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This paper presents a 20-Gb/s automatic gain control (AGC) amplifier in a 0.18-μm SiGe BiCMOS for high-speed applications. The proposed AGC amplifier compactly consists of a folded Gilbert variable-gain amplifier (VGA), a post amplifier (PA), a 50-Ω output buffer, and AGC loop including an open-loop peak detector (PD), a RC low-pass filter (LPF), and an error amplifier (EA). The AGC amplifier achieves the broadband characteristic by utilizing inductive peaking and capacitive degeneration as well as fT-doubler techniques to overcome the large parasitic capacitances. The proposed AGC circuits together with a linear VGA exhibits a wide gain control range of 45 dB for the received signal strength indication (RSSI). The measured AGC amplifier achieves a maximum gain of 21 dB and a -3-dB bandwidth (BW) of 20.6 GHz, which can support up to 25.4-Gb/s data rate. For the pseudorandom bit sequence (PRBS) length 231–1 with a bit-error rate (BER) of 10−12 at 20 Gb/s, the measured input dynamic range is 26 dB (20–400mVpp) and the peak-to-peak data jitter is less than 8 ps. The AGC amplifier consumes a power of 160 mW from a 3.3-V supply voltage and occupies an area of 850 μm × 850 μm.

Skin injury is a major problem threatening human physical and mental health, and how to promote wound healing has been the focus. Developing new wound dressings is an important strategy in skin regeneration. Aloe vera is a medicinal plant with a long history, complex constituents, and various pharmacological activities. Many studies have shown that A. vera plays an important role in promoting wound healing. Adding A. vera to wound dressing has become an ideal way. This review will describe the process of skin injury and wound healing and analyze the role of A. vera in wound healing. In addition, the types of wound dressing and the applications of A. vera in wound dressing will be discussed.

Background Metabolic syndrome (MetS) is a cluster of multiple cardiometabolic risk factors that increase the risk of type 2 diabetes and cardiovascular diseases. Identifying novel biomarkers of MetS and their genetic associations could provide insights into the mechanisms of cardiometabolic diseases. Methods Potential MetS-associated metabolites were screened and internally validated by untargeted metabolomics analyses among 693 patients with MetS and 705 controls. External validation was conducted using two well-established targeted metabolomic methods among 149 patients with MetS and 253 controls. The genetic associations of metabolites were determined by linear regression using our previous genome-wide SNP data. Causal relationships were assessed using a one-sample Mendelian Randomization (MR) approach. Findings Nine metabolites were ultimately found to be associated with MetS or its components. Five metabolites, including LysoPC(14:0), LysoPC(15:0), propionyl carnitine, phenylalanine, and docosapentaenoic acid (DPA) were selected to construct a metabolite risk score (MRS), which was found to have a dose-response relationship with MetS and metabolic abnormalities. Moreover, MRS displayed a good ability to differentiate MetS and metabolic abnormalities. Three SNPs (rs11635491, rs7067822, and rs1952458) were associated with LysoPC(15:0). Two SNPs, rs1952458 and rs11635491 were found to be marginally correlated with several MetS components. MR analyses showed that a higher LysoPC(15:0) level was causally associated with the risk of overweight/obesity, dyslipidaemia, high uric acid, high insulin and high HOMA-IR. Interpretation We identified five metabolite biomarkers of MetS and three SNPs associated with LysoPC(15:0). MR analyses revealed that abnormal LysoPC metabolism may be causally linked the metabolic risk. Funding This work was supported by grants from the National Key Research and Development Program of China (2017YFC0907004).

AimsTo investigate the frequency of USH2A mutation and the clinical and genetic differences between Usher syndrome type II (USH2) and retinitis pigmentosa (RP) in a large cohort of Chinese patients.MethodsA total of 1381 patients with inherited retinal disease (IRD) were recruited. The phenotypic and genotypic information of patients with USH2A mutations was evaluated.ResultsThe prevalence of patients with USH2A mutations was 15.75%, which was the most frequently detected gene in this cohort of patients. Hotspot of USH2A mutations was c.8559-2A >G and c.2802T >G. Patients with USH2 had an earlier and more serious decline of visual function and damage to retina structure than did patients with RP in the first 10 years (p0.05). Missense variants had less severe consequences and were found more commonly in RP, whereas more deleterious genotypes were associated with an earlier onset of disease and were found more commonly in USH2.ConclusionsThis study provides detailed clinical–genetic assessment of patients with USH2A mutations of Chinese origin, enabling precise genetic diagnoses, better management of these patients and putative therapeutic approaches.

Cardiovascular diseases (CVDs) pose a serious threat to human health, which are characterized by high disability and mortality rate globally such as myocardial infarction (MI), atherosclerosis, and heart failure. Although stem cells transplantation and growth factors therapy are promising, their low survival rate and loss at the site of injury are major obstacles to this therapy. Recently, the development of hydrogel scaffold materials provides a new way to solve this problem, which have shown the potential to treat CVD. Among these scaffold materials, environmentally responsive hydrogels have great prospects in repairing the microenvironment of cardiovascular tissues and vascular regeneration. They provide a new method for the treatment of cardiovascular tissue repair and space-time control for the release of various therapeutic drugs, including small-molecule drugs, growth factors, and stem cells. Herein, this article reviews the occurrence and current treatment of CVD, as well as the repair of cardiovascular injury by several environmental responsive hydrogels systems currently used, mainly focusing on the delivery of growth factors or the application of cell therapy to revascularization. In addition, we will also discuss the enormous potential and personal perspectives of environmentally responsive hydrogels in cardiovascular repair.

Purpose To characterize the genetic landscape of patients with suspected retinitis pigmentosa (RP) in the Chinese population. Design Cohort study. Participants A total of 1243 patients of Chinese origin with clinically suspected RP and their available family members (n = 2701) were recruited. Methods All patients and available family members were screened using multigene panel testing (including 586 eye disease-associated genes), followed by clinical variant interpretation. Main Outcome Measures Diagnostic yield, the 17 most commonly implicated genes, age at onset, de novo mutations, and clinical usefulness of genetic testing. Results Overall, 72.08% of patients received a molecular diagnosis, and the 17 top genes covered 75.63% of diagnostic cases. Diagnostic yield was higher among patients in the early-onset subgroup (≤5 years old, 79.58%) than in the childhood or adolescence-onset subgroup (6–16 years old, 73.74%) and late-onset subgroup (≥17 years old, 65.99%). Moreover, different genes associated with different onset ages and subgroups with different onset ages showed a diverse mutation spectrum. Only 11 de novo mutations (3.18%) were identified. Furthermore, 16.84% of the patients who received a molecular diagnosis had refinement of the initial clinical diagnoses, and the remaining 83.16% received definite genetic subtypes of RP. Conclusions This large cohort study provides population-based data of the genome landscape of patients with suspected RP in China. The diagnostic yield was significantly higher than that in previous studies, and the mutation spectrum is completely different with other populations. Genetic testing improves the chance to establish a precise diagnosis, identifies features not previously determined, and allows a more accurate refinement of risk to family members. Our results not only expand the existing genotypic spectrum but also serve as an efficient reference for the design of panel-based genetic diagnostic testing and genetic counseling for patients with suspected RP in China.

BackgroundBestrophin-1 (BEST1) gene is associated with a wide range of ocular phenotypes, collectively termed as bestrophinopathy. The aim of the current study was to identify the mutation spectrum ofBEST1in a large cohort of Chinese patients with bestrophinopathy.MethodsPatients clinically suspected of bestrophinopathy were screened using multigene panel testing. AllBEST1variants were confirmed by Sanger sequencing, and validated in the families.FindingsA total of 92 patients (Best vitelliform macular dystrophy (BVMD)=77; autosomal recessive bestrophinopathy (ARB)=15) from 58 unrelated families of Chinese origin and their available family members (n=65) were recruited. Overall, 39 distinct disease-causingBEST1variants were identified, including 13 novel variants, and two reported variants but novel for ARB. Of them, 14 were associated with ARB, 23 with BVMD and two (c.604C>T and c.898G>A) with both BVMD and ARB. Most mutations associated with BVMD were missense (97.78%), while ARB was associated with more complex mutations, including missense (88.46%), splicing effect (3.85%), and frameshifts (15.38%).BEST1hotspots were c.898G>A and c.584C>T among BVMD and ARB patients, respectively. Hot regions were located in exons 8, 2 and 6 in BVMD patients, and in exons 5 and 7 in ARB patients. The overall penetrance ofBEST1in our cohort was 71.30%, no de novo mutations were identified.ConclusionThis is the largest study to date that provides major population-based data of theBEST1mutation spectrum in China. Our results can serve as a well-founded reference for genetic counselling for patients with bestrophinopathy of Chinese origin.

In this paper, a new method for manufacturing flexible and repeatable sensors made of silicon solar cells is reported. The method involves depositing the noble metal film directly onto the Si template and stripping out the substrate with a pyramid morphology by using an adhesive polymer. In order to evaluate the enhancement ability of the substrate, Rhodamine 6G (R6G) were used as surface-enhanced Raman scattering (SERS) probe molecules, and the results showed a high sensitivity and stability. The limit of detection was down to 10−12 M for R6G. The finite-difference time domain (FDTD) was used to reflect the distribution of the electromagnetic field, and the electric field was greatly enhanced on the surface of the inverted pyramidal substrate, especially in pits. The mechanism of Raman enhancement of two types of pyramidal SERS substrate, before and after stripping of the noble metal film, is discussed. By detecting low concentrations of plasmid DNA, the identification of seven characteristic peaks was successfully realized using a noble metallic pyramidal substrate.

An active bidirectional mixer performing the up/down conversion has been proposed at K band with a 130-nm CMOS in this paper. With 2-dBm local oscillator drives, the mixer achieves the conversion gain, noise figure, and output P ldB of −2.5~-1.2 dB, 14.2~16 dB, and −9.2~-8 dBm from 23 to 25 GHz in up-conversion mode, respectively. In down-conversion mode, the mixer exhibits the conversion gain, noise figure, and input PldB of 1.3~3 dB, 15.2~19.3 dB, and −0.6~0 dBm from 23 to 25 GHz, respectively. The chip area is 0.75 × 0.8 mm2, which consumes 10.5 mW from a supply of 1.5 V.

Background To date, certain efforts have been made to investigate the clinical and genetic characteristics of patients with EYS mutations. However, data for Chinese patients are limited. Objectives To perform a detailed phenotyping and genetic characterization of 55 Chinese patients with EYS-RD, and to identify risk factors for these clinical data. Methods A total of 55 patients with EYS-RD were recruited. Best-corrected visual acuity (BCVA), patient age, age at symptom onset, disease duration, and genetic information were collected. Results Thirty-six novel variants, three hot mutations of EYS (30.3%, c.6416G>A, c.6557G>A, c.7492G>C) and one hot region (49.06%, Laminin G domains) were identified. In all, 36.84% of the mutations occurred at base G site, and majority of mutations (56.56%) were missense. Late-truncating mutations are significantly more prevalent (41.30%). The mean age of onset was 15.65 ± 14.67 years old; it had no significant correlation with genotype. The average BCVA was 0.73 ± 0.93 LogMAR, and 61.8% of eyes had a BCVA better than 0.52 logMAR. BCVA was positively correlated with disease duration time. The mean MD was 23.18 ± 7.34 dB, MD showed a significant correlation with genotype and age. Cataract was present in 56.45% of patients, and 42.59% of patients showed an absence of pigmentation in the retina. Cataract and hyperpigmentation both showed a significant correlation with age. Conclusions EYS-RD is associated with a moderate phenotype with onset around adolescence, but great variability. Our study largely enhances the current knowledge of phenotypic and genotypic characteristics of EYS-RD, which could pave the way for better management of these patients.

Background The retinoid isomerohydrolase RPE65 has received considerable attention worldwide since a successful clinical gene therapy was approved in 2017 as the first treatment for vision loss associated with RPE65-mediated inherited retinal disease. Identifying patients with RPE65 mutations is a prerequisite to assessing the patients’ eligibility to receive RPE65-targeted gene therapies, and it is necessary to identify individuals who are most likely to benefit from gene therapies. This study aimed to investigate the RPE65 mutations frequency in the Chinese population and to determine the genetic and clinical characteristics of these patients. Results Only 20 patients with RPE65 mutations were identified, and RPE65 mutations were determined to be the 14th most common among all patients with genetic diagnoses. Ten novel variants and two hotspots associated with FAP were identified. A literature review revealed that a total of 57 patients of Chinese origin were identified with pathogenic mutations in the RPE65 gene. The mean best Snellen corrected visual acuity was worse (mean 1.3 ± 1.3 LogMAR) in patients older than 20 years old than in those younger than 15 years old (0.68 ± 0.92 LogMAR). Bone spicule-like pigment deposits (BSLPs) were observed in six patients; they were older than those without BSLP and those with white-yellow dots. Genotype–phenotype analysis revealed that truncating variants seem to lead to a more severe clinical presentation, while best corrected visual acuity testing and fundus changes did not correlate with specific RPE65 variants or mutation types. Conclusions This study provides a detailed clinical-genetic assessment of patients with RPE65 mutations of Chinese origin. These results may help to elucidate RPE65 mutations in the Chinese population and may facilitate genetic counseling and the implementation of gene therapy in China.

Purpose: Autosomal dominant polycystic kidney disease (ADPKD) is characterized by progressive development of kidney cysts and enlargement and dysfunction of the kidneys. The Consortium of Radiologic Imaging Studies of the Polycystic Kidney Disease (CRISP) cohort revealed that 89.1% had either a PKD1 or PKD2 mutation. Of the CRISP patients with a genetic cause detected, mutations in PKD1 accounted for 85%, while mutations in the PKD2 accounted for the remaining 15%. Here, we report exome sequencing of 16 Saudi patients diagnosed with ADPKD and 16 ethnically matched controls. Methods: Exome sequencing was performed using combinatorial probe-anchor synthesis and improved DNA Nanoballs technology on BGISEQ-500 sequencers (BGI, China) using the BGI Exome V4 (59 Mb) Kit. Identified variants were validated with Sanger sequencing. Results: With the exception of GC-rich exon 1, we obtained excellent coverage of PKD1 (mean read depth = 88) including both duplicated and non-duplicated regions. Of nine patients with typical ADPKD presentations (bilateral symmetrical kidney involvement, positive family history, concordant imaging, and kidney function), four had protein truncating PKD1 mutations, one had a PKD1 missense mutation, and one had a PKD2 mutation. These variants have not been previously observed in the Saudi population. In seven clinically diagnosed ADPKD cases but with atypical features, no PKD1 or PKD2 mutations were identified, but rare predicted pathogenic heterozygous variants were found in cystogenic candidate genes including PKHD1, PKD1L3, EGF, CFTR, and TSC2. Conclusions: Mutations in PKD1 and PKD2 are the most common cause of ADPKD in Saudi patients with typical ADPKD. Abbreviations: ADPKD: Autosomal dominant polycystic kidney disease; CFTR: Cystic fibrosis transmembrane conductance regulator; EGF: Epidermal growth factor; MCIC: Mayo Clinic Imaging Classification; PKD: Polycystic kidney disease; TSC2: Tuberous sclerosis complex 2

Purpose To provides the clinical and genetic characteristics of a series of Chinese patients with X-linked juvenile retinoschisis (XLRS) through multimodal imaging and next-generation sequencing.Methods Thirty patients (60 eyes) from 29 unrelated families of Chinese origin with XLRS were screened using multigene panel testing, and underwent a complete clinical evaluation. All variants identified in this study and reported in the Human Gene Mutation Database were analysed.Results Twenty-five distinct variants in the retinoschisin gene were identified, of which eight were novel, and one was de novo. Missense mutations were the most prevalent type, and mutation hot spot was localized in the discoidin domain. The mean Snellen best-corrected visual acuity was 0.28 +/- 0.17. Of all eyes presenting with schisis, 92.86% had lamellar schisis and 62.5% had peripheral schisis. Schisis changes mostly involved inner and outer nuclear layers. X-linked juvenile retinoschisis (XLRS) patients had a high incidence of complications, and peripheral schisis was a risk factor for it. No obvious genotype-phenotype association was observed.Conclusion This study provides comprehensive analyses of the genetic and clinical characteristics of XLRS in a cohort of Chinese patients. The fourth de novo mutation in RS1 was identified. And we show that XLRS has a wide spectrum of clinical characteristics; hence, molecular diagnosis is crucial for its diagnosis, differential diagnosis and genetic counselling. Peripheral schisis is a risk factor for the high incidence of complications, and no clear genotype-phenotype correlations were found.

Burns, mechanical injuries, skin defects, poor wound healing and scars caused by chronic diseases are serious clinical issues that affect millions of people around the world. Hyaluronic acid (HA) is one of the main components of extracellular matrix, which is widely distributed in human body. Because of its unique physical and chemical properties and diversity of physiological functions, hyaluronic acid is widely used in tissue engineering and regenerative medicine. This paper reviews the application of HA and HA based scaffolds in the regeneration and repair of skin tissue, as well as the application of HA in the fields of skin filler, wound healing, beauty, etc.

Background To report the clinical and genetic findings from seven Chinese patients with choroideremia. Methods Five hundred seventy-eight patients with a clinically suspected diagnosis of retinitis pigmentosa (RP) underwent comprehensive ophthalmic examinations. Next-generation sequencing (NGS) was performed on samples from all patients. Detailed clinical characteristics of the patients with choroideremia identified in this study were assessed using multimodal imaging. Results Seven patients with choroideremia were identified, and six novel variants in CHM (c.1960 T > C p.Ter654Gln, c.1257del p.Ile420*fs1, c.1103_1121delATGGCAACACTCCATTTTT p.Tyr368Cysfs35, c.1414-2A > T, and c.1213C > T p.Gln405Ter, c.117-1G > A) were revealed. All variants were deleterious mutations: two were frameshifts, two were nonsense mutations, two were splicing mutations, and one was a readthrough mutation. The clinical phenotypes of these patients were markedly heterogeneous, and they shared many common clinical features with RP, including night blindness, constriction of the visual field and gradually reduced visual acuity. However, patients with choroideremia showed pigment hypertrophy and clumping, and chorioretinal atrophy, and a majority of patients with choroideremia presented with retinal tubulations in the outer layer of the retina. Conclusions We provide a detailed description of the genotypes and phenotypes of seven patients with choroideremia who were accurately diagnosed using NGS. These findings provide a better understanding of the genetics and phenotypes of choroideremia.

Purpose To investigate the clinical and genetic characteristics of occult macular dystrophy (OMD) based on a Chinese patient cohort. Methods Fifteen Chinese OMD patients from nine unrelated families underwent genetic testing, and all of them harbored a pathogenic RP1L1 variant. Comprehensive ophthalmic examinations were performed in nine probands, including spectral-domain optical coherence tomography (SD-OCT), near-infrared reflectance (NIR), fundus autofluorescence (AF), and multifocal electroretinography. Results The RP1L1 variants p.R45W and p.S1199C were identified in 13 patients and two patients, respectively, and one was a de novo mutation. Among the nine probands, the median ages at onset and examination were 25.0 years (range, 6-51 years) and 27.0 years (range, 14-55 years), respectively. The median decimal visual acuity was 0.20 (range, 0.04-0.5). Foveal photoreceptor thickness and visual acuity showed a significant correlation (r = 0.591; P = 0.01). All eyes presented with an absent interdigitation zone and blurred ellipsoid zone of photoreceptors when examined by SD-OCT. In addition, central round lesions with low NIR reflectance were observed in 66.7% (12/18) of eyes by NIR reflectance imaging, corresponding to the regions with abnormal photoreceptor microstructures observed by SD-OCT. Of the 18 eyes, only four eyes showed ring-like faint hyperfluorescence around the macula by AF. Conclusions To the best of our knowledge, this is the largest study in a cohort of Chinese OMD patients with RP1L1 mutations. Our findings revealed that the two recurrent RP1L1 variants are related to OMD in the Chinese population. Furthermore, multimodal imaging combined with genetic testing is valuable for diagnosing and monitoring OMD progression.

Background Panel‐based targeted exome sequencing was used to analyze the genetic and clinical findings of targeted genes in a cohort of northeast Chinese with retinitis pigmentosa. Methods A total of 87 subjects, comprising 23 probands and their family members (total patients: 32) with confirmed retinitis pigmentosa were recruited in the study. Panel‐based targeted exome sequencing was used to sequence the patients and family members, all subjects with retinitis pigmentosa underwent a complete ophthalmologic examination. Results Of the 23 probands, the clinical manifestations include night blindness, narrowing of vision, secondary cataracts, choroidal atrophy, color blindness, and high myopia, the average age of onset of night blindness is 12.9 ± 14 (range, 0–65; median, 8). Posterior subcapsular opacities is the most common forms of secondary cataracts (nine cases, 39.1%), and peripheral choroidal atrophy is the most common form of secondary choroidal atrophy (12 cases, 52.2%). Of these probands with complication peripheral choroidal atrophy, there were eight probands (66.7%, 8/12) caused by the pathogenic variation in USH2A gene. A total of 17 genes and 45 variants were detected in 23 probands. Among these genes, the commonest genes were USH2A (40%; 18/45), RP1 (15.6%; 7/45), and EYS (8.9%; 4/45), and the top three genes account for 56.5% (13/23) of diagnostic probands. Among these variants, comprising 22 (48.9%) pathogenic variants, 14 (31%) likely pathogenic variants, and nine (20%) uncertain clinical significance variants, and 22 variants was discovered first time. Most of the mutations associated with RP were missense (53.3%, 24/45), and the remaining mutation types include frameshift (35.6%, 16/45), nonsense (6.7%, 3/45), and spliceSite (4.4%, 2/45). Among the probands with mutations detected, compound heterozygous forms was detected in 13 (56.5%, 13/23) probands, and digenic inheritance (DI) forms was detected in five (21.7%, 5/23) probands. Conclusion Panel‐based targeted exome sequencing revealed 23 novel mutations, recognized different combinations forms of variants, and extended the mutational spectrum of retinitis pigmentosa and depicted common variants in northeast China., We applied panel‐based targeted exome sequencing to explore the pathogenic variation spectrum and genetic characteristics of retinitis pigmentosa populations in northeast China, and have a deeper understanding of the relationship between clinical manifestations and genotypes.

Background Panel‐based targeted exome sequencing was applied to identify the pathogenic variants and genetic characteristics of retinitis pigmentosa (RP) in two Chinese families, and to gain a deeper understanding of the relationship between clinical manifestations and genotypes. Methods A total of 17 subjects, comprising two probands (total patients: four subjects) and their family member, were recruited in this study. All subjects underwent comprehensive ophthalmic examinations and clinical evaluations, and the complete history and medical records were collected according to the standard procedures. All participants were screened using the multigene panel test (Target_Eye_792_V2 chip), and Sanger sequencing was used to confirm the candidate variants. Results Among these two families, a total of three novel mutations in the EYS gene were identified in patients, including a homozygous frameshift mutation c.9252_9253insT detected in two patients in one family, and the compound heterozygous splicesite mutation c.5644+2T>C and frameshift mutation c.1920_1923delTGAG detected in two patients in the another family. All patients in both families had early onset of night blindness and poor visual acuity, and with typical posterior capsule opacification. The mutation co‐segregated within all recruited individuals. In addition, one patient with compound heterozygous mutations was found to have typical blue‐blindness symptoms and detected a previously reported disease‐causing mutation c.235G>A in OPN1SW gene, which caused blue blindness manifestations and was first discovered in patient combined with RP causative genes. Conclusions Panel‐based targeted exome sequencing was used to identify three novel variants of RP causative gene, and we also detected a known pathogenic variants of blue‐blindness causative genes in two patients. Our finding will provide a powerful basis for genetic counseling and enhance our current understanding of the genetics factors for RP families., We applied panel‐based targeted exon sequencing to explore the pathogenic variation spectrum and genetic characteristics of retinitis pigmentosa populations in two Chinese families, and have a deeper understanding of the relationship between clinical manifestations and genotypes.

Two-dimensional (2D) ordered micro/nanostructured arrays have attracted intense interest for potential applications in a wide variety of fields, such as surface-enhanced Raman scattering, chemical and biological sensing, catalysis, energy storage, and conversion. In this paper, MoS2/TiO2 nanohole arrays are prepared by combing colloidal lithography and dip-coating method. The decorating of MoS2 nanosheets can significantly improve the photoelectrochemical and photocatalytic activity of TiO2 nanohole arrays in the visible light region. The photocurrent density of the optimized MoS2/TiO2 sample is 17.8 times higher than that of the pristine TiO2 film, while the enhancement factor of the corresponding kinetic constant in photocatalytic degradation is about 5.2. Our first-principles calculation results are in good agreement with the experimental observations. On the basis of the experimental and theoretical results, such enhanced performances can be assigned to two reasons: one is the improved visible light h...

Wounds have become one of the causes of death worldwide. The metabolic disorder of the wound microenvironment can lead to a series of serious symptoms, especially chronic wounds that bring great pain to patients, and there is currently no effective and widely used wound dressing. Therefore, it is important to develop new multifunctional wound dressings. Hydrogel is an ideal dressing candidate because of its 3D structure, good permeability, excellent biocompatibility, and ability to provide a moist environment for wound repair, which overcomes the shortcomings of traditional dressings. This article first briefly introduces the skin wound healing process, then the preparation methods of hydrogel dressings and the characteristics of hydrogel wound dressings made of natural biomaterials and synthetic materials are introduced. Finally, the development prospects and challenges of hydrogel wound dressings are discussed.

Background Familial exudative vitreoretinopathy (FEVR) is a severe clinically and genetically heterogeneous retinal disorder characterized with failure of vascular development of the peripheral retina. The symptoms of FEVR vary widely among patients in the same family, and even between the two eyes of a given patient. The purpose of this study was to investigate the molecular mechanisms by which the start codon mutation of the TSPAN12 causes difference in clinical manifestations between individuals in the same family. Methods Next‐generation sequencing (NGS)‐based target capture sequencing was performed in proband with a diagnosis of FEVR and their normal visual acuity family members. Cosegregation analysis of the candidate causative variant was performed in additional family members by using Sanger sequencing. Complete fundus examination, fundus fluorescein angiography (FFA), and family history collection were performed in all family members. Potential candidate causative variants were verified with reference to guidelines and standards from the American College of Medical Genetics and Genomics. Results We identified a novel heterozygous missense mutation (c.1A>G, p.M1V) localized in the start codon of the TSPAN12 and was detected as a potentially disease‐causing variant for the proband. Retrospective analysis of clinical data, fundus examination, and FFA showed that the mutant carrier presented peripheral retinal vascular anomalies in early stages, and visual acuity did not show significant effects. However, the proband who carried this mutation and his cousin showed typical high‐stage FEVR fundus changes coupled with a sharp decline in vision. Conclusions We report a novel start codon mutation (c.1A>G, p.M1V) in the TSPAN12 that causes clinically heterogeneous manifestations. Our results expand the mutation spectrums of TSPAN12, and will be valuable for disease diagnosis, prognosis, genetic counseling, and enriching our understanding of the role of the tetraspanin‐12 protein in the pathogenesis of FEVR.

PURPOSE To explore an early, rapid and precise diagnosis of Stickler syndrome type I (STL1) and to enrich the spectrum of COL2A1 mutations in the Chinese population, which is poorly studied at present. METHODS In the current study, we analysed 115 patients with high myopia by next-generation sequencing and identified five STL1 patients from four unrelated Chinese families. The clinical features of all patients were reviewed in detail. RESULTS Four variants of COL2A1 were identified, including two novel variants (c.1435delG and c.184delG) and two previously reported variants (c.1221+1G>A and c.1030C>T). Three variants caused premature termination codons which were common in STL1. In addition, we proposed a new diagnostic tactic to improve early diagnostics of STL1 in patients. CONCLUSION In this study, our findings expanded the spectrum of COL2A1 mutations with two novel variants and provided a new diagnostic tactic for reference, which was of great significance. Precise diagnosis on the basis of clinical manifestations and genetic testing will become the gold standard to diagnose inherited ocular disorders or syndromes in the future.

Background Heimler syndrome (HS) is a rare hereditary systemic disorder, partial clinically overlapping with Usher syndrome. So far, our knowledge of HS is very limited, many cases are misdiagnosed or may not even be diagnosed at all. This study aimed to analyze the clinical and genetic characteristics of HS, and to evaluate potential phenotype–genotype correlations. Results Two HS cases caused by PEX1 mutations were identified, and a novel likely pathogenic mutation, PEX1 c.895_896insTATA, was found. The main ophthalmic finding of the two patients was consistent with retinitis pigmentosa accompanied by cystoid macular edema, but short axial length and hyperopia were also observed as two previously unreported ocular phenotypes. Analysis of the literature showed that of the 29 HS patients previously reported, 12 had PEX6 mutations, 10 had PEX1 mutations, two had PEX26 mutations, and the remaining patients were not genetically tested. Three novel genotype–phenotype correlations were revealed from analysis of these patients. First, most genotypes of every HS patient include at least one missense variant; second, at least one mutation in PEX1 or PEX6 gene affects the AAA-ATPase region in every HS patient with retinal dystrophy, suggesting AAA-ATPase region is a hypermutable region in patients with a retinal dystrophy; third, there are no significant differences between PEX1-, PEX6-, and PEX26-associated phenotypes. Conclusion Next-generation sequencing is important for the diagnosis of HS. This study expands the clinical and genetic spectrum of HS, and provides additional insights into genotype–phenotype correlations, which is vital for accurate clinical practice, genetic counseling, and pathogenesis studies.

Objective Congenital hypogonadotropic hypogonadism (CHH) and constitutional delay of growth and puberty (CDGP) represent rare and common forms of GnRH deficiency, respectively. Both CDGP and CHH present with delayed puberty, and the distinction between these two entities during early adolescence is challenging. More than 30 genes have been implicated in CHH, while the genetic basis of CDGP is poorly understood. Design We characterized and compared the genetic architectures of CHH and CDGP, to test the hypothesis of a shared genetic basis between these disorders. Methods Exome sequencing data were used to identify rare variants in known genes in CHH (n = 116), CDGP (n = 72) and control cohorts (n = 36 874 ExAC and n = 405 CoLaus). Results Mutations in at least one CHH gene were found in 51% of CHH probands, which is significantly higher than in CDGP (7%, P = 7.6 × 10−11) or controls (18%, P = 5.5 × 10−12). Similarly, oligogenicity (defined as mutations in more than one gene) was common in CHH patients (15%) relative to CDGP (1.4%, P = 0.002) and controls (2%, P = 6.4 × 10−7). Conclusions Our data suggest that CDGP and CHH have distinct genetic profiles, and this finding may facilitate the differential diagnosis in patients presenting with delayed puberty.

This paper presents a 320-GHz 1 $\times$ 4 fully integrated phased array transmitter using 0.13- $\mu$ m SiGe BiCMOS technology. The 1 $\times$ 4 array transmitter is aiming for terahertz wireless communication and is based on RF beam forming architecture. By integrating a 20-GHz phase-locked-loop (PLL) frequency synthesizer, an 80-GHz quadrupler, a 1:4 Wilkinson power divider network, four-way 80-GHz tunable attenuators, amplifiers, analog phase shifters, 320-GHz frequency quadruplers/modulators, and on-chip antenna arrays, the transmitter chip achieves a maximal EIRP of 10.6 dBm at 320 GHz with the 3-dB bandwidth of 20 GHz, and ${\pm} {\hbox{12}}^{\circ}$ beam scanning range is obtained. The dc consumption of the whole chip is ${\sim} $ 1000 mW and the total chip size is 8 $\times$ 4.3 mm $^{2}$ .

The aim of this study is to investigate a food effect on the single-dose pharmacokinetics and tolerability of subutinib maleate capsules in healthy Chinese volunteers. The author evaluated the effect of being under a fasting or fed state at the time of drug intake on the single-dose of subutinib maleate capsules in a randomized, balanced, single-dose, 2-treatment (fasting and fed), 2-period design with a 3-week washout period. The end points were the maximum plasma drug concentration (Cmax) and areas under the plasma-concentration curve (AUC) for 336 h exposure (AUC0-336) and total exposure (AUC0-∞). All volunteers completed the whole study without side effects being observed. For subutinib, Cmax were 6.13 and 5.04 ng·mL(-1), and AUC0-336 were 278.4 and 304.5 h·ng·mL(-1) in the fasting and the fed state, respectively. For active metabolite, Cmax were 0.90 and 0.61 ng·mL(-1), and AUC0-336 were 65.5 and 56.4 h·ng·mL(-1) in the fasting and the fed state, respectively. The authors showed that food intake was associated with a slight increase in AUC values but decrease in Cmax of subutinib, and it was associated with a decrease both in AUC and Cmax of active metabolite.

Purpose Leber hereditary optic neuropathy (LHON) and autosomal dominant optic atrophy (ADOA) are the two commonest forms of hereditary optic neuropathy. The aim of this study was to comprehensively investigate the incidence and spectrum of mutations in patients with suspected hereditary optic neuropathy by combining mitochondrial DNA (mtDNA) genome-wide and targeted exon sequencing. Methods A cohort of 1101 subjects were recruited to participate in the study, comprising 177 families (177 probands and their family members, a total of 537 subjects, including 254 patients) and 164 sporadic cases with suspected hereditary optic neuropathy, and 400 unrelated control subjects for genetic analysis: all subjects (including control subjects) underwent a comprehensive ophthalmologic examination and were subjected to sequencing analysis of mtDNA genome-wide and targeted exon. Overall, targeted exon sequencing was used to screen 792 genes associated with common hereditary eye diseases, and the mtDNA genome-wide were screened by next-generation sequencing. Results We found variants detected in 168 (40.2%, 168/418) of the 418 patients screened. Among these, 132 cases (78.6%, 132/168) were detected with known LHON disease-causing mtDNA variants; 40 cases (23.8%, 40/168) were detected with nuclear DNA (ntDNA) variants, which included 36 cases (21.4%, 36/168) with detected OPA1 mutations, 4 patients (2.4%, 4/168) with detected OPA3 mutations, and 2 patients (1.2%, 2/168) with detected TMEM126A homozygous mutation. Coexistence variation (mtDNA/mtDNA [n = 16], ntDNA/ntDNA [n = 4], mtDNA/ntDNA [n = 7]) was found in 27 patients (16.4%, 27/165), including mtDNA/ntDNA coexistence variation that was detected in seven patients. Among these ntDNA mutations, 38 distinct disease-causing variants, including autosomal recessive heterozygous mutations, were detected, which included 22 novel variants and two de novo variants. Total haplogroup distribution showed that 34.5% (29/84) and 28.6% (24/84) of the affected subjects with m.11778G>A belonged to haplogroup D and M, with a high frequency of subhaplogroups D4, D5, and M7. Conclusions The LHON-mtDNA mutations are the commonest genetic defects in this Chinese cohort, followed by the OPA1 mutations. To our knowledge, this is the first comprehensive study of LHON, ADOA, and autosomal recessive optic atrophy combined with mtDNA genome-wide and targeted exon sequencing, as well as haplogroup analysis, in a large cohort of Chinese patients with suspected hereditary optic neuropathy. Our findings provide a powerful basis for genetic counseling in patients with suspected hereditary optic neuropathy. Translational Relevance We applied mtDNA genome-wide sequencing combined with panel-based targeted exon sequencing to explore the pathogenic variation spectrum and genetic characteristics of patients with suspected hereditary optic neuropathy, providing a comprehensive research strategy for clinical assistant diagnosis, treatment, and genetic counseling.

A 7.7---12 GHz fully monolithic transformer-coupled cascode power amplifier (PA) was designed for X-band phase array radar application. This PA was fabricated in a 0.25-$$\upmu $$μm SiGe BiCMOS technology with chip size of $$2\times 2$$2×2 mm$$^{2}$$2. The best choice of the cascode topology for PA design is discussed and the possible stability issue of this configuration is analyzed. The distributed capacitor structure which is connected to the base of cascode transistor is proposed to reduce the base series inductance and hence, improve circuit stability and boost gain. Moreover, circuit/layout co-design for above structure is completed through full 3D simulation. The PA features a three-stage cascode architecture that includes both medium-speed (medium breakdown voltage) and high breakdown voltage (low-speed) SiGe transistors, and a 1:2 input splitter and a 4:1 output combiner which are designed for a low insertion loss and compact dimensions on-chip. The proposed PA achieves a measured small signal gain of 26.6---29.6 dB from 7.7 to 12 GHz with a 5.0 V DC supply. A 28 dBm maximum output power with an 18.5 % power-added efficiency at 10 GHz have also been achieved.

Multidrug-resistant Acinetobacter baumannii becomes an increasing challenge due to the overuse of antibiotics. Combination therapies are considered as effective options to overcome this matter. The present study was to investigate the synergistic activity of meropenem combined with other antibiotics in vitro and in vivo. Checkerboard assay and time-kill assay were performed to study the combination effects in vitro. For the animal model, a murine sepsis model injected with inoculums intraperitoneally was used. Susceptibility test showed that all the twelve strains in this study were resistant to most of the antibiotics except rifampicin. In combination, meropenem plus rifampicin exhibited synergistic activity against six of twelve strains. In the sepsis model, meropenem monotherapy had no therapeutic effect in this model while it can enhance the activity of rifampicin in both survival rate and bacterial clearance from blood. Moreover, combination therapy significantly reduced plasma IL-6 levels compared with rifampicin monotherapy. Pharmacokinetic analysis of rifampicin was also performed in this study. These data above showed that there was synergistic activity between meropenem and rifampicin against multidrug-resistant Acinetobacter baumannii both in vitro and for experimental model of sepsis. It suggested that combining meropenem with rifampicin may be appropriate in treating multidrug-resistant Acinetobacter baumannii infections.

A 5 GHz transformer-feedback power oscillator with novel frequency modulation (FM) up to 10 MHz is presented in this paper. The novel FM is achieved by a CMOS transistor between transformer and ground, which is designed for varying the equivalent inductance and mutual inductance of the transformer and shows no DC connection with the oscillation circuit. The major frequency tuning is realized by the variable capacitor which is controlled by a phase lock loop. The RF VCO with 210 MHz tuning range operates in class-E mode to achieve a cost-effective transmitter, which demonstrates a high DC-to-RF conversion efficiency of 39 %. A RF power of 15.1 dBm and phase noise better than $$-$$ - 109 dBc/Hz @ 100 kHz from the central frequency of 5.5 GHz is obtained with the biasing conditions V $$_\mathrm{ds}$$ ds = 1.8 V and V $$_\mathrm{gs}$$ gs = 0.65 V. The VCO also demonstrates an ultra-low voltage operation capability: with V $$_\mathrm{ds}$$ ds = V $$_\mathrm{gs}$$ gs = 0.6 V and DC power consumption of 9 mW, the output power is 4.5 dBm and the phase noise better than $$-$$ - 93 dBc/Hz @ 100 kHz. The die size of the transformer-feedback power oscillator is only $$0.4\times 0.6$$ 0.4 × 0.6 mm $$^{2}$$ 2 .

In this paper, a 42GHz frequency synthesizer fabricated with 0.13"m SiGe BiCMOS technology is presented, which consists of an integer-N fourth-order type-II phase locked loop (PLL) with a LC tank VCO and a frequency doubler. The core PLL has three-stage current mode logic (CML) and flve stage true single phase clock (TSPC) logic in the frequency divider. Meanwhile, a novel balanced common-base structure is used in the frequency doubler design to widen the bandwidth and improve the fundamental rejection. The doubler shows a 41% fractional 3dB bandwidths with a fundamental rejection better than 25.7dB. The synthesizer has a maximum output power of 0dBm with a DC power consumption of 60mW. The worst phase noise at 100kHz, 1MHz and 10MHz ofiset frequencies from the carrier is i71dBc/Hz, i83dBc/Hz and i102:4dBc/Hz, respectively.

The aim of this study is to investigate a food effect on the single-dose pharmacokinetics and tolerability of clinofibrate tablets in 12 Chinese healthy volunteers. The authors evaluated the effect of being under a fasting or fed state at the time of drug intake on the single-dose of clinofibrate 400 mg tablets in a randomized, balanced, single-dose, two-treatment (fed and fasting), two-period, two-sequence study design with a 7-day washout period. The end points were the maximum plasma drug concentration (Cmax) and areas under the plasma-concentration curve (AUC) for 72 hours exposure (AUC0-72) and total exposure (AUC0-∞). All participants completed the whole study without side effects being observed. The Cmax mean of clinofibrate glucuronides and parent clinofibrate were 21.91, 17.85 μ/ml for the fasting state and 13.14, 11.25 μ/ml for the fed state, respectively. The AUC0-72 and AUC0-∞ of clinofibrate glucuronides and parent clinofibrate were 381.60, 307.07 μ/ ml and 404.55, 342.24 μ/ml for the fasting state and 379.02, 321.14 μ/ml and 432.24, 351.80 μ/ml for the fed state. The authors showed that food intake was associated with a significant decrease in Cmax, but no significant change in AUC values.

Leigh syndrome is a subacute necrotising encephalomyopathy proven by post-mortem analysis of brain tissue showing spongiform lesions with vacuolation of the neuropil followed by demyelination, gliosis and capillary proliferation caused by mutations in one of over 75 different genes, including nuclear- and mitochondrial-encoded genes, most of which are associated with mitochondrial respiratory chain function. In this study, we report a patient with suspected Leigh syndrome presenting with seizures, ptosis, scoliosis, dystonia, symmetrical putaminal abnormalities and a lactate peak on brain MRS, but showing normal MRC enzymology in muscle and liver, thereby complicating the diagnosis. Whole exome sequencing uncovered compound heterozygous mutations in NADH dehydrogenase (ubiquinone) flavoprotein 1 gene (NDUFV1), c.1162+4A>C (NM_007103.3), resulting in skipping of exon 8, and c.640G>A, causing the amino acid substitution p.Glu214Lys, both of which have previously been reported in a patient with complex I deficiency. Patient fibroblasts showed a significant reduction in NDUFV1 protein expression, decreased complex CI and complex IV assembly and consequential reductions in the enzymatic activities of both complexes by 38% and 67%, respectively. The pathogenic effect of these variations was further confirmed by immunoblot analysis of subunits for MRC enzyme complexes in patient muscle, liver and fibroblast where we observed 90%, 60% and 95% reduction in complex CI, respectively. Together these studies highlight the importance of a comprehensive, multipronged approach to the laboratory evaluation of patients with suspected Leigh syndrome.

This paper presents a fully integrated 166-GHz frequency synthesizer (FS) in 0.13-μm SiGe BiCMOS technology. The proposed FS consists of a 20-GHz phase-locked loop (PLL) and a frequency multiplier including a doubler (×2) and a quadrupler (×4). The FS generates the D-band output signals from 164.08 to 166.19 GHz. At 166.19 GHz, the measured phase noises at 100-kHz and 1-MHz offset frequencies are −54.07 dBc/Hz and −72.29 dBc/Hz, respectively. The total dc power dissipation of the FS is around 110 mW and the chip area is 2.16 × 0.57 mm2 including all testing pads. To the best of authors' knowledge, the proposed FS achieves the lowest power dissipation above 100 GHz to date and has great potential to be used for high-integration D-band applications.

This paper presents a 340 GHz 4-way fully integrated phased array transmitter using 0.13um SiGe BiCMOS technology. The chip integrates a 21.25 GHz synthesizer, a quadrupler together with a 1:4 Wilkinson network, power amplifiers, analog phase shifters, 20Gbps OOK modulators, and 2×2 on-chip antenna arrays on each channel. Simulated patterns show scanning to ±12° and >12dBi gain in E-plane. The chip size of the fully integrated phased array transmitter is 8×4.3 mm2.

A 27-41 GHz monolithic balanced frequency doubler fabricated using the 0.13 μm SiGe BiCMOS technology is presented in this letter. The balanced doubler consists of a balun, a driver amplifier (DA), a common-base (CB) doubling core and a medium power amplifier. The CB topology is used to increase the bandwidth and for the ease of matching with the balun. The proposed frequency doubler attained a measured gain of 16.8-19.8 dB, an output power of 1.3-4.3 dBm, and a fundamental rejection of better than 25.7 dB (from 27 to 41 GHz) at an input power of 15 5 dBm. An maximum output power of 8 dBm with dc power consumption of 35 mW and corresponding power added efficiency (PAE) of 16.9% have also been achieved. The chip size is 0.75 mm × 0.45 mm.

A 8-12 GHz fully monolithic transformer-coupled cascode power amplifier (PA) with the chip size of 2 × 2 mm2 fabricated using the 0.25-μm SiGe:BiCMOS technology is presented in this paper. Through circuit/layout co-design, the distributed capacitor structure which is connected to the base of cascode transistor is proposed to reduce the base connection inductance for solving circuit instability and improving the gain in the design. Moreover, the PA features a three-stage cascode architecture that includes both high-speed (low breakdown voltage) and high breakdown voltage (low-speed) SiGe transistors. The proposed PA attained a measured small signal gain of 27.6-29.6 dB from 7.7 to 12 GHz with a 5.0 V dc supply. A 28 dBm maximum output power with an 18.5% power-added efficiency at 10 GHz have also been achieved.

A 20-GHz voltage-controlled oscillator (VCO) for phase-locked loop (PLL) synthesizer is presented in this paper. The VCO and PLL synthesizer have been implemented using only CMOS devices of a 0.13-μπι SiGe BiCMOS technology with the chip area of 0.22 mm2 and 0.48 mm2, respectively. The measured tuning range of the VCO is 2.21 GHz from 19.9 to 22.11 GHz; the PLL synthesizer can generate output frequencies from 20.51 to 21.27 GHz successfully and the measured phase noise at 100-kHz and 1-MHz offset frequencies is −68.66 dBc/Hz and −97.17 dBc/Hz, respectively. At a 1.5-V supply, the power dissipation of the VCO and PLL synthesizer is 27 mW and 40 mW, respectively.

A frequency doubler from 27 to 41 GHz fabricated in 0.13-µm SiGe BiCMOS technology with a maximum output power of 8 dBm and a power added efficiency (PAE) of 17.5% at dc power consumption of 35 mW is presented. It consists of a balun, a driver amplifier (DA), a common-base (CB) core and a medium power amplifier. The CB topology with balun is designed for wider bandwidth and better matching. The measured results showed that the doubler presents a gain of 16.8–19.8 dB, an output power of 1.3–4.3 dBm, and a fundamental rejection of better than 25.7 dB from 27 to 41 GHz with −15.5 dBm input power. The chip size is 0.75 × 0.45 mm2.

Wideband directional couplers with high isolation are designed for millimeter-wave applications and implemented in two different in-house Si-based technologies processes — Si-benzocyclobutene (Si-BCB) process and LIGA-like process (lithography, electroplating, and molding). Two 3D tandem directional couplers for millimeter-wave/THz applications have been constructed using the Si-BCB process. The coupling and isolation of tandem coupler have been analyzed from circuit topology. A branch-line coupler is also constructed using the LIGA-like process. The electrical characteristics of these couplers have been simulated in 3D simulator. By comparing the results, the proposed Si-BCB process is noted to provide flexibilities in both the design and implementation of passive components.

This paper presents a comprehensive analysis of the electrical performance of the bonding-wire interconnection up to 170 GHz. The effects of the wire length, loop height and pad area have all been analyzed. An electrical model for the bonding-wire is discussed. By reducing interconnection distance and optimizing pad area, the performance of the bonding-wire can be enhanced. The acceptable measurement results of the bonding-wire up to 170 GHz are obtained.

In this paper, a novel 60 GHz flip-chip bandpass filter in standard CMOS technology is proposed. An insertion loss of 0.69 dB/mm for microstrip line is obtained at 60 GHz by using cascaded THRU de-embedding method. By deploying the gap between the flip-chip bump and the flipped chip, an endcoupled, half-wavelength resonator filter is designed and fabricated. The measured insertion loss of 3.3 dB and return loss of >13 dB with a bandwidth of 63% at centre frequency of 60 GHz clearly demonstrates that the proposed flip-chip filter is a promising candidate for 60 GHz integrated circuits applications.

In this paper, an improved correlation method is proposed to detect the phase difference between two signals in high frequency in a polarimetric radar system. The mean value of the correlation of two sampled signals is calculated based on Field Programmable Gate Array (FPGA) to give a more accurate result of the detection. The method is simulated in Simulink®, and the blocks are then converted into a Quartus II project and compiled to show the occupied resources. The basic principle of the method is described in detail and the results of the simulation provide some evidences that the method can be applied in the radar system for real time processing. Some notes are also given to improve the performance in practical applications.

The effect of rod distortion on the flow and heat transfer in a rod (fuel) bundle similar to those in an Advanced Gas-cooled Reactor (AGR) is investigated using carefully constructed CFD models. The results are of relevance to various other engineering applications, for example heat exchangers. The distorted element contracts gradually over the first half of the element, reaching a minimum at half high then subsequently increasing back to its normal value over the second half of the element. In this paper, the results for forced convection are presented. Changes in the rod profiles divert flow to regions of less resistance, resulting in strong cross flow recirculation regions. The resultant three dimensional flow is also accompanied by large scale swirling flow around the fuel pins. The hotspot at any height coincides with the leeward side of the cross flow. It is rather surprising that the peak can temperature at the location of worst bundle distortion (i.e middle height) is actually slightly lower than that of intact fuel. The overall peak can temperature in the damaged bundle is however much higher than that in the intact fuel, and this occurs towards the top of the bundle.

Background Aristolochiae Fructus (AF) and honey-fried Aristolochiae Fructus (HAF) have been used in China for a long time as anti-tussive and expectorant drugs. Few clinical cases have been reported to be associated with the toxicity of AF and HAF, although relatively high amounts of aristolochic acids (AAs) have been found in them. Our previous experiments have verified from the chemical changes and from traditional toxicology that honey-processing can significantly reduce the toxicity of AF. To further elucidate the detoxification mechanism of honey-processing, comparative pharmacokinetics of AAs in AF and HAF are performed in this study. Methods An HPLC-MS/MS (high-performance liquid chromatography-tandem mass spectrometry) method was developed and validated for the determination of AA I, AA II, AA C, AA D and 7-OH AA I in rat plasma. The multi-component pharmacokinetics of AAs in AF and HAF extracts were investigated after the oral administration of three doses to rats. The relative pharmacokinetic parameters were compared systematically. Results The five AAs shared a similar nonlinear PK (pharmacokinetic) process. They involve rapid absorption and elimination, and they were fit into a two-compartmental open model. Some significant pharmacokinetic differences were observed between the AF and HAF groups: the C max and AUC values of AA I and AA II in the AF groups were much higher than those of the HAF groups. Conclusions Honey-frying technology can reduce the toxicity of AF by significantly decreasing the absorption of AA I and AA II. The PK parameters obtained in this work could provide valuable references for the toxicity research and clinical use of Aristolochiaceae herbs, including AF and HAF. Graphical abstract Process diagram of comparative pharmacokinetics study Electronic supplementary material The online version of this article (doi:10.1186/s12906-017-1626-2) contains supplementary material, which is available to authorized users.