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Response inhibition, a crucial component of executive function, is closely related to personal impulse control, social adaption, and mental health. Previous studies have found response inhibition deficit in patients with major depressive disorder, but whether it also exists in individuals with subclinical depression (SD) remains unclear. This study aimed to identify the ability of response inhibition to emotional face stimuli both under explicit and implicit conditions in individuals with SD. Thirty-six subclinical depressed college students and 39 healthy individuals were recruited and administered the non-emotional, explicit, and implicit emotional stop-signal tasks (SSTs). Mixed-model analyses of variance were used to analyze the differences between and within groups. In implicit emotional SST, the results showed a significant longer stop-signal response time, a shorter stop-signal delay time, a shorter go reaction time, and a similar proportion of stop success in the SD group compared to healthy controls. However, the above indices showed no significant difference between the two groups in the non-emotional SST and explicit emotional SST. These findings suggest a possible defect of response inhibition in implicit emotional processing in individuals with SD, which may potentially serve as a marker of susceptibility to depression and thus be applied to early screening and intervention for major depressive disorder.

Precise regulation of chromosome separation through spindle assembly checkpoint (SAC) during oocyte meiosis is critical for mammalian reproduction. The kinetochore plays an important role in the regulation of SAC through sensing microtubule tension imbalance or missing microtubule connections. Here, we report that kinetochore scaffold 1 (KNL1, also known as CASC5), an outer kinetochore protein, plays a critical role in the SAC function of mouse oocytes. KNL1 localized at kinetochores from GVBD to the MII stage, and microinjection of KNL1-siRNA caused accelerated metaphase-anaphase transition and premature first meiosis completion, producing aneuploid eggs. The SAC was prematurely silenced in the presence of unstable kinetochore-microtubule attachments and misaligned chromosomes in KNL1-depleted oocytes. Additionally, KNL1 and MPS1 had a synergistic effect on the activation and maintenance of SAC. Taken together, our results suggest that KNL1, as a kinetochore platform protein, stabilizes SAC to ensure timely anaphase entry and accurate chromosome segregation during oocyte meiotic maturation.

Background/Aims Pancreatic ductal adenocarcinoma (PDAC) is associated with high mortality, even after surgical resection. The existing predictive models for survival have limitations. This study aimed to develop better nomograms for predicting overall survival (OS) and cancer‐specific survival (CSS) in PDAC patients after surgery. Methods A total of 6323 PDAC patients were retrospectively recruited from the Surveillance, Epidemiology, and End Results (SEER) database and randomly allocated into training, validation, and test cohorts. Multivariate Cox regression analysis was conducted to identify significant independent factors for OS and CSS, which were used for construction of nomograms. The performance was evaluated, validated, and compared with that of the 8th edition AJCC staging system. Results Ten independent factors were significantly correlated with OS and CSS. The 1‐, 3‐, and 5‐year OS rates were 40%, 20%, and 15%, and 1‐, 3‐, and 5‐year CSS rates were 45%, 24%, and 19%, respectively. The nomograms were calibrated well, with c‐indexes of 0.640 for OS and 0.643 for CSS, respectively. Notably, relative to the 8th edition AJCC staging system, the nomograms were able to stratify each AJCC stage into three prognostic subgroups for more robust risk stratification. Furthermore, the nomograms achieved significant clinical validity, exhibiting wide threshold probabilities and high net benefit. Performance assessment also showed high predictive accuracy and reliability. Conclusions The predictive ability and reliability of the established nomograms have been validated, and therefore, these nomograms hold potential as novel approaches to predicting survival and assessing survival risks for PDAC patients after surgery., In the present study, we constructed and validated nomograms for predicting the 1‐, 3‐, and 5‐year OS and CSS rates after surgical resection of PDAC. The nomograms established in the present study showed good performance for the prediction of OS and CSS, which was superior to that of the existing, conventional AJCC staging system with an improved net benefit. Therefore, these nomograms hold promise as novel prognosis models for improving the prediction of individualized postoperative survival and improving the care of PDAC patients following surgical resection.

The American Joint Committee on Cancer (AJCC) staging system is inadequate for an accurate prognosis in nasopharyngeal carcinoma (NPC). Thus, new biomarkers are under intense investigation. Here, we investigated whether the density of TILs could predict prognosis in NPC. First, we used 1490 cases of nasopharyngeal carcinoma samples from two independent cohorts to evaluate the density and distribution of tumor-infiltrating lymphocytes (TILs). Second, in one cohort, we assessed associations between TILs and clinical outcomes in 593 randomly selected samples (defined as the training set) and validated findings in the remaining 593 samples (defined as the validation set). Furthermore, we confirmed the prognostic value of TILs in a second independent cohort of 304 cases (defined as the independent set). Based on multivariable Cox regression analysis, we also established an effective prognostic nomogram including TILs to improve accuracy in predicting disease-free survival (DFS) for patients with nondisseminated NPC. We found that high TILs in the training set were significantly associated with favorable DFS [hazard ratio (HR) 0.41, 95% confidence interval (CI) 0.28-0.58, p < 0.001], overall survival (OS, HR 0.42, 95% CI 0.27-0.64, p < 0.001), distant metastasis-free survival (DMFS, HR 0.37, 95% CI 0.23-0.58, p < 0.001) and local-regional recurrent free survival (LRRFS, HR 0.43, 95% CI 0.25-0.73, p = 0.002). Multivariate analysis showed that TILs are an independent prognostic indicator for DFS in all cohorts. In summary, this study indicated that TILs may reflect the immunological heterogeneity of NPC and could represent a new prognostic biomarker.

Blue light plays an important role during the growth of Ganoderma lucidum, one of the best-known medicinal macrofungi in China. In the present study, we cloned Glwc-1 and Glwc-2, the homologue of the blue light photoreceptors Ncwc-1 and Ncwc-2 of Neurospora crassa, from G. lucidum. The deduced amino acid sequence of Glwc-1 contained the similar function domains as NcWC-1 including LOV, PAS B, PAS C, and PAC domains. The deduced amino acid sequence of Glwc-2 contained PAS domain and GATA-type zinc finger (Znf) domain as well as NcWC-2. Phylogenetic analysis based on fungal WC-1 and WC-2 supported GlWC-1 and GlWC-2 were blue light receptors. The expression of Glwc-1 and Glwc-2 indicated that they might play an important role during the primordium differentiation process of G. lucidum, and the external blue light stimulation increased the expression of Glwc-1 and Glwc-2.

Piccolo is a lightweight block cipher proposed at CHES 2011. This paper firstly gives the zero-correlation linear approximations over 7-round Piccolo and studies the security of Piccolo-128 against multidimensional zero-correlation linear cryptanalysis. Based on the statistic used in multidimensional linear cryptanalysis to detect the right key and wrong keys, this paper gives the data complexity when using this statistic in multidimensional zero-correlation linear cryptanalysis. Finally, with partial sum technique and the relation between the round keys in Piccolo-128, the first known-plaintexts attacks on round 0-12/round, 15-28/round, and 14-28 of Piccolo-128 are proposed; the data complexities of those attacks are 256.8/252.43/255.6 known plaintexts, respectively; and the time complexities are 2117.2,2123.09,2126.55, respectively. Copyright © 2016 John Wiley & Sons, Ltd.

Infantile hemangiomas can present a therapeutic challenge to clinicians, especially when associated with severe pain and feeding difficulties. The standard therapeutic management includes corticosteroids and propranolol. However, the clinical response is not always satisfactory. We present six cases of infantile hemangiomas successfully treated with oral itraconazole approximately 5 mg/kg per day. In the first month, the red color of the lesions became a little lighter and the growth of the lesions was controlled in all cases. An obvious clinical improvement was noted in all cases during the 3-month period, with 80-100% improvement in each patient at the end of the treatment, which was judged by both their parents and the dermatologists. Compliance with treatment instructions of oral itraconazole in infants was judged to be very good. Side-effects were mild and limited. Although itraconazole can inhibit angiogenesis and tumor growth in vitro and in vivo associated with some cancers, further research is required to understand the pathogenesis of infantile hemangiomas and the mechanism of itraconazole.

Trichophyton violaceum is a pathogen of tinea capitis and usually cause infection of scalp and hair in children. To investigate the parasitic form of T. violaceum in the human hair tissue, the infected hair strands were collected from a 9-year-old boy with tinea capitis due to T. violaceum and observed under both the scanning electron microscope (SEM) and transmission electron microscope (TEM). The SEM and TEM findings revealed that T. violaceum parasitically lives in the hair shaft in various forms and the morphological transformation of the fungus from hyphae into arthrospores was noted. The involved hair shaft was damaged to the great extent and its ultrastructural changes were evident. Those morphological characteristics of T. violaceum and the three-dimensional ultastructure changes of infected hairs give a better knowledge about the host-fungus relationship in tinea capitis.

Dunaliella salina, a unicellular green alga, has the potential to grow in hypersaline environments via one of its gene products, superoxide dismutase (SOD). The superoxide radicals (O2 (-) ) produced by environmental stresses can cause damage to cells, and SOD catalyzes the turnover of such free radicals to protect cells. In this study, the gene coding for SOD in D. salina was cloned and the product was further identified and characterized. The open reading frame of this gene was 651 bp long, encoding for 217 amino acids. According to the sequence alignment using BLAST, native polyacrylamide electrophoresis for SOD activity analysis, and atomic absorption spectroscopy analysis, this protein belongs to the manganese-containing superoxide dismutase (MnSOD) family. Complementation analysis, performed by introducing plasmids carrying an inducible version of the D. salina gene encoding for MnSOD into an SOD-deficient mutant of E.coli, revealed that this gene could not only complement the defects in SOD activity, but was also capable of providing a stronger tolerance to restrictive growth conditions, such as high salt and prolonged UV exposure, compared to the tolerance of wild-type strains.

RA175/SynCAM1/Cadm1 (Cadm1), a member of the immunoglobulin superfamily, is a synaptic cell adhesion molecule that has a PDZ-binding motif at the C-terminal region. It promotes the formation of presynaptic terminals and induces functional synapses in the central nervous system. Cadm1-deficient (knockout [KO]) mice show behavioral abnormalities, including excessive aggression and anxiety, but do not show any symptoms of neuromuscular disorder, although neuromuscular junctions (NMJs) have structures similar to synapses. We have examined the expression of members of the Cadm family in the mouse muscle tissues. Cadm4 and Cadm1 were major components of the Cadm family, and Cadm3 was faintly detected, but Cadm2 was not detected by RT-PCR. Cadm4 as well as Cadm1 colocalized with alpha-bungarotoxin at the NMJs and interacted with the multiple PDZ domain protein Mupp1. Cadm4 was expressed in Cadm1-KO mice and might compensate for Cadm1 loss through interactions with Mupp1.

Mutations in the parkin gene are the major cause of early-onset familial Parkinson’s disease (PD). We previously reported the generation and analysis of a knockout mouse carrying a deletion of exon 3 in the parkin gene. F1 hybrid pa+ ⁄‐ mice were backcrossed to wild-type C57Bl ⁄6 for three more generations to establish a pa‐ ⁄‐(F4) mouse line. The appearance of tyrosine hydroxylase-positive neurons was normal in young and aged pa‐ ⁄‐ (F4) animals. Loss of parkin function in mice did not enhance vulnerability of dopaminergic neurons to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity. However, the pa‐ ⁄‐ (F4) mice displayed impaired exploration and habituation to a new environment and exhibited thigmotaxis behaviour in the open field and Morris water maze. Abnormal anxiety-related behaviour of pa‐ ⁄‐ (F4) mice was also observed in the light ⁄dark exploration test paradigm. Dopamine metabolism was enhanced in the striatum of pa‐ ⁄‐ (F4) mice, as revealed by increased homovanillic acid (HVA) content and a reduced ratio of dihydroxyphenylacetic acid (DOPAC) ⁄HVA. The alterations found in the dopaminergic system could be responsible for the behavioural impairments of pa‐ ⁄‐ (F4) mice. Consistent with a recent observation of cognitive dysfunction in parkin-linked patients with PD, our findings provide evidence of a physiological role of parkin in non-motor behaviour, possibly representing a disease stage that precedes dopaminergic neuron loss.

Mutations in a protein designated Parkin were shown to be involved in the pathogenesis of autosomal recessive juvenile parkinsonism. Nothing is known about its regional and subcellular distribution in the mouse. In order to elucidate the Parkin mRNA and protein distribution in the adult mouse, the mouse cDNA was cloned and polyclonal antisera were generated against the N-terminal part of mouse Parkin. The antibodies were shown to be specific using Western blot analysis, immunostaining of cells transfected with mouse Parkin and pre-absorption tests. The Parkin protein expression profile was studied using immunohistochemistry and Western blot analysis and was compared with that of the mRNA yielded by in situ hybridization and RT-PCR analysis. Parkin protein was widely distributed in all subdivisions of the mouse brain. Low levels were found in the telencephalon and diencephalon, while the brainstem contained a large number of cells heavily expressing Parkin. Ultrastructural analysis and double immunohistochemistry revealed that the majority of Parkin-expressing cells were neurons, while only single glial cells exhibited immunostaining. The protein was distributed nonhomogeneously throughout the entire cytoplasm. A subpopulation of Parkin-immunopositive cells displayed speckled immunodeposits in the nucleus. Dopaminergic cells of the substantia nigra pars compacta exhibited high levels of Parkin mRNA but no Parkin protein, while the striatum contained immunopositive profiles but no mRNA signals. Our data indicate that Parkin is neither restricted to a single functional system nor associated with a particular transmitter system. The speckled nuclear distribution of Parkin immunoreactivity strongly suggests a role for Parkin in gene expression.