[Efficacy analysis of laparoscopic sleeve gastrectomy in morbidly obese patients aged 10-21 years].

Objective: To investigate the efficacy of laparoscopic sleeve gastrectomy (LSG) in morbidly obese patients aged 10 to 21 years. Methods: We conducted a retrospective analysis of clinical data from 89 out of 200 patients who underwent LSG at the Gastrointestinal Surgery/Weight Loss Center of the First Affiliated Hospital of Jinan University between January 2015 and December 2020. The primary outcome measures were the completion rate of LSG, the incidence of perioperative complications, and weight-related indicators 3, 6, 12, and ≥24 months postoperatively. Additionally, we compared glucose metabolism, lipid metabolism, vitamin levels, liver function, and other relevant biochemical variables before and after surgery. Normally distributed continuous data are presented as x±s. Because the numbers of patients at each follow-up time point were not identical with the number of patients in the study cohort preoperatively, independent sample t-tests were used for intergroup comparisons. Non-normally distributed continuous data are presented as M(Q1, Q3), and Mann-Whitney U tests were used for intergroup comparisons. Results: Among the 89 patients, 35 were male (39.3%), the mean age was (18±2) years, and mean body mass index (BMI) 38.5±4.8 kg/m²; 37 of the patients having a BMI greater than 40 kg/m². Additionally, 63 patients (70.8%) had fatty livers, 34 (38.2%) hyperuricemia, 31(34.8%) sleep apnea syndrome, 20 (22.4%) gastroesophageal reflux, eight (8.9%) type 2 diabetes, and two (2.2%) hypertension. All 89 patients underwent LSG surgery successfully, with no conversions to open surgery. During the perioperative period, there were no cases of major bleeding, gastric leakage, or infections. Notable postoperative symptoms included nausea, vomiting, and pain, most of which improved by the second postoperative day. BMI values 3, 6, and 12 months postoperatively had decreased to 31.5±5.8 kg/m², 28.6±4.3 kg/m², and 26.3±4.4 kg/m², respectively. All of these BMI values differed significantly from preoperative values (all P<0.05). At 12 and ≥24 months postoperatively, the percentages of total weight loss were (31.3±9.3)% and (33.1±10.5)%, respectively, both differing significantly from 3 months postoperatively (20.5±5.1)% (all P<0.05). The percentages of excess weight loss at 12 and ≥24 months postoperatively were 91% (70%, 113%) and 95% (74%, 118%) , respectively, both differing significantly from the percentage of total weight loss 3 months postoperatively (56% [45%, 72%]) (both P<0.05). Alanine transaminase and aspartate transaminase serum concentrations decreased from preoperative values of 44.4 (25.5, 100.5) U/L and 29.0 (9.5, 48.0) U/L to 14.0 (10.8, 18.3) U/L and 13.0 (10.5, 17.3) U/L, respectively, ≥24 months postoperatively. Hemoglobin A1c decreased from 5.6 (5.3, 5.8)% preoperatively to ≥24 months postoperatively 5.3 (5.0, 5.4)%. High-density lipoprotein increased from 1.0 (0.9, 1.2) mmol/L preoperatively to 1.4 (1.1, 1.6) mmol/L ≥24 months postoperatively. Vitamin B12 decreased from 350.0 (256.8, 441.3) µg/L preoperative to 230.3(195.4, 263.9) µg/L ≥24 months postoperatively. All differed significantly from preoperative values (all P<0.05). Conclusion: LSG has favorable efficacy in morbidly obese patients aged 10 to 21 years. However, further confirmation is required through long-term, multicenter, randomized, controlled trials.

[Advances in endoscopic sleeve gastroplasty for the treatment of obesity and metabolic disease].

Obesity poses a serious threat to human health, and although bariatric surgery has been proven effective treatment for morbidly obese patients, its surgical risks and high medical costs limit its clinical application and popularity. Endoscopic sleeve gastroplasty (ESG), as a relatively new endoscopic surgery technique for weight loss, has satisfactory weight loss effects compared to laparoscopic sleeve gastrectomy and lifestyle interventions, while preserving the normal structure of the stomach. Its weight loss effects and safety have been validated in multicenter studies abroad. Although, ESG has not yet been widely performed in China, with the gradual maturity of this technique, its prospects are worth attention in the field of weight loss. In the future, large-scale, long-term, multi-center studies are urgently needed in China to clarify the long-term effects, remission of comorbidities, and occurrence of complications of ESG surgery in obese and metabolic disease patients.

[Effects of over-expressing heat shock protein 60 on marrow mesenchymal stem cells in the treatment of phosgene-induced acute lung injury].

Objective: To investigate the effect of heat shock protein 60 (HSP60) overexpression on the ability of bone marrow mesenchymal stem cells (MSCs) and its therapeutic effect on rats with phosgene induced acute lung injury. Methods: HSP60 was transfected into MSCs by adenovirus. Western blot was used to measure the expressions of HSP60 before and after transfection. CCK-8 assay was used to detect the activity of MSCs, flow cytometry was used to detect the apoptotic ability of MSCs, and Transwell assay was used to observe the migration ability of MSCs. Sixty SPF grade male SD rats were randomly divided into control group, phosgene exposure group (inhalation of phosgene for 5 min) , MSCs group (phosgene exposure, MSCs treatment group) and transfected MSCs group (phosgene exposure, overexpression of HSP60 MSCs treatment group) . The pathological changes of lung were observed by lung pathological section, lung wet dry ratio, the degree of pulmonary edema, the total cell count and total protein content of alveolar lavage fluid, the inflammatory changes of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in BALF and serum were observed. The data were analyzed by Graphpad Prism 8.0 software. Paired comparisons were performed by non paired t-test. One way ANOVA was used for comparison between groups. Results: The proliferation ability of MSCs transfected with HSP60[A= (0.69±0.05) ] was significantly higher than that of MSCs not transfected with HSP60[A= (0.27±0.02) ] (P<0.05) . Compared with the phosgene exposure group, the pulmonary edema and inflammatory factor infiltration of MSCs group and MSCs transfected group were reduced. However, compared with MSCs group, the degree of pulmonary edema in MSCs transfected group was significantly improved, the levels of inflammatory factors IL-6 and TNF-α were significantly decreased, and the total protein content and total cell count in bronchoalveolar lavage fluid were less (P<0.05) . Conclusion: MSCs transfected with HSP60 can enhance the ability of proliferation, anti apoptosis, migration and the curative effect in rats with phosgene induced acute lung injury.

MiR-101a attenuates myocardial cell apoptosis in rats with acute myocardial infarction via targeting TGF-ß/JNK signaling pathway.

The article "MiR-101a attenuates myocardial cell apoptosis in rats with acute myocardial infarction via targeting TGF-ß/JNK signaling pathway, by F.-Q. Zhou, X.-F. Zhao, F.-Y. Liu, S.-S. Wang, H.-L. Hu, Y. Fang, published in Eur Rev Med Pharmacol Sci 2019; 23 (10): 4432-4438-DOI: 10.26355/eurrev_201905_17952-PMID: 31173319" has been withdrawn from the authors. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/17952.

MiR-101a attenuates myocardial cell apoptosis in rats with acute myocardial infarction via targeting TGF-ß/JNK signaling pathway.

OBJECTIVE: To investigate the effect of micro ribonucleic acid (miR)-101a on myocardial cell apoptosis in the rat model of acute myocardial infarction (AMI) and its regulatory mechanism. MATERIALS AND METHODS: A total of 30 Sprague-Dawley (SD) rats were randomly divided into the Sham group, Model group, and miR-101a mimic group, with 10 rats in each group. The rat model of AMI was established by the ligation of the anterior descending coronary artery. The rat left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) were detected using a color Doppler ultrasonic apparatus. Subsequently, the miRNA online database (TargetScan) was adopted to predict miRNAs that could be able to regulate TGF-ß1. Hematoxylin and eosin (H&E) staining was conducted to reveal the histopathological morphology changes in the rat heart. The serum levels of cysteinyl aspartate specific proteinase-3 (Caspase-3) and Bcl-2-associated X protein (Bax) in rats were detected via enzyme-linked immunosorbent assay (ELISA). Moreover, the expression levels of the transforming growth factor-beta l (TGF-ß1) and c-Jun N-terminal kinase (JNK) in rat heart were measured via Western blotting. RESULTS: Through searching miRNA database, miR-101a and TGF-ß1 messenger RNAs (mRNAs) had binding sites in the 3' untranslated region (3'UTR). Compared with those in Sham group, the rat LVEDV and LVESV were notably elevated, the histopathological morphology of the heart was seriously damaged, the apoptotic rate of myocardial cells and the levels of TGF-ß1 and JNK proteins significantly increased in the Model group. Additionally, compared with those in the Model group, the LVEDV and LVESV of rats in miR-101a mimic group were significantly reduced, the histopathological morphology of the heart was markedly improved, and the apoptotic rate and the levels of TGF-ß1 and JNK in rat heart were remarkably decreased. CONCLUSIONS: The myocardial cell apoptosis in AMI rats can be suppressed by overexpression of miR-101a by inhibiting the TGF-ß1/JNK signaling pathway.

[The effects of methylprednisolone on NLRP3 inflammasome in rats with acute lung injury Induced by Phosgene].

Objective: To investigate the effects of methylprednisolone on NOD-like receptor hot protein domain-associated protein 3 (NLRP3) inflammasome in phosgene-induced acute lung injury. Methods: Rats were randomly divided into four groups, 10 rats in Air group (inhalation of air of the same volume as the phosgene group) , 10 rats in Phosgene group (inhalation of 8.33 mg/L with 100% purity phosgene for 5 min) , 10 rats in Saline control group (inhalation of the same dose of phosgene and 2 mg/kg saline via tail vein injection one hour later) , 10 rats in MP group (inhalation of the same dose of phosgene and 2 mg/kg MP via tail vein injection one hour later) . The specimens of serum, bronchoalveolar lavage fluid (BALF) and lung tissue were collected after 6h. Morphological changes were observed by HE staining. The expression of NLRP3 in the lung of four groups was detected by immunohistochemistry. NLRP3、ASC and caspase-1 expression in the lung tissue was quantified by Western blot. Reverse transcription-polymerase chain reaction (RT-PCR) were used to detect the expression of NLRP3、ASC and caspase-1 mRNA in the lung tissue. The concentrations of IL-1ß、IL-18 and IL-33 in the serum and BALF were measured by enzyme-linked immunosorbent assay. Results: We successfully replicated the model of phosgene-induced ALI in rats. Morphological of HE staining after phosgene exposure to 6 h observed inflammatory cell infiltration in lung tissue in Phosgene group. Immunohistochemical staining results showed that there were many NLRP3 positive cells in lung tissue in Phosgene group. The levels of NLRP3, caspase-1 mRNA and protein expression in lung were significantly increased (P<0.05) in Phosgene group compared with Air group; compared with Phosgene group, The levels of NLRP3 and caspase-1 mRNA and protein expression in MP group were significantly decreased (P<0.05) . Compared with Air group, The levels IL-1ß、IL-18 and IL-33 mRNA protein expression in the serum and BALF were significantly increased (P<0.05) in Phosgene group. Compared with Phosgene group, The levels IL-1ß、IL-18 and IL-33 mRNA protein expression in the serum and BALF were significantly decreased (P<0.05) in MP group. Conclusion: Methylprednisolone can effectively protect the rats from phosgene-induced acute lung injury by inhibiting the expression of the NLRP3 inflammasome and reducing the release of inflammatory factors such as interleukin-1ß (IL-1ß) mediated by it.

MicroRNA-26a supports mammalian axon regeneration in vivo by suppressing GSK3ß expression.

MicroRNAs are emerging to be important epigenetic factors that control axon regeneration. Here, we report that microRNA-26a (miR-26a) is a physiological regulator of mammalian axon regeneration in vivo. We demonstrated that endogenous miR-26a acted to target specifically glycogen synthase kinase 3ß (GSK3ß) in adult mouse sensory neurons in vitro and in vivo. Inhibition of endogenous miR-26a in sensory neurons impaired axon regeneration in vitro and in vivo. Moreover, the regulatory effect of miR-26a was mediated by increased expression of GSK3ß because downregulation or pharmacological inhibition of GSK3ß fully rescued axon regeneration. Our results also suggested that the miR-26a-GSK3ß pathway regulated axon regeneration at the neuronal soma by controlling gene expression. We provided biochemical and functional evidences that the regeneration-associated transcription factor Smad1 acted downstream of miR-26a and GSK3ß to control sensory axon regeneration. Our study reveals a novel miR-26a-GSK3ß-Smad1 signaling pathway in the regulation of mammalian axon regeneration. Moreover, we provide the first evidence that, in addition to inhibition of GSK3ß kinase activity, maintaining a lower protein level of GSK3ß in neurons by the microRNA is necessary for efficient axon regeneration.

Expression of EpCAM and Wnt/ ß-catenin in human colon cancer.

The aims of this study were to explore the correlation between the expression of EpCAM and the Wnt/ß-catenin pathway in human colon cancer and its clinical significance for the evaluation of cancer prognosis. Samples from colon cancer, para-carcinoma, or benign intestinal tissue from individual patients (50) and from normal intestinal mucosal tissues (20) were obtained from the Pathology Department of the Shandong Province Binzhou People's Hospital (Shandong, China). Immunohistochemistry was used to detect the expression levels of EpCAM and ß-catenin proteins in these tissues, and the prognoses of the patients from whom the samples were derived were determined on follow-up examination. The corresponding in vitro mechanistic siRNA experiments were subsequently performed in the human colon cancer cell line HCT116 to observe the regulatory effects of silencing EpCAM expression on the Wnt/ß-catenin pathway. From these analyses, we determined that the expression levels of EpCAM and ß-catenin were higher in cancer tissues compared with other tissues from the same patient, and that the expression of EpCAM and Wnt/ß- catenin in colon cancers were positively correlated. The prognostic analysis showed an inverse correlation between EpCAM and Wnt/ß- catenin expression and patient prognosis. A further examination of cellular mechanisms confirmed that the silencing of EpCAM led to decreased expression of Wnt/ß-catenin, and thus reduced proliferation and increased the apoptosis ratio in the cells. These results suggest that suppression of EpCAM might be a new approach for treating colon cancer.

Intrinsic functional plasticity of the sensory-motor network in patients with cervical spondylotic myelopathy.

Several neuroimaging studies have suggested brain reorganisation in patients with cervical spondylotic myelopathy (CSM); however, the changes in spontaneous neuronal activity that are associated with connectedness remain largely unknown. In this study, functional connectivity strength (FCS), a data-driven degree centrality method based on a theoretical approach, was applied for the first time to investigate changes in the sensory-motor network (SMN) at the voxel level. Comparatively, CSM not only showed significantly decreased FCS in the operculum-integrated regions, which exhibited reduced resting-state functional connectivity (rsFC) around the Rolandic sulcus, but it also showed increased FCS in the premotor, primary somatosensory, and parietal-integrated areas, which primarily showed an enhanced rsFC pattern. Correlation analysis showed that altered FCS (in the left premotor-ventral/precentral-operculum, right operculum-parietale 4, and right S1) was associated with worsening Japanese Orthopaedic Association scores and that the rsFC pattern was influenced by cervical cord micro-structural damage at the C2 level. Together, these findings suggest that during myelopathy, the intrinsic functional plasticity of the SMN responds to the insufficient sensory and motor experience in CSM patients. This knowledge may improve our understanding of the comprehensive functional defects found in CSM patients and may inspire the development of new therapeutic strategies in the future.

Advantages of pyruvate over lactate in peritoneal dialysis solutions.

This review discusses effects of both lactate and pyruvate, and high glucose in peritoneal dialysis solutions (PDS) on leukocytes, mainly on intracellular pH ([pH](i)), glucose metabolic pathways, and apoptosis. Lactate-based PDS (L-PDS) are bioincompatible primarily due to the low pH, high lactate, and glucose excess in both individual and combination. High lactate in an acidi milieu would induce severe intracellular acidosis of leukocytes, and high glucose may disturb glucose metabolic pathways and activate protein kinase C (PKC) and nuclear factor-kappa B (NF-kappaB) of the cells, leading to apoptosis. Pyruvate-based PDS (P-PDS) are novel experimental PDS. Evidence shows that P-PDS are superior in biocompatibility. Pyruvate protection of cells has been confirmed in many fields besides the PDS area. Although the underlying mechanism whereby P-PDS preserve cell function is not fully understood, it may be associated with the maintenance of [pH](i) close to physiological, due to its low buffering capacity, improvement of cellular glucose metabolic pathways and redox state, and sustainment of intracellular calcium ([Ca2+]i) homeostasis in high glucose concentrations. It may also inhibit PKC and NF-kappaB activation in high glucose. In addition, pyruvate is a strong antioxidant, a scavenger of hydrogen peroxide (H2O2). However, exogenous pyruvate in PDS could not be an energy source for cells and also the Crabtree effect might not occur in neutrophils. Pyruvate is a hopeful candidate of buffers in PDS in the near future. Further observation of P-PDS is strongly needed with peritoneal cells to verify the cell protection both in vitro and in vivo before clinic trials.

Novel designs for sampled grating-based multiplexers demultiplexers.

Novel multiplexers-demultiplexers for dense wavelength-division multiplexing systems that use interleaved sampled gratings are presented. It is shown that, with the appropriate design, configurations ranging from hybrid to add-drop as well as all-grating-based multiplexers can easily be realized.

Neutrophilic transient acidification and superoxide production in peritoneal dialysate.

AIM: To elucidate whether an inhibited superoxide production (O2-) of neutrophils induced by commercial lactate-based peritoneal dialysates (PDS) could be corrected after a transient intracellular acidosis. METHODS: The intracellular pH ([pHi]) of human neutrophils incubated in PDS was monitored with a spectrofluorometer with a pH-sensitive dye (BCECF-AM). Neutrophilic O2- stimulated by zymosan was determined in PDS with the superoxide dismutase inhibitable ferricytochrome c reduction, using a spectrophotometer. RESULTS: The severe intracellular acidosis induced within 5 min by PDS at an extracellular pH of 5.2 could be promptly and completely recovered by a neutralization of the pH of media. However, O2- by neutrophils exposed to the PDS for as little as 5 min was drastically and persistently inhibited, even the acidic [pHi] of cells had been fully returned for 1 h. CONCLUSIONS: The intracellular acidification of cells in the initial phase could be transient and reversible, but impaired cell functions, at least in part including O2- generating system, might be consistent and irreversible in the early stage of the cellular acidosis in the peritoneal cavity of CAPD patients. The findings above may be of particular importance in both clinic and cell biology.

Pyruvate-based peritoneal dialysate preserves neutrophilic oxygen consumption.

AIM: To investigate effects of pyruvate- or lactate-based peritoneal dialysis solutions (P-PDS or L-PDS) on neutrophilic oxygen consumption and the role of the extracellular pH (pHe) in cells' oxygen uptake. METHODS: Human neutrophils were incubated in P-PDS or L-PDS containing pyruvate or lactate 35-38 mmol.L-1 at various pHe, respectively. Oxygen consumption rates by opsonized zymosan (OZ)-stimulated cells were measured polarographically, using a Clark-type oxygen electrode. RESULTS: L-PDS at an initial pH 5.2 dramatically inhibited the rate of oxygen consumption (2.2 nmol.min-1/10(6) cells) by neutrophils, while the equally acidic P-PDS markedly improved the rate (6.4 nmol.min-1/10(6) cells) (P < 0.01). However, P-PDS at pHe 5.2 severely impaired the rate by cells, the same as pHe 5.2 L-PDS. CONCLUSION: P-PDS preserved an oxygen consumption rate by OZ-stimulated human neutrophils, but in an acidi milieu it comparably deteriorated the ability of cells to consume oxygen, indicating that the pHe of PDS plays an essential role in cellular oxidative metabolism. The superior biocompatibility of an acidic P-PDS was associated with its lower buffering capacity.

Effects of pyruvate-based or lactate-based peritoneal dialysis solutions on neutrophil intracellular pH.

Acidic (pH 5.2) incubation mixtures containing pyruvate-based or lactate-based peritoneal dialysis solutions (PDSN's) induced comparable degrees of intracellular acidosis in neutrophils. However, addition of an acidic (pH 5.2), pyruvate-based PDSN to a pH-7.4, neutrophil/phosphate-buffered saline mixture brought about higher extracellular and intracellular (neutrophil) pH values when compared to the introduction of an equally acidic, lactate-based PDSN. This poor ability of acidic (pH 5.0-5.5), pyruvate-based PDSN's to resist alkalinizing influences is the cause for the above higher pH values. The higher intracellular pH levels so obtained may be a reason behind why acidic, pyruvate-based PDSN's appear to be more biocompatible than their equally acidic, lactate-based counterparts.

[Glutamate causes release of nitric oxide from chicken spinal cord in vitro].

Nitric oxide (NO) has been identified to have profound effects on many systems, especially the neural tissues. Many studies suggest that NO mediate the neurotoxicity of glutamate (Glu). In order to determine in vitro whether Glu causes release of NO from chicken spinal cord, different concentrations of Glu (0.1, 0.5, 1.0 mmol.L-1) were added to the primary cultured chicken spinal cord cells, and the quantity of NO- (the metabolism product of NO) in medium was detected. The result shows that Glu can enhance obviously the concentration of NO in primary cell cultures (212% compared with the control). If the spinal cord cells were pretreated with NO synthases (NOS) inhibitor--L-NOARG, the [NO-] was decreased compared with those treated with Glu only, and, on the contrary, the viability of cells was increased. All of the results above indicate that NO may play an important role in the neurotoxicity of Glu on nervous cells. It might be that Glu can instigate the activity of NO synthases, then induce a series of changes within cell and finally lead to the toxic effect on cells.

Effects of a pH 7.4, lactate-based and a pH 7.4, bicarbonate-based peritoneal dialysis solutions on neutrophil superoxide generation.

Neutrophil superoxide formation was similar when cells were incubated in self-made, non-autoclaved pH 7.4, lactate-based peritoneal dialysis solutions or in their self-made, non-autoclaved, pH 7.4, bicarbonate-based counterparts. On the other hand, commercially available, autoclaved, pH 7.4, lactate-based peritoneal dialysis solutions resulted in inhibition of superoxide production when compared to their self-made, non-autoclaved, pH 7.4, lactate-based or bicarbonate-based counterparts. The cause for this inhibition of superoxide generation is at present unknown.

Collection of a representative fraction of total spent hemodialysate.

We describe a method of obtaining a small representative fraction of spent dialysate by placing a side tube in the dialysate drainage tube. The side tube, capped with a small-gauge needle, is used to collect the specimen. Fractions obtained in this fashion are found to have a composition similar to that of the remaining spent dialysate.