We investigated the effects of electrical stimulation of the stomach on gastric emptying and the electrical activity of the stomach in 10 dogs. A model of gastroparesis was developed in five dogs using truncal vagotomy combined with injections of glucagon. Glucagon also induced electrical dysrhythmias. Bipolar electrodes were implanted in the stomach and the duodenum for electrical stimulation and for recording electrogastrograms. Gastric emptying of an isotope-labeled solid meal was assessed for 2 h. External electrical stimulation was delivered to the corpus of the stomach at its own physiological frequency to investigate whether it could restore normal gastric emptying. Such stimulation had no significant effect on gastric emptying in intact animals (45 vs. 43%: retention of isotope after 2 h) or when only vagotomy was performed (78 vs. 66%), but it significantly accelerated gastric emptying in animals with vagotomy and glucagon (from 86 to 68%). From this model of delayed gastric emptying, we suggest that electrical stimulation of the stomach at its own intrinsic frequency may recoordinate uncoupled slow wave activity induced by glucagon after vagotomy thus improving the rate of gastric emptying.
To cite this article: Rinde LB, Lind C, Sm abrekke B, Njølstad I, Mathiesen EB, Wilsgaard T, Løchen M-L, Hald EM, Vik A, Braekkan SK, Hansen J-B.Impact of incident myocardial infarction on the risk of venous thromboembolism: the Tromsø Study. J Thromb Haemost 2016; 14: 1183-91.
Essentials• Registry-based studies indicate a link between arterialand venous thromboembolism (VTE).• We studied this association in a cohort with confounder information and validated outcomes.• Myocardial infarction (MI) was associated with a 4.8-fold increased short-term risk of VTE.• MI was associated with a transient increased risk of VTE, and pulmonary embolism in particular.
Summary.Background: Recent studies have demonstrated an association between venous thromboembolism (VTE) and arterial thrombotic diseases. Objectives: To study the association between incident myocardial infarction (MI) and VTE in a prospective population-based cohort. Methods: Study participants (n = 29 506) were recruited from three surveys of the Tromsø Study (conducted in 1994-1995, 2001-2002, and 2007-2008) and followed up to 2010. All incident MI and VTE events during follow-up were recorded. Cox regression models with age as the time scale and MI as a time-dependent variable were used to calculate hazard ratios (HRs) of VTE adjusted for sex, body mass index, blood pressure, diabetes mellitus, HDL cholesterol, smoking, physical activity, and education level. Results: During a median follow-up of 15.7 years, 1853 participants experienced an MI and 699 experienced a VTE. MI was associated with a 51% increased risk of VTE (HR 1.51; 95% confidence interval [CI] 1.08-2.10) and a 72% increased risk of pulmonary embolism (PE) (HR 1.72; 95% CI 1.07-2.75), but not significantly associated with the risk of deep vein thrombosis (DVT) (HR 1.36; 95% CI 0.86-2.15). The highest risk estimates for PE were observed during the first 6 months after the MI (HR 8.49; 95% CI 4.00-18.77). MI explained 6.2% of the PEs in the population (population attributable risk) and 78.5% of the PE risk in MI patients (attributable risk). Conclusions: Our findings indicate that MI is associated with a transient increased VTE risk, independently of traditional atherosclerotic risk factors. The risk estimates were particularly high for PE.
Background-Growing evidence supports an association between venous thromboembolism (VTE) and arterial thrombotic diseases (ie, myocardial infarction and ischemic stroke). We aimed to study the association between VTE and future arterial events and to determine the population attributable risk of arterial events by VTE in a large prospective cohort recruited from the general population. Methods and Results-In 1994 to 1995 and 1993 to 1997, 81 687 subjects were included in the Tromsø Study and in the Diet, Cancer and Health Study and followed up to the date of incident venous and arterial events (myocardial infarction or ischemic stroke), death or migration, or to the end of the study period (2010 and 2008, respectively). There were 1208 cases of VTE and 90 subsequent arterial events during a median follow-up of 12.2 years. An association between VTE and future arterial events was found in all women and men aged <65 years but not in men aged >65 years. Women <65 years old with VTE had 3.3-fold higher risk of arterial disease (adjusted hazard ratio, 3.28; 95% confidence interval, 1.69-6.35) compared with women of the same age without VTE. The corresponding hazard ratio in men aged <65 years was 2.06 (95% confidence interval, 1.32-3.20). Only 0.9% of the arterial events were attributed to VTE, and the VTE explained 63.8% of the risk of arterial events among VTE patients. Conclusions-Our findings imply that women and young men with VTE have higher risk of arterial thrombotic disease than those without VTE. However, only 1% of the arterial thrombotic events in the population are attributed to VTE. (Circulation. 2014;129:855-863.)
Background
Postoperative endophthalmitis is a rare but dreaded complication of intraocular surgery and often results in severe visual impairment or blindness. The present study describes the clinical course, treatment and visual outcome of an outbreak of Burkholderia contaminans endophthalmitis following cataract surgery.
Methods
Among 290 patients who underwent uneventful phacoemulsification cataract surgery at one outpatient clinic between January 4th and 28th 2019, 6 cases developed Burkholderia contaminans endophthalmitis. Clinical data were collected by retrospective review of patient records. Microbiological samples from vitreous aspirates, intraocular lenses (IOL) and lens capsules were cultured, and recA and draft whole genome sequences analysed.
Results
The recA sequences of all Burkholderia contaminans isolates and the allelic profile of the isolates were identical. All cases had a similar clinical presentation with rapid development of endophthalmitis symptoms with variable time to onset. The mean time to admission was 34 days (12–112 days). All cases had a seemingly favourable response to intravitreal antibiotics. However, acute recurrences occurred after long time periods (12–71 days). The cases experienced between 0 and 3 recurrences. Due to persistent infection, the cases received between 5 and 15 treatments (mean 7.8) including IOL and lens capsule explantation in 5 of 6 cases. Burkholderia contaminans was detected in all explanted lens capsules. The final corrected distance visual acuity (CDVA, Snellen chart) was between 0.8 and 1.2 and all cases had final CDVA ≥0.8.
Conclusions
A persistent and intensive treatment approach including total lens capsule and IOL explantation is recommended for Burkholderia contaminans endophthalmitis following cataract surgery and may lead to a favourable visual result.
Background-A family history of myocardial infarction (FHMI) has been shown to increase the risk of venous thromboembolism (VTE). The mechanism underlying the association remains unclear. Therefore, we aimed to determine the risks of MI and VTE by FHMI using a cause-specific model and to explore whether atherosclerotic risk factors could explain the association between FHMI and VTE in a population-based cohort.
There is evidence in human populations that exposure to manganese (Mn), or Mn in combination with excessive noise exposure, results in hearing loss. Quantitative reverse-transcriptase polymerase chain reaction revealed expression of the metal transporters DMT1, ZIP8, and ZIP14 in control mouse ears. ZIP8 is known to have a high affinity (K m = 2.2 μM) for Mn transport, and ZIP8 protein was localized to the blood vessels of the ear by immunohistochemistry. We treated mice (strains C57BL/ 6J and DBA/2J) with Mn (100 mg/kg MnCl 2 , by subcutaneous injection, on three alternating days), and Mn was significantly elevated in the ears of the treated mice. Mn concentrations remained elevated over controls for at least 2 weeks after treatment. These studies demonstrate that metal transporters are present in the mouse ear and that Mn can accumulate in the ear following systemic exposure. Future studies should focus on whether Mn exposure is associated with hearing deficits.
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