Multiple Infectious Diseases Research Articles

CFD Simulation of Spread Risks of Infectious Disease due to Interactive Wind and Ventilation Airflows via Window Openings in High-Rise Buildings.

One of the concerns is that there may exist multiple infectious disease transmission routes across households in high‐rise residential buildings, one of which is the natural ventilative airflow through open windows between flats, caused by buoyancy effects. This study presents the modeling of this cascade effect using computational fluid dynamics (CFD) technique. It is found that the presence of the pollutants generated in the lower floor is generally lower in the immediate upper floor by two orders of magnitude, but the risk of infection calculated by the Wells‐Riley equation is only around one order of magnitude lower. It is found that, with single‐side open‐window conditions, wind blowing perpendicularly to the building may either reinforce or suppress the upward transport, depending on the wind speed. High‐speed winds can restrain the convective transfer of heat and mass between flats, functioning like an air curtain. Despite the complexities of the air flow involved, it is clear that this transmission route should be taken into account in infection control.

“Self-Nonself” Peptides in the Design of Vaccines

What makes a peptide an epitope? This is a central question in immunology. The clear identification of precise molecular characteristics of epitopes would help define the basic mechanisms of self/non-self distinction and lead to a greater understanding of phenomena such as tolerance, autoimmunity, allergy, and tumor escape of immune surveillance. Importantly, clarifying the properties an epitope is paramount to the development of diagnostic and therapeutic vaccines. This review analyzes recent reports on experimentally identified B cell epitopes associated with multiple infectious disease pathologies, cancer, autoimmunity, hypertension, obesity, and allergy. It illustrates data that further support the notion that only a low level of sequence similarity to the host proteome is needed to modulate the B cell epitope-specific peptidome. Amino acid sequences that are unique to the antigen and are not shared with the host proteome are specifically targeted by the humoral immune response. Therefore, low-similarity peptides may be significant to the rational development of peptide-based clinical treatments in cancer, autoimmunity, infection, and allergy. Biologically, the low-similarity hypothesis further supports sequence uniqueness as the molecular signature of "nonselfness" in the currently ongoing self/non-self debate.

VIRUS ANTIBODY LEVELS IN SERUM SPECIMENS FROM PATIENTS WITH OPTIC NEURITIS AND FROM MATCHED CONTROLS

Virus antibody levels in serum specimens taken in acute and convalescent phases from 77 patients with optic neuritits were tested by measles hamagglutination inhibition (HI), measles hemolysis inhibition (HLI), rubella HI, parainfluenza-1 HI, Epstein-Barr immunofluorescence (IF), and against 11 other viruses and mycoplasma pneumoniae with the complement fixation (CF) technique. The virus antibody levels were indicated to be usually very stable, and a fourfold change in virus antibody levels was demonstrated in only eight patients. The virus antibody levels were compared with specimens from two carefully selected control groups. The first control group consisted of 71 healthy persons matched in age, sex and place of residence with the patients with optic neuritis. The other control group consisted of 58 patients with various neurological diseases other than multiple sclerosis (MS) or infectious diseases of the central nervous system. The patients with optic neuritis had significantly higher measles antibody titres than the two control groups in both measles HI and measles HLI tests. Also in 33 patients with optic neuritis of unknown cause, the measles antibody levels were higher than in the control groups. On the other hand, various other antibody tests showed no statistically significant differences between patients with optic neuritis and the control group.

Myelitis in the course of systemic lupus erythematosus. Review

Myelopathy manifested clinically as acute longitudinal or transverse myelitis constitutes one of the most severe and rare neuropsychiatric manifestations of systemic lupus erythematosus (SLE) (1-3% of patients). Myelitis has been observed less commonly in other connective tissue diseases, mostly in antiphospholipid syndrome, and rarely in Sjögren's syndrome, Behçet's disease and mixed connective tissue disease. Acute transverse myelitis (ATM) may also be present in diseases of various etiology, including multiple sclerosis, sarcoidosis, infectious diseases and malignancies. Myelitis in SLE is manifested as a dramatic spinal cord injury leading to paralysis or muscular paresis, sensory deficits, and smooth muscle dysfunction usually in the form of sphincter dysfunction. The imaging technique of choice in case of suspected ATM is magnetic resonance imaging with intravenous contrast agent (gadolinium diethylenetriamine-pentaacid). Cerebrospinal fluid (CSF) examination in patients with ATM in the course of SLE indicate usually pleocytosis with prevalence of granulocytes, increased protein levels, low glucose levels, significantly hindering differential diagnosis in the early stage of the disease. Observations made by the authors (2 female patients with SLE) show that antibodies specific to SLE can be found in the CSF collected in the acute phase of myelitis. These observations have not yet been confirmed by other researchers. Early introduction of intravenous immunosuppression with large doses of cyclophosphamide and glucocorticosteroids improves the long-term prognosis. Other therapeutic approaches have been also used in more severe cases. Even with appropriate therapy, prognosis in this disease is uncertain.

Brain-specific Proteins Decline in the Cerebrospinal Fluid of Humans with Huntington Disease

We integrated five sets of proteomics data profiling the constituents of cerebrospinal fluid (CSF) derived from Huntington disease (HD)-affected and -unaffected individuals with genomics data profiling various human and mouse tissues, including the human HD brain. Based on an integrated analysis, we found that brain-specific proteins are 1.8 times more likely to be observed in CSF than in plasma, that brain-specific proteins tend to decrease in HD CSF compared with unaffected CSF, and that 81% of brain-specific proteins have quantitative changes concordant with transcriptional changes identified in different regions of HD brain. The proteins found to increase in HD CSF tend to be liver-associated. These protein changes are consistent with neurodegeneration, microgliosis, and astrocytosis known to occur in HD. We also discuss concordance between laboratories and find that ratios of individual proteins can vary greatly, but the overall trends with respect to brain or liver specificity were consistent. Concordance is highest between the two laboratories observing the largest numbers of proteins.

Interactions of Multiple Strain Pathogen Diseases in the Presence of Coinfection, Cross Immunity, and Arbitrary Strain Diversity

A model for coinfection in multiple strain infectious diseases is developed to incorporate coinfection statuses, immune and infection history, and cross immunity. It is solved for the symmetric interior equilibrium through the use of a ladder operator formalism inspired by quantum mechanical methods. We find that coinfection can fundamentally affects transmission dynamics with important epidemiologic and evolutionary consequences. It can significantly shift the distribution of age at infection for highly antigenically diverse pathogens so that in small host populations, an evolutionary strategy maximizing individual strain transmissibility might be less optimal than one which maximizes the total prevalence of all strains in the system. Alternatively, mechanisms which inhibit coinfection and thus increase total infection prevalence may be evolutionarily advantageous.

Prevalence of malnutrition in paediatric hospital patients

Childhood malnutrition has severe adverse effects on growth and development, but only limited information is available on the prevalence of malnutrition in paediatric hospital patients. We determined the prevalence of malnutrition in a series of unselected patients consecutively admitted as inpatients to a large tertiary care children's hospital in Germany. Data for weight and height upon admission were recorded in 475 unselected children aged 7.9+/-5 years (mean+/-SD). Weight for height 81-90 of median values were considered to indicate mild malnutrition, 70-80% moderate malnutrition and <70% severe malnutrition according to cut-off points defined by Waterlow. Some 24.1% of the patients were malnourished, with 17.7% of all patients who were mildly, 4.4% who were moderately and 1.7% who were severely malnourished. The largest proportion of malnourished patients was found among patients with multiple diagnoses (42.8% malnourished), mental retardation (40.0%), infectious diseases (34.5%) and cystic fibrosis (33.3%). The very high prevalence of malnutrition among children admitted to a children's hospital is considered intolerable, given the adverse consequences for short- and long-term health and well-being. Strategies for systematic screening and treatment of malnutrition in paediatric patients need to be refined and implemented.

Hybrid Cell Vaccination ResolvesLeishmania donovaniInfection by Eliciting a Strong CD8+Cytotoxic T-Lymphocyte Response with Concomitant Suppression of Interleukin-10 (IL-10) but Not IL-4 or IL-13

There is an acute dearth of therapeutic interventions against visceral leishmaniasis that is required to restore an established defective cell-mediated immune response. Hence, formulation of effective immunotherapy requires the use of dominant antigen(s) targeted to elicit a specific antiparasitic cellular immune response. We implemented hybrid cell vaccination therapy in Leishmania donovani-infected BALB/c mice by electrofusing dominant Leishmania antigen kinetoplastid membrane protein 11 (KMP-11)-transfected bone marrow-derived macrophages from BALB/c mice with allogeneic bone marrow-derived dendritic cells from C57BL/6 mice. Hybrid cell vaccine (HCV) cleared the splenic and hepatic parasite burden, eliciting KMP-11-specific major histocompatibility complex class I-restricted CD8+ cytotoxic T-lymphocyte (CTL) responses. Moreover, splenic lymphocytes of HCV-treated mice not only showed the enhancement of gamma interferon but also marked an elevated expression of the Th2 cytokines interleukin-4 (IL-4) and IL-13 at both transcriptional and translational levels. On the other hand, IL-10 production from splenic T cells was markedly suppressed as a result of HCV therapy. CD8+ T-cell depletion completely abrogated HCV-mediated immunity and the anti-KMP-11 CTL response. Interestingly, CD8+ T-cell depletion completely abrogated HCV-induced immunity, resulting in a marked increase of IL-10 but not of IL-4 and IL-13. The present study reports the first implementation of HCV immunotherapy in an infectious disease model, establishing strong antigen-specific CTL generation as a correlate of HCV-mediated antileishmanial immunity that is reversed by in vivo CD8+ T-cell depletion of HCV-treated mice. Our findings might be extended to drug-nonresponsive visceral leishmaniasis patients, as well as against multiple infectious diseases with pathogen-specific immunodominant antigens.

Roles of solar UV radiation and vitamin D in human health and how to obtain vitamin D

Exposure to solar UV radiation is a double-edged sword: the benefits include vitamin D3 production and tanning, while the risks include diseases linked to free-radical production and DNA damage. Research during the past few years has demonstrated that the health benefits of solar UVB (290–315 nm), the primary source of vitamin D3 for many people, now include reduced risk for bone diseases, many types of cancer and, to a lesser extent, autoimmune diseases such as multiple sclerosis and infectious diseases such as tuberculosis and influenza. Solar UVB may also play a beneficial role in other diseases and conditions. Recent studies indicate that the daily vitamin D3 requirement for optimal health is between 1000 and 4000 IU. The adverse health effects include skin cancer and melanoma, cataract development, premature skin aging and other lesser effects. However, the risk of melanoma seems to be due primarily to UVA (315–400 nm), and use of sunscreen that successfully blocks erythemal UV but does not provide g...

Sensitive and Specific Real-Time Polymerase Chain Reaction Assays to Accurately Determine Copy Number Variations (CNVs) of Human Complement C4A, C4B, C4-Long, C4-Short, and RCCX Modules: Elucidation of C4 CNVs in 50 Consanguineous Subjects with Defined HLA Genotypes

Recent comparative genome hybridization studies revealed that hundreds to thousands of human genomic loci can have interindividual copy number variations (CNVs). One of such CNV loci in the HLA codes for the immune effector protein complement component C4. Sensitive, specific, and accurate assays to interrogate the C4 CNV and its associated polymorphisms by using submicrogram quantities of genomic DNA are needed for high throughput epidemiologic studies of C4 CNVs in autoimmune, infectious, and neurological diseases. Quantitative real-time PCR (qPCR) assays were developed using TaqMan chemistry and based on sequences specific for C4A and C4B genes, structural characteristics corresponding to the long and short forms of C4 genes, and the breakpoint region of RP-C4-CYP21-TNX (RCCX) modular duplication. Assignments for gene copy numbers were achieved by relative standard curve methods using cloned C4 genomic DNA covering 6 logs of DNA concentrations for calibrations. The accuracies of test results were cross-confirmed internally in each sample, as the sum of C4A plus C4B equals to the sum of C4L plus C4S or the total copy number of RCCX modules. These qPCR assays were applied to determine C4 CNVs from samples of 50 consanguineous subjects who were mostly homozygous in HLA genotypes. The results revealed eight HLA haplotypes with single C4 genes in monomodular RCCX that are associated with multiple autoimmune and infectious diseases and 32 bimodular, 4 trimodular, and one quadrimodular RCCX. These C4 qPCR assays are proven to be robust, sensitive, and reliable, as they have contributed to the elucidation of C4 CNVs in >1000 human samples with autoimmune and neurological diseases.

The Troll in Toll: Mal and Tram as bridges for TLR2 and TLR4 signaling

Signaling by two of the most important bacteria-sensing TLRs, TLR2 and TLR4, involves two adaptor proteins, MyD88 adaptor-like (Mal) and Toll/IL-1 receptor (TIR) domain-containing adaptor-inducing IFN-beta (Trif)-related adaptor molecule (TRAM). Recently, new insights into the functioning of these two adapters have emerged. Mal is required by both TLRs to act as a bridge to recruit the adaptor MyD88, leading ultimately to NF-kappaB activation. Similarly, TRAM acts as a bridge to recruit TRIF to the TLR4 complex, leading to activation of the transcription factor IFN regulatory factor 3. Consistent with Mal and TRAM being key points of control, recent evidence suggests that they are subject to regulation by phosphorylation. Further, a variant in Mal in humans has been found to protect against multiple infectious diseases. Finally, another TIR domain-containing adaptor, sterile alpha and HEAT/armadillo motif protein (SARM), has been shown to act as an inhibitor of TRIF-dependent signaling. These recent discoveries add to the complexity of TLR signaling and highlight specific control mechanisms for TLR2 and TLR4 signaling.

Human genetics of infectious diseases: a unified theory

Since the early 1950s, the dominant paradigm in the human genetics of infectious diseases postulates that rare monogenic immunodeficiencies confer vulnerability to multiple infectious diseases (one gene, multiple infections), whereas common infections are associated with the polygenic inheritance of multiple susceptibility genes (one infection, multiple genes). Recent studies, since 1996 in particular, have challenged this view. A newly recognised group of primary immunodeficiencies predisposing the individual to a principal or single type of infection is emerging. In parallel, several common infections have been shown to reflect the inheritance of one major susceptibility gene, at least in some populations. This novel causal relationship (one gene, one infection) blurs the distinction between patient-based Mendelian genetics and population-based complex genetics, and provides a unified conceptual frame for exploring the molecular genetic basis of infectious diseases in humans.

What is the best control strategy for multiple infectious disease outbreaks?

Effective control of infectious disease outbreaks is an important public health goal. In a number of recent studies, it has been shown how different intervention measures like travel restrictions, school closures, treatment and prophylaxis might allow us to control outbreaks of diseases, such as SARS, pandemic influenza and others. In these studies, control of a single outbreak is considered. It is, however, not clear how one should handle a situation where multiple outbreaks are likely to occur. Here, we identify the best control strategy for such a situation. We further discuss ways in which such a strategy can be implemented to achieve additional public health objectives.

Prédisposition génétique et infections de l'enfant

The classic primary immunodeficiencies confer predisposition to multiple infectious diseases. However since ten years severe pediatric infections which were idiopathic have now molecular explanation. Indeed, defects in several genes confer a predisposition to infection with specific pathogenes in otherwise healthy individuals. These children present a new kind of hereditary immunodeficiency with severe and/or recurrent infections caused by only one microorganisms family, in opposition of others patients with “classic” primary immunodeficiency.

Dynamics of epidemics in homogeneous/heterogeneous populations and the spreading of multiple inter-related infectious diseases: Constant-sign periodic solutions for the discrete model

We consider the following model that describes the dynamics of epidemics in homogeneous/heterogeneous populations as well as the spreading of multiple inter-related infectious diseases: u i ( k ) = ∑ ℓ = k - τ i k - 1 g i ( k , ℓ ) f i ( ℓ , u 1 ( ℓ ) , u 2 ( ℓ ) , … , u n ( ℓ ) ) , k ∈ Z , 1 ⩽ i ⩽ n . Our aim is to establish criteria such that the above system has one or multiple constant-sign periodic solutions ( u 1 , u 2 , … , u n ) , i.e., for each 1 ⩽ i ⩽ n , u i is periodic and θ i u i ⩾ 0 where θ i ∈ { 1 ,- 1 } is fixed. Examples are also included to illustrate the results obtained.

The human cationic host defense peptide LL-37 mediates contrasting effects on apoptotic pathways in different primary cells of the innate immune system

The human cathelicidin LL-37 is a cationic host defense peptide (antimicrobial peptide) expressed primarily by neutrophils and epithelial cells. This peptide, up-regulated under conditions of inflammation, has immunomodulatory and antimicrobial functions. We demonstrate that LL-37 is a potent inhibitor of human neutrophil apoptosis, signaling through P2X(7) receptors and G-protein-coupled receptors other than the formyl peptide receptor-like-1 molecule. This process involved modulation of Mcl-1 expression, inhibition of BID and procaspase-3 cleavage, and the activation of phosphatidylinositol-3 kinase but not the extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase pathway. In contrast to the inhibition of neutrophil apoptosis, LL-37 induced apoptosis in primary airway epithelial cells, demonstrating alternate consequences of LL-37-mediated modulation of apoptotic pathways in different human primary cells. We propose that these novel immunomodulatory properties of LL-37 contribute to peptide-mediated enhancement of innate host defenses against acute infection and are of considerable significance in the development of such peptides and their synthetic analogs as potential therapeutics for use against multiple antibiotic-resistant infectious diseases.

Extra-Cellular DNA in Cord Blood (CB) Plasma: Use for Sample Identification [short Tandem Repeat (STR) Analysis] and for Infectious Disease Screening in CB Banks.

Introduction: A commitment of CB banks is to test CB units and maternal blood for multiple genetic and infectious disease markers. As a consequence, several aliquots of blood, mononuclear cells and plasma are taken during processing for immediate and delayed testing. Whereas control of identity between aliquots containing cells can be performed by DNA assays, identity controls for plasma aliquots rely only on bar-coded label systems. We hypothesize that there is soluble extra-cellular DNA (EC-DNA) and that it can be used for identity control of plasma aliquots. The aims of our study were;to determine the concentration of EC-DNA in CB-plasma,to evaluate whether genetic identity testing by STR analysis is feasible andto investigate whether EC-DNA allows infectious disease screening by nucleic acid testing (NAT).Methods: CB (n=20) was collected, processed (Rubinstein et al, PNAS 1995) and EC-DNA from 200 μl of 0.45μm-filtered plasma was extracted both with the Qiagen and the High Pure Viral Nucleic Acid method (Roche). Presence of EC-DNA was evaluated by detection of HLA-DR and ALU gene sequences and by STR analysis (AmpFlSTR-Profiler Plus-Applied Biosystems). Purified HBV was added to CB and peripheral blood (PB) plasma, EC-DNA recovered as above and HBV-DNA assessed by real time PCR.Results: All 20 samples were positive for HLA-DR by PCR and for ALU sequence by real time PCR, confirming the presence of EC-DNA in CB-plasma in concentrations of 0.022 +/− 0.012 ng/μl at the time of CB collection, rising to 0.124 +/− 0.025 ng/μl 33 hrs later; p<0.016. Concentrations observed in CB-plasma were higher than those of adult donor plasma (PB-plasma 0.005+/−0.0065 ng/μl). STR analysis was validated on cellular DNA and, when applied for EC-DNA, showed good signal strengths and low backgrounds, allowing accurate automatic allele identification with no manual corrections (genemapper software, Applied Biosystems). An increase in STR-PCR product concentration was observed when we analyzed EC-DNA samples from CB after 33hs (7017.6 +/− 2014 RFU/μl at time of CB collection and 30290.9 +/− 3164 RFU/μl after 33 hs; RFU = relative fluorescence units). HBV was recovered from all spiked units, in correspondence with the viral concentrations added. Recovery of HBV was 96 +/− 21% with high and low viral concentrations. Three mothers with HBAg/HBcore positive had also HBV-DNA in PB-plasma. Six with anti-HBcore only and 70 with anti-HBs were negative. HBV-DNA was also negative in CB-plasma for all seventy nine respective newborns.Conclusions: there is infant EC-DNA in CB-plasma and viral nucleic acids can be obtained using the same extraction method. There is an increase of EC-DNA in CB over time that may reflect cell death. STR assay of EC-DNA can be a useful molecular tool for the identification of plasma aliquots used for infectious disease testing in CB banks.

Hyperconcentrated (Dry) Versus Standard Platelet Apheresis: An In Vitro Quality Study.

Introduction: Platelet concentrates (PC) collected by apheresis are effective in supporting deeply thrombocytopenic patients. The reduced risk of multiple allogeneic exposure and transmissible infectious diseases together with the high WBC depletion and diminished transfusion reactions are the main advantages offered by PC transfusion. At moment, the availability of several synthetic solutions for platelets storage permits to prepare hyperconcentrate(dry) apheresis platelets with the advantage of reducing febrile non-hemolytic transfusion reactions and, in low body weight patients the citrate toxicity, without the necessity of further manipulations. The aim of this study was to test the quality of 20 dry platelets (DP) in comparison to 20 standard plateletpheresis (SP) concentrates.Materials and methods: A total of 40 apheresis procedures were performed by the single-needle Cobe Trima separation device (Gambro BCT, Lakewood, CO, USA) collecting either DP or SP concentrates. Within 1h after collection, the bag containing DP was added with the appropriate amount (70% of DP final volume) of synthetic solution for platelets storage (SSP, MacoPharma). Both DP and SP concentrates were stored at room temperature with gentle agitation for 4 days. For both concentrates, platelet yield was calculated and in vitro studies of membrane glycoproteins expression and aggregation at day +1 and day +4 were carried out.Results: The comparison between 20 DP and 20 SP concentrates in terms of ability to aggregate in vitro and membrane glycoproteins expression at day +1 and day +4 of storage is reported in table A and B respectively.Conclusions: The in vitro tests documented a major activation of dry platelets. In particular, the ability to aggregate was reduced in the 20 DP concentrates analised and this phenomenon was more evident at day +4 of storage. The alteration of membrane glycoproteins expression (markers of storage lesion) confirms the lower in vitro quality of DP concentrates. The effectiveness of this new blood component in vivo should be evaluated in a controlled clinical trial.Table AAt collectionDay +1Day +4SPDPSPDPSPDPCollagen μg/ml 4938897828053ADP 10 μM32112416165Ristocetin 1.5 mg/ml919777817152Collagen 10 μg/ml + Adrenaline 10 μM989593949380ADP 10 μM + Adrenaline 10 μM877276615730Table BAt collectionDay +1Day +4SPDPSPDPSPDPGPIb alfa (MFI)5.065.756.316.135.264.54GPIIb-IIIa (MFI)35.4736.7134.6137.731.7640.9GP IV (MFI)11.4911.411.6710.2811.6511.38GP 5324.2327.1121.7425.9121.4631.84GMP 14021.7929.2922.6530.3820.5834.89

Short-lived plasma blasts are the main B cell effector subset during the course of multiple sclerosis

Multiple sclerosis is a chronic inflammatory and demyelinating disorder of the CNS with an unknown aetiology. Although intrathecal immunoglobulin G (IgG) synthesis is a key feature of the disease, little is still known about the B cell response in the CNS of multiple sclerosis patients. We analysed the phenotype and kinetics of different B cell subsets in patients with multiple sclerosis, infectious disease (IND) and non-inflammatory neurological disease (NIND). B cells were detected in the CSF of multiple sclerosis and IND patients, but were largely absent in NIND patients. In the CSF, the majority of B cells had a phenotype of memory B cells and short-lived plasma blasts (PB); plasma cells were absent from the compartment. The proportion of PB was highest in multiple sclerosis patients and patients with acute CNS infection. While PB disappeared rapidly from the CSF after resolution of infection in IND patients, these cells were present at high numbers throughout the disease course in multiple sclerosis patients. CSF PB numbers in multiple sclerosis patients strongly correlated with intrathecal IgG synthesis and inflammatory parenchymal disease activity as disclosed by MRI. This study identifies short-lived plasma blasts as the main effector B cell population involved in ongoing active inflammation in multiple sclerosis patients.

Micromachined polymerase chain reaction system for multiple DNA amplification of upper respiratory tract infectious diseases

This paper presents a micro polymerase chain reaction (PCR) chip for the DNA-based diagnosis of microorganism genes and the detection of their corresponding antibiotic-resistant genes. The micro PCR chip comprises cheap biocompatible soda–lime glass substrates with integrated thin-film platinum resistors as heating/sensing elements, and is fabricated using micro-electro-mechanical-system (MEMS) techniques in a reliable batch-fabrication process. The heating and temperature sensing elements are made of the same material and are located inside the reaction chamber in order to ensure a uniform temperature distribution. This study performs the detection of several genes associated with upper respiratory tract infection microorganisms, i.e. Streptococcus pneumoniae, Haemopilus influenze, Staphylococcu aureus, Streptococcus pyogenes, and Neisseria meningitides, together with their corresponding antibiotic-resistant genes. The lower thermal inertia of the proposed micro PCR chip relative to conventional bench-top PCR systems enables a more rapid detection operation with reduced sample and reagent consumption. The experimental data reveal that the high heating and cooling rates of the system (20 and 10 °C/s, respectively) permit successful DNA amplification within 15 min. The micro PCR chip is also capable of performing multiple DNA amplification, i.e. the simultaneous duplication of multiple genes under different conditions in separate reaction wells. Compared with the large-scale PCR system, it is greatly advantageous for fast diagnosis of multiple infectious diseases. Multiplex PCR amplification of two DNA segments in the same well is also feasible using the proposed micro device. The developed micro PCR chip provides a crucial tool for genetic analysis, molecular biology, infectious disease detection, and many other biomedical applications.