Hagansteenberg7307

Rotavirus vaccine performance appears worse in countries with high rotavirus genotype diversity. Evidence suggests diminished vaccine efficacy (VE) against G2P[4], which is heterotypic with existing monovalent rotavirus vaccine formulations. Carboxyfluorescein succinimidyl ester Most studies assessing genotype-specific VE have been underpowered and inconclusive.

We pooled individual-level data from ten Phase II and III clinical trials of rotavirus vaccine containing G1 and P[8] antigens (RV1) conducted between 2000 and 2012. We estimated VE against both any-severity and severe (Vesikari score ≥11) rotavirus gastroenteritis (RVGE) using binomial and multinomial logistic regression models for non-specific VE against any RVGE, genotype-specific VE, and RV1-typic VE against genotypes homotypic, partially heterotypic, or fully heterotypic with RV1 antigens. We adjusted models for concomitant oral poliovirus and RV1 vaccination and the country's designated child mortality stratum.

Analysis included 87,644 infants from 22 countries in the Americas, Europe, Africa, and Asia. For VE against severe RVGE, non-specific VE was 91% (95% confidence interval (CI) 87-94%). Genotype-specific VE ranged from 96% (95% CI 89-98%) against G1P[8] to 71% (43-85%) against G2P[4]. RV1-typic VE was 92% (95% CI 84-96%) against partially heterotypic genotypes but 83% (67-91%) against fully heterotypic genotypes. For VE against any-severity RVGE, non-specific VE was 82% (95% CI 75-87%). Genotype-specific VE ranged from 94% (95% CI 86-97%) against G1P[8] to 63% (41-77%) against G2P[4]. RV1-typic VE was 83% (95% CI 72-90%) against partially heterotypic genotypes but 63% (40-77%) against fully heterotypic genotypes.

RV1 VE is comparatively diminished against fully heterotypic genotypes including G2P[4].

RV1 VE is comparatively diminished against fully heterotypic genotypes including G2P[4].Magnetic resonance imaging (MRI) assessment of fetal blood oxygen saturation (SO2 ) can transform the clinical management of high-risk pregnancies affected by fetal growth restriction (FGR). Here, a novel MRI method assesses the feasibility of identifying normally grown and FGR fetuses in sheep and is then applied to humans. MRI scans are performed in pregnant ewes at 110 and 140 days (term = 150d) gestation and in pregnant women at 28+3 ± 2+5 weeks to measure feto-placental SO2 . Birth weight is collected and, in sheep, fetal blood SO2 is measured with a blood gas analyzer (BGA). Fetal arterial SO2 measured by BGA predicts fetal birth weight in sheep and distinguishes between fetuses that are normally grown, small for gestational age, and FGR. MRI feto-placental SO2 in late gestation is related to fetal blood SO2 measured by BGA and body weight. In sheep, MRI feto-placental SO2 in mid-gestation is related to fetal SO2 later in gestation. MRI feto-placental SO2 distinguishes between normally grown and FGR fetuses, as well as distinguishing FGR fetuses with and without normal Doppler in humans. Thus, a multi-compartment placental MRI model detects low placental SO2 and distinguishes between small hypoxemic fetuses and normally grown fetuses.Due to the continuous rise in biofilm-related infections, biofilms seriously threaten human health. The formation of biofilms makes conventional antibiotics ineffective and dampens immune clearance. Therefore, it is important to understand the mechanisms of biofilm formation and develop novel strategies to treat biofilms more effectively. This review article begins with an introduction to biofilm formation in various clinical scenarios and their corresponding therapy. Established biofilm models used in research are then summarized. The potential targets which may assist in the development of new strategies for combating biofilms are further discussed. The novel technologies developed recently for the prevention and treatment of biofilms including antimicrobial surface coatings, physical removal of biofilms, development of new antimicrobial molecules, and delivery of antimicrobial agents are subsequently presented. Finally, directions for future studies are pointed out.

Dialysis patients have strong intracoronary calcification, accelerated by secondary hyperparathyroidism as well as atherosclerosis. We evaluated the association of intact parathyroid hormone (iPTH) level with intracoronary calcification evaluated by intravascular ultrasound (IVUS), and its impact on both stent expansion after percutaneous coronary intervention (PCI) and long-term clinical outcomes, in dialysis patients with coronary artery disease (CAD).Methods and Results A total of 116 patients on dialysis, who underwent PCI with IVUS guidance between March 2012 and December 2020, were enrolled. Patients were divided into 2 groups based on their median iPTH level. The degree of intracoronary calcification was evaluated by calcification score using grayscale IVUS in the target lesions. Preprocedural calcification scores were significantly higher in the high iPTH group compared with the low iPTH group (2.9±1.1 vs. 2.1±0.7, P<0.001). After PCI, the high iPTH group had a significantly lower stent expansion index (0.6±0.2 vs. 0.7±0.1, P<0.001) and stent symmetry index (0.5±0.1 vs. 0.7±0.1, P<0.001) compared with the low iPTH group. The incidence of major adverse cardiac or cerebrovascular events within 3 years was significantly higher in the high iPTH group (log-rank P<0.05).

High iPTH level is likely to increase intracoronary calcification, and cause inadequate stent expansion, which may be associated with increased risk of future adverse events in dialysis patients with CAD requiring PCI.

High iPTH level is likely to increase intracoronary calcification, and cause inadequate stent expansion, which may be associated with increased risk of future adverse events in dialysis patients with CAD requiring PCI.A 65-year-old man was admitted to our hospital with a 6-year history of painful muscle stiffness in his trunk and lower limbs, preventing him from walking. Stiff-person syndrome (SPS) was diagnosed because the patient had symptoms of painful muscle spasms elicited by tactile stimulation without joint contracture. Although SPS- related autoantibodies in the serum, including anti-glycine R, anti-amphiphysin, anti-glutamic acid decarboxylase (GAD), anti-dipeptidyl peptidase-like protein (DPPX) and anti-γ-aminobutyric acid-A (GABAA) R, were negative, the ACTH and cortisol levels were low. On the basis of additional loading tests for anterior pituitary function and ACTH, isolated ACTH deficiency (IAD) was diagnosed. Hormonal replacement therapy with hydrocortisone at 15 mg/day ameliorated the condition quickly, and the patient became asymptomatic after three months. Flexion contractures have been reported as musculoskeletal symptoms of IAD, but are not usually evident in patients with SPS. The present case illustrates that the painful muscle spasms elicited by tactile stimulation without joint contracture characteristic of SPS can also be symptoms of IAD.A 71-year-old man had persistent cervical pain secondary to thunderclap headache during sleep. MRI conducted the next morning revealed subdural hematoma and convexity subdural hemorrhage on the right occipital region, and the patient was hospitalized. MRA showed vascular narrowing in the bilateral PCA. Follow-up MRA on day 8 of admission showed aggravated vascular narrowing of PCA, indicative of reversible cerebral vasoconstriction syndrome (RCVS). The patient was treated with a calcium-channel antagonist. Post-discharge MRA showed improvement of PCA narrowing, and the diagnosis of RCVS was confirmed.A 60-year-old man developed dyspnea without apparent limb weakness. He had cardiomyopathy in his 30s and was treated for chronic heart failure since 42. He was diagnosed as having four and a half LIM domains 1 (FHL1) mutation at 53 following the same diagnosis of his younger brother. He was first admitted to the cardiology department for possible worsening of chronic cardiac failure. Blood gas analysis showing respiratory acidosis prompted his treatment with a respirator. Neurological examination revealed that he had mild weakness limited to the shoulder girdle muscles and contracture at jaw, spine, elbows and ankles. Skeletal muscle CT showed truncal atrophy. He, as well as his younger brother, was diagnosed with FHL1 myopathy resulting in ventilation failure and was discharged after successful weaning from the respirator in the daytime. The present sibling cases are the first with FHL1 mutation to develop respiratory failure without limb weakness and suggest that FHL1 myopathy as a differentially diagnosis of hereditary myopathies with early respiratory failure.We describe an unusual case of a 73-year-old man with amaurosis fugax. He had repeated transient monocular symptoms, one of which features lighting bolt-shaped glittering in the full visual field of the right eye since medical treatment for hypertension and diabetes mellitus started. A few days later, he felt difficulty in speech as well as sensory and motor disturbance in the left upper extremity, which finally brought him to our hospital. An MR scan unveiled subacute infarctions dotted in the right cerebral hemisphere and severe carotid stenosis on the same side with a delayed distal flow. He was hospitalised with diagnosed an ischemic stroke. Despite being treated with antithrombotic agents, he had suffered similar visual symptoms repeatedly and therefore, carotid artery stenting was performed on Day 16 starting from the onset. The right ophthalmic artery and choroidal crescent became depicted angiographically after our surgery had been completed. His visual disturbance has never appeared since then. Consequently, it is suggested that the optic disorders were attributed to a hemodynamically precarious state in the area of the ophthalmic artery.A 59-year-old woman presented with right hemiparesis and was transported from outside hospital. MRI revealed acute infarction and the left middle cerebral artery M2 occlusion. Intravenous infusion of recombinant tissue-type plasminogen activator, and mechanical thrombectomy (MT) were performed. The cause of cerebral infarction was diagnosed as Libman-Sacks endocarditis. She discharged without sequelae. After 10 months later, she presented with mild cognitive decline, and MRI showed new white matter lesion in left deep white matter. In magnetic resonance spectroscopy, the lesion showed an increased rate of choline/creatine, and a decreased rate of N-acetylaspartate/creatine, elevated lactate peak. When new higher brain dysfunction presented after recanalization by MT, it might be related to the delayed white matter lesion.A 47-year-old woman was admitted to our hospital for scrutiny of limb weakness and orthostatic hypotension that had progressed from childhood. She had been treated for alacrima and esophageal achalasia from childhood. On admission, she had hyperreflexia of upper and lower extremities, distal predominant muscle atrophy in the lower extremities, decreased sensation of the distal extremities, and autonomic neuropathy. Her blood test results ruled out adrenal insufficiency, but Schirmer's test was positive. Given the lacrimation symptoms, esophageal achalasia, and neuropathy, the patient was diagnosed with triple A syndrome in whom a c.463C>T mutation (p.R155C) was found in the AAAS gene by genetic testing. Triple A syndrome is an autosomal recessive inherited disease caused by mutations in the AAAS gene. Genetic testing of the AAAS gene should be considered in patients with one or two of main symptoms of triple A syndrome.