C-reactive protein (CRP) is an acute-phase protein produced by hepatocytes. The plasma concentration of CRP peaks around 48 hours following stimulation. A rapid decrease in CRP levels is observed when the stimuli end. Considering these characteristics of CRP, it is used to evaluate acute inflammatory responses in clinics. In addition, as it reflects the degree of surgical trauma, measuring the CRP concentration is an effective method of evaluating tissue damage depending upon the surgical method. As CRP is also an acute-phase protein in dogs, the purpose of the present study was to compare the factors related to acute inflammatory responses between dogs undergoing elective general surgery (GS) and orthopedic surgery (OS). A total of 44 healthy dogs were included in this study. The sex ratio of dogs that underwent OS was similar. Both groups showed increased CRP levels and white blood cell (WBC) counts on post-operative day (POD) 1-2. The CRP level in the OS group on POD 1-2 was significantly higher than that of the GS group and it was increased about 16-fold compared to the pre-operative value. No significant difference in WBC counts was observed between the two groups. Although a slight increase in the WBC count was observed on POD 1-2 in both groups, it was near the reference range during follow-up. Thus, measuring CRP levels can be more effective in evaluating acute inflammatory responses than WBC counts. Although a high level of post-operative serum CRP concentrations was observed in the OS group, it rapidly decreased to a level similar to the pre-operative value if there were no post-operative complications.

Colon cancer has been considered a leading cause of cancer-associated death. Folic acid is a vitamin necessary for cellular physiological functions and cell viability. However, the association between folic acid intake and colon cancer has been examined in several prospective cohort studies are controversial. This study investigated the effects of folate intake on colon carcinogenesis and oxidative stress in an azoxymethane (AOM)/dextran sodium sulfate (DSS) institute for cancer research (ICR) mouse model. Thirty male ICR mice (5 weeks old) were divided into the control group and the experimental group supplied 0.03% folic acid via drinking water (50 mL/week/mouse) for 6 weeks. To induce colonic pre-neoplastic lesions, the animals were subcutaneously injected three times weekly with AOM (10 mg/kg body weight), followed by 2% DSS in drinking water for a week. Folic acid supplementation significantly suppressed the total number of aberrant crypt foci and aberrant crypts. Histological image data showed that folic acid supplementation attenuated neoplastic change. In addition, we measured the thiobarbituric acid reactive substances concentration of dry feces samples to identify the effect of folic acid on reactive oxygen accumulation. The folic acid supplementation group had reduced reactive oxygen species levels in dry feces compared to the control group. In conclusion, these findings indicate that folic acid suppresses colon carcinogenesis and oxidative stress in an AOM/DSS mouse model.

Alzheimer’s disease (AD) is an irreversible and progressive neurodegenerative disease accompanied by aging, followed by memory impairment and cognitive decline. Although numerous attempts have been made to develop treatments for AD, most clinical trials have failed to delay or stop the progression of AD. Electroacupuncture (EA) is a complementary alternative medicine technique widely used to treat pain, inflammation, and neurodegenerative diseases. Additionally, blood-brain barrier (BBB) disruption is a known pathophysiology of neurodegenerative diseases, including AD. Moreover, amyloid beta deposition increases BBB permeability and produces inflammatory cytokines induced by glial activation. However, our previous study revealed that EA treatment at the Taegye acupoints (KI3) improves memory impairment through anti-neuroinflammation and increases glucose metabolism in 5XFAD mice. Therefore, we evaluated whether EA treatment at KI3 regulates BBB dysfunction in the prefrontal cortex of 5XFAD mice. For this study, 6.5-month-old 5XFAD mice were treated with EA stimulation at KI3 three times a week for two weeks. Western blotting, immunohistochemistry, and flow cytometry were used to evaluate the effects of EA treatment on BBB dysfunction. We found that EA stimulation attenuates BBB integrity by protecting BBB tight junction proteins (CD31, aquaporin 4, occludin, and claudin 5) in the prefrontal cortex of 5XFAD mice. In addition, EA treatment regulated inflammatory cytokines (IL-1α, IL-1β, IL-17, IL-23, IFN-ɣ, monocyte chemoattractant protein 1 (MCP-1), granulocyte-macrophage colony stimulating factors [GM-CSF], and IL-10) in the peripheral circulation of 5XFAD mice. Therefore, our data suggest that EA treatment could be a therapeutic agent for enhancing BBB dysfunction in AD.

Naturally occurring left ventricular hyperplasia is a rare but lethal disease. There are very few reports of this cardiac disease in captive nonhuman primates. In a colony of Macaca mulatta (Rhesus monkey) at California National Primate Research Center, a large number of rhesus macaques were diagnosed by autopsy with naturally occurring left ventricular hypertrophy without obvious underlying diseases over a 22-year period. The confirmatory diagnosis of ventricular hypertrophy was based on findings of notable left ventricular concentric hypertrophy with reduced left ventricular lumen, which is very similar to human ventricular hypertrophy cases. This report discusses an 11-year-old Macaca fascicularis monkey (Cynomolgus monkey, crab-eating macaque), weighing 2.95 kg, that was presented for enrollment in a pharmacokinetic (PK) study. During the PK experiment, the monkey died following a sudden decrease in percutaneous oxygen saturation and heart rate. Gross and histological examinations of the heart were performed. On gross pathology, the left ventricular wall was thickened, and the chamber lumen was reduced. In histopathological examination using hematoxylin- eosin and Masson-trichrome stains, fibrosis and myocyte disarray were not observed, but an increased cell density, compared to the normal heart, was confirmed. The autopsy results confirmed left ventricular hyperplasia as the major cause of death.

A 19-year-old male Siberian tiger was presented with inappetence and paralysis of hind limbs. In a computed tomography (CT) scan, intervertebral disk disease at L3–L4 was detected. Cardiac arrest occurred during the surgery. At autopsy, myxomatous mitral valve degeneration (MMVD) and eccentric hypertrophy of the left heart were noted. The diagnosis was congestive heart failure caused by MMVD. Microscopically, myocardial and pulmonary fibrosis were observed in addition to the disintegration of the fibrosa layer and accumulation of glycosaminoglycans and proteoglycans in the spongiosa layer of the mitral valve. This is the first case of congestive heart failure with MMVD in a Siberian tiger.