Danggui Buxuetang， derived from Clarifying Doubts about Damage from Internal and External Causes （Volume 2）： Treatise on Heat Injury to Stomach Qi（《内外伤辨惑论卷中·暑伤胃气论》） by LI Dongyuan in the Jin and Yuan dynasties， is a classic and famous formula for tonifying qi and generating blood that has been inherited and promoted by successive generations of medical practitioners and has been included in the "Catalogue of Ancient Classical Prescriptions （First Batch）" published by the National Administration of Traditional Chinese Medicine in 2018. The paper analyzed the historical origin， composition， dosage， processing， preparation， decocting， and taking methods， efficacy， and application of the classic formula Danggui Buxuetang by consulting ancient and modern literature and combining the key information examination principles of ancient classic prescriptions. A total of 604 pieces of information on relevant ancient literature were collected， including 186 ancient Chinese medical books， of which 40 （five in the Jin and Yuan dynasties， 19 in the Ming Dynasty， and 16 in the Qing Dynasty） had detailed records of composition， processing， and dosage. Danggui Buxuetang is mainly comprised of Astragali Radix and Angelicae Sinensis Radix. According to the ancient and modern dose conversion， there are 37.3-38.1 g of Astragali Radix and 7.5-7.6 g of Angelicae Sinensis Radix in the formula. Astragali Radix is preferably fried with honey and Angelicae Sinensis Radix with wine. Astragali Radix and Angelicae Sinensis Radix are decocted with 600 mL of water to 300 mL， and taken warm before meals. The main effect of this formula are described in ancient books as blood deficiency and fever， with symptoms of muscle fever， dryness and heat， irritability and thirst， red eyes and face， sleeplessness in daytime and night， and surging and feeble pulse which is weak under hard pressing， and it is a famous formula for replenishing qi and generating blood. Modern research shows that Danggui Buxuetang is commonly used in the treatment of various kinds of anemia， diabetic nephropathy， tumors， and cardiovascular and cerebrovascular diseases. The above research results can provide a reference for the subsequent development and research on the classic formula Danggui Buxuetang.

Objective:To explore the occurrence of medication errors (MEs) involving cytotoxic drugs in pharmacy intravenous admixture service (PIVAS).Methods:All the prescriptions containing cytotoxic drugs from January 2016 to December 2019 in PIVAS in Peking University Cancer Hospital were collected using the hospital information system. ME records found by pharmacists during the prescription review were screened out (defined as prescription error) and "the medication error record book" was searched to screen out MEs in PIVAS (defined as admixture errors) in the same period. Descriptive analysis was conducted on the grade, classification, links in which the MEs occurred, people who triggered, ME content, and the involved cytotoxic drugs of these MEs. In addition, the MEs that were not found in PIVAS but passed to the next link were defined as out-door errors.Results:A total of 347 367 prescriptions involving cytotoxic drugs were received in PIVAS in our hospital during the study period, in which 1 080 MEs were found, and the incidence of ME was 0.31%. The 1 080 MEs were all grade B errors that did not cause patient harm, of which 841 (77.87%) were prescription errors and 239 (22.13%) were admixture errors. Five MEs were not intercepted and led to out-door errors and the incidence of out-door errors was 0.01‰(5/347 367). The top 5 ME contents were wrong solvent (63.15%, 682/1 080), incomplete prescription (11.67%, 126/1 080), wrong number (8.80%, 95/1 080), wrong dose (6.11%, 66/1 080), and wrong method in intravenous administration (4.35%, 47/1 080). A total of 32 cytotoxic drugs were involved in 1 080 MEs and the top 5 were paclitaxels (23.24%, 251/1 080), fluorouracil (12.59%, 136/1 080), doxorubicin (6.39%, 69/1 080), cisplatin (5.46%, 59/1 080), and etoposide (5.37%, 58/1 080).Conclusions:The incidence of ME was 0.31% in PIVAS in our hospital, all of which were grade B errors. The errors mainly were prescription errors, the main contents were wrong solvent, and the main drugs involved were paclitaxels, fluorouracil, doxorubicin, cisplatin, and etoposide.

Objective:To explore the occurrence of medication errors (MEs) involving cytotoxic drugs in pharmacy intravenous admixture service (PIVAS).Methods:All the prescriptions containing cytotoxic drugs from January 2016 to December 2019 in PIVAS in Peking University Cancer Hospital were collected using the hospital information system. ME records found by pharmacists during the prescription review were screened out (defined as prescription error) and "the medication error record book" was searched to screen out MEs in PIVAS (defined as admixture errors) in the same period. Descriptive analysis was conducted on the grade, classification, links in which the MEs occurred, people who triggered, ME content, and the involved cytotoxic drugs of these MEs. In addition, the MEs that were not found in PIVAS but passed to the next link were defined as out-door errors.Results:A total of 347 367 prescriptions involving cytotoxic drugs were received in PIVAS in our hospital during the study period, in which 1 080 MEs were found, and the incidence of ME was 0.31%. The 1 080 MEs were all grade B errors that did not cause patient harm, of which 841 (77.87%) were prescription errors and 239 (22.13%) were admixture errors. Five MEs were not intercepted and led to out-door errors and the incidence of out-door errors was 0.01‰(5/347 367). The top 5 ME contents were wrong solvent (63.15%, 682/1 080), incomplete prescription (11.67%, 126/1 080), wrong number (8.80%, 95/1 080), wrong dose (6.11%, 66/1 080), and wrong method in intravenous administration (4.35%, 47/1 080). A total of 32 cytotoxic drugs were involved in 1 080 MEs and the top 5 were paclitaxels (23.24%, 251/1 080), fluorouracil (12.59%, 136/1 080), doxorubicin (6.39%, 69/1 080), cisplatin (5.46%, 59/1 080), and etoposide (5.37%, 58/1 080).Conclusions:The incidence of ME was 0.31% in PIVAS in our hospital, all of which were grade B errors. The errors mainly were prescription errors, the main contents were wrong solvent, and the main drugs involved were paclitaxels, fluorouracil, doxorubicin, cisplatin, and etoposide.

Objective To study the effect of glutamine (Gln) on the intestinal mucosa inflammatory reaction and permeability after intestine ischemia-reperfusion injury in rats.Methods The rat model of intestinal ischemia-reperfusion injury was established by clamping the mesenteric superior artery and then restoring blood flow.Forty-eight model rats were divided into control group (n =24) and model + Gln group (n =24)according to the stochastic indicator method.Both groups were given enteral nutrition with equal energy and nitrogen [energy 125.4 kJ/ (kg · d) and nitrogen 0.2 g/ (kg · d)].The model +Gln group was fed with enteral nutrition plus 3％ Gln,while the control group was fed with enteral nutrition plus 3％ soybean protein.The experiment lasted 8 days after modeling.The intestinal mucosa and the plasma levels of nuclear factor-κB (NF-κB),tumor necrosis factor-α (TNF-α),interleukin-6 (IL-6),Gln,D-LACtic acid and diamine oxidase (DAO) were observed in rats before and after modeling and on the 3rb and 8rd day of the experiment.Changes in the morphology of intestinal mucosa were observed by electron microscopy.Results After modeling in control and model + Gln group,the level of NF-κB in intestinal mucosa [18 cases (75.0％) and 17 cases (70.8％)] were significantly higher than those before modeling [0 case (0.0％),P =0.013,P =0.019],the level of IL-6 in intestinal mucosa [(313.27±75.28) pg/g and (321.75±76.46) pg/g] were significantly higher than those before modeling [(227.52 ±58.13) pg/g,P =0.023,P =0.043],and the level of TNF-α in intestinal mucosa [(241.28 ±65.29) pg/g and (240.35 ±64.86) pg/g] were significantly higher than those before modeling [(172.45 ±33.76) pg/g,P=0.036,P=0.011].The plasma level of IL-6 [(150.32 ± 18.74) ng/L and (148.21 ±20.19) ng/L] were significantly higher than those before modeling [(116.37 ± 14.59) ng/L,P =0.032,P =0.025],the plasma level of TNF-α [(127.62 ± 14.24) ng/Land (123.86 ± 13.75) ng/L] were significantly higher than those before modeling [(85.18 ± 8.84) ng/L,P =0.018,P =0.035],and the plasma level of D-LAC [(0.46 ±0.03) mmol/L and (0.51 ±0.04) mmol/L]were significantly higher than those before modeling [(0.27 ±0.02) mmol/L,P =0.041,P =0.018],and the plasma level ofDAO [(2.76±0.57) U/ml and (2.58 ±0.51) U/ml] were significantly higher than those before modeling [(1.52±0.24) U/ml,P=0.015,P=0.037],while the plasma level of Gln [(0.18 ±0.01) g/L and (0.21 ± 0.01) g/L] were significantly lower than those before modeling [(0.39 ± 0.03) g/L,P =0.026,P =0.031].On the 3rd and 8th days of the experiment in the control group,the level of NF-κB in intestinal mucosa [16 cases (66.7％),15 cases (62.5％)] were significantly higher than those before modeling (P =0.027,P =0.002),the level of TNF-α in intestinal mucosa [(226.23 ±55.35) pg/g and (214.76 ±54.82) pg/g] were significantly higher than those before modeling (P=0.042,P =0.038)],the level of IL-6in intestinal mucosa [(297.56 ± 71.39) pg/g and (291.49 ± 68.46) pg/g] were significantly higher than those before modeling (P =0.031,P =0.012).On the 3rd and 8th days in the control group,the plasma level of IL-6[(147.38 ± 17.25) ng/L and (144.65 ± 15.32) ng/L] were significantly higher than those before modeling (P =0.016,P =0.034),the plasma level of TNF-α [(121.75 ± 13.72) ng/L and (113.83 ± 11.69) ng/L] were significantly higher than those before modeling (P =0.025,P =0.041),the plasma level of D-LAC [(0.41 ±0.03) mmol/L and (0.53 ±0.05) mmol/L)] were significantly higher than those before modeling (P =0.029,P =0.030),the plasma level of DAO [(2.51 ± 0.52) U/ml and (1.76 ± 0.34) U/ml] were significantly higher than those before modeling (P =0.034,P =0.016).The plasma level of Gln [(0.22 ±0.01) g/L and (0.21 ±0.03) g/L] were significantly lower than those before modeling (P =0.042,P =0.035).On the 3rd day of the experiment in the model + Gln group,the levels of NF-κB,TNF-α,and IL-6 in intestinal mucosa [14 cases (58.3％),(213.78 ±43.76) pg/g,(293.72 ±69.86) pg/g] were significantly higher than those before modeling (P =0.038,P =0.026,P =0.013) ; the plasma level of IL-6,TNF-α,D-LAC,and DAO [(135.61 ±14.25) ng/L,(117.35 ±11.29) ng/L,(0.45 ±0.03) mmol/L,and (2.26 ± 0.43) U/ml] were significantly higher than those before modeling (P =0.021,P =0.032,P =0.032,P =0.025).On the 8th day of the experiment in the model + Gln group,the levels of NF-κB,TNF-α,and IL-6 in intestinal mucosa [9 cases (37.5％),(184.53 ± 42.16) pg/g,and (236.83 ±66.52) pg/g] were significantly lower than those after modeling and those in the control group (P =0.024,P=0.027; P=0.026,P=0.039; P=0.013,P=0.028) ; the plasma levels of IL-6,TNF-α,D-LAC,and DAO [(126.35±12.74) ng/L,(92.76±9.42) ng/L,(0.31 ±0.02) mmol/L,and (1.76±0.34) U/ml]were significantly lower than those after modeling and those in the control group (P =0.021,P =0.030; P =0.032,P =0.025 ; P =0.024,P =0.037 ; P =0.022,P =0.036) ; the plasma level of Gln [(0.40 ±0.03) g/L] was significantly higher than those after modeling and in the control group (P =0.028,P =0.032).Under the electron microscope,the structure of villus and recess was damaged after modeling,villi were sparse and short,with a lot of inflammatory cell infiltration in the lamina propria.Lymphangiectasia and edema occured after modeling.On the 8th day,compared with after modeling and the control group,intestinal villi and recess structure were significantly restored in the model + Gln group; compared with the after-modeling status,the recovery of intestinal mucosa villi and recess structure was not obvious,and the inflammatory cell infiltration in the lamina propria persisted in the control group.Conclusion Gln repairs ischemia-reperfusion injury in the intestinal mucosa by regulating intestinal mucosa inflammatory cytokine release,inhibitng inflammatory response,and reducing the permeability of the intestinal mucosa.

ObjectiveTo investigate the clinic and pathologic features of one patient diagnosed with neurocutaneous melanosis ( NCM ) by biopsy.MethodsA 21-year-old woman presented with a 2-month history of tinnitus,headache,vomiting and 1-month history of impaired vision.At birth,a massive nevus covering most of the posterior abdomen had been noted as well as the presence of multiple smaller lesions all over the body.Magnetic resonance imaging demonstrated a posterior fossa cyst compatible with the Dandy-Walker syndrome and extensive leptomeningeal enhancement. Surgery was performed to cystectomy and to obtain pathologic specimens from the leptomeninges. Biopsy and immunohistochemical study was performed.ResultsAt surgery,diffuse black pigmentation of the leptomeninges and the cyst was found.Under microscope,the cyst and leptomeninges were composed with melanocytes with variable pigmentation.Those cells positive for HMB45,MelanA,S100 and vimentin.Ki-67 positive cells ＜ 1％.The pathologic diagnosis wasleptomeningeal diffusemelanocytosis. Thepatientdied 2months after thesurgery.ConclusionsNCM is characterized by a focal or diffuse proliferation of melanin-producing cells in both the skin and the leptomeninges.NCM could be compatible with the Dandy-Walker syndrome.Definite diagnosis relies upon the histological data obtained by mean of biopsy.

Objective： To study the changes of water molecular diffusion in the ischemic region by using MR dephase technique and discuss the potential mechanism of the diffusion changes at early stage. Methods: Totally 43 cases were studied retrospectively. There were 10 cases whose MRI examinations were performed within 6 hours，12 cases from 7－24 hours，7 cases from 2－7 days, 8 cases from 8－14 days, 6 cases from 15 days to 2 months. The apparent diffusion coefficients in the ischemic region were calculated. Results: The ADCav in the grey matter was 8.61×10－4mm2*s－1. The ADCav decreased to (4.72×10－4±1.51×10－4) mm2*s－1 in ischemic region at superacute stage, ADCav ratio to contralateral corresponding region was 0.55±0.18, and ADCav increased to (5.68×10－4±1.22×10－4) mm2*s－1 during the time range of 2-7 days, （9.22×10－4±2.07×10－4） during the time range of 8－14 days, and approaching （26.42×10－4+9.65×10－4） mm2*s－1 during the time range of 2 months. The pearson product- moment correlation between the changes of diffusion value and time was sighificent (r=0.95, P<0.001). ADCv increased at superacute stage and decreased over time. Conclusion: The diffusion of water molecules in ischemic region decreased at superacute stage, and the ADC increased over time. The anisotropy increased at superacute stage and decreased as the course developed. DWI could detect ischemic lesion much earlier than CT and routine MR examination. DWI has great value in the diagnosis of superacute stroke. The mechanism of the diffusion changes at early stage may be the intracellular toxicity edema.

Objective To investigate the MR postprocessing workstation on PC level.To discuss the hardware enviroment suitble for the lab MR postprocessing and the correspongding clinical diagnostic value. Methods MR diffuison-weighted imaging and routine MRI were performed in 6 normal adults.The ADC and AI parameter images were rebuilt by using Perfect-Tech (version 2.0) software on the market saled PC computer. Results The process and analysis could be performed sucessfully on the the market saled PC computer. On the ADCav images,the boundary between the grey matter(GM)and white matter(WM) was blurring and showed the similar intensity.The anistropy in white matter was averaged out on the ADCav images.The ADC value was (7.59?1.12)?10 -4 mm 2/s in WM and (10.50?4.34)?10 -4 mm 2/s in GM. On the AI images,there was sharp boundary between GM and WM,with hypointensity in GM and hyperintensity in WM. The anistropy contrast was enhanced on AI images. AI was 0.20?0.09 in WM and 0.09?0.07 in GM with statistically significant difference between them(t=4.13,P

Objective To summarize the appearances of MS lesions on DWI, and to quantitatively study the ADC and AI values in different clinical MS subgroups Methods One hundred and eighty seven lesions were studied in 18 cases of MS at different clinical stages Routine MR and DWI were performed in all cases ADC and AI were calculated in the lesions,NAWM, and normal control group Results Hyperintensity (edema like on T 2WI) was demonstrated on DWI at acute primary progressive MS lesions Hyperintense ring sign was found at acute relapse MS lesions ADC increased in all subgroups of MS Significant difference of ADC was demonstrated among MS lesions, NAWM, and normal control groups Significant decrease of AI was demonstrated at later stages Hyperintensity was found in all MS lesions on T 2WI The hyperintensity lesions on DWI had enhanced or non enhanced appearances on CE T 1WI The ADC value of enhanced MS lesions was less than that of the non enhanced lesions ( t =4 19, P 0 05) Conclusion DWI could give quantitative information for different pathological changes in MS lesions of different clinical subgroups Quantitative measurement of diffusion has great potential value in the diagnosis, differential diagnosis, and the prediction of prognosis in MS

Objective To summarized the diseases which were demonstrated as hyperintensity lesions on high diffusion sensitive gradien(high b value) diffusion weighted imaging(DWI) To investigate the differential diagnosis of the diseases and to discuss the corresponding biophysics mechanism Methods 90 cases were studied, which were clinically highly suspected of brain ischemic stroke onset and in which hyperintensity lesions were demonstrated on DWI The patients were divided to 2 groups according to the time between the onset and the MR examination:group A(1 5-6 0 h)with 13cases, group B(7 h to 8 d)with 77cases The appearances of the lesions on conventional MRI, ADC values and anistropy(CV )of the lesions were studied Results hyperintensity lesions on high b value DWI were demonstrated in following diseases: acute ischmia, hematoma, abcesses, mengioma, mutiple sclerosis(MS) The ADC value was decreased to(5 87?1 02)(10 -4 mm 2/s in superacute cerebral ischemia, while the ADC value increased to (8 08?1 15)?10 -4 mm 2/s in active MS The CV in cerebral ischemia lesions was higher than the control group( P

Objective Calcium overload has important effect on cell injury in the ischemic stroke MR DWI/PWI mismatch may display the ischemic penumbra We try to explain the relationship between the characters of MR DWI/PWI and intracellular Ca 2+ in the different ischemic region through the model of focal cerebral ischemia Methods Twenty-eight rabbits underwent permanent middle cerebral artery occlusion (MCAo) From 0 5 h to 36 h after the onset of occlusion, diffusion-, perfusion-, and T 2-weighted MR imaging were performed to generate ADC, CBF, CBV parameters and anatomic images After the MR scanning, the same brain slices were incubated with Fluo-3/AM followed by the examination using laser confocal scanning microscope (LCSM) At different ischemic time, fluorescence intensity (FI) of the intracellular Ca 2+ in the DWI/PWI match region and mismatch one was recorded FI match /FI contralateral and FI mismatch /FI contralateral were produced and analyzed Results (1) MR outcome: The DWI/PWI match was located in the lateral caudoputamen and the DWI/PWI mismatch was mainly located in the frontoparietal cortex At 0 5 h after MCAo, CBF and CBV of lateral caudoputamen and frontoparietal cortex in the affected side deceased marked and the rCBF and rCBV of lateral caudoputamen were less then that of frontoparietal cortex in all groups ( t =-11 74, P