Altered dynamic functional connectivity of the thalamus subregions in patients with schizophrenia.

BACKGROUND: Previous neuroimaging studies indicated that patients with schizophrenia showed impaired thalamus and thalamo-cortical circuits. However, the dynamic functional connectivity (dFC) patterns of the thalamus remain unclear. In this study, we explored the dFC of the thalamus in SZ patients and whether clinical features are correlated with altered dFC. METHODS: Forty-three patients with schizophrenia and 31 healthy controls underwent 3.0 T rs-fMRI. Based on the human Brainnetome atlas, the thalamus is divided into 8 subregions. Subsequently, we performed flexible least squares method to calculate the dFC of each thalamus subregions. RESULTS: Compared with healthy controls, patients with schizophrenia exhibited increased dFC between the thalamus and cerebellar, visual-related cortex, sensorimotor-related cortex, and frontal lobe. In addition, we found that the dFC of the thalamus and the right fusiform gyrus was negatively associated with age of onset. CONCLUSIONS: Our findings demonstrated that the dFC of specific thalamus sub-regions is altered in patients with schizophrenia. Our results further suggested the dysconnectivity of thalamus plays an important role in the pathophysiology of schizophrenia.

Abnormal dynamic functional network connectivity in first-episode, drug-naïve patients with major depressive disorder.

Dynamic functional network connectivity (dFNC) could capture temporal features of spontaneous brain activity during MRI scanning, and it might be a powerful tool to examine functional brain network alters in major depressive disorder (MDD). Therefore, this study investigated the changes in temporal properties of dFNC of first-episode, drug-naïve patients with MDD. A total of 48 first-episode, drug-naïve MDD patients and 46 age- and gender-matched healthy controls were recruited in this study. Sliding windows were implied to construct dFNC. We assessed the relationships between altered dFNC temporal properties and depressive symptoms. Receiver operating characteristic (ROC) curve analyses were used to examine the diagnostic performance of these altered temporal properties. The results showed that patients with MDD have more occurrences and spent more time in a weak connection state, but with fewer occurrences and shorter dwell time in a strong connection state. Importantly, the fractional time and mean dwell time of state 2 was negatively correlated with Hamilton Depression Rating Scale (HDRS) scores. ROC curve analysis demonstrated that these temporal properties have great identified power including the fractional time and mean dwell time in state 2, and the AUC is 0.872, 0.837, respectively. The AUC of the combination of fractional time and mean dwell time in state 2 with age, gender is 0.881. Our results indicated the temporal properties of dFNC are altered in first-episode, drug-naïve patients with MDD, and these changes' properties could serve as a potential biomarker in MDD.

Proposed protocol for the investigation of the safety and efficacy of the COVID-19 vaccine for patients with psychosis, with pilot safety findings from a Chinese psychiatrist's self-experiment.

We present a study protocol designed to test the safety and efficacy of the 2019 coronavirus disease (COVID-19) vaccine in patients with major psychotic disease. A secondary objective is to investigate optional vaccination methods for these patients. In a self-experiment, a Chinese psychiatrist examined the safety and efficacy of the COVID-19 vaccine under clinical use of typical antipsychotic agents and sedatives (olanzapine, duloxetine, and diazepam). For patients with extremely drug-resistant conditions, the safety of the COVID-19 vaccine under electroconvulsive therapy was also investigated. The entire study process was recorded on high-definition video. This clinical study protocol is, to our knowledge, the first of its kind. Our findings will shed new light on the protection of patients with psychotic diseases from COVID-19 infection. The protocol was registered at Chinese clinical trial registry (www.chictr.org.cn, ChiCTR2100051297).

Alterations of dynamic functional connectivity between visual and executive-control networks in schizophrenia.

Schizophrenia is a chronic mental disorder characterized by continuous or relapsing episodes of psychosis. While previous studies have detected functional network connectivity alterations in patients with schizophrenia, and most have focused on static functional connectivity. However, brain activity is believed to change dynamically over time. Therefore, we computed dynamic functional network connectivity using the sliding window method in 38 patients with schizophrenia and 31 healthy controls. We found that patients with schizophrenia exhibited higher occurrences in the weakly and sparsely connected state (state 3) than healthy controls, positively correlated with negative symptoms. In addition, patients exhibited fewer occurrences in a strongly connected state (state 4) than healthy controls. Lastly, the dynamic functional network connectivity between the right executive-control network and the medial visual network was decreased in schizophrenia patients compared to healthy controls. Our results further prove that brain activity is dynamic, and that alterations of dynamic functional network connectivity features might be a fundamental neural mechanism in schizophrenia.

The Prevalence, Risk Factors and Clinical Correlates of QTc Prolongation in Chinese Hospitalized Patients With Chronic Schizophrenia.

Background: The QTc interval may be significantly prolonged in schizophrenia patients taking antipsychotics. Few studies have addressed QTc prolongation (QTP) in Chinese patients. Objectives: This study was designed to evaluate the prevalence of QTP and its clinical correlates in Chinese hospitalized patients with chronic schizophrenia. Methods: A total of 436 inpatients and 291 normal controls matched with age and sex were included. QTc prolongation was defined as 2 standard deviations (SD) above the mean value of normal controls. Positive and Negative Syndrome Scale (PANSS) and its five-factor model were used to evaluate psychopathological symptoms. Results: QTc interval was significantly longer in patients than in normal controls. The prevalence of QTP is 8.26% in Chinese hospitalized patients with chronic schizophrenia. More women than men displayed QTP. Compared with patients without QTP, the patients with QTP had significantly higher concrete/disorganized subscore, lower low density lipoprotein (LDL) and lower total protein (TP). Furthermore, binary logistic regression analysis showed that higher number of hospitalizations, higher concrete/disorganized subscore and lower LDL were risk factors for QTP. Correlation analysis indicated significant association between QTc interval and the following variables: sex, age, duration of illness, the number of hospitalizations, PANSS total score, fasting blood glucose (FPG). Finally, a multiple regression analysis showed that older age, antipsychotic polypharmacy, higher PANSS total score, and lower LDL were risk factors for QTP. Among them, LDL seemed to be a protective factor for QTP. Conclusions: QTc interval was longer in schizophrenia patients than in normal controls. The prevalence of QTP is 8.26% in Chinese hospitalized patients with chronic schizophrenia. Some clinical characteristics were risk factors for QTP. And LDL seemed to be a protective factor for QTP.

Safety and Efficacy of High-Dose Vitamin B6 as an Adjunctive Treatment for Antipsychotic-Induced Hyperprolactinemia in Male Patients With Treatment-Resistant Schizophrenia.

This study aimed to investigate the safety and efficacy of high-dose vitamin B6 (vB6) as an adjunct treatment for antipsychotic-induced hyperprolactinemia (AIHP) in male patients with treatment-resistant schizophrenia (TRS). In this randomized double-blinded controlled study, patients were randomized (1:1) into a control group given aripiprazole (ARI; 10 mg/day; n = 100) or an intervention group given vB6 (300 mg/12 h for 16 weeks; n = 100). Prolactin levels, psychotic symptoms [Positive and Negative Syndrome Scale (PANSS)], cognitive function [MATRICS Consensus Cognitive Battery (MCCB)], liver function, kidney function, growth hormone level, micronutrient levels, blood lipids, and adverse secondary effects (ASEs)[Treatment Emergent Symptom Scale (TESS) and Barnes-Akathisia scale] were monitored. After a 16-week treatment period, the vB6 group showed a 68.1% reduction in serum prolactin levels (from 95.52 ± 6.30 µg/L to 30.43 ± 18.65 µg/L) while the ARI group showed only a 37.4% reduction (from 89.07 ± 3.59 µg/L to 55.78 ± 7.39 µg/L). During weeks 1-4, both treatments reduced prolactin similarly. Subsequently, the ARI effect plateaued, while the vB6 effect remained robust. The vB6 group showed better alleviation of psychotic symptoms and cognitive impairment. No serious ASEs were observed; ASEs were more frequent in the ARI group. AIHP reduction efficacy of vB6 was associated with baseline prolactin and triglyceride levels, total vB6 dosage, and education level. In conclusion, compared with the ARI group, TRS patients given vB6 showed better attenuation of AIHP, lower ASE scores, and greater improvements in clinical symptoms and cognitive impairments. These results support further consideration of vB6 as a putative treatment for AIHP. Trial Registration: ChiCTR1800014755.

Clozapine induces metformin-resistant prediabetes/diabetes that is associated with poor clinical efficacy in patients with early treatment-resistant schizophrenia.

BACKGROUND: Two distinct subtypes of treatment-resistant schizophrenia (TRS) have been recently reported, including early-treatment resistance (E-TR) and late-treatment resistance (L-TR). This study was to assess clozapine-induced metformin-resistant prediabetes/diabetes and its correlation with clinical efficacy in schizophrenia E-TR subtype. METHODS: This prospective cohort study enrolled 230 patients with schizophrenia E-TR subtype and they were treated with adequate doses of clozapine for 16 weeks, during which patients with prediabetes/diabetes were assigned to receive add-on metformin. The main outcomes and measures included incidence of clozapine-induced prediabetes/diabetes and metformin-resistant prediabetes/diabetes, and the efficacy of clozapine as assessed by the Positive and Negative Syndrome Scale (PANSS) score. RESULTS: Clozapine-induced prediabetes/diabetes occurred in 76.52% of patients (170 prediabetes and 6 diabetes), of which the blood sugar of 43 (24.43%) patients was controlled with metformin. Despite add-on metformin, 47.06% (74/170) of prediabetes patients progressed to diabetes. In total, the incidence of clozapine-induced metformin-resistant prediabetes/diabetes was 75.57% (133/176). On completion of 16-week clozapine treatment, 16.52% (38/230) patients showed clinical improvement with PANSS scores of ≥50% declining. Furthermore, clozapine-induced prediabetes/diabetes was significantly correlated with the poor clinical efficacy of clozapine for schizophrenia E-TR subtype. CONCLUSIONS: The incidence of clozapine-induced metformin-resistant prediabetes/diabetes was considerably high in the schizophrenia E-TR subtype. Clozapine-induced metformin-resistant prediabetes/diabetes represents an independent risk factor that adversely affects the clinical efficacy of clozapine for the schizophrenia E-TR subtype. This study provided new evidence for re-evaluating the use of clozapine for TRS, especially E-TR subtype, and the use of metformin for the glycemic control of clozapine-induced prediabetes/diabetes.

Platelet-rich plasma attenuates intervertebral disc degeneration via delivering miR-141-3p-containing exosomes.

Oxidative stress mediated apoptotic and pyroptotic cell death contributes to intervertebral disc (IVD) degeneration, and platelet-rich plasma (PRP) exerts protective effects to attenuate IVD degeneration. Hence, the present study aimed to validate this issue and uncover the potential underlying mechanisms. The mice and cellular models for IVD degeneration were established by using puncture method and H2O2 exposure, respectively, and we evidenced that NLRP3-mediated cell pyroptosis, apoptosis and inflammatory responses occurred during IVD degeneration progression in vitro and in vivo. Then, the PRP-derived exosomes (PRP-exo) were isolated and purified, and we noticed that both PRP-exo and ROS scavenger (NAC) reversed the detrimental effects of H2O2 treatment on the nucleus pulposus (NP) cells. Further results supported that PRP-exo exerted its protective effects on H2O2 treated NP cells by modulating the Keap1-Nrf2 pathway. Mechanistically, PRP-exo downregulated Keap1, resulting in the release of Nrf2 from the Keap1-Nrf2 complex, which further translocated from cytoplasm to nucleus to achieve its anti-oxidant biological functions, and H2O2 treated NP cells with Nrf2-deficiency did not respond to PRP-exo treatment. In addition, miR-141-3p was enriched in PRP-exo, and miR-141-3p targeted the 3' untranslated region (3'UTR) of Keap1 mRNA for its degradation, leading to Nrf2 translocation. Furthermore, overexpression of miR-141-3p ameliorated the cytotoxic effects of H2O2 on NP cells, which were abrogated by upregulating Keap1 and silencing Nrf2. Taken together, we concluded that PRP secreted exosomal miR-141-3p to activate the Keap1-Nrf2 pathway, which helped to slow down IVD degeneration.

Integrating 3D-printed PHBV/Calcium sulfate hemihydrate scaffold and chitosan hydrogel for enhanced osteogenic property.

We developed the 3D-printed poly(3-hydroxybutyrate-co-3-hydroxyvalerate)/calcium sulfate hemihydrate (PHBV/CaSH) scaffolds by using fused deposition modelling (FDM) technique and then coated the scaffolds with chitosan (CS) acetic acid solution. After drying and neutralization, CS hydrogel was formed on the surface of the scaffolds. The resultant PHBV/CaSH/CS scaffolds could promote the adhesion and proliferation of rat bone marrow stromal cells (rBMSCs) and enhance the osteogenesis of rBMSCs by up-regulating the expression level of osteogenic genes compared to the PHBV and PHBV/CaSH scaffolds. In vivo studies further demonstrated the PHBV/CaSH/CS scaffolds could effectively promote new bone formation. Therefore, integrating 3D-printed PHBV/CaSH scaffold and CS hrydogel represents a novel strategy to promote osteogensis property, showing full potential for bone defects repair.

MicroRNA-411 promoted the osteosarcoma progression by suppressing MTSS1 expression.

MicroRNAs (miRNAs) play crucial roles in the progression of different tumors. In our study, we investigated the expression and roles of miR-411 in human osteosarcoma. In this study, we first confirmed that the miR-411 expression was higher in the serum of patients with osteosarcoma than in the serum of healthy volunteers. In addition, we found that the miR-411 expression was upregulated in the osteosarcoma tissues compared to that in the matched normal bone tissues. We also demonstrated that the miR-411 expression was upregulated in the four osteosarcoma cell lines. Elevated expression of miR-411 promoted osteosarcoma cell proliferation and migration. Moreover, we identified that metastasis suppressor protein 1 (MTSS1) was a direct target gene of miR-411 in the osteosarcoma cell. We also demonstrated that the MTSS1 expression was downregulated in the osteosarcoma tissues compared to that in the matched normal bone tissues. In addition, MTSS1 expression level was inversely correlated with miR-411 expression in the osteosarcoma tissues. Furthermore, elevated expression of miR-411 enhanced the osteosarcoma cell proliferation and migration through inhibiting the MTSS1 expression. These data suggested that miR-411 played as oncogene in the osteosarcoma partly by inhibiting the MTSS1 expression.

MicroRNA-492 overexpression exerts suppressive effects on the progression of osteosarcoma by targeting PAK7.

MicroRNAs (miRNAs or miRs), which are a class of non-coding RNAs, have emerged as effective modulators of various aspects of biological processes. Accumulating evidence has established significant associations between the dysregulation of miRs and tumorigenesis in various types of cancer. However, the role of miR­492, particularly in osteosarcoma (OS) remains elusive. In present study, we demonstrated that miR­492 functions as putative tumor suppressor miR in OS. The level of miR­492 was frequently downregulated in both OS tissues and cell lines. Moreover, the ectopic overexpression of miR­492 effectively inhibited the proliferation, migration and invasion of OS cell lines. Furthermore, transfection with a miR­492 overexpression vector also strongly attenuated the growth of xenograft tumors in vivo. p21-activated kinase (PAK7) was identified as the putative target of miR­492 in OS, and we further found a significantly inverse correlation between PAK7 and miR­492 in OS specimens. Taken together, our study has unraveled a novel role for miR­492 in OS and may help in establishing the rationale for more effective treatment strategies for OS via miR regulation.

Pim-2 Modulates Aerobic Glycolysis and Energy Production during the Development of Colorectal Tumors.

Tumor cells have higher rates of glucose uptake and aerobic glycolysis to meet energy demands for proliferation and metastasis. The characteristics of increased glucose uptake, accompanied with aerobic glycolysis, has been exploited for the diagnosis of cancers. Although much progress has been made, the mechanisms regulating tumor aerobic glycolysis and energy production are still not fully understood. Here, we demonstrate that Pim-2 is required for glycolysis and energy production in colorectal tumor cells. Our results show that Pim-2 is highly expressed in colorectal tumor cells, and may be induced by nutrient stimulation. Activation of Pim-2 in colorectal cells led to increase glucose utilization and aerobic glycolysis, as well as energy production. While knockdown of Pim-2 decreased energy production in colorectal tumor cells and increased their susceptibility to apoptosis. Moreover, the effects of Pim-2 kinase on aerobic glycolysis seem to be partly dependent on mTORC1 signaling, because inhibition of mTORC1 activity reversed the aerobic glycolysis mediated by Pim-2. Our findings suggest that Pim-2-mediated aerobic glycolysis is critical for monitoring Warburg effect in colorectal tumor cells, highlighting Pim-2 as a potential metabolic target for colorectal tumor therapy.

Decreased functional expression of Grp78 and Grp94 inhibits proliferation and attenuates apoptosis in a human gastric cancer cell line in vitro.

The aim of the present study was to determine the effect of downregulating the expression of glucose-regulated protein 78 (Grp78) and Grp94 upon the rate of proliferation and apoptosis in the human gastric cancer SGC-7901 cell line. The SGC-7901 cells were divided into three groups as follows: i) An experimental group co-transfected with the small interfering RNA vectors, psiSTRIKE™/Grp78 and psiSTRIKE/Grp94; ii) a negative control group, in which only Lipofectamine 2000™ was used to transfect the cells; and iii) a blank control group, in which cells were left untouched and not transfected with any agent. The transcriptional expression of Grp78 and Grp94 was assayed by reverse transcription polymerase chain reaction, and the protein expression of Grp78 and Grp94 was determined using an immunofluorescence assay at 24, 48 and 72 h post-transfection. The rates of cellular proliferation and apoptosis were assayed using MTT and flow cytometry analyses, respectively. The mRNA and protein expression of Grp78 and Grp94 in the gastric cancer cells was downregulated at 72 h post-transfection. In addition, the results of the MTT assay revealed that the proliferation rate of the gastric cancer cells in the co-transfected group was significantly inhibited at 72 h post-transfection compared with the control groups (P<0.05). The apoptosis ratio was significantly increased in the experimental group compared with the control groups (P<0.05). The co-transfection of the SGC-7901 cells with psiSTRIKE/Grp78 and psiSTRIKE/Grp94 markedly reduced the expression of Grp78 and Grp94, respectively. Furthermore, the reduction in the expression of Grp78 and Grp94 inhibited cellular proliferation and significantly downregulated the rate of apoptosis in the SGC-7901 cells in vitro.

MicroRNA-33b suppresses migration and invasion by targeting c-Myc in osteosarcoma cells.

MicroRNAs have emerged as fundamental regulators in gene expression through silencing gene expression at the post-transcriptional and translational levels. Osteosarcoma is the most common type of primary malignant bone tumor and is characterized by complex genetic changes and resistance to conventional treatments. In our study, the role of miR-33b in the progression and metastasis of osteosarcoma was investigated. Our results showed that miR-33b was significantly downregulated in osteosarcoma tissue and cell lines. Overexpression of miR-33b significantly inhibited cell proliferation, migration, and invasion in the MG-63 osteosarcoma cell line. Moreover, we also showed that c-Myc was negatively regulated by miR-33b at the posttranscriptional level, via a specific target site within the 3'UTR. Overexpression of c-Myc impaired miR-33b-induced inhibition of proliferation and invasion in osteosarcoma cells. The expression of c-Myc was frequently downregulated in osteosarcoma tumors and cell lines and was inversely correlated with miR-33b expression. Thus, our findings suggest that miR-33b inhibits osteosarcoma cells migration and invasion by targeting the c-Myc gene, acting as tumor suppressor. The findings of this study contribute to current understanding of the functions of miR-33b in osteosarcoma.

Construction of adipose scaffold for bone repair with gene engineering bone cells.

The bone defect repairing is still a challenge in orthopedics. As the gene engineering bones have been used in the bone repairing clinic, the scaffold construction is a critical fact to be considered. This study aims to construct optimal scaffolds using adipose tissue in the bone repair together with the gene engineering osteocytes. Rat adipose stem cells (ASC) were prepared; the cells were transduced with the OCT-4 gene carrying lentiviral vectors (OCT-4-Lv). Artificial bone defects were created in the rat femoral bone. The bone defects were filled up with adipose scaffolds and shaped by using surrounding muscles and supported with orthopedic splints. ASCs with or without transducing the OCT-4-Lv were injected into the adipose scaffolds. The rats were sacrificed 12 weeks after the surgery. After receiving the OCT-4-Lv, the expressions of OCT-4, RUNX2 and osteocalcin were detected in the ASCs. X-ray examination showed that rats received the OCT-4-Lv transduced ASCs together with the adipose pad had new bone formation in the defect area; none of the control rats showed any new bone formation in situ. The results were supported by histological assessment. Using adipose scaffold and OCT-4-modified ASC transplantation can repair bone defects.

Effects of zinc transporter on differentiation of bone marrow mesenchymal stem cells to osteoblasts.

The differentiation of bone marrow mesenchymal stem cells (MSCs) into osteoblasts is a crucial step during bone formation. However, the exact mechanisms regulating the early stages of osteogenic differentiation remain unknown. In the present study, we found that ZnT7, a member of the zinc transporter family SLC30A(ZnTs), was downregulated during dexamethasone-induced differentiation of rat MSCs into osteoblasts. Dexamethasone treatment resulted in significantly lower levels of ZnT7 compared with cocultured cells without dexamethasone. Differentiation was evaluated by measuring alkaline phosphatase (ALP) activity and staining for ALP, von Kossa, collagen type I, and osteocalcin. Overexpression of ZnT7 decreased the expression of the osteoblast alkaline phosphatase, type I collagen, as well as calcium deposition in mesenchymal cells. In contrast, knockdown of ZnT7 using siRNA promoted gene expression associated with osteoblast differentiation and matrix mineralization in vitro. Moreover, according to the ZnT7 inhibition or activation experiments, Wnt and ERK signaling pathways were found to be important signal transduction pathways in mediating the osteogenic effect of MSCs, and this effect is intensified by a decrease in the level of ZnT7 induced by dexamethasone. These findings suggest that ZnT7 is involved in the switch from the undifferentiated state of MSC to an osteogenic program, and marking the expression level of ZnT7 may be useful in the detection of early osteogenic differentiation.

Glutathione S-transferase polymorphisms and bone tumor risk in China.

AIM: We aimed to study the potential role of GSTM1 and GSTT1 in the risk of osteosarcoma in Chinese population. METHODS: We collected 110 osteosarcomas by pathologic examination and 226 controls from the First Affiliated Hospital of Harbin Medical University during December 2008 to December 2010. Genotyping was based upon duplex polymerase-chain-reaction with the PCR-CTPP method. RESULTS: Individuals carrying null GSTM1 and GSTT1 had 1.50 and 2.07 fold risks of osteosarcoma when compared with non-null genotypes, respectively. The increased risk associated with the GSTT1 polymorphism seemed more evident among males (Null GSTT1 genotype vs. non-null genotype, adjusted OR= 2.43, 95% CI: 1.29-3.30) than females (adjusted OR =1.66, 95% CI: 1.02-2.78). The increased risk was also more evident among individuals aged 15 years or less (adjusted OR for null GSTT1 genotype vs. non-null genotype = 2.24, 95% CI: 1.20-3.24) than those aged more than 15 years (adjusted OR = 1.82, 95% CI: 1.07-2.95). CONCLUSION: Our study of the association between polymorphisms in GSTM1 and GSTTI and the risk of osteosarcoma in a Chinese population provided evidence that null GSTTI might be a useful marker of susceptibility to osteosarcoma development, especially for male sand young age individuals.

[Surgical treatment and prognosis of cancer of hepatic flexure of colon invading the duodenum in 65 patients].

OBJECTIVE: To discuss surgical treatment of right colon carcinoma of hepatic flexure invading the duodenum. METHODS: Sixty-five patients with right colon carcinoma of hepatic flexure invading the duodenum, treated in our department from 1987 to 2007, were included in this study. Their clinicopathological data were retrospectively reviewed and analyzed. All the cases were divided into three types (local invasion, regional invasion, and cancer with internal fistula) according to duodenal defect, including local invasion (< 2.0 cm), wide invasion (> 2.0 cm) and the presence of internal fistula. RESULTS: 25 patients with local invasion underwent en bloc resection of the duodenal wall. Pedicled ileal flap was used to cover the large duodenal defect measuring 2.0 - 3.0 cm in 5 patients. Dudenojejunostomy was used to reconstruct the large defect measuring more than 5 cm in 3 patients. Conservative resection of right-sided colon was performed in 18 patients with wide invasion. 4 patients underwent pancreaticoduodenectomy combined with right hemicolectomy for colon cancer involving the pancreatic head. 10 underwent duodenal diverticularization. One patient with anastomotic leakage healed within 3 weeks. Other patients were cured without postoperative complications. The total 3-year and 5-year survival rates after surgery were 53.8% and 9.2%, respectively. CONCLUSION: The surgical procedure to be performed is usually decided according to the cancer location, extent, and duodenal defect and invasion, which are important for prolonging life time, improving of quality of life and prognosis in these patients.

[Diagnosis and surgical treatment of carcinoid tumors of the appendix in 64 patients].

OBJECTIVE: To summarize the experience in the diagnosis and surgical treatment of carcinoid tumors of the appendix. METHODS: From 1972 to 2006, 64 patients with carcinoid tumors of the appendix received surgical treatment in our hospitals. The clinical data of those patients were retrospectively analyzed. RESULTS: Of the 64 cases, only 6 cases (9.4%) were correctly diagnosed preoperatively, while 58 (90.6%) not confirmed, with a misdiagnosis rate of 90.6%. All patients underwent surgical treatment, including appendectomy in 54, ileocecectomy in 4, right hemicolectomy in 2 and right hemicolectomy with regional lymph node dissection in 4 cases. The operation modes were determined according to the doctor's judgments based on the age of the patients, the nature, size, location, infiltration depth and lymph node metastasis of the tumors. Of the 64 patients, 58 were followed up with a longest follow-up period of 13 years, while 6 lost follow-up. Fifty-seven of those were still surviving, only one died of liver metastasis at 13 years after operation. CONCLUSION: Carcinoid tumor of the appendix is rare with a high rate of misdiagnosis before operation. Surgical resection is the only effective treatment for this disease and proper operation mode is the key to achieve good survival.

Assessment of duodenal circular drainage in treatment of superior mesenteric artery syndrome.

AIM: To assess the clinical value of duodenal circular drainage for superior mesenteric artery syndrome (SMAS). METHODS: Forty-seven cases of SMAS were treated with duodenal circular drainage from 1959 to 2001. Clinical data were analyzed retrospectively. RESULTS: In this group, good effects were achieved in 39 cases treated with duodenal circular drainage after 2-15 years of follow-up. The other eight cases were first treated with anterior repositioning of the duodenum (two cases), duodenojejunostomy (five cases), subtotal gastrectomy and billroth II gastrojejunostomy (one case), but vomiting was not relieved until duodenal circular drainage was performed again. A follow-up study of 8-10 years revealed satisfactory results in these eight patients. CONCLUSION: In SMAS, if the reversed peristalsis is strong and continuous, and vomiting occurs frequently, the symptom can not be relieved even if the obstruction of duodenum is removed surgically. The key treatment is the relief of reversed peristalsis. The duodenal circular drainage can resolve the drainage direction of duodenal content, thus relieving the symptom of vomiting.