A 2.4-GHz full-duplex (FD) transceiver, which employs multiple self-interference (SI) cancellation techniques, is presented for future wideband wireless communication. The proposed FD radio features ...broadband SI suppression, cancellers calibrated for enhanced linearity, and the ability to cancel long-delay spread SI. A prototype chip is fabricated in a Taiwan Semiconductor Manufacturing Company's (TSMC) 40-nm CMOS process and works with a Xilinx RFSoC evaluation kit to complete the calibration loop for the radio analog front end (AFE). The FD AFE chip integrates an electrical-balanced duplexer (EBD) with a tuned impedance matching network (<inline-formula> <tex-math notation="LaTeX">{Z} </tex-math></inline-formula>Bal), two broadband five complex-tap continuous-time finite impulse response (FIR)-based RF cancellation filters, and a mixed-signal baseband cancellation path operating with a field-programmable gate array (FPGA) to complete a long-delay spread (<inline-formula> <tex-math notation="LaTeX">\tau =+174 </tex-math></inline-formula> ns) SI canceller. A fourth-order <inline-formula> <tex-math notation="LaTeX">{Z} </tex-math></inline-formula>Bal is employed to reduce SI group delay and improves the cancellation bandwidth (BW) when used with complex filters. This work reports a measured SI suppression of 62 dB across +120-MHz BW for delay spreads between 0 and 0.28 ns and SI cancellation of 23 dB across +120-MHz BW for delay spreads between 0.4 and 174 ns. The EBD achieves an enhanced common-mode rejection exceeding 55 dB through the use of a center-tap capacitor (<inline-formula> <tex-math notation="LaTeX">{C} </tex-math></inline-formula>CT) with minimal additional area. The RF canceller, calibrated by digitally controlled current digital-to-analog converters (DACs), demonstrates a maximum input-referred third order intercept point (IIP3) of +42 dBm. The receiver (RX) has a measured noise figure (NF) of 6.8 dB and an IIP3 of −21 dBm at the maximum gain setting of 40 dB. An integrated harmonic-rejection power amplifier (PA) achieves a measured maximum output power <inline-formula> <tex-math notation="LaTeX">{P} </tex-math></inline-formula>Sat and a PAE of 19.1 dBm and 27%, respectively. The overall FD transceiver, including an integrated phase-locked loop (PLL), occupies an area of 3.2 mm2 and consumes a total power of 373/78 mW including/excluding the PA.
The genome of the multihost bacteriophage ΦK64-1, capable of infecting
capsular types K1, K11, K21, K25, K30, K35, K64, and K69, as well as new capsular types KN4 and KN5, was analyzed and revealed ...that 11 genes (
,
,
,
,
,
,
,
,
,
, and
) encode proteins with amino acid sequence similarity to tail fibers/spikes or lyases.
previously was shown to encode a K64 capsule depolymerase (K64dep). Specific capsule-degrading activities of an additional eight putative capsule depolymerases (S2-4 against K1, S1-1 against K11, S1-3 against K21, S2-2 against K25, S2-6 against K30/K69, S2-3 against K35, S1-2 against KN4, and S2-1 against KN5) was demonstrated by expression and purification of the recombinant proteins. Consistent with the capsular type-specific depolymerization activity of these gene products, phage mutants of
,
,
, or
lost infectivity for KN4, K25, K35, or K30/K69, respectively, indicating that capsule depolymerase is crucial for infecting specific hosts. In conclusion, we identified nine functional capsule depolymerase-encoding genes in a bacteriophage and correlated activities of the gene products to all ten hosts of this phage, providing an example of type-specific host infection mechanisms in a multihost bacteriophage.
We currently identified eight novel capsule depolymerases in a multihost
bacteriophage and correlated the activities of the gene products to all hosts of this phage, providing an example of carriage of multiple depolymerases in a phage with a wide capsular type host spectrum. Moreover, we also established a recombineering system for modification of
bacteriophage genomes and demonstrated the importance of capsule depolymerase for infecting specific hosts. Based on the powerful tool for modification of phage genome, further studies can be conducted to improve the understanding of mechanistic details of
phage infection. Furthermore, the newly identified capsule depolymerases will be of great value for applications in capsular typing.
Despite the increasingly recognized impact of novel coronavirus disease (COVID-19), caused by severe acute respiratory syndrome (SARS) coronavirus 2 (SARS-CoV-2), on many aspects of health in adults ...and children, its effects on neonates born to infected mothers remain unclear. We conducted this study to investigate the outcomes of neonates born to mothers with COVID-19.
We searched the medical databases from inception to March 31, 2020 to perform a systematic review of outcomes in neonates born to mothers with COVID-19. Data were pooled using a random effects regression model. Primary and secondary outcomes were neonatal clinical outcomes and infectious status, respectively.
Fourteen studies involving 105 neonates fulfilling the study criteria were identified. The rates of preterm neonates and those small for gestational age (SGA) were 25 (23.8%) and 10 (11.2%), respectively. Among 91 neonates who were tested, 8 (8.8%) were positive for nucleic acids or antibodies for SARS-CoV-2. Additionally, 28 (26.7%) of the neonates were symptomatic and two test-negative neonates died, including one stillbirth. Between test-positive and test-negative groups, the rates of SGA, preterm delivery, duration between maternal symptom onset and delivery, and perinatal complication were not significantly different; but the rate of symptomatic after birth reached significant difference (62.5% vs 20.5%, p = 0.008).
Most neonates born to infected mothers had favorable outcomes. Although direct evidences of intrauterine infection were scarce, the risk of intrauterine infection should be considered based on a positive test in 8.8% of the neonates. Symptomatic neonates born to infected mothers should receive tests for SARS-CoV-2 to initiate appropriate treatment and quarantine. Further studies are warranted to assess the outcomes of COVID-19 in neonates.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
The prevalence of skin diseases and diabetes mellitus (DM) are prominent around the world. The current scope of knowledge regarding the prevalence of skin diseases and comorbidities with type 2 DM ...(T2DM) is limited, leading to limited recognition of the correlations between skin diseases and T2DM.
We collected 383 subjects from the Da Qing Diabetes Study during the period from July 9th to September 1st, 2016. The subjects were categorized into three groups: Normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and T2DM. The prevalence and clinical characteristics of skin diseases were recorded and investigated.
In this cross-sectional study, 383 individuals with ages ranging from 53 to 89-year-old were recruited. The overall prevalence of skin diseases was 93.5%, and 75.7% of individuals had two or more kinds of skin diseases. Additionally, there were 47 kinds of comorbid skin diseases in patients with T2DM, of which eight kinds of skin diseases had a prevalence >10%. The prevalence of skin diseases in NGT, IGT, and T2DM groups were 93.3%, 91.5%, and 96.6%, respectively; stratified analysis by categories showed a statistically significant difference in "disturbances of pigmentation" and "neurological and psychogenic dermatoses". The duration of T2DM also significantly associated with the prevalence of "disturbances of pigmentation" and "neurological and psychogenic dermatoses". Subsequently, the prevalence of "disturbances of pigmentation" was higher in males than females in NGT (P < 0.01) and T2DM (P < 0.01) groups. In addition, the difference in the prevalence of "disturbances of pigmentation" was also significant in NGT and T2DM groups (P < 0.01).
There was a high prevalence of skin diseases in the Da Qing Diabetes Study. To address the skin diseases in the Da Qing Diabetes Study, increased awareness and intervention measures should be implemented.
Information on the efficacy of pegylated interferon (PEG-IFN) treatment of chronic hepatitis B (CHB) patients and predictors of the response based on real-world data is limited. Consecutive 201 ...patients who underwent PEG-IFN treatment for CHB were reviewed. A virological response (VR) was defined as a serum HBV DNA of <2000 IU/mL, and a combined response (CR) was defined a VR accompanied by serological response for hepatitis B e antigen (HBeAg)-positive CHB. For HBeAg-positive CHB patients, the HBeAg seroconversion rate and CR rate were 30.5% and 21.2% at 48 weeks after end of treatment (EOT), respectively. Baseline alanine aminotransferase (ALT) level was associated with HBeAg seroconversion, while baseline hepatitis B s antigen (HBsAg) levels of <250 IU/mL and HBV DNA <2.5 × 10(7) IU/mL were strongly associated with sustained off-treatment CR. For HBeAg-negative CHB, the VR rates were 85.5%, and 27.7% at EOT, and 48 weeks after EOT, respectively; a baseline HBsAg <1,250 IU/mL was associated with sustained off-treatment VR. PEG-IFN treatment has durable HBeAg seroconversion in HBeAg-positive CHB, but results in a high risk of relapse among HBeAg-negative CHB patients. Pre-treatment HBsAg level is an important predictor of VR in CHB patients undergoing PEG-IFN treatment.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Pompe disease usually has muscle weakness due to glycogen accumulation. Heckmatt scale is commonly used to grade the pertinent findings of ultrasound. Nonetheless, it is difficult to detect subtle ...changes of the muscle. Besides, no ultrasonographic parameter has been proposed to predict the motor functions of Pompe disease. Therefore, we aimed to find out an ultrasonographic parameter that can quantify the muscle involvement and correlate with the motor functions in Pompe disease.
Eighteen patients with Pompe disease were enrolled. The echo heterogeneity index (standard deviation divided by mean echogenicity values by ImageJ analysis) and shear modulus were recorded from rectus femoris, biceps femoris, tibialis anterior, medial gastrocnemius, biceps brachii and triceps brachii muscles. Motor functions, including manual muscle strength, 6-min walk and four-limb stair climb tests were assessed. Correlations between ultrasonographic parameters and Heckmatt scale and motor functions were analyzed.
The echo heterogeneity index, but not the shear modulus, was negatively correlated with the Heckmatt scale rating in all muscles. The echo heterogeneity indices of tibialis anterior (r = 0.698, p = 0.008) and medial gastrocnemius (r = 0.615, p = 0.025) muscles showed positive correlations with the walking distance. Besides, the echo heterogeneity indices of four lower limb muscles were negatively correlated with the duration of stair climbing.
The echo heterogeneity index but not the shear modulus can be used to quantitatively describe the muscle involvement in Pompe disease. In addition, lower echo heterogeneity indices of lower limb muscles are associated with worse motor functions in these patients.
•Echo heterogeneity (EH) index is negatively correlated with the Heckmatt scale grades.•There is an inconsistent relationship between shear modulus and the Heckmatt scale.•Lower EH indices of lower limb muscles are associated with worse motor functions in Pompe disease.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
•An immunoprecipitation coupled with LC‒MS/MS was applied to globally identify cellular.•Factors that interact with the PA proteins of the influenza A H1N1, 2009 pandemic H1N1, and H3N2 viruses.•The ...interactome analysis demonstrated that proteins located in the mitochondrion, proteasome, nucleus are associated with the PA protein.•PA protein of influenza A virus is partly located in mitochondria and impacts on mitochondrial function and autophagy.•The mitochondrial protein PYCR2 interacts with the PA protein of influenza A virus and negatively regulates the replication of influenza A virus.
Influenza A virus can infect respiratory tracts and may cause severe illness in humans. Proteins encoded by influenza A virus can interact with cellular factors and dysregulate host biological processes to support viral replication and cause pathogenicity. The influenza viral PA protein is not only a subunit of influenza viral polymerase but also a virulence factor involved in pathogenicity during infection. To explore the role of the influenza virus PA protein in regulating host biological processes, we performed immunoprecipitation and LC‒MS/MS to globally identify cellular factors that interact with the PA proteins of the influenza A H1N1, 2009 pandemic H1N1, and H3N2 viruses. The results demonstrated that proteins located in the mitochondrion, proteasome, and nucleus are associated with the PA protein. We further discovered that the PA protein is partly located in mitochondria by immunofluorescence and mitochondrial fractionation and that overexpression of the PA protein reduces mitochondrial respiration. In addition, our results revealed the interaction between PA and the mitochondrial matrix protein PYCR2 and the antiviral role of PYCR2 during influenza A virus replication. Moreover, we found that the PA protein could also trigger autophagy and disrupt mitochondrial homeostasis. Overall, our research revealed the impacts of the influenza A virus PA protein on mitochondrial function and autophagy.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
•Risk factors for in vivo emergence of colistin resistance in carbapenem-resistant K. pneumoniae (CRKP) were studied.•Colistin exposure is the only independent risk factor for in vivo emergence of ...colistin resistance in CRKP.•Alteration in mgrB was the predominant mechanism for in vivo emergence of colistin resistance in CRKP.•Mechanisms of colistin resistance in some CRKP strains remained undiscovered.
Colistin is one of the last-resort antibiotics for treating carbapenem-resistant Klebsiella pneumoniae (CRKP). However, colistin resistance in CRKP poses a global antimicrobial crisis, as therapeutic options are limited. We investigated risk factors for in vivo emergence of colistin resistance in CRKP and explored the underlying resistance mechanisms. We conducted this matched case–control study of patients with sequential CRKP clinical strains at a medical centre in Taiwan between October 2016 and June 2019. The case group included patients with an index colistin-resistant CRKP (ColR-CRKP) strain and a previous colistin-susceptible CRKP (ColS-CRKP) counterpart. The control group encompassed patients with both an index and previous ColS-CRKP strains. Cases and controls were matched according to the time at risk, and conditional logistic regression was used to evaluate potential risk factors. Alterations in genes associated with resistance were compared between ColR-CRKP and ColS-CRKP strains. We identified 24 CRKP cases with in vivo-emergent colistin resistance, matched in a 1:2 ratio with controls. Multivariate analysis showed that colistin exposure is the only independent risk factor predisposing to colistin resistance (adjusted odds ratio = 19.09, 95% confidence interval 1.26–290.45; P = 0.034). Alteration in the mgrB gene was the predominant mechanism for emergent colistin resistance (17/24; 71%). In conclusion, colistin use is a risk factor for in vivo emergence of colistin resistance in CRKP. Given the lack of a rapid and reliable method to detect colistin resistance in daily practice, physicians should be vigilant for the emergence of resistance during colistin treatment.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
UVC irradiation-caused DNA lesions are repaired in mammalian cells solely by nucleotide excision repair (NER), which consists of sequential events including initial damage recognition, dual incision ...of damage site, gap-filling, and ligation. We have previously shown that gap-filling during the repair of UV-induced DNA lesions may be delayed by a subsequent treatment of oxidants or prooxidants such as hydrogen peroxide, flavonoids, and colcemid. We considered the delay as a result of competition for limiting protein/enzyme factor(s) during repair synthesis between NER and base excision repair (BER) induced by the oxidative chemicals. In this report, using colcemid as oxidative stress inducer, we showed that colcemid-caused delay of gap-filling during the repair of UV-induced DNA lesions was attenuated by overexpression of PCNA but not ligase-I. PCNA knockdown, as expected, delayed the gap-filling of NER but also impaired the repair of oxidative DNA damage. Fen-1 knockdown, however, did not affect the repair of oxidative DNA damage, suggesting repair of oxidative DNA damage is not of long patch BER. Furthermore, overexpression of XRCC1 delayed the gap-filling, and presumably increase of XRCC1 pulls PCNA away from gap-filling of NER for BER, consistent with our hypothesis that delay of gap-filling of NER attributes the competition between NER and BER.
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FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, UL, UM, UPUK
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