Postoperative abdominal herpes zoster complicated by intestinal obstruction: A case report.

BACKGROUND: Intestinal obstruction is a common occurrence in clinical practice. However, the occurrence of herpes zoster complicated by intestinal obstruction after abdominal surgery is exceedingly rare. In the diagnostic and treatment process, clinicians consider it crucial to identify the primary causes of its occurrence to ensure effective treatment and avoiding misdiagnosis. CASE SUMMARY: Herein, we present the case of a 40-year-old female patient with intestinal obstruction who underwent laparoscopic appendectomy and developed herpes zoster after surgery. Combining the patient's clinical manifestations and relevant laboratory tests, it was suggested that the varicella zoster virus reactivated during the latent period after abdominal surgery, causing herpes zoster. Subsequently, the herpes virus invaded the visceral nerve fibers, causing gastrointestinal dysfunction and loss of intestinal peristalsis, which eventually led to intestinal obstruction. The patient was successfully treated through conservative treatment and antiviral therapy and subsequently discharged from the hospital. CONCLUSION: Pseudo-intestinal obstruction secondary to herpes zoster infection is difficult to distinguish from mechanical intestinal obstruction owing to various causes. In cases of inexplicable intestinal obstructions, considering the possibility of a viral infection is essential to minimize misdiagnosis and missed diagnoses.

[Ozone Formation and Key VOCs of a Continuous Summertime O3 Pollution Event in Ji'nan].

In the summer of 2019, field measurements of ozone (O3) and its precursors[volatile organic compounds (VOCs) and nitrogen oxides (NOx)] were carried out at an urban site in Ji'nan. We found that the daily maximum 8-hour averages φ(O3) were (103.0±14.5)×10-9. The average φ(NOx) and φ(VOCs), which are ozone precursors, were (16.7±11.3)×10-9and (22.4±9.4)×10-9, respectively. The ·OH reactivity of VOCs was determined (9.6±3.8) s-1. Ji'nan suffered from serious O3 pollution. An observation-constrained chemical box model was deployed to evaluate in situ photochemical O3 production, which indicated that chemical reactions made positive contributions to O3 production rates between 07:00 and 19:00 LT, with the average hourly O3 production rate of 35.6×10-9 h-1. To evaluate the effectiveness of various ozone precursor control strategies in reducing ozone pollution, we combined the observation-based model (OBM) with the relative incremental reactivity (RIR) method. The key indicators that affect the local ozone production rate were identified. Ji'nan was under VOC-limited conditions and the key VOC precursors were alkenes. The O3 formation mechanism changed from the VOC-limited regime in the morning to the transitional regime in the afternoon. Correspondingly, the simulated local O3 production rate was increased from 18.3×10-9 h-1 to 29.6×10-9 h-1. To further explore the role of anthropogenic emissions in ozone pollution, we used the positive matrix factorization (PMF) model to identify the major sources contributing to VOCs. The major sources in Ji'nan were vehicular exhaust and gasoline evaporation, accounting for more than 50% of the observed VOCs. Therefore, constraints on vehicular emissions is the most effective strategy to control O3 pollution in Ji'nan.

Ultrasound, CT, and MR Imaging for Evaluation of Cystic Renal Masses.

Cystic renal masses are often encountered during abdominal imaging. Although most of them are benign simple cysts, some cystic masses have malignant characteristics. The Bosniak classification system provides a useful way to classify cystic masses. The Bosniak classification is based on the results of a well-established computed tomography protocol. Over the past 30 years, the classification system has been refined and improved. This paper reviews the literature on this topic and compares the advantages and disadvantages of different screening and classification methods. Patients will benefit from multimodal diagnosis for lesions that are difficult to classify after a single examination.

Increased TRPM4 Activity in Cerebral Artery Myocytes Contributes to Cerebral Blood Flow Reduction After Subarachnoid Hemorrhage in Rats.

Cerebral blood flow (CBF) reduction underlies unfavorable outcomes after subarachnoid hemorrhage (SAH). Transient receptor potential melastatin-4 (TRPM4) has a pivotal role in cerebral artery myogenic tone maintenance and CBF regulation under physiological conditions. However, the role of TRPM4 in CBF reduction after SAH is unclear. In this study, we aimed at testing whether TRPM4 would contribute to CBF reduction after SAH in vivo and determining underlying mechanisms. Rat SAH model was established by stereotaxic injection of autologous nonheparinized arterial blood at the suprasellar cistern. A TRPM4 blocker, 9-phenanthrol (9-Phe), was infused through an intraventricular catheter connected to a programmed subcutaneous pump to evaluate the contribution of TRPM4 to SAH outcomes. TRPM4 expression and translocation in cerebral artery myocytes were detected by immunoblotting. Macroscopic currents in cerebral artery myocytes were determined by whole-cell patch clamp. Myogenic tone of cerebral arteries was studied by pressurized myography. Cortical and global CBFs were measured via laser Doppler flowmetry and fluorescent microspheres, respectively. After SAH, TRPM4 translocation and macroscopic current density increased significantly. Furthermore, TRPM4 accounted for a greater proportion of myogenic tone after SAH, suggesting an upregulation of TRPM4 activity in response to SAH. Cortical and global CBFs were reduced after SAH, but were restored significantly by 9-Phe, implying that TRPM4 contributed to CBF reduction after SAH. Collectively, these discoveries show that increased TRPM4 activity has a pivotal role in CBF reduction after SAH, and provide a novel target for the management of cerebral perfusion dysfunction following SAH.

MicroRNA-128 Protects Dopamine Neurons from Apoptosis and Upregulates the Expression of Excitatory Amino Acid Transporter 4 in Parkinson's Disease by Binding to AXIN1.

BACKGROUND/AIMS: Parkinson's disease (PD) is a frequently occurring condition that resulted from the loss of midbrain neurons, which synthesize the neurotransmitter dopamine. In this study, we established mouse models of PD to investigate the expression of microRNA-128 (miR-128) and mechanism through which it affects apoptosis of dopamine (DA) neurons and the expression of excitatory amino acid transporter 4 (EAAT4) via binding to axis inhibition protein 1 (AXIN1). METHODS: Gene expression microarray analysis was performed to screen differentially expressed miRNAs that are associated with PD. The targeting relationship between miR-128 and AXIN1 was verified via a bioinformatics prediction and dual-luciferase reporter gene assay. After separation, DA neurons were subjected to a series of inhibitors, activators and shRNAs to validate the mechanisms of miR-128 in controlling of AXIN1 in PD. Positive protein expression of AXIN1 and EAAT4 in DA neurons was determined using immunocytochemistry. miR-128 expression and the mRNA and protein levels of AXIN1 and EAAT4 were evaluated via RT-qPCR and Western blot analysis, respectively. DA neuron apoptosis was evaluated using TUNEL staining. RESULTS: We identified AXIN1 as an upregulated gene in PD based on the microarray data of GSE7621. AXIN1 was targeted and negatively mediated by miR-128. In the DA neurons, upregulated miR-128 expression or sh-AXIN1 increased the positive expression rate of EAAT4 together with mRNA and protein levels, but decreased the mRNA and protein levels of AXIN1, apoptosis rate along with the positive expression rate of AXIN1; however, the opposite trend was found in response to transfection with miR-128 inhibitors. CONCLUSION: Evidence from experimental models revealed that miR-128 might reduce apoptosis of DA neurons while increasing the expression of EAAT4 which might be related to the downregulation of AXIN1. Thus, miR-128 may serve as a potential target for the treatment of PD.