Therapy-induced bone changes in oncology imaging with 18F-sodium fluoride (NaF) PET–CT

Annals of Nuclear Medicine - 18F-Sodium fluoride (18F-NaF) is a PET tracer that is mostly used in the evaluation of bone metastasis in oncology cases. Recently, 18F-NaF PET/CT is gaining wide...     

Cone beam computed tomography findings in temporomandibular joint of chronic qat chewers: Dimensional and osteoarthritic changes

The social habit of chewing qat (also known as khat) is widely practised in East Africa and the Arabian Peninsula. It has been linked with various oro-facial conditions, including temporomandibular joint disorders (TMD). This cross-sectional, comparative study sought to investigate the effects of qat chewing on temporomandibular joint (TMJ), using cone beam computed tomography (CBCT). A total of 85 Yemeni males were included. The participants were divided into two groups: Qat chewers (QC; n = 41) and non-qat chewers (NQC; n = 44). Relevant data were obtained using a structured questionnaire and standardised clinical examination. Additionally, CBCT images of the TMJs were obtained, and then, osteoarthritic changes and TMJ dimensions were analysed. SPSS 21 was used for statistical analyses, with a significant level was set at 0.05. Compared to NQC, a significantly higher proportion of QC presented with clinical signs of TMDs. The qualitative CBCT findings revealed significantly higher osteoarthritic changes in QC than in NQC: osteophyte (51.2% vs 22.7%; P = .008), subcortical sclerosis (48.8% vs 27.3%; P = .047), articular surface flattening (46.3% vs 6.8%; P = .009) and subcortical cysts (43.9% vs 4.5%; P < .001). However, CBCT quantitative findings (condylar dimensions) did not show significant differences between the two groups. The chewing side of the QC group showed slightly more changes compared to the non-chewing side. The results demonstrate that qat chewing has detrimental effects on TMJ manifested mainly as osteoarthritic changes. Further large-scale studies are recommended.     

Effects of intermittent hypoxia on sympathetic activity and blood pressure in humans

Sympathetic nerve activity and arterial pressure are frequently elevated in patients with obstructive sleep apnea (OSA). The mechanisms responsible for chronic sympathetic activation and hypertension in OSA are unknown. To determine whether repetitive apneas raise sympathetic nerve activity and/or arterial pressure, awake and healthy young subjects performed voluntary end-expiratory apneas for 20 s per min for 30 min (room air apneas). To accentuate intermittent hypoxia, in a separate group of subjects, hypoxic gas (inspired O2 10%) was added to the inspiratory port for 20 s before each apnea (hypoxic apneas). Mean arterial pressure (MAP) and muscle sympathetic nerve activity (MSNA, peroneal microneurography) were determined before and up to 30 min following the repetitive apneas. Following 30 hypoxic apneas (O2 saturation nadir 83.1+/-1.2%), MSNA increased from 17.4+/-2.7 to 23.4+/-2.5 bursts/min and from 164+/-28 to 240+/-35 arbitrary units respectively (P<0.01 for both; n=10) and remained elevated while MAP increased transiently from 80.5+/-3.7 to 83.1+/-3.9 mm Hg (P<0.05; n=11). In contrast, in the subjects who performed repetitive apneas during room air exposure (O2 saturation nadir 95.1+/-0.8%), MAP and MSNA did not change (n=8). End-tidal CO2 post-apnea, an index of apnea-induced hypercapnia, was similar in the 2 groups. In a separate control group, no effect of time on MAP or MSNA was noted (n=7). Thus, repetitive hypoxic apneas result in sustained sympathetic activation and a transient elevation of blood pressure. These effects appear to be due to intermittent hypoxia and may play a role in the sympathetic activation and hypertension in OSA.     

P50 inhibitory gating deficit is correlated with the negative symptomatology of schizophrenia

Abnormal sensory gating in schizophrenia has frequently been reported. The strength of central inhibitory pathways was measured using the P50 component of the auditory evoked potential in a conditioning-testing paradigm. The relationships between a relative decrease in P50 amplitude to repeated auditory stimuli and clinical symptoms remain controversial. Using the Positive and Negative Syndrome Scale, we studied the P50 auditory conditioning-testing paradigm in 81 schizophrenic subjects, categorized into subgroups with and without prominent negative symptoms, in comparison with 88 control subjects. We found increased ratios of testing stimuli to conditioning stimuli in both schizophrenic subgroups relative to findings in the control group. In addition, we found significantly increased mean latencies of the P50 responses to conditioning (C) and testing (T) stimuli and significantly increased T/C ratios in the subgroup with negative symptoms compared with the subgroup with non-negative symptoms.     

Vitamin D status and elevated red cell distribution width in community-dwelling adults: Results from the National Health and Nutrition Examination Survey 2001–2006

Objectives

Elevated red cell distribution width (RDW) is associated with morbidity and mortality in community-dwelling individuals. Although RDW is traditionally used to diagnose anemia, it may also be a marker of systemic inflammation. Since vitamin D is a potent modulator of inflammatory cytokines our goal was to investigate whether 25-hydroxyvitamin D levels (25OHD) are associated with RDW in non-hospitalized adults.

Design

To investigate this association, we conducted a cross-sectional study. Stepwise multivariable linear and logistic regression models were used to assess the independent association of 25OHD with RDW. Elevated RDW was defined as >14.5%.

Setting

Nationwide sample of non-hospitalized adults within the United States.

Participants

Individuals from the National Health and Nutrition Examination Survey from 2001-2006.

Results

15,162 individuals comprised the analytic cohort. Mean 25OHD was 24.9 ng/mL (SE 0.4) and the prevalence of elevated RDW was 6.3%. Linear regression analysis, controlling for age, sex, race, mean corpuscular volume, albumin, and neutropenia, demonstrated that 25OHD was inversely associated with RDW (β=-0.01; 95%CI -0.01 to -0.01). Logistic regression analysis, controlling for the same covariates, also demonstrated an inverse association of 25OHD with elevated RDW (OR 0.96; 95%CI 0.94-0.99). Individuals with 25OHD <30 ng/mL were more likely to have elevated RDW (OR 1.65; 95%CI 1.13-2.40) compared to those individuals with levels ≥30ng/mL.

Conclusions

In a nationwide sample of non-hospitalized adults within the United States, low 25OHD was associated with increased likelihood of elevated RDW. Further studies are needed to determine whether optimizing vitamin D status can reduce the prevalence of elevated RDW, and thereby reduce morbidity and mortality in the general population.

     

Quantitative bacterial micro-assay for rapid detection of serum phenylalanine on dry blood-spots: application in phenylketonuria screening.

Phenylketonuria is an inherited metabolic disease, which is characterized by an increased level of serum phenylalanine. Quantitative measurement of phenylalanine in the serum of phenylketonuria patients is necessary to confirm the disease, and to distinguish phenylketonuria from other forms of hyperphenylalaninemia. In this study, we report a rapid and inexpensive micro-assay for simultaneous detection and quantitative measurement of serum phenylalanine on dry blood-spots. Analysis of the standard curve showed a broad linear range for phenylalanine from 120 to 1800 micromol/L. Application of this method, the standard Guthrie bacterial inhibition assay and a high-performance liquid chromatography (HPLC) method for analysis of 34 samples from phenylketonuria patients and control samples produced comparable results, with the regression equation Y = 0.994X + 0.996. The advantage of this method over the Guthrie bacterial inhibition assay is its ability to measure serum phenylalanine quantitatively without false positive results. The method was successfully applied to dried blood-spots, serum and whole blood. The cost per sample is approximately 20-50 US cents, which is much less than for HPLC and commercial enzyme kits. The method can be automated, and is thus suitable for neonatal and mass screening for phenylketonuria, especially in developing countries where funding is a limiting factor.