Immunoglobulin has been widely used in a variety of diseases, including primary and secondary immunodeficiency diseases, neuromuscular diseases, and Kawasaki disease. Although a large number of clinical trials have demonstrated that immunoglobulin is effective and well tolerated, various adverse effects have been reported. The majority of these events, such as flushing, headache, malaise, fever, chills, fatigue and lethargy, are transient and mild. However, some rare side effects, including renal impairment, thrombosis, arrhythmia, aseptic meningitis, hemolytic anemia, and transfusion-related acute lung injury (TRALI), are serious. These adverse effects are associated with specific immunoglobulin preparations and individual differences. Performing an early assessment of risk factors, infusing at a slow rate, premedicating, and switching from intravenous immunoglobulin (IVIG) to subcutaneous immunoglobulin (SCIG) can minimize these adverse effects. Adverse effects are rarely disabling or fatal, treatment mainly involves supportive measures, and the majority of affected patients have a good prognosis.

Cerebral venous thrombosis (CVT), also called cerebral venous sinus thrombosis (CVST), is a cerebrovascular disease with diverse clinical manifestations that often affects young adults, women of childbearing age, and children. It's most common clinical manifestations are headache, seizures, altered consciousness, and neurological focal signs on physical examination. CVT can manifest as a single symptom, or it can present as a syndrome consisting of multiple symptoms. This non-specific clinical picture makes diagnosing CVT difficult. Although the mortality rate of CVT has been significantly reduced by improvements in treatment and diagnostic techniques, the mortality rate of severe CVT remains as high as 34.2%. Survivors of this type of CVT have varying degrees of residual symptoms and are not able to return to their previous work. Hence, we performed a comprehensive literature search in the PubMed, EMBASE, and Medline databases to review the diagnosis and treatment of CVT.

It is often alleged that mutations conferring herbicide resistance have a negative impact on plant fitness. A mutant ACCase1781 allele endowing resistance to the sethoxydim herbicide was introgressed from a resistant green foxtail (Setaria viridis (L.) Beauv) population into foxtail millet (S. italica (L.) Beauv.). (1) Better and earlier growth of resistant plants was observed in a greenhouse cabinet. (2) Resistant plants of the advanced BC7 backcross generation showed more vigorous juvenile growth in the field, earlier flowering, more tillers and higher numbers of grains than susceptible plants did, especially when both genotypes were grown in mixture, but their seeds were lighter than susceptible seeds. (3) Field populations originating from segregating hybrids had the expected allele frequencies under normal growth conditions, but showed a genotype shift toward an excess of homozygous resistant plants within 3 years in stressful conditions. Lower seed size, lower germination rate and perhaps unexplored differences in seed longevity and predation could explain how the resistant plants have the same field fitness over the whole life cycle as the susceptible ones although they produce more seeds. More rapid growth kinetics probably accounted for higher fitness of the resistant plants in adverse conditions. The likelihood of a linkage with a beneficial gene is discussed versus the hypothesis of a pleiotropic effect of the ACCase resistance allele. It is suggested that autogamous species like Setaria could not develop a resistant population without the help of a linkage with a gene producing a higher fitness.

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Adolescent suicide behaviour should be a serious problem. Measures can be taken to prevent suicide by observing the factors significantly linked to suicidal behaviour. Steps can then be taken to identify adolescents who have serious suicidal ideation so that intervention can be taken to reduce the suicidal rate.

BackgroundPim-1 kinase is a proto-oncogene and its dysregulation contributes to tumorigenesis and progression of a variety of malignancies. Pim-1 was suggested as a therapeutic target of cancers. The functional relevance of Pim-1 and the mechanism underlying its dysregulation in lung tumorigenesis remained unclear. This study aimed to investigate if Pim-1 has important functions in non-small-cell lung cancer (NSCLC) by: 1) evaluating the clinicopathologic significance of Pim-1 through analysing its expression in 101 human NSCLCs tissues using quantitative PCR, Western Blot and immunohistochemical studies, 2) determining its role in NSCLC and drug resistance using in vitro assays, and 3) investigating the regulatory mechanism of Pim-1 dysregulation in lung tumorigenesis.ResultsPim-1 was upregulated in 66.2% of the lung tumor tissues and its expression was significantly related to advanced stage (P = 0.019) and lymph node metastasis (P = 0.026). Reduced Pim-1 expression suppressed NSCLC cell growth, cell cycle progression and migration in vitro. Pim-1 was a novel target of miR-486-5p determined by luciferase report assay, and ectopic miR-486-5p expression in cancer cells reduced Pim-1 expression. Furthermore, eukaryotic translation initiation factor 4E (eIF4E) controlled the synthesis of Pim-1 in NSCLC cells, and its expression was positively associated with that of Pim-1 in NSCLC tissue specimens (r = 0.504, p < 0.001). The downregulated miR-486-5p and upregulated eIF4E in NSCLC cells led to the overexpression of Pim-1 by relieving the inhibitory effect of the 3′-UTR or 5′-UTR of Pim-1 mRNA, respectively. Moreover, Pim-1 knockdown sensitized NSCLC cells to cisplatin and EGFR tyrosine kinase inhibitor, gefitinib.ConclusionsPim-1 kinase could be a critical survival signaling factor in NSCLC, and regulated by miR-486-5p and eIF4E. Pim-1 kinase may provide a potential target for diagnosis and treatment for lung cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/1476-4598-13-240) contains supplementary material, which is available to authorized users.

GPR40 modulates epileptic seizure and NMDA receptor function through the regulation of NR2A and NR2B surface expression.

Alzheimer's disease (AD) is one of the most common causes of neurodegenerative diseases in the elderly. The accumulation of amyloid‐β (Aβ) peptides is one of the pathological hallmarks of AD and leads to the impairments of synaptic plasticity and cognitive function. The transient receptor potential vanilloid 1 (TRPV1), a nonselective cation channel, is involved in synaptic plasticity and memory. However, the role of TRPV1 in AD pathogenesis remains largely elusive. Here, we reported that the expression of TRPV1 was decreased in the brain of APP23/PS45 double transgenic AD model mice. Genetic upregulation of TRPV1 by adeno‐associated virus (AAV) inhibited the APP processing and Aβ deposition in AD model mice. Meanwhile, upregulation of TRPV1 ameliorated the deficits of hippocampal CA1 long‐term potentiation (LTP) and spatial learning and memory through inhibiting GluA2‐containing α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptor (AMPAR) endocytosis. Furthermore, pharmacological activation of TRPV1 by capsaicin (1 mg/kg, i.p.), an agonist of TRPV1, dramatically reversed the impairments of hippocampal CA1 LTP and spatial learning and memory in AD model mice. Taken together, these results indicate that TRPV1 activation effectively ameliorates cognitive and synaptic functions through inhibiting AMPAR endocytosis in AD model mice and could be a novel molecule for AD treatment.