Can the Non-pneumatic Anti-Shock Garment (NASG) reduce adverse maternal outcomes from postpartum hemorrhage? Evidence from Egypt and Nigeria

<p>Abstract</p> <p>Background</p> <p>Postpartum hemorrhage (PPH) is the leading cause of maternal mortality and severe maternal morbidity. The Non-pneumatic Anti-Shock Garment (NASG), a first-aid lower-body compression device, may decrease adverse outcomes from obstetric hemorrhage. This article is the first to report the effect of the NASG for PPH.</p> <p>Methods</p> <p>This pre-intervention/NASG study of 854 women was conducted in four referral facilities in Nigeria and two in Egypt between 2004-2008. Entry criteria were women with PPH due to uterine atony, retained placenta, ruptured uterus, vaginal or cervical lacerations or placenta accreta with estimated blood loss of ≥ 750 mL and one clinical sign of shock. Differences in demographics, conditions on study entry, treatment and outcomes were examined. The Wilcoxon rank-sum test and relative risks with 95% confidence intervals were calculated for primary outcomes - measured blood loss, emergency hysterectomy, mortality, morbidity (each individually), and a combined variable, "adverse outcomes", defined as severe morbidity and mortality. A multiple logistic regression model was fitted to test the independent association between the NASG and the combined severe morbidity and mortality outcome.</p> <p>Results</p> <p>Measured blood loss decreased by 50% between phases; women experienced 400 mL of median blood loss after study entry in the pre-intervention and 200 mL in the NASG phase (p < 0.0001). As individual outcomes, mortality decreased from 9% pre-intervention to 3.1% in the NASG phase (RR 0.35, 95% CI 0.19-0.62); severe morbidity decreased from 4.2% to 1%, in the NASG phase (RR 0.24, 95% CI 0.09-0.67). As a combination, "adverse outcomes," decreased from 12.8% to 4.1% in the NASG phase (RR 0.32, 95% CI 0.19-0.53). In a multiple logistic regression model, the NASG was associated with the combined outcome of severe maternal morbidity and mortality (OR 0.42, 95% CI 0.18-0.99).</p> <p>Conclusion</p> <p>In this non-randomized study, in which bias is inherent, the NASG showed promise for reducing blood loss, emergency hysterectomy, morbidity and mortality associated with PPH in referral facilities in Egypt and Nigeria.</p

Clinical Outcome of Carotid Body Paraganglioma Management: A Review of 10-Year Experience

Background. Carotid body paragangliomas are rare neoplasms usually benign, however sometimes presenting as highly aggressive tumors. Surgery is the main line of treatment. Purpose. To study and describe clinical presentations, surgical approaches, postoperative complications, and treatment outcomes. Materials and Methods. A single-institution retrospective analysis of 19 cases with carotid body paragangliomas who were candidates for surgery from January 2009 through January 2019 with a mean follow-up period of 58.8 months. Results. The mean age was 46 years with the female predominance of 63%. The mean size of the tumor was 4.3 cm. All cases were presented with a painless pulsating neck lump located anteriorly at the level of the hyoid bone. Neck US was done in all cases as a primary screening investigation. CT scanning was the second main investigation performed in 17 cases (89.5%) revealing tumors attached to the carotid artery at its bifurcation. Urinary catecholamine metabolites were measured in all cases to rule out familial functioning types. 5 cases (26.3%) were malignant. All cases were surgically approached through transcervical transverse incision. 11, 5, and 3 cases were classified as Shamblin’s type II, III, and I, respectively. All tumors were R0 resected with nodal neck dissection conducted in the malignant group. Major complications occurred in 4 cases (21%) during tumor dissection from the adventitia of carotid bifurcation. ECA ligation was performed in one case (5.3%). 2 patients (10.5%) suffered XII nerve paralysis. Carotid artery blowout occurred in one patient (5.3%) and was immediately controlled. No operative mortality occurred. All patients were free of disease during the follow-up period. 4 malignant cases (21%) suffered a systemic relapse to bone and lung metastasis justifying adjuvant chemotherapy, radiotherapy, or both. Conclusions. Surgery is the treatment of choice for carotid body paragangliomas. Complete R0 resection should be justified especially in case of malignancy. Adjuvant chemotherapy or radiotherapy is an option for patients with primary malignancy or relapse

Negative optokinetic afternystagmus in larval zebrafish demonstrates set-point adaptation

Motor learning is essential to maintain accurate behavioral responses. We used a larval zebrafish model to study ocular motor learning behaviors. During a sustained period of optokinetic stimulation in 5-day-old wild-type zebrafish larvae the slow-phase eye velocity decreased over time. Then interestingly, a long-lasting and robust negative optokinetic afternystagmus (OKAN) was evoked upon light extinction. The slow-phase velocity, the quick-phase frequency, and the decay time constant of the negative OKAN were dependent on the stimulus duration and the adaptation to the preceding optokinetic stimulation. Based on these results, we propose a sensory adaptation process during continued optokinetic stimulation, which, when the stimulus is removed, leads to a negative OKAN as the result of a changed retinal slip velocity set point, and thus, a sensorimotor memory. The pronounced negative OKAN in larval zebrafish not only provides a practical solution to the hitherto unsolved problems of observing negative OKAN, but also, and most importantly, can be readily applied as a powerful model for studying sensorimotor learning and memory in vertebrates

The role of biofeedback in the rehabilitation of veno-occlusive erectile dysfunction

Background Pelviperineal muscles play a role in erection through the enhancement of blood flow to the penis. Hence, the reinforcement of the power of such muscles through noninvasive visual pressure biofeedback rehabilitation may be helpful in erectile function improvement. Aim The aim of this study was to assess the value of pelviperineal muscles′ visual pressure biofeedback rehabilitation in the treatment of organic veno-occlusive erectile dysfunction (ED). Materials and methods This study included 30 patients with veno-occlusive ED. Exclusion criteria were neurological, psychological, endocrinal, and arterial insufficiency ED. Also, patients with malignancies, chronic renal failure, liver cell failure, urological congenital abnormalities, pelvic surgery, pelvic radiation, or trauma and patients on medications known to cause ED were excluded. All patients performed visual pressure biofeedback strengthening of the pelviperineal muscles three times weekly for 3 months. In addition to clinical and laboratory evaluations, patients were assessed by a self-administered questionnaire, a neurophysiological examination, a pharmacopenile duplex ultrasound, and the anal hold pressure. Results According to the self-administered questionnaire, 16/30 patients (53.3%) showed either partial or complete improvement (11 and five patients, respectively). On comparing prerehabilitation and postrehabilitation Results of the pharmacopenile duplex ultrasound, 18/30 patients (60%) showed either partial or complete improvement (13 and five patients, respectively). The anal hold pressure improved from 120.7 to 189.9 after biofeedback rehabilitation. Conclusion Pelviperineal muscles′ visual pressure biofeedback rehabilitation is effective, inexpensive, noninvasive, safe, and easily applicable in the treatment of venogenic ED and does not have as much side effects as medication

Negative optokinetic afternystagmus in larval zebrafish demonstrates set-point adaptation

Motor learning is essential to maintain accurate behavioral responses. We used a larval zebrafish model to study ocular motor learning behaviors. During a sustained period of optokinetic stimulation in 5-day-old wild-type zebrafish larvae the slow-phase eye velocity decreased over time. Then interestingly, a long-lasting and robust negative optokinetic afternystagmus (OKAN) was evoked upon light extinction. The slow-phase velocity, the quick-phase frequency, and the decay time constant of the negative OKAN were dependent on the stimulus duration and the adaptation to the preceding optokinetic stimulation. Based on these results, we propose a sensory adaptation process during continued optokinetic stimulation, which, when the stimulus is removed, leads to a negative OKAN as the result of a changed retinal slip velocity set point, and thus, a sensorimotor memory. The pronounced negative OKAN in larval zebrafish not only provides a practical solution to the hitherto unsolved problems of observing negative OKAN, but also, and most importantly, can be readily applied as a powerful model for studying sensorimotor learning and memory in vertebrates.ISSN:2045-232

INTS13 variants causing a recessive developmental ciliopathy disrupt assembly of the Integrator complex

International audienceAbstract Oral-facial-digital (OFD) syndromes are a heterogeneous group of congenital disorders characterized by malformations of the face and oral cavity, and digit anomalies. Mutations within 12 cilia-related genes have been identified that cause several types of OFD, suggesting that OFDs constitute a subgroup of developmental ciliopathies. Through homozygosity mapping and exome sequencing of two families with variable OFD type 2, we identified distinct germline variants in INTS13 , a subunit of the Integrator complex. This multiprotein complex associates with RNA Polymerase II and cleaves nascent RNA to modulate gene expression. We determined that INTS13 utilizes its C-terminus to bind the Integrator cleavage module, which is disrupted by the identified germline variants p.S652L and p.K668Nfs*9. Depletion of INTS13 disrupts ciliogenesis in human cultured cells and causes dysregulation of a broad collection of ciliary genes. Accordingly, its knockdown in Xenopus embryos leads to motile cilia anomalies. Altogether, we show that mutations in INTS13 cause an autosomal recessive ciliopathy, which reveals key interactions between components of the Integrator complex