Clinical Characteristics and Risk Factors of Nosocomial Infection in 472 Patients with Non-Hodgkin Lymphoma / 中国实验血液学杂志

OBJECTIVE@#To investigate the clinical characteristics and risk factors of nosocomial infection in patients with non-Hodgkin lymphoma (NHL), in order to guide better clinical prevention and treatment of nosocomial infection.@*METHODS@#The incidence of nosocomial infection, infection site, characteristics of pathogenic bacteria, drug sensitivity test results and infection risk factors of 472 non-Hodgkin lymphoma patients admitted to the Second Affiliated Hospital of Fujian Medical University from January 2015 to September 2020 were retrospectively analyzed.@*RESULTS@#Among the 472 patients, 97 (20.6%) had nosocomial infection, mainly in the lower respiratory tract (41.2%), followed by oral cavity, upper respiratory tract, urogenital tract, and blood. A total of 71 strains of pathogenic bacteria were isolated, including Gram-negative (G@*CONCLUSION@#NHL patients show high nosocomial infection rate and lower respiratory tract infection is common. Hospital day, clinical stage, presence of bone marrow invasion, and neutrophil count in peripheral blood are independent risk factors.

Advances in the study of p53 in response to DNA damage / 药学学报

p53 (encoded by TP53) is undoubtedly one of the most extensively studied genes and proteins. It is a highly potent transcription factor which, under normal circumstances, is maintained at low level. Both genotoxic and non-genotoxic stresses can induce p53 stabilized leading to changes in the expression of p53-responsive genes. The biological outcome inducing this pathway can be either growth arrest and apoptosis or senescence to maintain the integrity of the genome or to delete the damaged cells. The biochemical activity of p53 itself and the cellular environment govern the choice between these outcomes in a cell type- and stress-specific manner. So, p53 is a pivotal tumour suppressor and a mainstay of our body's natural anticancer defence. This review could provide some useful information for further study on the mechanisms of tumorigenesis and its progression, and also could contribute to the discovery of antitumor agents.

Neurodegenerative conformational disease and heat shock proteins / 药学学报

Many major neurodegenerative diseases are associated with proteins misfolding and aggregation, which are also called "neurodegenerative conformational disease". The interaction of gene mutation and environmental factors are probably primary events resulting in oligomer and aggregate formations of proteins. Moreover, the dysfunctions of protein control systems, i.e. the ubiquitin-proteasome system and autophagy-lysosomal system, also contribute to the neurodegenerative process. The present review mainly summarizes protein misfolding and aggregation in the development of neurodegenerative conformational disease and the underling mechanisms, as well as upregulation of heatshock proteins as a promising treatment method for this kind of disease.

The role of vitagene in aging and Alzheimer's disease and relevant advances of pharmacological study / 药学学报

Free radical hypothesis of aging emphasized that the age-related accumulation of free radicals results in cell injury. Alzheimer's disease (AD) is the most common form of neurodegenerative disease characterized by impaired cognition and memory of the elderly. Aging is a key risk factor in AD. Substantial evidence suggests that imbalance between free radical formation and clearance promotes AD pathogenesis. The brain overcomes oxidative stress by inducing expression of a set of genes called vitagenes. The protein products of vitagenes include heat shock proteins, heme oxygenases and thioredoxin systems, which serve as endogenous lifeguard of cells. This paper is a review of the expression and function of vitagenes in aging and AD brain, as well as relevant pharmacological study.

Association of gene polymorphism in promoter region of adiponectin gene and carotid artery intima-media thickness in patients with type 2 diabetes mellitus of Fujian / 中华内分泌代谢杂志

Objective To explore the association of-11377 site single nucleotide polymorphism in promoter region of adiponectin gene and carotid intima-media thickness(CIMT)in patients with type 2 diabetes mellitus.Methods The adiponectin gene-11377C→G polymorphism was identified by PCR-restriction fragment length polymorphism(RFLP)in 504 patients with type 2 diabetes mellitus(250 patients with increased CIMT and254 Datients with normal CIMT). Serum lipid and fasting plasma glucose were detected by full automatic biochemical analysor.fasting serum insulin(FINS) was measured by radioimmunoassay,and serum adiponectin level was assessed by ELISA.Results The frequencies of adiponectin gene-11377C→G genotype and allele were different between type 2 diabetic patients with normal and increased CIMT(P<O.01).In type 2 diabetic patients, the values of CIMT,diastolic blood pressure,low-density lipoprotein cholesterol (LDL-C)and homeostasis model assessment of insulin resistance (HOMA-IR) in-11377CC group were significantly lower than those in-11377CG +GG group(P<0.05 or P<O.01),but serum adiponectin level was higher in-11377CC group than that in -11377CG+GG group [(5.70 ±3.58 vs 4.72±2.34)mr/L,P<O.01].Variation at adiponectin gene-11377C→G was associated with increased CIMT in type 2 diabetic patients independent of serum adiponectin level(P= 0.037).Conclusion In type 2 diabetic patients of Fujian,the-11377C→G polymorphism of the adiponectin gene is associated with CIMT.

Effect and mechanism of Coeloglossum viride var. bracteatum extract on scopolamine-induced deficits of learning and memory behavior of rodents / 药学学报

The aim of the present study is to investigate the effect and mechanism of Coeloglossum viride var. bracteatum extract (CE) on scopolamine-induced learning and memory deficits. Learning and memory deficits of mice were evaluated by step-down passive avoidance test. Long-term potentiation of rats was detected in the dentate gyrus of hippocampus. Brain acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) activities were also determined. The results showed that scopolamine impaired learning and memory performance and LTP induction in hippocampus. Oral administration of CE (5, 10, and 20 mg x kg(-1)) significantly alleviated scopolamine-induced memory deficits measured by step-down test (P < 0.05). CE (5 mg x kg(-1), ip) significantly reversed the inhibitory effect of scopolamine on LTP in rats. In addition, CE was found to increase the activity of ChAT in rat brain. These results suggested that CE could alleviate scopolamine-induced learning and memory deficits, which might be due to the LTP-improvement and ChAT activity enhancement.

The roles of Kupffer cells in the development and regression of liver fibrosis / 药学学报

Hepatic fibrosis results from iterative hepatic injury with sustained inflammation, formation of scar tissue, loss of tissue architecture and organ failure. There is no doubt, from both human and animal studies, that too much or too protracted inflammation in the liver leads to excess scarring. During liver injury, Kupffer cells can quickly flood the hepatic milieu with soluble mediators, including oxidants, cytokines, and proteinases, which can affect stellate cell proliferation, migration, and differentiation. On the other hand, the contribution of Kupffer cells to regression of hepatic fibrosis has been demonstrated. These findings underscore the potential importance of hepatic macrophages in regulating both stellate cell biology and extracellular material degradation during regression of hepatic fibrosis. Therefore, biological characterization of Kupffer cells, their interactions with stellate cells in the cytokine environment are essential to understand the mechanisms underlying the progressive development of excessive scarring in the liver as well as the ability of the liver for tissue repair and recovery.

Biology of thioredoxin and its association with Alzheimer's disease and Parkinson's disease / 药学学报

Thioredoxin (Trx) is a crucial protein for antioxidative defense, as well as a redox regulator of the intra- and extracellular signaling pathways and transcription factors. In this review, we focus on mammalian Trx and its association with Alzheimer's disease (AD) and Parkinson's disease (PD). Based on the evidence of neuroprotective effects of Trx, up-regulation of Trx may be a good strategy for prevention and treatment of AD and PD.

Heat shock proteins: new target in cytoprotective and tumor therapy / 药学学报

Heat shock proteins (HSPs) form the most ancient defense system in all living organisms. These proteins act as molecular chaperones by helping the refolding of misfolded proteins and assisting their elimination if they become irreversibly damaged. HSPs interact with a number of cellular systems and form efficient cytoprotective mechanisms. HSPs allow cells to adapt to gradual changes in their environment and to survive in otherwise lethal conditions. The events of cell stress and cell death are linked, and HSPs induced in response to stress appear to function at key regulatory points in the control of apoptosis. HSPs include antiapoptotic and proapoptotic proteins that interact with a variety of cellular proteins. Their expression levels can determine the fate of the cell in response to death stimulus. On the other hand, HSPs are overexpressed in tumor cells, and the inhibition of HSP90 has recently been regarded as a very promising tool to combat various cancers. HSPs can be secreted to circulatory system from a variety of cell types in response to stress. The secreted exogenous proteins act as cytokines and have potential modulatory functions in immune system. Cell surface-bound HSP70 can render tumor cell more sensitive to natural killer cell-mediated cytolytic attack. Therefore, modulator of chaperone activities is becoming a new target of drug development, such as in apoptosis and tumor immunity fields.

Therapeutic evaluation of gliclazide-MR on blood glucose excursion by self-monitoring of blood glucose in type 2 diabetic patients / 中华内分泌代谢杂志

A total of 123 type 2 diabetics was randomised into 3 groups to receive gliclazide-MR, gliclazide or glibenclamide treatments for 16 weeks.All the subjects took self-monitoring of blood glucose (SMBG) during the trial.The effect of therapy was similar in 3 groups.The subtraction value between maximum and minimum blood glucose, mean postprandial maximum blood glucose, postprandial 2 h blood glucose, postprandial 2 h serum insulin and hypoglycaemia events were lower in gliclazide-MR group than those in glibenclamide group (all P＜0.01).The data suggest that SMBG is an useful method to evaluate blood glucose excursion.

Protective action of ulinastatin against lipopolysaccharides-induced acute lung injury in mice and the relation of it to iNOS and c-Jun expressions / 药学学报

<p><b>AIM</b>To study the protective action of ulinastatin against lipopolysaccharide (LPS)-induced acute lung injury in mice and the mechanism of its action.</p><p><b>METHODS</b>Mice were intraperitoneally injected with ulinastatin (50 and 100 ku x kg(-1)) or saline at a period of 12 h, separately, 30 min after the last injection of ulinastatin, except normal control, all mice of other groups were injected a dose of LPS 15 mg x kg(-1) via tail vein. The levels of TNFalpha in serum and lung were measured by ELISA. The expression of TNFalpha mRNA and iNOS mRNA in lung was assayed by RT-PCR. The expression of c-Fos and c-Jun protein in lung was measured by Western blotting method. And the NO2- / NO3- level in serum and MDA in lung were measured with kits.</p><p><b>RESULTS</b>The levels of NO2- / NO3- and TNFalpha in serum, MDA and TNFa in lung all increased after iv injection of LPS. The expressions of TNFa mRNA, iNOS mRNA, c-Fos and c-Jun in lung of LPS-injected mice were enhanced. Pretreatment with ulinastatin 100 ku x kg(-1) decreased the levels of NO2- / NO3- in serum and lung, reduced the index of lung, and inhibited the expressions of iNOS mRNA and c-Jun in lung induced by LPS in mice, while ulinastatin showed no effect on TNFa level in serum and lung.</p><p><b>CONCLUSION</b>Ulinastatin protected mice from acute lung injury induced by lipopolysaccharides via inhibiting the activation of c-Jun and iNOS mRNA expression.</p>

Xanthones from Tibetan medicine Halenia elliptica and their antioxidant activity / 中国医学科学院学报

<p><b>OBJECTIVE</b>To investigate the xanthones from Tibetan medicine Halenia elliptica and their antioxidant activity.</p><p><b>METHODS</b>Column chromatography over normal phase silica gel, reversed phase silica gel, Sephadex LH-20, and recrystallization techniques were used to isolate and purify constituents from Halenia elliptica. Infrared spectrometry, mass spectrometry, and nuclear magnetic resonance spectrometry were used to identify the structure of compounds. The antioxidant activity was evaluated by measuring the content of malondialdehyde product in mice liver cell microsomal induced by ferrous-cysteine.</p><p><b>RESULTS</b>Eight xanthones (compound I-VIII) were isolated and identified from the ethyl acetate extract of Halenia elliptica, among which 1,7-dihydroxy-2,3,5-trimethoxyxanthone was a novel compound. Compound I, III at 10 microg/ml and 100 microg/ml could inhibit the production of malondialdehyde in mouse liver microsomes in vitro.</p><p><b>CONCLUSION</b>Eight xanthones were isolated and they have certain antioxidant activity.</p>

Synthesis and antioxiactivity of squamosamide cyclic analogs / 中国医学科学院学报

<p><b>OBJECTIVE</b>To design and synthesize a series of squamosamide cyclic analogues and to test their antioxidation activity.</p><p><b>METHODS</b>Eleven 3-substituted indole-2-one derivatives were designed and synthesized through 9 steps with p-hydroxyphenylacetic acid as the starting material and their structures were confirmed by nuclear magnetic resonance and mass spectrometry.</p><p><b>RESULTS</b>Eleven compounds showed antioxidation activity and the activities of compounds 9 and 13 matches the positive control FLZ-52.</p><p><b>CONCLUSION</b>Cyclic reconstruction with FLZ-52 as the lead compound have some antioxidation activity.</p>

Damaging effect of cigarette smoke extract on primary cultured human umbilical vein endothelial cells and its mechanism / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the cellular effects of cigarette smoke extract (CSE) on primarily cultured human umbilical vein endothelial cells (HUVEC).</p><p><b>METHODS</b>The effects of CSE (5%-20%) and nicotine (10(-4) mol/L) on HUVEC viability, proliferation, angiogenesis and apoptosis were observed.</p><p><b>RESULTS</b>CSE decreased HUVEC survival rate and angiogenesis after 24 h as well as its proliferation after 48 h in a dose-dependent manner. Moreover, CSE induced apoptosis of HUVEC as indicated in condensation of nuclear chromatin and the presence of hypodiploid DNA. HUVEC incubated with CSE for 24 h gave a significant decrease in the expression of Bcl-2 as well as the decline in the Bcl-2/Bax ratio accompanied with the loss of mitochondrial membrane potential and excess cytosolic calcium. Our study also observed that p53 protein level decreased, rather than increased in cells treated with CSE. Nicotine had no discernible inhibitory effects on the above indices of HUVEC.</p><p><b>CONCLUSION</b>Exposure to CSE other than nicotine causes inhibition of viability, proliferation and differentiation of HUVEC. CSE-induced HUVEC injury is mediated in partthrough accelerated apoptosis but independent of p53 pathway. It appears that mitochondria have played a key role in the apoptosis of HUVEC induced by CSE.</p>

Injury of mouse brain mitochondria induced by cigarette smoke extract and effect of vitamin C on it in vitro / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the toxicity of cigarette smoke extract (CSE) and nicotine on mouse brain mitochondria as well as the protective effect of vitamin C in vitro.</p><p><b>METHOD</b>Mouse brain mitochondria in vitro was incubated with CSE or nicotine in the absence or presence of vitamin C for 60 minutes, and the changes of mitochondrial function and structure were measured.</p><p><b>RESULTS</b>CSE inhibited mitochondrial ATPase and cytochrome C oxidase activities in a dose-dependent manner. However, no significant changes in the peroxidation indices were observed when mitochondrial respiratory enzymes activity was inhibited, and protection of mitochondria from CSE-induced injury by vitamin C was not displayed in vitro. The effect of CSE on mouse brain mitochondria swelling response to calcium stimulation was dependent on calcium concentrations. CSE inhibited swelling of mitochondria at 6.5 mumol/L Ca2+, but promoted swelling response at 250 mumol/L Ca2+. Nicotine, the major component of cigarette smoke, showed no significant damage in mouse brain mitochondria in vitro. The CSE treatment induced mitochondrial inner membrane damage and vacuolization of the matrix, whereas the outer mitochondrial membrane appeared to be preserved.</p><p><b>CONCLUSION</b>The toxic effect of CSE on brain mitochondria may be due to its direct action on enzymatic activity rather than through oxygen free radical injury. Nicotine is not the responsible component for the toxicity of CSE to brain mitochondria.</p>

Inhibition of human low-density lipoprotein oxidation by salvianolic acid-A / 药学学报

<p><b>AIM</b>Oxidized low-density lipoprotein (LDL) is involved in the development of atherosclerosis. Oxidative modulation of serum LDL is related to oxygen free radicals. Antioxidants have beneficial effects on oxidative modulation of LDL and development of atherosclerosis. Salvia miltriorhiza (Danshen) preparations have been widely used in the treatment of cardio-cerebral vascular diseases in China. Salvianolic acid A (Sal-A), one of the components of Salvia miltriorhiza, was shown to have strong antioxidative activity. The aim of this investigation was to evaluate the effect of Sal-A on human LDL oxidative modulation mediated by copper ions.</p><p><b>METHODS</b>Oxidation of human LDL was performed in pH 7.4 phosphate-buffered saline with 10 mumol.L-1 CuSO4 at 37 degrees C water for 20 h. The content of malondialdehyde (MDA), lipofuscin and vitamin E in LDL as well as the rate of electrophoretic mobility (REM) of LDL were measured. The generation of free radicals during LDL oxidation was detected by low level-chemiluminescence (LL-CL). The chelation of Cu2+ by Sal-A was detected by UV-spectrum scanning.</p><p><b>RESULTS</b>Sal-A (10(-6) to 10(-4) mol.L-1) was shown to markedly reduce the production of MDA and lipofuscin as well as the consumption of vitamin E during LDL oxidation. Sal-A (10(-4) mol.L-1) was also shown to inhibit the increase of REM of LDL caused by oxidative modification. In addition, the spectrum of LL-CL showed that Sal-A (10(-6) to 10(-5) mol.L-1) decreased the generation of free radicals during LDL oxidation in a dose dependent manner. The differential UV-spectrum of Sal-A in the presence of Cu2+ indicated that Sal-A could chelate copper ions.</p><p><b>CONCLUSION</b>Sal-A has inhibitory effect on Cu2+ mediated human LDL oxidation through chelating Cu2+ and scavenging free radicals.</p>

Endogenous subclinical hyperthyroidism: needs it to be intervened? / 中华内分泌代谢杂志

Objective To explore the effects of subclinical hyperthyroidism (SH) on heart and bone and the optionof treatment. Methods Forty-three patients with endogenous SH were divided into two groups by the TSH level: group A (21 cases,TSH 0.03-0.60 mIU/L) and group B (22 cases, TSH