Mechanistic pathways for the degradation of SMX drug and floatation of degraded products using F–Pt co-doped TiO2 photocatalysts

This work presents smart pathways to enhance the photocatalytic activity of TiO₂via co-doping with fluorine (F) and platinum (Pt) to form F–Pt co-doped TiO₂ photocatalysts and investigates the unique and unusual fluorination of the floated products. Our investigations indicate that the crystalline structure of the photocatalysts was a mixture of anatase and brookite phases and that the nanoparticles of the synthesized nanocomposites had nanometric sizes (4–25 nm). The F–Pt co-doped TiO₂ nano-photocatalysts demonstrated degradation of sulfamethoxazole (SMX) drug of >93% within 90 min under direct solar light and 58% degradation within 360 min under a solar simulator. Thus, co-doping TiO₂ with F and Pt atoms to form F–Pt co-doped TiO₂ nanocomposite is an efficient pathway to achieve high photocatalytic performance escorted with the formation of floating metal-fluoropolymer, unlike pristine TiO₂ which has less photocatalytic degradation and no generation of a floating polymer. Our photocatalytic protocol demonstrates that the degradation of SMX started with redox reactions of oxygen and water absorbed on the surface of the prepared nanocomposites to form superoxide anions (O₂˙⁻) and hydroxy radicals (˙OH) which have oxidation superpower. The resultant products were subsequently fluorinated by fluoride radical ions and floated as metal-fluoropolymer.

This work presents smart pathways to enhance the photocatalytic activity of TiO₂via co-doping with fluorine (F) and platinum (Pt) to form F–Pt co-doped TiO₂ photocatalysts and investigates the unique and unusual fluorination of the floated products.     

Transient versus surgically managed small bowel intussusception in children: Role of ultrasound

Background:

To evaluate and compare the ultrasound (US) features of transient small bowel intussusception (SBI) with those which required surgical management.

Materials and Methods:

US features of 26 children with 32 intussusceptions from January 2014 to August 2014 were recorded and compared with follow-up imaging or surgical findings.

Results:

Transient SBI when compared to surgically managed intussusception has shorter length of intussusception (mean 2.25 cm, range 1.8-4.5 cm vs. mean 5.6 cm, range, 2.3-7.8 cm), smaller transverse diameter (mean, 1.2 cm, range 0.8-2.3 cm vs. mean, 3.3 cm, range 2.9-5.4 cm) and thin wall (mean, 3.3 mm, 2.3-4.9 mm vs. mean, 6.8 mm, range, 4.3-11.2 mm). Four out of five surgically managed intussusceptions were associated with the lead point while none of the transient SBI had any lead point. Peristalsis was absent in all surgically managed intussusceptions.

Conclusion:

Transient SBI is associated with a shorter length of intussusception, smaller transverse diameter, thin walls, absence of the lead point and visible peristalsis. All these findings may help in distinguishing it from those requiring surgical management.Key words: Children, surgically managed small bowel intussusception, transient small bowel intussusception, ultrasound     

Superolateral Dislocation of the Mandibular Condyle: A Series of Seven Cases

Introduction

Anterior and anteromedial dislocations of the mandibular condyle are seen frequently in mandibular fractures. Less frequent are dislocations of the condylar head in the lateral, medial and posterior direction whereas superior dislocation into the middle cranial fossa is rare. We report a series of seven cases encountered over the years, which, incidentally, is the largest case series reported till date with lateral and superolateral dislocation of the condyle after a traumatic injury.

Materials and method

In all cases but one, the condyle was reduced by manual manipulation with the patient in general anaesthesia. In all cases but one there was simultaneous fracture in the mandibular symphyseal region. The associated fractures were reduced and fixed with bone plates and screws.

Results

Patients were generally free from any long term complications of injury or surgery except for facial nerve paresis of a transient nature in one case.

Conclusion

To our knowledge, this clinical series presents the first reported case of superolateral dislocation which required open reduction. The etiology and mechanism of dislocation has been discussed along with a brief review of the literature.

Electronic supplementary material

The online version of this article (doi:10.1007/s12663-015-0770-9) contains supplementary material, which is available to authorized users.     

Indian tick typhus presenting as Purpura fulminans

Seriously ill patients presenting with purpura fulminans, sepsis and multi-organ failure often require extensive diagnostic workup for proper diagnosis and management. Host of common infections prevalent in the tropics, e.g. malaria, dengue; other septicemic infections e.g. meningococcemia, typhoid, leptospirosis, toxic shock syndrome, scarlet fever, viral exanthems like measles, infectious mononucleosis, collagen vascular diseases (Kawasaki disease, other vasculitis) diseases, and adverse drug reactions are often kept in mind, and the index of suspicion for rickettsial illness is quite low. We present a case of Indian tick typhus presenting with purpura fulminans (retiform purpura all over the body), sepsis and multiorgan failure without lymphadenopathy and eschar, successfully treated with doxycycline and discharged home. Hence, a high index clinical suspicion and prompt administration of a simple therapy has led to successful recovery of the patient.     

Reversibility of Retinal Microvascular Changes in Severe Falciparum Malaria

Malarial retinopathy allows detailed study of central nervous system vascular pathology in living patients with severe malaria. An adult with cerebral malaria is described who had prominent retinal whitening with corresponding retinal microvascular obstruction, vessel dilatation, increased vascular tortuosity, and blood retinal barrier leakage with decreased visual acuity, all of which resolved on recovery. Additional study of these features and their potential role in elucidating the pathogenesis of cerebral malaria is warranted.The pathogenesis of coma in falciparum malaria and its rapid reversibility are potential targets for adjunctive therapies, but they are not well-understood. Microvascular obstruction is probably an important contributor. The brain microvasculature is relatively inaccessible; it can be studied in detail only at post-mortem. Similarly, microvascular obstruction in the retina is thought to be a major contributor to the unique retinopathy of severe falciparum malaria, and, because it is easily visualized in living subjects, in-depth study is providing new and valuable insights. We describe an adult patient with cerebral malaria who had prominent retinal changes with some previously unrecognized features that resolved on recovery.A 24-year-old male truck driver from Orissa, India was admitted with severe Plasmodium falciparum malaria (parasitemia = 0.3%) with coma, generalized convulsions, hyperlactatemia, renal failure, and black urine. He had no prior medical history. Retinal photography showed bilateral patchy macular whitening with corresponding capillary non-perfusion and leakage of fluorescein caused by blood retinal barrier breakdown on fluorescein angiography (Figure 1). He was treated with intravenous artesunate, and from recovery of consciousness on day 3 to discharge, his visual acuity was markedly reduced (counting digits only), with loss of red–green color vision. Repeat examination on day 55 showed that the retinal changes, angiogram abnormalities, and visual deficits had resolved (acuity 6/9 bilaterally and normal color vision). Blood vessel tortuosity measured in three arteries and three veins by a single blinded observer tracing the center line of vessels between branch points in matched pairs of retinal photographs using Adobe Photoshop CS4 (Adobe Systems, San Jose, CA)¹ was greater on day 0 than day 55 (mean ratios of vessel widths measured at 10 points in each vessel; 1.226 in arteries and 1.172 in veins; vessel lengths were 1.043 and 1.035). These differences are similar to those found previously in diabetic macular edema.¹Open in a separate windowFigure 1.(A and B) Retinal photographs and (C and D, arterial phase; E and F, late phase) fluorescein angiograms of the left eye. On day 3, increased vessel thickness and tortuosity plus (A) patchy macular whitening with corresponding areas of (C) reduced perfusion and (E) fluorescein leakage were seen. On day 55, normal vessels, (B) no whitening, and (D) normal perfusion around the fovea with (F) no leakage of fluorescein were seen.Malarial retinal whitening is thought to be caused by hypoxic opacification of the retina after obstruction of small blood vessels by sequestered parasites.^2,3 It is similar to patchy ischemic retinal whitening (PIRW), a transient early sign of central retinal vein occlusion (CRVO)² thought to represent intracellular edema of overlying retinal intermediary neurones.⁴ The degree of retinal whitening in adults and children correlates with severity of malaria and peripheral blood lactate.^5,6 Hyperlactatemia is common in severe malaria and at least partly caused by obstruction of the systemic microcirculation by sequestered parasites. Cerebrospinal fluid lactate concentrations are also raised in cerebral malaria, and in those cases it is predictive of mortality.⁷The appearance and distribution of retinal whitening are unique to severe falciparum malaria. Typically, there are multiple small lesions most prominent in the macula, particularly temporal to the fovea. This area is a watershed between the superior and inferior retinal vascular arcades and particularly vulnerable to ischemic insults. Midperipheral involvement in malaria distinguishes it from PIRW, Purtscher''s retinopathy, and cotton wool spots (sometimes also seen in malaria), which are distributed particularly around the optic disk and typically more opaque. Malarial retinopathy is considered reversible,^8,9 but this case is the first published photographic evidence of reversibility.The angiogram in this patient showed that the whitening corresponds closely to capillary non-perfusion. This finding has not been described previously in adults but is common in Malawian children with cerebral malaria.¹⁰ Post-mortem studies in Malawi have found retinal blood vessels in cerebral malaria to be packed with sequestered parasites,¹¹ similar to findings in the brain in adults.¹² Because retinal whitening⁹ and central nervous system (CNS) sequestration^13,14 are particularly prominent in patients with malarial coma (cerebral malaria), this finding suggests that small blood vessel CNS ischemia plays a major role in pathogenesis. In survivors, malarial coma is rapidly reversible and, as seen in the retina in this case, reversal of blood vessel obstruction is a plausible contributor.This patient had mildly increased tortuosity of retinal blood vessels that decreased on recovery. Although increased vascular tortuosity has not been well-described in malaria, it is a recognized feature of other vascular occlusive diseases of the retina. Vessel tortuosity is caused by a combination of vessel dilation from radial stretching and the vessel taking a more serpentine path because of longitudinal stretching.¹⁵ Several pathogenic mechanisms have been proposed for increased retinal vascular tortuosity. They include (1) increased blood flow in anemia, (2) early angiogenesis caused by ischemia or inflammation and (3) dysregulation of vascular tone caused by microvascular obstruction and relative hypoxia in diabetic retinopathy, and (4) venous congestion causing elevated vascular pressure and dilatation of blocked vessels in CRVO and raised intracranial pressure resulting in central retinal vein compression. In malaria, anemia is common, uninfected red blood cells have reduced deformability, and sequestered parasites cause microvascular and venular obstruction. Angiogenesis is probably unimportant over the short timescale.¹Increased vascular tortuosity has not been well-described previously in severe falciparum malaria, possibly because the normal appearance of retinal vessels varies significantly between individuals and subtle changes are difficult to identify. Ophthalmoscopy revealed engorgement and tortuosity of retinal veins in 26% of children with cerebral malaria in Ghana, which mostly resolved by 1 week.⁸ In our patient, comparison of retinal photographs provided a more objective measure. Means of quantifying vessel tortuosity using computer-aided image processing are under development.The angiogram in this patient showed focal leakage of fluorescein across the blood–retinal barrier (BRB) in areas of non-perfusion, suggesting a common etiology. The BRB is analogous to the blood–brain barrier, which is also mildly disrupted in cerebral malaria. Leakage from larger retinal vessels crossing ischemic areas is a well-known phenomenon in retinal ischemia. The significance of this finding as a contributor to the pathogenesis of malarial coma is not known. More angiographic studies are needed.This patient had decreased visual acuity, which had resolved at follow-up. Although it is not possible to give a cause, it is the first report of an association between macular retinal whitening and decreased visual acuity with subsequent recovery.Additional studies of malarial retinopathy have great potential to enhance our understanding of vascular changes in severe malaria. To maximize their impact, studies should use retinal photography, where possible, to allow detailed examination of the full range of fundus signs by multiple blinded observers. This examination should be done both acutely and at follow-up. Fluorescein angiography provides a highly detailed map of CNS retinal perfusion. There is a need for additional detailed studies to include assessment of vascular tortuosity to investigate its role as a potential early and sensitive marker in studies of severe malaria.The rate of reversibility of malarial retinopathy has potential as an end point in intervention studies of severe malaria, particularly for adjunctive therapies that directly target the pathogenesis. Additional information on the speed of reversibility of the various components of malarial retinopathy is needed, and studies are underway to investigate this.     

Aneurysmally dilated major aorto-pulmonary collateral in tetralogy of Fallot

Haemodynamically significant systemic-to-pulmonary artery collaterals may present as a cause of cardiorespiratory compromise in tetralogy of Fallot (TOF) with pulmonary atresia. We present here a case of TOF with pulmonary atresia with aneurysmally dilated aorto-pulmonary collateral causing compression over trachea, presenting as dry irritating cough who died suddenly with haemoptysis probably due to rupture of hypertrophied bronchial collaterals or direct erosion of large major aorto-pulmonary collateral arteries (MAPCA) into the respiratory tract.     

Ingestion of a carbonated beverage decreases lower esophageal sphincter pressure and increases frequency of transient lower esophageal sphincter relaxation in normal subjects

Transient lower esophageal sphincter relaxation (tLESR) and decreased basal lower esophageal sphincter (LES) pressure are postulated mechanisms of gastroesophageal reflux (GER). There is conflicting evidence on the effect of carbonated drinks on lower esophageal sphincter function. This study was conducted to assess the effect of a carbonated beverage on tLESR and LES pressure. High resolution manometry tracings (16 channel water-perfused, Trace 1.2, Hebbard, Australia) were obtained in 18 healthy volunteers (6 men) for 30 min each at baseline, and after 200 mL of chilled potable water and 200 mL of chilled carbonated cola drink (Pepsi [Pepsico India Ltd]). The sequence of administration of the drinks was determined by random number method generated by a computer. The analysis of tracings was done using TRACE 1.2 software by a physician who was unaware of the sequence of administration of fluids. The mean (SD) age of the participant was 37.3 (12.9) years. The median (range) frequency of tLESr was higher after the carbonated beverage (10.5 [0-26]) as compared to baseline (0 [0-3], p?=?0.005) as well as after water (1 [0-14], p?=?0.010). The LES pressure decreased after ingestion of the carbonated beverage (18.5 [11-37] mmHg) compared to baseline (40.5 [25-66] mmHg, p?=?0.0001) and after water (34 [15-67] mmHg, p?=?0.003). Gastric pressure was not different in the three groups. Ingestion of a carbonated beverage increases tLESr and lowers LES pressure in healthy subjects.