2008-05Acute kidney injury criteria predict outcomes of critically ill patients

Feature Articles

Acute kidney injury criteria predict outcomes of critically ill patients*

Fidel Barrantes,MD;Jianmin Tian,MD,MPH;Rodrigo Vazquez,MD;Yaw Amoateng-Adjepong,MD,PhD;Constantine A.Manthous,MD

R

enal dysfunction is a common cause or complication of crit-ical illness and is associated with excess morbidity and

mortality (1–11).To date,there is no universally accepted de?nition for acute

kidney dysfunction.Varying terms,in-cluding acute renal failure ,renal insuf?-ciency ,kidney injury ,and renal impair-ment ,and various de?nitions (e.g.,percent or absolute increments of creat-inine,or decrements of urine output)have been used in previous publications.To the extent that nonuniform de?ni-tions hinder scienti?c inquiry (11,12),formulation of robust,scienti?cally valid de?nitions may expedite future studies of the epidemiology,pathophysiology,and treatment of renal failure.

The Acute Kidney Injury Network (AKIN)consists of nephrologists and in-tensive care physicians who have orga-nized efforts to promote a single,scien-ti?cally valid de?nition to promote the quality of further scienti?c inquiry into the pathogenesis of renal failure.In Sep-tember 2005,AKIN invited representa-tives of international nephrology and critical care societies to Amsterdam for a 3-day conference,the purpose of which was to review the medical literature and formulate/ratify a consensus working def-inition of acute kidney injury (AKI).After 2days of scienti?c presentations,the group deliberated and rati?ed the follow-ing interim diagnostic criteria of AKI:“An abrupt (within 48hrs)reduction in kidney function currently de?ned as an absolute increase in serum creatinine of either ?0.3mg/dL (?26.4?mol/L)or a percentage increase of ?50%(1.5-fold from baseline)or a reduction in urine output (documented oliguria of ?0.5mL/kg/hr for ?6hrs)”(12).It was ex-plicitly suggested that these criteria should be used in “the context of the

*See also p.1641.

Dr.Barrantes and Dr.Tian share ?rst authorship.From Bridgeport Hospital and Yale University School of Medicine,Bridgeport,CT.

The research was not supported by external funding.

The authors have not disclosed any ?nancial or intellectual con?icts of interest relevant to this re-search.

For information regarding this article,E-mail:Pcmant@https://www.sodocs.net/doc/7611151459.html,

Copyright ?2008by the Society of Critical Care Medicine and Lippincott Williams &Wilkins DOI:10.1097/CCM.0b013e318168fbe0

Objective:The Acute Kidney Injury Network’s proposed de?ni-tion for acute kidney injury (increment of serum creatinine >0.3mg/dL or 50%from baseline within 48hrs or urine output <0.5mL/kg/hr for >6hrs despite ?uid resuscitation when applicable)predicts meaningful clinical outcomes.Design:Retrospective cohort study.

Setting:A 350-bed community teaching hospital.

Patients:The study population consisted of 471patients with no recent history of renal replacement therapy who were admitted to the medical intensive care unit during 1yr.

Interventions:Medical records of all patients were reviewed using a data abstraction tool.Demographic information,diag-noses,risk factors for acute kidney disease,physiologic and laboratory data,and outcomes were recorded.

Measurements and Main Results:Of 496patients,471were not receiving renal replacement therapy in the weeks before medical intensive care unit admission;213had changes >.3mg/dL in serum creatinine within 48hrs and/or urine output of <.5mL/kg/hr for >6hrs.Detailed ?uid challenge information was available for only 123patients,who met acute kidney injury criteria,and three patients reversed after administration of >500mL of intravenous ?uid and/or blood products.All patients whose creatinine increased >50%also had increments >0.3mg/dL.The 120patients with acute kidney injury were older (mean ?SE :69.3?1.7vs.62.9?1.3,p <.01),were more ill (Acute Physiology and Chronic Health Evaluation II score 18.7?.6vs.13.3?.4,p <.01),and had multiple comorbidities (two or more organs,65%vs.51.3%,p <.01)compared with those without acute kidney injury.The mortality rate of patients who met criteria for acute kidney injury was signi?cantly higher than that of patients who did not have acute kidney injury (45.8vs.16.4%,p <.01).In multivariate logistic regression analyses,acute kidney injury was an indepen-dent predictor of mortality (adjusted odds ratio 3.7,95%con?-dence interval 2.2–6.1).Acute kidney injury was a better predictor of in-hospital mortality than was Acute Physiology and Chronic Health Evaluation II score,advanced age,or presence of nonrenal organ failures.Median hospital stay was twice as long in patients with acute kidney injury (14vs.7days,p <.01),and only patients with acute kidney injury required hemodialysis during hospital-ization.The oliguria criterion of acute kidney injury did not affect the odds of in-hospital mortality.

Conclusions:The Acute Kidney Injury Network de?nition of acute kidney injury predicts hospital mortality,need for renal replacement therapy,and prolonged hospital stay in critically ill patients.An increment of serum creatinine >0.3mg/dL in 48hrs alone predicts clinical outcomes as well as the full Acute Kidney Injury Network de?nition.(Crit Care Med 2008;36:1397–1403)K EY W ORDS :acute kidney injury;renal failure;renal insuf?-ciency;critical care;critical illness

clinical presentation and following ad-equate?uid resuscitation when applica-ble”(12).In this study,we hypothesized that AKI predicts in-hospital mortality, need for renal replacement therapy (RRT),and prolonged hospital stays of critically ill patients.

MATERIALS AND METHODS Study Design and Settings.This retrospec-tive cohort study was conducted at Bridgeport Hospital,Yale New Haven-Health,a350-bed community teaching hospital.The Institu-tional Review Board approved the study and waived the requirement for informed consent for this retrospective review of medical records.All patients admitted to the medical intensive care unit(MICU)from January1, 2005,to December31,2005,were eligible for the study.Patients were excluded if they were receiving any form of RRT(dialysis)in the weeks before MICU admission or if they re-quired dialysis in the?rst48hrs after admis-sion.

Data Extraction.Demographic informa-tion,principal admission diagnoses,primary and secondary discharge diagnoses,and co-morbidities,including coronary artery disease, heart failure,hypertension,gout,glomerulo-nephritis,cirrhosis,and chronic kidney dis-ease,were recorded from the medical records.

Risks for kidney dysfunction were also re-corded and included vomiting,diarrhea,hem-orrhage,hyperthermia,and use of nephrotoxic medications,including nonsteroidal anti-in?ammatory medications,angiotensin-convert-ing enzyme inhibitors,angiotensin receptor blockers,radiologic contrast agents,thiazides, loop diuretics,trimethoprim-sulfamethoxazole, and aminoglycosides.

The Acute Physiology and Chronic Health Evaluation(APACHE)II score,a modi?ed APACHE II score that excluded creatinine in-crements,and the number and types of organ failures were also computed/https://www.sodocs.net/doc/7611151459.html,an failures were de?ned using criteria recom-mended by Marshall and colleagues(13)(Ap-pendix1).Additionally,hourly urine outputs of all patients,routinely recorded on all MICU patients,were surveyed.

Physiologic data including blood pressures (lowest),heart rates(highest),respiratory rate (highest),Glasgow Coma Scale score,white blood cell count,hematocrit,serum electro-lytes,blood urea nitrogen,serum creatinine

(Scr),pH,P O

2,and P CO

2

were recorded using

customized data entry forms.Electrolytes, blood urea nitrogen,Scr,and complete blood counts were measured at least once daily(at 4–5am)in all patients;the highest blood urea nitrogen and Scr were recorded for each day. These data were recorded for MICU admission (baseline),24hrs before meeting criteria for AKI,at the time of AKI,24hrs after AKI,and ?48hrs after AKI.Recorded outcomes in-cluded in-hospital mortality,RRT,and MICU

and hospital lengths of stay(LOS).

Data Analysis.Patients were classi?ed as

having AKI if they had an increment of Scr

?0.3mg/dL or?50%increase within any48

hr interval and/or an episode of?0.5mL/

kg/hr urine output for?6hrs despite?uid

challenge of?500mL of normal saline,when

https://www.sodocs.net/doc/7611151459.html,rmation on?uid challenge

was incomplete for90patients who otherwise

would have ful?lled criteria for AKI.These

patients were excluded from the primary

analysis.

In-hospital mortality,need for RRT,and

hospital and intensive care unit LOS of pa-

tients with and without AKI were compared.

Analysis was performed using SAS version8.2

software.Categorical variables,described as

proportions,were compared with chi-square

tests.Continuous variables are reported as

mean?SE or as medians with the interquar-

tile ranges.Means were compared using Stu-

dent’s t-test if a normal distribution was de-

tected.Nonparametric variables were compared

with Wilcoxon’s rank-sum tests.A two-tailed

p?.05was considered statistically signi?cant.

To adjust for confounding and assess pos-

sible effect modi?cation,multiple logistic re-

gression,multiple linear regression,and strat-

i?ed analyses were performed when

appropriate.Given that the APACHE II score

includes information on renal dysfunction,a

modi?ed APACHE II score was calculated by

omitting the creatinine component in the to-

tal score.The modi?ed APACHE score was

used in multivariate analyses involving AKI.

Variables were included in the regression anal-

yses if they demonstrated signi?cant associa-

tion with outcomes of interest in the univar-

iate analyses and/or if prior studies suggested

they were potential confounders or effect

modi?ers.Both backward elimination and

stepwise regression methods were used to ar-

rive at the?nal model.

Additional sensitivity analyses were per-

formed including all of the patients who were

excluded from the primary analyses because of

the lack of information on?uid challenge.

They were reclassi?ed as having AKI and the

analyses were repeated.Similarly,the analyses

were repeated excluding the requirement of

?uid challenge in the de?nition of AKI.Addi-

tional analyses were done using only the rel-

ative contributions of creatinine increment or

changes in urine output as a basis for de?ning

AKI.Sensitivity,speci?city,positive predictive

value,and negative predictive value of AKI for

predicting mortality were calculated.The

Youden index(sensitivity?speci?city?1),a

measure of overall validity(14,15),was also

calculated.The predictive utility of the AKIN

criteria for in-hospital mortality was com-

pared with APACHE II score(?20),advanced

age(?65yrs),multisystem organ failure(two

or more nonrenal organ failures),and in-

creases in serum creatinine?0.3mg/dL and

?0.5mg/dL in48hrs.

RESULTS

There were496MICU admissions dur-

ing the study period.Fourteen patients

were excluded because they were already

receiving RRT at the time of admission,

and11were excluded because they re-

quired RRT within48hrs of admission.

Of the remaining471patients,213had

an increment of Scr?0.3mg/dL within

48hrs and/or urine output?0.5mL/

kg/hr for?6hrs.All patients whose Scr

increased?50%also had increments

?0.3mg/https://www.sodocs.net/doc/7611151459.html,plete information on

?uid challenge was available for only123

of these213patients.Only three of these

123patients had resolution of their ele-

vated Scr and/or decreased urine output

after?uid challenge.Thus,120patients

met AKI criteria and97of these devel-

oped AKI in the?rst48hrs of admission.

Eight of97who developed AKI in the?rst

48hrs later had Scr less than or equal to

their admission value,whereas none of

the23who developed AKI later in the ICU

stay returned to less than or equal to

their admission Scr.The control group,

261patients,included those who did not

meet changes in Scr and/or urine output

and the three patients whose increment

of Scr or decreased urine output resolved

after?uid challenge.The90patients who

had increments of Scr?0.3mg/dL

within48hrs and/or urine output?0.5

mL/kg/hr urine output for?6hrs but

lacked information on?uid challenge

were excluded from the primary analysis.

Patient Characteristics.The cohort

was predominantly white(69.8%),with a

median age of67(mean?SE64.9?1.0).

The majority of patients(56.7%)were

men.The median APACHE II score was

15.0for the cohort as a whole.The main

primary diagnoses necessitating ICU ad-

mission or transfer were respiratory fail-

ure(35.2%),sepsis(19.4%),gastrointes-

tinal bleeding(5.5%),and acute coronary

syndrome(4.5%).Overall median hospi-

tal and ICU lengths of stay were9and3

days,respectively.One third(31.5%)of

the cohort met criteria for AKI.

Table1shows characteristics of pa-

tients with and without AKI.Patients

with AKI were older(69.3?1.7vs.62.9?

1.3,p?.01),were more ill(APACHE II

score18.7?0.6vs.13.3?0.4,p?.01),

and had multiple comorbidities(two or

more organs,67.5%vs.48.3%,p?.01)

compared with those without AKI.Pa-

tients with AKI were more likely to have

been admitted with sepsis(27.5%vs.

15.7%,p?.01)and/or developed sepsis

at some point in their MICU stay(56.6% vs.26.4%,p?.01).Patients with AKI were also more likely to have multisys-tem organ failure compared with those without AKI(two or more nonrenal or-gan failures,67.5%vs.48.3%,p?.01).

AKI and Outcomes.The unadjusted

mortality rate of patients with AKI was

45.8%,nearly three times the mortality

rate of those without AKI(45.8%vs.

16.4%;risk ratio2.8,95%con?dence in-

terval[CI] 2.0–3.9)(Table2).The in-

creased mortality observed among pa-

tients with AKI was consistent across

categories of age,gender,modi?ed

APACHE II score,sepsis,nephrotoxic

medication exposures(see Materials and

Methods section),comorbidities,organ

failures,and abnormal baseline Scr(Ta-

ble3).In multiple logistic regression

analyses,AKI emerged as the most potent

predictor of mortality(adjusted odds ra-

tio3.7,95%CI2.2–6.1;Table4).The

modi?ed APACHE II score(i.e.,excluding

renal components)was not predictive of

mortality.Similarly,two or more nonre-

nal organ failures were not predictive of

mortality in the multivariate model.

All of the18patients who required

hemodialysis after48hrs of hospitaliza-

tion met criteria for AKI,and the mortal-

ity rate of this group was39%(95%CI

17.3–64.3%;Appendix2).

Median hospital and MICU lengths of

stay were2and1.7times higher,respec-

tively,in patients with AKI(hospital LOS,

14vs.7days,p?.01;MICU LOS,5vs.3

days,p?.01)compared with those with-

out AKI.Among those who died,there

were no statistically signi?cant differ-

ences in hospital or MICU LOS(hospital

LOS,14vs.9days,p?.25;MICU LOS,5

vs.4.5days,p?.71).In multivariate

linear regression analyses,AKI and sepsis

emerged as potent predictors of increased

LOS(Table5).

Sensitivity Analyses.Kidney dysfunc-

tion was associated with mortality when

we used various combinations of the two

major AKI criteria(odds ratios ranged

from2.72to3.73;Table6).The AKI def-

inition was moderately speci?c(77%)but

less sensitive(56%)in predicting in-

hospital mortality(Table7).Nonetheless,

it was a better predictor of in-hospital

mortality than was the traditional

APACHE II score,advanced age,or mul-

tisystem organ failure.All of these mea-

sures,including AKI criteria,were weak

predictors of mortality,with Youden in-

dexes ranging from0.13to0.33(where0

is a useless test and1.0is a perfect test).

DISCUSSION

This is the?rst study to examine

whether the Acute Kidney Injury Net-

work’s interim consensus de?nition for

AKI is associated with clinically meaning-

ful outcomes.Our cohort,consisting of a

year’s admissions to a community hospi-

tal MICU,demonstrates that patients

meeting this de?nition of AKI were three

times as likely to die during hospitaliza-

Table1.Demographic characteristics of study patients

Total AKI Non-AKI p Value Frequency,n(%)381(100)120(31.5)261(68.5)NA

Race,white,n(%)266(69.8)83(69.2)183(70.1).77

Gender,male,n(%)216(56.7)60(50.0)156(59.7).06

Age,yrs

Mean?SE64.9?1.069.3?1.762.9?1.3?.01

Median(25–75%range)67(53–80)73(61–82)64(51–83)?.01

Modi?ed APACHE II a

Mean?SE13.3?.315.3?.512.4?.3?.01

Median(25–75%range)13(10–17)15(11.5–19)12(9–16)?.01

APACHE II

Mean?SE15.0?.318.7?.613.3?.4?.01

Median(25–75%range)15(10–19)18(14–23)13(9–17)?.01

NROF,n(%)

Respiratory failure194(50.9)69(57.5)125(47.9).06

Hepatic/GI failure134(35.2)51(42.5)83(31.8).03

Cardiac failure130(34.1)53(44.2)77(29.5)?.01

CNS failure109(28.6)38(31.6)71(27.2).47

Hematological failure98(25.7)38(31.6)60(22.9)?.01?2NROFs(%of NROFs b)207(54.3)81(67.5)126(48.3)?.01 Sepsis,n(%)137(35.9)68(56.6)69(26.4)?.01

Most common primary diagnosis,n(%)

Respiratory failure134(35.2)49(40.8)85(32.5).22

Sepsis74(19.4)33(27.5)41(15.7)?.01

GI bleeding21(5.5)5(4.2)16(6.1).45

Acute coronary syndrome17(4.5)4(3.3)13(5.0).48

Comorbidities,n(%of?2)212(55.6)78(65.0)134(51.3)?.01?1nephrotoxic medications,n(%)c159(41.7)59(49.2)100(38.3).03

AKI,acute kidney injury;APACHE,Acute Physiology and Chronic Health Evaluation;NROF, nonrenal organ failure;GI,gastrointestinal;CNS,central nervous system.

a Modi?ed APACHE did not include renal components;

b NROFs did not include renal failure;

c number of nephrotoxic medications include

d angiotensin receptor antagonists,aminoglycosides, nonsteroidal anti-in?ammatory medications,and contrast agents.Confounding factors included age, comorbidities,modi?ed APACHE II score,and NROF.

https://www.sodocs.net/doc/7611151459.html,parison of mortality and lengths of stay among patients with and without acute kidney

injury(AKI)

Outcome Total AKI Non-AKI p Value

RRT rate,n(%)18(4.7)18(15.0)0(0.00)?.01 Hospital LOS,median

Survived8.014.07.0?.01 Died11.014.09.0.25 Total9.014.07.0?.01 MICU LOS,median

Survived 3.0 6.0 3.0?.01 Died 5.0 5.0 4.5.71 Total 3.0 5.0 3.0?.01 Mortality,n(%)

?2NROFs66(31.9)41(50.6)25(19.8)?.01?2NROFs32(18.4)14(35.8)18(13.3)?.01 1NROF19(15.8)9(34.6)10(10.6)?.01 2NROFs25(22.5)16(44.4)9(12.0)?.01 3NROFs27(40.9)19(59.4)8(23.1)?.01 4NROFs11(44.0)6(54.5)5(35.7)?.01 Total98(25.7)55(45.8)43(16.4)?.01

RRT,renal replacement therapy;LOS,length of stay;MICU,medical intensive care unit;NROF, nonrenal organ failure.

tion.They were signi?cantly more likely to require dialysis and had prolonged hospital stays compared with those who did not meet criteria.Thus,the current interim de?nition of AKI passes this lit-mus test of predicting the meaningful outcomes of mortality,prolonged hospi-tal stays,and the need for RRT.

These associations were expected.Previ-ous studies that examined the impact of acute renal failure in intensive care popu-lation documented increased mortality and prolonged hospital stay,using other de?ni-tions of acute renal failure (9,12,16).The 2nd International Consensus Conference of the Acute Dialysis Quality Initiative (16)found 44studies published before 2004that used ?20different diagnostic criteria for renal injury or failure.Owing to the vari-ability of de?nitions and patient demo-graphics,mortality associated with renal dysfunction ranged from ?5%for non-ICU patients to ?50%for ICU patients with concurrent organ dysfunction/failure.Def-initions based on the need for acute RRT are most common in the literature and demonstrate the strongest association with in-hospital mortality,ranging from 50%to ?70%.The mortality of this subcohort in our study was 39%(95%CI 17.3%to 64.3%).Uchino and colleagues (3)reported outcomes of 29,269critically ill patients admitted to 54hospitals in 23countries.The criteria for acute renal failure used in their study included need for RRT,oliguria (?200mL/12hrs),or blood urea nitrogen ?84mg/dL.In-hospital mortality was 60%.However,it is nearly impossible to compare our study with theirs,despite similar co-horts.This highlights the dif?culty in this ?eld;nonuniform and,in many cases,arbi-trary de?nitions hinder direct comparisons between studies and prevent valid quanti-tative aggregation (e.g.,meta-analyses)of results from different studies.A group of clinicians,some of whom represented AKIN at the Amsterdam conference,earlier proposed the risk,injury,failure,loss,and end-stage kidney disease (RIFLE)criteria (17).RIFLE is a classi?cation system that includes temporary and permanent anuric renal failure as stages of renal dysfunction.Since these last stages of loss and end-stage disease constituted outcomes in our study,it is not appropriate to compare RIFLE with AKI.Moreover,RIFLE was developed be-fore publication of Chertow and colleagues’(1)data demonstrating that smaller incre-ments (0.3mg/dL)of creatinine than those cited in RIFLE (1–3times elevation)were associated with outcomes of hospitalized patients.While RIFLE may allow studies of

Table 3.Relative risk of mortality of patients strati?ed across demographic and physiologic variables

Variables

AKI

Non-AKI Strati?ed

Total Dead Total Dead RR 95%CI Age,yrs ?65793613429 2.1 1.4–3.1?65411912714 4.2 2.3–7.6Gender Male 603315625 3.4 2.2–5.2Female 602210518 2.1 1.2–3.7Comorbidities ?2783613425 2.5 1.6–3.80or 1

411912818 3.3 1.9–5.7Modi?ed APACHE II ?1567318721 1.9 1.2–3.1?155******** 3.6 2.2–5.9Sepsis Sepsis 69346917 3.1 1.9–5.0No sepsis 512119326 2.0 1.3–3.3Organ failure Respiratory Yes 693512529 2.2 1.5–3.2No

512013614 3.9 2.2–7.1Hepatic/GI Yes 51268314 3.0 1.7–5.2No

692917829 2.6 1.7–4.1Hematological Yes 38166010 2.5 1.3–5.0No 823920133 4.3 2.3–8.0CNS Yes 38187115 2.2 1.3–4.0No 823719028 3.1 2.0–4.6Cardiac Yes 53277719 2.1 1.3–3.3No

672818424 3.3 2.0–5.2Multisystem NROFs ?2814112625 2.5 1.7–3.8?1

391413518 2.5 1.3–5.0Nephrotoxic medications ?1592710012 3.8 2.1–7.0None

612816131 2.4 1.6–3.7Scr on admission ?24120389 2.1 1.1–4.0?2

79

35

222

34

2.9

2.0–4.3

AKI,acute kidney injury;RR,risk ratio;CI,con?dence interval;APACHE,Acute Physiology and Chronic Health Evaluation;GI,gastrointestinal;CNS,central nervous system;NROF,nonrenal organ failure;Scr,serum creatinine.

Crude risk ratio for AKI and mortality was 2.78;95%CI ?2.0–3.9.

Table 4.Predictors of in-hospital mortality by univariate and multivariate analyses

Risk Ratio

95%CI

Univariate analysis AKI

2.8 2.0–

3.9APACHE II modi?ed (?15) 1.7 1.2–2.4Comorbidities (?2)

1.30.9–1.9Nephrotoxic medications (?1)0.90.6–1.3NROF (?2) 1.7 1.2–

2.5Sepsis

1.9 1.4–

2.7Odds Ratio

95%CI Multivariate logistic regression AKI 3.7 2.2–6.1Sepsis

1.8

1.8–

2.9

CI,con?dence interval;AKI,acute kidney injury;APACHE,Acute Physiology and Chronic Health Evaluation;NROF,nonrenal organ failure.

prognostication for each stage of kidney injury,the current data suggest that RIFLE criteria for risk and/or injury may be ren-dered more sensitive if revised to the now more evidence-based AKI parameters.

The natural courses of the many partic-

ular diseases that cause AKI have not been

suf?ciently characterized because so few

studies have studied the same patients us-

ing the same de?nitions.Nonuniformity is

equally problematic for interventional stud-

ies.For example,imagine the dif?culty in-

herent in studies examining the ef?cacy of

N-acetyl-cysteine for AKI if every study de-

?ned success or failure(i.e.,renal failure)

differently.Nonuniform de?nitions hinder

the progress of science.

The2005AKIN consensus de?nition

was chosen understanding that kidney dys-

function is a continuum of disease,and in

order to study it most broadly,the initial

interim diagnosis should be as sensitive as

possible.Also,it was recognized that intra-

vascular volume status in?uences both

urine output and Scr.Prerenal azotemia

due to intravascular depletion can lead to

decrements of urine output and incre-

ments of Scr before tubular injury,but if of

suf?cient duration and magnitude,intra-

vascular contraction can cause tubular

ischemia and infarction unto oliguria and

azotemia that can then be independent of

subsequent volume repletion.Accordingly,

the consensus in Amsterdam was to assert

that AKI be de?ned“only after an optimal

state of hydration had been achieved...if

appropriate.”No speci?c amount of?uid

resuscitation was suggested given that dif-

ferent clinical conditions and patient prob-

lems demand varying magnitudes of?uid

challenge.Assessing whether an optimal

hydration state had been achieved was ex-

tremely dif?cult in this retrospective study.

To certify that the patient’s volume status

was optimal,we required administration of

a minimum of500mL of volume expander

(saline,colloid,or blood)during?1hr in

response to oliguria or increments of Scr.

Complete information on?uid challenge

was unavailable in about42%of our pa-

tients.The association of AKI with in-

hospital mortality was still signi?cant(odds

ratio2.7;95%CI1.7–4.2),discarding the

“appropriate?uid challenge”requirement.

The de?nition for AKI was not in-

tended to be?nal.Rather,it was proposed

Table5.Predictors of length of stay(LOS)

Predictors of Hospital LOS Risk Ratio95%CI Univariate analysis

AKI 2.2 1.7–3.0 APACHE II modi?ed(?15) 1.3 1.0–1.8 Comorbidities(?2) 1.10.8–1.5 Nephrotoxic medications(?1) 1.00.8–1.4 NROF(?2) 1.5 1.1–2.1 Sepsis 2.0 1.5–2.6 Multivariate linear regression Coef?cient SE AKI 3.0 1.9 Sepsis8.0 1.8 Predictors of MICU LOS Risk Ratio95%CI Univariate analysis

AKI 2.0 1.4–2.7 APACHE II modi?ed(?15) 1.5 1.1–2.1 Comorbidities(?2)0.90.7–1.3 Nephrotoxic medications(?1) 1.10.8–1.5 NROF(?2) 1.7 1.2–2.4 Sepsis 1.9 1.4–2.6 Multivariate linear regression Coef?cient SE AKI 2.2 1.1 Sepsis 3.1 1.0 CI,con?dence interval;AKI,acute kidney injury;APACHE,Acute Physiology and Chronic Health Evaluation;NROF,nonrenal organ failure;MICU,medical intensive care unit.

Cutoff point for hospital stay was13.9days,the75%percentile of all hospital LOS.Cutoff point for MICU stay was6.7days,the75%percentile of all MICU LOS.

Table6.Mortality using various permutations of acute kidney injury(AKI)diagnostic criteria

Mortality,n(%)Logistic Regression OR95%CI

AKI(both1Scr and oliguria)55(45.8) 3.7 2.2–6.2

Permutations

Oliguria44(46.8) 3.0 1.8–5.1

1Scr55(45.8) 3.7 2.3–6.2

Both1Scr and oliguria present44(46.8) 3.0 1.8–5.1

Including90patients without?uid challenge as AKI88(42.1) 2.8 1.8–4.4

Discarding?uid challenge from AKI de?nition85(42.5) 2.7 1.7–4.2

OR,odds ratio;CI,con?dence interval;1,increased;Scr,serum creatinine.

https://www.sodocs.net/doc/7611151459.html,parative predictors of mortality

Total Mortality,%Sensitivity,%Speci?city,%Youden Index a PPV,%NPV,%Accuracy b APACHE II(?20)5851.70.340.800.130.370.780.68 AKI12045.80.560.770.330.460.840.72 Age?65yrs21430.40.660.480.140.310.800.52 NROF(?2NROF)20831.70.670.500.170.320.820.54 Scr increase?0.3c7648.70.380.860.240.490.800.74 Scr increase?0.5c5851.70.310.900.210.530.790.75 RRT1838.90.070.960.030.390.750.73 PPV,positive predictive value;NPV,negative predictive value;APACHE,Acute Physiology and Chronic Health Evaluation;AKI,acute kidney injury; NROF,nonrenal organ failure;Scr,serum creatinine;RRT,renal replacement therapy.

a Youden index?sensitivity?speci?city?1;

b accuracy?(true results/all results);

c Scr increase as the only criterion without requiring?ui

d challeng

e or48-hr window o

f development.

with the presumption that it would be tested and re?ned based on scienti?c data.Our data indicate that the AKI def-inition is an excellent beginning.How-ever,simplifying the de?nition of AKI to include only serum creatinine elevation of?0.3mg/dL produced the greatest as-sociation with in-hospital mortality and captured all who required acute RRT.Of the patients with AKI who either died or required RRT,none had decreased urine volume without a concomitant increase in serum creatinine.Since the absolute increment in Scr criterion is so small(0.3 mg/dL),it captured all patients who had Scr increases?50%.(This may be more germane to children,who were not in-cluded in our study.)Using only an in-crease in Scr?0.3mg/dL within48hrs as the sole criterion for AKI has the added advantage of not requiring measurement of hourly urine output,a task not rou-tinely done outside an ICU.The study by Chertow et al.(1)?rst demonstrated that a change of Scr?0.3mg/dL,up or down, was associated with increased mortality. The study by Chertow et al.(1)?rst dem-onstrated that a change of Scr?0.3 mg/dL any time during hospitalization was associated with increased mortality. Our study differs because AKI is de?ned as an increment of0.3mg/dL in a48-hr period.Our data support not only that such small changes of creatinine are as-sociated with meaningful differences in outcome but also that acute increments ?0.3mg/dL predict outcomes.This clin-ically practical de?nition of AKI bene?ts from its simplicity and robust association with patient outcomes and therefore may be most appropriate for future epidemio-logic and therapeutic studies.

This study has several limitations. First,it describes a relatively small co-hort of relatively homogeneous(i.e., medically,critically ill)patients.It does not include trauma,postoperative,and other surgical patients.This limits the generalizability of our?ndings.Perhaps our?ndings can be generalized to pa-tients in other MICUs since our commu-nity hospital admits patients with a broad range of medical problems,with a similar breadth of pathology admitted to other MICUs.However,these data should be generalized cautiously to surgical pa-tients and those who are hospitalized but less ill.Insofar as these data are consis-tent with the more heterogeneous cohort described by Chertow et al.(1),it is likely that future studies will con?rm the utility of the AKI de?nition in broader popula-tions of hospitalized patients.Moreover,

our cohort included very few patients with

glomerulonephritis,interstitial nephritis,

and obstructive uropathies.Accordingly,

our?ndings should be generalized care-

fully,if at all,to these populations.

Second,the retrospective nature of

this study hindered the completeness of

data acquisition(e.g.,no data were avail-

able regarding“appropriate?uid chal-

lenge”in90patients).We could not reli-

ably determine whether assessment of

volume status was performed for oliguria

and,if so,whether it was followed by

administration of an appropriate volume

of intravenous?uid challenge or dose of

diuretic.We could ascertain that only

three of123patients who received?500

mL of normal saline or other volume

expander had reversal of AKI criteria(i.e.,

persistent oliguria or failure of creatinine

to decrease).It is impossible to ascertain

post hoc whether AKI persisted due to the

wrong therapeutic response or an insuf-

?cient therapeutic response.There is no

gold standard for a?uid challenge,and

practitioners vary considerably in their

approach.

Third,due to our relatively small co-

hort,we did not perform an extensive

analysis in patients who had AKI super-

imposed on an abnormal baseline Scr.In

our cohort,the strati?ed relative risk of

mortality of patients with AKI adjusted to

initial Scr?2mg/dL was2.1(CI1.1–

4.0).Similarly,Chertow et al.(1)re-

ported an increased odds ratio of death

(4.1),adjusted for chronic renal disease

(1).The AKIN de?nition of AKI,despite

its strong association with mortality,was

not suf?ciently sensitive(56%).It was

moderately speci?c(77%),thus yielding

a Youden index of only0.33.Nonetheless,

the moderate speci?city suggests that pa-

tients with AKI deserve careful attention

(and,potentially,interventions)to avoid

poor outcomes.Despite the poor Youden

index,AKI was more highly predictive of

in-hospital mortality than was the widely

used APACHE II score.

Fourth,the outcomes we selected—

in-hospital mortality,need for RRT,and

LOS—may not necessarily capture all rel-

evant consequences of AKI.Other conse-

quential effects include increased re-

source utilization within and outside of

the MICU,subsequent development of

chronic kidney disease,and the future

need for RRT due to successive acute,

chronic,or acute on chronic injuries.

These could not be assessed in this study.

CONCLUSIONS

This study demonstrates that the in-

terim consensus de?nition of AKI is clin-

ically valid in that it independently pre-

dicts meaningful clinical outcomes.

Additional studies at other centers and

with broader cohorts of patients are re-

quired to con?rm this?nding and/or to

re?ne the de?nition further.The AKIN

initiative is likely to yield a robust,evi-

dence-based de?nition that clinicians and

scientists can embrace in future clinical

care and inquiry.

ACKNOWLEDGMENTS

We are grateful to Shailendra Up-

adhyay,MD,Artur Grigoriyan,MD,and

Santhi Adigopula,MD,for many hours of

assistance gathering data from medical

records for this report.

REFERENCES

1.Chertow GM,Burdick E,Honour M,et al:

Acute kidney injury,mortality,length of stay

and costs in hospitalized patients.J Am Soc

Nephrol2005;16:3365–370

https://www.sodocs.net/doc/7611151459.html,ssnigg A,Schmidlin D,Mouhieddine M,et

al:Minimal changes of serum creatinine pre-

dict prognosis in patients after cardiotho-

racic surgery:A prospective cohort study.

J Am Soc Nephrol2004;15:1597–1605

3.Uchino S,Kellum JA,Bellomo R,et al:Acute

renal failure in critically ill patients:A mul-

tinational,multicenter study.JAMA2005;

294:813–818

4.Liano F,Pascual J,The Madrid Acute Renal Fail-

ure Study Group:Epidemiology of acute renal

failure:A prospective,multicenter,community-

based study.Kidney Int1996;50:811–818

5.Metnitz PGH,Krenn CG,Steltzer H,et al:Effect

of acute renal failure requiring renal replacement

therapy on outcome in critically ill patients.Crit

Care Med2002;30:2051–2058

6.Conlon PJ,Stafford-Smith M,White WD,et

al:Acute renal failure following cardiac sur-

gery.Nephrol Dial Transplant1999;14:

1158–1162

7.Mangano CM,Diamondstone LS,Ramsay JG,

et al:Renal dysfunction after myocardial re-

vascularization:Risk factors,adverse out-

comes and hospital resource utilization.Ann

Intern Med1998;128:194–203

8.Chertow GM,Levy EM,Hammermeister KE,

et al:Independent association between acute

renal failure and mortality following cardiac

surgery.Am J Med1998;104:343–348

9.Uchino S,Bellomo R,Goldsmith D,et al:An

assessment of RIFLE criteria for acute renal

failure in hospitalized patients.Crit Care

Med2006;34:1913–1917

10.Mehta RL,Pascual MT,Soroko S,et al:

Diuretics,mortality and nonrecovery of re-

nal function in acute renal failure.The

PICARD study group.JAMA2002;288: 2547–2553

11.Thakar CV,Liangos O,Yared JP,et al:ARF

after open-heart surgery:In?uence of gender and race.Am J Kidney Dis2003;41:742–751 12.Mehta RL,Kellum JA,Shah SV,et al:Acute

kidney injury network(AKIN):Report of an initiative to improve outcomes in acute kid-ney injury.Crit Care2007;11:R31

13.Marshall JC,Cook DJ,Christou NV,et al:

Multiple organ dysfunction score:A reliable descriptor of a complex clinical outcome.

Crit Care Med1995;23:1638–1652

14.Perkins NJ,Schisterman EF:The Youden In-

dex and the optimal cut-point corrected for measurement error.Biom J2005;47:428–441 15.Youden WJ:Index for rating diagnostic tests.

Cancer1950;3:32–35

16.Bouman C,Kellum JA,Lamiere N,et al:

De?nition for acute renal failure.Acute Di-alysis Quality Initiative Web site.http:// https://www.sodocs.net/doc/7611151459.html,/adqi/ADQI2/ADQI2g1.pdf.

Accessed April9,200717.Bellomo R,Ronco C,Kellum JA,et al:Acute renal

failure—de?nition,outcome measures,animal

models?uid therapy and information technology

needs:The second international consensus con-

ference of the Acute Dialysis Quality Initiative

(ADQI)group.Crit Care2004;8:R204–R212

APPENDIX1

Following are criteria used to de?ne

nonrenal organ failures,modi?ed from

Marshal et al(13).

Cardiac/circulatory failure

Systolic blood pressure?90mm Hg or

mean arterial pressure?70mm Hg for

?1hr despite adequate volume resuscita-

tion,or use of vasopressors to achieve the

same goals

Ventricular tachycardia or?brillation

Respiratory failure

Hypercapnia(Pa CO2?55mm Hg)

Hypoxemia(Pa O2?60mm Hg)

Pa O2/F IO2?250if other organ dysfunc-

tion present or?200if the lung is the

only dysfunctional organ

Hematologic failure

Platelet count?80,000or decreasing

50%during3days

Evidence of disseminated intravascular

coagulation

Hepatic failure

Rising hepatic enzymes(1.5times)

Hyperbilirubinemia(1.5times)

Gastrointestinal failure

Overt gastrointestinal bleeding

Neurologic failure

Depressed level of consciousness(Glas-

gow Coma Scale score?6)

Seizures

APPENDIX2.Predictors of in-hospital need for acute hemodialysis

Risk Ratio95%CI Univariate analysis

AKI NA a NA a APACHE-II modi?ed(?15) 1.5.6–3.7 Co-morbidities(?2) 2.1.8–5.7 Nephrotoxic medications(?1) 1.1.5–2.8 Non-renal organ failure(NROF)(?2) 1.3.5–3.2 Sepsis 1.8.7–4.4 Multivariate logistic regression b

AKI,acute kidney injury;APACHE,Acute Physiology and Chronic Health Evaluation;CI,con?-dence interval;NA,not available.a No patient in non-AKI group had renal replacement therapy.

b Multivariate logisti

c regression was not performe

d becaus

e no patients in the Non-AKI group had renal replacement therapy.

2011年四川大学华西药学院706药学综合

2011年四川大学华西药学院706药学综合（转自小木虫） 一部分：物理化学 单选题14道3分一道，每章节都涉及 计算题1道8分，参看第四章完全不互溶双液体系水蒸气消耗系数蒸出有机物的百分质量分数 二部分：分析化学 1~10题单选11~20多选均3分一道 判断题20道2分一道总体难度不大，但个别几道比较偏。分析化学覆盖面相当的广泛，无论书上有无现成的都很可能考到，要求考生复习过程中看书要多注意细节，多做练习题，真题等，不仅仅是四川大学的练习题。 三部分：有机化学 排序题5道4分一道，难度不是很大，要求考生复习多注意细节，多做练习题，第五版教材和第六版教材结合看。 化学方程式50分5分一道，个别题偏难 合成题30分10分一道，11年的第二道比较难的原因涉及磷酸基的去除，仅看教材的话（非常抱歉我看了那么多遍人卫版的教材包括药科大的练习册真的没见过磷酸基的去除，曾经见过一博士师兄的笔记本他还说磷酸基是易离去基，可能刑其毅的书有讲到），其余两道难度适中，但这都是主观题，要求不仅仅是做出来。 四部分：生物化学 名词解释12分2分一道，其中信号肽和反义核酸我见过但没仔细记过，所以到最后一刻为了不开天窗乱编的，其余难度不大。 选择题填空题呵呵这两道单分多少忘记了，总体难度适中，个别细节问题有时候是很难把握的。简答题15分5分一道酶的比活力及其意义；遗传中心法则；造成蛋白质变性的主要原因及在蛋白质分离提纯过程中的注意事项....O(∩_∩)O~《药物分析生物学》这本书的考试内容是融合在生物化学书中的，各个学校学的不一样，有些生物化学学得比较远把遗传这些都学了的，就不用再花时间看《药物分子生物学》了。 2012年的同学多多加油哦O(∩_∩)O~仔细复习打牢基础是关键，多做练习特别是真题是王道，复习过程是非常艰辛的，特别是分析化学是看完一遍几天不看又会忘记，细节实在太多了，有些题考得也是在太偏太细了有时候只能靠猜，但直觉也需要实力做基础，总之就是无论复习有多困难要相信自己！祝大家考研成功！有梦想的人很伟大，为梦想而踏实奋斗的人更伟大！ 2009年四川大学华西药学院药学综合考研试题（转自小木虫） 09华西药学综合 物理化学部分 25道选择题，每个章节均有3，4题，但是主要是考基础，不用过多的做难题，抓住课本基础是关键 分析化学部分 60分选择题，10个单选，10个多选，也不是很难，多选题考得会比较广，不是看书就可以搞定的也会比较细，40分20道选择题 有机化学部分 30分排序题，这部分不是很难，40分方程式，比较难，和以前真题有较大出入，30分合成题也是很难，有机建议多做题找感觉

华西药学院-天然药物化学题目分享及参考答案【精华】

关于天然药物化学的一些原题分享和参考答案 2013年1月22日 写在前面：此分享凡出现页码均为人卫版第五版书上页码，为让用新教材的同学方便查阅 考证，将会附上章节，另外对于生物碱这一章的教学内容是不按教材上的，是按老版第五版 的内容上，不过到时上这块的王锋鹏老师会给我们人手复印一份的，不用担心哈！另外对于 天然药化的学习，个人没有什么好的见解，按老师给的思考题来看书应该效率会比较高，另 外最好加上习题集的题目，可以选择性做，因为我们10级这次考试就是习题集上每章的题 目加上00、01、03、87、91级的几份考题的综合，其中习题集大概占了30%，01级的题 目占了60%，其他考卷占了有10%.所以大家到时一定要多多做原题哈！ 另外，这份题目里的答案只是参考答案，不一定都是对的，如有谬误，还请见谅哈！好了， 不多说了，开始进入正题！ 01级题目及其他题目 一、写出下列化合物的结构类型： 1 a. 第七章 第四节 Vs b. 答案：1a.齐墩果烷型五环三萜 1b.乌苏烷型五环三萜（P278） 2.a Vs b. . （大概是这个，可以看一下01级 (这个10级考到了) 的纸质版，上面有哈） 答案：a 托品烷类生物碱 （P357 第九章第三节） Vs b.单萜类吲哚生物碱 注：还有一个可能考的是简单吲哚类生物碱，回去看一看 3. a. Vs b. P149 第四章 第一节 四 HO 4310813141720H H 125679111215161819212223 24252627282930HO 4310813141720H H 192324252627282930

2013华西药学院706药学综合回忆版

华西药学院706药学综合回忆版 有机化学 今年的仍然没有变，1.性质比较2.写产物3.大合成 没啥好说的，每年都出的不一样，把习题册弄活吃透，都做会就差不多了，反正也不难。要强调的一点是，历年真题中的有机题也要都做懂，今年就考了几个往年真题中的让大多数考生似是而非的的题。 今年的有机化学相对比较简单吧。 分析化学 今年分化题型略有改变，增添了名词解释，1.名词解释2.选择（单选，多选）3.判断题 名解虽然是新题型，但是都考的比较基础，只要平时看分化时将一些重点概念掌握了就没问题了，我记得应该有：振动弛豫，化学位移，荧光效率等一共十个，每个两分，都很基础，大家不用担心。 至于选择题，我想给学弟学妹们重点强调的是，一定要把历年分化选择题做个遍！一定要每个题都弄懂！因为分化出题老师实在是太懒了！！！今年选择题有90%以上都是原题，连答案都没变啊！！！有木有！！！但是，话又说回来，川大历来没有公布标准答案，这就需要我们自己下功夫，一定要把每个题都弄懂，要有根有据，强烈建议提前一点整理准备，不懂得大胆地向老师请教！ 判断题的话也大多都是原题，40%左右的新题，比较基础，但是考的都是细节，所以要求我们复习分化时一定要注意细节，多看，多总结！这也是历年来学姐学长们所强调的。 物理化学 今年物理化学题型与去年又有变化，今年物化取消了去年坑爹的填空题，重回正轨，具体有1.单选题2.计算题 单选题的话大多数都是原题，少于30%的新题，知识点与往年相比也没有变化，还是那句话，使用好真题你就能拿下药综，在复习物化时一定要关注知识点，而不是答案，切记！。。。虽然考试时答案也没变- -！ 计算题今年有两道16分，第一题是有关能量效率计算什么的（抱歉我真的忘了，因为这题完全看不懂，做不会T oT），这题确实不会只好瞎写了，希望有战友能回忆起来的话帮我添上谢谢。第二题是相平衡的计算，先要求画图，然后是产率的计算，非常基础和简单，应该是习题册的原题，同时也是去年的原题。。。。。12年考过。 生物化学 今年生物化学的题型的改动，取消了名词解释和简答题（真劲爆啊），1.英译汉2.选择题3.填空题 英译汉大家不用担心，非常简单，全部考的重要的概念和技术的英文全称，要求你写出英文简写与汉语即可，比如PCR ,VLDL 等，大家在复习时只要对重点概念的英文全称加以留意即可。 选择题都比较基础，有原题但不多，且分值也不高。 今年最大的变化时简答题没了，师兄我苦逼的日日夜夜都白瞎了。。。。填空题的话也都比较基础，多看看书也就能做个七七八八了。

Hibernate中Criteria的完整用法

QBE (Query By Example) Criteria cri = session.createCriteria(Student.class); cri.add(Example.create(s)); //s是一个Student对象 list cri.list(); 实质：创建一个模版，比如我有一个表serial有一个giftortoy字段，我设置serial.setgifttoy("2"), 则这个表中的所有的giftortoy为2的数据都会出来 2: QBC (Query By Criteria) 主要有Criteria,Criterion,Oder,Restrictions类组成 session = this.getSession(); Criteria cri = session.createCriteria(JdItemSerialnumber.class); Criterion cron = Restrictions.like("customer",name); cri.add(cron); list = cri.list(); ============================== 比较运算符 HQL运算符QBC运算符含义 = Restrictions.eq() 等于 <> Restrictions.not(Exprission.eq()) 不等于 > Restrictions.gt() 大于 >= Restrictions.ge() 大于等于 < Restrictions.lt() 小于 <= Restrictions.le() 小于等于 is null Restrictions.isnull() 等于空值 is not null Restrictions.isNotNull() 非空值 like Restrictions.like() 字符串模式匹配 and Restrictions.and() 逻辑与 and Restrictions.conjunction() 逻辑与 or Restrictions.or() 逻辑或 or Restrictions.disjunction() 逻辑或 not Restrictions.not() 逻辑非 in(列表) Restrictions.in() 等于列表中的某一个值 ont in(列表) Restrictions.not(Restrictions.in())不等于列表中任意一个值 between x and y Restrictions.between() 闭区间xy中的任意值 not between x and y Restrictions.not(Restrictions..between()) 小于值X或者大于值y 3: HQL String hql = "select https://www.sodocs.net/doc/7611151459.html, ,avg(s.age) from Student s group by https://www.sodocs.net/doc/7611151459.html,"; Query query = session.createQuery(hql); list = query.list(); .... 4: 本地SQL查询 session = sessionFactory.openSession(); tran = session.beginTransaction();

presentation evaluation criteria

Professional Studies Presentation Evaluation Criteria The numbers in the top of the boxes are points in a continuum. For example, you can assign 20 points for Organization. As long as you do not give more points than suggested in the leftmost box, the score will range between 0 and 100 when you add up the numbers. Organization (20%) 20 Consistently clear, concise, well organized. Points were easy to follow because of the organization. Transitions between sections smooth and coordinated. 15Usually clear, concise, well organized. Most of the presentation was easy to follow. Transitions between sections usually coordinated. 10Not always clear or concise. Organization was adequate, but weak. Occasionally wandered and was sometimes difficult to follow. Transitions between sections weak. 5Often unclear and disorganized, rambled too much. The presentation was confusing and difficult to follow. Transitions between sections awkward. Topic Knowledge (20%) 20Displayed an excellent grasp of the material. Demonstrated excellent mastery of content, application and implications. Excellent research depth. 15Displayed a general grasp of the material. Demonstrated good mastery of content, application and implications. Good research depth. 10Displayed some grasp of the material. Demonstrated adequate mastery of content, application and implications. Research not very deep. 5Displayed a poor grasp of the material. Demonstrated a superficial handling of content, application and implications. Little depth of research. Creativity (10%) 10Very creative and original. Imaginative design and use of materials. Novel handouts, visual aids, or methods. 8 Exhibited some originality and creativity. 5 Routine treatment, minimal thought given to originality or creativity. 3Lacked creativity. Very ordinary and mundane. Visual Aids (15%) 15Simple, clear, easy to interpret, easy to read. Well coordinated with content, well designed, used very effectively. Excellent example of how to prepare and use good visual aids 11Usually clear, easy to interpret, easy to read. Generally well coordinated with content, design was okay, generally used effectively. Demonstrated some understanding of how to use visual aids. 8 Marginally acceptable, too complex, crowded, difficult to read or interpret. Adequate coordination with content. Used only adequately. Showed little understanding of how to prepare and use visual aids. 4Poor quality visual aids (or none), hard to read, technically inaccurate, poorly constructed. Poor coordination with content. Used poorly. The presenter did not seem to know how to prepare or use visual aids effectively. Summary (15%) 15Clear, concise, major points emphasized, clear recommendations, strong conclusion or call for action. 11Referred to main points, recommendations weak or missing, weak conclusion or call for action. 8Vague mention of major points, no recommendations, weak conclusion, weak or no call for action. 4No summary, no recommendations, no conclusions, no call for action. Stage Presence (20%) 20 Excellent stage presence. Confident, used notes well, at ease, excellent gestures, good audience attention, good eye contact. 15Good stage presence. Fairly confident, used notes fairly well, good gestures, acceptable audience attention and eye contact. 10 Adequate stage presence. Read parts, fumbled with notes, several distracting mannerisms, minimal gestures, minimal eye contact, too many um=s. 5Poor stage presence. Unprepared, awkward, shuffled papers, poor eye contact, lots of um=s, turned from audience to read overheads, shuffled feet, fidgeted. Poor gestures. TOTAL POINTS COMMENTS:

华西药学院 历年分子生物学 考题及参考答案

华西药学院2009-2010学年上学期分子生物学考题答案 2013年1月22日晚 使用说明：此答案仅供参考，如有谬误，还请见谅！ 一、英文翻译【12*0.5=6分】 1 SNP 单核苷酸多态性 2 Transposon 转座子 3 RNA splicing RNA剪接 4 Attenuator 衰减子 5 determination of DNA sequence DNA序列测定 6 Interrupted gene 断裂基因 7 DDRP DNA指导的DNA聚合酶8 CRP 分解代谢基因活化蛋白 9 site-specific in vitro mutation 体外定向突变10 frameshift mutation 移码突变（这个过时了，不考） 11 translocation 移位12 primase 引物酶 二、名词解释【10*2=20分】 1 Enhancer 增强子：指远离转录起点，决定基因表达的时空特异性，增强启动子转录活力的一段DNA序列。 2 Molecular chaperone 分子伴侣：细胞内能够帮助新生肽链正确折叠和装配组装成为成熟蛋白质的一类蛋白因子，在真核生物和原核生物中广泛存在。 3 semidiscontinous replication 半不连续复制：一条链上的DNA在DNA聚合酶的作用下以5'-3'方向连续合成一条长的DNA链，而另一条另一条链的DNA合成是不连续的，即先合成一段段短的DNA片段，再将这些短片段连成DNA长片段，这样的过程称为半不连续复制 4 supergene family 超基因家族: 来源相同、结构相似，但功能却不尽相同的一大批基因，这一大批基因分属于不同的基因家族，总称为超基因家族 5 promoter 启动子：RNA聚合酶识别、结合和开始转录的一段DNA序列，是RNA聚合酶起始转录需要的辅助因子 6 mic RNA 干扰mRNA的互补RNA，即反义RNA，通过碱基互补和特定mRNA的SD序列、起始密码子AUG以及它们的上下游的部分核苷酸序列结合，从而抑制mRNA的翻译 7 reverse transcription 逆转录：以RNA为模板合成DNA，这与通常转录过程遗传信息从DNA到RNA的方向相反，故称为逆转录作用，通常又叫做RNA指导的DNA合成。 8 stringent response 严紧反应（这个过时了，不考） 9 gRNA（这个过时了，不考） 10 physical map物理图谱:以一段已知的核苷酸序列的DNA为“位标”，以碱基对Mb或Kb 等物理距离为图距的基因组图。 三、填空【60*0.5=30分】 1、RNA生物合成抑制剂有【】、【】、【】三种，其中碱基类似物是属于【】（这个过时了，不考） 2、Southern印迹杂交是鉴别【DNA 】靶分子的杂交，Northern印迹杂交是鉴别【RNA】靶分子的杂交，而Western印迹杂交可以用来分析【蛋白质】 3、端粒的复制依赖【端粒酶】的催化，以【RNA】为模板通过【逆转录】方式来完成 4、RNA聚合酶对转录起始的调控主要是通过【σ亚基替换】来调控，这是因为【σ因子】能够识别DNA分子上的RNA合成的起始信号，不同的【σ因子】会竞争性的与核心酶结合，而且【环境】的变化可以诱导产生特定的【σ因子】，从而开启特定的基因。 5、DNA复制后修复主要有【重组修复】和【SOS修复】两大类，其中【SOS修复】属于差错倾向性修复。 6、根据突变带来的效果，DNA突变可分为【无义突变】、【同义突变】和【错义突变】，

华西药学院大一上下学期各科课程介绍及一些经验(精)

关于华西药学院大一上下学期各科课程介绍及一些经验分享 (如有谬误,还请见谅 2011年9月至10月首先,我先讲下大一下的概况。我们大一下学期有两种课, 一类是必修课,一类是选修课。09级是不管评奖学金还是保研都只看必修的成绩(只能第一次的成绩,每一学年的评奖都不能挂科,但下年无挂科可参加,SO,大家第一次就考高分最好了!,而我们10级却不太一样,我们保研跟09一样,但评奖学金却还要算选修的成绩,当然,这里不包括中华文化和其他自己选的课,是指你课表里预置的选修课,我不知道你们11级会怎样(到时你们可以问问你们的辅导员,但如果想拿奖学金的同学就要重视选修的学习了,争取拿高分,这样对以后的评奖有帮助!好了,现在开 始各科介绍! 必修篇 上学期 本人于10年进入华西药学院,至今刚好在药海混了一年,想起当年我的惨痛经历,深知经验的重要性,故此,作此篇,让11级的同学能够知己知彼,充分做好相关准备,利用好时间,提高效率,希望对药学院的同志们有所帮助。本篇参考了一些学长的资料,主要文献来源于10级共享文件中宁健凯的《转大一课程介绍》,在此特别感谢! 1、大学英语 主要内容:一般就是用PPT讲讲课文,讲讲课后练习,做点听力练习,看看电影。 附加:新生进校后有英语分班考试【10级,11级是否有还不知道】,根据高考考试成绩分为A、B班,根据上课情况,我们10级学生普遍认为差距不太大,还有外教 的课,不过挺简单的,就是期末会有一个个人展示,要算分的! 重要性:这门课上课没啥重要内容,期末考试也比较简单,但学分非常重,4个学分,是本专业学分最多的一门学科,我那一届的老师经常跟我们说:“因为我们以后要与国际接轨,所以一定要学好英语”,个人觉得很对,毕竟现在英语是国际语言,学好对于以

Design Criteria

Design Criteria Building optimization must be followed by design criteria; these design criteria are given by the corresponding code. With the aim to determine the optimization criteria I personally have chosen the IBC 2013 Code with the corresponding related codes, such as ACI 318 and ASCE-7, concrete and load codes. Firstly we should determine the basic requirements for a high-rise building with shear wall structure and deep foundation as a foundation system, being this kind of building the objective of the study in situ. ?Building use and occupancy: (CHAPTER 3)Residential group R-2, residential occupancies containing sleeping units or more than two dwelling units where the occupants are primarily permanent in nature, including: Apartment houses, Boarding houses (non-transient), Convents, Dormitories, Fraternities and sororities, Hotels (non-transient), I Live/work units, Monasteries, Motels (non-transient), Vacation timeshare properties. ?Requirements based on occupancy:(CHAPTER 4) 1. For buildings not greater than 420 feet (128 m) in building height, the fire-resistance rating of the building elements in Type IA construction shall be permitted to be reduced to the minimum fire-resistance ratings for the building elements in Type IB. 2. In other than Group F-1, M and S-1 occupancies, the fire-resistance rating of the building elements in Type IB construction shall be permitted to be reduced to the fire-resistance ratings in Type IIA. 3. Bond strength:

criteria范文

criteria范文 我抄袭作业的原因是因为我想早点写完作业早点玩，谁都想玩，但是假如为了玩就抄 作业的话太不值了，现在玩只能玩一会，假如学习不好，以后找不着工作，没钱吃饭，还 谈的上玩吗我抄袭作业抱有一种作业是做给老师看的这种想法，其实根本不是，我们不 做作业，老师就不用批改作业，反而更轻松。所以，作业是为自己做的，我这么想辜负了 老师的一片好心，所以，我向老师表现出深深地歉意! One point is clear that different issues have different objective criteria. For example, criteria of price talking will include factors of cost, market situation, depreciation, price competition and other necessary factors. In other negotiations, exper ts’ opinions, international conventions and norms and legal documents will all serve as objective criteria. 为解决本人衣服无人洗，饭菜无人做，花钱无节制，生活无压力的现状，本人新引进 一招商项目，将于2020年02月20(26)日17时30分举行盛大的庆典活动，请亲朋好友准时参加! In the Sino—US negotiation on China’s accession into WTO, the two parties disputed over China’s developing country status. US took the position that China should be treated as a developed country. To back US stance, American negotiators cited China’s growing exports and large foreign reserve holdings. They a rgued that in developing countries China’s sophisticated technology in launching and retrieving satellites had no parallel. One American negotiator even compared the situation in China with that in India and some African countries. He said when he opened the door of a family in a poorest area randomly chosen by the Chinese government and asked the people if they had their breakfast, he was told they did, and he went on asking if lunch and supper were guaranteed, the answer was yes. However he had a very different story in some African countries and even in some areas in India. People there had little food for breakfast, not mention lunch and supper. The two countries insisted on their own standards and it was hard to bridge the discrepancy. Here the focus is which criterion to apply to for resolving the dispute. In fact there is a ready criterion provided by the World Bank, which is measured by per capita GNP. According to the World Bank’s standard, countries whose per capita GNP below $785 (1996) are the poorest countries. China’s per capita GNP in 1997 was $750, which is among the poorest countries. 甲方聘用乙方的月薪为_____元(含养老、医疗、住房公积金)。试用期满后，并经考 核合格，可根据平等协商的原则，签订正式劳动合同。

全国五大药学院之四川大学华西药学院

全国五大药学院校简介（一）——四川大学华西药学院 首先是我就读的学校，四川大学的华西药学院。 华西药学院最强的是药剂、药化，药分等也不错，临床药学更是中国首创的，据说目前国内高校用的临床药学的教材全是在我们的基础上编的。 华西药学院还有个特点，那就是面积大，据说是全国各个药学院中最大的，无数其他的药学院羡慕不已。 华西药学院前身为华西协合大学理学院药学系，创建于1932年，是我国最早的全日制本科高等药学院系之一。1953年，更名为四川医学院药学系，随后设立药学和药物化学两个专业；1985年，四川医学院药学系随学校改名为华西医科大学药学系，1987年3月，在原药学系和药物研究所的基础上建立药学院；1989年，在国内率先招收临床药学专业的本科学生；2000年10月，原华西医科大学与四川大学合并，组建新的四川大学，随之更名为四川大学华西药学院。 华西药学院现有建筑面积27000平方米的教学楼和实验楼，分布在风景如画的华西钟楼和荷花池畔。现有十一个教研室，一个药物研究所，三个中心，即：药物化学教研室、药剂学教研室、天然药物化学教研室、生药学教研室、药物分析学教研室、药理学教研室、生物制药学教研室、物理药学教研室、临床药学教研室、药事管理学教研室、中药制剂学教研室；四川大学药物研究所；现代药学专业教学中心实验室、分析测试中心和药事管理培训中心，1个生药标本馆和药用植物园。药学院现有教职工134人，其中教授25人，研究员1人，副教授23人，副研究员和高级实验师等13人，讲师27人，助理研究员和实验师等16人；省学科带头人4名，博士研究生导师18人，硕士研究生导师26人。目前每年招收本科生200名左右，博士生、硕士生160余人，全院在校生1200余人。 华西药学院现设药学本科专业，下设药物化学、药学和临床药学三个专业方向。为药学一级学科博士学位授权单位，有药学博士后流动站1个，二级学科博士授权点3个（药物化学、药剂学、药物分析学），二级学科硕士授权点6个（药物化学、药剂学、药物分析学、生药学、微生物与生化药物和药理学）。可招收博士的学科包括：药物化学、药剂学、生药学、药物分析、药理学、临床药学、药事管理学、天然药物化学。可招收硕士的学科包括：药物化学、药剂学、生药学、药物分析、微生物与生化药学、药理学、临床药学、药事管理学、天然药物化学。有省重点学科2个：药物化学和药剂学，教育部重点实验室1个：靶向药物及传递系统重点实验室（建设），省重点实验室2个：靶向药物与新型给药系统实验室和天然药物学实验室。

条件类Criteria的用法

复合查询主要是处理，具有关联关系的两个实体怎样进行关联查询，比如User 实体对象与Addres实体对象具有一对多的关联关系，我们可以如下构造 符合查询： Criteria criteria=session.createCriteria(User.class); Criteria addcriteria=criteria.createCriteria(“addresses”);(1) addcriteria.add(Express.like(“address”,”%tianjin%”)); List list=criteria.list(); for(int i=0;i User user=(User)list.get(i); System.out.println(user.getName()+”\n”); Set addresses=user.getAddresses(); Iterator it=addresses.iterator(); while(it.hasNext(){ Address address=(Address)it.next(); Syste m.out.println(address.getAddress()+”\n”); } } 当执行到了（1）处时，表明要针对User对象的addresses属性添加新的查询条件，因此当执行criteria.list()时，Hibernate会生成类似如下的SQL语句： Select * from user inner join address on user.id=address.id where address.address like …%shanghai%?; 正如我们所见，我们可以通过向Criteria中添加保存关联对象的集合属性（addresses属性保存与User对象相关联的Address对象），来构造复合查询，在数据库一端是通过内连接查询来实现。 Hibernate QBC查询 QBC查询：

华西药学院2015届推免研究生评分细则(试行)

四川大学华西药学院推免研究生实施办法 （试行） 一、推免原则及推免条件 参照教育部文件（教学厅〔2014〕5号）、四川省教育厅文件（川招考委〔2014〕59号）和四川大学推荐优秀应届本科毕业生免试攻读研究生的实施办法（川大教〔2014〕178号）执行。 二、评分要求及细则 1．综合成绩的计算方法 综合成绩＝学业成绩×65％＋科研创新潜质、专业能力倾向成绩×30％＋社会活动成绩×5％； 其中科研创新潜质、专业能力倾向成绩=科研能力成绩×1/3+专家面试×2/3 2．科研能力与社会活动范围的认定 2.1科研能力 （1）科研成果：主要指发表在与药学专业有关的公开刊物上的研究论文；主编或参编与药学专业有关的著作；参研与药学相关的项目；获省级及以上奖励。 （2）科学竞赛：主要指省级及以上科技、知识类竞赛奖励（如大学生英语竞赛、大学生电子设计竞赛、挑战杯竞赛、数学建模竞赛、课外科技竞赛、创业设计大赛、 机器人大赛等）。 （3）发明创造：主要指发明专利。 2.2社会活动 社会活动：包括文艺活动（主要指省级及以上文学、艺术类竞赛奖励）、体育活动（主要指省级及以上体育类竞赛奖励）、社会活动（主要指承担校内学生组织、社团活动、实践活动），以及校外公益活动并获校级及以上奖励。 3．科研能力计分办法 （1）凡经我院实验教学（必修实验课程）培养得优良（80分及以上）者，其科研能力的基础分为8分。若未达到优良，学分在2学分（含2学分）以下的实验课程每门扣除0.05分，学分在2学分以上的实验课程每门扣除0.1分。 （2）在校期间，在四川大学相关实验室或研究室进行科研训练，并在各类与药学有关的公开刊物上发表研究论文（需见刊，并附上指导教师的情况证明）。其中发表药学类SCI收录论文的第一作者至第四作者加分依次为1, 0.5，0.2, 0.1分；在药学类核心刊物上发表论文的第一作者至第四作者加分依次为0.5，0.2, 0.1, 0.05分；在其

2003华西药学综合

四川大学 2003年攻读硕士学位研究生入学考试试题 科目：药学综合 代玛：706# 专业：药理学、药物化学、药剂学、生药学、药物分析学微生物与生化药学、生物化学与分子生物学、生物医学工程；（试题共13页） (答案必须写在答题纸上,写在试题上不给分） 有机化学部分（40分) 一、有机化合物的命名 1.用系统命名法命名下列化合物（4分） 2.写出下列化合物的结构式（4分） （1）反-4-甲氮基环己基甲醛 (优势构想) (2)二苯基并-18-冠-6 （3）1,4-二甲基本环[2.2.2]辛烷（4）3-羟甲基-4-羟基吡啶 二、完成下列反应（若为立体选择性反应，须写出产物的的立体构型 (毎小 题2分.共16分） 1、 2、 3、

4、 5、 6、 7、 8、 三、由指定原料合成下列化合物(其他试剂任选.毎小题5分.共10分） 四.推荐下列化含物的结构（共6分） 化合物 A (C6H10O) 与 Br2/CCl4 ，Na ，苯肼均不发生反应。A 不溶于水，但在酸或碱催化下可水解得到B（C8H12O2）。B与等摩尔的高锰酸作用可得到甲醛和C(C6H10O)。 C有碘仿反应。试写出A、 B. C的可能结构及相关反应式。

分析化学部分（40分) 一、填空题 (30分.毎空1分） 1、写出NH4H2PO4在水溶液中的质子条件式__________________________________。 2、HC104和HC1的酸强度不同，但在水中，二者的强度差别消失。水是二者的_____；而HC1和HAc在水中表现出不两的酸强度，水在这里起到了____________效应。 3.结合滴定中的封闭现象是指_____________,可加入__________消除干扰。 4.药典規定测定CuSO4·5H2O含量的方法为：取样0.5g，精密称定，置碘瓶中，加水50ml 溶解后，加HAc 4ml，KI2g，用Na2S2O3（0.1mol/L）滴定，近终点时加入淀粉指示液，继续滴定至兰色消失，即达终点。问： ①取0.5g左右样品的原因是________；②写出取下列溶剂和试剂所用量器或容器；50ml 水_______, 4mlHAc_______, 2gKI_______:③近终点时加入淀粉指示液的原因是______ __(CuSO4? 5H2O的分子量为249.7) 5.指示电扱是指电位随_________________________的电极，参比电极的电位___________。 6.离子对色谱是在流动相中加入_________试剂。被分析的样品离子在流动相中与___________,从而増加样品在非极性固定相中的溶解度，使分配系数增加，改善分离效果；离子抑制色谱则是通过调节流动相的_____，抑期_______，增加样品在固定相中的溶解度，以达到分离有机弱酸碱的目的。 7.称取维生素C 0.05g 溶于100ml的0.005mol/L 硫酸溶液中，在准确量取此溶液2.0ml 稀释至100ml，取此溶液于1cm吸收池中，在λ______245nm（）处测得A 值为0.551，样品中维生素C的百分含量为___________,在λ_____处测定的原因是___________。 8.用pH汁测定溶液的pH值.用pH=4.00缓冲液，25℃时测得电动势为0.209V.改用未知溶液代替缓冲溶液，测得电动势为0.312V.该未知溶液PH值为________________。 9.测定含量可用三种方法：其中化学分析法为_______法，滴定剂为_____指示剂为_____；两种仪器分析法为______和________。其选择依据分别是_______和_______ 10．偏高Beer定律的光学因素有__________、__________、___________和____________。 二、选择题（10分，每题1分） 1.测定头发中徽量锌含量, 应选择（） A. EDTA 滴定法 B.离子选择性电极法 C原子吸收分光光度法 2.用NaOH溶液滴定苯甲酸溶液，应选指示剂为（) A.甲基红 B.酚酞 C.结晶紫 3.指出下列关于吸附色谱叙述错误的是（） A.姐分极性增加，从溶液中被吸附的作用越强 B.流动相的极性越强，溶质越容易被固定相所吸附 C.吸附剂的活度级数越小.对溶质的吸附力越大 4. GC进行定量分析时，最常用的方法是（ ) A.内标法 B.归一化法 C.外标一点法