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Under the threat of quantum computers’ expected powerful computational capacity, the study on post-quantum cryptography is becoming urgent nowadays. Lattice-based cryptography is one of the most promising candidates of post-quantum cryptography. To give a secure instantiation for practical applications, it is necessary to understand the complexity of the best-known attacks. Most of the attacks to lattice-based cryptography use basis reduction algorithms. For instance, the most commonly used practical basis reduction algorithms are variants of the block Korkin–Zolotarev (BKZ) algorithm. In this paper, we study the effect of applying the quick reordering technique (QRT) to lattice algorithms, mainly the enumeration algorithm and the BKZ algorithm. We show that QRT is a simple method to improve these two algorithms with respect to cutting down the number of search nodes and thus reducing the total runtime. For improving on the LLL algorithm with dimensions smaller than 30, the success rate is larger than 10%, and for the BKZ algorithm with blocksize smaller than 30, the success rate is larger than 40%. At first, we observe that reordering the LLL-reduced basis vectors by increasing norm orders will change the distribution of search nodes in the enumeration tree, which gives a chance to reduce the enumeration search nodes with a certain probability. The experimental results show that the runtime of the enumeration algorithm can be accelerated approximately by a factor of two. We further explain this phenomenon from a theoretical point of view, which follows Gama–Nguyen–Regev’s analysis (Gama et al., in: Advances in cryptology—EUROCRYPT 2010, proceedings of 29th annual international conference on the theory and applications of cryptographic techniques, pp 257–278, 2010). Then we apply this reordering technique to the implementation of the BKZ algorithm in the open-source library NTL. Our experimental results in dimensions 100–120 with blocksize 15–30 show that on the LLL-reduced bases, our modified NTL-BKZ outputs a vector shorter than the original NTL-BKZ with rate 40.91%-45.73% by setting the LLL approximation factor by δLLL=0.99. Furthermore, in the instances where the improved BKZ found one same or shorter vector, the runtime is up to 2.02 times faster than the original NTL-BKZ when setting the blocksize β=25 with δLLL=0.99.

Multivariate public‐key cryptography (MPKC) is considered a leading candidate for post‐quantum cryptography (PQC). It is based on the hardness of the multivariate quadratic polynomial (MQ) problem, which is a problem of finding a solution to a system of quadratic equations over a finite field. In this paper, we survey some recent progress in the security analysis of MPKC. Among various existing multivariate schemes, the most important one is the Rainbow signature scheme proposed by Ding et al. in 2005, which was later selected as a finalist in the third round of the PQC standardization project by the National Institute of Standards and Technology. Under the circumstances, some recent research studies in MPKC have focussed on the security analysis of the Rainbow scheme. In this paper, the authors first explain efficient algorithms for solving the MQ problem and the research methodology for estimating their complexity in MPKC. Then, the authors survey some recent results related to the security analysis of the Rainbow scheme. In particular, the authors provide a detailed description of the complexity analysis for solving the bi‐graded polynomial systems studied independently by Nakamura et al. and Smith‐Tone et al., and then expound the rectangular MinRank attack against Rainbow proposed by Beullens.

Schnurri-2 (Shn-2), an nuclear factor-κB site-binding protein, tightly binds to the enhancers of major histocompatibility complex class I genes and inflammatory cytokines, which have been shown to harbor common variant single-nucleotide polymorphisms associated with schizophrenia. Although genes related to immunity are implicated in schizophrenia, there has been no study showing that their mutation or knockout (KO) results in schizophrenia. Here, we show that Shn-2 KO mice have behavioral abnormalities that resemble those of schizophrenics. The mutant brain demonstrated multiple schizophrenia-related phenotypes, including transcriptome/proteome changes similar to those of postmortem schizophrenia patients, decreased parvalbumin and GAD67 levels, increased theta power on electroencephalograms, and a thinner cortex. Dentate gyrus granule cells failed to mature in mutants, a previously proposed endophenotype of schizophrenia. Shn-2 KO mice also exhibited mild chronic inflammation of the brain, as evidenced by increased inflammation markers (including GFAP and NADH/NADPH oxidase p22 phox), and genome-wide gene expression patterns similar to various inflammatory conditions. Chronic administration of anti-inflammatory drugs reduced hippocampal GFAP expression, and reversed deficits in working memory and nest-building behaviors in Shn-2 KO mice. These results suggest that genetically induced changes in immune system can be a predisposing factor in schizophrenia.

Background Laparoscopic cholecystectomy (LC) is one of the most commonly undertaken procedures worldwide for cholecystolithiasis and cholecystitis. Accessory liver lobe (ALL) is a developmental anomaly defined as an excessive liver lobe composed of a normal liver parenchyma. Some ALL exist on the serosal side of the gallbladder. We herein present two cases of ALL incidentally detected during LC. Case presentation The first case was a 69-year-old woman diagnosed with chronic cholecystitis. LC was performed. ALL was observed anterior to the wall of the gallbladder and resected after clipping. Pathological findings revealed liver tissue with Glisson’s capsule and a lobular structure in ALL. However, communication between the bile ducts of ALL and the main liver was unclear due to surgical heat degeneration. The second case was a 56-year-old woman diagnosed with acute cholecystitis. LC was performed approximately one month after the attack, and ALL attached to the wall of gallbladder. ALL was clipped and completely resected. Pathological findings showed that the bile ducts of ALL might be connected within the wall of gallbladder. Conclusions We presented two cases of ALL attached to the gallbladder encountered during LC. Since ALL contains a normal liver parenchyma, postoperative bleeding or bile leakage may occur if it is inefficiently resected. Therefore, the complete resection of ALL is important to prevent these postoperative complications.

Molecular mechanisms regulating animal seasonal breeding in response to changing photoperiod are not well understood. Rapid induction of gene expression of thyroid-hormone-activating enzyme (type 2 deiodinase, DIO2 ) in the mediobasal hypothalamus (MBH) of the Japanese quail ( Coturnix japonica ) is the earliest event yet recorded in the photoperiodic signal transduction pathway. Here we show cascades of gene expression in the quail MBH associated with the initiation of photoinduced secretion of luteinizing hormone. We identified two waves of gene expression. The first was initiated about 14 h after dawn of the first long day and included increased thyrotrophin (TSH) β-subunit expression in the pars tuberalis; the second occurred approximately 4 h later and included increased expression of DIO2 . Intracerebroventricular (ICV) administration of TSH to short-day quail stimulated gonadal growth and expression of DIO2 which was shown to be mediated through a TSH receptor–cyclic AMP (cAMP) signalling pathway. Increased TSH in the pars tuberalis therefore seems to trigger long-day photoinduced seasonal breeding. Spring in their step In spring, many animals start to become reproductively active. They are generally responding to the longer day lengths at this time of the year, but the molecular pathways that mediate the response are not fully understood. Experiments in the Japanese quail, a well established model for studying photoperiodism, have identified the expression of the thyroid-stimulating hormone thyrotrophin in the pars tuberalis, part of the anterior lobe of the pituitary gland, as a critical event in triggering this photoperiodic response. Two waves of gene expression are involved, the first at about 14 hours after dawn on the first 'long' day, and a second a few hours later. This paper examines the changes in gene expression during the first exposure to a long day (such as those found in spring) in Japanese quails and find that two waves of genes are induced as part of the photoperiodic response. This paper also identifies thyrotrophin expression in the pars tuberalis as a critical event in triggering this photoperiodic response.

BackgroundTrifluridine/tipiracil (TAS-102) is an anticancer drug for metastatic colorectal cancer (CRC). This study aimed to analyze the effects and risk factors about effects of TAS-102 in real-world patients with metastatic CRC (the EROTAS-R study).MethodsThis study retrospectively analyzed 271 patients aged ≥ 20 years who underwent TAS-102 for metastatic CRC at nine related institutions from 2014 to 2021. Therapeutic results of TAS-102 + bevacizumab (Bev) and TAS-102, effect predictors, adverse events (AE), and AE predictors were examined.ResultsThe backgrounds of all cases were as follows: average age, 66.7 ± 10.9 years; male ratio, 59.5%; performance status (PS) 0/1/2, 43.5%/50.6%/5.9%; and tumor site right/left, 25.5%/74.5%. The therapeutic results of 109 cases receiving TAS-102 + Bev and 162 cases receiving TAS-102 were as follows: disease control rate, 53.2% vs. 28.0% (p < 0.01); progressive free survival (PFS), 6.2 vs. 4.2 months (p < 0.01); and overall survival (S), 11.8 vs. 9.3 months (p = 0.03). Multivariate analysis for effect-related factors (odds ratio (OR), 95%confidence interval (CI)) showed the following: PS1 + 2 (0.257, 0.134–0.494, p < 0.01) and a combination of Bev (3.052, 1.598–5.827, p < 0.01). The rates of grade 3 AE for TAS-102 + Bev and TAS-102 were 53.2% and 48.8%, respectively (p = 0.47). Various AE predictors were as follows: male sex (p = 0.69), age ≥ 75 years (p = 0.59), PS1 + 2 (p = 0.20), body surface area < 1.53 m2 (p = 0.26), eGFR < 50 ml/min (p = 0.02), and AST ≥ 50 IU/L (p = 0.64).ConclusionA better OS and PFS comparing TAS-102 + Bev to TAS-102 for CRC was achieved in a large number of real-world patients.

The dentate gyrus of the hippocampus has been implicated in the pathophysiological basis of neuropsychiatric disorders including schizophrenia. We have identified several mouse models of neuropsychiatric disorders with robust molecular and functional defects in the dentate gyrus. Among them, mice lacking Schnurri-2 (Shn2 or HIVEP2) have been proposed as a model of schizophrenia and intellectual disability. Shn2 knockout mice exhibit behavioral abnormalities resembling symptoms of schizophrenia and HIVEP2-related intellectual disability as well as marked functional alterations in the soma and output synapse of the dentate granule cells (GCs). Although robust abnormalities were also observed in the dendritic spine morphology in the GCs, their functional correlates remain unknown. In the present study, we performed electrophysiological analyses of synaptic transmission at the medial perforant path (MPP) input onto the GCs in Shn2 knockout mice. While the basal synaptic efficacy was preserved, short-term synaptic depression induced by paired-pulse or low-frequency stimulation was reduced in the mutant mice. High-frequency tetanic stimulation induced lasting synaptic potentiation in both wild-type and mutant mice. However, the decaying synaptic potentiation shortly after the tetanic stimulation was significantly reduced in the mutant mice. These results indicate that the Shn2 deficiency attenuates bidirectional short-term synaptic plasticity at the MPP-GC synapse, thereby rendering the synapse more static. Our finding further supports a possible role of the dentate gyrus dysfunction in pathophysiology of schizophrenia and may also provide important information in interpreting morphology changes of the brain synapses in neuropsychiatric disorders.

Accumulating evidence suggests that subcellular-scale structures such as dendritic spine and mitochondria may be involved in the pathogenesis/pathophysiology of schizophrenia and intellectual disability. Previously, we proposed mice lacking Schnurri-2 (Shn2; also called major histocompatibility complex [MHC]-binding protein 2 [MBP-2], or human immunodeficiency virus type I enhancer binding protein 2 [HIVEP2]) as a schizophrenia and intellectual disability model with mild chronic inflammation. In the mutants’ brains, there are increases in C4b and C1q genes, which are considered to mediate synapse elimination during postnatal development. However, morphological properties of subcellular-scale structures such as dendritic spine in Shn2 knockout (KO) mice remain unknown. In this study, we conducted three-dimensional morphological analyses in subcellular-scale structures in dentate gyrus granule cells of Shn2 KO mice by serial block-face scanning electron microscopy. Shn2 KO mice showed immature dendritic spine morphology characterized by increases in spine length and decreases in spine diameter. There was a non-significant tendency toward decrease in spine density of Shn2 KO mice over wild-type mice, and spine volume was indistinguishable between genotypes. Shn2 KO mice exhibited a significant reduction in GluR1 expression and a nominally significant decrease in SV2 expression, while PSD95 expression had a non-significant tendency to decrease in Shn2 KO mice. There were significant decreases in dendrite diameter, nuclear volume, and the number of constricted mitochondria in the mutants. Additionally, neuronal density was elevated in Shn2 KO mice. These results suggest that Shn2 KO mice serve as a unique tool for investigating morphological abnormalities of subcellular-scale structures in schizophrenia, intellectual disability, and its related disorders.

Our previous work identified human immunodeficiency virus type I enhancer binding protein 1 (HIVEP1) as a putative driver of LPS-induced NF-κB signaling in humans in vivo . While HIVEP1 is known to interact with NF-ĸB binding DNA motifs, its function in mammalian cells is unknown. We report increased HIVEP1 mRNA expression in monocytes from patients with sepsis and monocytes stimulated by Toll-like receptor agonists and bacteria. In complementary overexpression and gene deletion experiments HIVEP1 was shown to inhibit NF-ĸB activity and induction of NF-ĸB responsive genes. RNA sequencing demonstrated profound transcriptomic changes in HIVEP1 deficient monocytic cells and transcription factor binding site analysis showed enrichment for κB site regions. HIVEP1 bound to the promoter regions of NF-ĸB responsive genes. Inhibition of cytokine production by HIVEP1 was confirmed in LPS-stimulated murine Hivep1 -/- macrophages and HIVEP1 knockdown zebrafish exposed to the common sepsis pathogen Streptococcus pneumoniae . These results identify HIVEP1 as a negative regulator of NF-κB in monocytes/macrophages that inhibits proinflammatory reactions in response to bacterial agonists in vitro and in vivo .

Many symptoms induced by isolation rearing of rodents may be relevant to neuropsychiatric disorders, including depression. However, identities of transcription factors that regulate gene expression in response to chronic social isolation stress remain elusive. The transcription factor ATF‐7 is structurally related to ATF‐2, which is activated by various stresses, including inflammatory cytokines. Here, we report that Atf‐7 ‐deficient mice exhibit abnormal behaviours and increased 5‐HT receptor 5B ( Htr5b ) mRNA levels in the dorsal raphe nuclei. ATF‐7 silences the transcription of Htr5B by directly binding to its 5′‐regulatory region, and mediates histone H3‐K9 trimethylation via interaction with the ESET histone methyltransferase. Isolation‐reared wild‐type (WT) mice exhibit abnormal behaviours that resemble those of Atf‐7 ‐deficient mice. Upon social isolation stress, ATF‐7 in the dorsal raphe nucleus is phosphorylated via p38 and is released from the Htr5b promoter, leading to the upregulation of Htr5b . Thus, ATF‐7 may have a critical role in gene expression induced by social isolation stress.