Thank you for downloading using multivariate statistics. As you may know, people have look hundreds times for their favorite novels like this using multivariate statistics, but end up in infectious downloads. Rather than reading a good book with a cup of tea in the afternoon, instead they juggled with some harmful bugs inside their laptop. using multivariate statistics is available in our digital library an online access to it is set as public so you can download it instantly. Our books collection saves in multiple locations, allowing you to get the most less latency time to download any of our books like this one. Merely said, the using multivariate statistics is universally compatible with any devices to read.

Using Multivariate Statistics

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

https://biblio.ugent.be/publication/8555786/file/8555788.pdf

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

中枢神経系疾患の治療は正常細胞（ニューロン）の機能維持を目的とするが，脳血管障害のように機能障害の原因が細胞の死滅に基づくことは多い．一方，脳腫瘍の治療においては薬物療法や放射線療法といった腫瘍細胞の死滅を目標とするものが大きな位置を占める．いずれの場合にも，細胞死の機序を理解することは各種病態や治療法の理解のうえで重要である．現在のところ最も研究の進んでいる細胞死の型はアポトーシスである．そのなかで重要な位置を占めるミトコンドリアにおける反応および抗アポトーシス因子について概要を紹介する．

Neuroscience 細胞死：最近の知見

In 2009, the Nomenclature Committee on Cell Death (NCCD) proposed a set of recommendations for the definition of distinct cell death morphologies and for the appropriate use of cell death-related terminology, including 'apoptosis', 'necrosis' and 'mitotic catastrophe'. In view of the substantial progress in the biochemical and genetic exploration of cell death, time has come to switch from morphological to molecular definitions of cell death modalities. Here we propose a functional classification of cell death subroutines that applies to both in vitro and in vivo settings and includes extrinsic apoptosis, caspase-dependent or -independent intrinsic apoptosis, regulated necrosis, autophagic cell death and mitotic catastrophe. Moreover, we discuss the utility of expressions indicating additional cell death modalities. On the basis of the new, revised NCCD classification, cell death subroutines are defined by a series of precise, measurable biochemical features.

/pdf/molecular-definitions-of-cell-death-subroutines-q5g428rlyi.pdf

Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012

(Macro)autophagy is a bulk degradation process that mediates the clearance of long-lived proteins and organelles. Autophagy is initiated by double-membraned structures, which engulf portions of cytoplasm. The resulting autophagosomes ultimately fuse with lysosomes, where their contents are degraded. Although the term autophagy was first used in 1963, the field has witnessed dramatic growth in the last 5 years, partly as a consequence of the discovery of key components of its cellular machinery. In this review we focus on mammalian autophagy, and we give an overview of the understanding of its machinery and the signaling cascades that regulate it. As recent studies have also shown that autophagy is critical in a range of normal human physiological processes, and defective autophagy is associated with diverse diseases, including neurodegeneration, lysosomal storage diseases, cancers, and Crohn's disease, we discuss the roles of autophagy in health and disease, while trying to critically evaluate if the coincidence between autophagy and these conditions is causal or an epiphenomenon. Finally, we consider the possibility of autophagy upregulation as a therapeutic approach for various conditions.

https://www.physiology.org/doi/pdf/10.1152/physrev.00030.2009

Regulation of Mammalian Autophagy in Physiology and Pathophysiology

As a basic syndrome of Chinese medicine, the study of characteristic syndrome spectrum of Qi deficiency syndrome is of great significance for the standardization of clinical diagnosis and modern material basis research. Suitable operators and algorithms were chosen to dig out the relationship between diseases, syndromes, symptoms, detection indicators and etiologist from the literature of Chinese clinical and basic research by literature mining method of frequency statistics, association rules and complex network analysis. Moreover, the information system of Institute of Information on Traditional Chinese Medicine, China Academy of Chinese Medical Sciences was taken as the tools of data mining. The objective was to study the characteristic spectrum of Qi deficiency syndrome and to explore the characteristics of Qi deficiency syndrome. The results showed that the syndrome of fatigue, dietary were the main factors. The main pathogenesis of coronary heart disease, heart failure, chronic obstructive pulmonary disease, diabetes and stroke the disease were Qi deficiency. The clinical features of Qi deficiency syndrome were fatigue, shortness of breath and pale tongue. The biological indicators of Qi deficiency related were blood lipids, ECG, blood rheology, inflammatory reaction, NO, ET and NF-κB signalling pathway. The Qi deficiency syndrome on the level of syndrome spectrum was studied by the method of literature mining, which would provide reliable characteristic guidance data for the research on the substantial basis of Qi deficiency, the research on standard of diagnosis, establishment of syndrome model, the study on combination of disease and syndrome and the mechanism of prescriptions.

Research of characteristic spectrum of Qi deficiency syndrome based on literature mining technology

OBJECTIVE To observe the protective effect of serum containing Tanyu Tongzhi formula (TYTZF) on ox-LDL-induced human umbilical vein endothelial cells (HUVECs) injury and detect its mechanism on anti-artherosclerosis. METHOD HUVECs were pretreated with serum containing TYTZF and simvastatin respectively for 2 hours and then added with 100 mg x L(-1) of ox-LDL and laid aside for 24 hours. The activity of HUVECs were measured by the methyl thiazolyl tetrazolium (MTF) method and the NO content in cell culture supernatants were examined by the Griess method. The mRNA levels of Cav-1 and eNOS were measured by the Real-time PCR method. The protein expression of Cav-1 and eNOS were detected by Western blotting. RESULT The activity of HUVECs was significantly decreased after ox-LDL treatment (P < 0.01) and this decrease was significantly inhibited by serum containing TYTZF and simvastatin of different doses (P < 0.05). They could enhance the NO content in cell culture supernatants, down-regulate the expression of Cav-1 and up-regulate the expression of eNOS at mRNA and protein levels, which was especially notable after treatment with serum containing TYTZF and simvastatin in large doses. CONCLUSION TYTZF has the protective effect on HUVECs by increasing the production of NO and up-regulating Cav-1 expression and down-regulating eNOS expression.

[Effects of serum containing Tanyu Tongzhi formula on production of NO, caveolin-1 and eNOS in HUVECs injured by ox-LDL].

OBJECTIVE Animal model of Qi deficiency and blood stasis was established by muti-factor stimulation in rats. METHOD Healthy SD rats were chronically stimulated randomly by muti-factor methods (chronic sleep deprivation and feed with moderately high lipid and sugar food). Then the indices of hemorheology, plasma total lipids, vasoactive molecules, blood pressure (BP) and ventricular pressure (VP) were measured. RESULT The results as well as the analysis of etiology and pathology suggested that model rats could objectively reflect the clinical characteristics of Qi deficiency and blood stasis syndrome. Blood viscosity at low level, plasma content of angiotensin II (Ang II) and endothelin (ET) significantly increased in model rats, while BP and VP significantly decreased (P < 0.05). On the other hand, Buyang Huanwu decoction could lower down the level of AngII in serum and blood viscosity at low level in rats induced by some stimulus, whereas BP and VP elevated significantly (P < 0.05). CONCLUSION Animal model of Qi deficiency and blood stasis induced by muti-factor stimulation including chronic sleep deprivation and feed with moderately high lipid and sugar food could facilitate further study on blood stasis syndrome and screening of Chinese herbal drugs in promoting blood circulation and removing blood stasis.

[Experimental study on Qi deficiency and blood stasis induced by muti-factor stimulation in rats].

[A study of antitumor chemotherapeutic agents -synthesis of cantharidine derivatives (author's transl)].

Myocardial ischemia is a pathological state of heart with reduced blood flow to heart and abnormal myocardial energy metabolism. This disease occurs commonly in middle aged and elderly people. Several studies have indicated that the rat was an appropriate animal model used to study myocardial ischemia. In this study, in order to gain insights into the pathogenesis of myocardial ischemia, we sequenced the transcriptomes of three normal rats as control and the same number of myocardial ischemia rats. We sequenced the genomes of 6 rats, including 3 cases (myocardial ischemia) and 3 controls using Illumina HiSeq 2000. Then we calculated the gene expression values and identified differentially expressed genes based on reads per kilobase transcriptome per million (RPKM). Meanwhile we performed a GO enrichment analysis and predicted novel transcripts. In our study, we found that 707 genes were up-regulated and 21 genes were down-regulated in myocardial ischemia rats by at least 2-fold compared with controls. By the distribution of reads and the annotation of reference genes, we found 1,703 and 1,552 novel transcripts in cases and controls, respectively. At the same time, we refined the structure of 9,587 genes in controls and 10,301 in cases. According to the results of GO term and pathway analysis of differentially expressed genes, we found that the immune response, stimulus response, response to stress and some diseases may be associated with myocardial ischemia. Since many diseases, especially immune diseases, are associated with myocardial ischemia, we should pay more attention to the complications which might result from myocardial ischemia.

/pdf/transcriptomic-analysis-of-myocardial-ischemia-using-the-2m31qxvzqv.pdf

Jian-Xun Liu

Papers

Research of characteristic spectrum of Qi deficiency syndrome based on literature mining technology

[Effects of serum containing Tanyu Tongzhi formula on production of NO, caveolin-1 and eNOS in HUVECs injured by ox-LDL].

[Experimental study on Qi deficiency and blood stasis induced by muti-factor stimulation in rats].

[A study of antitumor chemotherapeutic agents -synthesis of cantharidine derivatives (author's transl)].

Transcriptomic Analysis of Myocardial Ischemia Using the Blood of Rat