One stage surgical management of hydatid cyst of lung &; liver—by right thoracotomy &; phrenotomy

Introduction Hydatid cysts of the lung are quite frequent in our country. Some patients have additional cysts in the liver. Though most of the liver cysts remain asymptomatic for long time, but may be symptomatic with increasing size. Surgical removal is the treatment of choice for both lung & liver cysts. Aim of the study was to establish suitability of one stage surgery for pulmonary & hepatic hydatid cysts. Methods From 1996 through 2003 we operated on 216 pulmonary hydatid cysts, out of which 42 patients had hydatid cysts in the right lung as well as in the right lobe of liver. Right thoracotomy was done to remove the lung hydatids followed by phrenotomy to remove the liver cysts. Results Right thoracotomy was done in 42 patients having hydatid cysts of lung & liver. In 36 patients, cysts were removed, bronchial leaks were sutured & residual cavities were obliterated. Out of rest 6 patients, having dense adhesions or destruction of pulmonary parenchyma, 4 had segmentectomy & 2 had lobectomy. Right phrenotomy was then done with radial incision above the palpated liver cysts. Hydatid cyst was removed from liver. Cavity and remaining pericystic liver tissue was inverted with sutures. Water seal chest drain & subdiaphragmatic drain were placed. Post operative albendazole was continued for 3 months in the dose of 10–20 mg/kg with a gap of 2 weeks after each month. Post operative recovery was uneventful in most of the cases. However, air leak continued for almost 3 weeks in 4 patients & 3 months in one patient. There was no death. Conclusion Surgical management of pulmonary and hepatic hydatids with one stage right thoracotomy & phrenotomy is a suitable option. It avoids additional laparotomy and thereby additional cost & hospital stay. Results are quite satisfactory.     

Mitochondrial calcium uniporter regulator 1 (MCUR1) regulates the calcium threshold for the mitochondrial permeability transition

During the mitochondrial permeability transition, a large channel in the inner mitochondrial membrane opens, leading to the loss of multiple mitochondrial solutes and cell death. Key triggers include excessive reactive oxygen species and mitochondrial calcium overload, factors implicated in neuronal and cardiac pathophysiology. Examining the differential behavior of mitochondrial Ca²⁺ overload in Drosophila versus human cells allowed us to identify a gene, MCUR1, which, when expressed in Drosophila cells, conferred permeability transition sensitive to electrophoretic Ca²⁺ uptake. Conversely, inhibiting MCUR1 in mammalian cells increased the Ca²⁺ threshold for inducing permeability transition. The effect was specific to the permeability transition induced by Ca²⁺, and such resistance to overload translated into improved cell survival. Thus, MCUR1 expression regulates the Ca²⁺ threshold required for permeability transition.The mitochondrial permeability transition (MPT) pore is large, and its opening collapses the mitochondrial membrane potential (ΔΨ), depleting the matrix of solutes <1.5 kDa. The osmotic imbalance swells and disrupts mitochondria, leading to cell death. The molecular structure of the MPT pore is unknown, although cyclophilin D [peptidyl-prolyl isomerase F (PPIF)], the ADP/ATP translocase, the F1-FO-ATP synthase, and spastic paraplegia 7 are key for its function (1–5).Key triggers for the MPT include oxidative damage and Ca²⁺ overload. Reactive oxygen species attack a cysteine residue in mammalian PPIF (6, 7), but how Ca²⁺ overload activates the pore is unknown. Elimination of the known regulators typically inhibits the sensitivity of the MPT globally, not favoring any particular trigger (8–10). Because Ca²⁺ overload promotes cell death in excitable cells, targeting this pathway selectively may prove beneficial.To discover novel regulators specific to mitochondrial Ca²⁺ overload, we studied MPT in Drosophila S2R+ cells, a system where screens have identified molecules involved in Ca²⁺ transport (11–13). We found that mitochondria within these cells were resistant to Ca²⁺ overload (14) but did possess an MPT. Moreover, we identified a mammalian gene, mitochondrial calcium uniporter regulator 1 (MCUR1), with no known Drosophila homolog, which is able to alter the MPT Ca²⁺ threshold. Inhibiting this gene confers resistance from cell death mediated by mitochondrial Ca²⁺ overload.     

Mechanisms underlying the antihypertensive effects of garlic bioactives

Cardiovascular disease remains the leading cause of death worldwide with hypertension being a major contributing factor to cardiovascular disease–associated mortality. On a population level, non-pharmacological approaches, such as alternative/complementary medicine, including phytochemicals, have the potential to ameliorate cardiovascular risk factors, including high blood pressure. Several epidemiological studies suggest an antihypertensive effect of garlic (Allium sativum) and of many its bioactive components. The aim of this review is to present an in-depth discussion regarding the molecular, biochemical and cellular rationale underlying the antihypertensive properties of garlic and its bioactive constituents with a primary focus on S-allyl cysteine and allicin. Key studies, largely from PubMed, were selected and screened to develop a comprehensive understanding of the specific role of garlic and its bioactive constituents in the management of hypertension. We also reviewed recent advances focusing on the role of garlic bioactives, S-allyl cysteine and allicin, in modulating various parameters implicated in the pathogenesis of hypertension. These parameters include oxidative stress, nitric oxide bioavailability, hydrogen sulfide production, angiotensin converting enzyme activity, expression of nuclear factor–κB and the proliferation of vascular smooth muscle cells. This review suggests that garlic and garlic derived bioactives have significant medicinal properties with the potential for ameliorating hypertension and associated morbidity; however, further clinical and epidemiological studies are required to determine completely the specific physiological and biochemical mechanisms involved in disease prevention and management.     

Video assisted thoracoscopic (VATS) Thymectomy-a better alternative

Background With the introduction of video imaging technique in late 1980s the field of thoracoscopy was expanded into video assisted thoracic surgery (VATS) in 1990. VATS has several unique advantages like reducing repiratory complications, hospital stay and post operative pain due to avoidance of thoracotomy/sternotomy. It is indicated in almost all thoracic surgical procedures-both diagnostic and therapeutic. VATS thymectomy is being practised more and more replacing conventional thymectomy with thoracotomy/sternotomy. Methods From 2000 to 2003 we have performed 22 cases of VATS thymectomy in Myesthenia Gravis. Surgery was performed in supine decubitus under General anaesthesia with Double Lumen E T Tube for epsilateral Lung Collapse. Three ports were made on the right chest at 2nd space parasternal, 4th space anterior axillary line and at 5th space just below the nipple. At the end of the procedure a chest drain was introduced through the lowest port. Results Out of 22 patients 12 were females and 10 males. Median age was 36 years (Range 16 years to 64 years). Median operating time was 2 hours and drainage was 200 ml. Median ventillation time was 6 hours. Median hospital stay was five days. There was no mortality and no major complications. Conclusion VATS thymectomy is a suitable alternative to conventional thymectomy with thoracotomy/sternotomy. Results are comparable. VATS is now developing into an exciting adjunct in thoracic surgery. The morbidity associated with this procedure is extremely low. VATS has become an essential component of all thoracic surgical units and more and more thoracic surgical dieases will be managed with this minimally invasive technique in future.     

Central nervous system lesions in Malawian children: identifying the treatable

In Malawi, children with central nervous system (CNS) tumours are seldom able to be treated with curative intent. A study was undertaken of 29 children who underwent CNS MRI during a two year period. A combination of neoplastic and non-neoplastic diagnoses were noted, seven of which were revised on review. As a result an effective system has been set up for remote urgent review to guide prognosis and treatment. The opinion of a paediatric neuro-radiologist greatly assists in differentiating infectious and non infectious causes of CNS lesions and can enable the local team to effectively triage patients.     

Is clonidine useful for treatment of clozapine-induced sialorrhea?

Clozapine has shown superior efficacy in treatment of refractory schizophrenia, but its use is limited by emergent side-effects. Among other adverse effects, sialorrhea is a troublesome side-effect, its stigmatizing nature results in poor treatment compliance. Several hypotheses have been put forward in the etiology of clozapine-induced sialorrhea. 2 adrenergic antagonism is hypothesized to be involved in its pathophysiology, based on the response to clonidine and lofexidine. Oral clonidine (50 to 100 g/day) was tried on 12 stable outpatients of schizophrenia maintained on clozapine. Wet area over the pillow as reported by the patients was recorded at baseline and at 4 weeks of treatment along with the subjective response after the treatment. Most of the patients reported a decrease in sialorrhea without any adverse events. We describe encouraging results in an open case series of oral clonidine for clozapine-induced sialorrhea.     

TUBA1A mutation-associated lissencephaly: case report and review of the literature

Lissencephaly is a disorder of neuronal migration resulting in abnormal cerebral cortical sulcation and gyration. Affected children present with microcephaly, developmental delay, and early-onset epileptic seizures. Recently, de novo missense mutations in the tubulin α-1A (TUBA1A) gene were identified as causing a distinctive radiologic phenotype comprising of posteriorly predominant lissencephaly with dysgenetic corpus callosum, cerebellar and brainstem hypoplasia, and more recently, polymicrogyria. We describe a 14-month-old girl with TUBA1A mutation-associated lissencephaly, and summarize the clinical and neuroradiologic findings of 19 cases in the literature.