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Objective: To evaluate the feasibility and safety of temporary ileostomy via median specimen extraction site in the lower abdomen. Methods: Twenty-two patients who underwent laparoscopic radical resection for rectal cancer and needed temporary ileostomy were prospectively enrolled. Temporary ileostomy was placed on the median specimen extraction site of the lower abdomen. Intraoperative and postoperative conditions, stoma-related complications and ileostomy reversal surgery were observed. d. Results: Among the 22 patients, there were 14 female patients and 8 male patients: the average age was 56 ±14 years; the average body mass index was 22.0 ±3.4 kg/m2; the average tumour size was 4.4 ±2.2 cm; the average distance between the tumour and the dentate line was 5.9 ±2.3 cm; the average time of laparoscopic low anterior resection was 221 ±56 minutes; the average blood loss was 168 ±91 ml; and the average postoperative hospital stay was 9.9 ±3.9 days. The average ileostomy reversal surgery time was 72 ±15 minutes, the average blood loss was 50 ±27 ml, and the average postoperative hospital stay was 5.9 ±1.0 days. Stoma-related complications occurred in 5 patients, of which one was treated by emergency surgery. Conclusion: In laparoscopic low anterior resection, patients with temporary ileostomy via the median specimen extraction site did not have serious complications that required surgical intervention during hospitalization, and there was no mortality during the perioperative period. It is safe and feasible to perform temporary ileostomies via the median specimen extraction site in the lower abdomen, but for permanent ileostomies, the median site in the lower abdomen should be carefully selected as the ileostomy site.

BACKGROUND: Previous studies have identified LCP1 as a diagnostic and prognostic marker in several cancers. However, the role of LCP1 in gastric cancer (GC) and its effect on tumor immune infiltration remain unclear. OBJECTIVE: The aim was to explore the role of LCP1 in GC and its effect on tumor immune infiltration. METHODS: We explored the expression of LCP1 relative to clinicopathology in GC patients by bioinformatics analysis and immunohistochemistry. Using cBioportal database, we analyzed the characteristic genetic variations of LCP1 in GC. In addition, we evaluated the correlation between LCP1 expression and tumor-infiltrating lymphocytes (TILs) using R software, TIMER and TISIDB databases. Finally, we analyzed the biological functions in which LCP1 may participate and the signaling pathways it may regulate. RESULTS: Here, we showed that LCP1 expression is significantly correlated with tumor aggressiveness and poor prognosis in GC patients. Additionally, the results indicated that LCP1 was associated with TILs, including both immunosuppressive and immunosupportive cells, and was strongly correlated with various immune marker sets in GC. GSEA analysis demonstrated that LCP1 expression played an important role in lymphocyte formation and immune reaction. CONCLUSIONS: LCP1 may be a potential prognostic biomarker for GC patients and a marker for tumor immunotherapy.

Acne rosacea is a type of chronic dermatosis with the characteristics of erubescence, angiotelectasis and pustule formation. However, current treatment methods are limited due to the side effects. Artesunate demonstrated a promising therapeutic efficacy with a high safety margin. HaCaT cells were treated with antibacterial peptide LL‑37 to simulate rosacea caused by Demodex folliculorum (D. folliculorum) infection. Cell Counting kit 8 and flow cytometry assays were performed to measure cellular proliferation, apoptosis, the stage of the cell cycle and reactive oxygen species generation in order to determine the level of cell damage. Then the damaged cells were treated with different concentrations of artesunate and doxycycline to determine the therapeutic effect of artesunate. Pro‑inflammatory cytokines tumor necrosis factor‑α (TNF‑α), interleukin (IL)‑6, IL‑8 and C‑C motif chemokine 2 (MCP‑1) were measured using an ELISA, while western blotting was used to detect the expression of Janus kinase 2 (JAK2) and signal transducer and transcription activator (STAT3). As a result, LL‑37 treated HaCaT cells decreased in cell viability, had an increased apoptotic rate and cell cycle arrest, indicating that cell damage caused by rosacea was simulated. In addition, upregulated concentrations of the pro‑inflammatory cytokines TNF‑α, IL‑6, IL‑8 and MCP‑1 were attenuated in the artesunate group in a dose‑dependent fashion, indicating the therapeutic effect of artesunate. Furthermore, higher concentrations of artesunate exhibited an improved effect compared with the doxycycline group. In addition, increased expression levels of JAK2 and STAT3 following treatment with LL‑37 suggested that rosacea caused by D. folliculorum infection may lead to inflammation through the JAK/STAT signaling pathway. In conclusion, the potential mechanism by which damage occurs in rosacea was revealed and a promising therapeutic method against rosacea was demonstrated.

The effects of early deprivation (ED, which involves both dam and littermate deprivation) on anxiety and memory are less investigated in comparison with maternal separation (MS), and it is not yet clear how ED affects long-term potentiation (LTP) in the hippocampal Schaffer collateral pathway. By using a series of behavioral tests, enzyme-linked immunosorbent assay and field potential recording, we explored the effect of pre-weaning daily 3-h ED on anxiety, memory and potential mechanisms in adult male rats. Compared with control, ED rats spent longer time in open arms of elevated plus maze and in light compartment of light-dark transition box. Consistently, stress-induced blood plasma corticosterone level was also lower in ED rats. Moreover, ED rats showed better performance in social recognition and Morris water maze test. In accordance with results in memory tests, the threshold of LTP induction in hippocampal CA3-CA1 pathway of ED rats was also reduced. Our results indicate ED reduced anxiety, but enhanced social recognition and spatial reference memory. We suggest the diminished hypothalamic-pituitary-adrenal axis response and facilitated hippocampal LTP may contribute to the anxiety-reducing and memory-enhancing effects of ED, respectively.

Cerebellar dysfunction causes ataxia characterized by loss of balance and coordination. Until now, the molecular and neuronal mechanisms of several types of inherited cerebellar ataxia have not been completely clarified. Here, we report that leucine-rich G protein-coupled receptor 4 (Lgr4/Gpr48) is highly expressed in Purkinje cells (PCs) in the cerebellum. Deficiency of Lgr4 leads to an ataxia-like phenotype in mice. Histologically, no obvious morphological changes were observed in the cerebellum of Lgr4 mutant mice. However, the number of PCs was slightly but significantly reduced in Lgr4(-/-) mice. In addition, in vitro electrophysiological analysis showed an impaired long term depression (LTD) at parallel fiber-PC (PF-PC) synapses in Lgr4(-/-) mice. Consistently, immunostaining experiments showed that the level of phosphorylated cAMP-responsive element-binding protein (Creb) was significantly decreased in Lgr4(-/-) PCs. Furthermore, treatment with forskolin, an adenylyl cyclase agonist, rescued phospho-Creb in PCs and reversed the impairment in PF-PC LTD in Lgr4(-/-) cerebellar slices, indicating that Lgr4 is an upstream regulator of Creb signaling, which is underlying PF-PC LTD. Together, our findings demonstrate for first time an important role for Lgr4 in motor coordination and cerebellar synaptic plasticity and provide a potential therapeutic target for certain types of inherited cerebellar ataxia.

Background Mucopolysaccharidosis IIIB (MPS IIIB) is a genetic disease characterized by mutations in the NAGLU gene, deficiency of α-N-acetylglucosaminidase, multiple congenital malformations and an increased susceptibility to malignancy. Because of the slow progressive nature of this disease and its atypical symptoms, the misdiagnosis of MPS IIIB is not rare in clinical practice. This misdiagnosis could be avoided by using next-generation sequencing (NGS) techniques, which have been shown to have superior performance for detecting mutations underlying rare inherited disorders in previous studies. Case presentation Whole exome sequencing (WES) was conducted and the putative pathogenic variants were validated by Sanger sequencing. The activity of MPS IIIB related enzyme in the patient's blood serum was assayed. A heterozygous, non-synonymous mutation (c.1562C>T, p.P521L) as well as a novel mutation (c.1705C>A, p.Q569K) were found in the NAGLU gene of the patient. The two mutations were validated by Sanger sequencing. Our data showed that this patient's c.1562C>T, p.P521L mutation in the NAGLU gene was inherited from his father and c.1705C>A, p.Q569K was from his mother. The diagnosis was further confirmed by an enzymatic activity assay after patient recall and follow-up. Conclusions Our results describe an atypical form of MPS IIIB and illustrate the diagnostic potential of targeted WES in Mendelian disease with unknown etiology. WES could become a powerful tool for molecular diagnosis of MPS IIIB in clinical setting.

Considerable evidence indicates that the noradrenergic system of the basolateral amygdala (BLA) participates in the consolidation of various types of emotionally arousing memories. We previously reported that administration of an anesthetic-dose of sevoflurane immediately after continuous multiple-trail inhibition avoidance (CMIA) training impaired memory consolidation. This experiment investigated whether posttraining noradrenergic activation of the BLA is sufficient to reverse the memory impairing effect of sevoflurane. Adult male Sprague-Dawley rats received bilateral injections of norepinephrine (NE 0.3, 1.0, or 3.0 μg/0.5 μl) or normal saline (NS 0.5 μl) immediately after training in a CMIA paradigm. Subsequently, the rats were exposed to sevoflurane (2% inspired) or air for 2h. Norepinephrine produced a dose-dependent enhancement of memory consolidation on a 24-h retention test. The highest dose of NE tested (3.0 μg/0.5 μl) blocked sevoflurane-induced impairment of memory consolidation and reversed the inhibitory effect of sevoflurane on activity-regulated cytoskeletal protein (Arc) expression in the hippocampus 2h after training. These findings provide evidence that the mechanism mediating the memory-impairing effect of sevoflurane involves a network interaction between the BLA noradrenergic system and modulation of Arc protein expression in the hippocampus.

A novel stomach-derived peptide, ghrelin, is down-regulated in sepsis and its IV administration decreases proinflammatory cytokines and mitigates organ injury. In this study, we wanted to investigate the effects of ghrelin on proinflammatory responses and cognitive impairment in septic rats.Prospective, randomized, controlled experiment.Animal basic science laboratory.Sprague-Dawley rats, weighing 250-300 g.Sepsis was induced by cecal ligation and puncture. Animals were randomly divided into four groups: sham, sham + ghrelin, cecal ligation and puncture, and cecal ligation and puncture + ghrelin. Saline was given subcutaneously (30 mL/kg) at 4 and 16 hours after surgery for all rats. Septic rats were treated with ceftriaxone (30 mg/kg) and clindamycin (25 mg/kg) subcutaneously at 4 and 16 hours after surgery. Ghrelin (80 μg/kg) was administrated intraperitoneally 4 and 16 hours after surgery in sham + ghrelin group and cecal ligation and puncture + ghrelin group.The levels of proinflammatory cytokines in hippocampus were measured by enzyme-linked immunosorbent assay, and cleaved caspase-3 was detected by Western blot 24 hours after surgery. Neuronal apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nick-end labeling staining 48 hours after surgery. Additional animals were monitored to record survival and body weight changes for 10 days after surgery. Survival animals underwent behavioral tasks 10 days after surgery: open-field, novel object recognition, and continuous multiple-trial step-down inhibitory avoidance task. Ghrelin significantly decreased the levels of proinflammatory cytokines and inhibited the activation of caspase-3 in the hippocampus after cecal ligation and puncture. The density of terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive apoptotic neurons was significantly lowered by ghrelin. In addition, ghrelin improved the survival rates after cecal ligation and puncture. There were no differences in the distance and move time between groups in open-field task. However, the survivors after cecal ligation and puncture were unable to recognize the novel object and required more training trials to reach the acquisition criterion. All these long-term impairments were prevented by ghrelin.Ghrelin inhibited proinflammatory responses, improved the survival rate, and prevented cognitive impairment in septic rats.

BACKGROUND: Curcumin has been demonstrated to have many neuroprotective properties, including improvement of cognition in humans and neurogenesis in animals, yet the mechanism of such effects remains unclear. METHODOLOGY: We assessed behavioural performance and hippocampal cell proliferation in aged rats after 6- and 12-week curcumin-fortified diets. Curcumin enhanced non-spatial and spatial memory, as well as dentate gyrate cell proliferation as compared to control diet rats. We also investigated underlying mechanistic pathways that might link curcumin treatment to increased cognition and neurogenesis via exon array analysis of cortical and hippocampal mRNA transcription. The results revealed a transcriptional network interaction of genes involved in neurotransmission, neuronal development, signal transduction, and metabolism in response to the curcumin treatment. CONCLUSIONS: The results suggest a neurogenesis- and cognition-enhancing potential of prolonged curcumin treatment in aged rats, which may be due to its diverse effects on genes related to growth and plasticity.