Frank Christopher Howarth

Prof. Frank Christopher Howarth

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Research Focus & Metrics

Academic Career Length

26Years (2001-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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4 November 2005 in Experimental Physiology
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FHFrank Christopher Howarth
Frank Christopher Howarth
MJM. Jacobson
M. Jacobson
MSM. Shafiullah
M. Shafiullah
Ernest AdeghateErnest Adeghate
Ernest Adeghate
In vivo biotelemetry studies have demonstrated that short‐term streptozotocin (STZ)‐induced diabetes is associated with a reduction in heart rate (HR) and heart rate variability (HRV) and prolongation of QT and QRS intervals. This study investigates the long‐term effects of STZ‐induced diabetes on the electrocardiogram (ECG), physical activity and body temperature. Transmitter devices were surgically implanted in the peritoneal cavity of young adult male Wistar rats. Electrodes from the transmitter were arranged in Einthoven bipolar lead II configuration. ECG, physical activity and body temperature data were continuously recorded with a telemetry system before and following the administration of STZ (60 mg kg−1) for a period of 22 weeks. HR, physical activity and body temperature declined rapidly 3–5 days after the administration of STZ. The effects became conspicuous with time reaching a new steady state approximately 1–2 weeks after STZ treatment. HR at 4 weeks was 268 ± 5 beats min−1 in diabetic rats compared to 347 ± 12 beats min−1 in age‐matched controls. HRV at 4 weeks was also significantly reduced after STZ treatment (18 ± 3 beats min−1) compared to controls (33 ± 3 beats min−1). HR and HRV were not additionally altered in either diabetic rats (266 ± 5 and 20 ± 4 beats min−1) or age‐matched controls (316 ± 6 and 25 ± 4 beats min−1) at 22 weeks. Reduced physical activity and/or body temperature may partly underlie the reductions in HR and HRV. In addition, the increased power spectral low frequency/high frequency ratio from 4 weeks after STZ treatment may indicate an accompanying disturbance in sympathovagal balance.

29 October 2014 in Molecular and Cellular Biochemistry
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Journal Article
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NHN. N. Hamouda
N. N. Hamouda
VSV. Sydorenko
V. Sydorenko
MQM. A. Qureshi
M. A. Qureshi
JAJ. M. Alkaabi
J. M. Alkaabi
MOM. Oz
M. Oz
FHFrank Christopher Howarth
Frank Christopher Howarth

28 January 2011 in Experimental Physiology
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Journal Article
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FHFrank Christopher Howarth
Frank Christopher Howarth
MQM. A. Qureshi
M. A. Qureshi
ZHZ. Hassan
Z. Hassan
LKL. T. Al Kury
L. T. Al Kury
DID. Isaev
D. Isaev
Ernest AdeghateErnest Adeghate
Ernest Adeghate

1 June 2002 in Pflügers Archiv - European Journal of Physiology
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FHFrank Christopher Howarth
Frank Christopher Howarth
MQM. Qureshi
M. Qureshi
EWE. White
E. White

11 January 2008 in Experimental Physiology
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Journal Article
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FHFrank Christopher Howarth
Frank Christopher Howarth
MJMichael Jacobson
Michael Jacobson
MSMohamed Shafiullah
Mohamed Shafiullah
Ernest AdeghateErnest Adeghate
Ernest Adeghate
In vivo biotelemetry studies have demonstrated a variety of heart rhythm disturbances in type 1 diabetes mellitus. In the streptozotocin (STZ)‐induced diabetic rat, these disturbances have included reductions in heart rate (HR) and heart rate variability (HRV) and an electrocardiogram that displays prolonged QRS duration and Q–T interval. The aim of this study was to investigate the chronic effects of type 2 diabetes mellitus on heart rhythm in the Goto–Kakizaki (GK) rat. Transmitter devices were surgically implanted in the peritoneal cavity of young male GK and age‐matched Wistar control rats. Electrodes from the transmitter were arranged in Einthoven bipolar lead II configuration. Electrocardiogram, physical activity and body temperature data were recorded in rats from age 2 to 15 months. Data were acquired for 2 weeks each month. Non‐fasting blood glucose, glucose tolerance and body weight were measured periodically. In GK rats, growth rate and maximal attained body weight were significantly reduced and non‐fasting blood glucose was progressively increased compared with age‐matched Wistar control animals. Heart rate was significantly lower in GK compared with control rats at 2, 7 and 15 months of age. At 2 months of age, HR was 316 ± 6 beats min−1 in GK rats compared with 370 ± 7 beats min−1 in Wistar control animals. There was a progressive age‐dependent decline in HRV in Wistar control rats; however, HRV in GK rats did not alter significantly with age. Heart rate variability was significantly reduced in GK compared with Wistar control rats at 2 and 7 months. At 2 months of age, HRV was 28 ± 2 beats min−1 in GK rats compared with 38 ± 3 beats min−1 in Wistar control rats. Reduced HR in GK rats may be an inherited characteristic. The absence of age‐dependent reductions in HRV in GK rats may be a consequence of an underlying impairment of autonomic control which manifests at early age.

26 April 2013 in Molecular and Cellular Biochemistry
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KSK. A. Salem
K. A. Salem
MQM. A. Qureshi
M. A. Qureshi
VSV. Sydorenko
V. Sydorenko
KPK. Parekh
K. Parekh
PJP. Jayaprakash
P. Jayaprakash
FHFrank Christopher Howarth
Frank Christopher Howarth