An adaptive grid voltage/frequency tracking method based on SOGIs on a shipboard PV-diesel-battery hybrid power system

This paper addresses the unbalanced voltage, subharmonic/dc-offset voltage, and low-frequency (LF)/high-frequency (HF) harmonics of a grid voltage tracking method based on second-order generalized integrators (SOGIs) in high voltage/frequency swing on a shipboard photovoltaic (PV)-diesel-battery hybrid power system. To perform this work, a kind of shipboard PV–diesel-battery hybrid power system structure was first analyzed, emphasizing both the active and reactive power (PQ) control strategy and the sensitivity of the phase-locked loop (PLL) that is crucial to the vessel’s electrical networks. Then, the effect of grid voltage harmonics in SOGIs and of voltage/frequency swing on SOGI frequency-locked loop (SOGI-FLL) was studied. Meanwhile, aiming to the adverse power qualities of a shipboard power system (SPS), a SOGI-based structure with prefilter, a dc-offset block, and a positive sequence extractor (SOGI-FDE) was proposed. Finally, to overcome all of the vessel’s grid problems, a new SOGI-based voltage tracking structure, SOGI-FDE-FLL, consisting of SOGI-FDE and SOGI-FLL, was proposed to achieve accurate grid voltage tracking rapidly. This proposed schematic was used as an adaptive grid voltage tracking method to a three-phase three-wire shipboard PV–diesel-battery hybrid power system. Experimental results were obtained validating this proposal

Time bound of atomic adiabatic evolution in the accelerated optical lattice

The accelerated optical lattice has emerged as a valuable technique for the investigation of quantum transport physics and has found widespread application in quantum sensing, including atomic gravimeters and atomic gyroscopes. In our study, we focus on the adiabatic evolution of ultra-cold atoms within an accelerated optical lattice. Specifically, we derive a time bound that delimits the duration of atomic adiabatic evolution in the oscillating system under consideration. To experimentally substantiate the theoretical predictions, precise measurements to instantaneous band populations were conducted within a one-dimensional accelerated optical lattice, encompassing systematic variations in both lattice's depths and accelerations. The obtained experimental results demonstrate a quantitatively consistent correspondence with the anticipated theoretical expressions. Afterwards, the atomic velocity distributions are also measured to compare with the time bound. This research offers a quantitative framework for the selection of parameters that ensure atom trapped throughout the acceleration process. Moreover, it contributes an experimental criterion by which to assess the adequacy of adiabatic conditions in an oscillating system, thereby augmenting the current understanding of these systems from a theoretical perspective

A six-generation Chinese family in haplogroup B4C1C exhibits high penetrance of 1555A > G-induced hearing Loss

<p>Abstract</p> <p>Background</p> <p>The 1555A > G mutation is the most common cause of aminoglycoside-induced and non-syndromic deafness. However, the variable clinical phenotype and incomplete penetrance of A1555G-induced hearing loss complicate our understanding of this mutation. Environmental factors, nuclear genes, mitochondrial haplotypes/variants and a possible threshold effect have been reported to may be involved in its manifestation.</p> <p>Methods</p> <p>Here, we performed a clinical, molecular, genetic and phylogenic analysis in a six-generation Chinese family.</p> <p>Results</p> <p>A clinical evaluation revealed that affected individuals without aminoglycoside exposure developed hearing loss extending gradually from 12000 Hz to 8000 Hz and then to 4000 Hz. Using pyrosequencing, we detected an identical homoplasmic 1555A > G mutation in all individuals except one. We did not find any correlation between the mutation load and the severity of hearing loss. T123N coexisted with the 1555A > G mutation in six affected subjects in our pedigree. Analysis of the complete mtDNA genome of this family revealed that this family belonged to haplotype B4C1C and exhibited high penetrance. Upon the inclusion of subjects that had been exposed to aminoglycosides, the penetrance of the hearing loss was 63.6%.; without exposure to aminoglycosides, it was 51.5%. This pedigree and another reported Chinese pedigree share the same haplotype (B4C1C) and lack functionally significant mitochondrial tRNA variants, but nevertheless they exhibit a different penetrance of hearing loss.</p> <p>Conclusions</p> <p>Our results imply that the factors responsible for the higher penetrance and variable expression of the deafness associated with the 1555A > G mutation in this pedigree may not be mtDNA haplotype/variants, but rather nuclear genes and/or aminoglycosides.</p

Effect of liver histopathology on islet cell engraftment in the model mimicking autologous islet cell transplantation

Background: The inflammatory milieu in the liver as determined by histopathology is different in individual patients undergoing autologous islet cell transplantation. We hypothesized that inflammation related to fatty-liver adversely impacts islet survival. To test this hypothesis, we used a mouse model of fatty-liver to determine the outcome of syngeneic islet transplantation after chemical pancreatectomy. Methods: Mice (C57BL/6) were fed a high-fat-diet from 6 weeks of age until attaining a weight of ≥28 grams (6–8 weeks) to produce a fatty liver (histologically > 30% fat);steatosis was confirmed with lipidomic profile of liver tissue. Islets were infused via the intra-portal route in fatty-liver and control mice after streptozotocin induction of diabetes. Outcomes were assessed by the rate of euglycemia, liver histopathology, evaluation of liver inflammation by measuring tissue cytokines IL-1β and TNF-α by RT-PCR and CD31 expression by immunohistochemistry. Results: The difference in the euglycemic fraction between the normal liver group (90%, 9/10) and the fatty-liver group (37.5%, 3/8) was statistically significant at the 18th day post- transplant and was maintained to the end of the study (day 28) (p = 0.019, X2 = 5.51). Levels of TNF–α and IL-1β were elevated in fatty-liver mice (p = 0.042, p = 0.037). Compared to controls cytokine levels were elevated after islet cell transplantation and in transplanted fatty-liver mice as compared to either fatty- or islet transplant group alone (p = NS). A difference in the histochemical pattern of CD31 could not be determined. Conclusion: Fatty-liver creates an inflammatory state which adversely affects the outcome of autologous islet cell transplantation

Effectiveness of Traditional Chinese Medicine Compound JieDuTongLuoShengJin Granules Treatment in Primary Sjögren’s Syndrome: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial

Objective. To evaluate the clinical therapeutic efficacy and safety of JieDuTongLuoShengJin granules + HCQ in patients with pSS. Methods. 40 patients with low-activity-level pSS and without visceral involvement participated in this study and were randomized to receive either JieDuTongLuoShengJin granules with HCQ or placebo with HCQ. Patients and investigators were blinded to treatment allocation. The primary endpoint was week 12 ESSPRI score, while secondary endpoints included ESSDAI, salivary and lacrimal gland function, and some laboratory variables. Safety-related data were also assessed. Results. Comparing with the placebo group, the treatment group experienced statistically significant improvement in the mean change from baseline for the primary endpoint of ESSPRI score and also in PGA. Moreover, in comparison with baseline values, the treatment group had significantly improved ESSDAI score, unstimulated saliva flow rate, and several laboratory variables. However, upon comparison of the two groups, there were no significant differences for them. The incidence of AEs was 10.0%, one in treatment group and three in placebo group. Conclusion. Treatment with a combination of JieDuTongLuoShengJin granules with HCQ is effective in improving patients’ subjective symptoms and some objective indicators of pSS. These results indicate that JieDuTongLuoShengJin is promising as a safe and effective treatment of pSS

Low genetic diversity in captive populations of the critically endangered Blue-crowned Laughingthrush (Garrulax courtoisi) revealed by a panel of novel microsatellites

Background Captive populations permit research and conservation of endangered species in which these efforts are hardly implemented in wild populations. Thus, analysing genetic diversity and structure of captive populations offers unique opportunities. One example is the critically endangered Blue-crowned Laughingthrush, Garrulax courtoisi, which has only two known wild populations in Wuyuan, Jiangxi and Simao, Yunnan, China. We carried out the first conservation genetic study, in order to provide useful implications that allow for successful ex situ conservation and management of the Blue-crowned Laughingthrush. Methods Using the novel microsatellite markers developed by whole-genome sequencing, we genotyped two captive populations, from the Ocean Park Hong Kong, which are of unknown origin, and the Nanchang Zoo, which were introduced from the Wuyuan wild population since the year 2010–2011, respectively. The genetic diversity of captive Blue-crowned Laughingthrush populations was estimated based on genetic polymorphisms revealed by a new microsatellite data set and mitochondrial sequences. Then, we characterised the population structure using STRUCTURE, principal coordinates analysis, population assignment test using the microsatellite data, and haplotype analysis of mitochondrial data. Additionally, we quantified genetic relatedness based on the microsatellite data with ML-Relate. Results Our results showed equally low levels of genetic diversity of the two captive Blue-crowned Laughingthrush populations. The population structure analysis, population assignment test using the microsatellite data, and haplotype analysis of the mitochondrial data showed weak population structuring between these two populations. The average pairwise relatedness coefficient was not significant, and their genetic relatedness was quantified. Discussion This study offers a genetic tool and consequently reveals a low level of genetic diversity within populations of a critically endangered bird species. Furthermore, our results indicate that we cannot exclude the probability that the origin of the Hong Kong captive population was the wild population from Wuyuan. These results provide valuable knowledge that can help improve conservation management and planning for both captive and wild Blue-crowned Laughingthrush populations

Mutations in TUBB8 and Human Oocyte Meiotic Arrest

BACKGROUND Human reproduction depends on the fusion of a mature oocyte with a sperm cell to form a fertilized egg. The genetic events that lead to the arrest of human oocyte maturation are unknown. METHODS We sequenced the exomes of five members of a four-generation family, three of whom had infertility due to oocyte meiosis I arrest. We performed Sanger sequencing of a candidate gene, TUBB8, in DNA samples from these members, additional family members, and members of 23 other affected families. The expression of TUBB8 and all other β-tubulin isotypes was assessed in human oocytes, early embryos, sperm cells, and several somatic tissues by means of a quantitative reverse- transcriptase–polymerase-chain-reaction assay. We evaluated the effect of the TUBB8 mutations on the assembly of the heterodimer consisting of one α-tubulin polypeptide and one β-tubulin polypeptide (α/β-tubulin heterodimer) in vitro, on microtubule architecture in HeLa cells, on microtubule dynamics in yeast cells, and on spindle assembly in mouse and human oocytes. RESULTS We identified seven mutations in the primate-specific gene TUBB8 that were responsible for oocyte meiosis I arrest in 7 of the 24 families. TUBB8 expression is unique to oocytes and the early embryo, in which this gene accounts for almost all the expressed β-tubulin. The mutations affect chaperone-dependent folding and assembly of the α/β-tubulin heterodimer, disrupt microtubule behavior on expression in cultured cells, alter microtubule dynamics in vivo, and cause catastrophic spindle-assembly defects and maturation arrest on expression in mouse and human oocytes. CONCLUSIONS TUBB8 mutations have dominant-negative effects that disrupt microtubule behavior and oocyte meiotic spindle assembly and maturation, causing female infertility. (Funded by the National Basic Research Program of China and others.