Cristofer Zarate-Calderon

Objective: We aimed to determine whether sexual experience modulates the soleus H-reflex in male rats and to assess the specific contribution of vermis lobules 6a and 7 to cerebellar-dependent spinal plasticity. Methods: Thirty-six male Wistar rats were divided into sexually inexperienced (SI) and sexually experienced (SE) groups and assigned to one of three cerebellar conditions: intact control, lobule 6a lesion, or lobule 7 lesion. SE rats underwent repeated mating sessions until they achieved efficient copulatory performance. Subsequently, targeted electrolytic lesions were made, and electromyographic recordings of the soleus H-reflex were obtained under urethane anesthesia to quantify H-wave amplitude and temporal parameters. Results: The global linear mixed model yielded no significant main effects of sexual experience, cerebellar condition, or their interaction on H-wave amplitude. Planned contrasts revealed a near-significant trend toward higher H-wave amplitude in sexually experienced intact animals compared with inexperienced controls (p = 0.061, Cohen’s d = 0.592, 95% CI [−1.44, 0.04] V), and significant amplitude reductions following lobule 6a (p = 0.029, d = 1.450, 95% CI [0.13, 2.33] V) and lobule 7 (p = 0.002, d = 2.256, 95% CI [0.74, 3.08] V) lesions specifically in sexually experienced animals. Neither sexual experience nor lesions significantly affected H-wave latency or duration, suggesting that modulation primarily targets synaptic excitability rather than axonal conduction. M-wave latency showed a significant effect of sexual experience (p = 0.026, d = 1.405, 95% CI [0.03, 0.45] ms). Conclusions: Sexual experience appears to be associated with cerebellar-dependent modulation of soleus H-reflex excitability; lobules 6a and 7 of the cerebellar vermis contribute to this effect specifically in experienced animals. Shorter M-wave latency in experienced animals suggests parallel peripheral motor reorganization. Adequately powered confirmatory studies are needed to characterize the mechanisms underlying this association.

Background: Iron overload cardiomyopathy (IOC) is a major determinant of outcomes in hemochromatosis, and conventional echocardiography may miss early myocardial toxicity. Comparative data on primary (PH) versus secondary hemochromatosis (SH) using myocardial work (MW) indices are limited. Methods: We performed a retrospective cross-sectional study of 34 adults (16 PH and 18 SH patients) at a tertiary center. They all underwent echocardiography with speckle-tracking to obtain LV global longitudinal strain (GLS) and non-invasive MW indices from pressure-strain loops: global work index (GWI), global constructive work (GCW), global wasted work (GWW), and global work efficiency (GWE). Echocardiographic phenotypes were classified as a Normal, Dilated, Restrictive, or right ventricular/pulmonary hypertension (RVPH) phenotype. Results: SH patients showed higher iron burden and neurohormonal activation than PH patients (maximum ferritin 2954 vs. 444 ng/mL; BNP 93 vs. 13.5 pg/mL; both p < 0.001) and accounted for all deaths (33% vs. 0%) despite similar 3D LVEFs and GLSs. PH patients predominantly exhibited Normal phenotypes (81%), whereas SH patients more often showed advanced phenotypes, mainly RVPH and Dilated. GWI correlated inversely with ferritin (ρ ≈ −0.40), particularly ferritin at echocardiography in SH patients, while PH patients showed no significant correlations. GWW was higher in Dilated/RVPH compared to Normal phenotypes, and in SH patients, higher maximum ferritin was associated with impaired right ventricular free-wall strain. Conclusions: PH and SH patients exhibit distinct IOC phenotypes, with SH patients showing more advanced remodeling and worse outcomes. In this exploratory analysis, MW indices showed modest associations with iron burden markers, suggesting they may provide complementary information beyond LVEF and GLS. These preliminary findings require validation in larger, prospective studies.

Parkinsonian symptoms such as tremors, rigidity, bradykinesia, and postural instability typically arise from basal ganglia dysfunction, but growing evidence suggests cerebellar circuits also play a key role. Here, we investigated multiunit activity (MUA) in the inferior olive (IO), dentate nucleus (DN), and Crus II of the cerebellum in a rat model of tract lesion-induced parkinsonism triggered by ventrolateral striatum (VLS) injury. Thirty-six male Wistar rats were divided into a Lesion group and an Intact group. Monopolar electrodes were implanted to record MUA in IO, DN, or Crus II for four consecutive weeks. Basal and tremor-associated signals were analyzed using generalized linear models and post hoc comparisons. In rats with VLS lesions, IO activity initially increased and then declined over time, whereas DN activity remained consistently elevated, suggesting compensatory upregulation. Crus II showed no significant shifts in baseline activity. During tremor episodes, all three structures exhibited distinct temporal fluctuations in MUA. These findings reveal cerebellar structure-specific responses to striatal injury and highlight the cerebellum’s role in both the acute and chronic phases of Parkinsonian motor dysfunction. Careful consideration of possible inflammatory responses to electrode implantation remains essential for future studies.

Background: Keloid scarring is a fibroproliferative disorder driven by a complex interplay of genetic, epigenetic, and environmental factors, resulting in significant cosmetic and functional impairment. Despite its high prevalence in African, Asian, and Hispanic populations, the molecular mechanisms underlying ancestry-dependent susceptibility remain incompletely understood. Methods: This narrative review synthesizes current genomic, epigenetic, and multi-omic evidence related to keloid scarring. Relevant literature was identified through a targeted, structured, non-systematic search of PubMed, Scopus, Web of Science, SciELO, and Google Scholar up to August 2025, focusing on genetic susceptibility loci, epigenetic regulation, and ancestry-related differences. PRISMA-ScR guidelines were used as a reporting framework to enhance transparency, without implying a formal systematic review methodology. Results: This synthesis identifies recurrent susceptibility loci at 1q41, 3q22.3, and 15q21.3 across multiple populations. Variants in NEDD4 and regulatory regions near BMP2 emerge as key modulators of profibrotic signaling pathways, including TGF-β/SMAD and NF-κB. Additionally, epigenetic reprogramming and long non-coding RNA networks, such as CACNA1G-AS1, appear to sustain fibroblast hyperactivation. A persistent limitation is the marked underrepresentation of Latin American populations in current genomic studies. Conclusions: Integrating ancestry-specific genomic variation with epigenetic markers is essential for advancing precision diagnostic and therapeutic strategies in keloid scarring. Future research should prioritize diverse, multicenter cohorts and integrative multi-omics approaches to improve risk stratification and enable targeted interventions for this disfiguring condition.

Background: Parkinsonism entails pronounced basal ganglia dysfunction, but emerging research suggests that broader subcortical networks, specifically the cerebellum, play a vital role in functional motor compensation following circuit-level destabilization. This study sought to characterize the electrophysiological dynamics of Multi-Unit Activity (MUA) amplitude in Crus II, the dentate nucleus (DN), and the inferior olive (IO) following a focal mechanical lesion of the ventrolateral striatum (VLS) as a circuit-level perturbation model during spontaneous behaviors. Methods: Bilateral mechanical VLS lesions were induced in 24 male Wistar rats. MUA signals were chronically recorded over a four-week protocol during self-grooming, horizontal locomotion, and rearing behaviors. Results: Crus II and the IO exhibited a structure-specific “dynamic transition,” shifting from early-stage hyperexcitability to significant late-stage attenuation by W4 (p < 0.001), reflecting a divergence from control trajectories rather than internal temporal drift within the lesioned state. Conversely, the DN showed sustained hypoactivity compared to healthy controls throughout the recording period (p < 0.05). Despite these robust neurophysiological shifts, the syntactic organization of grooming and exploratory patterns remained phenotypically preserved, indicating functional sufficiency despite underlying circuit noise. Conclusions: VLS injury triggers a rapid distributed reorganization across the striato-cerebellar network. The cerebellum acts as an active adaptive node, recalibrating internal network gain to mask early Parkinsonian-like circuit dysfunction at the level of functional sufficiency and maintain motor performance through active homeostatic gain regulation.

Background: Neuropathic pain represents a substantial global burden with limited effective therapeutic options. Pulsed Electromagnetic Field (PEMF) therapy has emerged as a potential non-invasive adjuvant, though clinical evidence remains inconsistent. This systematic review and meta-analysis evaluated PEMF efficacy and safety, specifically analyzing the influence of etiology and stimulation parameters. Methods: Following PRISMA 2020 guidelines (PROSPERO: CRD420251184151), five databases (Cochrane, PubMed, Scopus, Web of Science, and LILACS) were searched for Randomized Controlled Trials (RCTs) comparing PEMF versus sham. Risk of bias was assessed via Cochrane RoB 2, and heterogeneity was explored through detailed subgroup analyses. Results: Thirteen RCTs met the inclusion criteria (N = 688). While global analysis indicated a statistically significant pain reduction (SMD: −1.01; p = 0.03), it exhibited extreme statistical heterogeneity (I² = 92.8%) and instability. After adjusting for missing studies using the Trim-and-Fill method, global significance disappeared. However, subgroup analysis resolved this inconsistency, revealing a massive, clinically meaningful effect in Spinal/Radicular pain (SMD: −2.35; 95% CI: −4.42 to −0.29), whereas Peripheral Neuropathy showed no significant reduction (SMD: −0.38; 95% CI: −0.86 to 0.10). Conclusions: The PEMF evidence base for neuropathic pain is currently highly fragmented. Extreme heterogeneity and publication bias render “one-size-fits-all” efficacy estimates invalid and potentially misleading. Instead, our data reveals a critical etiological divergence: PEMF appears highly effective for spinal/radicular pathology, likely due to the mechanical nature of the lesion, but demonstrates limited efficacy for diffuse peripheral neuropathy. Future research must abandon generic protocols in favor of etiology-specific trials, prioritizing high-frequency parameters and rigorous bias control.

In the original publication, there was a mistake in the legend for Table 1

Background: Parkinsonism, characterized by motor symptoms, is typically attributed to basal ganglia dysfunction. Recent evidence suggests that the cerebellum may also influence these symptoms. This study investigated Crus II, the dentate nucleus (DN), and the inferior olive (IO) in a rat model of parkinsonism induced by a bilateral ventrolateral striatal (VLS) lesion. Materials and Methods: Twenty-four male Wistar rats were divided into control (n = 12) and experimental (n = 12) groups. Monopolar electrodes were implanted in target structures. The experimental group received a bilateral VLS lesion. Animals underwent four weekly sessions of electrophysiological recordings and blind behavioral assessments (resting, grooming, locomotion, rearing, sniffing) via video tracking. Power spectral density (PSD) in the 300–500 Hz band was computed. Statistical analyses included Mann–Whitney U, Friedman with Wilcoxon post hoc, and Spearman correlation tests. Results: During weeks one and two, there were significant PSD increases in the experimental group compared to the control, particularly in Crus II—grooming (p = 0.005), locomotion (p = 0.007), and rearing (p = 0.026); in IO—sniffing (p = 0.0167); and in DN—grooming (p < 0.001) and locomotion (p = 0.0008). Additionally, intragroup analysis revealed significant PSD elevations relative to baseline in these structures. Significant correlations were observed only for grooming (negative correlations) and sniffing (positive correlations) across all cerebellar regions. Conclusions: These findings suggest compensatory cerebellar hyperactivity induced by VLS lesion, potentially modulating hypokinetic symptoms and highlighting dynamic network interactions. Interpretation warrants caution due to limitations inherent to the acute lesion model and experimental duration.

BACKGROUND AND OBJECTIVES: The greater occipital nerve (GON) and lesser occipital nerve (LON) have gained importance because of conditions such as occipital neuralgia and cervicogenic headaches. To a great depth, their anatomy is essential for performing viable diagnostic and therapeutic procedures such as nerve blocks and decompression procedures. This research involves identifying key anatomic landmarks and the potential compression points of the GON and LON using cadaveric dissections for possible surgical approaches. METHODS: Five fresh, untreated cadavers, 3 male and 2 female, were dissected bilaterally to trace the pathways of the GON and LON. Anatomic measurements were made using ImageJ software, and coordinates were analyzed with K-means clustering for optimal intervention points. These dissections focused on determining in detail the relation of these nerves to surrounding muscular and fascial structures. RESULTS: The study shows that for GON, there were many points possible for compression, such as where it pierced through the semispinalis and trapezius muscles along the course of the occipital artery. For the LON, however, the potential compression sites were contact points along the course of the occipital artery. After applying K-means clustering, 4 centroids (M1, M2, M3, and M4) were identified. M1 and M3 correspond to the LON, while M2 and M4 correspond to the GON. These centroid locations lie near the nerves' most common compression sites, suggesting they could serve as strategic landmarks for surgical approaches. Cluster quality measures (inertia and silhouette coefficients) showed well-defined clusters. CONCLUSION: This study yields anatomic information about the GON and LON anatomy and illustrates key compression points and optimal sites for therapeutic interventions. Within the constraints of sample size, these findings provide preliminary anatomic insights that can guide more precise nerve block and decompression techniques for occipital neuralgia and related headaches.