Dual-Energy Computed Tomography Pulmonary Angiography: Comparison of Vessel Enhancement between Linear Blended and Virtual Monoenergetic Reconstruction Techniques

Introduction

Optimal opacification of the pulmonary vasculature is a fundamental factor of a diagnostic quality computed tomography pulmonary angiogram (CTPA). This retrospective study examined the feasibility of utilising a noise-optimised monoenergetic reconstruction of the dual-energy computed tomography pulmonary angiogram (DE-CTPA) as an additional protocol to increase vessel opacification.

Hemodialysis-associated amyloidosis presenting as lingual nodules

Hemodialysis has permitted long-term survival of patients with kidney failure, but not without many complications, such as mineral loss from bones, secondary hyperparathyroidism, and increased risk of infection. Recently a new form of amyloidosis, AB2M, has been characterized that is specifically associated with long-term dialysis. The tissues and organs affected by deposits of AB2M appear to differ from those affected by the other major types of amyloidosis; AB2M affects mainly the carpal ligament, synovia of large joints, juxtaarticular bone, and intervetebral disks, while involvement of the oral tissues has been rare. We present here a case in which the biopsy of superficial lingual deposits of AB2M led to the recognition that the patient had developed hemodialysis-associated amyloidosis. It is suggested that periodic inspection of the oral soft tissues for signs or symptoms of amyloidosis should become a part of the dental care of patients undergoing dialysis.     

Salivary procalcitonin and periodontitis in diabetes

Periodontitis and type 2 diabetes are co-morbid conditions, both characterized by infectious susceptibility. We investigated procalcitonin (ProCT) levels in the serum and saliva of persons with periodontitis and type 2 diabetes (n = 20), to determine if these levels are altered by periodontitis activity or by hyperglycemia. Persons with severe periodontitis showed higher levels of salivary-ProCT than did those with moderate periodontitis (241 +/- 71 vs. 77 +/- 516 pg/mL, p = 0.02) and higher levels than did healthy control individuals (118 +/- 26 pg/mL, p = 0.05). Salivary-ProCT levels were correlated with bleeding-on-probing (r = 0.45, p = 0.05), as well as with HgbA(1c) (r = 0.49, p = 0.03). Salivary levels of ProCT were higher than serum levels for the periodontitis/diabetes group (152 +/- 37 vs. 78 +/- 17 pg/mL, p = 0.02) and the control group (118 +/- 146 vs. 48 +/- 17 pg/mL, p = 0.01). Persons with periodontitis and type 2 diabetes have salivary-ProCT levels that reflect their degree of periodontitis activity and hyperglycemia. This study demonstrates, for the first time, the presence of procalcitonin (ProCT), an established serum marker of infection, in saliva.     

Effect of clonidine on secretion of fluid and ions by the parotid and submandibular glands of the rat

Secretion in response to this alpha 2-adrenergic agonist was evaluated in the presence and absence of several adrenergic antagonists, reserpine and sympathectomy (Sx). In both glands, the response was qualitatively but not quantitatively similar to that induced by the alpha 1-adrenergic agonist, phenylephrine, in the presence of propranolol. With clonidine, the volume of submandibular saliva was much higher but the Ca concentration was 3-4 times lower than that of the parotid; both salivas had low Na but high K concentrations. Clonidine-induced secretion was almost completely blocked by the alpha 1-adrenergic antagonist, prazosin and a mixed alpha-adrenergic antagonist, phentolamine, and markedly reduced by the alpha 2-adrenergic antagonist, yohimbine, but unaffected by the beta-adrenergic antagonist, propranolol. Reserpine reduced the parotid, but enhanced the submandibular secretory response to clonidine. Results in Sx glands were similar. Thus, in the rat glands clonidine may activate alpha 1-rather than alpha 2-adrenoceptors, which appear to play a part similar to alpha 1-adrenoceptors only after reserpine or Sx.     

Physostigmine-induced salivary secretion in the rat

The purpose of this study was to see if physostigmine, a reversible cholinesterase inhibitor, affects the secretion and composition of saliva of the major salivary glands of the rat. Low doses of physostigmine did not elicit secretion. At higher doses there was significant flow from the parotid and submandibular glands within 5 min; however, no sublingual secretion was observed. The submandibular flow rate was highest for the first 5 min, then declined rapidly. The parotid flow rate initially was one-fifth of the maximum submandibular rate and then gradually decreased. The concentrations of Ca, Na and K of physostigmine-induced parotid saliva, and the Na of submandibular saliva, were similar to those with carbachol stimulation. The Ca and K concentrations of submandibular saliva were significantly higher than with carbachol or parasympathetic stimulation, and resembled those of alpha-adrenergic stimulation. The protein concentrations of physostigmine-evoked saliva from both glands were similar. The amylase activity of physostigmine-evoked parotid saliva was much higher than that of carbachol or parasympathetic stimulation. Physostigmine-evoked secretion was completely blocked by atropine, a cholinergic antagonist, and by reserpine, partially blocked by phentolamine, an alpha-adrenergic antagonist and not affected by surgical sympathectomy. Morphologically, physostigmine resulted in a moderate decrease in the number of acinar, but not ductal, secretory granules of both the parotid and submandibular glands, while the sublingual gland was unaffected. Numerous patches of parotid acini also developed vacuoles or vesicles. These results suggest that physostigmine-induced salivary secretion is mediated primarily by direct effects on cholinergic and alpha-adrenergic receptors.     

Cancer-promoting effect of Taiwan betel quid in hamster buccal pouch carcinogenesis

OBJECTIVE: To investigate the cancer-promoting effect of Taiwan betel quid in hamster buccal pouch carcinogenesis.
MATERIALS AND METHODS: Two hundred and fifty-two non-inbred mate adult Syrian golden hamsters were randomly divided into six groups, each containing forty-two animalS. A treatment regimen over a 14-week experimental period was employed with six animals per group being killed at seven different periods (every 2 weeks). The right buccal pouch of each animal was painted three times a week with various combinations of 7, 12-dimethylbenz[a]anthracene (DMBA), Taiwan betel quid extract, dimethyl sulfoxide (DMSO) and mineral oil.
RESULT: Both the number and size of tumors in animals concurrently treated with DMBA and betel quid were significantly higher than those in animals treated with DMBA alone in each killing period of 8, 10, 12 and 14 weekS. No visible tumors but hyperkeratosis and acanthosis were observed in pouches treated with betel quid alone for all killing periods.
CONCLUSION: Our results indicate Taiwan betel quid may be a co-carcinogen in human oral carcinogenesis, if extrapolation can be made from the current animal study.     

The KEL24 and KEL14 alleles of the Kell blood group system

BACKGROUND: The Kell blood group system consists of at least 21 antigens, which may be classified into five sets of alleles and at least 10 independently expressed antigens. The molecular basis of four of the five sets of alleles has been described; point mutations in KEL leading to amino acid substitutions characterize the alleles. In this study, the point mutation associated with the remaining allele, KEL14/KEL24, was determined. STUDY DESIGN AND METHODS: The 19 exons of KEL were amplified from genomic DNA by a polymerase chain reaction (PCR) procedure. The PCR products were sequenced. DNA sequences from unrelated KEL:14,24 and KEL:-14,24 individuals were compared to the DNA sequence of the common KEL:14,-24 phenotype. RESULTS: DNA from the KEL:14,24 person yielded both G and C at nt 659, indicating an Arg and Pro polymorphism in amino acid residue 180 of Kell protein. DNA from the KEL:-14,24 person had a G659C mutation in exon 6, indicating an Arg180Pro substitution. The G659C change introduces an Hae III restriction enzyme site, which was used to confirm the base mutations by restriction fragment length polymorphism analysis of the PCR products. CONCLUSION: A G659C mutation, predicting an Arg180Pro change in Kell protein, is associated with the KEL14/KEL24 allele.