Betaine prevents cognitive dysfunction by suppressing hippocampal microglial activation in chronic social isolated male mice.

Chronic social isolation (SI) stress, which became more prevalent during the COVID-19 pandemic, contributes to abnormal behavior, including mood changes and cognitive impairment. Known as a functional nutrient, betaine has potent antioxidant and anti-inflammatory properties in vivo. However, whether betaine can alleviate the abnormal behavior induced by chronic SI in mice remains unknown. In this study, we investigated the efficacy of betaine in the treatment of behavioral changes and its underlying mechanism. Three-week-old male mice were randomly housed for 8 weeks in either group housing (GH) or SI. The animals were divided into normal saline-treated GH, normal saline-treated SI, and betaine-treated SI groups in the sixth week. The cognitive and depression-like behavior was determined in the eighth week. We found that long-term betaine administration improved cognitive behavior in SI mice but failed to prevent depression-like behavior. Moreover, long-term betaine administration inhibited hippocampal microglia over-activation and polarized microglia toward the M2 phenotype, which effectively inhibited the expression of inflammatory factors in SI mice. Finally, the protective effect of betaine treatment in SI mice might not be due to altered activity of the hypothalamic-pituitary-adrenal axis. Collectively, our findings reveal that betaine can improve SI-induced cognitive impairment, thus providing an alternative natural source for the prevention of memory loss caused by SI or loneliness.

The effects of nuclear factor-kappa B in pancreatic stellate cells on inflammation and fibrosis of chronic pancreatitis.

The activation of pancreatic stellate cells (PSCs) plays a critical role in the progression of pancreatic fibrosis. Nuclear factor-kappa B (NF-κB) is associated with chronic pancreatitis (CP). Previous evidence indicated that NF-κB in acinar cells played a double-edged role upon pancreatic injury, whereas NF-κB in inflammatory cells promoted the progression of CP. However, the effects of NF-κB in PSCs have not been studied. In the present study, using two CP models and RNAi strategy of p65 in cultured PSCs, we found that the macrophage infiltration and MCP-1 expression were increased, and the NF-κBp65 protein level was elevated. NF-κBp65 was co-expressed with PSCs. In vitro, TGF-ß1 induced overexpression of the TGF-ß receptor 1, phosphorylated TGF-ß1-activated kinase 1 (p-TAK1) and NF-κB in the PSCs. Moreover, the concentration of MCP-1 in the supernatant of activated PSCs was elevated. The migration of BMDMs was promoted by the supernatant of activated PSCs. Further knockdown of NF-κBp65 in PSCs resulted in a decline of BMDM migration, accompanied by a lower production of MCP-1. These findings indicate that TGF-ß1 can induce the activation of NF-κB pathway in PSCs by regulating p-TAK1, and the NF-κB pathway in PSCs may be a target of chronic inflammation and fibrosis.

Respective roles of the mitogen-activated protein kinase (MAPK) family members in pancreatic stellate cell activation induced by transforming growth factor-ß1 (TGF-ß1).

Activated pancreatic stellate cells (PSCs) play a crucial role in the progression of pancreatic fibrosis. Transforming growth factor-ß (TGF-ß) is one of the strongest stimulator inducing fibrosis. The mitogen-activated protein kinase (MAPK) proteins (including ERK, JNK and p38 MAPK) are known to contribute to PSC activation and pancreatic fibrosis. Previous studies have identified PSC activation induced by TGF-ß1 is related to MAPK pathway, but the respective role of MAPK family members in PSC activation still unclear, and which family member may be the key mediator in mice PSC activation still controversial. In this study, we investigated the influence of different MAPK family member (JNK, ERK, and p38 MAPK) on mice PSC activation using an in vivo and in vitro model. The results showed p-JNK, p-ERK and p-p38 MAPK were all over-expressed in CP group, and p-JNK, p-ERK, and p-p38 MAPK were co-expressed with activated PSC. In vitro, TGF-ß1 induced JNK and ERK over-expression in PSCs. In contrast, p38 MAPK expression in PSC showed only a very weak increase. JNK- and ERK-specific inhibitors inhibited FN and α-SMA mRNA expression in PSCs, and a p38 MAPK inhibitor had no effect on PSC activation. These findings indicate that JNK and ERK were directly involved in the PSCs activation induced by TGF-ß1 and the development of pancreatic fibrosis. p38 MAPK participate in the progression of CP, but it does not respond to TGF-ß1 directly and may not be regarded as the target of TGF-ß1 induced PSC activation.

Blockade of GLUT1 by WZB117 resensitizes breast cancer cells to adriamycin.

The tolerance to adriamycin of cancer as a common and stubborn obstacle occurred during curing breast cancer patients needs to be overcome. In the present study, we explored whether inhibiting the glucose transporter 1 (GLUT1) could restore the activity of adriamycin in breast cancer cell line MCF-7 resistant to adriamycin and the possible underlying mechanisms. Adriamycin-resistant cell line MCF-7/ADR was selected stepwise from the parental MCF-7 cells and the level of GLUT1 was measured. Then, the MCF-7/ADR cells were incubated with adriamycin, WZB117 (a specific GLUT1 inhibitor), or both. The viability, proliferation and apoptosis of cells and the level of glucose and lactate were measured, respectively. Finally, the cytosolic and mitochondrial proteins were isolated and the activity of the adenosine monophosphate-activated protein kinase (AMPK)/phosphorylated AMPK, mammalian target of rapamycin (mTOR)/phosphorylated mTOR, and apoptotic-related protein BCL-2-associated X protein (BAX), Bcl-2 was assayed by western blot. We found that WZB117 resensitized MCF-7/ADR to adriamycin and increased BAX translocated to mitochondria, which through activation of AMPK and inhibition of mTOR in a high probability. Inhibition of the GLUT1 could partially restore the antineoplastic effects of adriamycin in the adriamycin-resistant MCF-7 cell line possibly through activating the AMPK, downregulating the mTOR pathway, and increasing the BAX translocation to mitochondria.

Quantum teleportation between remote atomic-ensemble quantum memories.

Quantum teleportation and quantum memory are two crucial elements for large-scale quantum networks. With the help of prior distributed entanglement as a "quantum channel," quantum teleportation provides an intriguing means to faithfully transfer quantum states among distant locations without actual transmission of the physical carriers [Bennett CH, et al. (1993) Phys Rev Lett 70(13):1895-1899]. Quantum memory enables controlled storage and retrieval of fast-flying photonic quantum bits with stationary matter systems, which is essential to achieve the scalability required for large-scale quantum networks. Combining these two capabilities, here we realize quantum teleportation between two remote atomic-ensemble quantum memory nodes, each composed of ∼10(8) rubidium atoms and connected by a 150-m optical fiber. The spin wave state of one atomic ensemble is mapped to a propagating photon and subjected to Bell state measurements with another single photon that is entangled with the spin wave state of the other ensemble. Two-photon detection events herald the success of teleportation with an average fidelity of 88(7)%. Besides its fundamental interest as a teleportation between two remote macroscopic objects, our technique may be useful for quantum information transfer between different nodes in quantum networks and distributed quantum computing.

Association between vitamin B1 intake and hyperuricemia in adults.

Studies investigating the relationship between dietary vitamin B1 intake and risk of Hyperuricemia (HU) are scarce, the present study aimed to examine the association of dietary vitamin B1 intake and HU among adults. This cross-sectional study included 5750 adults whose data derived from National Health and Nutrition Examination Survey (NHANES) from March 2017 to March 2020. The dietary intake of vitamin B1 was assessed using 24-h dietary recall interviews. The characteristics of study participants were grouped into five levels according to the levels of vitamin B1 quintile. Multivariate logistic regression analysis was used to estimate the odds ratio (OR) and 95% confidence interval (CI) of HU, according to the vitamin B1 intake quintile for male and female separately. The dose-response relationship was determined by the restricted cubic spline (RCS). Smoothed curve fitting was used to assess serum uric acid concentration versus dietary vitamin B1 intake in the study population. The prevalence of hyperuricemia was 18.90% (20.15% and 17.79% for males and females, respectively) in the United States from March 2017 to March 2020. Multiple logistic regression analyses showed that in the male population, the HU ratio (OR) of vitamin B1 intake in Q2 to Q5 compared with the lowest quintile (Q1) was 0.75 (95% CI 0.52, 1.09), 0.70 (95% CI 0.48, 1.02), 0.66 (95% CI 0.44, 0.99) and 0.55 (95% CI 0.34, 0.90). The P for trend was 0.028. In women, the ORs for vitamin B1 intake Q2 to Q5 were 0.87 (95% CI 0.64, 1.19), 0.97 (0.68-1.38), 1.05 (0.69-1.60) and 0.75 (0.42-1.34), respectively. The P for trend was 0.876. The RCS curve revealed a linear relationship between vitamin B1 intake and the risk of hyperuricemia in men (P nonlinear = 0.401). Smoothed curve fitting demonstrated a negative association between vitamin B1 intake and serum uric acid concentration in men, whereas there was no significant association between dietary vitamin B1 intake and the risk of hyperuricemia in women. In the US adult population, dietary vitamin B1 intake was negatively associated with hyperuricemia in males.

The diagnostic value of neutrophil to lymphocyte ratio, albumin to fibrinogen ratio, and lymphocyte to monocyte ratio in Parkinson's disease: a retrospective study.

Background: Parkinson's disease (PD) is a prevalent disorder of the central nervous system, marked by the degeneration of dopamine (DA) neurons in the ventral midbrain. In the pathogenesis of PD, inflammation hypothesis has been concerned. This study aims to investigate clinical indicators of peripheral inflammation in PD patients and to explore the diagnostic value of neutrophil-to-lymphocyte ratio (NLR), albumin-to-fibrinogen ratio (AFR), and lymphocyte-to-monocyte ratio (LMR) in assessing PD risk. Methods: This study included 186 patients with PD and 201 matched healthy controls (HC) with baseline data. Firstly, the differences of hematological indicators between PD group and healthy participants were compared and analyzed. Univariate and multivariate regression analyses were then conducted. Smooth curve fitting was applied to further validate the relationships between NLR, LMR, AFR, and PD. Subsequently, subgroup analysis was conducted in PD group according to different duration of disease and Hoehn and Yahr (H&Y) stage, comparing differences in clinical indicators. Finally, the receiver operating characteristic (ROC) curve was employed to assess the diagnostic value of NLR, LMR, and AFR in PD. Results: Compared to the HC group, the PD group showed significantly higher levels of hypertension, diabetes, neutrophil count, monocyte count, CRP, homocysteine, fibrinogen, and NLR. Conversely, levels of LMR, AFR, lymphocyte count, HDL, LDL, TG, TC, uric acid, and albumin were significantly lower. The multivariate regression model indicated that NLR (OR = 1.79, 95% CI: 1.39-2.31, p < 0.001), LMR (OR = 0.75, 95% CI: 0.66-0.85, p < 0.001), and AFR (OR = 0.79, 95% CI: 0.73-0.85, p < 0.001) were significant factors associated with PD. Smooth curve fitting revealed that NLR was positively linked to PD risk, whereas AFR and LMR were inversely associated with it. In ROC curve analysis, the AUC of AFR was 0.7290, the sensitivity was 63.98%, and the specificity was 76.00%. The AUC of NLR was 0.6200, the sensitivity was 50.54%, and the specificity was 71.50%. The AUC of LMR was 0.6253, the sensitivity was 48.39%, and the specificity was 73.00%. The AUC of the combination was 0.7498, the sensitivity was 74.19%, and the specificity was 64.00%. Conclusion: Our findings indicate that NLR, LMR, and AFR are significantly associated with Parkinson's disease and may serve as diagnostic markers.

Cluster headache: understandings of current knowledge and directions for whole process management.

Cluster headache (CH) is a common primary headache that severely impacts patients' quality of life, characterized by recurrent, severe, unilateral headaches often centered around the eyes, temples, or forehead. Distinguishing CH from other headache disorders is challenging, and its pathogenesis remains unclear. Notably, patients with CH often experience high levels of depression and suicidal tendencies, necessitating increased clinical attention. This comprehensive assessment combines various reports and the latest scientific literature to evaluate the current state of CH research. It covers epidemiology, population characteristics, predisposing factors, and treatment strategies. Additionally, we provide strategic insights into the holistic management of CH, which involves continuous, individualized care throughout the prevention, treatment, and rehabilitation stages. Recent advances in the field have revealed new insights into the pathophysiology of CH. While these findings are still evolving, they offer a more detailed understanding of the neurobiological mechanisms underlying this disorder. This growing body of knowledge, alongside ongoing research efforts, promises to lead to the development of more targeted and effective treatments in the future.

Chronic social isolation leads to abnormal behavior in male mice through the hippocampal METTL14 mediated epitranscriptomic RNA m6A modifications.

BACKGROUND: Social isolation not only increases the risk of mortality in later life but also causes depressive symptoms, cognitive and physical disabilities. Although RNA m6A modifications are suggested to play key roles in brain development, neuronal signaling and neurological disorders, both the roles of m6A and the enzymes that regulate RNA m6A modification in social isolation induced abnormal behavior is unknown. The present study aims to explore the possible epitranscriptomic role of RNA m6A modifications and its enzymes in social isolation induced impaired behavior. METHODS: 3-4 weeks mice experiencing 8 weeks social isolation stress (SI) were used in the present study. We quantified m6A levels in brain regions related to mood and cognitive behavior. And the expression of hippocampal m6A enzymes was also determined. The role of hippocampal m6A and its enzymes in SI induced abnormal behavior was further verified by the virus tool. RESULTS: SI led to not only depressive and anxiety-like behaviors but also cognitive impairment, with corresponding decreases in hippocampal m6A and METTL14. Hippocampal over-expression METTL14 with lentivirus not only rescued these behaviors but also enhanced the hippocampal m6A level. Hippocampal over-expression METTL14 resulted in increased synaptic related genes. CONCLUSIONS: We provide the first evidence that post-weaning social isolation reduces hippocampal m6A level and causes altered expression of m6A enzyme in mice. Importantly, hippocampal METTL14 over-expression alleviated the SI-induced depression/anxiety-like and impaired cognitive behaviors and enhanced m6A level and synaptic related genes expression.

[Port-owned Mobile Source Air Pollutant Emission Inventory].

Based on the comprehensive development of the emission inventory of air pollution sources, the emission inventory of self-owned mobile sources of Tianjin coastal ports was researched and formulated. In this study, a gridded emission inventory with a resolution of 3 km×3 km was established for six types of air pollutants from road and non-road mobile sources. The spatial and temporal distribution characteristics of pollutant emissions were analyzed, and the uncertainty of the inventory was analyzed using the Monte Carlo method. The results showed that in 2020, the self-owned mobile sources of coastal ports emitted 148.22 t PM10, 135.34 t PM2.5, 1061.04 t SO2, 4027.16 t NOx, 756.60 t CO, and 237.07 t VOCs, of which the total emissions of road and non-road mobile sources accounted for 6.66% and 93.34% of the mobile source emissions, respectively. The main contributors to motor vehicle pollutant emissions from road mobile sources in the whole port area were small, medium, and large passenger vehicles (gasoline) and heavy trucks (diesel). The main contributors to the pollutants emitted by non-road mobile sources were ships and construction machinery. Uncertainty analysis results showed that the overall uncertainty of mobile sources ranged from -13.3% to 16.53%.

PPARα is involved in high-fat diet-induced risk avoidance impairment via the regulation of hippocampal BDNF.

Risk avoidance behaviors are essential for survival. "Uncontrollable" risk-taking behaviors in animals or humans may have severe adverse consequences. In humans, a large proportion of psychiatric disorders are accompanied by impairments in risk avoidance. Obesity is associated with psychiatric disorders. Peroxisome proliferator-activated receptor α (PPARα) takes part in regulating lipid metabolism and neuronal function. Here, we investigated the effect of high-fat diet (HFD)-induced obesity on risk avoidance and the role of PPARα in this behavior. Male PPARα-null (KO) mice and wild-type (WT) mice were assigned to four different groups: WT-CON and KO-CON (normal diet); WT-HFD and KO-HFD (high fat diet). The HFD began at week 6 and was continued until sampling. A series of behavioral tests were performed at week 11. We found that WT but not KO mice fed with a HFD exhibited weight gain and risk avoidance impairment, compared with the mice fed with a normal diet. The staining of c-Fos revealed that the hippocampus was the main brain region involved in risk avoidance behavior. Moreover, biochemical analysis suggested that the decreased levels of the brain-derived neurotrophic factor (BDNF) in the hippocampus might contribute to risk avoidance impairment induced by a HFD. These results indicated that PPARα is involved in HFD-induced risk avoidance impairment via the regulation of hippocampal BDNF.

Lateral septal nucleus, dorsal part, and dentate gyrus are necessary for spatial and object recognition memory, respectively, in mice.

Introduction: Cognitive impairment includes the abnormality of learning, memory and judgment, resulting in severe learning and memory impairment and social activity impairment, which greatly affects the life quality of individuals. However, the specific mechanisms underlying cognitive impairment in different behavioral paradigms remain to be elucidated. Methods: The study utilized two behavioral paradigms, novel location recognition (NLR) and novel object recognition (NOR), to investigate the brain regions involved in cognitive function. These tests comprised two phases: mice were presented with two identical objects for familiarization during the training phase, and a novel (experiment) or familiar (control) object/location was presented during testing. Immunostaining quantification of c-Fos, an immediate early gene used as a neuronal activity marker, was performed in eight different brain regions after the NLR or NOR test. Results: The number of c-Fos-positive cells was significantly higher in the dorsal part of the lateral septal nucleus (LSD) in the NLR and dentate gyrus (DG) in the NOR experiment group than in the control group. We further bilaterally lesioned these regions using excitotoxic ibotenic acid and replenished the damaged areas using an antisense oligonucleotide (ASO) strategy. Discussion: These data reinforced the importance of LSD and DG in regulating spatial and object recognition memory, respectively. Thus, the study provides insight into the roles of these brain regions and suggests potential intervention targets for impaired spatial and object recognition memory.

A high-quality model for predicting the prognosis of breast neuroendocrine carcinoma to help clinicians decide on appropriate treatment methods: A population-based analysis.

BACKGROUND: Breast neuroendocrine carcinoma (NEC) is a rare malignancy with unclear treatment options and prognoses. This study aimed to construct a high-quality model to predict overall survival (OS) and breast cancer-specific survival (BCSS) and help clinicians choose appropriate breast NEC treatments. PATIENTS AND METHODS: A total of 378 patients with breast NEC and 349,736 patients with breast invasive ductal carcinoma (IDC) were enrolled in the Surveillance, Epidemiology, and End Results (SEER) database between 2010 and 2018. Propensity score matching (PSM) was performed to balance the clinical baseline. Prognostic factors determined by multivariate Cox analysis were included in the nomogram. C-index and calibration curves were used to verify the performance of the nomogram. RESULTS: Nomograms were constructed for the breast NEC and breast IDC groups after PSM. The C-index of the nomograms ranged from 0.834 to 0.880 in the internal validation and 0.818-0.876 in the external validation, indicating that the nomogram had good discrimination. The risk stratification system showed that patients with breast NEC had worse prognoses than those with breast IDC in the low-risk and intermediate-risk groups but had a similar prognosis that those in the high-risk group. Moreover, patients with breast NEC may have a better prognosis when undergoing surgery plus chemotherapy than when undergoing surgery alone or chemotherapy alone. CONCLUSIONS: We established nomograms with a risk stratification system to predict OS and BCSS in patients with breast NEC. This model could help clinicians evaluate prognosis and provide individualized treatment recommendations for patients with breast NEC.

Targeting PERK mediated endoplasmic reticulum stress attenuates neuroinflammation and alleviates lipopolysaccharide-induced depressive-like behavior in male mice.

Neuroinflammation plays a key role in the development of depression-like behaviors.Endoplasmic reticulum (ER) stress,defined as accumulation of unfolded proteins in the ER,is suggested tocollaboratewithinflammation process to drive sustained neuroinflammation. Protein kinase R-like endoplasmic reticulum kinase (PERK) is ofparticularly attractive target because it plays key rolein the regulation of ER stress-induced neuroinflammation, however, little isknown whether PERKmediatedER stress is implicated in LPS-induced depression-like behaviors.Thus, we aimed to evaluate the induction of PERK pathwayin mice with depression-like behaviors induced by LPS, as well as the alterations in depression-like behaviorsfollowing the blocking of PERK pathway.We found that LPS challenges resulted in enhanced PERK in the hippocampus, with no alteration in the prefrontal cortex. Importantly, we found that PERKinhibitorISRIB reducedthe proinflammatory responsesof microglia in the context of acute LPS-induced brain inflammation, and subsequent the preserved hippocampal neurogenesis, and improvement in depression-like behavioroutcomes following LPS challenges.It was also worth mentioning thatISRIB treatmentreduced the peripheral pro-inflammatory cytokines includingIL-1ß, IL-6 and IL-18. Thus, targetingPERK mediated Endoplasmic reticulum stress may be a promising antidepressant and anti-inflammatory candidate drug for the alleviation of neuroinflammationmediated depression, and PERKinhibitorISRIBmay havebenefits for combating major depressive disorder.

Aspirin Ameliorates Pancreatic Inflammation and Fibrosis by Inhibiting COX-2 Expression in Experimental Chronic Pancreatitis.

Aim: Chronic pancreatitis (CP) is a complex and intractable disease mainly manifested as chronic inflammation and fibrosis. Aspirin(acetylsalicylic acid, ASA) has been reported to be used in the treatment of acute pancreatitis (AP), but its effectiveness on CP is unclear. This study aimed to investigate the therapeutic effects of ASA in CP mice. Methods: A murine model of CP was induced by intraperitoneal injection with 20% L-arginine. After one week of L-arginine administration, mice in the ASA treatment group were administered aspirin (100mg/kg/d) by intragastric gavage. At two, four, and six weeks after the first injection of L-arginine, mice were euthanized and the pancreas was collected for histological and molecular analysis. A second model of CP (caeruelin-induced) was used as a validation experiment to test the effect of ASA. Results: L-arginine-induced CP resulted in over-expression of the inflammatory enzyme cyclooxygenase (COX)-2. COX-2 expression decreased after ASA treatment. Pancreatic-injury inflammatory response (measured by changes in amylase, CK-19, F4/80, CD3, MCP-1, IL-6) and fibrosis degree (measured by expression of COL1A1, MMP-1 and TIMP-1) was reduce in ASA -treated mice model. The therapeutic effect of ASA was also observed in caeruelin-induced CP. Conclusion: ASA has an ameliorating effect in murine models of CP through inhibition of pancreatic inflammation and fibrosis, which may be a promising option for clinical treatment.

Predicting the survival benefit of local surgery in patients aged 70 years or older with stage IV breast cancer: A population-based analysis.

PURPOSE: The aim of this study was to establish individualized nomograms to predict survival outcomes in older female patients with stage IV breast cancer who did or did not undergo local surgery, and to determine which patients could benefit from surgery. METHODS: A total of 3,129 female patients with stage IV breast cancer aged ≥70 years between 2010 and 2015 were included in the Surveillance, Epidemiology, and End Results program. Multivariate Cox regression analysis was used to identify risk factors for overall survival (OS) and breast cancer-specific survival (BCSS). Survival analysis was performed using the Kaplan-Meier plot and log-rank test. Nomograms and risk stratification models were constructed. RESULTS: Patients who underwent surgery had better OS (HR = 0.751, 95% CI [0.668-0.843], P < 0.001) and BCSS (HR = 0.713, 95% CI [0.627-0.810], P < 0.001) than patients who did not undergo surgery. Patients with human epidermal growth factor receptor 2-positive, lung or liver metastases may not benefit from surgery. In the stratification model, low-risk patients benefited from surgery (OS, HR = 0.688, 95% CI [0.568-0.833], P < 0.001; BCSS, HR = 0.632, 95% CI [0.509-0.784], P < 0.001), while patients in the high-risk group had similar outcomes (OS, HR = 0.920, 95% CI [0.709-1.193], P = 0.509; BCSS, HR = 0.953, 95% CI [0.713-1.275], P = 0.737). CONCLUSION: Older female patients with stage IV breast cancer who underwent surgery had better OS and BCSS than those who did not in each specific subgroup. Patients in low- or intermediate-risk group benefit from surgery while those in the high-risk group do not.

[Effect of liquid resuscitation on homeostasis of patients with severe acute pancreatitis].

OBJECTIVE: To evaluate the effect of liquid resuscitation on acid-base balance and electrolytes of patients with severe acute pancreatitis (SAP). METHODS: According to the target of liquid resuscitation, 22 patients with SAP involved in this self-controlled prospective study received sufficient liquid resuscitation in acute stage of acute pancreatitis. The results of blood gas analysis, acid-base balance and electrolytes were compared before and after liquid resuscitation. The correlation between the volume of liquid used in resuscitation and the level of blood chlorine was analyzed. RESULTS: The mean resuscitation duration was (15.0±2.4) hours, and the volume of liquid resuscitation was 3 4594 203 ml, with mean volume (3 910± 102) ml in 22 patients; blood sodium (mmol/L) and chlorine (mmol/L) levels were both significantly higher after resuscitation compared with those before resuscitation (Na(+): 145.83±1.85 vs. 139.67±2.25, Cl(-): 117.33±1.64 vs. 101.83±1.77, both P<0.05). Blood pH value, hematocrit (Hct), anion gap (AG, mmol/L), blood lactic acid (mmol/L) were slightly lowered after resuscitation (pH value: 7.39±0.02 vs. 7.42±0.02, Hct: 35.63±1.58 vs. 46.85±2.38, AG: 8.02±1.21 vs. 14.47±0.89, blood lactic acid: 1.10±0.18 vs. 1.97±0.15, P<0.05 or P <0.01). In addition, the level of blood chlorine was significantly correlated with the volume of liquid used in resuscitation (r=0.720 8,P<0.01). CONCLUSION: The target of liquid resuscitation in patients with SAP should be cautiously determined, including control of the volume of liquid for resuscitation, in order to avoid acid-base imbalance or hyperchloraemia. At the same time, the change in internal environment should be monitored.

[The clinical effectiveness of percutaneous drainage and laparotomy for patients with infective pancreatic necrosis].

OBJECTIVE: To compare the clinical effectiveness of percutaneous US- or CT-guided drainage and laparotomy for patients with infective pancreatic necrosis. METHODS: Data of 90 infective pancreatic necrosis patients admitted from January 2008 to December 2009 were included. They were divided into two groups by the different treatment choices. Twenty-seven patients in the percutaneous group received percutaneous US- or CT-guided drainage as first choice. After that a sump suction apparatus was applied for controlled drainage. If no improvement was achieved after 3 days, they would received operation soon. While patients in the laparotomy group received surgical drainage at the time when the diagnosis of infected pancreatic necrosis was confirmed. Continuous drainage was also applied for these ones. RESULTS: The percutaneous group had a significant low rate of reoperation (7.1% vs. 14.3%, P < 0.05) and postoperative residual abscesses (7.1% vs. 28.6%, P < 0.05). Furthermore, 48.1% of patients in percutaneous group successfully avoid laparotomy. In the regard of complications, the percutaneous group presented lower incidence of both single organ dysfunction (7.4% vs. 28.6%, P < 0.05), intestinal fistula (7.4% vs. 27.0%, P < 0.05) and long-term complications (3.7% vs. 22.2%, P < 0.05). In addition, the percutaneous group costed less medical resources as evidenced by shorter ICU duration (21.2 ± 9.7 vs. 28.7 ± 12.1, P < 0.01), shorter hospital duration (48.2 ± 12.5 vs. 59.6 ± 17.5, P < 0.05) and less expenditure (191 762 ± 5892 vs. 341 689 ± 10 854, P < 0.05). CONCLUSIONS: Percutaneous drainage can effectively lower the surgical rates and the rates of complications and reoperations in patients with infective pancreatic necrosis. Besides that, it could also reduce the cost of medical resources.

The application of carbon nanoparticles in the lymph node biopsy of cN0 papillary thyroid carcinoma: A randomized controlled clinical trial.

OBJECTIVE: We applied carbon nanoparticle suspensions to the papillary thyroid carcinoma cases with no clinical regional lymph node metastasis (cN0) to show the lymph flow from primary tumors, and evaluated its value in the lymph node biopsy of cN0 papillary thyroid carcinoma and protection of parathyroid. PATIENTS AND METHODS: One hundred and fourteen patients with cN0 papillary thyroid carcinoma were randomly assigned to experimental and control groups. The experimental group received carbon nanoparticles injection around the primary tumor, while the control group received no injection. Both groups subsequently received standard lateral thyroid gland resection, isthmus resection, subtotal thyroidectomy, or clearance of lymph nodes (LNs) of the central compartment. RESULTS: A total of 342 LNs of the central compartment were dissected in the experimental group (6.00 ± 0.98 per patient) with 81 LNs confirmed to be positive (0.95 ± 0.77 per patient), whereas 261 LNs of the same area were dissected in the control group (4.58 ± 0.60 per patient) with 27 confirmed to be positive (0.47 ± 0.50 per patient). There is a significant difference between experimental and control groups in the average number of LNs dissected per patient (6.00 ± 0.98 vs. 4.58 ± 0.60, p < 0.001) but not the positive LNs per patient (0.95 ± 0.77 vs. 0.47± 0.50, p = 0.11). Parathyroid was found in two patients from the experimental group and in seven patients in the control group (p = 0.29). Three patients in the experimental group and seven patients in the control group had hypocalcemia (p = 0.21), and four patients in each group had hoarseness (p = 0.58). CONCLUSIONS: Carbon nanoparticle suspensions can be used to stain central lymph nodes of cN0 papillary thyroid carcinoma without staining of parathyroid and leakage, and improve the resection of LNs.

[Therapeutic effects of Chai Qin Cheng Qi decoction on severe acute pancreatitis complicated liver damage in rats and its mechanisms].

OBJECTIVE: To study the effects of Chai Qin Cheng Qi Decoction(CQCQD)(Traditional Chinese Medicine)on severe acute pancreatitis (SAP)complicated liver damage in rats. METHODS: Seventy-two SD rats were randomly divided into three groups(n=24):Sham group, SAP group and CQCQD treatment group. SAP model was induced by retrograde injection with sodium taurocholate. The rats in CQCQD group received treatment with CQCQD. After modeling 1 h, 5 h, 10 h, pancreas and liver histopathological changes were observed. The serum levels of interleukin-6(IL-6), amylase(AMS), alanine aminotransferase(ALT) and aspartate transaminase(AST) were detected. IL-6 and monocyte chemotactic protein 1(MCP-1)mRNA in pancreas and liver were assayed. RESULTS: Compared with sham group, the activities of AMS,ALT and AST and the serum level of IL-6 in SAP group were increased significantly. The levels of MCP-1 and IL-6 mRNA in pancreas and liver tissue were increased (P<0.05). Compared with SAP group, the activities of AMS,ALT and AST and the level of IL-6 in CQCQD group were reduced significantly (P<0.05). The pancreas and liver tissue pathological damage alleviated. The levels of IL-6 and MCP-1mRNA in pancreas and liver were decreased significantly(P<0.05). CONCLUSIONS: MCP-1 takes part in the progression of SAP complicated liver damage; CQCQD can significantly inhibit the expression of pancreas and liver MCP-1, alleviate pathological damage of pancreas and liver in SAP and play a therapeutic role in SAP complicated liver damage.