This study investigates the repurposing potential of the anesthetic ketamine (KET) as a preventive agent, both alone and in combination with the azoles fluconazole (FLC) and itraconazole (ITR), against Candida spp. biofilms adhering to fragments of peripheral venous catheters. The activity was assessed in vitro through cell viability and colonization assays of impregnated catheter segments, while morphological alterations were analyzed using scanning electron microscopy (SEM). KET, both alone and in association with ITR, significantly reduced (p < 0.05) the adherence of C. albicans to the impregnated fragments. Furthermore, the combinations KET + FLC and KET + ITR frequently exhibited greater efficacy in reducing biofilm viability than the agents used individually, suggesting additive/synergistic interactions. SEM revealed structural damage to the treated fungal cells. These findings indicate that KET exhibits preventive activity against Candida spp. biofilms, including on catheter surfaces, and may enhance the activity of azoles, positioning it as a promising candidate for repurposing in the treatment of biofilm-associated fungal infections.

Despite the therapeutic potential of ketamine (KET) as a psychoactive drug, off-dose use or abuse may lead to irreversible consequences, ranging from mild to severe dependency, cardiovascular complications, and even death. Thus, its accurate detection in human biological samples is essential. In this study, a novel opto-electrochemical sensor is developed based on a scalable indium tin oxide (ITO) surface modified with molecularly imprinted polymer (MIP) using β-cyclodextrin (β.CD) and polyaniline (PANI) for the selective detection of KET. In the embedded sensing interface, the β.CD serves as a host molecule to form specific cavities for KET entrapment, and PANI acts as an electrochromic material. This strategy enables visual detection via vivid color changes that correspond to KET concentration, along with electrochemical outputs. The sensor exhibits a linear response range from 1 to 700 nM, with a detection limit of 0.33 nM (S/N = 3) and a limit of quantification of 3.3 nM (± 0.002 nM) across electrochemical, optical, and RGB signals. Selectivity tests against structurally similar drugs confirm negligible cross-reactivity toward KET. Real sample analysis in human urine and saliva, with recoveries between 99.45% and 101.68%, validates the sensor's reliability. The dual-mode capability-electrochemical and visual-combined with green chemistry compliance (AGREE score: 0.84) promises the sensor's potential to provide technical support for point-of-care applications in clinical diagnostics and forensic medicine.

Unveiling the role of single versus repeated low-dose ketamine in attenuating doxorubicin-induced chemobrain and depression in rats: differential modulation of neuroinflammation, phosphorylated GLT-1, SERT, DAT, and BDNF/TrkB signaling.

This study investigated perioperative Th1/Th2 cytokine polarization and biochemical changes in cats undergoing ovariohysterectomy under three different anesthesia protocols. Twenty-four healthy mixed-breed female cats were randomly allocated into three groups (n = 8/group): propofol–isoflurane (Group I), xylazine–ketamine hydrochloride (Group II), and xylazine–isoflurane (Group III). Venous blood samples were collected preoperatively (0 h) and at 6 and 12 h postoperatively. Serum concentrations of TNF-α, IFN-γ, IL-2, IL-4, IL-5, and IL-10 were quantified using feline-specific ELISA kits, and biochemical variables were measured with an automated analyzer. In Group I, tumor necrosis factor (TNF)-α, increased postoperatively (12.64 ± 2.28 ng/mL) compared to preoperative levels (6.79 ± 0.74 ng/mL; p < 0.05). In Group II, both interferon (IFN)-γ and interleukin (IL)-2 levels decreased after the operation compared to pre-op 0 h (p < 0.05). Group III showed a decrease in IL-4 and IL-10 postoperatively (124.21 ± 23.45 pg/mL and 106.05 ± 5.25 ng/mL, respectively) compared to pre-op 0 h (197.28 ± 14.40 pg/mL and 113.14 ± 11.19 ng/mL, respectively; p < 0.05). IL-5 concentrations did not change significantly in any group. Postoperative biochemical changes were transient and remained within reference ranges, with no clinical complications observed. These findings indicate that anesthesia protocols differentially influence perioperative immune responses in cats. The xylazine–ketamine combination induced the greatest cytokine fluctuations, whereas xylazine–isoflurane best preserved Th1/Th2 balance. Anesthetic selection may play a critical role in minimizing perioperative immune modulation. The xylazine–isoflurane protocol may be a preferable option for feline ovariohysterectomy, particularly in patients where immune stability is clinically relevant. These findings indicate that anesthesia protocols are associated with distinct short-term perioperative immune profiles in cats undergoing elective ovariohysterectomy. The observed differences should be interpreted as preliminary and hypothesis-generating, and larger studies with standardized pain assessment and longer follow-up are warranted to clarify clinical implications.

Less than 150 chemicals have been evaluated for their potential to cause developmental neurotoxicity (DNT) using OECD rodent-based test guidelines. The DNT in vitro battery (DNT IVB), comprised of 17 human or rodent cell-based assays, is a proposed alternative. Recent work identified three false negative compounds that are developmentally neurotoxic in rodent or human studies but negative in the DNT IVB (5,5-diphenylhydantoin, maneb, nicotine). We hypothesized that multi-behavioral phenotyping in early-life stage zebrafish can complement the DNT IVB. Zebrafish embryos or larvae were acutely (40 min) or developmentally (1-5 days post-fertilization) exposed to 12 DNT positive chemicals 5,5-diphenylhydantoin, BDE-99, chlorpyrifos, haloperidol, hexachlorophene, ketamine hydrochloride, maneb, nicotine, PFOA, tebuconazole, trichlorfon, or triethlytin bromide or to 0.4% DMSO. Behavior was evaluated using the Visual and Acoustic Motor Response (VAMR) assay, comprised of 26 behavioral endpoints including visual and acoustic startle responses, non-associative habituation learning, and memory retention. Five proposed DNT negative compounds were also evaluated under both exposure paradigms. To fit concentration response data, generalized additive and linear mixed effects modeling strategies were combined with Fréchet distance calculations. Hit calls were identified such that inclusion of the zebrafish VAMR assay within the DNT IVB would potentially increase battery sensitivity without compromising battery specificity. Hits in the VAMR assay were typically detected at 1-4 orders of magnitude lower concentrations relative to the DNT IVB. Taken together, the zebrafish behavior-based VAMR assay can add value to the DNT IVB by increasing test battery sensitivity and enhancing potency detection.

Background: Noninvasive transdermal insulin delivery using ultrasound technology has gained attention for improving the glycemic control of insulin-dependent patients. Methods: Indirect functional comparison and evaluation of insulin dosage, between noninvasive ultrasound-mediated transdermal delivery and needle injection methods, was achieved utilizing in vivo blood glucose measurements of temporary hyperglycemic rabbits. Nine rabbits were divided into three groups: (i) untreated control, (ii) subcutaneous injection and (iii) ultrasound-mediated transdermal delivery. Animals were anesthetized using a combination of ketamine hydrochloride and sodium xylazine to produce temporary hyperglycemic rabbits during the experiments. The rabbits in the control group did not receive insulin, while the animals in the ultrasound group received insulin transdermally for 10 min utilizing a customized single-element piston-shaped ultrasound transducer operated by multi-frequency electrical signals from 100 to 200 kHz. Rabbits in the direct subcutaneous injection group were anesthetized and injected with 0.25 units/kg of insulin. Results: With an initial blood glucose baseline level of 228.7 ± 13.1 (mg/dL) for all rabbits, the in vivo results of control group showed an increase above the baseline by 129.7 ± 27.3 (mg/dL) at the end of the in vivo experimental period (80 min). However, the ultrasound-mediated delivery and subcutaneous injection groups showed noticeable statistically significant percentage reductions in blood glucose levels by 43.9 ± 5.4 and 42.7 ± 6.6, respectively, compared to the control group by the end of the in vivo experiments. Conclusions: In vivo glucose response results confirmed that piston-shaped ultrasound transducers achieved indirectly similar insulin dosage delivery by ultrasound energy for tested animals with no statistically significant differences once compared to the results of the subcutaneous needle injection group.

Ketamine (KET) exhibits potential anticancer activity, with enhanced cytotoxicity against melanoma cells when combined with the permeation enhancer dodecyl maltoside (DDM). To support clinical translation, this study evaluated the embryotoxicity, effects on angiogenesis, and cytocompatibility of KET, DDM, and their combination (KET + DDM) using a chicken embryo model. The chorioallantoic membrane (CAM) assay was used to assess angiogenesis following treatment with KET (1000 µM), DDM (19.6 µM), or KET + DDM in fertilized eggs. Embryonic survival and morphology were monitored for five days. Quantitative PCR analysis of heart, lung, kidney, and brain tissues evaluated apoptosis-related genes (Caspase 3, Caspase 8, Caspase 9, BAX) and VEGF expression. Cytocompatibility was examined in primary embryonic fibroblasts (EFBs) using AlamarBlue assays and morphological assessment. The results showed no significant differences in vascular density, vessel length, or branching in the CAM assay across all treatments. Embryos treated with KET or KET + DDM showed normal survival and morphology, while DDM alone reduced viability. Apoptotic and angiogenic gene expression remained unchanged in major organs. In vitro, KET and KET + DDM did not reduce EFB viability or alter morphology. Overall, KET and KET + DDM did not produce detectable adverse effects in embryonic and cellular models, preserving angiogenesis and development. Notably, the KET + DDM combination showed no detectable adverse effects, supporting the preliminary safety of this combination for further anticancer investigation.Supplementary InformationThe online version contains supplementary material available at 10.1038/s41598-026-46828-9.

Straightforward screening of ketamine in forensic samples using voltammetry with screen-printed carbon graphite electrodes.

• MSG induced significant cardiotoxicity through SERCA2a downregulation, calcium dysregulation, and oxidative stress in male Wistar rats. • L-arginine treatment restored SERCA2a expression and normalized plasma and cardiac calcium homeostasis in MSG-treated animals. • L-arginine enhanced antioxidant defense mechanisms by increasing NADPH, G6PDH, and GPx activities while reducing lipid peroxidation. • MSG dysregulated VEGF-PI3K growth factor signaling, while L-arginine normalized these pathways to prevent apoptosis. • L-arginine demonstrated multi-target cardioprotection through simultaneous modulation of calcium handling, redox balance, and survival signaling pathways. L-arginine is a semi-essential amino acid that is produced endogenously and can be obtained through dietary supplements. Monosodium glutamate (MSG) is an umami flavor enhancer used in packaged and processed food and has been associated with cardiotoxicity and inflammation. The sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a (SERCA2a) is a key player in the Ca2+ cycle of cardiac regulation. This study aims to evaluate the effect of L-arginine on SERCA2a in MSG-induced cardiac toxicity. Twenty male Wistar rats weighing 100-120g were divided into four groups (n=5/group) and were fed as group1; control- rat chow + olive oil (vehicle); group 2; rat chow+ L-arginine (150 mg/kg), group 3; MSG (120mg/kg) + vehicle, group 4; MSG+ L-Arginine daily for 6 weeks respectively. At the end of the experiment, rats were anaesthetized with 0.3ml of I.M ketamine hydrochloride (50mg/ml), and blood was collected by cardiac puncture. Serum and cardiac tissue homogenate were analyzed, and values expressed as mean ± SEM with p-values < 0.05 accepted as significant. The results showed that MSG, compared with the control, significantly decreased plasma and cardiac NO, NADPH, GPx, Ca2+, cardiac SERCA2 activity, VEGF, and PI3K, and increased plasma and cardiac MDA and uric acid (P<0.05). However, L-arginine significantly increased NO, NADPH, GPx, and cardiac SERCA2 activity, as well as VEGF and PI3K, compared with the control and MSG-treated groups. In conclusion, L-arginine attenuated MSG-induced cardiotoxicity by restoring calcium handling and redox balance, as well as modulating VEGF–PI3K/Akt survival signaling to reduce apoptotic and metabolic dysfunctions.

Treatment-resistant depression (TRD), defined by unsuccessful response to multiple antidepressants, affects approximately one-third of individuals with major depressive disorder, yet its underlying molecular mechanisms remain poorly understood. Here, we developed a preclinical model of TRD in which mice exposed to chronic social defeat stress were sequentially treated with fluoxetine (FLX) and ketamine (KET), allowing behavioral stratification into antidepressant responsive and non-responsive mice. RNA sequencing of the nucleus accumbens (NAc) and prefrontal cortex (PFC) revealed transcriptional signatures associated with treatment outcomes. Prior exposure to FLX exerted a priming effect that facilitated molecular and behavioral responsiveness to KET in a subset of animals. However, this priming effect was absent in non-responders, despite identical treatment regimes, suggesting a transcriptional divergence in both the NAc and PFC in underlying differential outcomes. Gene co-expression network analysis identified modules enriched for differentially expressed genes unique to stress-susceptible and FLX-KET nonresponsive mice, as well as modules overlapping with both stress susceptibility and antidepressant resistance. These findings suggest that failed antidepressant treatment can shape the brain’s molecular landscape in a way that influences subsequent treatment outcomes, and that resistance arises not simply from treatment failure but from an absence of adaptive molecular priming. This work provides insight into the gene networks contributing to antidepressant non-response and highlights a mechanistic framework for modeling antidepressant resistance in preclinical systems. By identifying molecular correlates of sequential pharmacological resistance, our findings may inform the development of novel therapeutic strategies for individuals with TRD.

As one of the most prevalent drugs, ketamine (KT) presents a significant social risk, making the development of a specific and ultrasensitive detection tool essential. Herein, the molecular dynamics (MD) simulation calculation-based molecularly imprinted polymer (MIP) with excellent recognition capability and the ZnO-CuO p-n heterojunction with efficient charge separation were prepared to fabricate a novel molecularly imprinted photoelectrochemical (MIP-PEC) sensor for the specific and ultrasensitive detection of KT. Impressively, compared with traditional MIP preparation methods that suffer from limited selectivity and inefficient trial-and-error component screening, MD simulation calculations enable the rational design of highly selective MIP, reducing costs and enhancing efficiency. Specifically, the binding energy of KT with functional monomers and cross-linkers, along with the solvation energy of solvents, were analyzed by MD simulation calculations, ultimately identifying the methacrylic acid (MAA), ethylene glycol dimethacrylate (EGDMA), and acetonitrile (ACN) as the optimal components to build MIP with precisely recognized cavities, which effectively improved the detection selectivity of the designed sensor. Furthermore, the ZnO-CuO p-n heterojunction with a precisely matched band effectively reduced the recombination rate of carriers, enhancing photoelectric response and stability. As a result, the constructed MIP-PEC sensor successfully achieved a specific and ultrasensitive assay of KT with a low detection limit down to 0.746 nM, an imprinting factor (IF) of 8.75, and a selectivity factor (SF) of 4.70, surpassing previous reports and enabling successful application in urine, saliva, and wastewater samples. This study provides a distinctly specific and ultrasensitive analytical platform for the assay of illegal drugs in the field of social security.

BackgroundConventional ketamine hydrochloride solutions are acidic and hyperosmotic, limiting their tolerability for subcutaneous (SC) delivery. BB106 is a novel ketamine formulation using the multitude of sulfobutylether-beta-cyclodextrin (SBECD) anionic substitutions as ionic counterions to achieve a new ketamine-SBECD salt in solution at near-physiologic pH and isotonicity, thereby enabling SC administration. To support its development for pain and neuropsychiatric indications, we conducted nonclinical toxicology studies in rats and minipigs.MethodsA 2-week repeated-dose SC injection study in rats and a 4-week continuous SC infusion study in Göttingen minipigs were performed, each with a 2-week recovery phase. Assessments included clinical observations, body weights, food consumption, ophthalmology, electrocardiography, clinical pathology, toxicokinetics (TK), and histopathology.ResultsBB106 was well-tolerated in both species. No mortality or dose-limiting systemic toxicity occurred. Clinical signs were consistent with ketamine pharmacology (eg, transient ataxia) and resolved after dosing. Local site reactions were minimal, histologically mild, and reversible. No treatment-related lesions were observed in any of the systemic tissues examined (including liver, kidney, bladder, and brain). TK analyses confirmed consistent systemic exposure without accumulation. SBECD itself produced no adverse effects at the exposure levels tested.ConclusionRepeated SC bolus injections in rats and continuous SC infusion in minipigs demonstrated favorable local and systemic safety profiles for BB106. These findings support its feasibility as an alternative to intravenous ketamine for pain and psychiatric disorders. To our knowledge, this is the first toxicology report of SC administration of an SBECD salt formulation and the results support continued consideration as a potential medicine.

Abstract Background Stenotrophomonas maltophilia is an opportunistic pathogen that disproportionately affects vulnerable patients in high-acuity settings. These individuals often receive sedation for pain, agitation, and ventilation. The interaction between sedatives and antibiotics against S. maltophilia is unclear. This study evaluated whether common sedatives alter antibiotic activity and growth suppression against S. maltophilia. Methods Seven clinical S. maltophilia isolates (MB16829, MB16852, MB17662, MB17666 from hematologic malignancy patients at MD Anderson; SM6, SM9, SM10 from lung disease patients at UK Healthcare) were exposed to 8 antibiotics—levofloxacin (LEV), ciprofloxacin (CIP), trimethoprim/sulfamethoxazole (TMP/SMX), minocycline (MIN), omadacycline (OMC), eravacycline (ERV), aztreonam/avibactam (ATM/AVI), and cefiderocol (FDC)—alone or with haloperidol (HAL), hydromorphone (HMP), fentanyl (FEN), dexmedetomidine (DEX), ketamine (KET), or midazolam (MID). Growth (OD600) was measured every 15 minutes for 24 hours at 37°C. Significant changes were defined as ≥0.1 absorbance difference vs. antibiotic alone. Results Sedative–antibiotic interactions altered S. maltophilia growth in 43 regimens (Figure 1). MID increased growth in 11 combinations, followed by FEN (10). DEX was the only sedative linked to decreased growth (6 regimens). ERV and OMC were most impacted, with 9 and 8 increased-growth combinations; 3 of 6 decreases also involved OMC. SM9 showed increased growth in 8 combinations, mainly with OMC and MID. Isolate 16852 showed decreased growth in 6 combinations—all with DEX. ATM/AVI and FDC remained stable, except in 16829, where 3 FDC combinations (+DEX, KET, MID) increased growth (Figure 2). ERV+MID increased growth in 17666 (0.538), 17662 (0.581), SM6 (0.418), and SM9 (1.016) vs. ERV alone (0.353, 0.353, 0.173, 0.114; Figure 3). In Figure 4, OMC combinations in 17662 (A) and SM9 (B) showed isolate-specific responses, with MID and FEN driving the greatest increases. Conclusion MID and FEN most often increased S. maltophilia growth, especially with OMC and ERV in SM9 and 17662. DEX reduced growth in all six decreased regimens in 16852. FDC increased growth only in 16829. Findings highlight sedative effects on antibiotic activity in critical care. Disclosures All Authors: No reported disclosures

Ketamine-induced re-organisation of neural oscillations across health, MDD, and TRD: A systematic review of magnetoencephalography insights.

Methamphetamine (METH)-induced agitation, a major concern in acute METH intoxication, is currently treated with benzodiazepines. Due to current polysubstance use patterns in METH consumption, this treatment may fatally exacerbate respiratory depression produced by opioid adulterants or intentionally co-administered opioids. We previously showed that the α2-agonist dexmedetomidine (DEX), which does not potentiate opioid-induced respiratory depression in clinical practice, can be safely and effectively co-administered with naloxone to attenuate METH-induced agitation following naloxone reversal in METH-fentanyl co-intoxicated rats. While the unique arousability of DEX-induced sedation is clinically useful, the current study tested the safety and efficacy of DEX and adjunctive ketamine (KET) in producing deeper, less arousable sedation when needed (i.e., for severe agitation or to facilitate an intricate procedure). Fifteen minutes after 1mg/kg METH administration in male rats (simulating treatment of naloxone-unmasked agitation with a delay), low-dose (0.032mg/kg) DEX ± (56mg/kg) KET, high-dose (0.18mg/kg) DEX, or saline was administered. Key measurements included METH-induced locomotor activity (a rat model of agitation), the rat coma scale (a quantification of arousability), and α2-agonist class side effects. Both high-dose DEX and DEX-KET almost completely attenuated METH-induced locomotor activity for 90min after administration, but with the combination the sedation was deeper during the most intense METH-induced stimulation, and the α2-agonist side effects were less intense and of shorter duration. These data provide proof-of-concept support for the potential use of DEX-KET in producing deeper sedation in METH-induced agitation.

Aim/Background: A five-month-old female Duroc pig was presented with a rare case of extra-large ventral abdominal hernia for surgical correction at a private farm in Makurdi, Benue State. The chief complaint was a swelling on the ventral abdomen immediately caudal to the umbilicus near the preputial area. The swelling, first noticed before one month of age, gradually increased in size to a “handball shape” by the time of presentation. The hernia had previously been corrected about a month earlier but reoccurred, appearing larger than the initial swelling. Methods: Clinical examination revealed a soft, pliable, and completely reducible hernia mass with a hernia ring measuring approximately 10 cm in width. Following aseptic preparation and concurrent fluid therapy to stabilize the patient, sedation was achieved using xylazine at 3 mg/kg body weight, and general anesthesia was induced with ketamine hydrochloride at 35 mg/kg body weight. An elliptical incision was made at the hernia site to prevent accidental puncture. Blunt dissection was employed to separate abdominal contents from mild adhesions involving muscle, fascia, and peritoneum. The contents were reduced gently into the abdominal cavity, and herniorrhaphy was performed by apposing the edges of the hernia ring with chromic catgut (size 2-0) in three layers using interrupted suture patterns. Post-operative management included antibiotic and Dexanor (anti-inflammatory analgesic) therapy for five days. Results: The pig recovered uneventfully, and complete healing was observed by the 12th day post-operation. No complications were recorded throughout the recovery period. Conclusion: Successful surgical management of a recurrent extra-large ventral abdominal hernia was achieved through careful aseptic preparation, appropriate anesthesia, and layered herniorrhaphy, resulting in full recovery without postoperative complications.

Male cat (tomcat) neutering is a common surgical procedure performed to control overpopulation and reduce undesirable behaviors such as aggression, roaming, vocalization, and urine spraying. This case study documents the surgical sterilization of a 2.3-kg tomcat presented to the PMAC Veterinary Teaching Hospital, Sylhet, Bangladesh. Although both surgical and non-surgical sterilization techniques are available, permanent surgical removal of the testicles remains the most widely practiced and reliable method. In this case, bilateral orchiectomy was performed under general anesthesia following proper aseptic preparation and shaving of the operative site. General anesthesia was achieved using a combination of xylazine hydrochloride (1.1 mg/kg), atropine sulfate (0.04 mg/kg), and ketamine hydrochloride (15 mg/kg). Both testicles were removed, and the spermatic cords were ligated using absorbable sutures. Post-operative management included a five-day course of antibiotics and anti-inflammatory drugs. No post-surgical complications were observed, and the surgical wound healed uneventfully without the use of skin sutures. This case demonstrates that routine surgical neutering of tomcats, when performed using proper aseptic techniques and appropriate anesthetic protocols, is a safe, feasible, and effective procedure. Furthermore, it highlights the importance of surgical sterilization in population control and behavioral management while emphasizing the advantages of surgical neutering as a permanent sterilization method. Res. Agric. Livest. Fish. Vol. 12, No. 3, December 2025: 501-506

The use of anesthetics may cause damage to the human nervous system, leading to cognitive and motor dysfunction in severe cases. The role of lncRNAs in anesthesia-induced nerve injury have been reported, but their specific regulatory mechanism remains to be explored. By analyzing the GSE160299 and GSE235357 datasets, LINC01187 was screened as our target lncRNA. With the aid of bioinformatics methods, hsa-miR-6069 and IGF2BP3 were predicted as possible downstream molecules of LINC01187. Their expressions were detected by RT-qPCR or western blotting. The dual-luciferase reporter assay was used to determine the targeted association among them. The CCK-8, Annexin V/PI staining, and ROS detection kit were used to evaluate the viability, apoptosis, and oxidative damage of cells. The Rota-Rod and Morris water maze tests were used to measure the motor and learning abilities of rats. LINC01187 showed a low expression in propofol (PPF)- or ketamine (KTM)-treated human cortex neuron cells (hCNCs) and in the hippocampal tissues of KTM-treated rats. Overexpression therapy with LINC01187 alleviated the damage caused by KTM to the motor and learning abilities of rats. LINC01187 targeted hsa-miR-6069 and downregulated it. Hsa-miR-6069 inhibited IGF2BP3 expression by binding to its mRNA. The overexpression of LINC01187 rescued the viability decrease, apoptosis increase, and oxidative damage in PPF/KTM-induced hCNCs by inhibiting hsa-miR-6069 to promote IGF2BP3 expression. In conclusion, intrathecal injection therapy of the LINC01187 vector restored the impairment of motor and learning abilities in KTM-treated rats. LINC01187 protected nerve cells and rats from anesthetic-induced impairment by regulating the hsa-miR-6069/IGF2BP3 axis.

This study aimed to investigate the impact of cerebrospinal fluid (CSF) from single-prolonged stress (SPS) model mice on the neurobehavioral outcomes in normal mice, and to explore the underlying mechanisms. CSF was extracted from SPS mice (SPS-CSF), and norepinephrine (NE) levels were measured using high-performance liquid chromatography-electrochemical detection (HPLC-ECD). A cannula was used for direct hippocampal injection of SPS-CSF, followed by behavioral experiments such as the elevated plus maze and fear extinction tests to assess changes in anxiety and fear memory in SPS-CSF injected mice. Hematoxylin and eosin (HE) staining was employed to evaluate neuronal pathology in the hippocampus. Western blotting and immunofluorescence were used to detect changes in the expression of astrocytic and synaptic proteins. Transmission electron microscopy (TEM) was adopted for synaptic ultrastructural analysis. Additionally, the effect of intraperitoneal ketamine (KET) injection on the behavioral changes induced by SPS-CSF was assessed. The results showed that SPS mice exhibited typical anxiety-like behavior, and NE levels in the CSF of SPS mice were significantly higher than those in control animals. Repeated injections of SPS-CSF into normal mice led to anxiety-like behavior and impaired fear memory extinction. After SPS-CSF administration, neuronal damage was observed in the hippocampus, along with decreased glial fibrillary acidic protein (GFAP) expression and reduced synaptic protein levels. Interestingly, the behavioral changes induced by SPS-CSF persisted for several weeks, and these changes could be blocked by KET. These findings suggest that stereotactic injection of SPS-CSF into the hippocampus can induce anxiety-like behavior and abnormal fear memory in normal mice, with mechanisms involving the regulation of astrocytes and synapses. This model indicates a potential "infectious" nature of SPS-CSF and provides a novel approach for future research on post-traumatic stress disorder (PTSD).

A rat snake was presented with the history of rescue from a rural household. It was said to have some hit injury and was dull and reluctant to move. Bubbling of nasal discharge from the nostril, open mouth breathing and copious salivation were noticed. On auscultation deep breathing was observed; respiratory distress was noticed. The snake was medicated with ketamine hydrochloride and Diazepam and prepared for endoscopic assessment. A 2.8mm thin flexible endoscopy was used to assess the trachea, lungs and air sac area. In the middle of respiratory tract, occlusion with Pentastomid worm was noticed which was retrieved using grasping forceps. Dextrose Normal Saline was administered orally using feeding tubes and ivermectin was given subcutaneously. The snake recovered uneventfully after endoscopy and later rehabilitated and released in to a non-human habitat area.