Background: Although serum osmolal gap can be a useful diagnostic tool, clinicians are not familiar with its use in clinical practice.
Objectives: The review presents in a series of questions-answers and under a clinical point of view the current data regarding the use of osmolal gap.
Discussion: The definition and the best formula used for the calculation of osmolal gap, the main causes of increased osmolal gap with or without increased anion gap metabolic acidosis, as well as the role of concurrent lactic acidosis or ketoacidosis are presented under a clinical point of view.
Conclusions: The calculation of osmolal gap is crucial in the differential diagnosis of many patients presenting in emergency departments with possible drug or substance overdose as well as in comatose hospitalized patients. 相似文献
Eating disorders are associated with significant illness burden and costs, yet access to evidence-based care is limited. Greater use of programme-led and focused interventions that are less resource-intensive might be part of the solution to this demand-capacity mismatch.
Method
In October 2022, a group of predominantly UK-based clinical and academic researchers, charity representatives and people with lived experience convened to consider ways to improve access to, and efficacy of, programme-led and focused interventions for eating disorders in an attempt to bridge the demand-capacity gap.
Results
Several key recommendations were made across areas of research, policy, and practice. Of particular importance is the view that programme-led and focused interventions are suitable for a range of different eating disorder presentations across all ages, providing medical and psychiatric risk are closely monitored. The terminology used for these interventions should be carefully considered, so as not to imply that the treatment is suboptimal.
Conclusions
Programme-led and focused interventions are a viable option to close the demand-capacity gap for eating disorder treatment and are particularly needed for children and young people. Work is urgently needed across sectors to evaluate and implement such interventions as a clinical and research priority. 相似文献
Between January 1990 and December 2003, 117 patients were surgically treated for tympanosclerosis at a tertiary referral center.
The objective of our study was to review the hearing results in this cohort. The patients were divided into three groups:
predominant involvement of tympanic membrane (33 cases), predominant fixation of malleus or/and incus (72 cases), and stapedial
fixation (12 cases). Preoperative and postoperative air–bone gap (ABG), and pure tone average (PTA) were compared after short-term
and long-term follow-up, and statistical significance was determined. After surgery, air–bone gap was improved by 11.7 dB
after short-term, and by 10.9 dB after long-term observation period. The improvement of ABG was not significantly different
between the groups. Pure tone average (PTA) was improved by 15.2 dB in short-term period, with decrease of results in the
long-term follow-up to 10.3 dB. Successful hearing result as judged by ABG was obtained in 66.7% with affected tympanic membrane,
in 65.3% with malleus or/and incus fixation, and in 50.0% with stapedial fixation. Statistical analysis confirmed significant
improvement of hearing for all groups. Highly significant difference was noted for low frequency ABG (0.5, 1, and 2 kHz).
Hearing improvement on ABG was preserved after long-term observation. No significant sensorineural hearing loss was seen in
this series. Surgery for tympanosclerosis results in significant improvement of ABG and PTA. Most of the improvement is obtained
in lower frequencies. Long-term results are comparable to short-term results, with slight hearing deterioration in stapedial
fixation. 相似文献
BackgroundLeft-sided repair for long gap esophageal atresia (LGEA) has been described for patients with a large leftward upper pouch, no thoracic tracheoesophageal fistula (TEF) nor tracheobronchomalacia (TBM), or as salvage plan after prior failed right-sided repair. We describe our experience with left-sided MIS traction induced growth process.MethodsWe retrospectively reviewed patients who underwent Foker process for LGEA at two institutions between December 2016 and November 2021. Patient characteristics, surgical techniques, and outcomes were reviewed.Results71 patients underwent Foker process. Of 34 MIS cases, 28 patients (82%) underwent left-sided repair (median gap length 5 cm) at median age 4 months with median 3 (range 2–8) operations and median 13.5 (IQR 11–21) days on traction until esophageal anastomosis. 9 patients (32%) underwent completely MIS approach, whereas 5 patients (18%) converted to open at first operation and 14 patients (50%) converted to open later in the traction process. Traction was internal in 68%, external in 11%, and combination in 21%. Median follow-up was 15.4 (IQR 7.5–31.7) months after anastomosis. 14% had anastomotic leak managed with antibiotics and/or esophageal vacuum therapy. Median number of esophageal dilations was 3.5 (range 0–13). 18% required stricture resection. 39% underwent Nissen fundoplication. None have needed esophageal replacement.ConclusionsFor multiple reasons including the tendency of both esophageal pouches to have a leftward bias, less tracheal compression by upper pouch, and clean field of surgery for reoperative cases, we now more commonly use left-sided approach for MIS LGEA repair compared to right side, regardless of left aortic arch.Level of evidenceLevel IV Treatment Study. 相似文献
Aedes aegypti is a major vector of arthropod-borne viruses such as yellow fever virus and dengue viruses. Efforts to discern the function of genes involved in important behaviours, such as vector competence and host seeking through reverse genetics, would greatly benefit from the ability to generate targeted gene disruptions. Homing endonucleases are selfish elements which catalyze double-stranded DNA (dsDNA) breaks in a sequence-specific manner. In this report we demonstrate that the homing endonucleases I- Ppo I, I- Sce I, I- Cre I and I- Ani I are all able to induce dsDNA breaks in adult female Ae. aegypti chromosomes as well as catalyze the somatic excision of a transgene. These experiments provide evidence that homing endonucleases can be used to manipulate the genome of this important disease vector. 相似文献
Effect of Stretch on Conduction and Cx43 . Introduction: In disease states such as heart failure, myocardial infarction, and hypertrophy, changes in the expression and location of Connexin43 (Cx43) occur (Cx43 remodeling), and may predispose to arrhythmias. Stretch may be an important stimulus to Cx43 remodeling; however, it has only been investigated in neonatal cell cultures, which have different physiological properties than adult myocytes. We hypothesized that localized stretch in vivo causes Cx43 remodeling, with associated changes in conduction, mediated by the renin–angiotensin system (RAS). Methods and Results: In an open‐chest canine model, a device was used to stretch part of the right ventricle (RV) by 22% for 6 hours. Activation mapping using a 312‐electrode array was performed before and after stretch. Regional stretch did not change longitudinal conduction velocity (post‐stretch vs baseline: 51.5 ± 5.2 vs 55.3 ± 8.1 cm/s, P = 0.24, n = 11), but significantly reduced transverse conduction velocity (28.7 ± 2.5 vs 35.4 ± 5.4 cm/s, P < 0.01). It also reduced total Cx43 expression, by Western blotting, compared with nonstretched RV of the same animal (86.1 ± 32.2 vs 100 ± 19.4%, P < 0.02, n = 11). Cx43 labeling redistributed to the lateral cell borders. Stretch caused a small but significant increase in the proportion of the dephosphorylated form of Cx43 (stretch 9.95 ± 1.4% vs control 8.74 ± 1.2%, P < 0.05). Olmesartan, an angiotensin II blocker, prevented the stretch‐induced changes in Cx43 levels, localization, and conduction. Conclusion: Myocardial stretch in vivo has opposite effects to that in neonatal myocytes in vitro. Stretch in vivo causes conduction changes associated with Cx43 remodeling that are likely caused by local stretch‐induced activation of the RAS. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1276‐1283, November 2010)相似文献