Sepsis and septic shock are common critical diseases in the ICU, which have a high mortality and seriously affect the patients'' quality of life.The pathogenesis of sepsis is very complicated and involves the changes in the functions of multiple systems and organs.Recently, the investigation into the potential mechanisms underlying the development of sepsis is becoming a hotspot all over the world.The author presents an overview on the advances in the studies of the pathogenesis of sepsis, relating to the imbalance of inflammatory response, immune dysfunction, abnormal blood coagulation, nerve-endocrine-immunity network, mitochondrial function damage, endoplasmic reticulum stress, autophagy, and genetic polymorphism, in order to provide some theoretical evidence for the prevention and treatment of sepsis in clinical practice.

BACKGROUND: Resistin is an adipocyte-derived polypeptides. While central obesity can result in insulin resistance and type 2 diabetes mellitus.OBJECTIVE: To compare the expression of resistin protein in subcutaneous adipose tissue of normal human abdominal and thigh, and to investigate the role of resistin in central obesity bringing insulin resistance.DESIGN: Controlled observational experiment.SETTING: Department of Endocrinology, Tongji Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology.PARTICIPANTS: Totally 20 patients hospitalized between January and April 2003 at the Department of Surgery of Tongji Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology were selected. All cases were divided into abdominal fat group with 12 cases and thigh fat group with 8 cases based on the site of fat tissue.METHODS: ①Blood pressure, height, body mass were measured and body mass index (BMI), percentage of body fat (BF%) in vivo (according to formulas induced by data from white people) were calculated: Male=1.2×body mass (kg)+height-2 (M-2)+0.23×age-16.2; Female =1.2× body mass (kg)×height-2 (m-2)+0.23×age-5.4. ②Fasting blood glucose was measured with glucose oxidase assay. ③Protein was isolated with lysis buffer and protein concentration was identified with Bradford method; The expression of resistin protein was measured with Western-blot method.MAIN OUTCOME MEASURES: Blood pressure, BMI, BF%; fasting blood glucose and expression of resistin protein of all cases of the two groups.RESULTS: Totally 20 patients were involved the result analysis. ①There were no significant difference in fast blood glucose, systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index (BMI) and BF%between two groups (P ＞ 0.05). ②Expression levels (A) of resistin protein in abdominal subcutaneous adipose tissues was (14 942±6 076), which was more higher than that in thigh subcutaneous adipose tissues (39 421±6 087). There was markedly significant difference (P ＜ 0.01).CONCLUSION: The expression of resistin protein is much greater in abdominal fat depots than in thigh fat depots, which has evaluative value for studying the episode of central obesity-induced insulin resistance and type 2 diabetes mellitus.

Aim To study the active constituents for the treatment of rheumatoid arthritis from the ethyl acetate extracts of the roots of Lasianthus acuminatissimus Merr. Methods Various chromatographic techniques were used to separate and purify the constituents. Their structures were established on the basis of 1D, 2D NMR and HRMS spectroscopic analyses and their preliminary evaluation of anti-inflammation effect on the release of β-glucuronidase was carried out. Results Eight compounds were isolated and identified as lasianthuslactone A ( 1 ) , codonolactone ( 2 ), 2, 5-dimethoxy-1,4-benzoquinone ( 3 ) ,uncargenin A (4) , nonadecyl alcohol (5) , 13-docosenoic acid (6) , tetracosanoic acid (7) and β-sitosterol (8). Compound 3 showed a significant inhibitory effect on release of β-glucuronidase rat polymorphous nuclear leukocytes activated by platelet activating factor (PAF). Conclusion Compound 1is a new one, the others were isolated from the plant for the first time and 3 is one of active antiinflammation compound in the plant.

Objective To investigate the effect of inhibition of endoplasmic reticulum stress (ERS) in ischemic preconditioning-induced cerebral ischemia tolerance.Methods A total of 120 adult male SpragueDawley rats were randomly allocated into three groups:sham operation,global cerebral ischemic and ischemic preconditioning groups (ischemic preconditioning for 3 minutes,and global cerebral ischemia for 15 minutes after 2 days).Three time points (day 1,day 3 and day 7) were set.Sugawara method was used to observe the changes of neurological behavior in rats.TUNEL staining was used to observe the conditions of cortical neuronal apoptosis.Immunofluorescence staining and Western blot analysis were used to detect the expression levels of ERS-related protein CHOP,GRP78,and caspase-12.Results The neurological behavior score showed that the sham operation group did not have neurological deficits.Both the global cerebral ischemic group and the ischemic preconditioning group had obvious neurological deficits,and they improved gradually with the passage of time,but after modeling,the neurological scores at each time point in the global cerebral ischemic were significantly lower than those in the ischemic preconditioning group:at day 1∶11.00 ±0.63 vs.14.33 ±0.33 (t =21.74,P＝0.001); at day 3∶ 12.17±0.31vs.15.17±0.48 (t=27.93,P =0.000); at day 7:14.67±0.49 vs.16.33 ±0.33 (t =7.81,P=0.020).TUNEL staining showed that at day 7 after ischemia,the positive cell count per mm2 in the sham operation,global cerebral ischemic and ischemic preconditioning groups were 4.83 ±1.85vs.395.67± 43.43 and 146.17± 27.38 respectively (F=23.62,P=0.001).The ischemic preconditioning group was significantly lower than that in the global cerebral ischemic group (P =0.001).Immunofluorescence staining showed that at day 7 after ischemia,the numbers of positive cells of CHOP (26.50±3.89vs.82.33±4.25; P=0.000),GRP78 (15.00±2.02vs.35.67±2.99; t=0.000),and caspase-12 (22.33 ± 2.76 vs.66.50± 7.25; P=0.000) in the ischemic preconditioning group were significantly less than those in the global cerebral ischemic group.Western blotting showed that at day 7 after ischemia,the expression levels of CHOP (1.22 ± 0.38 vs.3.22 ± 0.51; t =24.50,P =0.001),GRP78 (1.78 ± 0.45 vs.3.16 ± 0.76; t =14.29,P =0.005),and caspase-12 (2.89 ± 0.53 vs.5.96 ± 0.67; t =77.73; P =0.000) in the ischemic preconditioning group were significantly lower than those in the global cerebral ischemic group.Conclusions Ischemic preconditioning demonstrated a neuroprotective effect for the second lethal ischemia,its mechanism may be associated with the relief of ERS and downregulation of ERS-related protein.

Objective To investigate the clinical curative effects of duloxetine combined with thioctic acid on diabetic painful peripheral neuropathy. Methods Sixty-two patients with diabetic painful peripheral neuropathy were divided into three groups by random digits table: group A(22 patients, duloxetine combined with thioctic acid group), group B (20 patients,duloxetine group) and group C (20 patients,thioctic acid group). The other treatments were same. All patients were treated for six weeks. The pain remission level and nerve conductive velocity were compared among three groups. Results The pain level in three groups was significantly alleviated after treatment (P ＜ 0.01 ). The general effective rate was 86.4%(19/22),70.0% (14/20) and 50.0% (10/20) in group A,group B and group C,respectively (P ＜ 0.05). Visual analogue scales (VAS) in group A was significantly lower than that in group B and group C from the second week after treatment (P ＜ 0.05 ). Nerve conductive velocity was improved in both group A and group C after treatment (P＜0.01),but there was no significant difference between two groups (P＞0.05). In group B,compared with that before treatment,nerve conductive velocity had no significantly improved after treatment (P＞ 0.05). Conclusion Duloxetine combined with thioctic acid can enhance the clinical curative effects on diabetic painful peripheral neuropathy.

AIM: To investigate the protective effects of diltiazem (Dil) on liver, pancreas and small intestines in hemorrhagic-shock canines and its mechanism. METHODS: The canines were bled to a mean arterial pressure (MAP) of 5.33-6.67 kPa for 30 min to produce the model of shock. During the shock, the dogs received water-soluble calcium channel blocker Dil or normal saline. The MAP was kept at the level for 90 min, then the total blood which was bled previously was reperfused . They were observed for 240 min. RESULTS: Dil could significantly elevated MAP of the hemorrhagic-shock canines ( P

ObjectiveTo investigate the relationship between sepsis induced high mobility group 1 (HMG 1) gene expression and endotoxemia in rats. MethodsSepsis was induced by cecal ligation puncture (CLP). One hundred Wistar model rats were randomly divided into four groups: normal control group ( n =10), sham operation (SO) group ( n =10), CLP group (further subdivided into 2?h, 6?h, 12?h, 24?h, 48?h and 72?h post CLP, n =10 in each subgroup), and bactericidal/permeability increasing protein(rBPI 21 ) treatment group (further subdivided into 12?h, 24?h post CLP, n =10 in each subgroup). Tissue samples from the liver, lungs and kidneys were harvested for the measurement of endotoxin concentrations and HMG 1 mRNA expression by RT PCR. Results Compared to normal control and SO groups the HMG 1 mRNA levels significantly increased in tissues during 6～72?h post CLP ( P

Objective To investigate the change on monoamine neurotransmitter in cerebral cortex motor area of traumatic asphyxia canines and provide scientific basis for its therapy.Methods The model of canine traumatic asphyxia was established,the change on monoamine neurotransmitter in cerebral cortex (motor area) and the products of metabolism during different time were tested with HPLC DC method.Results At 2 h after damage in cerebral cortex 5 hydroxyindolecetic acid (5 HIAA) elevated remarkably; At 8 h after da mage 5 hydroxytryptamine (5 HT), homovanillic acid (HVA) elevated; but there was no obvious change on norepinephrine(NE) and 3,4 dihydroxyphenyl acetic acid (DOPAC).Conclusion The monoamine neurotransmitters might play an important role in the pathological course of secondary brain injury after traumatic asphyxia.The utilization of 5 HT antagonists or compound inhibitor at early stage was a reliable method for treating brain injury after traumatic asphyxia.

Abstract Sepsis and related syndromes are the major cause of multiple organ failure and death in patients with critical illnesses.Neuroendocrine dysfunction has long been thought to be an important event in sepsis.In clinic,optimal management of the hormones could alleviate severe complications in sepsis.In this article,we review the dysfunction of neuroendocrine system as well as autonomic nervous system in sepsis,and summarize the respective therapy strategies.

ObjectiveTo observe the effect of mometasone furoate on serous eotaxin in children with allergic rhinitis.MethodsThe observation group included 30 cases who got allergic rhinitis and treated by mometasone furoate.The level of eotaxin before and after treatment was detected by ELISA,and was compared with normal children in control group.ResultsBefore treatment,the signs scores of observation group was (9.4 ± 2.3 ),and after treatment was(3.1 ± 1.8),the difference was statistically significant(t =2.148,P ＜0.05).The treatment effect contained 19 cases(63.3％ ) 9 cases(30.0％ ) effective and 2 cases(6.7％ ) ineffective.Before treatment,the level of eotaxin in observation group was remarkably higher than control group [ (221.41 ± 137.96 ) ng/L vs ( 128.71 ± 60.73 ) ng/L,t =- 2.721,P ＜ 0.05 ],after treatment,symptom and sign was mitigated and eotaxin level was remarkably lower than before treatment[ ( 115.50 ± 52.71 ) ng/L vs (221.41 ± 137.96 ) ng/L,t =- 3.661,P ＜ 0.05 ].There was no serious adverse reaction in observation group.ConclusionTreated allergic rhinitis by corticosteroids could inhibit the allergic inflammation and down-regulate the eotaxin level.