Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.

Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.

Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.

Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.

Background: Dynamic parameters used for predicting fluid responsiveness require special equipment and are minimally invasive. Therefore, recent interest in the use of carotid artery ultrasound parameters, such as carotid corrected flow time (FTc) and peak velocity variation (ΔVpeak) has grown. Therefore, we performed this systematic review and meta-analysis to assess the ability of carotid FTc and/or ΔVpeak to accurately predict fluid responsiveness. Methods: We searched the PubMed and Embase databases for articles evaluating the diagnostic accuracy of carotid FTc or ΔVpeak for predicting fluid responsiveness. Two independent authors performed the search and selected studies published until May 2022. The studies were assessed for the inclusion and exclusion criteria using Rayyan (Rayyan Systems Inc., 2022). Results: Ten studies (n=438) that fulfilled the inclusion criteria were selected. Studies were divided into those assessing carotid FTc and those assessing carotid ΔVpeak. Five studies (six datasets) assessed FTc. The pooled sensitivity and specificity of carotid FTc were 0.76 and 0.88, respectively. The summary receiver operating characteristic (SROC) curve for carotid FTc had an area under the curve (AUC) of 0.9092, with a Q value of 0.8412. Seven studies calculated carotid ΔVpeak. The pooled sensitivity and specificity for ΔVpeak were 0.83 and 0.81, respectively. The SROC curve had an AUC of 0.8941 and a Q value of 0.8250. Conclusions Our meta-analysis showed that both carotid FTc and ΔVpeak are useful for predicting fluid responsiveness in anesthesia and critical care settings with good specificity and sensitivity.

OBJECTIVES: Dengue is a mosquito-borne viral disease globally transmitted by Aedes aegypti. The most effective method to prevent the transmission of the disease is proficient vector control. Understanding the breeding behaviour of the responsible vectors is very pertinent in this regard; therefore, the present study was conducted to understand Ae. aegypti behaviour regarding the selection of containers for oviposition in the megacity of Delhi. METHODS: A household survey in different localities within Delhi was carried out during 2018-2019. All available containers were inspected for the presence of immature Ae. aegypti. In entomological surveillance, the ovipositional preference of Aedes was computed using the breeding preference ratio, container index in the field, and laboratory settings, and associations of dengue cases with monthly variation in environmental factors and container type were also calculated. RESULTS: The household larval survey in 40 localities showed that 40% of 27,776 water-holding containers in 3,400 houses were plastic, followed by overhead tanks (26.2%), and coolers (12.1%). The most preferred breeding habitat was clay pots (9.3%), followed by metallic containers (8.5%) and solid waste (7.1%). A laboratory-based study showed that Aedes preferred clay containers (81.8%) over 4 other types of containers (plastic, paper, metal, and glass). CONCLUSIONS The present study provides a rationale for using clay containers as a possible surveillance tool (ovitraps) or as a vector control tool. This information might aid researchers in developing novel traps and targeting preferred containers for larval control activities during transmission and non-transmission seasons.

Pediatric glioblastoma (pGBM) is a rare entity accounting for only approximately 3% of all childhood brain tumors. Treatment guidelines for pGBM have been extrapolated from those in adult glioblastoma. Rarity of pGBM and underrepresentation of pediatric population in major studies precludes from defining the ideal treatment protocol for these patients. Maximum safe resection is performed in most of the cases followed by postoperative radiotherapy in children over 3 years of age. Benefit of temozolomide is unclear in these patients. Here, we present the clinicopathological details and outcome of six pGBM patients treated at our institute in 2018–2019.

Pediatric glioblastoma (pGBM) is a rare entity accounting for only approximately 3% of all childhood brain tumors. Treatment guidelines for pGBM have been extrapolated from those in adult glioblastoma. Rarity of pGBM and underrepresentation of pediatric population in major studies precludes from defining the ideal treatment protocol for these patients. Maximum safe resection is performed in most of the cases followed by postoperative radiotherapy in children over 3 years of age. Benefit of temozolomide is unclear in these patients. Here, we present the clinicopathological details and outcome of six pGBM patients treated at our institute in 2018–2019.

Background: The effect of dexmedetomidine as an adjuvant in the adductor canal block (ACB) and sciatic popliteal block (SPB) on the postoperative tramadol-sparing effect following spinal anesthesia has not been evaluated. Methods: In this randomized, placebo-controlled study, ninety patients undergoing below knee trauma surgery were randomized to either the control group, using ropivacaine in the ACB + SPB; the block Dex group, using dexmedetomidine + ropivacaine in the ACB + SPB; or the systemic Dex group, using ropivacaine in the ACB + SPB + intravenous dexmedetomidine. The primary outcome was a comparison of postoperative cumulative tramadol patient-controlled analgesia (PCA) consumption at 48 hours. Secondary outcomes included time to first PCA bolus, pain score, neurological assessment, sedation score, and adverse effects at 0, 5, 10, 15, and 60 minutes, as well as 4, 6, 12, 18, 24, 30, 36, 42, and 48 hours after the block. Results: The mean ± standard deviation of cumulative tramadol consumption at 48 hours was 64.83 ± 51.17 mg in the control group and 41.33 ± 38.57 mg in the block Dex group (P = 0.008), using Mann–Whitney U-test. Time to first tramadol PCA bolus was earlier in the control group versus the block Dex group (P = 0.04). Other secondary outcomes were comparable. Conclusions Postoperative tramadol consumption was reduced at 48 hours in patients receiving perineural or systemic dexmedetomidine with ACB and SPB in below knee trauma surgery.

Purpose: Hypofractionated radiotherapy (RT) is becoming a new standard in postoperative treatment of patients with early stage breast cancer after breast conservation surgery. However, data on hypofractionation in patients with advanced stage disease who undergo mastectomy followed by local and regional nodal irradiation (RNI) is lacking. In this retrospective study, we report late-term effects of 3 weeks post-mastectomy hypofractionated local and RNI with two-dimensional (2D) technique in patients with stage II and III breast cancer. Methods: Between January 1990 and December 2007, 1,770 women with breast cancer who were given radical treatment with mastectomy, systemic therapy and RT at least 10 years ago were included. RT dose was 35 Gy/15 fractions/3 weeks to chest wall by two tangential fields and 40 Gy in same fractions to supraclavicular fossa (SCF) and internal mammary nodes (IMNs). SCF and IMNs dose was prescribed at dmax and 3 cm depth, respectively. Chemotherapy and hormonal therapy was given in 64% and 74% patients, respectively. Late-term toxicities were assessed with the Radiation Therapy Oncology Group (RTOG) scores and LENT-SOMA scales (the Late Effects Normal Tissue Task Force-Subjective, Objective, Management, Analytic scales). Results: Mean age was 48 years (range, 19 to 75 years). Median follow-up was 12 years (range, 10 to 27 years). Moderate/marked arm/shoulder pain was reported by 254 (14.3%) patients. Moderate/marked shoulder stiffness was reported by 219 (12.3%) patients. Moderate/marked arm edema was seen in 131 (7.4%) patients. Brachial plexopathy was not seen in any patient. Rib fractures were noted in 6 (0.3%) patients. Late cardiac and lung toxicity was seen in 29 (1.6%) and 23 (1.3%) patients, respectively. Second malignancy developed in 105 (5.9%) patients. Conclusion RNI with 40 Gy/15 fractions/3 weeks hypofractionation with 2D technique seems safe and comparable to historical data of conventional fractionation (ClinicalTrial.gov Registration No. XXXX).