Treatment of posterior interosseous nerve entrapment syndrome with ultrasound-guided hydrodissection: A case report.

BACKGROUND: Posterior interosseous nerve (PIN) entrapment syndrome is one of the causes of weakness and pain of the arm muscles, which is prone to missed diagnosis and misdiagnosis in clinic practice. This paper reports a case of PIN entrapment syndrome, with PIN injury indicated by electrophysiology. Musculoskeletal ultrasound was applied to identify that the entrapment point was located at the inlet of the Frohse arch and the outlet of the supinator muscle. Treatment with ultrasound-guided nerve hydrodissection was performed on the entrapment point, which significantly improved the symptoms. Ultrasound-guided nerve hydrodissection is an effective therapeutic method for PIN entrapment syndrome. CASE SUMMARY: A male patient, 35 years old, worked as an automobile mechanic. He felt slightly weak extension activity of his right fingers 2 years ago but sought no treatment. Later, the symptoms gradually became aggravated and led to finger drop, particularly severe in the right middle finger, accompanied by supination weakness of the right forearm. Neural electrophysiological examination showed that the patient had partial PIN injury of the right radius. Musculoskeletal ultrasound examination indicated PIN entrapment at the inlet of the Frohse arch and the outlet of the supinator muscle. Therefore, PIN entrapment syndrome was diagnosed. After treatment with ultrasound-guided nerve hydrodissection around the entrapment point, the dorsiflexion weakness of the right hand was significantly improved compared with before treatment. CONCLUSION: Ultrasound-guided hydrodissection is efficacious for PIN entrapment syndrome, with high clinical value and great application prospects.

Human Encephalitis Complicated With Ocular Symptoms Associated With Pseudorabies Virus Infection: A Case Report.

Pseudorabies virus (PRV) is an alpha herpesvirus found in many wild and domestic animals, and causes neurological diseases in humans. Several cases of PRV-induced human encephalitis accompanied with severe visual impairment have been reported. There is currently no effective treatment for severe visual impairment caused by PRV. We report a case of PRV encephalitis with severe visual impairment. The diagnosis and treatment experience of this patient is summarized to improve the awareness of clinicians. We present a 42-year-old man with PRV infection who was admitted due to intermittent fever for 5 days and unconsciousness for 1 day. He subsequently developed severe visual impairment during hospital stay. Empirical antiviral treatment with ganciclovir and sodium foscarnet was started on the day of admission and continued for > 50 days, which had significant treatment effect. Eye complications caused by PRV infection have been frequently reported in patients with PRV encephalitis. In this patient, based on the patient's condition, antiviral therapy was initiated on admission day, and according to the results of the next-generation sequencing of the cerebrospinal fluid, the duration of antiviral therapy was prolonged, which improved treatment efficacy and alleviated neurological symptoms and eye vision damage. To the best of our knowledge, this is the first report that describes partial restoration of acute vision loss associated with PRV infection after aggressive treatment. Our experience suggests that although prompt treatment cannot prevent the acute vision loss associated with PRV infection, timely anti-viral and anti-inflammatory treatment can alleviate ocular complications.

Identification of the Diagnostic Biomarker VIPR1 in Hepatocellular Carcinoma Based on Machine Learning Algorithm.

The purpose of this study was to identify the potential diagnostic biomarkers in hepatocellular carcinoma (HCC) by machine learning (ML) and to explore the significance of immune cell infiltration in HCC. From GEO datasets, the microarray datasets of HCC patients were obtained and downloaded. Differentially expressed genes (DEGs) were screened from five datasets of GSE57957, GSE84402, GSE112790, GSE113996, and GSE121248, totalling 125 normal liver tissues and 326 HCC tissues. In order to find the diagnostic indicators of HCC, the LASSO regression and the SVM-RFE algorithms were utilized. The prognostic value of VIPR1 was analyzed. Finally, the difference of immune cell infiltration between HCC tissues and normal liver tissues was evaluated by CIBERSORT algorithm. In this study, a total of 232 DEGs were identified in 125 normal liver tissues and 326 HCC tissues. 11 diagnostic markers were identified by LASSO regression and SVM-RFE algorithms. FCN2, ECM1, VIRP1, IGFALS, and ASPG genes with AUC>0.85 were regarded as candidate biomarkers with high diagnostic value, and the above results were verified in GSE36376. Survival analyses showed that VIPR1 and IGFALS were significantly correlated with the OS, while ASPG, ECM1, and FCN2 had no statistical significance with the OS. Multivariate assays indicated that VIPR1 gene could be used as an independent prognostic factor for HCC, while FCN2, ECM1, IGFALS, and ASPG could not be used as independent prognostic factors for HCC. Immune cell infiltration analyses showed that the expression of VIPR1 in HCC was positively correlated with the levels of several immune cells. Overall, VIPR1 gene can be used as a diagnostic feature marker of HCC and may be a potential target for the diagnosis and treatment of liver cancer in the future.

Inhibition of the CEBPß-NFκB interaction by nanocarrier-packaged Carnosic acid ameliorates glia-mediated neuroinflammation and improves cognitive function in an Alzheimer's disease model.

Neuroinflammation occurs early in Alzheimer's disease (AD). The initial stage of AD is related to glial dysfunction, which contributes to impairment of Aß clearance and disruption of synaptic connection. CEBPß, a member of the CCAAT-enhancer-binding protein (CEBP) family, modulates the expression of inflammation-associated genes, and its expression is elevated in brains undergoing degeneration and injured brains. However, the mechanism underlying CEBPß-mediated chronic inflammation in AD is unclear. In this study, we observed that increases in the levels of nuclear CEBPß facilitated the interaction of CEBPß with the NFκB p65 subunit, increasing the transcription of proinflammatory cytokines in the APP/PS1 mouse brain. Oral administration of nanocarrier-packaged carnosic acid (CA) reduced the aberrant activation of microglia and astrocytes and diminished mature IL-1ß, TNFα and IL-6 production in the APP/PS1 mouse brain. CA administration reduced ß-amyloid (Aß) deposition and ameliorated cognitive impairment in APP/PS1 mice. We observed that CA blocked the interaction of CEBPß with NFκB p65, and chromatin immunoprecipitation revealed that CA reduced the transcription of the NFκB target genes TNFα and IL-6. We confirmed that CA alleviated inflammatory mediator-induced neuronal degeneration and reduced Aß secretion by inhibiting the CEBPß-NFκB signalling pathway in vitro. Sulfobutyl ether-beta-cyclodextrin (SBEßCD) was used as the encapsulation agent for the CA-loaded nanocarrier to overcome the poor water solubility and enhance the brain bioavailability of CA. The CA nanoparticles (NPs) had no obvious toxicity. We demonstrated a feasible SBEßCD-based nanodelivery system targeting the brain. Our data provide experimental evidence that CA-loaded NPs are potential therapeutic agents for AD treatment.

Zinc oxide nanoparticles reduce the chemoresistance of gastric cancer by inhibiting autophagy.

BACKGROUND: Gastric cancer (GC) is a common malignancy that results in a high rate of cancer-related mortality. Cisplatin (DDP)-based chemotherapy is the first-line clinical treatment for GC therapy, but chemotherapy resistance remains a severe clinical challenge. Zinc oxide nanoparticle (ZnO-NP) has been identified as a promising anti-cancer agent, but the function of ZnO-NP in GC development is still unclear. AIM: To explore the effect of ZnO-NP on chemotherapy resistance during GC progression. METHODS: ZnO-NP was synthesized, and the effect and underlying mechanisms of ZnO-NP on the malignant progression and chemotherapy resistance of GC cells were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays, colony formation assays, transwell assays, wound healing assays, flow cytometry, and Western blot analysis in GC cells and DDP-resistant GC cells, and by tumorigenicity analyses in nude mice. RESULTS: Our data revealed that ZnO-NP was able to inhibit proliferation, migration, and invasion and induce apoptosis of GC cells. Meanwhile, ZnO-NP significantly reduced the half maximal inhibitory concentration (IC50) of DDP for the inhibition of cell proliferation of DDP-resistant SGC7901/DDP cell lines. Autophagy was increased in DDP-resistant GC cells, as demonstrated by elevated light chain 3-like protein 2 (LC3II)/LC3I and Beclin-1 expression and repressed p62 expression in SGC7901/DDP cells compared to SGC7901 cells. Mechanically, ZnO-NP inhibited autophagy in GC cells and treatment with DDP induced autophagy, which was reversed by ZnO-NP. Functionally, ZnO-NP attenuated the tumor growth of DDP-resistant GC cells in vivo. CONCLUSION: We conclude that ZnO-NP alleviates the chemoresistance of GC cells by inhibiting autophagy. Our findings present novel insights into the mechanism by which ZnO-NP regulates the chemotherapy resistance of GC. ZnO-NP may serve as a potential therapeutic candidate for GC treatment. The potential role of ZnO-NP in the clinical treatment of GC needs clarification in future investigations.

[A machine learning model based on initial gut microbiome data for predicting changes of Bifidobacterium after prebiotics consumption].

OBJECTIVE: To investigate the effects of prebiotics supplementation for 9 days on gut microbiota structure and function and establish a machine learning model based on the initial gut microbiota data for predicting the variation of Bifidobacterium after prebiotic intake. METHODS: With a randomized double-blind self-controlled design, 35 healthy volunteers were asked to consume fructo-oligosaccharides (FOS) or galacto-oligosaccharides (GOS) for 9 days (16 g per day). 16S rRNA gene high-throughput sequencing was performed to investigate the changes of gut microbiota after prebiotics intake. PICRUSt was used to infer the differences between the functional modules of the bacterial communities. Random forest model based on the initial gut microbiota data was used to identify the changes in Bifidobacterium after 5 days of prebiotic intake and then to build a continuous index to predict the changes of Bifidobacterium. The data of fecal samples collected after 9 days of GOS intervention were used to validate the model. RESULTS: Fecal samples analysis with QIIME revealed that FOS intervention for 5 days reduced the intestinal flora alpha diversity, which rebounded on day 9; in GOS group, gut microbiota alpha diversity decreased progressively during the intervention. Neither FOS nor GOS supplement caused significant changes in ß diversity of gut microbiota. The area under the curve (AUC) of the prediction model was 89.6%. The continuous index could successfully predict the changes in Bifidobacterium (R=0.45, P=0.01), and the prediction accuracy was verified by the validation model (R=0.62, P=0.01). CONCLUSION: Short-term prebiotics intervention can significantly decrease α-diversity of the intestinal flora. The machine learning model based on initial gut microbiota data can accurately predict the changes in Bifidobacterium, which sheds light on personalized nutrition intervention and precise modulation of the intestinal flora.

[Establishment of a neonatal piglet model of multiple organ dysfunction syndrome].

OBJECTIVE: To study the reliability of establishing a neonatal piglet model of multiple organ dysfunction syndrome (MODS) by cecal ligation and puncture (CLP). METHODS: Fourteen neonatal piglets were randomly assigned into Experiment group (n=9) and Control group (n=5). MODS model was established in the piglets from the Experiment group by CLP. The Control group underwent a sham-operation. Serum biochemical parameters (ALT, AST, ALB, BUN, Cr, CK-MB and lactic acid), blood platelet counting and blood gas analysis(PaO2 and PaCO2) were tested at 0, 24, 48, 72, 96, and 120 hrs after operation. The histomorphological changes of important vital organs were examined by hematoxylin-eosin staining under a light microscope. RESULTS: The levels of serum ALT, AST, BUN, Cr, CK-MB and lactic acid in the Experiment group began to increase 24 hrs after operation. Significant differences were observed between the Experiment and the Control group at 48 hrs in ALT (83.0 +/- 9.3 U/L vs 57.8 +/- 15.8 U/L), AST (348.8 +/- 132.9 U/L vs 106.4 +/- 12.5 U/L), BUN (10.5 +/- 2.5 micromol/L vs 4.3 +/- 1.0 micromol/L), Cr (79.2 +/- 9.0 micromol/L vs 53.6 +/- 6.8 micromol/L), CK-MB (5152.0 +/- 1 857.8 U/L vs 1243.0 +/- 354.5 U/L), and lactic acid (12.3 +/- 4.0 mmol/L vs 4.6 +/- 1.5 mmol/L) (P < 0.01). The high levels of the above parameters persisted until 96 hrs after operation in the Experiment group and then decreased but were still higher than those at 0 h after operation. After operation, the blood platelet counting decreased significantly at 96 hrs, and PaO2 decrease and PaCO2 increase were observed at 48 hrs in the Experiment group compared with the Control group. All animals, except one, in the Experiment group died within 120 hrs after operation (with the MODS incidence of 56%), while none died in the Control group. The tissue injuries with different degrees were observed in the lungs, liver, heart, kidneys and gastrointestinal tracts of the Experiment group. CONCLUSIONS: Neonatal piglet MODS model can be established successfully by CLP.

Postnatal high-protein diet improves learning and memory in premature rats via activation of mTOR signaling.

PURPOSE: The present study investigated whether a high-protein diet affects spatial learning and memory in premature rats via modulation of mammalian target of rapamycin (mTOR) signaling. METHODS: Pre- and full-term Sprague-Dawley pups were fed a normal (18% protein) or high-protein (30% protein) diet (HPD) for 6 or 8 weeks after weaning. Spatial learning and memory were tested in the Morris water maze at week 6 and 8. The activation of mTOR signaling pathway components was evaluated by western blotting. RESULTS: Spatial memory performance of premature rats consuming a normal and HPD was lower than that of full-term rats on the same diet at 6 weeks, and was associated with lower levels of ribosomal protein S6 kinase p70 subtype (p70S6K) and initiation factor 4E-binding protein 1 (4EBP1) phosphorylation in the hippocampus. Spatial memory was improved in 8-week-old premature rats on an HPD as compared to those on a normal diet. Premature rats on an HPD had p70S6K and 4EBP1 phosphorylation levels in the hippocampus that were comparable to those of full-term rats on an HPD. CONCLUSION: Long-term consumption of a protein-rich diet can restore the impairment in learning and memory in pre-term rats via upregulation of mTOR/p70S6K signaling.

Dysbiosis of Gut Microbiota With Reduced Trimethylamine-N-Oxide Level in Patients With Large-Artery Atherosclerotic Stroke or Transient Ischemic Attack.

BACKGROUND: Gut microbiota has been suggested to play a role in almost all major diseases including cardio- and cerebrovascular diseases. A possible mechanism is the transformation of dietary choline and l-carnitine into trimethylamine by gut bacteria. This metabolite is further oxidized into trimethylamine-N-oxide (TMAO) in liver and promotes atherogenesis. Nevertheless, little is known about gut microbial diversity and blood TMAO levels in stroke patients. METHODS AND RESULTS: We performed a case-control study of patients with large-artery atherosclerotic ischemic stroke and transient ischemic attack. TMAO was determined with liquid chromatography tandem mass spectrometry. Gut microbiome was profiled using Illumina sequencing of the 16S rRNA V4 tag. Within the asymptomatic control group, participants with and without carotid atherosclerotic plaques showed similar levels of TMAO without a significant difference in gut microbiota; however, the gut microbiome of stroke and transient ischemic attack patients was clearly different from that of the asymptomatic group. Stroke and transient ischemic attack patients had more opportunistic pathogens, such as Enterobacter, Megasphaera, Oscillibacter, and Desulfovibrio, and fewer commensal or beneficial genera including Bacteroides, Prevotella, and Faecalibacterium. This dysbiosis was correlated with the severity of the disease. The TMAO level in the stroke and transient ischemic attack patients was significantly lower, rather than higher, than that of the asymptomatic group. CONCLUSIONS: Participants with asymptomatic atherosclerosis did not exhibit an obvious change in gut microbiota and blood TMAO levels; however, stroke and transient ischemic attack patients showed significant dysbiosis of the gut microbiota, and their blood TMAO levels were decreased.

Treatment and prevention of lymphorrhea after radical gastrectomy of gastric cancer.

PURPOSE: Lymphorrhea is an uncommon complication of abdominal surgery. Here, we retrospectively investigate the treatment and prevention of lymphorrhea after radical gastrectomy. METHODS: From January 1995 to January 2007, a total of 1,596 patients who underwent surgery for gastric cancer were investigated. According to the AJCC cancer stage manual, tumor stages of 693 (43.4%) cases were T1 or T2 and 903 (56.6%) cases were T3 or T4. A total of 1,104 (69.2%) patients received grade D1 lymphadenectomy or grade D2, and 492 (30.8%) patients received grade D3 or D4. Ligation was used during the lymphadenectomy in 829 (51.9%) patients, and the electrotome cautery was used in 767 (48.1%) patients. Patients diagnosed of lymphorrhea were treated with total parenteral nutrition (TPN) alone before 2001, and with TPN plus octreotide after 2001. RESULTS: The incidence of lymphorrhea of patients with D1-2 lymphadenectomy was much lower than those with D3-4 lymphadenectomy (P < 0.01). For patients whose lymphatic vessels were ligated during the operation, the incidence of lymphorrhea was much lower than those lymphatic vessels were electrically cauterized (P < 0.01). No significant difference of incidence of lymphorrhea could be found between patients with T1-2 and T3-4 tumor stages (P > 0.05). Octreotide or TPN administration can reduce the quantity and duration of lymphorrhea,and the combination of Octreotide and TPN has a more significant effect on lymphorrhea than TPN alone (P < 0.01). CONCLUSION: The major cause of lymphorrhea following radical gastrectomy was the inappropriate management of lymphadenectomy. Avoiding an extensive lymphadenectomy at surgery and ligating the disrupted lymph vessels would reduce the incidence of lymphorrhea. The combination of Octreotide and TPN is an effective therapeutic modality for lymphorrhea.