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Articles by S Ahmad
Total Records ( 6 ) for S Ahmad
  G. S De Oliveira , S Ahmad , P. C Fitzgerald and R. J. McCarthy
  Background

Transcutaneous measurement of carbon dioxide (Tcco2) provides a non-invasive estimation of arterial carbon dioxide (Paco2). Nasal capnography (Pe'co2) is used to assess ventilation during monitored anaesthesia care (MAC) with sedation since it can readily detect apnoea. We compared the agreement between Tcco2 and Pe'co2 with Paco2 and the ability to detect hypercarbia in patients under deep sedation.

Methods

Forty healthy female subjects receiving deep sedation for hysteroscopy were studied. A Tcco2 (TOSCA 500, Radiometer, Inc., Westlake, OH, USA) electrode was applied to the earlobe and Pe'co2 capnography was monitored using nasal side-stream sampling. All subjects received oxygen (3 litre min–1). Subjects were evaluated at intervals using a modified Ramsay sedation score until they reached a score ≥5. Arterial blood gas values were compared with Tcco2 and Pe'co2 values. Bland–Altman, linear regression, and receiver operator characteristics analysis were performed.

Results

The mean (sd) absolute difference between the Tcco2, Pe'co2, and the Paco2 were 0.43 (0.35) and 1.06 (0.8) kPa, respectively (P=0.002). Tcco2 demonstrated a mean bias (2 sd) of 0.23 (0.07–0.4) kPa with Paco2 compared with –0.93 (–1.24 to –0.63) kPa for Pe'co2. One minute before blood sampling, the sensitivity of the Tcco2 monitor for detecting Paco2 >6.65 kPa was greater than for Pe'co2 (66.7% vs 33.3%, P<0.01).

Conclusions

Tcco2 demonstrated better agreement with Paco2 than Pe'co2 for patients under MAC with deep sedation. Tcco2 monitoring was more sensitive for detection of Paco2 >6.65 kPa than Pe'co2.

  C. F Barnett , E. J Bonura , S. D Nathan , S Ahmad , O. A Shlobin , K Osei , A. L Zaiman , P. M Hassoun , D. R Moller , S. D Barnett and R. E. Girgis
  Background:

Pulmonary hypertension (PH) is a common complication of sarcoidosis that is associated with increased mortality. The pathogenesis of PH in sarcoidosis is uncertain, and the role of pulmonary arterial hypertension (PAH)-specific therapies remains to be determined.

Methods:

We conducted a retrospective study of patients with sarcoidosis and PH at two referral centers. New York Heart Association (NYHA) functional class, exercise capacity, hemodynamic data, pulmonary function tests, and survival were collected and analyzed.

Results:

Twenty-two sarcoidosis patients treated with PAH-specific therapies were identified. After a median of 11 months of follow-up, NYHA class was improved in nine subjects. Mean 6-min walk distance (n = 18) increased by 59 m (p = 0.032). Patients with a higher FVC experienced a greater increment in exercise capacity. Among 12 patients with follow-up hemodynamic data, mean pulmonary artery pressure was reduced from 48.5 ± 4.3 to 39.4 ± 2.8 mm Hg (p = 0.008). The 1- and 3-year transplant-free survival rates were 90% and 74%, respectively.

Conclusions:

PAH-specific therapy may improve functional class, exercise capacity, and hemodynamics in PH associated with sarcoidosis. Prospective, controlled trials of PAH therapies for sarcoidosis are warranted to verify this apparent benefit. Mortality among the study population was high, highlighting the need for urgent evaluation at a lung transplant center.

  A Ahmed , T Fujisawa , X. L Niu , S Ahmad , B Al Ani , K Chudasama , A Abbas , R Potluri , V Bhandari , C. M Findley , G. K.W Lam , J Huang , P. W Hewett , M Cudmore and C. D. Kontos
 

Atherosclerosis is promoted by a combination of hypercholesterolemia and vascular inflammation. The function of Angiopoietin (Ang)-2, a key regulator of angiogenesis, in the maintenance of large vessels is unknown. A single systemic administration of Ang-2 adenovirus (AdAng-2) to apoE–/– mice fed a Western diet significantly reduced atherosclerotic lesion size (40%) and oxidized LDL and macrophage content of the plaques. These beneficial effects were abolished by the inhibition of nitric oxide synthase (NOS). In endothelial cells, endothelial NOS activation per se inhibited LDL oxidation and Ang-2 stimulated NO release in a Tie2-dependent manner to decrease LDL oxidation. These findings demonstrate a novel atheroprotective role for Ang-2 when endothelial cell function is compromised and suggest that growth factors, which stimulate NO release without inducing inflammation, could offer atheroprotection.

  S. A McCalmon , D. M Desjardins , S Ahmad , K. S Davidoff , C. M Snyder , K Sato , K Ohashi , O. M Kielbasa , M Mathew , E. P Ewen , K Walsh , H Gavras and F. J. Naya
 

Rationale: The vasoactive peptide angiotensin II (Ang II) is a potent cardiotoxic hormone whose actions have been well studied, yet questions remain pertaining to the downstream factors that mediate its effects in cardiomyocytes.

Objective: The in vivo role of the myocyte enhancer factor (MEF)2A target gene Xirp2 in Ang II–mediated cardiac remodeling was investigated.

Methods and Results: Here we demonstrate that the MEF2A target gene Xirp2 (also known as cardiomyopathy associated gene 3 [CMYA3]) is an important effector of the Ang II signaling pathway in the heart. Xirp2 belongs to the evolutionarily conserved, muscle-specific, actin-binding Xin gene family and is significantly induced in the heart in response to systemic administration of Ang II. Initially, we characterized the Xirp2 promoter and demonstrate that Ang II activates Xirp2 expression by stimulating MEF2A transcriptional activity. To further characterize the role of Xirp2 downstream of Ang II signaling we generated mice harboring a hypomorphic allele of the Xirp2 gene that resulted in a marked reduction in its expression in the heart. In the absence of Ang II, adult Xirp2 hypomorphic mice displayed cardiac hypertrophy and increased β myosin heavy chain expression. Strikingly, Xirp2 hypomorphic mice chronically infused with Ang II exhibited altered pathological cardiac remodeling including an attenuated hypertrophic response, as well as diminished fibrosis and apoptosis.

Conclusions: These findings reveal a novel MEF2A-Xirp2 pathway that functions downstream of Ang II signaling to modulate its pathological effects in the heart.

  S Ahmad , J. C Ellis , H Kamwendo and E. M. Molyneux
  Objective

To assess the impact of HIV infection and exposure on survival in critically ill children requiring resuscitation.

Methods

A 6-month descriptive prospective cohort study of all live admissions to the resuscitation room of an urban paediatric emergency department in Blantyre, Malawi.

Results

583 children were resuscitated, of whom 401 (69%) survived to hospital discharge. 26% of all children tested positive for HIV infection (152/576), and this was highest in patients presenting with shock (66%; 162/247), clinically diagnosed septicaemia (57%; 125/218) and malnutrition (40%; 24/60). Of 152 HIV-seropositive children, 30 (20%) died within 24 h, while among 424 seronegative children 36 (8.4%) died within 24 h (p<0.001). Later deaths (>24 h) were also more common in HIV-seropositive children compared with HIV-uninfected patients (24.3% vs 12.3%; p<0.001). Survival to 24 h was 80% (122/152) and to discharge 56% (85/152) in HIV-seropositive children. In HIV-uninfected children survival to 24 h was 92% (388/424) and to discharge 79% (336/424).

Conclusion

Early and late case death rates are greater in HIV-seropositive than in HIV-uninfected children. 80% of HIV-infected children survived the period most influenced by the process of resuscitation, that is, the first 24 h. HIV status alone should not influence the limitation of intervention decisions in the resuscitation room when faced with a critically ill child.

  B. J Blencowe , S Ahmad and L. J. Lee
 

Recent papers have described the first application of high-throughput sequencing (HTS) technologies to the characterization of transcriptomes. These studies emphasize the tremendous power of this new technology, in terms of both profiling coverage and quantitative accuracy. Initial discoveries include the detection of substantial new transcript complexity, the elucidation of binding maps and regulatory properties of RNA-binding proteins, and new insights into the links between different steps in pre-mRNA processing. We review these findings, focusing on results from profiling mammalian transcriptomes. The strengths and limitations of HTS relative to microarray profiling are discussed. We also consider how future advances in HTS technology are likely to transform our understanding of integrated cellular networks operating at the RNA level.

 
 
 
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