POTENTIAL ROLE OF WHOLE-BODY HYPERTHERMIA TO TREAT LYME DISEASE

1995 ◽  
Vol 88 ◽  
pp. S142
Author(s):  
L. M. Shecterle ◽  
P. Gasper ◽  
J. A. St. Cyr. Jacqmar
Pathogens ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1193
Author(s):  
Andrea De Bonis ◽  
Mariasole Colombo ◽  
Rossella Terragni ◽  
Barbara Bacci ◽  
Simone Morelli ◽  
...  

Canine hepatozoonosis caused by Hepatozoon canis is an emerging disease in Europe. Clinical pictures vary from subclinical to life-threatening and non-specific clinical signs are predominantly reported. A 2-month-old female puppy originating from Southern Italy was adopted and moved to Northern Italy. Then, the dog was brought to a local veterinary practice for gastrointestinal signs, migrating lameness and pruritic dermatitis, and then tested positive for Hepatozoon spp. gamonts at the blood smear. After treatment with imidocarb dipropionate and doxycycline, the dog showed an initial clinical improvement. However, gastrointestinal signs recurred, and diffuse superficial pyoderma appeared on the thoracolumbar region, along with fever, lethargy, and weight loss. Eight months from the first onset of clinical signs, the dog was referred to a veterinary clinic and subjected to complete blood count, urine and fecal analysis, along with abdominal ultrasonography, whole-body CT and gastroduodenal endoscopy. Skin biopsies and blood samples were subjected to a PCR-coupled sequencing protocol, which scored both positive for H. canis. Alterations were consistent with a pre-existing cholangiohepatitis and multiple acquired extrahepatic shunts secondary to portal hypertension. The dog was euthanatized due to a clinical worsening two months later. The potential role of H. canis in the systemic disease observed, clinic-pathological findings and epizootiological implications are discussed.


2021 ◽  
Author(s):  
Natalie J Haywood ◽  
Katherine I Bridge ◽  
Cheukyau Luk ◽  
Nele Warmke ◽  
Katie J Simmons ◽  
...  

SummaryThere are at least two distinct types of thermogenic adipocyte in mammals: a pre-existing form established during development, termed classical brown adipocytes and an inducible form, ‘beige’ adipocytes1–3. Various environmental cues can stimulate a process frequently referred to as ‘beiging’ of white adipose tissue (WAT), leading to enhanced thermogenesis and obesity resistance 4, 5. Whilst beiging of WAT as a therapeutic goal for obesity and obesity-related complications has attracted much attention6–9; therapeutics stimulating beiging without deleterious side-effects remain elusive10. The endothelium lines all blood vessels and is therefore in close proximity to all cells. Many studies support the possibility that the endothelium acts as a paracrine organ11–14. We explored the potential role of endothelial insulin-like growth factor-1 receptor (IGF-1R) as a paracrine modulator of WAT phenotype. Here we show that a reduction in endothelial IGF-1R expression in the presence of nutrient excess leads to white adipocyte beiging, increases whole-body energy expenditure and enhances insulin sensitivity via a non-cell autonomous paracrine mechanism. We demonstrate that this is mediated by endothelial release of malonic acid, which we show, using prodrug analogues, has potentially therapeutically-relevant properties in the treatment of metabolic disease.


1995 ◽  
Vol 118 (5) ◽  
pp. 1021-1029 ◽  
Author(s):  
T. Konishi ◽  
M. Nomoto ◽  
K. Shimizu ◽  
T. Abe ◽  
H. Itoh ◽  
...  

Author(s):  
H. Bender ◽  
J. P. Frohmann ◽  
M. Grapow ◽  
A. Schomburg ◽  
H-J. Biersack

1993 ◽  
Vol 2 (3) ◽  
pp. 225-228 ◽  
Author(s):  
E. Mayatepek ◽  
D. Hassler ◽  
M. Maiwald

The purpose of this study was to evaluate the potential role of LTB4and cysteinyl leukotrienes in Lyme disease (LD). Therefore, a total number of 34 patients divided into four groups was studied. The patients were classified as having Lyme arthritis (n = 7) or Lyme meningitis (n = 10), and as control groups patients with a noninflammatory arthropathy (NIA) (n = 7) and healthy subjects (n = 10). LTB4as well as LTC4secretion from stimulated polymorphonuclear leukocytes (PMNL) from all groups of patients showed no statistical differences. LTB4levels in synovial fluid were significantly increased in patients with Lyme arthritis (median 142 ng/ml, range 88–296) when compared to the control subjects with NIA (median 46 ng/ml, range 28–72) (p < 0.05). No statistical difference of urinary LTE4levels between all the different groups of patients was observed. These results show that cysteinyl leukotrienes do not play an important role in the pathogenesis of LD. In contrast to previous findings in rheumatoid arthritis, LTB4production from stimulated PMNL was not found to be increased in LD. However, the significantly elevated levels of LTB4in synovial fluid of patients with Lyme arthritis underline the involvement of LTB4in the pathogenesis of this disease.


1993 ◽  
Vol 264 (5) ◽  
pp. H1355-H1359 ◽  
Author(s):  
W. F. Taylor ◽  
V. S. Bishop

We have shown previously that an increase in ear blood flow velocity (EBF) in the conscious, chronically instrumented rabbit during whole body heating (WBH) involves active neurogenic vasodilation that is abolished by local nerve block. This study was designed to test the potential role of nitric oxide (NO) in rabbit ear neurogenic vasodilation during hyperthermia. Rabbits were instrumented for the measurement of arterial pressure, heart rate, and EBF (Doppler ultrasound). A catheter was also placed in the left lingual artery for administration of drugs to the left ear. WBH was achieved by circulating warm water through a rubber pad placed around the rabbit. Internal temperature was measured with a rectal thermocouple. During WBH, bolus injections of N omega-nitro-L-arginine (L-NNA), a false substrate for the formation of NO, were given via the lingual artery (10(-5) M, 4-5 ml total) to determine whether NO was involved in the increase in EBF. During WBH, left ear vascular conductance (EVC) increased from 0.07 +/- 0.03 to 5.87 +/- 0.73 kHz/100 mmHg and right EVC from 0.20 +/- 0.13 to 4.49 +/- 1.73 kHz/100 mmHg. When EVC was maximum, L-NNA was administered into the left lingual artery. EVC began to decrease after a latency of 23 min. At 56 +/- 8 min, left and right EVC had decreased to 0.18 +/- 0.10 and 0.23 +/- 0.11 kHz/100 mmHg, respectively (P < 0.05). Subsequent infusions of L-arginine, the true substrate for NO formation, restored EVC. These results suggest that NO is involved in active vasodilation during heating in the rabbit ear.


Vaccines ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 43
Author(s):  
Tina Y. Poussaint ◽  
Kerri L. LaRovere ◽  
Jane W. Newburger ◽  
Janet Chou ◽  
Lise E. Nigrovic ◽  
...  

A 12-year-old male was presented to the hospital with acute encephalopathy, headache, vomiting, diarrhea, and elevated troponin after recent COVID-19 vaccination. Two days prior to admission and before symptom onset, he received the second dose of the Pfizer-BioNTech COVID-19 vaccine. Symptoms developed within 24 h with worsening neurologic symptoms, necessitating admission to the pediatric intensive care unit. Brain magnetic resonance imaging within 16 h of admission revealed a cytotoxic splenial lesion of the corpus callosum (CLOCC). Nineteen days prior to admission, he developed erythema migrans, and completed an amoxicillin treatment course for clinical Lyme disease. However, Lyme antibody titers were negative on admission and nine days later, making active Lyme disease an unlikely explanation for his presentation to hospital. An extensive workup for other etiologies on cerebrospinal fluid and blood samples was negative, including infectious and autoimmune causes and known immune deficiencies. Three weeks after hospital discharge, all of his symptoms had dissipated, and he had a normal neurologic exam. Our report highlights a potential role of mRNA vaccine-induced immunity leading to MIS-C-like symptoms with cardiac involvement and a CLOCC in a recently vaccinated child and the complexity of establishing a causal association with vaccination. The child recovered without receipt of immune modulatory treatment.


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