The effect of narrative nursing on improving the negative emotions and quality of life of patients with moderate to severe cancer pain.

OBJECTIVE: This study aimed to explore the effect of narrative nursing on improving the negative emotions, sleep quality, and quality of life of patients with moderate to severe cancer pain. METHODS: A total of 80 patients with moderate to severe cancer pain who had been hospitalized in the lymphoma oncology department in our hospital from March 2019 to September 2021 were selected as the study subjects and randomly divided into the conventional nursing and narrative nursing groups, with 40 cases in each group. A conventional nursing intervention was conducted for one group, and narrative nursing was provided for the second group in addition to the conventional nursing. The anxiety and depression, sleep quality, quality of life, and satisfaction with pain management of the patients in the two groups were compared before and after the intervention. RESULTS: In the narrative nursing group, the self-rating anxiety scale and self-rating depression scale scores were significantly lower than those in the conventional nursing group after the intervention (P < 0.05). The scores for sleep quality, sleep duration, sleep efficiency, and daytime dysfunction and the total Pittsburgh Sleep Quality Index scores were significantly lower in the narrative nursing group compared with the conventional care group (P < 0.05). The scores for the physical function, living ability, social adaptation, and psychological status items in the Quality of Life Questionnaire Core 30 were significantly higher in the narrative nursing group than in the conventional care group (P < 0.05). The patients' satisfaction with pain management was higher in the narrative nursing group than in the conventional care group (P < 0.05). CONCLUSION: Narrative nursing can alleviate the negative emotions of anxiety and depression in patients with moderate to severe cancer pain and improve their sleep quality, quality of life, and pain management satisfaction.

Madelung's disease with alcoholic liver disease and acute kidney injury: A case report.

BACKGROUND: Madelung's disease (MD) is a rare disorder of lipid metabolism, characterized by the growth of unencapsulated masses of adipose tissue symmetrically deposited around the neck, shoulders, or other sites around the body. Its pathological mechanism is not yet known. One of the most common comorbidities in MD patients is liver disease, especially chronic alcoholic liver disease (CALD); however, no reports exist of acute kidney injury (AKI) with MD. CASE SUMMARY: We report a 60-year-old man who presented with complaint of edema in the lower limbs that had persisted for 3 d. Physical examination showed subcutaneous masses around the neck, and history-taking revealed the masses to have been present for 2 years and long-term heavy drinking. Considering the clinical symptoms, along with various laboratory test results and imaging characteristics, a diagnosis was made of MD with acute exacerbation of CALD and AKI. The patient was treated with liver function protection and traditional Chinese medicine, without surgical intervention. He was advised to quit drinking. After 10 d, the edema had subsided, renal function indicators returned to normal, liver function significantly improved, and size of subcutaneous masses remained stable. CONCLUSION: In MD, concomitant liver or kidney complications are possible and monitoring of liver and kidney functions can be beneficial.

The incidence of cytokine release syndrome and neurotoxicity of CD19 chimeric antigen receptor-T cell therapy in the patient with acute lymphoblastic leukemia and lymphoma.

Our objective was to summarize the side effect of chimeric antigen receptor (CAR)-T cell therapy in patients with acute lymphocytic leukemia (ALL) and lymphoma. Two independent reviewers extracted relevant data. A total of 35 hematologic malignancy studies with CD19 CAR-T cell were included (1412 participants). Severe cytokine release syndrome (sCRS) proportion was experienced by 18.5% (95% confidence interval [CI], 0.128-0.259; P = 0.000) of 982 patients with the National Cancer Institute/Lee/common terminology criteria for adverse events grading system. The pooled neurotoxicity proportion was 21.7% (95% CI, 0.167-0.287; P = 0.000) of 747 patients with the same grading system. For all of the 25 clinical trials with the same grading system, subgroup analysis was performed. Based on the different disease type, a pooled prevalence of 35.7% was observed with event rate (ER) of 0.358 (95% CI, 0.289-0.434; P = 0.000) for ALL in 12 clinical trials. For lymphoma, a pooled prevalence of 13% was observed with ER of 0.073 (95% CI, 0.028-0.179; P = 0.000) in eight clinical trials. It was demonstrated that the patients who were older than 18 years of age have the lower sCRS incidence of 16.1% (95% CI, 0.110-0.250; P = 0.000) compared with 28.6% of the remaining population who were younger than 18 years of age (95% CI, 0.117-0.462: P = 0.023) in our analysis. Based on the different co-stimulatory domain, the sCRS of 16.5% was observed with ER of 0.175 (95% CI, 0.090-0.312; P = 0.000) for 4-1BB. The sCRS of 22.2% was observed with ER of 0.193 (95% CI, 0.107-0.322; P = 0.000) for CD28. For both the CD28 and 4-1BB, the sCRS of 17.3% was observed with ER of 0.170 (95% CI, 0.067-0.369; P = 0.003). Sub-analysis sCRS of the impact with cell dose and specific disease indication were also demonstrated. Limitations include heterogeneity of study populations, as well as high risk of bias of included studies. These results are helpful for physicians, patients and the other stakeholders to understand the adverse events and to further promote the improvement of CAR-T cell therapy in the future.

Assessment of the efficacy of passive cellular immunotherapy for glioma patients.

To evaluate the therapeutic efficacy of passive cellular immunotherapy for glioma, a total of 979 patients were assigned to the meta-analysis. PubMed and the Cochrane Central Register of Controlled Trials were searched initially from February 2018 and updated in April 2019. The overall survival (OS) rates and Karnofsky performance status (KPS) values of patients who underwent passive cellular immunotherapy were compared to those of patients who did not undergo immunotherapy. The proportion of survival rates was also evaluated in one group of clinical trials. Pooled analysis was performed with random- or fixed-effects models. Clinical trials of lymphokine-activated killer cells, cytotoxic T lymphocytes, autologous tumor-specific T lymphocytes, chimeric antigen receptor T cells, cytokine-induced killer cells, cytomegalovirus-specific T cells, and natural killer cell therapies were selected. Results showed that treatment of glioma with passive cellular immunotherapy was associated with a significantly improved 0.5-year OS (p = 0.003) as well as improved 1-, 1.5-, and 3-year OS (p ≤ 0.05). A meta-analysis of 206 patients in one group of clinical trials with 12-month follow-up showed that the overall pooled survival rate was 37.9% (p = 0.003). Analysis of KPS values demonstrated favorable results for the immunotherapy arm (p < 0.001). Thus, the present meta-analysis showed that passive cellular immunotherapy prolongs survival and improves quality of life for glioma patients, suggesting that it has some clinical benefits.

Hirsutella sinensis inhibits NLRP3 inflammasome activation to block aristolochic acid-induced renal tubular epithelial cell transdifferentiation.

In recent years, kidney damage caused by ingestion of Chinese medicinal herbs containing Aristolochic acid (AA) has attracted extensive attention. However, whether the nephrotoxicity of AA is related to NLRP3 inflammasome has not been reported. Hirsutella sinensis (HS) has a certain therapeutic effect on aristolochic acid nephropathy (AAN) and is related to NLRP3 inflammasome. Therefore, this study explores whether HS plays a role in renal injury induced by AA through NLRP3 inflammasome pathway. AA-stimulated renal tubular epithelial cells showed that AA could promote the expression of NLRP3, ASC, and α-SMA, increase the secretion and expression of caspase-1, IL-1ß, and IL-18, and inhibit the expression of E-cadherin in a dose- and time-dependent manner. When NLRP3 was down-regulated, the expression of α-SMA and E-cadherin did not change significantly, but significantly blocked the regulation of α-SMA and E-cadherin expression by AA. When AA and HS were added to renal tubular epithelial cells at the same time, the effects of AA on the expression of NLRP3, ASC, caspase-1, IL-1ß, IL-18, and α-SMA gradually decreased to the level of control group with the increase of HS dosage. At the same time, HS can reduce the transdifferentiation of renal tubular epithelial cells by inhibiting the activation of NLRP3 inflammasome. These findings will provide important pharmacological references for the treatment of AAN and the clinical application of HS.

The efficacy of anti-CD19 chimeric antigen receptor T cells for B-cell malignancies.

Immunotherapy with chimeric antigen receptor T (CAR-T) cells has proved remarkably effective in recently published clinical trials. In this meta-analysis, we performed a systematic review in terms of the clinical response treated with CAR-T cells in acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL) and lymphomas patients. Thirty-eight published clinical studies including 665 patients were eligible for response rate (RR) evaluation. The overall pooled RR of CD19-CAR-T cells was 72% (95% confidence interval: 62-77%). The various clinical parameters were analyzed. RR was 81% in ALL, 68% in lymphoma and 70% in CLL. RR in patients who received interleukin (IL)-2 was 70%, whereas in those who did not receive IL-2, it was 74%. RR was 75% with lymphodepletion and 56% without lymphodepletion. RR with autologous cells was 76% and 57% with allogeneic cells. In conclusion, this meta-analysis showed a high clinical RR of CD19-CAR-T cell-based immunotherapy in patients with refractory B-cell malignancies.

[The Clinical Study of Comorbidities and Systemic Inflammation in COPD].

OBJECTIVE: To assess the association between chronic obstructive pulmonary disease (COPD) comorbidities and clinical characteristics, and to explore the inflammation mechanism. METHODS: 220 stable COPD patients were included. Clinical characteristics and comorbidities were recorded, and blood samples were collected. The relationship among the number and type of comorbidities, Charlson comorbidity index (CCI), clinical characteristics and the levels of plasma inflammatory markers [interleukin (IL)-6, high sensitivity C-reaction protein (hs-CRP), tumor necrosis factor-α (TNF-α), IL-8] were studied. RESULTS: The top five comorbidities were hypertension, metabolic syndrome and diabetes osteoporosis, bronchiectasis and peripheral vascular diseases. The level of plasma IL-6 was greater in higher CCI score (≥4) group compared with lower CCI score (<4) group ( P=0.011). Levels of IL-6 and IL-8 and the number of hospitalization in prior year were positively correlated with CCI and age adjusted CCI (r<0.03, P<0.05). There was a correlation between the COPD comorbidities and systemic inflammatory response (r<0.3, P<0.05). CONCLUSION: Patients with a higher CCI score had more severe symptoms, functional impairment and higher level of inflammatory factors and high frequency of hospital admission due to acute exacerbation. The mechanism by which COPD may play a role in systemic inflammatory response deserves further study.

Genetic screening and functional analysis of CASP9 mutations in a Chinese cohort with neural tube defects.

AIM: Neural tube defects (NTDs) are birth defects of the nervous system and are the second most frequent cause of birth defects worldwide. The etiology of NTDs is complicated and involves both genetic and environmental factors. CASP9 is an initiator caspase in the intrinsic apoptosis pathway, which in Casp9-/- mice has been shown to result in NTDs because of decreased apoptosis. The aim of this study was to evaluate the potential genetic contribution of the CASP9 gene in human NTDs. METHODS: High-throughput sequencing was performed to screen genetic variants of CASP9 genes in 355 NTD cases and 225 matched controls. Apoptosis-relevant assays were performed on transiently transfected E9 neuroepithelial cells or human embryonic kidney 293T cells, to determine the functional characteristics of NTD-specific rare variants under complete or low folic acid (FA) status. RESULTS: We found significant expression of CASP9 rare variants in NTDs and identified 4 NTD-specific missense variants. Functional assays demonstrated that a p.Y251C variant attenuates apoptosis by reducing CASP9 protein expression and decreasing activity of the intrinsic apoptosis pathway. From this, we conclude that this variant may represent a loss-of-function mutation. A 4-time recurrent p.R191G variant did not affect intrinsic apoptosis in complete medium, while it completely inhibited apoptosis induced by low FA medium. CONCLUSION: Our findings identify a genetic link for apoptosis in human NTDs and highlight the effect of gene-environment interactions in a complex disease.

[Efficacy Comparison of Different Salvage Treatment Regimens for Patients with Refractory/Relapsed Acute Myeloid Leukemia].

OBJECTIVE: To compare the efficacy and safety of 3 different regimens, namely MAC, FLAG and CAG, as the re-induction chemotherapy for acute myeloid leukemia(AML) patients with primary induction failure and relapse. METHODS: The clinical data of 156 AML patients with primary induction failure and relapse, except patients with acute promyelocytic leukemia(APL), treated with any of the above 3 regimens in our center from January 2008 to April 2016 were analyzed retrospectively. According to the treatment regimens, 156 patients were divided into MAC group (n=60), FLAG group (n=45) and CAG group (n=51). The complete remission(CR), partial remissison(PR), overall survival(OS), disease-free survival(DFS) and adverse events during the treatment were analyzed, so as to compare and evaluate the efficacy and safety of the 3 different regimens. RESULTS: After 1 course of re-induction chemotherapy, CR in MAC group was significantly higher than that in FLAG and CAG group (55.4% vs 34.1% vs 34.0%)(P<0.05). The OS was not statistically significantly different among 3 groups (P>0.05) with a median OS of 11 months, 5.46 months and 10.2 months, respectively. The myelosuppression was the main adverse event with no significant difference among the groups(P>0.05). More patients treated with MAC regimen underwent febrile neutropenia (93.3% vs 86.7% vs 64.7%)(P<0.001). However, the incidence of fatal infections was not signicantly different among 3 groups(5% vs 8.9% vs 5.9%)(P>0.05). CONCLUSION: Compared with FLAG and CAG regimen, the MAC regimen can enable more AML patients with primary induction failure and refractory to achieve CR without increasing severe adverse events,therefore,this regimen may provide a opportunity for patients to recieve hematopoietic stem cell transplantation.

Sonic Hedgehog Signaling Affected by Promoter Hypermethylation Induces Aberrant Gli2 Expression in Spina Bifida.

GLI2 is a key mediator of the sonic hedgehog (Shh) signaling pathway and plays an important role in neural tube development during vertebrate embryogenesis; however, the role of gli2 in human folate-related neural tube defects remains unclear. In this study, we compared methylation status and polymorphisms of gli2 between spina bifida patients and a control group to explore the underlying mechanisms related to folate deficiency in spina bifida. No single nucleotide polymorphism was found to be significantly different between the two groups, although gli2 methylation levels were significantly increased in spina bifida samples, accompanied by aberrant GLI2 expression. Moreover, a prominent negative correlation was found between the folate level in brain tissue and the gli2 methylation status (r = -0.41, P = 0.014), and gli2 hypermethylation increased the risk of spina bifida with an odds ratio of 12.45 (95 % confidence interval: 2.71-57.22, P = 0.001). In addition, we established a cell model to illustrate the effect of gli2 expression and the accessibility of chromatin affected by methylation. High gli2 and gli1 mRNA expression was detected in 5-Aza-treated cells, while gli2 hypermethylation resulted in chromatin inaccessibility and a reduced association with nuclear proteins containing transcriptional factors. More meaningful to the pathway, the effect gene of the Shh pathway, gli1, was found to have a reduced level of expression along with a decreased expression of gli2 in our cell model. Aberrant high methylation resulted in the low expression of gli2 in spina bifida, which was affected by the change in chromatin status and the capacity of transcription factor binding.

Renal Interstitial Arteriosclerotic Lesions in Lupus Nephritis Patients: A Cohort Study from China.

OBJECTIVE: The aim of this study was to evaluate renal arteriosclerotic lesions in patients with lupus nephritis and investigate their associations with clinical and pathological characteristics, especially cardio-vascular features. DESIGN: A retrospective cohort study. PARTICIPANTS: Seventy-nine patients with renal biopsy-proven lupus nephritis, diagnosed between January 2000 and June 2008 from Peking University First Hospital. RESULTS: In clinico-pathological data, patients with arteriosclerosis had higher ratio of hypertension and more severe renal injury indices compared with patients with no renal vascular lesions. More importantly, patients with renal arteriosclerosis had worse cardiac structure and function under transthoracic echocardiographic examination. Patients with renal arteriosclerosis tend to have higher ratios of combined endpoints compared with those of no renal vascular lesions, although the difference didn't reach statistical meanings (P = 0.104). CONCLUSION: Renal arteriosclerotic lesion was common and associated with vascular immune complex deposits in lupus nephritis. It might have a certain degree of association with poor outcomes and cardiovascular events, which needs further explorations.

Elevated expression of NEDD9 is associated with metastatic activity in gastric cancer.

OBJECTIVE: To investigate the protein and mRNA expression of NEDD9 in gastric cancer (GC) tissues, adjacent atypical hyperplasia tissues, and normal gastric mucosa tissues, and analyze its relationship with the pathological features and prognosis of GC. METHODS: Forty cases of GC tissues, 20 cases of adjacent atypical hyperplasia tissues, and 40 cases of normal gastric mucous tissues were collected. Immunohistochemistry and Western blot were used to examine the expression of NEDD9 protein in various tissues. Situ hybridization and reverse transcription polymerase chain reaction were applied to detect the expression of NEDD9 mRNA in various tissues. The correlation of NEDD9 expression with invasion and metastasis of GC was analyzed. RESULTS: The protein expression level of NEDD9 was significantly higher in GC tissues than in adjacent atypical hyperplasia tissues and normal gastric mucous tissues (P<0.05). The protein expression level of NEDD9 was positively related to the invasion depth of carcinoma and tumor lymph node metastasis (P<0.05), but unrelated to age, sex, tumor size, and clinical classification of cancer (P<0.05). The mRNA expression level of NEDD9 was also significantly higher in GC tissues than in adjacent atypical hyperplasia tissues and normal gastric mucous tissues (P<0.05), and positively related with the tumor lymph node metastasis and invasion depth of carcinoma (P<0.05). CONCLUSION: NEDD9 is involved in the occurrence and development of GC, and it may be an important biological marker of GC metastasis and infiltration.

Increased number of forkhead box P3+ tumor-infiltrating lymphocytes correlates with high preoperative albumin level and better survival in patients with stage II or III colorectal cancer.

Tumor-infiltrating lymphocytes (TILs) that test positive for forkhead box P3 (FOXP3) and elevated preoperative serum albumin levels have been positively associated with survival in colorectal cancer (CRC). This study aimed to investigate correlations among FOXP3+ TILs, preoperative serum albumin, overall survival, and other clinicopathological features of CRC patients. Surgical specimens from 340 stage II-III CRC patients were stained immunohistochemically for the presence of FOXP3+ TILs. Serum albumin levels were determined using an automatic biochemistry analyzer. Associations between various clinicopathological features and patient survival were analyzed via a Cox proportional hazards regression model. The correlation between FOXP3+ TILs and preoperative serum albumin was assessed using Pearson's correlation analysis. Survival curves were constructed by the Kaplan-Meier method. A high FOXP3+ TIL density (>15/five high-power fields), elevated preoperative serum albumin (≥35 g/L), and proximal colon carcinoma were significantly associated with better survival, and high FOXP3+ TIL number and elevated preoperative serum albumin were independent predictors of better survival. The correlation between the number of FOXP3+ TILs and preoperative serum albumin level was significant but neither of these correlated with gender, age, tumor size, tumor differentiation, mucinous tumor, T4 stage, postoperative chemotherapy, or tumor location. Our findings suggest that increased FOXP3+ TILs and high preoperative serum albumin levels are independent prognostic markers for improved survival in CRC patients. Furthermore, the number of FOXP3+ TILs correlates with preoperative serum albumin levels in these patients.

Arbutin, an intracellular hydroxyl radical scavenger, protects radiation-induced apoptosis in human lymphoma U937 cells.

Ionizing radiation (IR) can generate reactive oxygen species (ROS). Excessive ROS have the potential to damage cellular macromolecules including DNA, proteins, and lipids and eventually lead to cell death. In this study, we evaluated the potential of arbutin, a drug chosen from a series of traditional herbal medicine by measuring intracellular hydroxyl radical scavenging ability in X-irradiated U937 cells. Arbutin (hydroquinone-ß-D-glucopyranoside), a naturally occurring glucoside of hydroquinone, has been traditionally used to treat pigmentary disorders. However, there are no reports describing the effect of arbutin on IR-induced apoptosis. We confirmed that arbutin can protect cells from apoptosis induced by X-irradiation. The combination of arbutin and X-irradiation could reduce intracellular hydroxyl radical production and prevent mitochondrial membrane potential loss. It also could down-regulate the expression of phospho-JNK, phospho-p38 in whole cell lysate and activate Bax in mitochondria. Arbutin also inhibits cytochrome C release from mitochondria to cytosol. To verify the role of JNK in X-irradiation-induced apoptosis, the cells were pretreated with a JNK inhibitor, and found that JNK inhibitor could reduce apoptosis induced by X-irradiation. Taken together, our data indicate that arbutin plays an anti-apoptotic role via decreasing intracellular hydroxyl radical production, inhibition of Bax-mitochondria pathway and activation of the JNK/p38 MAPK pathway.

Isofraxidin, a potent reactive oxygen species (ROS) scavenger, protects human leukemia cells from radiation-induced apoptosis via ROS/mitochondria pathway in p53-independent manner.

Ionizing radiation (IR) leads to oxidizing events such as excessive reactive oxygen species (ROS) in the exposed cells, resulting in further oxidative damage to lipids, proteins and DNA. To screen the potential radio-protective drug, the intracellular ROS was measured in irradiated U937 cells pretreated with 80 candidate traditional herbal medicine, respectively. Isofraxidin (IF) was one possible radio-protector in these 80 drugs. This study investigated the radio-protective role of IF, a Coumarin compound, in human leukemia cell lines, for the first time. Results indicate that IF protects against IR-induced apoptosis in U937 cells in the time- and concentration- dependent manner. IF decreases IR-induced intracellular ROS generation, especially hydroxyl radicals formation, inhibits IR-induced mitochondrial membrane potential loss and reduces IR-induced high intracellular Ca(2+) levels regardless of ER stress. IF down-regulates the expression of caspase-3, phospho-JNK, phospho-p38 and activates Bax in mitochondria. IF inhibits cytochrome c release from mitochondria to cytosol. IF also moderates IR-induced Fas externalization and caspase-8 activation. IF also exhibits significant protection against IR-induced cell death in other leukemia cell lines such as Molt-4 cells and HL60 cells regardless of p53. Taken together, the data demonstrate that IF protects leukemia cells from radiation-induced apoptosis via ROS/mitochondria pathway in a p53-independent manner.

The relationship between mucin phenotype and clinicopathological factors, proliferative activity and p53 expression in gastric hyperplastic polyps.

AIMS: Gastric hyperplastic polyps (GHPs) are the most common polypoid lesion of the stomach, and their malignant potential has been demonstrated. In the present study, we evaluated the mucin phenotypes of GHPs and investigated the relationships among mucin phenotypes and clinical-pathological factors, proliferative activity and p53 expression in GHPs. METHODS: The CD10, MUC2, MUC5AC and MUC6 expression patterns of 238 GHPs were examined by immunohistochemical staining. The GHP mucin phenotypes were divided into 4 subtypes: the gastric mucin phenotype (G-type), the intestinal mucin phenotype (I-type), the mixed or gastrointestinal mucin phenotype (GI-type) and the unclassified mucin phenotype (U-type). RESULTS: The G and GI types were observed in 58% and 42% of the GHPs, respectively. However, no I or U type GHPs were found in the present study. The GI type was more common in lesions with dysplasia or carcinoma than in polyps without dysplasia or carcinoma (P<0.001). P53-positivity rate and high index of Ki-67 tumors were significantly more common in the GI-type than in the G-type polyps (P<0.001). CONCLUSIONS: The mucin phenotype may serve as a useful marker for the malignant potential of GHPs, and GI-type GHPs should be considered to be a lesion with malignant potential.

Dosimetric evaluation of volumetric-modulated arc therapy (RapidArc) for primary leiomyosarcoma in the spine.

This study aims to investigate the suitability of volumetric-modulated arc therapy (VMAT) with RapidArc for primary leiomyosarcoma (LMS) in the spine, and present a new method to improve the target coverage and organs at risk (OAR) sparing. Five patients with LMS were retrospectively reviewed. The intensity-modulated radiotherapy (IMRT) with five coplanar beams (5b-IMRT) or seven coplanar beams (7b-IMRT), and VMAT using four quasi-quarter coplanar arcs (4q-VMAT) or two full coplanar arcs (2f-VMAT) were generated. Planning target volume (PTV) dose coverage, OAR dose sparing, conformity index (CI), and homogeneity index (HI) were evaluated. A hollow-cylinder model (HCM) was also used for feasible optimal beam arrangements. The mean doses to PTV were 95.2% ± 1.0%, 93.0% ± 1.0%, 97.9% ± 1.0% and 96.2% ± 1.5% for 4q-VMAT, 2f-VMAT, 5b-IMRT and 7b-IMRT respectively, while the mean maximum doses to spinal cord (SC) were 43.7 ± 0.9 Gy, 42.0 ± 0.8 Gy, 41.4 ± 1.2 Gy and 40.6 ± 1.4 Gy. Compared to 5b-IMRT, the mean doses delivered to kidneys decreased by about 35.1% (8.5 Gy), 2.5% (0.6 Gy) and 35.5% (8.6 Gy) for 4q-VMAT, 2f-VMAT, and 7b-IMRT, respectively. The CI proposed by Baltas et al. was twice as good with IMRT than with 4q-VMAT, and the numbers of monitor units were increased five- and threefold with 7b-IMRT and with 5b-IMRT compared to VMAT. The unexpected results we presented here show that VMAT technique can't achieve highly conformal treatment plans while maintaining SC sparing for LMS in the spine. An approach is proposed based on a hollow-cylinder model, but it is difficult to apply to clinical practice. In this case, VMAT is not superior to IMRT except for significant reduction in delivery time.

[Organ toxicity and efficacy of high-dose daunorubicin-based chemotherapy in the treatment of acute leukemia].

OBJECTIVE: To evaluate the safety and therapeutic effect of high-dose daunorubicin-based (HD-DNR) chemotherapy in the treatment of acute leukemia (AL). METHODS: The clinical data of 25 AL patients, including 14 cases for induction chemotherapy, 8 for consolidation chemotherapy and 3 for reinduction therapy, which were treated with HD- DNR (DNR dosage of 90 mg/m(2)× 3 d) between June 2010 and August 2012 in our hospital were retrospectively analyzed, the adverse reaction of chemotherapy, especially cardiac toxicity and therapeutic effect were evaluated. RESULTS: Most of the adverse reactions were mild, including cardiac toxicity, and no patient discontinued therapy because of HD-DNR related toxicities. Grade 3 or higher adverse reactions occurred only in the infection (56%) and diarrhea (12%). Withdrawal or dose reduction due to strong adverse reactions was not observed in all patients. Adverse reactions of infections (92%), lower ejection fraction(52.6%), diarrhea (48%), nausea (36%), vomiting (36%), dental ulcer (36%) and myocardial ischemia (32%) were relatively more common. The median time of neutrophil count reached to ≥ 0.5 × 10(9)/L and platelet ≥ 20 × 10(9)/L were both 21 days(ranged 9-31 and 9-38 days). Nine patients were complicated with infections before chemotherapy and 14 after chemotherapy, mainly occurred in gastrointestinal tract and respiratory system. Gastrointestinal, liver and kidney toxicity was slight. The cardiac ejection decreased in 10 cases, but only 1 reached grade 2 without clinical symptoms. Of the 14 AL patients for induction chemotherapy, 13 achieved hematological complete remission. Eight patients received HD-DNR as consolidation chemotherapy remained complete remission, while 3 refractory/relapsed patients remained non-remission. CONCLUSION: The adverse reaction of HD-DNR based chemotherapy for AL treatment was mild, no obvious cardiac adverse reaction occurred. The treatment dose of DNR at 90 mg/m(2) × 3 d can be safely and effectively used to treat acute leukemia.

Inclusion of renal vascular lesions in the 2003 ISN/RPS system for classifying lupus nephritis improves renal outcome predictions.

The 2003 International Society of Nephrology/Renal Pathology Society (ISN/RPS) pathological classification system of lupus nephritis specified the importance of vascular damage and indicated this should be included in the diagnostic summary. Few pathological studies of lupus nephritis, however, focus on the patterns of renal vascular involvement. Here we assessed renal vascular lesions in lupus nephritis based on the 2003 ISN/RPS classification system and evaluated their association with clinical and pathological data in a large cohort from a single center in China. Among 341 patients with lupus nephritis, 279 were diagnosed with single or multiple renal vascular lesions that included 253 with vascular immune complex deposits, 82 with atherosclerosis, 60 with thrombotic microangiopathy, 13 with noninflammatory necrotizing vasculopathy, and 2 with true renal vasculitis. Patients with thrombotic microangiopathy had the poorest renal outcome. In multivariate Cox hazard analysis after inclusion of renal vascular lesions, the new chronicity index score became a significantly better independent risk factor for renal outcome (hazard ratio 2.32). Thus, renal vascular lesions are common in lupus nephritis and closely correlate with clinical disease activity and renal outcome. Inclusion of a detailed description of renal vascular lesions in the ISN/RPS classification of lupus nephritis may strengthen its predictive value for renal outcome.

The spectrum of renal thrombotic microangiopathy in lupus nephritis.

INTRODUCTION: Among various lupus renal vascular changes, thrombotic microangiopathy (TMA) presented with the most severe clinical manifestations and high mortality. The pathogenesis of TMA in systemic lupus erythematosus (SLE) was complicated. The aim of this study was to assess clinical manifestations, laboratory characteristics, pathological features and risk factors for clinical outcomes of lupus nephritis patients co-existing with renal TMA in a large cohort in China. METHODS: Clinical and renal histopathological data of 148 patients with biopsy-proven lupus nephritis were retrospectively analyzed. Serum complement factor H, A Disintegrin and Metalloprotease with Thrombospondin type I repeats 13 (ADAMTS-13) activity, antiphospholipid antibodies and C4d deposition on renal vessels were further detected and analyzed. RESULTS: In the 148 patients with lupus nephritis, 36 patients were diagnosed as co-existing with renal TMA based on pathological diagnosis. Among the 36 TMA patients, their clinical diagnoses of renal TMA were as followings: 2 patients combining with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome, 2 patients combining with anti-phospholipid syndrome, 2 patients with malignant hypertension, 1 patient with scleroderma and the other 29 patients presenting with isolated renal TMA. Compared with the non-renal TMA group, patients with renal TMA had significantly higher urine protein (7.09±4.64 vs. 4.75±3.13 g/24h, P=0.007) and serum creatinine (159, 86 to 215 vs. 81, 68 to 112 µmol/l, P<0.001), higher scores of total activity indices (AI) (P<0.001), endocapillary hypercellularity (P<0.001), subendothelial hyaline deposits (P=0.003), interstitial inflammation (P=0.005), glomerular leukocyte infiltration (P=0.006), total chronicity indices (CI) (P=0.033), tubular atrophy (P=0.004) and interstitial fibrosis (P=0.018). Patients with renal TMA presented with poorer renal outcome (P=0.005) compared with the non-TMA group. Renal TMA (hazard ratio (HR): 2.772, 95% confidence interval: 1.009 to 7.617, P=0.048) was an independent risk factor for renal outcome in patients with lupus nephritis. The renal outcome was poorer for those with both C4d deposition and decreased serum complement factor H in the TMA group (P=0.007). CONCLUSIONS: There were various causes of renal TMA in lupus nephritis. Complement over-activation via both classical and alternative pathways might play an important role in the pathogenesis of renal TMA in lupus nephritis.