Effect of nitrogen fertilizer on the quality traits of Indica rice with different amylose contents.

BACKGROUND: Nitrogen is a key factor affecting the quality of rice. Studying the impact of nitrogen fertilizer on the taste, physicochemical properties, and starch structure of Indica rice with different amylose contents is of great significance for scientifically fertilizing and cultivating high-quality rice varieties for consumption. RESULTS: The results indicate that increasing nitrogen fertilizer application reduces the amylose content and increases the protein content, resulting in a decrease in taste quality. Simultaneously, it reduces the intergranular porosity of starch particles, improving the appearance and milling quality of rice. Compared to the N1 treatment (nitrogen fertilizer application rate of 90 kg ha-1), the taste of low-amylose rice (Yixiangyou 2115) and high-amylose rice (Byou 268) decreased by 14.24% and 19.79%, respectively, under N4 treatment (nitrogen fertilizer application rate of 270 kg ha-1). The effect of nitrogen fertilizer on low-amylose rice is mainly reflected in increased rice hardness, enthalpy value, and setback viscosity, resulting in a decline in taste. The effect of nitrogen fertilizer on high-amylose rice is mainly reflected in a decrease in peak viscosity, an increase in gelatinization temperature, and crystallinity under high nitrogen levels. CONCLUSION: Increasing nitrogen fertilizer application can improve the appearance and milling quality of rice, but it also leads to an increase in protein content, hardness, gelatinization enthalpy, decrease in breakdown value, and a decline in palatability. In practical production, different production measures should be taken according to different production goals. © 2024 Society of Chemical Industry.

MicroRNA-218-5p regulates inflammation response via targeting TLR4 in atherosclerosis.

BACKGROUND: To investigate the expression of miR-218-5p in atherosclerosis patients and its effect on ox-LDL induced THP-1-derived macrophage inflammatory response. METHODS: RT-qPCR detected the expression of serum miR-218-5p, and the diagnostic value of miR-218-5p was analyzed by ROC curve. Pearson correlation coefficient was used to evaluate the correlation between miR-218-5p and CIMT and CRP. THP-1 cells were treated with ox-LDL to construct foam cell model. The expression of miR-218-5p was regulated by in vitro transfection technique, and the effects of miR-218-5p on cell viability, apoptosis and inflammation were investigated. Luciferase reporter genes were used to analyze target genes of miR-218-5p in cell models. RESULTS: The expression of miR-218-5p in the atherosclerosis cohort was significantly reduced, and miR-218-5p showed a good ability to distinguish patients from healthy people. Correlation analysis showed that the level of miR-218-5p was negatively correlated with the levels of CIMT and CRP. Cytological studies showed that the expression of miR-218-5p in macrophages decreased after ox-LDL induction. ox-LDL treatment on macrophages resulted in decreased cell viability, increased cell apoptosis and production of inflammatory cytokines, which contributed to the exacerbation of plaque formation. However, the above situation was reversed after upregulation of miR-218-5p. Bioinformatics analysis showed that TLR4 may be the target gene of miR-218-5p, and this hypothesis was proved by luciferase reporter gene assay. CONCLUSIONS: The expression of miR-218-5p is reduced in atherosclerosis, and it may regulate the inflammatory response of atherosclerotic foam cells by targeting TLR4, suggesting that miR-218-5p may be a promising target for clinical atherosclerosis therapy.

MiR-483-5p downregulation alleviates ox-LDL induced endothelial cell injury in atherosclerosis.

BACKGROUND: In light of the abnormal expression of microRNA (miR-483-5p) in patients with atherosclerosis (AS), its role in vascular endothelial cell injury was explored. And the mechanisms related to autophagy were also elucidated. METHODS: Human umbilical vein endothelial cells (HUVECs) were given 100 mg/L ox-LDL to induce endothelial injury. Cell transfection was done to regulate miR-483-5p levels. Cell viability and apoptosis were detected. qRT-PCR was employed for the mRNA levels' detection. RESULTS: Autophagic flux impairment of HUVECs was detected after ox-LDL treatment, along with the upregulation of miR-483-5p. Ox-LDL inhibited cell viability and promoted cell apoptosis, but these influences were changed by miR-483-5p downregulation. MiR-483-5p downregulation decreased the mRNA levels of IL-1ß, IL-6, ICAM-1 and VCAM-1. 3-MA, the autophagy inhibitor, reversed the beneficial role of miR-483-5p downregulation in ox-LDL-induced HUVECs' injury. TIMP2 acts as a target gene of miR-483-5p, and was downregulated in HUVEC models. CONCLUSION: MiR-483-5p downregulation alleviated ox-LDL-induced endothelial injury via activating autophagy, this might be related to TIMP2.

Icariin inhibits isoproterenol-induced cardiomyocyte hypertropic injury through activating autophagy via the AMPK/mTOR signaling pathway.

Icariin (ICA), a bioactive flavonoid compound derived from Epimedium, have been demonstrated possessing anti-oxidative stress, anti-inflammation in the cardiovascular disease. But its effects on cardiomyocyte hypertrophy and the underlying mechanisms remains unclear. Here we found that ICA alleviated ISO-induced H9c2 or NRCM myocytes hypertrophy, assessed by surface area and the expression of ANP, BNP and ß-MHC. Furthemore, ICA reversed cardiomcytes enlargment by suppresing apoptotic injury and increasing autophagic flux. By contrast, 3-MA, an autophagy inhibitor, could abolished the antihypertrophic and pro-autophagic flux effects of ICA. Mechanistically, ICA increased the phosphorylation levels of AMPK and autophagy-related markers beclin-1, Atg5 and the LC3II/I ratio, and decreased phosphorylated mTOR. But the effects of ICA on ISO-induced cardiomyocytes hypertrophy were attenuated by selective AMPK inhibitor Compound C. In conclusion, these findings indicated that ICA attenuated cardiomyocyte hypertrophy induced by ISO and prevented cell injury, and the specific mechanism was mediated by AMPK/mTOR pathway to enhance autophagy and reduce autophagy-related cardiomyocyte apoptosis.

Robotic colorectal cancer surgery in China: a nationwide retrospective observational study.

BACKGROUND: Robotic colorectal cancer surgery is widely accepted and applied. However, there is still no objective and comprehensive assessment on the data of nationwide multicenter series. METHOD: A total of 28 medical centers in Mainland China participated in this nationwide retrospective observational study. From the first case performed in each center to the last until December 2017, patients with robotic resection for primary tumor and pathologically confirmed colorectal adenocarcinoma were consecutively enrolled. Clinical, pathological and follow-up data were collected and analyzed. RESULTS: A total of 5389 eligible patients were finally enrolled in this study, composing 72.2% of the total robotic colorectal surgery volume of Mainland China in the same period. For resections of one bowel segment of primary tumor, the postoperative mortality rate was 0.08% (4/5063 cases), and the postoperative complication rate (Clavien-Dindo grade II or higher) was 8.6% (434/5063 cases). For multiple resections, the postoperative mortality rate was 0.6% (2/326 cases), and the postoperative complication rate was 16.3% (53/326 cases). Out of 2956 patients receiving sphincter-preserving surgery in only primary resection, 130 (4.4%) patients had anastomotic leakage. Traditional low anterior resection (tumor at middle rectum) (OR 2.384, P < 0.001), traditional low anterior resection (tumor at low rectum) (OR 1.968, P = 0.017) and intersphincteric resection (OR 5.468, P = 0.006) were significant independent risk factors for anastomotic leakage. Female gender (OR 0.557, P = 0.005), age ≥ 60 years (OR 0.684, P = 0.040), and preventive stoma (OR 0.496, P = 0.043) were significant independent protective factors. Body mass index, preoperative chemotherapy/radiotherapy, tumor size, and TNM stage did not independently affect the occurrence of anastomotic leakage. CONCLUSION: Robotic colorectal cancer surgery was safe and reliable and might have advantages in patients at high risk of anastomotic leakage.

Analysis of the association of interleukin-17 gene polymorphisms with gastric cancer risk and interaction with Helicobacter pylori infection in a Chinese population.

We aimed to explore the association between interleukin-17 (IL-17) polymorphisms, Helicobacter pylori infection, and subsites in gastric cancer risk in a Chinese population. We genotyped three promoter polymorphisms (rs2275913G>A, rs3748067C>T, and rs763780T>C) of IL-17 in a case-control study of 260 gastric cancer patients and 512 healthy controls. An unconditional multiple logistical regression model was used to calculate the effects of IL-17 gene polymorphisms on gastric cancer risk. The rs2275913 AA (adjusted OR = 1.69, 95 % CI = 1.15-2.49) and rs3748067 TT (adjusted OR = 1.73, 95 % CI = 1.03-2.94) genotypes were associated with an increased risk of gastric cancer. We observed a significant interaction among rs2275913G>A, rs3748067C>T, and H. pylori infection on the risk of gastric cancer (p for interaction of 0.036 and 0.048, respectively). H. pylori infection subjects carrying the rs2275913 AA (adjusted OR = 2.48, 95 % CI = 1.49-4.12) and rs3748067 TT (adjusted OR = 2.54, 95 % CI = 1.34-5.12) genotypes had a greatly increased risk of gastric cancer compared to negative H. pylori participants. Similarly, subjects carrying the rs2275913 AA (adjusted OR = 2.09, 95 % CI = 1.25-3.45) and rs3748067 TT (adjusted OR = 2.29, 95 % CI = 1.20-4.20) genotypes had a moderately increased risk of noncardia gastric cancer. A significant interaction was observed between the rs2275913G>A and rs3748067C>T genotype and subsites of gastric cancer (p for interaction of 0.044 and 0.008, respectively). The rs2275913G>A and rs763780T>C polymorphisms increase gastric cancer risk, and interact with H. pylori infection and subsites. These findings could be helpful in identifying individuals at increased risk for developing gastric cancer.

An achievement has been made in establishing an induced pluripotent stem cell line (SDPHi005-A) from a healthy Chinese male donor.

Successfully transforming isolated peripheral blood mononuclear cells (PBMCs) from a healthy male into induced pluripotent stem cells (iPSCs) was achieved using non-integrating episomal vectors containing OCT4, SOX2, c-MYC, KLF4, and BCL-XL. The iPSCs exhibited a normal karyotype, expressed pluripotency markers, and demonstrated the ability to differentiate into three germ layers in vitro. This iPSC line may be employed for subsequent research purposes.

Effective synergies in indium oxide loaded with zirconia mixed with silicoaluminophosphate molecular sieve number 34 catalysts for carbon dioxide hydrogenation to lower olefins.

Tandem catalysts consisting of metal oxides and zeolites have been widely studied for catalytic carbon dioxide (CO2) hydrogenation to lower olefins, while the synergies of two components and their influence on the catalytic performance are still unclear. In this study, the composite catalysts composed of indium oxide loaded with zirconia (In2O3/ZrO2) and silicoaluminophosphate molecular sieve number 34 (SAPO-34) are developed. Performance results indicate that the synergies between these two components can promote CO2 hydrogenation. Further characterizations reveal that the chabazite (CHA) structure and acid sites in the SAPO-34 are destroyed when preparing In-Zr/SAPO by powder milling (In-Zr/SAPO-M) because of the excessive proximity of two components, which inhibits the activation of CO2 and hydrogen (H2), thus resulting in much higher methane selectivity than the catalysts prepared by granule stacking (In-Zr/SAPO-G). Proper granule integration manner promotes tandem reaction, thus enhancing CO2 hydrogenation to lower olefins, which can provide a practicable strategy to improve catalytic performance and the selectivity of the target products.

Defluorination and directional conversion to light fuel by lithium synergistic vacuum catalytic co-pyrolysis for electrolyte and polyvinylidene fluoride in spent lithium-ion batteries.

To overcome the drawbacks of current recycling technologies and achieve clean utilization of toxic substances in spent lithium-ion batteries, a lithium synergistic vacuum catalytic co-pyrolysis method was proposed to defluorinate electrolyte and polyvinylidene fluoride with directional conversion to light fuel. The gas chromatography-mass spectrometry results indicated, compared to the control group, that adding CaO-ZSM-5 catalyst increased the light fuel (alcohols and hydrocarbons) content of the pyrolysis gas from 61.8 % to 91.47 % under the optimal conditions (530 °C and initial pressure of 100 Pa), whereas the total proportion of esters and toxic organic compounds decreased from 32.58 % to 3.99 %. Moreover, the ethylene carbonate and hexanedinitrile content of the electrolyte was enriched to 85 % in the pyrolysis oil. Notably, fluoride was not detected in the pyrolysis oil and gas, achieving a 98.16 % defluorination rate, implying that hazardous waste was transformed to ordinary waste, thereby greatly avoiding toxic emissions to the environment. The X-ray diffraction (XRD) and scanning electron microscopy/energy-dispersive X-ray spectroscopy data indicated that fluorine was fixed in the form of CaF2. X-ray photoelectron spectroscopy and XRD analysis of the catalytic pyrolysis residue confirmed that nonferrous metals in the cathode material were converted into simple substances and oxides. Finally, possible co-pyrolysis mechanisms of the organic compounds are proposed, including Li+ generation, chain initiation, catalytic pyrolysis, and directional conversion.

Home away from home: international students' experiences during the COVID-19 pandemic and the role of US higher education.

Introduction: This study focuses on the impact of the COVID-19 pandemic on international students' overall experiences. Method: We interviewed 22 international students from 11 countries and 17 universities in the US who participated in a large longitudinal study that aims to understand the physical and emotional wellbeing of young adults during the COVID-19 pandemic. Guided by Bronfenbrenner's ecological model, the findings suggested that students were impacted by the COVID-19 pandemic at interpersonal, institutional, political, and personal levels. Results: The results showed that the pandemic exacerbated existing stressors such as the lack of social support from family, various visa regulations, competitive and limited job opportunities, discrimination and xenophobia, particularly toward students from Asia, and financial burdens. Additionally, the findings highlighted students' perceived loss of the "American dream" and the uneven return on investment due to the pandemic. Discussion: This study reveals the importance of US higher education institutions in supporting international students during the pandemic, particularly in terms of their sense of belonging. Recommendations for institutions drawn from the findings are proposed to better support international students during times of COVID-19 and beyond.

International student stressors and mental health during the COVID-19 pandemic: a qualitative study.

OBJECTIVE: To identify stressors affecting international students' mental health during the COVID-19 pandemic. PARTICIPANTS: Twenty-two international students from 10 countries and 17 US institutions participated. METHODS: Participants were recruited from a larger study examining the wellbeing of young adults during the pandemic. RESULTS: Four main stressors were identified: (1) Uncertainty and anxiety induced by decisions and policies in response to COVID-19; (2) Fears regarding xenophobia; (3) Limited understanding by educators and school staff of international students' unique challenges; (4) Greater awareness of racial and cultural identity. CONCLUSION: The pandemic has contributed to additional stressors for international students. Educators and mental health professionals may help support international students' mental health by gaining basic knowledge about common stressors and directly acknowledging the challenges, educating international students on race and racism and supporting anti-racism efforts, and encouraging the creation of shared affinity spaces and increasing psychoeducation to promote resilience.

ANGPTL8 is a negative regulator in pathological cardiac hypertrophy.

Pathological cardiac hypertrophy is an independent risk factor for heart failure and is considered a target for the treatment of heart failure. However, the mechanisms underlying pathological cardiac hypertrophy remain largely unknown. We aimed to investigate the role of angiopoietin-like protein 8 (ANGPTL8) in pathological cardiac hypertrophy. We found that serum ANGPTL8 levels were significantly increased in hypertensive patients with cardiac hypertrophy and in mice with cardiac hypertrophy induced by Ang II or TAC. Furthermore, the secretion of ANGPTL8 from the liver was increased during hypertrophic processes, which were triggered by Ang II. In the Ang II- and transverse aortic constriction (TAC)-induced mouse cardiac hypertrophy model, ANGPTL8 deficiency remarkably accelerated cardiac hypertrophy and fibrosis with deteriorating cardiac dysfunction. Accordingly, both recombinant human full-length ANGPTL8 (rANGPTL8) protein and ANGPTL8 overexpression significantly mitigated Ang II-induced cell enlargement in primary neonatal rat cardiomyocytes (NRCMs) and H9c2 cells. Mechanistically, the antihypertrophic effects of ANGPTL8 depended on inhibiting Akt and GSK-3ß activation, and the Akt activator SC-79 abolished the antihypertrophic effects of rANGPTL8 in vitro. Moreover, we demonstrated that ANGPTL8 directly bound to the paired Ig-like receptor PIRB (LILRB3) by RNA-seq and immunoprecipitation-mass screening. Remarkably, the antihypertrophic effects of ANGPTL8 were largely blocked by anti-LILRB3 and siRNA-LILRB3. Our study indicated that ANGPTL8 served as a novel negative regulator of pathological cardiac hypertrophy by binding to LILRB3 (PIRB) and inhibiting Akt/GSK3ß activation, suggesting that ANGPTL8 may provide synergistic effects in combination with AT1 blockers and become a therapeutic target for cardiac hypertrophy and heart failure.

Robotic versus laparoscopic surgery for middle and low rectal cancer (REAL): short-term outcomes of a multicentre randomised controlled trial.

BACKGROUND: Robotic surgery for rectal cancer is gaining popularity, but evidence on long-term oncological outcomes is scarce. We aimed to compare surgical quality and long-term oncological outcomes of robotic and conventional laparoscopic surgery in patients with middle and low rectal cancer. Here we report the short-term outcomes of this trial. METHODS: This multicentre, randomised, controlled, superiority trial was done at 11 hospitals in eight provinces of China. Eligible patients were aged 18-80 years with middle (>5 to 10 cm from the anal verge) or low (≤5 cm from the anal verge) rectal adenocarcinoma, cT1-T3 N0-N1 or ycT1-T3 Nx, and no evidence of distant metastasis. Central randomisation was done by use of an online system and was stratified according to participating centre, sex, BMI, tumour location, and preoperative chemoradiotherapy. Patients were randomly assigned at a 1:1 ratio to receive robotic or conventional laparoscopic surgery. All surgical procedures complied with the principles of total mesorectal excision or partial mesorectal excision (for tumours located higher in the rectum). Lymph nodes at the origin of the inferior mesenteric artery were dissected. In the robotic group, the excision procedures and dissection of lymph nodes were done by use of robotic techniques. Neither investigators nor patients were masked to the treatment allocation but the assessment of pathological outcomes was masked to the treatment allocation. The primary endpoint was 3-year locoregional recurrence rate, but the data for this endpoint are not yet mature. Secondary short-term endpoints are reported in this article, including two key secondary endpoints: circumferential resection margin positivity and 30-day postoperative complications (Clavien-Dindo classification grade II or higher). The outcomes were analysed according in a modified intention-to-treat population (according to the original assigned groups and excluding patients who did not undergo surgery or no longer met inclusion criteria after randomisation). This trial was registered with ClinicalTrials.gov, number NCT02817126. Study recruitment has completed, and the follow-up is ongoing. FINDINGS: Between July 17, 2016, and Dec 21, 2020, 1742 patients were assessed for eligibility. 502 patients were excluded, and 1240 patients were enrolled and randomly assigned to receive either robotic surgery (620 patients) or laparoscopic surgery (620 patients). 69 patients were excluded (34 in the robotic surgery group and 35 in the laparoscopic surgery group). 1171 patients were included in the modified intention-to-treat analysis (586 in the robotic group and 585 in the laparoscopic group). Six patients in the robotic surgery group received laparoscopic surgery and seven patients in the laparoscopic surgery group received robotic surgery. 22 (4·0%) of 547 patients in the robotic group had a positive circumferential resection margin as did 39 (7·2%) of 543 patients in the laparoscopic group (difference -3·2 percentage points [95% CI -6·0 to -0·4]; p=0·023). 95 (16·2%) of patients in the robotic group had at least one postoperative complication (Clavien-Dindo grade II or higher) within 30 days after surgery, as did 135 (23·1%) of 585 patients in the laparoscopic group (difference -6·9 percentage points [-11·4 to -2·3]; p=0·003). More patients in the robotic group had a macroscopic complete resection than in the laparoscopic group (559 [95·4%] of 586 patients vs 537 [91·8%] of 585 patients, difference 3·6 percentage points [0·8 to 6·5]). Patients in the robotic group had better postoperative gastrointestinal recovery, shorter postoperative hospital stay (median 7·0 days [IQR 7·0 to 11·0] vs 8·0 days [7·0 to 12·0], difference -1·0 [95% CI -1·0 to 0·0]; p=0·0001), fewer abdominoperineal resections (99 [16·9%] of 586 patients vs 133 [22·7%] of 585 patients, difference -5·8 percentage points [-10·4 to -1·3]), fewer conversions to open surgery (10 [1·7%] of 586 patients vs 23 [3·9%] of 585 patients, difference -2·2 percentage points [-4·3 to -0·4]; p=0·021), less estimated blood loss (median 40·0 mL [IQR 30·0 to 100·0] vs 50·0 mL [40·0 to 100·0], difference -10·0 [-20·0 to -10·0]; p<0·0001), and fewer intraoperative complications (32 [5·5%] of 586 patients vs 51 [8·7%] of 585 patients; difference -3·3 percentage points [-6·3 to -0·3]; p=0·030) than patients in the laparoscopic group. INTERPRETATION: Secondary short-term outcomes suggest that for middle and low rectal cancer, robotic surgery resulted in better oncological quality of resection than conventional laparoscopic surgery, with less surgical trauma, and better postoperative recovery. FUNDING: Shenkang Hospital Development Center, Shanghai Municipal Health Commission (Shanghai, China), and Zhongshan Hospital Fudan University (Shanghai, China).

Baicalein Mediates Mitochondrial Autophagy via miR-30b and the NIX/BNIP3 Signaling Pathway in Parkinson's Disease.

Parkinson's disease (PD) is regarded as a severe neurodegenerative disorder. Baicalein is involved in the treatment of PD. This study explored the mechanism of baicalein in PD. The PD rat model was established using 6-hydroxydopamine. The neurologic score, dopamine (DA) content, apoptotic cells, and neuronal damage were evaluated after rats were treated with baicalein. Autophagy in PD rats was inhibited using 3-methyladenine (3-MA). The mitochondrial membrane potential (MMP) and autophagy-related proteins (LC3, P62) were detected. Next, agomiR-30b was transfected into PD rats. The targeting relation between miR-30b and NIX was predicted and verified. Then, sh-NIX was transfected into PD rats, and the effects of miR-30b and NIX on MMP, LC3, and P62 were assessed. When miR-30b was overexpressed using agomiR-30b, the NIX and BNIP3 levels were detected. Baicalein increased the neurological score and restored DA content, neurons, MMP, and mitochondrial autophagy protein levels. Baicalein inhibited miR-30b expression and miR-30b targeted NIX. miR-30b upregulation or NIX silencing reversed the effect of baicalein on MMP and mitochondrial autophagy. Baicalein upregulated NIX and BNIP3 expressions, while miR-30b overexpression inhibited NIX and BNIP3 expressions. In summary, baicalein mediated mitochondrial autophagy and restored neuronal activity by downregulating miR-30b and activating the NIX/BNIP3 pathway, thus protecting against PD.

Baicalein Induces Mitochondrial Autophagy to Prevent Parkinson's Disease in Rats via miR-30b and the SIRT1/AMPK/mTOR Pathway.

Parkinson's disease (PD) is a prevailing neurodegenerative disorder. Baicalein has neuroprotective effects on PD animals, but its mechanism is not clarified. We explored baicalein effects on PD rats. PD rat models were established by injecting 6-hydroxydopamine into the striatum of substantia nigra on the left side of the rat brain and treated with baicalein. Dopamine (DA) content, neuronal apoptosis, neuronal injury, neuronal mitochondria, and autophagy were assessed. Baicalein-treated PD rats were treated with autophagy inhibitor 3-methyladenine to identify the role of autophagy in PD. PD rats were injected with AgomiR-30b-5p or sh-SIRT1 plasmids and treated with baicalein. PD rats elicited decreased neurological score and DA secretion of the striatum, increased neuronal apoptosis, and injury, and reduced number of mitochondria and autophagy, whereas baicalein alleviated neuronal injury and partly recovered mitochondrial dysfunction, 3-methyladenine inhibited the protection of baicalein. miR-30b-5p was elevated and SIRT1 was diminished in PD rats and inhibited by baicalein. miR-30b-5p targeted SIRT1. miR-30b-5p overexpression or SIRT1 silencing annulled the protection of baicalein. The phosphorylation level of AMPK in the substantia nigra of PD rats was decreased and mTOR was increased, whereas baicalein annulled these trends. Briefly, baicalein activated mitochondrial autophagy via miR-30b-5p and the SIRT1/AMPK/mTOR pathway, thus protecting PD rats.

Learning curve of laparoscopic surgery for gastric cancer, a laparoscopic distal gastrectomy-based analysis.

BACKGROUND: The application of laparoscopic gastrectomy in management of gastric cancer is being propagated rapidly. Training and education play important role during this process. The purpose of this study is to define the learning curve of laparoscopic gastrectomy to obtain an insight into this training process. METHODS: All 362 cases of laparoscopic gastrectomy from January 1998 to July 2007 were enrolled and divided into 12 groups of 30 cases each in time sequence. The learning curve was defined with the split group method. Laparoscopic distal gastrectomy was extracted from the 12 groups and the means of operation time and intraoperative blood loss were compared to define the learning curve. Then general data and variables including occurrence of systematic inflammatory response syndrome (SIRS), complications, and conversion to open surgery were compared among the phases of learning curve. RESULTS: A three-phase learning curve of laparoscopic gastrectomy was defined from the laparoscopic distal gastrectomy-based analysis, which included a training phase for the first 120 cases of operation, an intermediate phase for the following 90 cases, and a well-developed phase for the last 152 cases. Learning was considered to be complete after 60-90 operations in the training phase. For most variables, the differences among three phases were statistically significant except for the rate of complications. CONCLUSIONS: There was a significant learning curve, composed of three phases. Experience of about 60-90 cases of operation was required for completion of learning.

Effects of repetitive transcranial magnetic stimulation on cognitive function and cholinergic activity in the rat hippocampus after vascular dementia.

Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive treatment that can enhance the recovery of neurological function after stroke. Whether it can similarly promote the recovery of cognitive function after vascular dementia remains unknown. In this study, a rat model for vascular dementia was established by the two-vessel occlusion method. Two days after injury, 30 pulses of rTMS were administered to each cerebral hemisphere at a frequency of 0.5 Hz and a magnetic field intensity of 1.33 T. The Morris water maze test was used to evaluate learning and memory function. The Karnovsky-Roots method was performed to determine the density of cholinergic neurons in the hippocampal CA1 region. Immunohistochemical staining was used to determine the number of brain-derived neurotrophic factor (BDNF)-immunoreactive cells in the hippocampal CA1 region. rTMS treatment for 30 days significantly improved learning and memory function, increased acetylcholinesterase and choline acetyltransferase activity, increased the density of cholinergic neurons, and increased the number of BDNF-immunoreactive cells. These results indicate that rTMS can ameliorate learning and memory deficiencies in rats with vascular dementia. The mechanism through which this occurs might be related to the promotion of BDNF expression and subsequent restoration of cholinergic system activity in hippocampal CA1 region.

Effect of transcranial magnetic stimulation on the expression of c-Fos and brain-derived neurotrophic factor of the cerebral cortex in rats with cerebral infarct.

The effect of transcranial magnetic stimulation (TMS) on the neurological functional recovery and expression of c-Fos and brain-derived neurotrophic factor (BDNF) of the cerebral cortex in rats with cerebral infarction was investigated. Cerebral infarction models were established by using left middle cerebral artery occlusion (MCAO) and were randomly divided into a model group (n=40) and a TMS group (n=40). TMS treatment (2 times per day, 30 pulses per time) with a frequency of 0.5 Hz and magnetic field intensity of 1.33 Tesla was carried out in TMS group after MCAO. Modified neurological severity score (NSS) were recorded before and 1, 7, 14, 21, and 28 day(s) after MCAO. The expression of c-Fos and BDNF was immunohistochemically detected 1, 7, 14, 21, and 28 day(s) after infarction respectively. Our results showed that a significant recovery of NSS (P<0.05) was found in animals treated by TMS on day 7, 14, 21, and 28 as compared with the animals in the model group. The positive expression of c-Fos and BDNF was detected in the cortex surrounding the infarction areas, while the expression of c-Fos and BDNF increased significantly in TMS treatment group in comparison with those in model group 7, 14, 21, and 28 days (P<0.05) and 7, 14, 21 days (P<0.01) after infarction, respectively. It is concluded that TMS has therapeutic effect on cerebral infarction and this may have something to do with TMS's ability to promote the expression of c-Fos and BDNF of the cerebral cortex in rats with cerebral infarction.

[Effects of transcranial magnetic stimulation on recovery of neural functions and changes of synaptic interface and dendritic structure in the contralateral brain area after cerebral infarction: experiment with rats].

OBJECTIVE: To evaluate the effects of transcranial magnetic stimulation (TMS) on the brain plasticity and its role in functional outcome in cerebral infarction. METHODS: Twenty male SD rats underwent suture of the unilateral middle cerebral artery (MCA) so as to establish focal cerebral infarction models and then were randomly divided into 2 equal groups: model group, to be reared in the original living state, and TMS group, given in addition TMS treatment 1 day after infarction 2 times per day and 30 pulses per time for 4 weeks. Twenty-eight days after the rats were killed. Four rats from each group underwent microscopy of the brain to measure the dendritic structure of the pyramidal cells quantitatively. Other 4 rats from each group underwent electron microscopy of the brain to measure the parameters of synaptic interface in the sensorimotor cortex. Neural function scoring was conducted 24 hours after the establishment of model and before being killed. RESULTS: There was no significant difference in the neural function 24 h after the establishment of models, however, 28 days after the score of neural function of the TMA group was 0.58 +/- 0.49, significantly lower than that of the model group (0.92 +/- 0.28, P < 0.05). The total dendritic length, number of dendritic branching points, and dendritic density in layer V pyramidal cells within the undamaged motor cortex of the TMS group were 898 microm +/- 127 microm, 6.6 +/- 1.5, and 0.75/microm +/- 0.19/microm, all significantly higher than those of the model group (788 microm +/- 112 microm, 5.8 +/- 1.5, and 0.60/microm +/- 0.16/microm, P < 0.05 or < 0.01). Electron microscopy showed that the synaptic curvatures and post-synaptic density of the TMS group were 1.06 +/- 0.08 and 64 +/- 13 respectively, both significantly higher than those of the model group (1.02 +/- 0.06 and 54 +/- 12 nm respectively, P < 0.05 and P < 0.01), and the synapse cleft width of the TMS group was 19.5 +/- 2.1, significantly narrower than that of the model group (23.3 +/- 2.3, P < 0.01). CONCLUSION: TMS promotes the improvement of neural functions of the rats with cerebral ischemia by the potential mechanism that TMS strengthen the compensatory roles of the synaptic interface and dendritic structure in the undamaged sensorimotor cortex area and increase synaptic plasticity.