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Study Design: Retrospective radiographic review.Objectives: Investigate and quantify transverse pedicle angle (TPA), the medial-to-lateral pedicle angulation, and its potential association with pelvic incidence (PI) in patients with isthmic lumbar spondylolisthesis (ISLS) and compare to those with degenerative lumbar spondylolisthesis (DSLS) and controls.Methods: A total of 200 patients (64 ISLS, 70 DSLS, 66 control) were included. TPA was calculated at the L3-5 vertebral levels using axial computed tomography slices. PI was measured on lateral radiographs. Two independent observers completed the measurements. As a sensitivity analysis, TPA was also measured at the most cranial and caudal aspects of the L3-5 vertebral levels of a subset of participants (29 ISLS, 31 DSLS, 35 control) and the cranial to caudal change (ΔTPA) was calculated.Results: TPA values (mean ± SD) at L4 and L5 for ISLS (L4: 17.3° ± 3.7°, L5: 26.0° ± 5.2°) were significantly higher than those for the DSLS (L4: 14.3° ± 3.8°, L5: 22.2° ± 5.0°) and control (L4: 14.5° ± 3.9°, L5: 20.7° ± 3.8°) groups. TPA in the DSLS group was significantly higher than controls at L5, but not L4. High PI predicted wider TPA at L5 in both DSLS and ISLS. ΔTPA (mean ± SD) increased sequentially proceeding through the L3-5 spinal levels for the ISLS (L3: 6.8° ± 4.4°, L4: 8.7° ± 5.2°, L5: 15.6° ± 9.0°), DSLS (L3: 8.2° ± 6.0°, L4: 8.3° ± 5.9°, L5: 18.3° ± 7.2°), and control (L3: 6.8° ± 4.4°, L4: 8.2° ± 4.7°, L5: 17.7° ± 7.0°) groups.Conclusions: TPA was significantly increased in ISLS compared with DSLS and controls. High PI significantly predicted high TPA at the L5 vertebral level in ISLS and DSLS. ΔTPA increased sequentially proceeding through the lumbar spine across groups.

Undetectable measurable residual disease (uMRD) is achievable in patients with chronic lymphocytic leukemia (CLL) with the BCL2-inhibitor venetoclax alone or combined with the Bruton’s tyrosine kinase inhibitor ibrutinib. This phase 2, multicenter, MRD-driven study was designed to discontinue treatment upon reaching uMRD4 (<10−4) in patients with relapsed/refractory CLL receiving venetoclax monotherapy or after the addition of ibrutinib. Primary end point of the study was proportion of uMRD4 with venetoclax ± ibrutinib. Secondary end points were overall response rate, partial response, complete response, progression-free survival, duration of response, overall survival, and safety of venetoclax ± ibrutinib. Patients with uMRD4 at Cycle 12 Day 1 discontinued venetoclax. MRD+ patients added ibrutinib and continued both drugs up to Cycle 24 Day 28/uMRD4/progression/toxicity. After Cycle 24 Day 28, MRD+ patients continued ibrutinib. Thirty-eight patients (29% with TP53 aberrations; 79% with unmutated IGHV) started venetoclax. Overall response rate with venetoclax was 36 (95%) of 38 patients (20 complete; 16 partial response). Seventeen patients (45%) with uMRD4 at Cycle 12 Day 1 discontinued venetoclax. Nineteen (55%) MRD+ subjects added ibrutinib. After a median of 7 months (range, 3-10 months) of combined treatment, 16 (84%) of 19 achieved uMRD4, thus stopping both drugs. Two MRD+ patients at Cycle 24 Day 28 continued ibrutinib until progression/toxicity. After a median follow-up of 36.5 months, median progression-free survival was not reached; 10 patients progressed (4 restarted venetoclax, 3 without treatment need, 2 developed Richter transformation, and 1 dropped out). Seven (22%) of 32 patients remain uMRD4 after 3 years of follow-up. Neutropenia was the most frequent grade 3 to 4 adverse event; no grade 5 events occurred on study. This sequential MRD-guided approach led to uMRD4 in 33 (87%) of 38 patients, with venetoclax monotherapy or combined with ibrutinib, delivering treatment combination only in a fraction, and ultimately identifying the few patients benefiting from continuous therapy. This trial was registered at www.clinicaltrials.gov as # NCT04754035.

Sudden unexplained death in epilepsy (SUDEP) is the most common cause of death in children and young adults with epilepsy with epileptic patients harboring a 27 times increased risk of death from SUDEP. Structural brain lesions are encountered in up to 50% of autopsy cases. In this case series, we report 3 previously undiagnosed structural causes of SUDEP discovered at autopsy at our institution including schizencephaly, ganglioglioma, and focal cortical dysplasia. Our major recommendation is in cases with suspected SUDEP, formal neuropathological examination and tissue sampling should be employed to identify and characterize specific potential anatomic etiologies.

•Proof of concept of miniaturized gas chromatograph.•First coupling of preconcentrator to Nano Gravimetric Detector.•Monitoring and long-survey of air quality pollutants using autonomous system.•Volatile Organic Compounds monitoring in extreme environments.

Food Pollen Allergy Syndrome is an IgE mediated reaction that occurs due to cross reactivity of pollen proteins (ex. Bet v1 in Birch tree) with specific fruits and vegetables due to conserved homologous regions (ex. Mal d1 in apple). Localized symptoms occur in pollen-sensitized individuals, but systemic reactions are rare. We present a case of a multi-system allergic reaction after fresh pressed apple cider consumption.

The heart has its own immune network, with numerous resident macrophages distributed throughout its structures. Macrophages conduct immunosurveillance of myocardial tissue, helping to orchestrate repair through multiple mechanisms. They secrete cytokines such as tumor necrosis factor (TNF) and interleukin 1 (IL-1) beta, which contribute to endothelial cell activation and inflammation. While these cytokines are helpful in moderation, inappropriate overactivation can be problematic. We discuss a rare case of immune-mediated endocarditis after cardiac surgery in a patient with Down Syndrome.