An analysis of contact tracing protocol in an over-dispersed SEIQR Covid-like disease.

The aim of this work is to study an over-dispersed SEIQR infectious disease and obtain optimal methods of contact tracing. A prototypical example of such a disease is that of the current SARS-CoV-2 pandemic. In consequence, this study is immediately applicable to the current health crisis. In this paper, we introduce both a discrete and continuous model for various modes of contact tracing. From the continuous model, we derive a basic reproductive number and study the stability of the equilibrium points. We also implement the continuous and discrete models numerically and further analyze the effectiveness of different types of contact tracing and their cost on society. Additionally, through these simulations, we also study the effect that various parameters of the disease have on its evolution.

Intranasal delivery of dexamethasone efficiently controls LPS-induced murine neuroinflammation.

Neuroinflammation is the hallmark of several infectious and neurodegenerative diseases. Synthetic glucocorticoids (GCs) are the first-line immunosuppressive drugs used for controlling neuroinflammation. A delayed diffusion of GCs molecules and the high systemic doses required for brain-specific targeting lead to severe undesirable effects, particularly when lifelong treatment is required. Therefore, there is an urgent need for improving this current therapeutic approach. The intranasal (i.n.) route is being employed increasingly for drug delivery to the brain via the olfactory system. In this study, the i.n. route is compared to the intravenous (i.v.) administration of GCs with respect to their effectiveness in controlling neuroinflammation induced experimentally by systemic lipopolysaccharide (LPS) injection. A statistically significant reduction in interleukin (IL)-6 levels in the central nervous system (CNS) in the percentage of CD45+ /CD11b+ /lymphocyte antigen 6 complex locus G6D [Ly6G+ and in glial fibrillary acidic protein (GFAP) immunostaining was observed in mice from the i.n.-dexamethasone (DX] group compared to control and i.v.-DX-treated animals. DX treatment did not modify the percentage of microglia and perivascular macrophages as determined by ionized calcium binding adaptor molecule 1 (Iba1) immunostaining of the cortex and hippocampus. The increased accumulation of DX in brain microvasculature in DX-i.n.-treated mice compared with controls and DX-IV-treated animals may underlie the higher effectiveness in controlling neuroinflammation. Altogether, these results indicate that IN-DX administration may offer a more efficient alternative than systemic administration to control neuroinflammation in different neuropathologies.

Brain-borne IL-1 adjusts glucoregulation and provides fuel support to astrocytes and neurons in an autocrine/paracrine manner.

It is still controversial which mediators regulate energy provision to activated neural cells, as insulin does in peripheral tissues. Interleukin-1ß (IL-1ß) may mediate this effect as it can affect glucoregulation, it is overexpressed in the 'healthy' brain during increased neuronal activity, and it supports high-energy demanding processes such as long-term potentiation, memory and learning. Furthermore, the absence of sustained neuroendocrine and behavioral counterregulation suggests that brain glucose-sensing neurons do not perceive IL-1ß-induced hypoglycemia. Here, we show that IL-1ß adjusts glucoregulation by inducing its own production in the brain, and that IL-1ß-induced hypoglycemia is myeloid differentiation primary response 88 protein (MyD88)-dependent and only partially counteracted by Kir6.2-mediated sensing signaling. Furthermore, we found that, opposite to insulin, IL-1ß stimulates brain metabolism. This effect is absent in MyD88-deficient mice, which have neurobehavioral alterations associated to disorders in glucose homeostasis, as during several psychiatric diseases. IL-1ß effects on brain metabolism are most likely maintained by IL-1ß auto-induction and may reflect a compensatory increase in fuel supply to neural cells. We explore this possibility by directly blocking IL-1 receptors in neural cells. The results showed that, in an activity-dependent and paracrine/autocrine manner, endogenous IL-1 produced by neurons and astrocytes facilitates glucose uptake by these cells. This effect is exacerbated following glutamatergic stimulation and can be passively transferred between cell types. We conclude that the capacity of IL-1ß to provide fuel to neural cells underlies its physiological effects on glucoregulation, synaptic plasticity, learning and memory. However, deregulation of IL-1ß production could contribute to the alterations in brain glucose metabolism that are detected in several neurologic and psychiatric diseases.

Usefulness of rhinomanometry in the identification and treatment of patients with obstructive sleep apnoea: an algorithm for predicting the relationship between nasal resistance and continuous positive airway pressure. a retrospective study.

OBJECTIVES: We tried to assess the relationship between nasal resistance measured by rhinomanometry and the pressure used in CPAP. DESIGN: Retrospective medical case series review, January 2004 to December 2014. SETTING: Tertiary care academic medical centre. PARTICIPANTS: Thirty-eight patients (m = 56.55 years; male = 90.5%) with CPAP settings ≤8 and 39 patients (m = 57.49 years; male = 74.9%) with pressure settings ≥12. MAIN OUTCOME MEASURES: Study variables were BMI, neck circumference, Epworth Sleepiness Scale score, nasopharyngeal examination and computerised anterior active rhinomanometry, sitting and supine, in basal conditions and after intranasal administration of oxymetazoline (0.05%). Nocturnal polysomnography was performed to calculate the apnoea-hypopnoea index without and with CPAP to analyse the effectiveness of the treatment. RESULTS: BMI and resistance in supine position after vasoconstriction at 150 Pa were useful variables to predict the pressure setting that should be used. We obtained an equation to calculate the probability that a patient requires a pressure >12 cm H2 O as a function of their BMI and total nasal airflow at 150 pascal in supine position after vasoconstriction. CONCLUSIONS: Rhinomanometry is useful to predict the impact of structural nasal modifications on the positive pressure to support decision-making in relation to surgery.

Prognosis and Outcomes in Early Stage Glottic Carcinoma Involving the Anterior Commissure Treated with Laser CO2 Surgery: A Retrospective Observational Analysis.

The anterior commissure (AC) is the area where the vocal cords attach to the thyroid cartilage through Broyles' ligament. Many authors argue that involvement of the anterior commissure in early stage glottic carcinoma (I, II) constitutes a risk factor for local recurrence. The objective of this study is to evaluate whether anterior commissure involvement in early stage glottis cancer is an independent risk factor for recurrence and mortality. The study included all those patients diagnosed with glottis carcinoma in stages I and II of the AJCC treated by transoral laser surgery at the Hospital San Pedro (Logroño, Spain) between 2005 and 2015. Patients were divided into two groups according to the presence (AC1) or absence (AC0) of involvement of the commissure. Of 29 patients treated, 44.8% were AC1. Patients with anterior commissure involvement had more local recurrence (p = 0.2701); higher mortality rate (p = 0.2256); lower disease-free survival (p = 0.0881) and a lower overall survival (p = 0.0331). The 5-year survival rate was 24.5% lower in patients with invasion of the anterior commissure. The involvement of the anterior commissure is an independent risk factor that should be considered in the prognosis of laryngeal cancer.

Role of prethymic cells in acquisition of self-tolerance.

The sequential character of T-lymphocyte development as it pertains to the stage at which self-tolerance is acquired was investigated. Three phases were studied, defined here as prethymic, intrathymic, and postthymic as determined by the timing of thymus implantation. The model utilized was the temporal pattern of skin graft rejection in thymusless BALB/c nude mice implanted with allogeneic, C57BL/6J, or syngeneic thymuses before or after skin grafting; in some instances, F(1) hybrid spleen cells were also given to newborns or young adults. These experiments in nude mice showed that, (a) self-tolerance could be established despite the absence of the host's own haplotype in the implanted thymus; (b) recently emigrated postthymic cells could already discriminate self from non-self; (c) specific neonatal tolerance could be induced in nudes by inoculation of F(1) hybrid cells; (d) nudes showed a higher capacity for induction of neonatal tolerance than did normal littermates. These findings indicate that the process of self-tolerance in the T cell's lineage begins during the prethymic state early in ontogeny.

Immunoregulatory feedback between interleukin-1 and glucocorticoid hormones.

The production and action of immunoregulatory cytokines, including interleukin-1 (IL-1), are inhibited by glucocorticoid hormones in vivo and in vitro. Conversely, glucocorticoid blood levels were increased by factors released by human leukocytes exposed to Newcastle disease virus preparations. This activity was neutralized by an antibody to IL-1. Therefore the capacity of IL-1 to stimulate the pituitary-adrenal axis was tested. Administration of subpyrogenic doses of homogeneous human monocyte-derived IL-1 or the pI 7 form of human recombinant IL-1 to mice and rats increased blood levels of adrenocorticotropic hormone (ACTH) and glucocorticoids. Another monokine, tumor necrosis factor, and the lymphokines IL-2 and gamma-interferon had no such effects when administered in doses equivalent to or higher than those of IL-1. The stimulatory effect of IL-1 on the pituitary-adrenal axis seemed not to be mediated by the secondary release of products from mature T lymphocytes since IL-1 was endocrinologically active when injected into athymic nude mice. These results strongly support the existence of an immunoregulatory feedback circuit in which IL-1 acts as an afferent and glucocorticoid as an efferent hormonal signal.

Corticotropin-releasing factor-producing neurons in the rat activated by interleukin-1.

Intraperitoneal administration of human recombinant interleukin-1 (IL-1) to rats can increase blood levels of corticosterone and adrenocorticotropic hormone (ACTH). The route by which IL-1 affects pituitary-adrenal activity is unknown. That the IL-1-induced pituitary-adrenal activation involves an increased secretion of corticotropin-releasing factor (CRF) is indicated by three lines of evidence. First, immunoneutralization of CRF markedly attenuated the IL-1-induced increase of ACTH blood levels. Second, after blockade of fast axonal transport in hypothalamic neurons by colchicine, IL-1 administration decreased the CRF immunostaining in the median eminence, indicating an enhanced release of CRF in response to IL-1. Third, IL-1 did not stimulate ACTH release from primary cultures of anterior pituitary cells. These data further support the notion of the existence of an immunoregulatory feedback circuit between the immune system and the brain.

The immune response evokes changes in brain noradrenergic neurons.

A decreased noradrenaline turnover in the hypothalami of rats was observed at the peak of the immune response to sheep red blood cells. The decrease in noradrenergic neuronal activity was mimicked by injection of soluble r mediators released by immunological cells activated in vitro. Noradrenaline also tended to decrease in the brainstem but not in the residual brain. It is suggested that products released from activated immunological cells during the immune response may induce the previously described autonomic and endocrine mechanisms that contribute to immunoregulation.

The neuro-endocrine-immune relationship in pulmonary and pleural tuberculosis: a better local profile in pleural fluid.

BACKGROUND: Tuberculosis (TB) is a major health problem worldwide. In TB, the immune and central nervous systems modulate each other. The two main components of this network are the hypothalamic-pituitary-adrenal axis (HPA) and autonomic nervous system (ANS). OBJECTIVE: To elucidate neuro-endocrine-immune (NEI) interactions in pulmonary (PTB) or pleural (PLTB) TB, we analysed the relationship among compounds from these systems. METHODS: We quantified levels of catecholamines, hormones and cytokines in plasma from patients with PTB (n = 46) or PLTB (n = 12) and controls (n = 32), and in the pleural fluid from PLTB patients. Transcript expression for genes involved in glucocorticoid-related function (quantitative real-time polymerase chain reaction) was also analysed in mononuclear cells (MCs) from peripheral blood (PBMC) or pleural effusion (PEMC) compartments. RESULTS: Both patient groups had increased plasma levels of pro- and anti-inflammatory cytokines, cortisol, growth hormone (GH) and dopamine, whereas insulin-like growth factor 1 (IGF-1) and dehydroepiandrosterone levels were decreased. The pleural fluid contained increased levels of pro-inflammatory cytokines, GH and IGF-1 and reduced levels of steroid hormones compared with their plasma counterparts. PBMCs from PTB patients had increased expression of transcripts for 11ß-hydroxysteroid dehydrogenase (11ßHSD1) and a decreased glucocorticoid receptor (GR) ratio (GRα/GRß). In PLTB cases, expression of 11ßHSD1 and GRα transcripts was higher in PEMCs. CONCLUSION: PTB patients seem to display adverse NEI dysregulation. Changes in pleural fluid are compatible with a more effective NEI reaction.

Modeling epidemics using cellular automata.

The main goal of this work is to introduce a theoretical model, based on cellular automata, to simulate epidemic spreading. Specifically, it divides the population into three classes: susceptible, infected and recovered, and the state of each cell stands for the portion of these classes of individuals in the cell at every step of time. The effect of population vaccination is also considered. The proposed model can serve as a basis for the development of other algorithms to simulate real epidemics based on real data.

[Functional recovery in hemifacial transplants in rats]. / Recuperación funcional del trasplante hemifacial en ratas.

INTRODUCTION: There are a number of different options open to the surgeon for the reconstruction of the face and scalp, but when tissue loss is very extensive, good aesthetic and functional recovery is not possible. Not only must the damaged tissues be replaced, but motor and sensorial functioning also has to be restored. AIM: To evaluate the functional recovery of hemifacial allografts in rats. MATERIALS AND METHODS: Twenty-one hemifacial flaps were transplanted from Long-Evans rats to Wistar-Lewis rats, under immunosuppression monotherapy with tacrolimus. Prior to the operation, anatomical and allograft viability studies were conducted. Two groups of transplanted rats were formed: with or without nerve repair. In the nerve repair group, end-to-end suture was employed to repair the infraorbital branch of the trigeminal nerve and the buccolabial, upper mandibular marginal and zygomatico-orbital branches of the facial nerve. Sensory recovery was evaluated by filming traction of the whiskers, whereas motor recovery was assessed by blind tests using electromyography studies of the mystacial muscles and electroneurography of the facial nerve. At eight weeks, the animals were sacrificed and biopsy samples were taken from the mystacial region. RESULTS: The facial flap was successfully lifted in 10 cases. In the nerve repair group both clinical and electrophysiological recovery were observed at six weeks, whereas biopsy samples taken in the eighth week showed recovery of the nerve fascicles. CONCLUSIONS: The hemifacial flap can be transplanted. By repairing the nerves of the allograft, it is possible to achieve its functional recovery, as can be confirmed clinically, electrophysiologically and histopathologically. To date, this is the first evidence of functional recovery following a hemifacial transplant in rats.

[The vestibulocollic reflex: assessment and characteristics of vestibular-evoked myogenic potentials analysed by age groups]. / Reflejo vestibulocervical. Valoracion y caracteristicas de los potenciales vestibulares miogenicos evocados analizados por tramos de edad.

INTRODUCTION: Obtaining vestibular-evoked myogenic potentials (VEMP) by means of the vestibulocollic reflex is a readily available technique that provides an image of vestibular functioning and is useful for evaluating the pathologies that involve compromise of the anatomical pathway of the reflex. Although normal patterns do exist, responses vary at different ages. AIM: To obtain reference values of the vestibulocollic reflex according to different age groups. SUBJECTS AND METHODS: We studied 40 volunteers with no symptoms of auditory or vestibular compromise. Each ear was stimulated separately by a series of clicks (sounds lasting 0.1 s; 3 pps; intensities of 100 dB nHL and 85 dB nHL) and recordings were made in the sternocleidomastoid muscles by means of surface electrodes as patients who were lying on their backs contracted these muscles as they lifted their heads. We studied the latency of the initial p13-n23 positive-negative potential and the peak-to-peak amplitude. The existence of later n34-p44 potentials was evaluated. RESULTS: No statistically significant differences were found between genders or between the two ears. We did not find any differences between the latencies of the waves according to the intensity of the stimulus, but there is a relationship between the amplitude of the p13-n23 potential and the intensity of the stimulus. The latencies of the responses in children under 10 years of age differ from those of the other groups, but no differences were found among those over the age of 11. CONCLUSIONS: The VEMP display steady and easily identifiable latencies. We obtained different reference values for latency in children under the age of 10 and those over 11 years old. The amplitude decreases with the intensity of the stimulus.

Immunological effects of behavioral activation with exercise in major depression: an exploratory randomized controlled trial.

Major depression (MD) is associated with peripheral inflammation and increased cardiovascular risk. Regular physical exercise can have anti-inflammatory effects. The present study examined whether behavioral activation with exercise affects inflammatory processes in MD. Ninety-eight patients with MD were randomly assigned to cognitive-behavioral therapy (CBT) emphasizing exercise during behavioral activation (CBT-E), CBT with pleasurable low-energy activities as an active control condition (CBT-C) or a passive waiting list control group (WL). Plasma levels of C-reactive protein (CRP), interleukin (IL)-6, IL-10, lipopolysaccharide (LPS)-stimulated IL-6 production, and blood immune cell counts were analyzed at baseline and weeks 8 (post-behavioral activation) and 16 (post-treatment). Thirty non-depressed age- and sex-matched controls were included to examine potential immunological alterations in MD at baseline. Patients with MD exhibited higher levels of CRP, higher neutrophil and monocyte counts, lower IL-10 levels and reduced LPS-stimulated IL-6 production compared to controls (P<0.001-0.045). Multilevel modeling indicated that CBT-E was associated with increased anti-inflammatory IL-10 at weeks 8 and 16 compared to CBT-C and WL (P=0.004-0.018). CBT-E did not significantly affect other immunological makers in the total sample. A subgroup analysis including patients with potentially higher cardiovascular risk (CRP ⩾1 µg ml-1) indicated that CRP was reduced in CBT-E compared to CBT-C (P<0.007) and marginally reduced compared to WL (P<0.085) after week 16. The present findings provide new insights into immunological effects of behavioral treatments against depression. Behavioral activation in conjunction with exercise may have the potential to reverse, in part, immunological alterations in MD.

[Simulation of an outbreak of Acinetobacter baumannii in hospitals]. / Simulación de la propagación de un brote por Acinetobacter baumannii en entornos hospitalarios.

OBJECTIVE: Acinetobacter baumannii infections have increased over time becoming a significant issue. Consequently, those applications that allow to predict the evolution of an outbreak and the relevance of the different control methods, are very important. The design of mathematical models plays a central role in this topic. METHODS: Development of a deterministic mathematical model based on ordinary differential equations whose variables and parameters are defined upon the basis of knowledge of the epidemiology and characteristics of A. baumannii. This model is analyzed from a qualitative point of view and, also, its computational implementation is derived. RESULTS: Several simulations were obtained developed from different initial conditions. The qualitative analysis of these simulations provides formal evidence of most effective control measures. CONCLUSIONS: The implementation of the computational model is an extremely useful tool in terms of managing A. baumannii outbreaks. There is mathematical proof of the fact that the observance of efficient hygiene and screening rules reduces the number of infected patients.

An adverse immune-endocrine profile in patients with tuberculosis and type 2 diabetes.

Diabetes is a risk factor for the development of pulmonary tuberculosis (TB) and both diseases present endocrine alterations likely to play a role in certain immuno-endocrine-metabolic associated disorders. Patients with TB, or with TB and type 2 diabetes (TB + T2DM) and healthy controls (HCo) were assessed for plasma levels of cortisol, dehydroepiandrosterone (DHEA), estradiol, testosterone, growth hormone (GH), prolactin, insulin-like growth factor-1 (IGF-1), cytokines (IL-6, IL-10, IFN-γ) and the specific lymphoproliferative capacity of peripheral blood mononuclear cells. All patients had higher levels of cortisol with a reduction in DHEA, thus resulting in an increased cortisol/DHEA ratio (Cort/DHEA). Increased prolactin and particularly GH levels were found in both groups of TB patients. This was not paralleled by increased concentrations of IGF, which remained within the levels of HCo. Estradiol levels were significantly augmented in patients TB, and significantly more in TB + T2DM, whereas testosterone levels were decreased in both groups of patients. IFN- γ and IL-6 concentrations were significantly increased in all TB, even further in TB + T2DM; while IL-10 was equally increased in both groups of TB patients. The in vitro specific proliferative capacity was decreased in both groups of patients as compared to that of HCo. The adverse immune-endocrine profile of TB seems to be slightly more pronounced in patients who also have T2DM.

Electric stimulation of the vagus nerve reduced mouse neuroinflammation induced by lipopolysaccharide.

BACKGROUND: Neuroinflammation (NI) is a key feature in the pathogenesis and progression of infectious and non-infectious neuropathologies, and its amelioration usually improves the patient outcome. Peripheral inflammation may promote NI through microglia and astrocytes activation, an increased expression of inflammatory mediators and vascular permeability that may lead to neurodegeneration. Several anti-inflammatory strategies have been proposed to control peripheral inflammation. Among them, electrical stimulation of the vagus nerve (VNS) recently emerged as an alternative to effectively attenuate peripheral inflammation in a variety of pathological conditions with few side effects. Considering that NI underlies several neurologic pathologies we explored herein the possibility that electrically VNS can also exert anti-inflammatory effects in the brain. METHODS: NI was experimentally induced by intraperitoneal injection of bacterial lipopolysaccharide (LPS) in C57BL/6 male mice; VNS with constant voltage (5 Hz, 0.75 mA, 2 ms) was applied for 30 s, 48 or 72 h after lipopolysaccharide injection. Twenty four hours later, pro-inflammatory cytokines (IL-1ß, IL-6, TNFα) levels were measured by ELISA in brain and spleen extracts and total brain cells were isolated and microglia and macrophage proliferation and activation was assessed by flow cytometry. The level of ionized calcium binding adaptor molecule (Iba-1) and glial fibrillary acidic protein (GFAP) were estimated in whole brain extracts and in histologic slides by Western blot and immunohistochemistry, respectively. RESULTS: VNS significantly reduced the central levels of pro-inflammatory cytokines and the percentage of microglia (CD11b/CD45low) and macrophages (CD11b/CD45high), 24 h after the electrical stimulus in LPS stimulated mice. A significantly reduced level of Iba-1 expression was also observed in whole brain extracts and in the hippocampus, suggesting a reduction in activated microglia. CONCLUSIONS: VNS is a feasible therapeutic tool to attenuate the NI reaction. Considering that NI accompanies different neuropathologies VNS is a relevant alternative to modulate NI, of particular interest for chronic neurological diseases.

Interleukin-6: a cytokine to forget.

It is known that proinflammatory cytokines such as interleukin-6 (IL-6) are expressed in the central nervous system (CNS) during disease conditions and affect several brain functions including memory and learning. In contrast to these effects observed during pathological conditions, here we describe a physiological function of IL-6 in the "healthy" brain in synaptic plasticity and memory consolidation. During long-term potentiation (LTP) in vitro and in freely moving rats, IL-6 gene expression in the hippocampus was substantially increased. This increase was long lasting, specific to potentiation, and was prevented by inhibition of N-methyl-D-aspartate receptors with (+/-)-2-amino-5-phosphonopentanoic acid (AP-5). Blockade of endogenous IL-6 by application of a neutralizing anti-IL-6 antibody 90 min after tetanus caused a remarkable prolongation of LTP. Consistently, blockade of endogenous IL-6, 90 min after hippocampus-dependent spatial alternation learning resulted in a significant improvement of long-term memory. In view of the suggested role of LTP in memory formation, these data implicate IL-6 in the mechanisms controlling the kinetics and amount of information storage.

On the mechanism of antiinflammation induced by tumor transplantation, surgery, and irritant injection.

Tumor transplantation, major surgery, and injection of nonspecific irritants elicit inflammation locally while suppressing inflammation induced subsequently and at distant sites. Such systemic antiinflammation in rodents occurs via corticosterone-independent and -dependent pathways. Based upon hormone measurements and the response to adrenalectomy, antiinflammation induced by irritants and certain surgical procedures is corticosterone independent while that which follows tumor transplantation is corticosterone dependent. However, injection of tumorous ascites stimulates both pathways since it contains two antiinflammatory factors: Factor A (molecular weight less than 2,000) does not alter hormone balance while Factor B (molecular weight 30,000-100,000) increases corticosterone levels and is corticosterone dependent. Desensitization of systemic antiinflammation develops rapidly regardless of whether it is corticosterone dependent (Factor B) or independent (Factor A or irritants). However, tumor transplantation resists desensitization possibly by inducing an immune response since lymphocytic mitogens prevent development of and break established desensitization. Nevertheless, abolition of tumor-induced antiinflammation follows injection of tumorous ascites by a mechanism that involves Factor B suppression of the corticosterone response to the tumor while Factor A apparently raises the threshold at which physiological increases in corticosterone inhibit leukocyte emigration. We conclude that systemic antiinflammation is a general consequence of a localized inflammatory reaction and that desensitization of such antiinflammation develops rapidly. Recent evidence indicates that certain mediators of inflammation are proinflammatory when administered intradermally but antiinflammatory when given intravenously. Thus, systemic antiinflammation may arise when chemical mediators of inflammation generated by a local reaction gain access to the circulation.

Preliminary study of the lymphatic drainage system of the nose and paranasal sinuses and its role in detection of sentinel metastatic nodes.

CONCLUSIONS: The normal nasal lymphatic drainage runs via the facial vessels into the neck lymphatic nodes of levels I-II and this drainage pattern was found in our patients with sinonasal tumors. We found only one true-positive sentinel lymph node (SLN). Our pathological material was very limited and so further investigations are required before any valid conclusions can be drawn concerning the clinical value of SLNs in nasal tumors. Objectives. To detect the lymph collection route of the nasal fossae and paranasal sinuses and to identify the first echelon in the tumor metastatic cascade in order to prevent the risk of occult metastases in N0 necks in patients with primary head and neck squamous cell carcinoma (SCC). MATERIAL AND METHODS: Our control group comprised 30 patients (20 females; age range 19-50 years) suffering from chronic otitis media who had an anatomically normal nose and a cNO neck on palpation. The pathological group comprised 6 patients (2 females; age range 40-85 years) suffering from sinonasal tumors: 3 SCC, 1 recurrent melanoma, 1 ameloblastoma and 1 inverted papilloma. All had a clinically staged cNO neck on palpation and CT. In the control group, lymphoscintigraphy was carried out by means of unilateral injection of radioactive gold into the head of the inferior turbinate. The tracer was identified using a gamma camera 3 and 6 h after the injection. In the pathological group the chosen tracer was technetium, which was administered 1 day prior to surgery by means of injections into the heads of the inferior and middle turbinates, into the nasal septum and into the retromaxillary gingival mucosa. The tracer was identified transcutaneously using a navigator probe in the gamma camera at 15 min, 30 min and 1 h post-injection. A mark was drawn on the skin corresponding to the hot spot of the SLN. The study was repeated 30 min before surgery. The neck incision was selected according to the location of the SLN. A hand-held gamma probe was used in the operating theatre to detect in situ the radioactivity of the surgical excisional nasal area and the cervical SLN. Once the SLN was excised its radioactivity was confirmed ex situ, taking into account that the activity counts were at least three times greater than background. Postoperatively, all SLNs were histopathologically examined and cytokeratin staining was carried out immunohistochemically using the monoclonal antibody cocktail AE1/AE3. Results. In the control group, intense activity at the injection tracer site and lower activity in the submandibular area (level I) were detected in 26.6% of cases. Nasal radioactivity persisted for 6 h post-injection and submandibular radioactivity increased, also reaching the area corresponding to neck node level II (70%). In two cases (6.6%), radioactivity was observed in the retropharyngeal nodes. In the pathological group, the SLN was found in the submandibular area (level I) in three cases, and in the ameloblastoma patient three SLNs were found at levels I-II. Three cases were false positives, and no metastases were detected using any of the histopathological procedures. The only one true positive corresponded to a female with an SCC of the maxillary infrastructure with invasion of the gingival mucosa. The histopathological code was 1 and a metastasis was detected on hematoxylin-eosin examination. In the other two cases no SLNs were detected.