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Rationale: Conventional computerized tomography (CT) examination can differentiate renal cortical tumor from urothelial carcinoma on the basis of the highly contrast-enhanced vessels in renal cortical tumors. However, the capillary distribution of renal cell carcinoma (RCC) has been under-investigated. Here, we present a micro-CT image of tumor tissue in a patient with RCC., Patient Concerns: The patient was a 72-year-old woman with a past history of diabetes mellitus and hypertension. She did not have tumor-related symptoms., Diagnosis and Interventions: The tumor was diagnosed using abdominal CT during her yearly routine health check. After radical nephrectomy, the tumor was subjected to pathological examination and micro-CT imaging. Pathological analysis confirmed a clear cell renal carcinoma. The capillary distribution of the tumor was significantly lesser than that of the normal cortex on micro-CT image., Lessons: Microvessels of RCC can be detected by micro-CT. We also found that the distribution of microvessels was uneven and lower than that in the normal cortex in this case. For a more general diagnosis, more micro-CT images of RCC tumors are needed.

Thyroid function may alter carbohydrate metabolism via influence of insulin, which may in terms of derangement of thyroid function and insulin function result in the development of type 2 diabetes mellitus (T2D). We investigated the association of thyroid disorders with T2D by a cohort study of the Taiwan nationwide health insurance database.A sub-dataset of the National Health Insurance Research Database (NHIRD) was used in this study. The thyroid disease (both hyper- and hypo-thyroidism) group was chosen from patients older than 18 years and newly diagnosed between 2000 and 2012. The control group consisted of randomly selected patients who never been diagnosed with thyroid disease and 4-fold size frequency matched with the thyroid disease group. The event of this cohort was T2D (ICD-9-CM 250.x1, 250.x2). Primary analysis was performed by comparing the thyroid disease group to the control group and the second analysis was performed by comparing the hyperthyroidism subgroup, hypothyroidism subgroup, and control group.The occurrence of T2D in the thyroid disease group was higher than the control group with hazard ratio (HR) of 1.23 [95% confidence interval (CI) = 1.16-1.31]. Both hyperthyroidism and hypothyroidism were significantly higher than control. Significantly higher HR was also seen in female patients, age category of 18 to 39-year-old (y/o) and 40 to 64 y/o subgroups. Higher occurrence of T2D was also seen in thyroid disease patients without comorbidity than in the control group with HR of 1.47 (95% CI = 1.34-1.60). The highest HR was found in the half-year follow-up.There was a relatively high risk of T2D development in patients with thyroid dysfunctions, especially in the period of 0.5 to 1 year after presentation of thyroid dysfunctions. The results suggest performing blood sugar tests in patients with thyroid diseases for early detection and treatment of T2D.

Between 1952 and 1992, more than 200 large radiobiology studies were conducted in research institutes throughout Europe, North America, and Japan to determine the effects of external irradiation and internal emitters on the lifespan and tissue toxicity development in animals. At Argonne National Laboratory, 22 external beam studies were conducted on nearly 700 beagle dogs and 50,000 mice between 1969 and 1992. These studies helped to characterize the effects of neutron and gamma irradiation on lifespan, tumorigenesis, and mutagenesis across a range of doses and dosing patterns. The records and tissues collected at Argonne during that time period have been carefully preserved and redisseminated. Using these archived data, ongoing statistical work has been done and continues to characterize quality of radiation, dose, dose rate, tissue, and gender-specific differences in the radiation responses of exposed animals. The ongoing application of newly-developed molecular biology techniques to the archived tissues has revealed gene-specific mutation rates following exposure to ionizing irradiation. The original and ongoing work with this tissue archive is presented here as a case study of a more general trend in the radiobiology megastudies. These experiments helped form the modern understanding of radiation responses in animals and continue to inform development of new radiation models. Recent archival efforts have facilitated open access to the data and materials produced by these studies, and so a unique opportunity exists to expand this continued research.

The comparative central nervous system (CNS) toxicity of serially administered intravenous doses of lidocaine, bupivacaine, etidocaine, and tetracaine was investigated in awake dogs. The mean cumulative dose required for convulsive activity was 4.0 mg/kg tetracaine, 5.0 mg/kg bupivacaine, 8.0 mg/kg etidocaine, and 22.0 mg/kg lidocaine. The cumulative convulsive dose of lidocaine was significantly greater than that of the other three agents (P less than 0.01). A comparison of the in vivo anesthetic potency and the acute CNS toxicity of these various agents suggests little difference in the therapeutic ratio between less potent anesthetics such as lidocaine and more potent drugs, i.e., tetracaine, bupivacaine, and etidocaine. The relative CNS toxicity of the different agents as determined in awake dogs in this study was compared with their relative cardiovascular toxicity previously evaluated in a series of ventilated dogs anesthetized with pentobarbital. The dose of lidocaine, etidocaine, tetracaine, and bupivacaine required to produce irreversible cardiovascular depression was 3.5-6.7 times greater than that which produced convulsions. These results suggest that the CNS is the primary target organ for the toxic effects of both highly lipid-soluble and highly protein-bound local anesthetics (i.e., bupivacaine, etidocaine, and tetracaine) and less lipid-soluble and less protein-bound drugs (i.e., lidocaine) following rapid intravenous administration.

Despite the increasing use of rectal methohexital as a premedicant-induction agent in pediatric anesthesia, there are no data to confirm the assumption that low plasma methohexital concentrations are the cause of inadequate sedation of children and that high concentrations are associated with the loss of consciousness. Plasma methohexital concentrations were determined in 20 ASA Class I children, ages 2-7 yr, after the rectal administration of methohexital (25 mg/kg). Seventeen of the 20 children in this study fell asleep after receiving the drug and achieved peak plasma concentrations greater than 2 micrograms/ml. The maximum plasma methohexital concentration in children that did not fall asleep was less than 2 micrograms/ml. The mean time to the onset of sleep after drug administration was 8.3 min (at which time the mean plasma concentration was 4.4 micrograms/ml). The mean peak plasma concentration and the mean time to peak plasma concentration were 4.7 micrograms/ml and 13.9 min, respectively. Loss of consciousness after rectal administration of methohexital correlates well with the plasma concentration of the drug.

To determine whether prematurely born infants with a history of idiopathic apneic episodes are more prone than other infants to life-threatening apnea during recovery from anesthesia, the authors prospectively studied 214 infants (173 full term, 41 premature) who received anesthesia. Fifteen premature infants had a preanesthetic history of idiopathic apnea. Six of these required mechanical ventilation because of idiopathic apneic episodes during emergence from anesthesia. Two were ventilated for other reasons, and seven recovered normally. Infants ventilated for apnea were younger (postnatal age 1.6 +/- 1.2 months, mean +/- SD; conceptual age 38.6 +/- 3.0 weeks) than those who recovered normally (postnatal age 5.6 +/- 2.7 months; conceptual age 55.1 +/- 11.3 weeks) (P less than 0.01). No other premature or full-term infant was ventilated because of postoperative apneic episodes. The authors conclude that anesthetics may unmask a defect in ventilatory control of prematurely born infants younger than 41-46 weeks conceptual age who have a preanesthetic history of idiopathic apnea.