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Objective: To investigate the phenomenon of epileptic spasms (ES) and focal seizures (FS) in a single ictal event (FS-ES phenomenon) and to study the etiology, manifestations, and prognosis of this phenomenon. Methods: The data of the 15 neonates who had ES and FS in a single ictal event, according to video-electroencephalography (VEEG) recording in Department of Neonatology of Children's Hospital of Fudan University during the period of January 2018 to December 2019, was analyzed retrospectively. Results: Of the 15 neonates, 7 were male and 8 were female. Gestational age was 39 (32-42) weeks. Birth weight was 3 100 (1 825-3 850) g. The initial onset age of convulsions was 2 (1-10) days. The age of the first discovery of FS-ES phenomenon was 25 (14-32) days. The age of seizure-free was 7(1-27) months. All of the initial seizure types were FS. The FS-ES phenomenon of 15 patients started with FS. The FS-ES phenomenon manifested in 2 forms: FS followed by ES (12 cases), ES appeared during an FS without interrupting FS (2 cases). In 1 neonate the spasm occurred in both forms. The etiology included genetic factors (9 cases), intracranial infection (1 case), abnormal brain tissue structure (2 cases), and etiology was unknown in 3 cases. All the neonates had a poor prognosis except one. Conclusions: The FS-ES phenomenon in the neonatal period starts with FS. There are various etiologies. Etiologies of most patients are genetic factors. Most of the patients have a poor prognosis.

Objective: To analyze the re-examination results of malaria cases captured from the National Notifiable Communicable Disease Reporting System in Hubei Provincial Malaria Diagnostic Reference Laboratory from 2017 to 2019, so as to pro- vide the scientific evidence for improving the malaria control capability in the province., Methods: Microscopy and nested PCR assay were performed to re-examine the diagnosis of malaria cases registered in the National Notifiable Communicable Disease Reporting System in Hubei Provincial Malaria Diagnostic Reference Laboratory from 2017 to 2019, and the coincidences of ma- laria diagnosis and malaria parasite species were evaluated., Results: A total of 410 malaria cases were reported in Hubei Province from 2017 to 2019 according to the data retrieved from the National Notifiable Communicable Disease Reporting System. Among the 407 samples re-examined by Hubei Provincial Malaria Diagnostic Reference Laboratory from 2017 to 2019, the diag- nosis 374 malaria cases were confirmed, with an overall coincidence of 91.89% (374/407) for malaria diagnosis and 89.04% (333/374) for parasite species identification. The coincidence rates of malaria diagnosis and parasite species identification were 50.00% to 100.00% and 66.67% to 100.00% in 16 cities (prefectures) of Hubei Province during the re-examinations, which both varied in regions ( χ 2 = 40.46 and 42.30, both P values < 0.01). The coincidence rates of Plasmodium falciparum , P. vivax , P. malariae and P. ovale identification were 95.80%, 100.00%, 58.33% and 51.92% during the re-examinations, respectively ( χ 2 = 76.66, P < 0.01). The consistency rate between microscopic and nested PCR results was 89.83% (362/403)., Conclusions: The overall diagnostic quality of malaria is high in medical institutions at all levels in Hubei Province; however, the diagnostic capability of malaria remains to be improved in some regions.

Objective: To analyze the hotspots of known pathogenic disease-causing variants of glucose-6-phosphate dehydrogenase (G6PD) and the phenotype spectrum of neonatal patients with known pathogenic disease-causing variants of G6PD. Methods: The known pathogenic disease-causing variants of G6PD were collected from Human Gene Mutation Database. Screening was performed for these variants among the 7 966 cases (2 357 neonatal, 5 609 non-neonatal) in the database of sequencing at Molecular Diagnosis Center, Children's Hospital of Fudan University. All these samples were from patients suspected with genetic disorder. The database contained Whole Exon Sequencing data and Clinical Exon Sequencing data. We screened out the patients with known pathogenic disease-causing variants of G6PD, analyzed the hotspot of G6PD and the phenotype spectrum of neonatal patients with known pathogenic disease-causing variants of G6PD. Results: (1) Among the next generation sequencing data of the 7 966 samples, 86 samples (1.1%) were detected as positive for the known pathogenic disease-causing variants of G6PD (positive samples set). In the positive sample set, 51 patients (33 males, 18 females) were newborn babies. Forty-three patients (26 males, 17 females) had the enzyme activity data of G6PD. (2) Among the 86 samples, Arg463His, Arg459Leu, Leu342Phe, Val291Met were the leading 4 disease-causing variants found in 72 samples (84%). (3) Male neonatal patients with the same variants had the statistically significant differences in enzyme activity: among 13 patients with Arg463His, enzyme activity of 9 patients was ranked as grade Ⅲ, 1 case ranked as Ⅳ, 3 cases had no activity data;among 10 patients with Arg459Leu, enzyme activity of 4 patients was ranked as Ⅱ, 4 cases ranked as Ⅲ, 2 cases had no activity data;among 2 patients with His32Arg, enzyme activity of one patient was ranked as Ⅱ, another was Ⅲ. Male neonatal patients with the same mutation and enzyme activity also had the statistically significant differences in phenotype spectrum: among 9 patients with Arg463His and level Ⅲ enzyme activity, 6 presented hyperbilirubinemia, 2 met the criteria for exchange transfusion therapy, 2 showed hemolysis;among 4 patients with Arg459Leu and level Ⅱ enzyme activity, 3 presented hyperbilirubinemia;among 4 patients with Arg459Leu and level Ⅲ enzyme activity, 2 presented hyperbilirubinemia, 1 met the standard of exchange transfusion therapy;among 3 patients with Val291Met and level Ⅲ enzyme activity, 1 presented hyperbilirubinemia. Conclusions: Arg463His, Arg459Leu, Leu342Phe, Val291Met were the hotspots variants for the G6PD. Patients with the same G6PD variants and sex present different phenotype, patients with the same G6PD variants, sex and enzyme activity also present different phenotype .

Nowadays, EGFR-TKIs are important treatment strategy in lung cancer, but the resistance to EGFR-TKIs remains an unsolved issue preventing the patients from further benefits. Recent studies have shown that casein kinase (CK2) plays an important role in carcinogenesis and development of cancer. CK2 inhibitor has also demonstrated anti-tumor effects. Here we reviewed the mechanism of EGFR-TKIs and the potential reasons of resistance. Interestingly, there is a crosstalk between CK2 and EGFR downstream signaling pathways, therefore, it may be possible that CK2 inhibitor can overcome the EGFR-TKIs resistance.

This review presented an introduction of the visual pathway related circadian rhythm regulation system: the intrinsically photosensitive retinal ganglion cells-suprachiasmatic nucleus-pineal gland-melatonin axis, and discussed the impact of light with different wave length and irradiation received by retina on circadian rhythm and sleep habit. A hypothesis was proposed consequently that the high morbidity of sleep disorder in elderly might be partially attributable to the long-term blue light blocking status induced by age-related cataract. A number of relative literatures were reviewed and a novel research direction was advanced on improving circadian rhythm and sleep condition in elderly based on the current knowledge. (Chin J Ophthalmol, 2016, 52: 309-314).

Objective: To explore whether quninalizarin, an specific inhibitor of protein kinase CK2, could sensitize icotinib in EGFR-TKIs (epithelial growth factor receptor-tyrosine kinase inhibitor)-resistant cell lines and uncover the underlying mechanisms., Methods: MTT assay was performed to evaluate the inhibitory effect of quninalizarin, icotinib or the combination of both on cell proliferation in several lung adenocarcinoma cell lines. Western blot assay was used to assess if combined inhibition of EGFR and protein kinase CK2 by icotinib and quninalizarin, exerts effect on the expression and phosphorylation of major proteins of EGFR signaling pathways., Results: The IC50 of HCC827, H1650, H1975 and A549 cells for icotinib were (8.07±2.00)μmol/L, (66.01±6.64)μmol/L, (265.60±9.47)μmol/L and (87.88±6.8)μmol/L, respectively, indicating that HCC827 cells are sensitive to icotinib, and the H1650, H1975 and A549 cells are relatively resistant to icotinib. When treated with both quninalizarin and icotinib in the concentration of 50 μmol/L, the viability of H1650, H1975 and A549 cells was (40.64±3.73)%, (65.74±3.27)% and (44.96±0.48)%, respectively, significantly lower than that of H1650, H1975 and A549 cells treated with 50 μmol/L icotinib alone (55.05±1.22)%, (71.98±1.60)% and (61.74±6.18)%, respectively (P<0.01 for all). When treated with both 100 μmol/L quninalizarin and 100 μmol/L icotinib, the viability of H1650, H1975 and A549 ells were (23.35±0.81)%, (55.70±1.03)%, (33.42±1.33)%, respectively, significantly lower than the viability of H1650, H1975 and A549 cells treated with 100 μmol/L icotinib alone (40.57±2.65)%, (62.40±2.05)% and (44.97±8.20)%, respectively, (P<0.01 for all). The two-way ANOVA analysis showed that compared with the viability of EGFR-TKIs-resistant cells (H1650, H1975, A549) treated with 50 μmol/L and 100 μmol/L icotinib alone, the viability of cells treated with icotinib and quinalizarin were significantly suppressed, and the differences were statistically significant (P<0.01). In addition, the phosphorylation form of Akt and ERK (namely p-Akt and p-ERK) were significantly down-regulated by treating with quninalizarin and icotinib together in the H1650 cells while the expression of Akt and ERK changed little., Conclusions: Quinalizarin, as a specific CK2 inhibitor, may overcome icotinib resistance by inhibiting proliferation mediated by Akt and ERK in human lung adenocarcinoma cell lines, and enhances the suppressive effect of icotinib on the proliferation of EGFR-TKIs-resistant human lung adenocarcinoma cells.

We recently reported that the first detectable expression of SMC-specific proteins during coronary smooth muscle cell (CoSMC) differentiation from isolated proepicardial cells was restricted to cells undergoing epithelial-to-mesenchymal transformation (EMT). The objectives of this study were to examine more closely the relation between actin cytoskeletal rearrangements and serum response factor (SRF)-dependent transcription, and to specifically test whether rhoA-GTPase signaling is required for CoSMC differentiation. We report here that PDGF-BB stimulates EMT and promotes SRF-dependent expression of SMC marker genes calponin, SM22alpha, and SMgamma(actin) (SMgammaA) in proepicardial cells. C3 exoenzyme or rhoGDI, inhibitors of rhoA signaling, blocked PDGF-BB-induced EMT, prevented actin reorganization into stress fibers, and inhibited CoSMC differentiation. Incubation with the selective p160 rho-kinase (p160RhoK) inhibitor Y27632 (RKI) blocked EMT, prevented the appearance of calponin and SMgammaA-positive cells, and abolished expression and nuclear localization of SRF. To test the role of RhoK signaling for CoSMC differentiation in vivo, quail proepicardial organs (PEOs) were pretreated with RKI or vehicle and then grafted into age-matched host chick embryos to produce a chimeric epicardium. The ability of grafted cells to participate in coronary vessel formation was monitored by staining with antibodies for quail cell nuclear antigen and SMC marker proteins. Proepicardial cells pretreated with RKI failed to form CoSMCs in vivo. Time course studies traced this deficiency to a failure of epicardial-derived mesenchymal cells to migrate into or survive within the myocardium. In summary, these data point to important roles for rhoA-RhoK signaling in molecular pathways controlling cytoskeletal reorganization, SRF-dependent transcription, and cell survival that are required to produce CoSMCs from proepicardial cells.

Clear differences exist in the incidence and severity of atherosclerotic plaques that arise in different segments of the arterial tree. Aortic homograft transplant experiments in dogs showed that the greater incidence of plaque formation in the abdominal versus the thoracic aorta was due to intrinsic differences in the cell populations in these two segments rather than to hemodynamic factors. What is the basis for SMC diversity within a common vessel wall? Recent lineage analysis studies in the avian and mammalian embryo indicate that two distinct SMC lineages contribute to the formation of the major elastic outflow arteries including the aorta. A mixture of unique SMC types of diverse developmental lineages within a common vessel wall raises new questions about the potential for SMC type-specific responses to growth factors and cytokines involved in human atherosclerosis and restenosis.

230 consecutive cases of multiple injuries (1978-1990) were evaluated retrospectively with AIS-ISS; the overall mortality was 16.96% (39 deaths); and of the 51 cases with MSOF, the mortality rate was 49% (25 deaths), It is suggested: (1) The mortality rate was directly related to ISS. In case the ISS was > 50, the mortality rate would increase in two-folds. (2) Prehospital support, intensive care, timely operation, prevention of MSOF consisted to be the crucial problems of increasing the survival rate and would be the basic factors of AIS-ISS. (3) Other factors such as patients age, delayed transport, systemic organ function, misdiagnosis, faulty management and limitation of medical facilities would all take part in the lack of efficiency of ISS.

Transcription of the narGHJI operon (encoding nitrate reductase) in Escherichia coli is primarily dependent on the activation of the pleiotropic transacting factor Fnr, which interacts with the promoter through a cis element (Fnr box) located near the transcription start site. Further stimulation of transcription occurs in the presence of nitrate and is dependent on activation of the transacting factor NarL and a cis-acting sequence (NarL box) located approximately 200 base pairs upstream from the transcription start site. To define the structure of the NarL box, alterations in the NarL box region, generated by saturation mutagenesis of the sequence from positions -184 to -202 in the narGHJI promoter of a narG::lacZ fusion-bearing plasmid, were analyzed for their effects on NarL-mediated stimulation of transcription. Single base substitutions that significantly reduced the NarL-mediated stimulation were restricted to a 6-base sequence, TACTCC, located at positions -193 to -198 in the narGHJI promoter. When 2 bases were modified, NarL-mediated stimulation was severely reduced when one or both alterations were located within the 6-base sequence. Attempts to restore NarL-mediated stimulation with an inverted NarL box were not successful. Although previous studies suggested that NarL-mediated stimulation of transcription may occur by a DNA looping mechanism, the results presented here demonstrate that it does not involve the passive formation of a simple DNA loop. Replacement of 94 or 108 bases of the approximately 150 base sequence between the Fnr box and the NarL box with an unrelated sequence resulted in elimination of NarL-mediated stimulation of transcription. Furthermore, shifting of most of the intervening sequence or defined segments of the sequence by 4 bases while maintaining the position of the NarL box relative to sequences required for Fnr-dependent, anaerobic transcription also eliminated the NarL-mediated stimulation. We conclude that in addition to the 6-base NarL box located on a specific face of the promoter DNA, the stimulation of transcription by NarL requires some specific sequences and/or higher order structure specified by the DNA that separates the NarL box from the Fnr box.