Introduction:  Glaucoma involves progressive neuropathy of the optic nerve, accompanied by structural changes to the optic nerve head or disk, ultimately resulting in functional changes to the visual field. The main aim of the study. Material and methods:  the present study was conducted after taking permission from institutional ethical committee. A total of 184 glaucoma patients under inclusion criteria there inform consent was taken and they were divided into four groups. Group A: Patients treated with latanoprost, Group B: Patients treated with bimatoprost, Group C: Patients treated with Pilocarpine and Group D: Patients treated with Timolol. All the patients were sociodemographical status, intraocular pressure, and blood pressure was notes at baseline. Every 4 hours ocular parameters were noted and named as after treatment.  Results: Age and gender distribution of the study population. Among the 184 patients, majority of the patients were male 136 (73.91%) with the age group of 55 (29.89%) were aged group of 41–50 years. Highlights the educational status of glaucoma and married status patients. The majority had a Senior Secondary Certificate (SSC) qualification, with 88 (47.82) patients and married 139, (75.54%). The patients reported that poor vision 167 (90.76%). Among them 124 (74.25%) were unable to read. 104 (54.52%) patients had less than six months. The study also observed that glaucoma patients had diabetes, hypertension. Ocular changes in glaucoma patients following treatment with ocular eye drops were assessed by measuring intraocular pressure (IOP). IOP readings were taken at 8:00 AM for all four groups and compared with readings taken at 8:00 PM after treatment. The results showed no significant differences (p > 0.05) between the four groups. Conclusion:  Bimatoprost shows decrease in intraocular pressure when compared with pilocarpine, travoprost and timolol in treatment of ocular glaucoma.

Introduction This study aimed to evaluate and compare the subfoveal choroidal thickness (SFCT) and peripapillary choroidal thickness (PPCT) in eyes affected by central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO), as well as to assess changes in these parameters after intravitreal anti-vascular endothelial growth factor (anti-VEGF) therapy.  Methods: A prospective longitudinal observational study was conducted on treatment-naive patients with CRVO (n=80) and BRVO (n=120) over a 9-month follow-up period. Demographic data, clinical characteristics, and spectral-domain optical coherence tomography (SD-OCT) measurements, including SFCT, PPCT, central macular thickness (CMT), and retinal nerve fiber layer (RNFL), were recorded at baseline, 3 months, and 9 months. Statistical comparisons were performed to evaluate changes in affected and fellow eyes.   Results: CRVO patients were younger than BRVO patients (58.0 ± 18.9 vs. 70.1 ± 10.1 years; *P* = 0.008). Baseline PPCT in affected eyes was significantly higher in CRVO compared to BRVO (155.38 ± 48.23 µm vs. 116.84 ± 51.29 µm; *P* = 0.017). SFCT also showed a trend toward greater thickness in CRVO but did not reach statistical significance (*P* = 0.129). Both conditions demonstrated significant reductions in SFCT and PPCT following anti-VEGF therapy, with CRVO showing greater baseline and post-treatment choroidal thickness compared to BRVO. Fellow eyes of CRVO patients exhibited consistently higher PPCT and SFCT at 9 months (*P* = 0.001 and *P* = 0.011, respectively).   Conclusions: CRVO is associated with greater baseline and post-treatment PPCT compared to BRVO, suggesting more pronounced choroidal involvement. The reduction in choroidal thickness following anti-VEGF therapy supports the hypothesis that VEGF and hydrostatic pressure contribute to choroidal changes in retinal vein occlusion (RVO). Further studies with extended follow-up are needed to explore the implications of these findings on disease management and prognosis

We present a case of lactic acidosis in a patient with acute severe asthma who did not have any overt signs of sepsis or tissue hypoperfusion. Mr IL was a 49 years old male who was known to have moderate asthma. He had multiple previous admissions to hospital with exacerbation of asthma but had never required an intensive care admission and had never been intubated. His other comorbidities included atrial fibrillation, ischemic heart disease and depression. His usual medications included salbutamol, budesonide and salmeterol inhalers, aspirin, atorvastatin and digoxin. He was a mechanic by trade with no obvious occupational sensitization. He had no pets at home. He was a smoker with a 20-pack year history. Recent lung function tests showed an FEV1/FVC of 0.68 with a post bronchodilator FEV1 of 4.17 L (95% predicted). He was admitted with a 1-week history of worsening shortness of breath, dry cough and wheeze. His baseline blood tests including full blood count, C reactive protein, liver and renal function were normal. Chest radiograph was unremarkable.

Patients with morbid obesity suffer a wide range of symptoms that relate to their oesophagus and stomach. It is rather paradoxical that patients who are overweight suffer the symptoms of difficulty in swallowing, pain during eating or pain after eating, because the symptoms of difficulty eating do not translate into weight reduction. There are a range of underlying causes that include gastro-oesophageal reflux disease, dysmotility in the oesophagus, peptic ulceration and the nature and pattern of dietary intake. In addition, the surgical treatments used for morbid obesity cause similar symptoms from gastric bands leading to dysphagia or reflux from being too tight or from erosion into the stomach, from balloons being displaced and bypass complications. Serious oesophageal conditions occur more frequently in patients with obesity such as Barrett’s oesophagus and Adenocarcinoma of the oesophagus. This article reviews the literature to highlight the range of potential problems from oesophageal symptoms and disease and how they can be managed in the context of morbid obesity.

Electroconvulsive Therapy (ECT) has been in use since 1938 and remains one of the most important and controversial treatments. The National Institute of Clinical Excellence in UK specifically recommends considering ECT as an option in treatment of severe depression (when life threatening and a rapid response is needed or when other treatments have failed), moderate depression (not responding to multiple treatments), catatonia and a prolonged and severe manic episode. For ECT to have a therapeutic response, it is now recognised that a generalised tonic-clonic seizure is essential. The degree by which the stimulus intensity exceeds the seizure threshold is an important determinant of both therapeutic effectiveness and cognitive side effects. This article attempts to discuss the significance of estimating the seizure threshold and the practical ways of lowering it, to reduce the side effects during the course of the treatment.

The phagocyte oxidase 47 (P47Phox) is produced by the NCF1 gene which is located on chromosome 7. The P47 Phox forms an important component of the NADPH oxidase complex enzyme which leads to the production of reactive oxygen species (ROS). The NCF1 gene exists in two versions, one is a wild type gene with GTGT at the start of exon 2. The other is a pseudogene and it has its GT deletion at the start of exon2 which leads to passive production of ROS. The role of ROS in malaria was studied through the restriction enzymeGeobacillus stearothermophilus GR75 (BsrG1) found in the NCF1 gene. This enzyme digests only the pseudogene and has no impact on the wild type gene. The comparison of 88 malarial patients with 100 healthy individuals proves that there was no association of NCF1 gene with malaria because the P value was greater than 0.05. Background: Malaria is a mosquito-borne infectious disease which is caused by a eukaryotic protist of the genus Plasmodium. The most fatal form of the disease is caused by Plasmodium falciparum. The neutrophil cytosolic factor 1 (NCF1), also known as p47 phox, is an important subunit of NADPH oxidase which plays a role in the production of ROS. The forming of ROS is a pivotal component of innate immunity against parasitic and bacterial infection. Aim: The aim of study was to find out that whether the NCF1 gene and ROS had a role in malaria. Method: Samples from 88 malarial patients and 100 healthy individuals were processed with the restriction enzyme BsrGI. Conclusion: It was found that the NCF1 gene and ROS have no association with malaria.

Introduction: Sedation is frequently administered by non-anaesthetic doctors in the emergency department whilst minor procedures are carried out. Guidelines and protocols exist but are non-anaesthetic doctors familiar with them? Methods: A questionnaire survey of 53 orthopaedic surgeons (registrars) in Bristol and Cardiff was carried out to ascertain their current clinical practice, knowledge, and training with regards to sedation. Results: Sedation had been administered by all the orthopaedic doctors surveyed at some stage in their careers to facilitate fracture or joint reduction or to apply traction in settings outside the operating room. Forty-five percent of respondents had read the sedation protocol for their hospital but fewer respondents ensured monitoring data forms were completed during and after the procedure (21% and 23% respectively). Morphine and other opioids were the most commonly used sedative medication. The pharmacology section of the questionnaire revealed a reasonable knowledge base for most trainees with a mean score of 4.29 out of 7. Whilst the majority of respondents had undergone advanced life support training (89%), only 30% of respondents had undergone formal training regarding sedation techniques. Conclusion: Sedation for minor procedures is widely performed by orthopaedic doctors. There is the potential for significant morbidity and mortality, so doctors need to be aware of and follow sedation guidelines. Adequate training needs to be incorporated into postgraduate training speciality programmes to ensure safe sedation practices.

In the RE-LY study2 (Randomized Evaluation of Long-term Anticoagulant Therapy), high-dose dabigatran (150mg twice a day) was found to be superior to warfarin for the prevention of stroke and systemic emboli, required no routine INR monitoring, and had few food and drug interactions. James Freeman and colleagues,3 using data from the RE-LY trial, found that high-dose dabigatran (150mg twice a day) was the most efficacious and cost-effective strategy compared with adjusted-dose warfarin among adults older than 65 with AF. Dabigatran has been shown to specifically and reversibly inhibit thrombin, the key enzyme in the coagulation cascade. Studies in healthy volunteers4 and in patients undergoing orthopaedic surgery have indicated that dabigatran has a predictable pharmacokinetic/pharmacodynamic profile, allowing for a fixed-dose regimen. Peak plasma concentrations of dabigatran are reached approximately two hours after oral administration in healthy volunteers, with no unexpected accumulation of drug concentrations upon multiple dosing. Excretion is predominantly via the renal route as unchanged drug. Dabigatran is not metabolized by cytochrome P450 isoenzymes. Though use of dabigatran for non-valvular AF and venous thromboembolism (VTE) is gaining practice,5 it remains far from being the standard of care