45513770
The acronym "PCP" is Pneumocystis pneumonia, not Pneumocystis carinii pneumonia.
33491888
Noninvasive ventilation in ARDS caused by Mycobacterium tuberculosis: report of three cases and review of literature
22528299
Pulmonary hypertension as a presenting manifestation of allergic bronchopulmonary aspergillosis.
The case of a 46-year-old lady who presented with respiratory failure and pulmonary hypertension in the absence of clinical signs of asthma or bronchiectasis, and in whom a diagnosis of allergic bronchopulmonary aspergilloma [ABPA] was made subsequently on the basis of radiological and laboratory investigations is reported. Symptomatic and objective improvement was seen with corticosteroid therapy. To the best of the authors' knowledge, such an occurrence has not been reported previously. This case highlights the importance of keeping a high index of suspicion while investigating a patient with pulmonary hypertension in whom the aetiology is not apparent on initial evaluation. Identification of the disease, in its early-stage, can prevent progression to bronchiectasis and fibrotic lung disease, and thus, patients can be saved from the morbidity related to end-stage disease.
45999589
Noninvasive ventilation in acute heart failure.
3038618
Is the mortality higher in the pulmonary vs the extrapulmonary ARDS? A meta analysis.
BACKGROUND AND AIM
ARDS can occur from the following two pathogenetic pathways: a direct pulmonary injury (ARDSp); and an indirect injury (ARDSexp). The predisposing clinical factor can influence the pathogenesis and clinical outcome of ARDS. This metaanalysis was aimed at evaluating whether there is any difference in mortality between the two groups.


METHODS
We searched the MEDLINE, EMBASE, and CINAHL databases for relevant studies published from 1987 to 2007, and included studies that have reported mortality in the two groups of ARDS. We calculated the odds ratio (OR) and 95% confidence interval (CI) to assess mortality in patients with ARDSp vs patients with ARDSexp and pooled the results using three different statistical models.


RESULTS
Our search yielded 34 studies. In all, the studies involved 4,311 patients with 2,330 patients in the ARDSp group and 1,981 patients in the ARDSexp group. The OR of mortality in ARDSp group compared to the ARDSexp group was 1.11 (95% CI, 0.88 to 1.39), as determined by the random-effects model; 1.04 (95% CI, 0.92 to 1.18), as determined by the fixed-effects model; and 1.04 (95% CI, 0.92 to 1.18), as determined by the exact method, indicating that mortality is similar in the two groups. The mortality was no different whether the studies were classified as prospective (OR, 1.15; 95% CI, 0.87 to 1.51) or retrospective (OR, 1.01; 95% CI, 0.61 to 1.69); small (OR, 1.11; 95% CI, 0.77 to 1.60) or large (OR, 1.1; 95% CI, 0.82 to 1.49); or observational (OR, 1.10; 95% CI, 0.82 to 1.49) or interventional (OR, 0.97; 95% CI, 0.79 to 1.19). There was methodological and statistical heterogeneity (I(2), 50.9%; 95% CI, 21.3 to 66.2%; chi(2) statistic, 67.22; p = 0.0004).


CONCLUSIONS
The results of this study suggest that there is no difference in mortality between these two groups. Further studies should focus on specific etiologies within the subgroups rather than focusing on the broader division of ARDSp and ARDSexp.
26068481
Efficacy and safety of iodopovidone pleurodesis through tube thoracostomy.
OBJECTIVE
To evaluate the efficacy and safety of iodopovidone as an agent for pleurodesis through tube thoracostomy in patients with recurrent pleural effusions and pneumothorax.


METHODS
This was a prospective study in which pleurodesis was performed with a solution of 20 mL 10% iodopovidone and 80 mL normal saline solution infused through a tube thoracostomy and left in the pleural cavity for 4 h.


RESULTS
A total of 64 patients (34 men) with a mean (+/-SD) age of 47.1 +/- 15.4 years were included. There were 37 cases of pleural effusion and 27 of pneumothorax. A complete response (neither reaccumulation of fluid nor recurrence of pneumothorax) was obtained in 32 (86.5%) patients with pleural effusion and 25 (92.6%) patients with pneumothorax. A second procedure (i.e. repeated pleurodesis) was attempted successfully in four patients in the pleural effusion group. All patients experienced chest pain to a varying degree as recorded on a Visual Analogue Scale (median 50.5, range 10-95). Seven patients developed fever and one immunocompromised patient developed empyema following the procedure. There were no recurrences at a median follow up of 5 months (range 3-15 months) in the pleural effusion group, and 13 months (range 6-24 months) in the pneumothorax group.


CONCLUSIONS
Iodopovidone can be used as an effective and safe agent for (chemical) pleurodesis (through tube thoracostomy), which is inexpensive and readily available.
38365589
Quantification of tumour initiating effect of jute batching oil and its distillates over mouse skin.
In order to identify the tumour initiating constituent(s) of a mineral oil, jute batching oil (JBO), used in the processing of jute fibres, it was fractionally distilled in various boiling range fractions. The latter were then subjected to in vivo assessment of their aryl hydrocarbon hydroxylase (AHH) inducing potential in mouse epidermis. Fractions with almost similar AHH inducing potential were regrouped and studied for their tumour initiating potential over mouse skin following two-stage initiation-promotion protocol and using 12-O-tetradecanoyl phorbol-13-acetate (TPA) as tumour promoter. It was noticed that: (1) JBO as initiator, provoked local development of benign skin tumours over mouse back; (2) fractions of JBO boiling below 335 degrees C and above 399 degrees C accounted for most of the tumour initiating potential of the oil; (3) the histological features of the tumours (i.e. benign papillomas and keratoacanthomas) initiated by these fractions were similar to those developed after being initiated with unfractionated or reconstituted JBO; (4) removal of these fractions from JBO may be attempted which could decontaminate the batch oil from most of its tumorigenic components and make it safer for industrial use.
44772256
The septospinal ligament in cleft lip nose deformity: study in adult unilateral clefts.
BACKGROUND
Septal deviation and alar cartilage deformities constitute an important component of both the aesthetic deformity and airway compromise in unilateral cleft lip nose deformity. The purpose of this study was to examine the retrocolumellar preseptal area in this deformity for evaluation of deforming forces in the adult population.


METHODS
Fifty-five patients aged 13 years or older presenting with unilateral cleft nasal deformity were included. The caudal border of the septum was accessed using an incision along the ipsilateral membranous septum. Perioperatively, the curved caudal septal edge was exposed and explored down to its attachment with the hypertrophied anterior nasal spine. The overlying tethering tissues were excised and submitted for histopathologic examination. The curved septal cartilage was straightened and the misplaced anterior nasal spine was excised. The remaining cleft nasal deformity was corrected depending on the specific presenting pathologic abnormality.


RESULTS
A well-defined, tough, fibrous band was detected extending from the deviated curved surface of the septal cartilage to the anterior nasal spine that was filling up the retrocolumellar area. Histopathologic examination revealed fibrous tissue in all cases studied, consistent with diagnosis of a ligament. Postoperatively, the nasal tip complex cosmetic result was considered to be good or very good in 89.7 percent, satisfactory in 8.1 percent, and poor in 2.0 percent of patients.


CONCLUSIONS
A well-defined ligament has been documented and demonstrated in adult patients with unilateral cleft lip nose deformity. The authors recommend that this septospinal ligament, previously unreported, should be excised in toto to achieve straightening of the septum, columellar centralization, and nasal sill symmetry in unilateral cleft lip nose deformity.
19302108
Gone astray: Imaging suggested an ovarian tumor, but physicians identified something quite different.
44919999
Asymptomatic incomplete left ventricular apical rupture diagnosed by cardiac magnetic resonance imaging.
66-year-old man presented with a fever of 103 °F, cough, and dyspnea, despite 3 days' treatment of pneumonia. Chest radiography revealed a normal cardiac silhouette and a small left pleural effusion. A baseline electrocardiogram (ECG) showed normal sinus rhythm with profound ST-segment elevation in the anterolateral leads. An ECG obtained 2 months earlier was normal. An echocardiogram showed severe hypokinesis of the anterior, anteroseptal, and apical segments without evidence of a pericardial effusion. Coronary angiography revealed complete occlusion of the proximal left anterior descending coronary artery with severe distal anterior hypokinesis. 
 
Forty-eight hours after admission, the patient had recurrent fever. A repeat transthoracic echocardiogram (Fig. 1) revealed a thin, aneurysmal, left ventricular (LV) apex with pericardium apparently adherent to the apex. In addition, a moderate-to-large, echo-free pericardial effusion was noted. Out of clinical concern for a possible contained LV rupture, cardiac magnetic resonance imaging (CMR) was performed for definitive evaluation and tissue characterization. 
 
 
 
Fig. 1 Transthoracic echocardiogram (4-chamber view at end-systole) reveals an apex-sparing pericardial effusion and an aneurysmal left ventricular apex. 
 
 
 
The CMR (Figs. 2 and 3) revealed evidence of a large myocardial infarction (MI) with subsequent aneurysm formation involving the distal half of the left anterior descending artery distribution and the entire apex, with an extensive amount of thrombus in the apex. A “hinge-point” involving the lateral and anterolateral walls was noted, raising the concern of a possible contained rupture of the LV apex. A large, predominantly simple-appearing pericardial effusion was noted circumferentially, but the apex was spared. The pericardium was hyperenhanced on viability/ scar imaging in the regions of infarct, suggesting post-MI pericarditis. 
 
 
 
Fig. 2 Cine cardiac magnetic resonance imaging demonstrates a large aneurysmal area involving the distal half of the left anterior descending coronary artery distribution with an extensive amount of thrombus at the apex. A hinge-point involving the lateral ... 
 
 
 
 
 
Fig. 3 Viability/scar imaging reveals a transmural infarction of the affected area. The remainder of the left ventricular myocardium appears to be of full thickness and viable. There is also hyperenhancement of the pericardium in the infarct regions, ... 
 
 
 
A follow-up echocardiogram performed 1 week later showed a slight decrease in the size of the pericardial effusion. Repair of the LV was deferred until effective surgical suturing could be performed on the infarcted area. 
 
Eight weeks later, the patient underwent successful LV endoaneurysmorrhaphy with a Dacron patch. Intraoperatively, a 3- × 4-cm balloon-like aneurysm was found to be fused to the pericardial sac. The aneurysm was excised, and subsequent microscopic evaluation revealed necrotic myocardium and reactive connective tissue (Fig. 4). The patient had an uneventful hospital course and was discharged from the hospital in stable condition. At a follow-up visit 2 months later, he reported a substantial increase in exercise tolerance and a return to usual daily activities. 
 
 
 
Fig. 4 Photomicrograph illustrates necrotic myocardium and adjacent reactive connective tissue. (H & E, orig. ×100)
8524964
Relationship between circadian blood pressure variation and circadian protein excretion in CKD.
Circadian blood pressure changes are blunted in patients with chronic kidney disease (CKD). Proteinuria is the most important correlate of hypertension in CKD. However, little is known about the influence of circadian blood pressure changes and variation in protein excretion rate. Furthermore, the impact of blood pressure components, e.g., mean arterial pressure and pulse pressure, on proteinuria has not been evaluated. To analyze the relationship of circadian changes in blood pressure on urinary protein excretion patterns, glomerular filtration rate was measured with iothalamate clearance and 24-h ambulatory blood pressure with SpaceLabs 90207 monitor in 22 patients with CKD. It was found that hourly protein excretion rates were 31% higher during the night. Excretion results of sodium, potassium, chloride, urea, and creatinine were also between 30 and 40% higher at night. Systolic, mean arterial, and pulse pressures but not diastolic pressure were related to daytime protein excretion rate. At night, the relationship of systolic, diastolic, and mean arterial pressures was significantly lower and essentially flat with respect to protein excretion rate, but the relationship of pulse pressure and proteinuria was not different from that seen during the day. Circadian variation in blood pressure did not impact circadian sodium excretion rate. In conclusion, these data suggest that patients with CKD have patterns of proteinuria that share different relationships with blood pressure components depending on the awake-sleep state. Pulse pressure is related to proteinuria independent of the awake-sleep state. Reducing mean arterial pressure during the day and pulse pressure during the day or night may be effective antiproteinuric strategies.