30 research outputs found
Human Placenta Extract Therapy for Feline Hepatic Lipidosis
Feline hepatic lipidosis (HL), the most common hepatobiliary disease in cats, is characterized by the accumulation of excessive triglycerides (TGs) in more than 80% of hepatocytes. Forced oral feeding is recommended as the only therapy for this disease but the prognosis is often poor. As human placenta extract (Laennec) has been used to improve hepatic metabolism, we investigated the efficacy of this drug for the treatment of cats with HL. Ten cats diagnosed with HL in this study were treated with Laennec as a therapeutic drug. An immediate improvement in clinical symptoms was observed in all 10 cases. A statistical analysis indicated that the blood level of ALT (P = 0.029), AST (P = 0.029), ALP (P = 0.005), and T-Bil (P = 0.012) decreased significantly after treatment. All 7 hospitalized cases were eventually discharged from the hospital with a mean hospitalization duration of 4.8 days. The results of this study suggest that Laennec preparation has potential as an effective medicine for feline HL
Screening of bacterial DNA in bile sampled from healthy dogs and dogs suffering from liver- or gallbladder-associated disease
Although the biliary system is generally aseptic, gallbladder microbiota has been reported in humans and some animals apart from dogs. We screened and analyzed the bacterial deoxyribonucleic acid in canine gallbladders using bile sampled from 7 healthy dogs and 52 dogs with liver- or gallbladder-associated disease. PCR screening detected bacteria in 17.3% of diseased dogs (9/52) and none in healthy dogs. Microbiota analysis of PCR-positive samples showed that the microbial diversity differed between liver- and gallbladder-associated disease groups. Thus, a specific bacterial community appears to occur at a certain frequency in the bile of diseased dogs
Clinicopathological Findings and Prognosis in Canine Cases Diagnosed As Primary Hypoplasia of the Portal Vein
Presumptive precursor-targeted immune-mediated anemia concurrent with gastrointestinal lymphoma in a cat
Clinicopathological Findings and Prognosis in Canine Cases Diagnosed As Primary Hypoplasia of the Portal Vein
Canine primary hypoplasia of the portal vein (PHPV) is a microscopic malformation of the hepatic vasculature. The prevalence, clinical signs, and clinicopathological findings of PHPV in dogs are unclear, because there are few reports concerning PHPV in the veterinary literature. This retrospective study reviewed clinical records and liver biopsy data from 48 dogs with hepatic disease that were examined at a private veterinary hospital in Japan between April 2011 and March 2014 to determine the prevalence of PHPV among dogs that underwent liver biopsy and to determine the clinical and clinicopathological findings of PHPV in dogs. Records for all 48 dogs that underwent liver biopsy were investigated. Collected data included signalment, clinical signs, physical examination findings, complete blood cell count, chemistry results, pre-and postprandial serum total bile acid concentrations, coagulation profiles (prothrombin time, activated partial thromboplastin time, fibrinogen, and antithrombin), and abdominal ultrasonography findings at the first medical examination. The diagnosis of PHPV was made on the basis of histological examination of hepatic biopsy specimens and portography or CT angiography. Among the 48 canine cases, 28 dogs (58.3%) were diagnosed with PHPV, which was the most common diagnosis. The most frequent clinical sign in dogs with PHPV was asymptomatic persistently increased liver enzymes (57.1%). Toy poodles were at a significantly higher risk of PHPV than other breeds among dogs that underwent liver biopsy (P < 0.001). The median survival time of dogs with PHPV was more than 5 years. Plasma fibrinogen concentration below the reference range was an indicator of PHPV in this study. Dogs with PHPV frequently had mild clinical signs and a favorable prognosis
Age-related change of the plasma fibrinogen concentration in dogs
The aim of the present study was to investigate whether canine plasma fibrinogen concentration changes with age. We also investigated sex differences in the plasma fibrinogen concentration. As a result, the plasma fibrinogen concentration was found to moderately increase with age (Spearman's r = 0.55, P < 0.001), whereas that of the male and female dogs did not differ to a statistically significant extent. This finding suggests the need to consider aging as a factor that affects the plasma fibrinogen concentration
Analysis of the Disease Potential of a Recombinant Retrovirus Containing Friend Murine Leukemia Virus Sequences and a Unique Long Terminal Repeat from Feline Leukemia Virus
We have molecularly cloned a feline leukemia virus (FeLV) (clone 33) from a domestic cat with acute myeloid leukemia (AML). The long terminal repeat (LTR) of this virus, like the LTRs present in FeLV proviruses from other cats with AML, contains an unusual structure in its U3 region upstream of the enhancer (URE) consisting of three tandem direct repeats of 47 bp. To test the disease potential and specificity of this unique FeLV LTR, we replaced the U3 region of the LTR of the erythroleukemia-inducing Friend murine leukemia virus (F-MuLV) with that of FeLV clone 33. When the resulting virus, F33V, was injected into newborn mice, almost all of the mice eventually developed hematopoietic malignancies, with a significant percentage being in the myeloid lineage. This is in contrast to mice injected with an F-MuLV recombinant containing the U3 region of another FeLV that lacks repetitive URE sequences, none of which developed myeloid malignancies. Examination of tumor proviruses from F33V-infected mice failed to detect any changes in FeLV U3 sequences other than that in the URE. Like F-MuLV-infected mice, those infected with the F-MuLV/FeLV recombinants were able to generate and replicate mink cell focus-inducing viruses. Our studies are consistent with the idea that the presence of repetitive sequences upstream of the enhancer in the LTR of FeLV may favor the activation of this promoter in myeloid cells and contribute to the development of malignancies in this hematopoietic lineage