation point cf 24 h postchallenge. CONCLUSION: Inhalation of LPS in healthy volunteers can be used as a safe and stable model of neutrophil inflammation. Blood/plasma and sputum indices can be employed to monitor the response to LPS. We suggest that this model may be used for initial human studies of novel COPD-active drugs.

Becoming a winner but staying the same: identities and consumption of lottery winners.

This article discusses how large lottery winnings are experienced and used by the winners. The study draws on a survey of 420 Swedish winners, which is analyzed against the background of previous research from the USA and Europe. The analyses show that winners are cautious about realizing any dreams of becoming someone else somewhere else. This result contradicts theories suggesting that identities are being liquefied by the commercially driven consumer culture in affluent Western societies. In contrast, the article concludes that winners generally try to stay much the same, but on a somewhat higher level of consumption. The critical situation that large winnings produce is generally met by an attempt to hold on to one's identity and social relations. In addition, the article shows that lump sum winners tend to save and invest large parts of their winnings, compared with winners of monthly installments who are more likely to spend on leisure and consumption. These results indicate that "wild" lump sums make winners "tame" their winnings more firmly, whereas "domesticated" monthly instalments can be spent more thoughtlessly without changing identity or becoming an unfortunate winner.

Treatment with the C5a receptor antagonist ADC-1004 reduces myocardial infarction in a porcine ischemia-reperfusion model.

BACKGROUND: Polymorphonuclear neutrophils, stimulated by the activated complement factor C5a, have been implicated in cardiac ischemia/reperfusion injury. ADC-1004 is a competitive C5a receptor antagonist that has been shown to inhibit complement related neutrophil activation. ADC-1004 shields the neutrophils from C5a activation before they enter the reperfused area, which could be a mechanistic advantage compared to previous C5a directed reperfusion therapies. We investigated if treatment with ADC-1004, according to a clinically applicable protocol, would reduce infarct size and microvascular obstruction in a large animal myocardial infarct model. METHODS: In anesthetized pigs (42-53 kg), a percutaneous coronary intervention balloon was inflated in the left anterior descending artery for 40 minutes, followed by 4 hours of reperfusion. Twenty minutes after balloon inflation the pigs were randomized to an intravenous bolus administration of ADC-1004 (175 mg, n = 8) or saline (9 mg/ml, n = 8). Area at risk (AAR) was evaluated by ex vivo SPECT. Infarct size and microvascular obstruction were evaluated by ex vivo MRI. The observers were blinded to the treatment at randomization and analysis. RESULTS: ADC-1004 treatment reduced infarct size by 21% (ADC-1004: 58.3 ± 3.4 vs control: 74.1 ± 2.9%AAR, p = 0.007). Microvascular obstruction was similar between the groups (ADC-1004: 2.2 ± 1.2 vs control: 5.3 ± 2.5%AAR, p = 0.23). The mean plasma concentration of ADC-1004 was 83 ± 8 nM at sacrifice. There were no significant differences between the groups with respect to heart rate, mean arterial pressure, cardiac output and blood-gas data. CONCLUSIONS: ADC-1004 treatment reduces myocardial ischemia-reperfusion injury and represents a novel treatment strategy of myocardial infarct with potential clinical applicability.

Budesonide prevents cytokine-induced decrease of the relaxant responses to formoterol and terbutaline, but not to salmeterol, in mouse trachea.

During asthma exacerbations, increased airway inflammation may impair the effects of beta(2)-adrenoceptor (beta(2)AR) agonists. It is unclear whether this impairment is prevented by inhaled glucocorticoids (GCs). We have investigated the relaxation of carbachol-contracted mouse tracheal segments to the beta(2)AR agonists formoterol, terbutaline, and salmeterol. The segments were pre-exposed for 4 days to the proinflammatory cytokines tumor necrosis factor alpha (100 ng/ml) and interleukin-1beta (10 ng/ml) with or without the GC, budesonide (1 microM). Formoterol and terbutaline induced greater maximal relaxation (R(max)) than salmeterol. The cytokines decreased R(max) of all beta(2)AR agonists, whereas budesonide had no effect. However, after concomitant treatment with cytokines and budesonide, the R(max) values of formoterol and terbutaline were not impaired, whereas budesonide did not prevent the decrease in the R(max) of salmeterol. A similar pattern was observed for cAMP production by the agonists. In tracheal smooth muscle, beta(2)AR mRNA was not affected by the cytokines but increased with budesonide. However, the cytokines markedly increased cyclooxygenase (COX)-2 mRNA expression, which may lead to heterologous desensitization of beta(2)AR. It is noteworthy that the cytokine-induced increase of COX-2 was blocked by concomitant budesonide suggesting that heterologous desensitization of beta(2)AR by the cytokines may be prevented by budesonide treatment. Budesonide prevented cytokine-induced impairment of the tracheal relaxation and beta(2)AR/cAMP signaling for formoterol but not for salmeterol. This suggests that differences exist between formoterol and salmeterol in beta(2)AR coupling/activation and/or signal transduction upstream of cAMP. These results imply that maximal bronchodilator effects of formoterol, but not of salmeterol, are maintained by budesonide treatment during periods with increased inflammation, such as asthma exacerbations.

5-FU uptake in peritoneal metastases after pretreatment with radioimmunotherapy or vasoconstriction: an autoradiographic study in the rat.

This study was conducted to test if tumour drug uptake could be increased in experimental colorectal cancer peritoneal metastases, by using pretreatment with peritoneal vasoconstriction or radioimmunotherapy. A total of 29 nude rats with peritoneal metastases were injected intraperitoneally (i.p.) with 14C-labelled 5-FU. The animals were randomly allocated to 5 groups. Six days prior to 5-FU, group I (control) received i.p. NaCl, group II was subjected to i.p. radioimmunotherapy (RIT) 131I-labelled anti-CEA monoclonal antibody (150 MBq) and group III received i.p. Norbormide 10 minutes before 5-FU. Two days prior to 5-FU group IV and V received i.p. NaCl (control) and RIT, respectively. 5-FU uptake was visualised with autoradiography and quantified by computer-based image analysis. Tumours in group III showed a higher uptake (mean+/-SD, 21.4+/-17) than in group I (11.8+/-10, p=0.04). This was also true when the analysis was restricted to larger tumours (> or = median 627 pixels) group III (23.2+/-19) vs. group I (11.8+/-7, p=0.002). Peritoneal tumours in group II were of smaller size (median area 308 pixels) than in group I (619 pixels), in group III (901 pixels), in group IV (769 pixels) and in group V (808 pixels). RIT decreased the tumour size whereas it did not affect 5-FU uptake. The uptake of 5-FU was potentiated by pretreating the animals with Norbormide. These results demonstrate that 5-FU uptake in experimental peritoneal metastases is increased when the peritoneal absorption of the drug is blocked using pretreatment with a vasoconstrictive agent. This principle may also be relevant when treating patients with colorectal cancer peritoneal metastases.

A sequential fluorescence method for neurotransmitter-specific retrograde tracing in the central nervous system of the rat; utilizing True Blue and immunohistochemistry in combination with computer-assisted photography.

Aiming to map the distribution of spinally projecting, hypothalamic neurons containing neuronal nitric oxide synthase (nNOS), True Blue (TB) is injected into the rat spinal cord. After survival times of 7-14 days the animals are anaesthetized and perfused transcardially with a solution containing paraformaldehyde and sucrose. After dissection, the injection site is further fixed for 4-8 h, cut in a cryostat, and documented by computer-assisted digital photography. The brain region of interest is fixed for 4 h, rinsed in phosphate buffer for 48 h, sectioned, and photographically documented utilizing filter settings for visualization of TB. The brain sections are then immunohistochemically processed using a primary antibody against nNOS and a Texas Red (TR)-labelled secondary antibody and once again photographically documented, now using filter settings for visualization of TB and TR, respectively. Utilizing the Photoshop program, the TB containing cells can then be exactly aligned and the presence of TB and/or TR fluorescence in the same cell bodies are evaluated. This method for neurotransmitter-specific retrograde tracing derives its high sensitivity from the optimization of fixation/rinsing parameters, the use of appropriate fluorophores, and sequential digital microphotography.

Effects of motor and sensory stimulation in stroke patients with long-lasting dysphagia.

Dysphagia is a common poststroke symptom with negative effects on recovery and rehabilitation. However, the orofacial regulation therapy, developed by Castillo Morales, comprising body regulation and orofacial regulation in combination with a palatal plate application has shown promising results in stroke patients. This therapy is based not only on muscle exercises but also on an improvement of the entire sensory-motor reflex arc involved in normal deglutition, and on the knowledge that the function of face and oropharynx at deglutition is closely interrelated with the entire body posture as well as with appropriate breathing. The treatment concept is relatively unknown to caregivers, partly due to lack of scientific evaluation of treatment results. The present investigation aimed to assess the effect of motor and sensory stimulation in stroke patients with dysphagia persisting for more than six months. Seven patients were evaluated with respect to orofacial and pharyngeal motility and sensory function before and two weeks after a five-week treatment period. The evaluation comprised a swallowing capacity test, a meal observation test, clinical examination of oral motor and sensory function, a velopharyngeal closure test, and videofluoroscopy. In addition, the symptoms were scored by the patients. An overall single-blind estimation showed objective and self-assessed swallowing improvement in all seven patients. Kappa coefficients are calculated on all reliability data, both inter- and intrarater reliabilities. Sensory and motor stimulation seems to be a promising therapy in stroke patients with long-lasting and persistent oropharyngeal dysphagia.

Whole-Body Autoradiography.

Ever since its introduction in the early 1950s whole-body autoradiography has been used quite extensively for mapping the fate of various substances in the body, especially in the fields of pharmacology and toxicology. A detailed description of the whole-body autoradiographic technique is given. Some factors of general interest are dealt with-such as radionuclides and labeled substances, followed by a number of illustrations providing details and specific references.