[Challenges and opportunities of remote diagnosis and treatment management of sleep disordered breathing under the normalization of epidemic situation].

Since the outbreak of coronavirus disease 2019 (COVID-19), the diagnosis and treatment of diseases has been greatly affected. Obstructive sleep apnea hypopnea syndrome (OSAHS) is a common chronic disease, whose diagnosis and treatment methods have changed dramatically during the epidemic period-from traditional outpatient diagnosis and treatment to online remote diagnosis and treatment based on Internet. The diagnostical capability of major sleep centers has increased instead of decreasing. But with the change of diagnosis and treatment mode, privacy, data security, medical insurance policy and other related issues also emerge as the times require. Under the normalization of epidemic situation, telemedicine not only creates new opportunities, but also faces unprecedented challenges.

[Feasibility study of telemedicine model for diagnosis and treatment of patients with obstructive sleep apnea hypopnea syndrome in China].

Objective: To explore the feasibility of applying telemedicine model in disease management for patients with obstructive sleep apnea hypopnea syndrome (OSAHS) in China. Methods: A total of 24 patients were enrolled with suspected OSAHS who were admitted to the Sleep Center of Peking University People's Hospital from October 2015 to September 2016. Patients were diagnosed by electronic questionnaire assessment and home sleep apnea monitoring (HSAT) and were treated with remote automatic positive airway pressure (APAP). After 1 week, 1 month and 3 months of treatment, the patients were followed up by video. The follow-up questionnaire was completed by the patients through an independent data management platform. The APAP treatment data and compliance data were obtained through a built-in digital card of the APAP device. Linear regression model was used to explore the factors related to patient compliance. One-way repeated-measure analysis of variance was used to compare the changes of APAP duration and apnea hypopnea index (AHI) among patients at different treatment time points. Paired t-test was used to compare the EPWORTH scale (ESS) scores before and after treatment. Results: A total of 22 patients were diagnosed with OSAHS, including 20 males (90.9%), aged (45.6±10.2) years and AHI before treatment was (46.9±20.4) times/h. A total of 20 OSAHS patients received APAP treatment, and the proportion of patients with good compliance after 1 week, 1 month and 3 months of treatment were 15/19, 10/19 and 8/18, respectively. The severity of sleepiness before treatment affected compliance. Each 1-point increase in ESS score was associated with a 6.16% (95%CI: 3.01%, 9.31%) increase in compliance. Age, body mass index and AHI before treatment had no effect on compliance (all P values>0.05). The AHI of the patients who had been treated for 1 week, 1 month and 3 months were (2.5±2.1), (2.2±1.6) and (1.9±1.0) times/h, respectively. (P=0.195). After 3 months of treatment, the ESS score was (7.0±3.3), lower than that before treatment (10.6±3.1) (P=0.079). Conclusion: Telemedicine mode of diagnosis and treatment of OSAHS patients has good therapeutic effect and patient compliance, which is practical and feasible.

Ultrafast relaxation of photoexcited superfluid He nanodroplets.

The relaxation of photoexcited nanosystems is a fundamental process of light-matter interaction. Depending on the couplings of the internal degrees of freedom, relaxation can be ultrafast, converting electronic energy in a few fs, or slow, if the energy is trapped in a metastable state that decouples from its environment. Here, we study helium nanodroplets excited resonantly by femtosecond extreme-ultraviolet (XUV) pulses from a seeded free-electron laser. Despite their superfluid nature, we find that helium nanodroplets in the lowest electronically excited states undergo ultrafast relaxation. By comparing experimental photoelectron spectra with time-dependent density functional theory simulations, we unravel the full relaxation pathway: Following an ultrafast interband transition, a void nanometer-sized bubble forms around the localized excitation (He[Formula: see text]) within 1 ps. Subsequently, the bubble collapses and releases metastable He[Formula: see text] at the droplet surface. This study highlights the high level of detail achievable in probing the photodynamics of nanosystems using tunable XUV pulses.

Desorption dynamics of heavy alkali metal atoms (Rb, Cs) off the surface of helium nanodroplets.

We present a combined ion imaging and density functional theory study of the dynamics of the desorption process of rubidium and cesium atoms off the surface of helium nanodroplets upon excitation of the perturbed 6s and 7s states, respectively. Both experimental and theoretical results are well represented by the pseudodiatomic model for effective masses of the helium droplet in the desorption reaction of meff/mHe ≈ 10 (Rb) and 13 (Cs). Deviations from this model are found for Rb excited to the 6p state. Photoelectron spectra indicate that the dopant-droplet interaction induces relaxation into low-lying electronic states of the desorbed atoms in the course of the ejection process.

Toward a density functional description of liquid pH2.

A finite-temperature density functional approach to describe the properties of parahydrogen in the liquid-vapor coexistence region is presented. The first proposed functional is zero-range, where the density-gradient term is adjusted so as to reproduce the surface tension of the liquid-vapor interface at low temperature. The second functional is finite-range and, while it is fitted to reproduce bulk pH(2) properties only, it is shown to yield surface properties in good agreement with experiments. These functionals are used to study the surface thickness of the liquid-vapor interface, the wetting transition of parahydrogen on a planar Rb model surface, and homogeneous cavitation in bulk liquid pH(2).

Gene expression profiles for the human pancreas and purified islets in type 1 diabetes: new findings at clinical onset and in long-standing diabetes.

Type 1 diabetes (T1D) is caused by the selective destruction of the insulin-producing beta cells of the pancreas by an autoimmune response. Due to ethical and practical difficulties, the features of the destructive process are known from a small number of observations, and transcriptomic data are remarkably missing. Here we report whole genome transcript analysis validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and correlated with immunohistological observations for four T1D pancreases (collected 5 days, 9 months, 8 and 10 years after diagnosis) and for purified islets from two of them. Collectively, the expression profile of immune response and inflammatory genes confirmed the current views on the immunopathogenesis of diabetes and showed similarities with other autoimmune diseases; for example, an interferon signature was detected. The data also supported the concept that the autoimmune process is maintained and balanced partially by regeneration and regulatory pathway activation, e.g. non-classical class I human leucocyte antigen and leucocyte immunoglobulin-like receptor, subfamily B1 (LILRB1). Changes in gene expression in islets were confined mainly to endocrine and neural genes, some of which are T1D autoantigens. By contrast, these islets showed only a few overexpressed immune system genes, among which bioinformatic analysis pointed to chemokine (C-C motif) receptor 5 (CCR5) and chemokine (CXC motif) receptor 4) (CXCR4) chemokine pathway activation. Remarkably, the expression of genes of innate immunity, complement, chemokines, immunoglobulin and regeneration genes was maintained or even increased in the long-standing cases. Transcriptomic data favour the view that T1D is caused by a chronic inflammatory process with a strong participation of innate immunity that progresses in spite of the regulatory and regenerative mechanisms.

Dendritic cells pulsed with antigen-specific apoptotic bodies prevent experimental type 1 diabetes.

Dendritic cells (DCs) are powerful antigen-presenting cells capable of maintaining peripheral tolerance. The possibility to generate tolerogenic DCs opens new therapeutic approaches in the prevention or remission of autoimmunity. There is currently no treatment inducing long-term tolerance and remission in type 1 diabetes (T1D), a disease caused by autoimmunity towards beta cells. An ideal immunotherapy should inhibit the autoimmune attack, avoid systemic side effects and allow islet regeneration. Apoptotic cells--a source of autoantigens--are cleared rapidly by macrophages and DCs through an immunologically silent process that contributes to maintaining tolerance. Our aims were to prevent T1D and to evaluate the re-establishment of peripheral tolerance using autologous DCs pulsed in vitro with apoptotic bodies from beta cells. Immature DCs derived from bone marrow of non-obese diabetic (NOD) mice were obtained and pulsed with antigen-specific apoptotic bodies from the beta cell line NIT-1. Those DCs that phagocytosed apoptotic cells diminished the expression of co-stimulatory molecules CD40 and CD86 and reduced secretion of proinflammatory cytokines. Moreover, these cells were resistant to increase the expression of co-stimulatory molecules after lipopolysaccharide activation. The administration of these cells to NOD transgenic mice expressing interferon-beta in their insulin-producing cells, a model of accelerated autoimmune diabetes, decreased diabetes incidence significantly and correlated positively with insulitis reduction. DCs pulsed with apoptotic cells that express disease-associated antigens constitutes a promising strategy to prevent T1D.

Natural killer cells are required for accelerated type 1 diabetes driven by interferon-beta.

The destruction of beta cells by the islet infiltrating lymphocytes causes type 1 diabetes. Transgenic mice models expressing interferon (IFN)-beta in beta cells, in the non-obese diabetic (NOD) strain and in a diabetes-free, major histocompatibility complex-matched, homologous strain, the non-obese resistant (NOR) mice, developed accelerated type 1 diabetes after 3 weeks of age. Our aim was to determine if natural killer (NK) cells could affect the acceleration of the disease. We determined the amount of NK cells in the pancreas, spleen and lymph nodes from NOD rat insulin promoter (RIP)-IFN-beta mice. Pancreatic cytokines were assessed by quantitative real-time polymerase chain reaction and protein arrays. To confirm the relevance of NK cells in the acceleration of autoimmune diabetes this subset was depleted with anti-asialo GM1 antibodies. An increase of intrapancreatic NK cells characterized the accelerated onset of diabetes both in NOD and NOR RIP-IFN-beta transgenic models. Cytokines involved in NK function and migration were found to be hyperexpressed in the pancreas from accelerated diabetic mice. Interestingly, the depletion of NK cells in vivo abolished completely the acceleration of diabetes. NK cells connect innate to adaptive immunity and might play a role in autoimmunity. We report here that NK cells are required critically in the pancreas for accelerated diabetes. This model links inflammation to acceleration of beta cell-specific autoimmunity mediated by NK cells.

Squeezing a helium nanodroplet with a Rydberg electron.

We have investigated, by means of density functional theory, the structure of a "scolium", that is, an electron circulating around a positively charged 4He nanodroplet, temporarily prevented from neutralization by the helium-electron repulsion. The positive ion core resides in the center of the nanodroplet where, as a consequence of electrostriction, a strong increase in the helium density with respect to its bulk value occurs. The electron enveloping the 4He cluster exerts an additional electrostatic pressure which further increases the local 4He density around the ion core. We argue that under such pressure, sufficiently small 4He nanodroplets may turn solid. The stability of a scolium with respect to electron-ion recombination is investigated.

Reg (regenerating) gene overexpression in islets from non-obese diabetic mice with accelerated diabetes: role of IFNbeta.

AIMS/HYPOTHESIS: The expression of IFNbeta in beta cells results in accelerated type 1 diabetes. The REG family of beta cell proliferation factors have been described as autoantigens in autoimmune diabetes. The aim of this study was to determine the effect of IFNbeta on Reg expression, and the implications of this in terms of autoimmunity. METHODS: Reg gene expression was determined in islets from non-obese diabetic (NOD) RIP-HuIFNbeta mice by cDNA microarray, quantitative real-time PCR and immunohistochemistry. The effect of IFNbeta on Reg1 and Reg2 expression was assessed in the NOD insulinoma cell line NIT-1. IL-6, known to induce Reg expression, was measured in the insulitis microenvironment. Morphological studies were carried out to determine islet enlargement in this model. RESULTS: Reg2 was upregulated in islets from the NOD RIP-HuIFNbeta mice at the onset of the autoimmune attack. IFNbeta upregulates Reg1 and Reg2 genes in NIT-1 cells. The expression of Il6 was increased in islets from transgenic mice and in NIT-1 cells exposed to HuIFNbeta. Moreover, islets from transgenic mice were enlarged compared with those from wild-type mice. CONCLUSIONS/INTERPRETATION: Reg overexpression correlates well with the acceleration of diabetes in this model. The upregulation of Reg suggests that islets try to improve hyperglycaemia by regenerating the cells lost in the autoimmune attack. Reg expression is regulated by several factors such as inflammation. Therefore, the overexpression of an IFNbeta-induced autoantigen (REG) in the islets during inflammation might contribute to the premature onset of diabetes.

Tolerance, Autoimmunity and Immune Regulation: Report from the Keystone Symposia, Breckenridge, Colorado (USA)

Los grupos internacionales más relevantes en tolerancia inmunológica y autoinmunidad participaron en el Simposio Keystone ‘Tolerancia, Autoinmunidad y Regulación Inmunológica’ en Breckenridge, Colorado, entre el 21 y el 26 de marzo de 2006. Las ponencias describieron los avances en la investigación en el campo de la tolerancia y la autoinmunidad. En este resumen se ha organizado la información en cinco áreas: 1) Genes y señalización en la regulación del sistema inmune, 2) Desencadenantes extrínsecos y aspectos intrínsecos de la autoinmunidad, 3) Supresión y regulación del sistema inmune, 4) Ensayos clínicos de inmunotolerancia, 5) Debate y reconocimientos a la trayectoria científica. Los resultados presentados en el simposio demuestran los continuos avances en el conocimiento de la tolerancia y ponen de manifiesto la necesidad de continuar investigando en esta línea. Esto contribuiría al desarrollo de ensayos clínicos de prevención de enfermedades autoinmunes en sujetos de riesgo

The most relevant international groups working in immunological tolerance and autoimmunity participated in the Keystone Symposia ‘Tolerance, Autoimmunity and Immune Regulation’ in Breckenridge, Colorado, between the 21st and 26th of March 2006. Lectures and abstracts described new research work and advances relevant to tolerance and autoimmunity. In this report, the information is organized in five areas: 1) Genes and signals in immune regulation, 2) Extrinsic triggers and intrinsic drivers of autoimmunity, 3) Suppression and regulation of the immune system, 4) Translating tolerance to the clinic, 5) Debate and awards. The results presented in the meeting demonstrate the continuous advances in the knowledge of tolerance and prove the need to pursue research on this field. This may help to develop clinical trials to prevent autoimmune diseases in at risk subjects

Syngeneic islet transplantation into seminal vesicles of diabetic rats.

Pancreatic islet transplantation has been proposed as an attractive option for the treatment of type I diabetes. Transplantation into different sites has been investigated, among them those that are immuno-logically privileged (e.g., thymus, uterus, brain, anterior eye chamber, and testicle). Because of their characteristics, seminal vesicles could be considered as immunologically privileged organs, but there is no worldwide experience that can confirm it. The purpose of the present study is to assess the viability and functionality of islet transplantation into seminal vesicles of diabetic rats. One hundred ninety inbred adult male syngeneic Lewis rats were used as donors (n = 72), receptors (n = 36), and controls(n = 11). Diabetes was chemically induced through a single intraperitoneal injection of streptozotocin. Groups of 1200 purified islets were introduced in the right seminal vesicle of diabetic rats. Diabetic control rats were sham transplanted. Body weight and glycemia were monitored every 2 d. Of transplanted rats, 16.7% achieved a good function due to islet engraftment, while 30.6% achieved a partially good response, and 52.7% were considered as nonresponding. This is the first report about islet transplantation into seminal vesicles of diabetic animals. Our results indicate that islet transplantation into rat seminal vesicles is technically possible, and that islets can function normally after engraftment into the wall of the seminal vesicle.

Viral infections and autoimmune diabetes

La diabetes tipo 1 (DT1) es una enfermedad autoinmunitariacausada por la destrucción de las células beta pancreáticas productorasde insulina. La patogénesis de DT1 es compleja, interviniendofactores genéticos, inmunológicos y ambientales. Lasinfecciones víricas serían uno de los factores ambientales que, juntamentecon la susceptibilidad genética, podrían estar implicadosen la patogénesis de la enfermedad. En la presente revisión, resumimoslas hipótesis de la contribución de los virus en las enfermedadesautoinmunes en general, centrándonos en la DT1: Mimetismomolecular, aumento del procesamiento y presentación antigénicade autoantígenos durante la infección o diseminación deepítopos (epitope spreading), efectos colaterales, reconocimientode epitopos crípticos por parte de linfocitos T autoreactivos, activaciónde linfocitos T con dos receptores (dual TCRs), reactivaciónde células T de memoria por mecanismos antígeno inespecíficos,anticuerpos anti-idiotípicos y superantígenos. Resultadosde estudios epidemiológicos, serológicos y experimentales sugierenla asociación entre varios virus y el desarrollo de DT1. Losdatos más convincentes son las variaciones estacionales de la incidenciade la enfermedad, el aumento de la frecuencia de diabetesen pacientes con rubeola congénita o infección por enterovirusy la detección de secuencias de DNA de citomegalovirus enlos linfocitos de pacientes con DT1. Sin embargo, los efectos causalesdirectos son muy dificiles de demostrar. El objetivo de lapresente revisión es resumir los datos sobre el papel de los virusen el desarrollo de la DT1

Type 1 diabetes (T1D) is an autoimmune disease that resultsfrom the destruction of insulin producing pancreatic islet betacells. The pathogenesis of T1D is complex and results from a combinationof genetic, immunologic and environmental factors. Virusesseem to play a role among the many environmental factorsthat, together with the genetic susceptibility, have been implicatedin the pathogenesis of T1D. Here we review the various hypothesesof the contribution of viruses to autoimmune diseases ingeneral, focusing on T1D: Molecular mimicry, increased processingand presentation of autoantigens during infection or epitopespreading, direct bystander effects, recognition of cryptic epitopesby autoreactive T cells, activation of T cells with dual TCRs,reactivation of memory T cells by nonantigen-specific mechanisms,anti-idiotypic antibodies and superantigens. Epidemiological,serological and experimental studies suggest the associationof several viruses to the development of autoimmune diabetes.The most convincing findings are the seasonal variationsin the incidence of the disease, the increased frequency of T1D inpatients with congenital rubella syndrome or enterovirus infectionand the detection of CMV DNA sequences in lymphocytesfrom T1D patients. However, direct causative effects are difficultto verify. The aim of the present review is to summarize the findingsregarding the role of viruses in the development of T1D

Viral infections and autoimmune diabetes

La diabetes tipo 1 (DT1) es una enfermedad autoinmunitaria causada por la destrucción de las células beta pancreáticas productoras de insulina. La patogénesis de DT1 es compleja, interviniendo factores genéticos, inmunológicos y ambientales. Las infecciones víricas serían uno de los factores ambientales que, juntamente con la susceptibilidad genética, podrían estar implicados en la patogénesis de la enfermedad. En la presente revisión, resumimos las hipótesis de la contribución de los virus en las enfermedades autoinmunes en general, centrándonos en la DT1: Mimetismo molecular, aumento del procesamiento y presentación antigénica de autoantígenos durante la infección o diseminación de epítopos (epitope spreading), efectos colaterales, reconocimiento de epitopos crípticos por parte de linfocitos T autoreactivos, activación de linfocitos T con dos receptores (dual TCRs), reactivación de células T de memoria por mecanismos antígeno inespecíficos,anticuerpos anti-idiotípicos y superantígenos. Resultadosde estudios epidemiológicos, serológicos y experimentales sugieren la asociación entre varios virus y el desarrollo de DT1. Los datos más convincentes son las variaciones estacionales de la incidencia de la enfermedad, el aumento de la frecuencia de diabetes en pacientes con rubeola congénita o infección por enterovirus y la detección de secuencias de DNA de citomegalovirus en los linfocitos de pacientes con DT1. Sin embargo, los efectos causales directos son muy dificiles de demostrar. El objetivo de la presente revisión es resumir los datos sobre el papel de los virus en el desarrollo de la DT1 (AU)

Type 1 diabetes (T1D) is an autoimmune disease that results from the destruction of insulin producing pancreatic is let betacells. The pathogenesis of T1D is complex and results from a combination of genetic, immunologic and environmental factors. Viruses seem to play a role among the many environmental factors that, together with the genetic susceptibility, have been implicatedin the pathogenesis of T1D. Here we review the various hypotheses of the contribution of viruses to autoimmune diseases in general, focusing on T1D: Molecular mimicry, increased processing and presentation of autoantigens during infection or epitopespreading, direct bystander effects, recognition of cryptic epitopesby autoreactive T cells, activation of T cells with dual TCRs, reactivation of memory T cells by nonantigen-specific mechanisms,anti-idiotypic antibodies and superantigens. Epidemiological,serological and experimental studies suggest the association of several viruses to the development of autoimmune diabetes.The most convincing findings are the seasonal variations in the incidence of the disease, the increased frequency of T1D in patients with congenital rubella syndrome or enterovirus infection and the detection of CMV DNA sequences in lymphocytes from T1D patients. However, direct causative effects are difficult to verify. The aim of the present review is to summarize the findings regarding the role of viruses in the development of T1D (AU)

Efectores inmunitarios de la destrucción de células beta en la diabetes mellitus tipo 1 / Inmunological effectors of beta cell damage in type 1 diabetes

Gran parte de lo que sabemos sobre el desarrollo de la diabetes mellitus tipo 1 (T1D), se lo debemos a los estudios realizados en el ratón NOD, actualmente uno de los mejores modelos experimentales de esta enfermedad. Estudios realizados en esta cepa murina han demostrado que los linfocitos T son los principales efectores de la destrucción de las células beta pancreáticas. Sin embargo, también se ha observado que otras células del sistema inmune están implicadas en el desarrollo de la enfermedad. Entre ellas, las células dendríticas, los macrófagos y los linfocitos B, son imprescindibles tanto en el inicio como en fases mas avanzadas de la enfermedad. El objetivo de la presente revisión es sintetizar los recientes conocimientos sobre el papel de estas poblaciones celulares como células efectoras en el desarrollo de la T1D (AU)

Avances en inmunología de la diabetes tipo 1: IDS7-2004, Cambridge (UK) / Advances on immunology of type 1 diabetes: IDS7-2004, Cambridge (UK)

El 7º Congreso Internacional de la Immunology of Diabetes Society (IDS), tuvo lugar en Cambridge (UK) entre el 28 y el 31de Marzo de 2004, con la participación de los grupos más relevantes que trabajan en la inmunología de la diabetes, la fisiología de la célula beta y el transplante de islotes. Se presentaron muy diversas novedades científicas en el campo de la diabetes tipo 1. A modo de compendio en este resumen, los trabajos se agruparon en 8 áreas: 1) Talleres de autoanticuerpos y linfocitos T, 2) utilidad de los modelos animales en diabetes tipo 1, 3) transplante de islotes en pacientes diabéticos, 4) hipótesis de la higiene, 5) contribución de la célula beta y los linfocitos T en el ataque autoinmune ("la víctima y el asesino"), 6) variaciones en la diabetes tipo 1 (forma fulminante en Japón), 7) nuevo modelo animal para el estudio de la diabetes tipo 1 y 8) simposio satélite de transplante. Los datos presentados reflejan los lentos pero constantes avances en el conocimiento de la diabetes tipo 1 y evidencian la necesidad de seguir investigando hasta llegar a comprender la etiopatogenia de esta enfermedad y poder desarrollar tanto ensayos de prevención en sujetos de riesgo como tratamientos eficaces y seguros para los pacientes (AU)

Diabetes mellitus tipo 1: autoinmunidad frente a la célula beta / Type 1 diabetes mellitus: autoimmunity to Beta-cells

La diabetes mellitus tipo 1 es una enfermedad de etiología desconocida causada por la destrucción de las células productoras de insulina por parte del sistema inmunitario. Se conocen factores genéticos y desencadenantes ambientales que confieren susceptibilidad de desarrollar la enfermedad, así como alteraciones inmunológicas asociadas al proceso inflamatorio de los islotes que se detallan en esta revisión. Estos datos, junto con los modelos animales desarrollados -espontáneos o genéticamente manipulados- y los ensayos clínicos para evitar la manifestación de la enfermedad, han generado conocimiento y multitud de hipótesis, pero hasta el momento no existe prevención efectiva frente a la diabetes autoinmune. Es de esperar que las investigaciones presentes y futuras sobre la diabetes tipo 1 consigan determinar la etiología de la enfermedad y lograr la prevención o tratamientos de tolerancia inmunológica eficaces (AU)

Evidence of expression of endotoxin receptors CD14, toll-like receptors TLR4 and TLR2 and associated molecule MD-2 and of sensitivity to endotoxin (LPS) in islet beta cells.

CD14, a GPI-linked membrane protein, is a component of the lipopolysaccharide (LPS) receptor complex, one of the pattern-recognizing receptors (PRR) expressed by myeloid lineage cells. Here we report that CD14, the functionally linked toll-like receptor molecules, TLR2 and TLR4, and the associated molecule MD-2 are expressed in endocrine cells of the human pancreatic islets. CD14 expression in human pancreatic islets was determined by immunofluorescence staining of tissue sections and primary cultures, and confirmed by flow cytometry of dispersed normal islets and SV40-transformed islet cells (HP62). The latter cells synthesized and secreted CD14 in response to lipopolysaccharide (LPS) in a time- and dose-dependent manner. Reverse transcription polymerase chain reaction (RT-PCR)-Southern was positive for CD14, TLR2, TLR4 and MD-2 in human pancreas, purified islets and HP62 cells. In vitro experiments using rat islets (also positive for CD14 by RT-PCR) and HP62 cells showed that LPS regulates glucose-dependent insulin secretion and induces inflammatory cytokines [interleukin (IL)-1alpha, IL-6 and tumour necrosis factor (TNF)-alpha]. The functional expression of CD14 and associated molecules in islet beta cells adds a new pathway that islet cells may follow to adjust their function to endotoxaemia situations and become vulnerable to the inflammatory events that occur during diabetogenic insulitis.

Bound states of 3He at the edge of a 4He drop on a cesium surface.

We show that small amounts of 3He atoms, added to a 4He drop deposited on a flat cesium surface at zero temperature, populate bound states localized at the contact line. These edge states show up for drops large enough to develop well defined surface and bulk regions together with a contact line, and they are structurally different from the well-known Andreev states that appear at the free surface and at the liquid-solid interface of films. We illustrate the one-body density of 3He in a drop with 1000 4He atoms, and show that for a sufficiently large number of impurities the density profiles spread beyond the edge, coating both the curved drop surface and its flat base and eventually isolating it from the substrate.