Systematic review of primary osseointegrated dental implants in head and neck oncology

The aim of this paper is to provide a systematic review of articles concerning primary osseointegrated dental implants in the head and neck oncology setting. We searched MEDLINE (1950 to March 2009) and Embase (1980 to March 2009) using the terms head and neck, oral, maxillofacial, craniofacial, jaws, mandible, maxilla, zygoma, dental implants, osseointegrated implants, implants, tumour, cancer, oncology, immediate, simultaneous, and primary. Two authors independently reviewed the abstracts, and all those written in the English language that referred to the placement of primary dental implants in patients with cancer of the head neck were included. Articles that referred to craniofacial or extraoral implants were excluded. Of 892 abstracts 83 were eligible for further consideration; the full articles were evaluated, and 41 that complied fully with the inclusion criteria are presented as a tabulated summary. There are three case reports, 13 reviews, and 25 clinical studies. Eight of the clinical studies refer solely to the insertion of dental implants at the time of primary oncological resection, and only two were of a prospective design. We have concisely summarised publications concerning primary dental implants, and our findings will help to inform head and neck cancer teams, particularly oncological surgeons, restorative dentists, and maxillofacial prosthodontists of the evidence base surrounding this approach to oral rehabilitation.     

Expression of specific granule markers on the cell surface of neutrophil cytoplasts

The widespread assumption that cytoplasts generated from human polymorphonuclear leukocytes (PMNs) are vesicles consisting solely of cytoplasm surrounded by plasma membrane and devoid of granule activity remains to be tested. PMN cytoplasts were prepared by centrifugation of intact cells on a Ficoll step gradient in the presence of cytochalasin B. Two granule membrane markers, Mol, a fluorometrically detectable antigen, and cytochrome b, both of which have been shown to translocate to the plasma membrane during granule release, were compared for their activity in cytoplasts and intact PMNs. We found that the amount of Mol detected on the plasma membrane of intact PMNs, as compared with other membrane markers (such as antigens LFA-1 and beta 2m), increased 1.6- fold upon exposure of PMNs to Ficoll plus cytochalasin B prior to centrifugation. Another twofold increase in Mol expression occurred upon cytoplast preparation. Release of the granule enzymes, vitamin B12- binding protein, and lysozyme were also followed and correlated well (r = .78 and .92) with the amount of Mol antigen present on the cell surface. Cytochrome b was also found to be higher (1.4-fold) on plasma membranes isolated from cytoplasts than on plasma membranes isolated from intact control cells. These results indicate that some fusion of granule membranes and plasma membranes occurred during treatment of PMNs with Ficoll plus cytochalasin b and during cytoplast preparation.     

Hepatic encephalopathy in cirrhotic and portacaval shunted dogs: lack of changes in brain GABA uptake, brain GABA levels, brain glutamic acid decarboxylase activity and brain postsynaptic GABA receptors

It has been suggested, from studies of a rabbit model of fulminant hepatic failure, that hepatic encephalopathy might be related to an increase in brain gamma-aminobutyric acid uptake through a more permeable bloodbrain barrier, leading to an overactivity of brain gamma-aminobutyric acid-mediated inhibitory neurotransmission. Five groups of dogs were studied: normal dogs, dogs with secondary biliary cirrhosis without and with hepatic encephalopathy and portacaval shunted dogs without and with hepatic encephalopathy. Brain gamma-aminobutyric acid and sucrose uptake was investigated using the multiple indicator dilution curve technique in unanesthetized dogs. Tracer doses of 99mTc-labeled albumin (extracellular reference substance), 3H-labeled gamma-aminobutyric acid and 14C-labeled sucrose prepared in autologous dog plasma were injected in one carotid artery, and dorsal sagittal sinus dilution curves were obtained. Uptake was calculated by comparing the areas under the 99mTc-labeled albumin and the [3H]gamma-aminobutyric acid (or [14C]sucrose) curves from appearance to peak height. After killing, brain gamma-aminobutyric acid levels were measured in the frontal cortex by high-performance liquid chromatography and glutamic acid decarboxylase activities using a radioenzymatic assay. Brain gamma-aminobutyric acid postsynaptic receptors were assessed using [3H]muscimol binding studies. There were no significant changes in cirrhotic and shunted dogs with or without hepatic encephalopathy with regard to brain gamma-aminobutyric acid and sucrose uptake, brain gamma-aminobutyric acid levels and glutamic acid decarboxylase activities. [3H]Muscimol binding studies did not show any changes in the number nor in the affinity of postsynaptic gamma-aminobutyric acid receptors.(ABSTRACT TRUNCATED AT 250 WORDS)     

Region-selective permeability of the blood-brain barrier to α-aminoisobutyric acid during thiamine deficiency and following its reversal

Thiamine deficiency (TD) results in focal lesions in several regions of the rat brain including the thalamus and inferior colliculus. Since alterations in blood-brain barrier (BBB) integrity may play a role in this damage, we have examined the influence of TD on the unidirectional blood-to-brain transfer constant (K_i) of the low molecular weight species α-aminoisobutyric acid (AIB) in vulnerable and non-vulnerable brain regions at different stages during progression of the disorder, and following its reversal with thiamine. Analysis of the regional distribution of K_i values showed early (day 10) increased transfer of [¹⁴C]-AIB across the BBB in the vulnerable medial thalamus as well as the non-vulnerable caudate and hippocampus. At the acute symptomatic stage (day 14), more widespread BBB permeability changes were detected in most areas including the lateral thalamus, inferior colliculus, and non-vulnerable cerebellum and pons. Twenty-four hours following thiamine replenishment, a heterogeneous pattern of increased BBB permeability was observed in which many structures maintained increased uptake of [¹⁴C]-AIB. No increase in the [³H]-dextran space, a marker of intravascular volume, was detected in brain regions during the progress of TD, suggesting that BBB permeability to this large tracer was unaffected. These results indicate that BBB opening i) occurs early during TD, ii) is not restricted to vulnerable areas of the brain, iii) is progressive, iv) persists for at least 24 h following treatment with thiamine, and v) is likely selective in nature, depending on the molecular species being transported.

     

The role of hemochromatosis susceptibility gene mutations in protecting against iron deficiency in celiac disease

BACKGROUND & AIMS: Celiac disease and hereditary hemochromatosis are common HLA-defined conditions in northwestern Europe. We sought to determine whether there is a genetic relationship between the 2 diseases and if hemochromatosis susceptibility gene (HFE) mutations are protective against iron deficiency in celiac disease. METHODS: Polymerase chain reaction amplification using sequence-specific primers capable of identifying the 2 HFE gene mutations (H63D and C282Y) and the HLA class I and II alleles was used to type 145 white patients with celiac disease and 187 matched controls. Hemoglobin and fasting serum iron levels in celiac patients were measured at diagnosis. RESULTS: HFE gene mutations, H63D or C282Y, were identified in 70 celiac patients (48.3%) and 61 controls (32.6%) (P = 0.004). The C282Y mutation was associated with HLA-A*03 and B*07 alleles in controls and with A*01, A*03, B*08, and DRB1*0301 alleles in celiac patients; the H63D mutation was associated with HLA-A*25 and DRB1*03 alleles in controls and A*29 and DRB1*03 alleles in celiac patients. At diagnosis, celiac patients with the C282Y mutation had higher mean hemoglobin and fasting serum iron levels compared with the HFE wild type (P = 0.0002 and 0.006, respectively). This was not observed with the H63D mutation. CONCLUSIONS: In celiac disease, HFE gene mutations are common and are in linkage disequilibrium with different HLA alleles compared with controls. A disease-specific haplotype that carries C282Y and DQB1*02 is suggested. We propose that HFE gene mutations provide a survival advantage by ameliorating the iron deficiency seen in celiac patients.     

Why semantic dementia drives you to the dogs (but not to the horses): A theoretical account

This paper describes a patient (IH) with semantic dementia and severe impairment in all semantic categories except for numerical knowledge, which was preserved. IH showed a severe deficit in reading and writing non-number words (e.g., candle, juice) and nonwords, and preservation of reading and writing number words (e.g., one, forty) and numerals (e.g., 1, 40). IH's pattern of performance can be explained by the combination of a selective sparing of one semantic category--i.e., numbers--with a total deficit of nonsemantic processes for mapping letters and sounds. As number was the only spared semantic category in the presence of these other nonsemantic deficits, it follows that the semantic route is sufficient for accurate reading and spelling. Our data clarify the nature of reading and writing processes and support the functional and neuroanatomical independence of the number domain.     

Dissociations in numerical abilities revealed by progressive cognitive decline in a patient with semantic dementia

This study describes a 3-year follow-up investigation of the deterioration of number abilities in a semantic dementia patient (IH). A few studies have previously reported the decline of number knowledge in patients with degenerative disorders, although almost never in semantic dementia (Diesfeldt, 1993; Girelli, Luzzatti, Annoni, & Vecchi, 1999; Grafman, Kempen, Rosenberg, Salazar, & Boller, 1989). These studies described the change of the patients’ performance mainly in terms of increased errors in number tasks. On the other hand, dissociations between different types of number abilities, or different arithmetical operations, have been reported in patients with focal lesions. In the present investigation, the cognitive basis of number processing was revealed throughout the patient's cognitive decline. Two major results emerged from a longitudinal study: First, the patient's conceptual knowledge of arithmetic was well preserved despite severe impairment of nonarithmetic conceptual knowledge. Second, the patient's progressive decline revealed patterns of dissociations between different number abilities. These were between (1) multiplication and other arithmetical operations, which particularly emerged in the use of algorithms; (2) impaired knowledge of number facts and procedures on one hand, and conceptual knowledge of arithmetic on the other; and (3) different types of transcoding skills. The implications of these dissociations for the cognitive architecture of number processing are discussed.