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Background The DTaP-IPV/Hib combination vaccine can replace the acellular tetanus vaccine, polio vaccine, and the Haemophilus influenzae type B vaccine. Data on the safety of DTaP-IPV/Hib vaccines are required. We aimed to evaluate the safety of the vaccination program. Methods Using the National Adverse Events Following Immunization (AEFI) surveillance system (CNAEFIS) in Guangzhou, China, a retrospective study was performed from May 11, 2011, to December 31, 2017. There were 376 cases of adverse events after vaccination with the DTaP IPV/Hib vaccine. The primary analysis indicators were the number of vaccines used, the number of AEFI reports received, and the reporting rate (per 100,000). Results From May 1, 2011, to December 31, 2017, 516,000 doses of vaccine were inoculated, and 376 cases of adverse reactions were reported; the reporting rate was 72.8 per 100,000 vaccines. There were eight cases of serious AEFIs (1.5 per 100,000), with four cases of thrombocytopenic purpura (0.8 per 100,000); three cases of cyanosis of the lips, stiffness, and flexion of limbs, and convulsions (0.6 per 100,000); and one case of a high fever (0.2 per 100,000). The highest incidence of AEFIs occurred after the fourth dose (n = 207, 55.0%, 40.1 per 100,000), followed by the first dose (n = 81, 21.5%, 15.7 per 100,000), second dose (n = 48, 12.8%, 9.3 per 100,000) and third dose (n = 40, 10.6%, 7.7 per 100,000). The AEFI incidence was higher after injection of the vaccine into the deltoid muscle of the upper arm (n = 276, 73.4%, 53.5 per 100,000) than after injection of the vaccine into the thigh (n = 100, 26.6%, 19.4 per 100,000). There was a significant difference between AEFIs after injection into the deltoid of the upper arm deltoid and the thigh (x2 = 164.8, P Conclusions Most of the reported AEFIs after DTaP-IPV/Hib vaccination are not serious. There were four cases of TP in this study; vaccination may be a rare cause of thrombocytopenic purpura.

This paper describes a 22-to-36.8 GHz low phase noise Colpitts voltage-controlled oscillator (VCO) array using 0.13-μm SiGe BiCMOS technology. The VCO array consists of four Colpitts VCO cores and three millimeter-wave (MMW) selectors. In the VCO core, in order to achieve the best phase noise and power consumption trade-off, an optimization method based on symbolic expressions is presented. In a further research, a switchable bias current technique is proposed to achieve lower phase noise. The MMW selectors are designed to select the desired VCO core and cover the whole frequency band with sufficient output power. The fabricated VCO array features a wide tuning range of 50.3%, low phase noise between −100.7 dBc/Hz and −95.3 dBc/Hz at 1 MHz offset and high output power of 4.5 dBm, which results in the FOMT between −183.2 dBc/Hz and −177.8 dBc/Hz.

In this paper, a new analytic approach is proposed for injection-locked ring oscillators (ILROs) design at millimeter waves (mm-waves). Using time and transfer constants (TTC) analysis, a two-pole model of the delay stage is applied into the injection-locking behavior model for an N-stage ring oscillator, and analytic expressions of the self-resonance frequency (SOF) and the locking range are derived. These expressions are concise and based solely on device-level circuit parameters, enabling fast and exact ILRO design through DC and AC simulations. In addition, a dual-input injection technique is investigated and a layout optimization technique is presented. Using a 0.13-μm SiGe BiCMOS process, a two-stage ring oscillator with dual-input injection is implemented for verification. The fabricated divider achieves a wide locking range from 16 to 67 GHz at −10-dBm input power. The divider core consumes a current of 3.9 mA from 3.3 V supply with an area of 45 × 60 μm2. The measured results agree well with theoretical analyses and simulated results.

A low voltage low power receiver supporting 780/868/915/2400 MHz ZigBee bands is presented in this paper. The receiver exploiting low-IF architecture consists of a RF-to-BB (baseband) current reuse front-end, a Gm-C based variable gain complex band-pass filter (CBPF) for image rejection and four stages of limiting amplifiers which saturate IF signal for demodulation. The proposed ZigBee receiver chip is implemented in TSMC 180 nm CMOS technology with metal-insulator-metal (MIM) capacitors. PCB measurement results show that the receiver has 45.9 dB conversion gain, 8.5 dB NF and −33.5 dBm out-of-band IIP3 at sub-GHz bands. When working in 2.4 GHz band, the gain is 38.4 dB, noise figure (NF) is 16.7 dB and the out-of-band IIP3 is −28.2 dBm. The S11 bandwidth (S11

A wideband 2–3 GHz three-stage low noise amplifier (LNA) featuring current reuse, cascaded L-type input matching network (IMN), and optimized multiple gated transistors method (MGTR) using 0.18- μ m CMOS technology is presented in this paper. The current-reused topology is employed in the first two stages to reduce power consumption. For a wideband input matching, the common gate (CG) topology is adopted. Moreover, the cascaded L-type IMN composed of two single L-type networks cascaded in series is proposed for the first time. To improve the linearity performance, the optimized MGTR taking both transconductance g m and third-order nonlinear coefficient g m ″ into consideration is proposed and applied to the output stage. The proposed LNA presents a maximum power gain of 28.0 dB, an input matching across 1.8–5.8 GHz and a high third-order input intercept point (IIP 3 ) of −9.89 dBm. A noise figure (NF) of 3.1–3.5 dB is obtained in the required band with a power dissipation of 6.49 mA from a 3 V power supply.

A low power 0.1–1 GHz RF receiver front-end composed of noise-cancelling trans-conductor stage and I/Q switch stage was presented in this paper. The RF receiver front-end chip was fabricated in 0.18 µm RF CMOS. Measurement results show the receiver front-end has a conversion gain of 28.1 dB at high gain mode, and the single-sideband (SSB) noise figure is 6.2 dB. In the low gain mode, the conversion gain of the receiver front-end is 15.5 dB and the IP1dB is −12 dBm. In this design, low power consumption and low cost is achieved by current-reuse and inductor-less topology. The receiver front-end consumes only 5.2 mW from a 1.8 V DC supply and the chip size of the core circuit is 0.12 mm2.

In this paper, a newly analytical method is proposed for the design of programmable frequency dividers. The more accurate transfer function of the current mode logic (CML) stage is used to analyze the injection-locking behavior models of the dual-modulus prescaler, and the general analytical expressions of the locking range of the prescaler are derived. Based on the analytical expressions that can be calculated using device-level circuit parameters obtained through DC and AC simulations, the dual-modulus prescaler design can be optimized quickly and accurately, thereby extending the frequency-division range of the programmable frequency divider. The proposed analytical method is verified by the measured results of the 2–22 GHz programmable divider, fabricated in 0.13-μm SiGe BiCMOS technology. By using heterojunction bipolar transistors (HBTs) in the dual-modulus prescaler and metal–oxidesemiconductor field-effect transistors (MOSFETs) in the pulse and swallow counters, the proposed programmable divider achieves the lowest power consumption of 63.3 mW and the best FOMT compared with previously works.

Human adenovirus type 12 (HAdV-12) displays a relatively low virulence and slow replication in cultured human cells, which is manifested by premature death of HAdV-12-infected cells. Whereas HAdV-2 induction of IFN-β expression was transient, HAdV-12-infected cells maintained high levels of IFN-β expression, protein kinase R (PKR) activation and eIF-2α phosphorylation throughout the infectious cycle. The importance of the IFN-inducible PKR kinase in restriction of HAdV-12 was supported by the enhanced growth of the virus following PKR knockdown in HeLa cells. Ectopic expression of HAdV-2 VA RNAI increased HAdV-12 hexon protein expression, suggesting that insufficient VA RNA expression contributes to the restricted growth of HAdV-12. Although some adenovirus species are known to persist in human lymphoid tissues, HAdV12 has so far not been found. Thus, it is possible that the inability of HAdV12 to evade the INF response may have implications for the virus to establish long-lasting or persistent infections.

Double-stranded RNA (dsRNA) plays a centrally important role in antiviral innate immunity, both for the production of interferon (IFN) and also in the actions of IFN. Among the IFN-inducible gene products are the protein kinase regulated by RNA (PKR) and the adenosine deaminase acting on RNA 1 (ADAR1). PKR is an established key player in the antiviral actions of IFN, through dsRNA-dependent activation and subsequent phosphorylation of protein synthesis initiation factor eIF2α thereby altering the translational pattern in cells. In addition, PKR plays an important role as a positive effector that amplifies the production of IFN. ADAR1 catalyzes the deamination of adenosine (A) in RNA with double-stranded (ds) character, leading to the destabilization of RNA duplex structures and genetic recoding. By contrast to the antiviral and proapoptotic functions associated with PKR, the actions of ADAR1 in some instances are proviral and cell protective as ADAR1 functions as a suppressor of dsRNA-mediated antiviral responses including activation of PKR and interferon regulatory factor 3.

Two size forms of ADAR1 adenosine deaminase are known, one constitutively expressed (p110) and the other interferon (IFN)-induced (p150). To test the role of ADAR1 in viral infection, HeLa cells with ADAR1 stably knocked down and 293 cells overexpressing ADAR1 were utilized. Overexpression of p150 ADAR1 had no significant effect on the yield of vesicular stomatitis virus. Likewise, reduction of p110 and p150 ADAR1 proteins to less than approximately 10 to 15% of parental levels (ADAR1-deficient) had no significant effect on VSV growth in the absence of IFN treatment. However, inhibition of virus growth following IFN treatment was approximately 1 log(10) further reduced compared to ADAR1-sufficient cells. The level of phosphorylated protein kinase PKR was increased in ADAR1-deficient cells compared to ADAR1-sufficient cells following IFN treatment, regardless of viral infection. These results suggest that ADAR1 suppresses activation of PKR and inhibition of VSV growth in response to IFN treatment.

ADAR1, an interferon inducible adenosine deaminase acting on RNA, catalyzes the C6 deamination of adenosine (A) to produce inosine (I) in RNA substrates with double-stranded character, leading to genetic recoding and altered RNA structure. Adar1 expression occurs from multiple promoters and encodes either an IFN-inducible p150 cytoplasmic protein or a constitutively expressed N-terminally truncated p110 nuclear protein. The roles of ADAR1 p150 and p110 in uninfected cells and during virus infection were examined using human cell clones made stably deficient in ADAR1, mouse cells genetically deficient in ADAR1, and by complementation strategies. The effects of ADAR1 deficiency on virus growth, IFNb induction, and stress responses including formation of stress granules (SG) and cell death were opposite to those established for dsRNA-dependent PKR kinase deficiency. Exemplified by measles virus (MV) infection, ADAR1 suppressed activation of PKR and IRF3 and protected cells from SG formation and cytopathic damage. MV-induced SG formation was PKR-dependent and impaired by catalytically active p150 but not p110 ADAR1. C KO mutant MV was an effective inducer of IFNb by IPS-1-dependent signaling that was amplified by PKR. RNA expression profiles were characterized by qPCR and RNA deep sequencing, with differences found between C KO mutant and parental MV, and untreated and IFN-treated cells. Significant amounts of dsRNA accumulate during C KO mutant infection. Results obtained with mouse cells genetically deficient in either adar1 or the related deaminase adar2 , or stat1 or stat2 , suggest a central role of ADAR1 in overall A-to-I editing and p150 in the IFN-induced editing. In summary, ADAR1 behaved as an anti-apoptotic host factor that, in some instances, suppressed innate immune activities and was pro-viral. Our findings furthermore implicate a balanced interplay between PKR and ADAR1 in modulating IFNb protein production and stress responses following virus infection. (Supported by NIAID, NIH).