Culling of guinea pigs can provide a large number of animals per year for meat production, but little information is available in the scientific literature on the carcass characteristics and non-carcass components of these animals. The objective of this study was to evaluate the carcass and non-carcass characteristics of cull guinea pigs in comparison to their fattening counterparts. Forty-eight fattening (3 months-age, 24 females and 24 males) and forty-eight cull (14 months-age, 24 females and 24 males) guinea pigs were slaughtered and carcass yield, linear measurements, tissular composition, and non-carcass components were evaluated. In general, cull guinea pigs had higher carcass, tissue, and non-carcass component weights. Cull male and both female guinea pig groups had similar carcass yields. Cull animals had higher carcass and hind leg lengths, lumbar and thoracic circumferences, and carcass compactness than their young counterparts. However, a sex effect was found for leg compactness depending on whether they were fattened or cull. Tissue percentages values were similar between fattening and culling animals of the same sex. However, females had a higher percentage of fat tissue than males. Fattening females had the best muscle to bone ratio, followed by cull males. The non-carcass elements were more represented in fattening animals than in culls, probably due to an allometric growth of the viscera in relation to the rest of the body. In commercial and cooking terms, this information is valuable for producers and researchers who need to understand the factors that influence carcass characteristics of guinea pigs.

This study aimed to develop and evaluate a guinea pig model for glaucoma, comparing resultant eyeball enlargement with an existing myopia model. Thirty guinea pigs underwent intracameral injection of magnetic microspheres to induce chronic ocular hypertension (COH). Intraocular pressure (IOP) was systematically monitored, revealing a successful induction of COH in 73.33% of the guinea pigs. The mean IOP increased from a baseline of 18.04 ± 1.33 mmHg, reaching a peak at week 3 (36.31 ± 6.13 mmHg) and remaining elevated for at least 7 weeks. All data are presented as mean ± standard deviation of the mean. Subsequently, detailed assessments were conducted to validate the established glaucoma model. Immunofluorescent staining demonstrated a significant decrease in the density of retinal ganglion cells (RGC) in the glaucoma group. Optic disc excavation and notable thinning of the lamina cribrosa (LC) were observed. The quantity of optic nerve ax·ons in glaucoma group gradually decreased from baseline (44553 ± 3608/mm2) to week 4 (28687 ± 2071/mm2) and week 8 (17977 ± 3697/mm2). Moreover, regarding the global enlargement of eyeballs, both the transverse and longitudinal axis in glaucomatous eyes were found to be significantly larger than that in myopic eyes, particularly in the anterior chamber depth (1.758 ± 0.113 mm vs. 1.151 ± 0.046 mm). These findings indicate distinct patterns of structural changes associated with glaucoma and myopia in the guinea pig model. This guinea pig model holds promise for future research aimed at exploring biomechanical mechanisms, therapeutic interventions, and advancing our understanding of the relationship between glaucoma and myopia.

Obesity is a major risk factor for the development of life-threatening malignant ventricular tachyarrhythmias (VT) and sudden cardiac death (SCD). Risks may be highest for patients with high levels of the proinflammatory cytokine interleukin (IL)-6. We used our guinea pig model of high-fat diet (HFD)-induced arrhythmias that exhibit a heightened proinflammatory-like pathology, which is also observed in human obesity arrhythmias, as well as immunofluorescence and confocal microscopy approaches to evaluate the pathological IL-6 trans-signaling function and explore the underlying mechanisms. Using blind-stick and electrocardiogram (ECG) techniques, we tested the hypothesis that heightened IL-6 trans-signaling would exhibit increased ventricular arrhythmia/SCD incidence and underlying arrhythmia substrates. Remarkably, compared to low-fat diet (LFD)-fed controls, HFD promoted phosphorylation of the IL-6 signal transducer and activator of transcription 4 (STAT4), leading to its activation and enhanced nuclear translocation of pSTAT4/STAT4 compared to LFD controls and pSTAT3/STAT3 nuclear expression. Overactivation of IL-6 trans-signaling in guinea pigs prolonged the QT interval, which resulted in greater susceptibility to arrhythmias/SCD with isoproterenol challenge, as also observed with the downstream Janus kinase (JAK) 2 activator. These findings may have potentially profound implications for more effective arrhythmia therapy in the vulnerable obese patient population.

Experimental evidence suggests that chronic intermittent hypoxia (CIH), a major hallmark of obstructive sleep apnea (OSA), boosts carotid body (CB) responsiveness, thereby causing increased sympathetic activity, arterial and pulmonary hypertension, and cardiovascular disease. An enhanced circulatory chemoreflex, oxidative stress, and NO signaling appear to play important roles in these responses to CIH in rodents. Since the guinea pig has a hypofunctional CB (i.e., it is a natural CB knockout), in this study we used it as a model to investigate the CB dependence of the effects of CIH on pulmonary vascular responses, including those mediated by NO, by comparing them with those previously described in the rat. We have analyzed pulmonary artery pressure (PAP), the hypoxic pulmonary vasoconstriction (HPV) response, endothelial function both in vivo and in vitro, and vascular remodeling (intima-media thickness, collagen fiber content, and vessel lumen area). We demonstrate that 30 days of the exposure of guinea pigs to CIH (FiO2, 5% for 40 s, 30 cycles/h) induces pulmonary artery remodeling but does not alter endothelial function or the contractile response to phenylephrine (PE) in these arteries. In contrast, CIH exposure increased the systemic arterial pressure and enhanced the contractile response to PE while decreasing endothelium-dependent vasorelaxation to carbachol in the aorta without causing its remodeling. We conclude that since all of these effects are independent of CB sensitization, there must be other oxygen sensors, beyond the CB, with the capacity to alter the autonomic control of the heart and vascular function and structure in CIH.

UNASSIGNED: Swallowing impairment is a crucial issue that can lead to aspiration, pneumonia, and malnutrition. Animal models are useful to reveal pathophysiology and to facilitate development of new treatments for dysphagia caused by many diseases. The present study aimed to develop a new dysphagia model with reduced pharyngeal constriction during pharyngeal swallowing.
UNASSIGNED: We analyzed the dynamics of pharyngeal swallowing over time with the pharyngeal branches of the vagus nerve (Ph-X) bilaterally or unilaterally transected, using videofluoroscopic assessment of swallowing in guinea pigs. We also evaluated the detailed anatomy of the pharyngeal constrictor muscles after the denervation.
UNASSIGNED: Videofluoroscopic examination of swallowing showed a significant increase in the pharyngeal area during swallowing after bilateral and unilateral sectioning of the Ph-X. The videofluoroscopy also showed significantly higher pharyngeal transit duration for bilateral and unilateral section groups. The thyropharyngeal muscle on the sectioned side was significantly thinner than that on the intact side. In contrast, the thickness of the cricopharyngeal muscles on the sectioned and intact sides were not significantly different. The mean thickness of the bilateral thyropharyngeal muscles showed a linear correlation to the pharyngeal area and pharyngeal transit duration.
UNASSIGNED: Data obtained in this study suggest that denervation of the Ph-X could influence the strength of pharyngeal contraction during pharyngeal swallowing in relation to thickness of the pharyngeal constrictor muscles, resulting in a decrease in bolus speed. This experimental model may provide essential information (1) for the development of treatments for pharyngeal dysphagia and (2) on the mechanisms related to the recovery process, reinnervation, and nerve regeneration following injury and swallowing impairment possibly caused by medullary stroke, neuromuscular disease, or surgical damage from head and neck cancer.

The guinea pig in Ecuador is synonymous with our ancestral gastronomy and cultural tradition, but because of the diet rich in L-canavanine (alfalfa) that they receive; could limit its consumption in patients with primary immune thrombocytopenia (ITP). Ingestion of alfalfa in humans can cause kidney failure and lupus-like syndrome. The John Hopkins Lupus Center recommends avoiding it in the diet of patients with Systemic Lupus Erythematosus (SLE), as it aggravates inflammation by stimulating immune activity (flares). We present two cases of patients with ITP linked to guinea pig ingestion. It is probable
El cuy en el Ecuador es sinónimo de nuestra gastronomía ancestral y de tradición cultural, pero por la alimentación rica en L-canavanina (alfalfa) que reciben; podría limitar su consumo en pacientes con trombocitopenia inmune primaria (PTI). La ingesta de alfalfa en humanos puede propiciar insuficiencia renal y síndrome lupus-like.  El centro de Lupus John Hopkins recomiendan evitarla en la dieta de los pacientes con Lupus Eritematoso Sistémico (LES), al agravar la inflamación por estimulación de la actividad inmune (flares). Presentamos dos casos de pacientes con PTI vinculados con la ingesta de cuy.  ¿Es probable?

UNASSIGNED: Lactate measurements have been utilized as diagnostic and prognostic tools for a variety of veterinary species. Reference intervals for lactate have not been published or validated in guinea pigs.
UNASSIGNED: Whole blood from 48 anesthetized laboratory guinea pigs (46 Dunkin Hartley [38 males, eight females]; two Strain 13 [two males]) was analyzed using two point of care instruments (iSTAT and Lactate Plus). There were two consecutive timepoints on the iSTAT (iSTAT time 1 and time 2) and three consecutive timepoints on the Lactate Plus (Lactate Plus time 1, time 2, and time 3).
UNASSIGNED: There was agreement with no constant or proportional bias between the two instruments compared at equivalent timepoints (iSTAT time 1 and Lactate Plus time 3) as determined by Bland-Altman (bias: -0.19; 95% LoA: -0.55 to 0.16) and Deming linear regression analyses (slope: 1.092, 95% confidence intervals (CI): -0.9 to 1.29; y-intercept: 0.09, 95% CI: -0.12 to 0.30). Reference intervals for iSTAT time 1 were 0.49 to 1.83 mmol/L and Lactate Plus time 1 were 0.60 to. 2.2 mmol/L. There was a significant increase in lactate values from iSTAT time 1 to iSTAT time 2 and from Lactate Plus time 1 to Lactate Plus time 3.
UNASSIGNED: This study found strong agreement between the point of care instruments. Reference intervals for lactate for both the iSTAT and Lactate Plus instruments were similar to canine and feline intervals. Analysis should occur within 5 minutes of sample collection. Future work should assess lactate as a prognostic indicator in guinea pigs.

A well-developed heart is essential for embryonic survival. There are constant interactions between cardiac tissue motion and blood flow, which determine the heart shape itself. Hemodynamic forces are a powerful stimulus for cardiac growth and differentiation. Therefore, it is particularly interesting to investigate how the blood flows through the heart and how hemodynamics is linked to a particular species and its development, including human. The appropriate patterns and magnitude of hemodynamic stresses are necessary for the proper formation of cardiac structures, and hemodynamic perturbations have been found to cause malformations via identifiable mechanobiological molecular pathways. There are significant differences in cardiac hemodynamics among vertebrate species, which go hand in hand with the presence of specific anatomical structures. However, strong similarities during development suggest a common pattern for cardiac hemodynamics in human adults. In the human fetal heart, hemodynamic abnormalities during gestation are known to progress to congenital heart malformations by birth. In this chapter, we discuss the current state of the knowledge of the prenatal cardiac hemodynamics, as discovered through small and large animal models, as well as from clinical investigations, with parallels gathered from the poikilotherm vertebrates that emulate some hemodynamically significant human congenital heart diseases.

OBJECTIVE: Alzheimer\'s disease (AD) is the most common form of dementia. However, while 150+ animal models of AD exist, drug translation from preclinical models to humans for treatment usually fails. One factor contributing to low translation is likely the absence of neurodegenerative models that also encompass the multi-morbidities of human aging. We previously demonstrated that, in comparison to the PigmEnTed (PET) guinea pig strain which models \"typical\" brain aging, the Hartley strain develops hallmarks of AD like aging humans. Hartleys also exhibit age-related impairments in cartilage and skeletal muscle. Impaired mitochondrial respiration is one driver of both cellular aging and AD. In humans with cognitive decline, diminished skeletal muscle and brain respiratory control occurs in parallel. We previously reported age-related declines in skeletal muscle mitochondrial respiration in Hartleys. It is unknown if there is concomitant mitochondrial dysfunction in the brain.
METHODS: Therefore, we assessed hippocampal mitochondrial respiration in 5- and 12-month Hartley and PET guinea pigs using high-resolution respirometry.
RESULTS: At 12 months, PETs had higher complex I supported mitochondrial respiration paralleling their increase in body mass compared to 5 months PETs. Hartleys were also heavier at 12 months compared to 5 months but did not have higher complex I respiration. Compared to 5 months Hartleys, 12 months Hartleys had lower complex I mitochondrial efficiency and compensatory increases in mitochondrial proteins collectively suggesting mitochondrial dysfunction with age.
CONCLUSIONS: Therefore, Hartleys might be a relevant model to test promising therapies targeting mitochondria to slow brain aging and AD progression.

BACKGROUND: Recombinant human Interleukin receptor antagonist (rhIL-Ra) can bind to the IL-1 receptor on the cell membrane and reversibly blocks the proinflammatory signaling pathway. However, its effect on allergic rhinitis (AR) and the underlying mechanism remains unknown. This study aims to investigate the efficacy of recombinant human interleukin-1 receptor antagonist (rhIL-1Ra) on AR guinea pigs.
METHODS: Guinea pigs were systemically sensitized by intraperitoneal injection and topical intranasal instillation with ovalbumin within 21 days. Animals administrated with saline served as the normal control. The AR animals were randomly divided into the model group and distinct concentrations of rhIL-1Ra and budesonide treatment groups. IL-1β and ovalbumin specific IgE levels were detected by ELISA kits. Nasal mucosa tissues were stained with hematoxylin & eosin (HE) for histological examination.
RESULTS: It was found that the numbers of sneezing and nose rubbing were remarkably reduced in rhIL-1Ra and budesonide-treated guinea pigs. Besides, rhIL-1Ra distinctly alleviated IgE levels in serum and IL-1β levels in nasal mucus, together with decreased exfoliation of epithelial cells, eosinophilic infiltration, tissue edema and vascular dilatation.
CONCLUSIONS: rhIL-1Ra is effective in AR guinea pigs and may provide a novel potential choice for AR treatments.