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Background: Urine leukocyte count under microscopy is one of the most frequently used routine screening tests for urinary tract infection (UTI). Nevertheless, it is observed that pyuria is lacking in 10-25% of children with UTI. This study aims to determine the factors related to pyuria-negative UTI in young infants aged under four months old. Method: This retrospective cross-sectional study was conducted on 157 patients aged under 4 months old with UTI. All subjects had paired urinalysis and urine culture, which were collected via transurethral catheterization. According to the results of their urinalysis, the patients were then classified as UTI cases with pyuria and UTI cases without pyuria. The clinical characteristics and outcomes of both groups were analyzed. Result: Among the 157 UTI patients, the prevalence of pyuria-negative UTI was 44%. Significant risk factors associated with pyuria-negative UTI included non-E.coli pathogens, younger age, shorter duration of fever prior to hospital visit, lower white blood cell (WBC) count upon hospital visit, and absence of microscopic hematuria. Conclusions: We found that non-E.coli uropathogens were the strongest factor related to pyuria-negative UTI. The absence of pyuria cannot exclude the diagnosis of UTI in young infants, and it’s reasonable to perform both urinalysis and urine culture as a part of the assessment of febrile or ill-looking young infants.

Abstract We implicated the X-chromosome THOC2 gene, which encodes the largest subunit of the highly-conserved TREX (Transcription-Export) complex, in a clinically complex neurodevelopmental disorder with intellectual disability as the core phenotype. To study the molecular pathology of this essential eukaryotic gene, we generated a mouse model based on a hypomorphic Thoc2 exon 37–38 deletion variant of a patient with ID, speech delay, hypotonia, and microcephaly. The Thoc2 exon 37–38 deletion male (Thoc2 Δ/Y ) mice recapitulate the core phenotypes of THOC2 syndrome including smaller size and weight, and significant deficits in spatial learning, working memory and sensorimotor functions. The Thoc2 Δ/Y mouse brain development is significantly impacted by compromised THOC2/TREX function resulting in R-loop accumulation, DNA damage and consequent cell death. Overall, we suggest that perturbed R-loop homeostasis, in stem cells and/or differentiated cells in mice and the patient, and DNA damage-associated functional alterations are at the root of THOC2 syndrome.

A comparison is presented on England's air quality management practices between rural and urban regions. Rural regions were found to face different challenges than those of urban areas, including airborne pollutants from sources outside rural boundaries, and a lack of history and experience in developing air quality management strategies.

BackgroundUrinary tract infection (UTI) is a potential cause of neonatal jaundice. Nevertheless, there remains a lack of consensus regarding appropriate screening practices for UTI in infants with hyperbilirubinemia. This study aimed to analyze a group of jaundiced infants to assess the prevalence of UTI, explore potential risk factors, and examine the impact of UTI on the course and severity of neonatal jaundice.MethodsThis retrospective case-control study was conducted on 150 jaundiced infants (aged

Traumatic brain injury (TBI) is associated with an increased risk of developing Parkinson’s disease (PD), though the exact mechanisms remain unclear. TBI triggers acute neuroinflammation and catecholamine dysfunction post-injury, both implicated in PD pathophysiology. The long-term impact on these pathways following TBI, however, remains uncertain. In this study, male Sprague-Dawley rats underwent sham surgery or Marmarou’s impact acceleration model to induce varying TBI severities: single mild TBI (mTBI), repetitive mild TBI (rmTBI), or moderate–severe TBI (msTBI). At 12 months post-injury, astrocyte reactivity (GFAP) and microglial levels (IBA1) were assessed in the striatum (STR), substantia nigra (SN), and prefrontal cortex (PFC) using immunohistochemistry. Key enzymes and receptors involved in catecholaminergic transmission were measured via Western blot within the same regions. Minimal changes in these markers were observed, regardless of initial injury severity. Following mTBI, elevated protein levels of dopamine D1 receptors (DRD1) were noted in the PFC, while msTBI resulted in increased alpha-2A adrenoceptors (ADRA2A) in the STR and decreased dopamine beta-hydroxylase (DβH) in the SN. Neuroinflammatory changes were subtle, with a reduced number of GFAP+ cells in the SN following msTBI. However, considering the potential for neurodegenerative outcomes to manifest decades after injury, longer post-injury intervals may be necessary to observe PD-relevant alterations within these systems.

IntroductionTraumatic brain injury (TBI) is now known to be a chronic disease, causing ongoing neurodegeneration and linked to increased risk of neurodegenerative motor diseases, such as Parkinson's disease and amyotrophic lateral sclerosis. While the presentation of motor deficits acutely following traumatic brain injury is well-documented, however, less is known about how these evolve in the long-term post-injury, or how the initial severity of injury affects these outcomes. The purpose of this review, therefore, was to examine objective assessment of chronic motor impairment across the spectrum of TBI in both preclinical and clinical models.MethodsPubMed, Embase, Scopus, and PsycINFO databases were searched with a search strategy containing key search terms for TBI and motor function. Original research articles reporting chronic motor outcomes with a clearly defined TBI severity (mild, repeated mild, moderate, moderate–severe, and severe) in an adult population were included.ResultsA total of 97 studies met the inclusion criteria, incorporating 62 preclinical and 35 clinical studies. Motor domains examined included neuroscore, gait, fine-motor, balance, and locomotion for preclinical studies and neuroscore, fine-motor, posture, and gait for clinical studies. There was little consensus among the articles presented, with extensive differences both in assessment methodology of the tests and parameters reported. In general, an effect of severity was seen, with more severe injury leading to persistent motor deficits, although subtle fine motor deficits were also seen clinically following repeated injury. Only six clinical studies investigated motor outcomes beyond 10 years post-injury and two preclinical studies to 18–24 months post-injury, and, as such, the interaction between a previous TBI and aging on motor performance is yet to be comprehensively examined.ConclusionFurther research is required to establish standardized motor assessment procedures to fully characterize chronic motor impairment across the spectrum of TBI with comprehensive outcomes and consistent protocols. Longitudinal studies investigating the same cohort over time are also a key for understanding the interaction between TBI and aging. This is particularly critical, given the risk of neurodegenerative motor disease development following TBI.