Analysis of vaccine messages on social media (Twitter) in Scandinavia.

Vaccine hesitancy is listed as one of the top 10 global health threats by the WHO. Existing studies investigating the relationship between vaccine hesitancy and social media have found that misinformation and vaccine concerns on social media can cause significant declines in vaccine coverage rates. The objective of this study was to provide insight into the dynamics of vaccine messages on Twitter in Scandinavia (Denmark, Norway, Sweden), by analyzing tweets in local languages during 2019. A validated measure, the 5C scale, was used to map relevant predictors of vaccination behavior, capturing the factors confidence (in vaccines and the system that delivers them), complacency (not perceiving diseases as high risk), constraints (structural and psychological barriers), calculation (engagement in extensive information searching) and collective responsibility (willingness to protect others). A total of 1794 tweets met the inclusion criteria (DK: 48%, NO: 15%, SE: 37%), predominantly tweeted by private users (86%). The HPV vaccine was mentioned in 81% of tweets. Tweets were classified as expressing confidence (61%), complacency (18%), constraints (15%), calculation (15%), and collective responsibility (4%). Confidence in vaccines and the system that delivers them was expressed in 57%. A lack of confidence was expressed in 4% of all tweets, in combination with calculation in 39%. Analyzing public sentiment toward vaccination on Twitter is a useful tool to leverage for better understanding of the dynamics behind vaccine hesitancy. This analysis could provide actionable information for healthcare professionals and public health authorities to mitigate online misinformation and public vaccine concerns.

Cheyne-Stokes respiration and supine dependency.

The influence of position during sleep on central apnoeas during Cheyne-Stokes respiration has not previously been studied systematically. The current authors aimed to study the effect of body position and sleep stages on central sleep apnoeas during Cheyne-Stokes respiration. A total of 20 consecutive patients with cardiovascular diseases and central sleep apnoea during Cheyne-Stokes respiration were investigated using nocturnal polysomnography, including a body position sensor mounted on the patient's sternum. The mean central apnoea-hypopnoea index was significantly higher in the supine position than in nonsupine positions (41+/-13 versus 26+/-12). The central apnoea-hypopnoea index was highest in sleep stages 1 and 2, and lowest in slow-wave sleep and rapid eye movement sleep. In every sleep stage, central apnoeas and hypopnoeas were more prevalent in the supine position compared with nonsupine positions. In conclusion, sleep in the supine body position increases the frequency of apnoeas and hypopnoeas in patients with Cheyne-Stokes respiration.

Mandibular advancement device in patients with obstructive sleep apnea : long-term effects on apnea and sleep.

STUDY OBJECTIVES: To evaluate the long-term effects on apneas and sleep and the tolerability of a mandibular advancement device in patients with obstructive sleep apnea. DESIGN: Prospective study. SETTING: Department of Respiratory Medicine, University Hospital, Umeå, Sweden. PATIENTS: Thirty-three consecutively treated patients. INTERVENTIONS: Individually adjusted mandibular advancement devices. MEASUREMENTS AND RESULTS: Polysomnographic sleep recordings on 1 night without the device and 1 night with the device were performed after 0.7 +/- 0.5 years (mean +/- SD) and after 5.2 +/- 0.4 years from the start of treatment. Nineteen of the 33 patients experienced a short-term satisfactory treatment result with an apnea-hypopnea index of < 10 events per hour and a satisfactory reduction in snoring. Fourteen patients were regarded as being insufficiently treated with the device. Seventeen of the short-term satisfactorily treated patients (90%) and 2 of the remaining patients continued treatment on a long-term basis. The apnea-hypopnea index was reduced by the device from 22 +/- 17 to 4.9 +/- 5.1 events per hour (p < 0.001) in these 19 long-term treatment patients, which did not differ from what was found at the short-term follow-up visits in these patients. Patients with their devices replaced or adjusted experienced a better long-term effect than patients still using their original devices (p < 0.05). CONCLUSIONS: The long-term effect and tolerability of a mandibular advancement device are good in patients who are recommended the treatment on the basis of a short-term sleep recording, provided that the device is continuously adjusted or replaced with a new one when needed. A short-term follow-up is valuable in the selection of patients who will benefit from long-term treatment with a mandibular advancement device.

The effect of a mandibular advancement device on apneas and sleep in patients with obstructive sleep apnea.

OBJECTIVE: To evaluate the effects of a mandibular advancement device on apneas and sleep in mild, moderate, and severe obstructive sleep apnea. DESIGN: Prospective study. SUBJECTS: Forty-four of 47 patients included. INTERVENTION: Individually adjusted mandibular advancement devices. MEASUREMENTS: Polysomnographic sleep recordings for 1 night without the device and 1 night with it, with a median of 1 day and no changes in weight, medication, or sleep position between the recordings. RESULTS: The device reduced the median obstructive apnea-hypopnea index from 11 (range, 7 to 19) to 5 (range, 0 to 17) (p<0.001) in 21 patients with mild sleep apnea, from 27 (range, 20 to 38) to 7 (range, 1 to 19) (p<0.001) in 15 patients with moderate sleep apnea, and from 53 (range, 44 to 66) to 14 (range, 2 to 32) (p<0.05) in 8 patients with severe sleep apnea. The arousal index decreased and the sleep stage patterns improved in all severity groups. Twenty-eight of 44 patients were successfully treated with an obstructive apnea-hypopnea index of below 10 and a subjective reduction in snoring. Nine of 16 patients with treatment failure still reported a reduction in snoring. The success rate correlated inversely to the disease severity (r=-0.41; p<0.01). CONCLUSIONS: A mandibular advancement device reduces apneas and improves sleep quality in patients with obstructive sleep apnea, especially in those with mild and moderate disease. A follow-up sleep recording during treatment is necessary because of the risk of silent obstructive apneas without subjective snoring with the device.

Reversal of central sleep apnea with oxygen.

OBJECTIVE: To examine the effect of oxygen on apneas and sleep quality in patients with frequent central apneas during sleep. DESIGN/SUBJECTS: Prospective intervention study of 20 consecutive patients with predominant central apnea identified from 570 patients referred for suspected sleep apnea syndrome. Sixteen patients had congestive heart failure and seven of them had a previous stroke. Three of the remaining four patients without heart failure had experienced a previous stroke, and one was being treated with morphine. SETTING: The Department of Pulmonary Medicine at Umeå (Sweden) University Hospital. INTERVENTIONS: The patients were investigated for one night receiving nasal oxygen and one night without it. MEASUREMENTS: Overnight polysomnography with transcutaneous PCO2 and arterial blood gases. RESULTS: Central apneas occurred during Cheyne-Stokes respiration in 18 of 20 patients and two patients had idiopathic central apneas. Without oxygen, the median number of all central apneas and hypopneas was 33.5 (range, 8.0 to 52.0) per hour of sleep. These episodes decreased to 5.0 (range, 0.0 to 31.0)(p < 0.01) during oxygen therapy. In 17 of 20 patients, the frequency of central apneas was reduced by more than 50%. Central apneas were reduced by oxygen irrespective of the presence or absence of heart failure or Cheyne-Stokes respiration. The arousal frequency was reduced during oxygen treatment. Daytime sleepiness, difficulty falling asleep, snoring, and self-scored awakenings were reduced in seven patients who were given nocturnal oxygen at home. Obstructive and mixed apneas were unaffected by oxygen. CONCLUSIONS: Oxygen effectively reduces central sleep apnea in eucapnic patients.

Sleep apnoea and nocturnal angina.

Hypoxaemia occurs with sleep apnoea and might induce nocturnal angina. Sleep apnoea was found in 9 of 10 patients with nocturnal angina pectoris. Nocturnal angina diminished during treatment of sleep apnoea by continuous positive airway-pressure, and the number of nocturnal myocardial ischaemic events measured by computerised vector-cardiography was reduced.

Changes in contractile response and effect of a calcium antagonist, nimodipine, in isolated intracranial arteries of baboon following experimental subarachnoid hemorrhage.

Isolated pial arteries from a previously well-characterized model of experimental subarachnoid hemorrhage (SAH) in baboon were tested for their contractile response to 5-hydroxytryptamine (5-HT), norepinephrine (NE), and prostaglandin F2 alpha (PGF2 alpha) and the effect of the calcium antagonist, nimodipine. Autologous blood was injected cisternally at three times with one-day intervals to a total amount of 11.5-29.5 ml (mean: 18.5 ml), and the animals were killed 7 days after the first injection. Untreated animals served as controls. The degree of maximum contraction (EAm) with 5-HT and NE in the control situation was for the three arteries tested in the order middle cerebral greater than anterior cerebral greater than basilar artery. Experimental SAH markedly increased EAm, by 190-370 percent above control values (depending on type of vessel) for 5-HT and 170-185 percent for NE. In addition, the sensitivity to 5-HT was significantly increased, as evidenced by a left-shift of the concentration-response curve. Previous exposure of the artery to 10(-6) M nimodipine reduced the contractile response of both amines to approximately half, the inhibition being slightly less pronounced post-SAH. When vessels were contracted beforehand with the amines or with PGF2 alpha, followed by administration of increasing amount of nimodipine (10(-9) M to 10(-6) M), a concentration-dependent relaxation was obtained by up to 60 percent of the original level. This relaxing effect was significantly less following SAH in the experiments with NE and PGF2 alpha compared to 5-HT; the contraction in the presence of 5-HT did not differ before and after experimental SAH. The experiments show that SAH markedly enhances the intrinsic activity for both 5-HT and NE. Nimodipine inhibits the contractile response less efficiently following experimental SAH. The difference in the responsiveness to 5-HT on the one hand, and to NE and PGF2 alpha on the other, could be due to differences in the blood-induced alterations of those calcium channels that are influenced by the calcium antagonist, nimodipine.

Ultrastructural cerebrovascular changes in a model of subarachnoid hemorrhage in baboon based on triple cisternal blood injection.

In a subarachnoid hemorrhage model in the baboon, achieved through three cisternal blood injections with 1-day intervals, the cerebral arteries were dissected out 7 days after the first blood injection for electron microscopy All the animals showed ultrastructural changes in the cerebral arteries: two with severe, one with moderate, and three with mild alterations in the vessel walls. The most constant findings were seen in the muscle cells of the media layer. Fragmentation of the nuclei was frequently observed together with cytoplasmic vacuoles. Scattered groups or single degenerated muscle cells were also noted. In the intima the changes included rounding of the nuclei along with the appearance of cytoplasmic vacuoles. Desquamation or flattening of the endothelium and loss of tight junctions were encountered in some vessel areas. Degenerating mitochondria were a common finding.

Nerves containing serotonin, its interaction with noradrenaline, and characterization of serotonin receptors in cerebral arteries of monkey.

1 Immunohistochemistry was applied to study the presence of 5-hydroxytryptamine (5-HT) and dopamine-beta-hydroxylase (DBH) in cerebrovascular nerves of monkeys, and serotonergic receptors were characterized in the vessels by in vitro pharmacology. 2 A well-developed plexus of 5-HT immunoreactive fibres was found to supply the pial arteries at the base of the brain. The network closely resembled the distribution of neural DBH, used as an index for noradrenergic nerves. 3 5-HT contracted the basilar artery (BA) and middle cerebral artery (MCA) with equal potency and intrinsic activity. The effect was not antagonized by phentolamine or propranolol. 4 The 5-HT2 receptor antagonist, ketanserin, inhibited the response to 5-HT in a competitive manner in both vessels, with pA2 values obtained from Schild plots of 9.15 in BA and 9.40 in MCA. 5 Electrical field stimulation elicited a neurogenic contraction that was completely blocked by 3 X 10(-7) M tetrodotoxin, 3 X 10(-6) M guanethidine, and 10(-6) M phentolamine. The response was also antagonized by ketanserin, but only in concentrations higher than those inhibiting the response to 5-HT. 6 In accordance with the findings during nerve stimulation, noradrenaline (NA) contracted the pial arteries, particularly MCA where the intrinsic activity closely resembled the value obtained with 5-HT. Ketanserin antagonized the response, but less efficiently than that induced by 5-HT. 7 5-HT had no effect on the (noradrenergic) neurogenic contraction obtained during electrical stimulation. Nor did 5-HT affect the contraction induced by exogenous NA. 8 It is concluded that 5-HT and NA may be co-localized in perivascular nerves of the monkey brain. 5-HT contracts pial arteries through postjunctional 5-HT2 receptors, but does not seem to interfere prejunctionally with the noradrenergic nerves or with exogenous NA.

Cerebrovascular and metabolic changes during the delayed vasospasm following experimental subarachnoid hemorrhage in baboons, and treatment with a calcium antagonist.

A model has been designed in baboons for simulating the clinical situation during the late phase of vasospasm in patients with subarachnoid hemorrhage (SAH). A total amount of 14-33 ml autologous blood was injected into the cisternal system on 3 occasions in the course of 4 days. Neurological symptoms were seen, and the mortality rate was 29%. Angiography 3 days after the last injection showed arterial vasoconstriction amounting to 23% in the vertebro-basilar system, and 11% (right) and 18% (left) in the carotid system. Cerebral blood flow (CBF) measured by the intra-arterial 133Xe technique and the cerebral metabolic rate of oxygen (CMRO2) were reduced by 18% and 11%, respectively. The hypercapnic CBF response was significantly impaired, from a mean of 3.90 ml/100 g/min to 1.72 ml/100 g/min of flow increase for each mm Hg elevation of paCO2. Autoregulation, tested by administration of angiotensin II, was also significantly affected as evidenced by a pressure-dependent increment of CBF during hypertension in 5 out of 7 animals tested. The impaired autoregulation was reflected in the autoregulatory index, which in the whole group increased from 0.06 ml/100 g/min for each mm Hg increase in MABP in the pre-SAH animals to 0.29 ml/100 g/min per mm Hg post-SAH. Treatment with the calcium antagonist, nimodipine (0.5 microgram/kg/min i.v. during 45 min), enhanced CBF significantly by 17% before experimental SAH, whereas after SAH the effect was slight and did not reach statistical significance; CMRO2 was not significantly affected in either group. Intravenous nimodipine combined with hypertension resulted in a marked increase in the autoregulatory index to 1.58 ml/100 g/min per mm Hg in pre-SAH animals and a less pronounced increment to 0.58 ml/100 g/min per mm Hg following experimental SAH. The beneficial effect of nimodipine reported in SAH patients is therefore, in view of our findings, more likely due primarily to a protective mechanism at the cellular level than to an influence on the vascular bed.

Changes in cerebral blood flow and metabolism following intraarterial or local administration of nimodipine, before and after experimental subarachnoid hemorrhage in baboons.

Experimental subarachnoid hemorrhage (SAH) was induced in baboons by repeated injections of autologous blood into cisterna chiasmatis and cisterna magna, a total of 14-33 ml being injected over 3-4 days. Cerebral blood flow (CBF; 133xenon clearance) and cerebral metabolic rate of oxygen (CMRO2) were measured before, and 7 days after, the first blood injection. The effect of the calcium channel blocker, nimodipine, used in a commercially available form for clinical application, was studied following continuous i.a. infusion (0.1 microgram X kg-1 X min-1) for an interval of 45 min, and also 20 and 60 min after intrathecal administration of 1 microgram X kg-1. During the infusion experiments, CBF was increased by 25-30% both before and after the cisternal blood injection. CMRO2 was also enhanced, but much less. Nimodipine in doses given did not alter systemic blood pressure. Following intrathecal application, CBF and CMRO2 slightly increased at 20 min only before experimental SAH.

Late cerebral arterial spasm: the cerebrovascular response to hypercapnia, induced hypertension and the effect of nimodipine on blood flow autoregulation in experimental subarachnoid hemorrhage in primates.

1. Late cerebral arterial spasm was induced by repeated injections of autologous blood in a total amount of 14-33 ml into the basal cisterns of baboons to mimick subarachnoid hemorrhage (SAH). Regional cerebral blood flow (CBF), sagittal sinus pressure, cerebral arterial caliber from angiograms, and cerebral metabolic rate of oxygen (CMRO2) were measured before and after the experimental SAH to determine responses to hypercapnia and induced hypertension. The effect of the calcium antagonist, Nimodipine, on CBF autoregulation pre- and post-SAH was tested. 2. One week after the blood injections were started there was about 10-20% reduction, depending on territory measured, in the arterial diameter of the carotid and vertebral systems. This was associated with an 18% reduction in CBF and 9% decrease in the brain metabolism. 3. During hypercapnia before and after experimental SAH the flow increased with a mean of 3.7 and 1.8 ml, respectively, for each mm Hg elevation of PaCO2. In control animals, graded angiotensin-induced hypertension did not overtly affect CBF. Following SAH, the CBF autoregulation was impaired in 5 of 6 animals tested. 4. I.v. infusion of Nimodipine markedly curtailed the CBF autoregulation in pre-SAH animals and, to a somewhat slighter extent, also in post-SAH animals.

Reduced noradrenaline uptake and retention in cerebrovascular nerves associated with angiographically visible vasoconstriction following experimental subarachnoid hemorrhage in rabbits.

Rabbits were injected with 1-2 ml autologous blood into the chiasmatic and basal cisterns to stimulate subarachnoid hemorrhage. Selective vertebral angiography performed at various time-periods following blood injection showed a 27 per cent reduction in basilar artery diameter within 3-5 days, followed by normalization so that pre-injection size was regained within 26 days after the treatment. Formaldehyde histofluorescence of the major basal pial arteries showed almost 75 per cent reduction in number and fluorescence intensity of visible perivascular adrenergic nerves at 3-7 days following blood injection. The noradrenaline fluorescence in a normal number of nerves returned to control values at 26 days after treatment. The noradrenaline reduction in the perivascular nerves was confirmed in fluorometric determinations. The presence of cisternal blood markedly impaired the neuronal uptake of 3H-noradrenaline at 3 days following the injection. The transmitter uptake had normalized 2 weeks later. The impaired neuronal uptake of noradrenaline in the presence of cisternal blood is in accordance with the net reduction in transmitter of the perivascular nerves, and may provide one pathophysiological factor in the development of angiographically visible vasoconstriction, having a time-course resembling that of the functional changes in the perivascular adrenergic nerves.

Increased sensitivity of the basilar artery to norepinephrine and 5-hydroxytryptamine following experimental subarachnoid hemorrhage.

The reactivity of rabbit basilar artery to norepinephrine and 5-hydroxytryptamine was tested in vitro three days following cisternal injection of 1.0 ml autologous blood to simulate subarachnoid hemorrhage. Following this treatment the artery became three to five times more sensitive to norepinephrine compared with vessels from untreated animals. This was reflected in a parallel shift of the log dose-response curve towards lower concentrations of norepinephrine in a way resembling that seen after cocaine treatment of sympathectomy and interpreted as a prejunctional supersensitivity of the vascular alpha-receptors. The injection of blood also increased the amount of vasoconstriction with 5-hydroxytryptamine to a level which was three times higher than that obtained in untreated vessels. The results suggest one type of mechanism whereby monoamines might be involved in cerebral vasospasm following subarachnoid hemorrhage.