Surgically induced astigmatism after laser in situ keratomileusis for spherical myopia

PURPOSE: To study risk factors for surgically induced astigmatism (SIA) after laser in situ keratomileusis (LASIK). METHODS: In a retrospective case control study of 104 eyes (52 patients) that underwent LASIK for myopia (spherical ablation alone), two groups were studied: 42/104 eyes with SIA, and controls (62/104 eyes). The main variables studied were preoperative refraction, corneal thickness, preoperative keratometric power, amount of ablation, ablation zone diameter, flap thickness, flap size, and the presence of complications. The effect of SIA on visual performance was also evaluated. RESULTS: The mean myopia for which LASIK was undertaken was -4.50 +/- 2.04 D. Mean scalar astigmatism induced was 0.35 +/- 0.50 D at 1 month, 0.33 +/- 0.40 D at 3 months, and 0.16 +/- 0.60 D at 6 months. SIA based on refractive cylinder was 0.66 +/- 0.29 D at 1 month, 0.54 +/- 0.32 D at 3 months, and 0.49 +/- 0.34 D at 6 months. Mean axis of vector induced astigmatism was 82.5 degrees +/- 57 degrees at 1 month, 98.86 degrees +/- 52.4 degrees at 3 months, and 113.9 degrees +/- 62.6 degrees at 6 months. Risk factors associated with the occurrence of SIA were preoperative keratometric power of >44 D [OR (95% CI); 1.97 (0.62 to 6.26)], ablation zone diameter of <6 mm [OR (95 % CI) 2.76; (0.6 to 12.6)], and suction ring diameter of 8.5 mm [OR (95% CI) 12.46; (2.0 to 77.38)]. The occurrence of SIA had no significant effect on uncorrected Snellen high contrast visual acuity, contrast sensitivity, and glare in comparison with controls. CONCLUSION: Surgically induced astigmatism was more likely to occur with the use of smaller suction rings of 8.5 mm and in ablation zones less than 6 mm. Parameters for visual performance were not affected by the presence of surgically induced astigmatism.     

Fear of missing out: A brief overview of origin,theoretical underpinnings and relationship with mental health

Fear of missing out (FoMO) is a unique term introduced in 2004 to describe a phenomenon observed on social networking sites. FoMO includes two processes; firstly, perception of missing out, followed up with a compulsive behavior to maintain these social connections. We are interested in understanding the complex construct of FoMO and its relations to the need to belong and form stable interpersonal relationships. It is associated with a range of negative life experiences and feelings, due to it being considered a problematic attachment to social media. We have provided a general review of the literature and have summarized the findings in relation to mental health, social functioning, sleep, academic performance and productivity, neuro-developmental disorders, and physical well-being. We have also discussed the treatment options available for FoMo based on cognitive behavior therapy. It imperative that new findings on FoMO are communicated to the clinical community as it has diagnostic implications and could be a confounding variable in those who do not respond to treatment as usual.     

Excitotoxicity: Bridge to various triggers in neurodegenerative disorders

Glutamate is one of the most prominent neurotransmitter in the body, present in over 50% of nervous tissue and plays an important role in neuronal excitation. This neuronal excitation is short-lived and is followed by depression. Multiple abnormal triggers such as energy deficiency, oxidative stress, mitochondrial dysfunction, calcium overload, etc can lead to aberration in neuronal excitation process. Such an aberration, serves as a common pool or bridge between abnormal triggers and deleterious signaling processes with which central neurons cannot cope up, leading to death. Excitotoxicity is the pathological process by which nerve cells are damaged and killed by excessive stimulation by neurotransmitters such as glutamate and similar substances. Such excitotoxic neuronal death has been implicated in spinal cord injury, stroke, traumatic brain injury, hearing loss and in neurodegenerative diseases of the central nervous system such as stroke, epilepsy, multiple sclerosis, Alzheimer disease, Amyltropic lateral sclerosis, Parkinson’s disease, Huntington disease and alcohol withdrawal. This review mainly emphasizes the triggering events which sustain neuronal excitation, role of calcium, mitochondrial dysfunction, ROS, NO, chloride homeostasis and eicosanoids pathways. Further, a brief introduction about the recent research occurring in the treatment of various neurodegenerative diseases, including a summary of the presumed physiologic mechanisms behind the pharmacology of these disorders.     

Plasmodium vivax remains responsive to chloroquine with primaquine treatment regimen: a prospective cohort study from tertiary care teaching hospital in southern India

We conducted this prospective study among 110 symptomatic Plasmodium vivax patients attending the Kasturba Hospital, Manipal, India, in order to evaluate their clinico-laboratory profile during July 2007-July 2009. Complications observed among patients were: anaemia (46.4%; 95% confidence interval [CI], 37.08-55.72%); thrombocytopenia (68.2%; 95% CI, 59.5-76.9%); leucopenia (29.1%; 95% CI, 20.61-37.59%); hyperbilirubinaemia (20%; 95% CI, 12.53-27.47%); non-oliguric renal failure (10.9%; 95% CI, 5.08-16.72%); elevated serum transaminases (33.6%; 95% CI, 24.77-42.43%); hypotension (8.2%; 95% CI, 3.07-13.33%); hepatomegaly (27.3%; 95% CI, 18.97-35.63%); and splenomegaly and jaundice in 12.7% (95% CI, 6.48-18.92%). The 99% chloroquine response and zero mortality observed in this study of vivax malaria are encouraging points for practicing physicians.     

Screening for Barrett's esophagus in colonoscopy patients with and without heartburn

BACKGROUND & AIMS: The population prevalence of Barrett's esophagus (BE) is uncertain. Our aim was to describe the prevalence of BE in a volunteer population. METHODS: Upper endoscopy (EGD) was performed in 961 persons with no prior history of EGD who were scheduled for colonoscopy. Symptom questionnaires were completed prior to endoscopy. Biopsy specimens were taken from the gastric cardia and any columnar mucosa extending > or =5 mm into the tubular esophagus and from the stomach for H. pylori infection in the last 812 patients. RESULTS: The study sample was biased toward persons undergoing colonoscopy, males, and persons with upper GI symptoms. The prevalence of BE was 65 of 961 (6.8%) patients, including 12 (1.2%) with long-segment BE (LSBE). Among 556 subjects who had never had heartburn, the prevalences of BE and LSBE were 5.6% and 0.36%, respectively. Among 384 subjects with a history of any heartburn, the prevalences of BE and LSBE were 8.3% and 2.6%, respectively. In a univariate analysis, LSBE was more common in those with any heartburn vs. those with no heartburn (P = 0.01), but the sample size was insufficient to allow multivariate analysis of predictors of LSBE. In a multivariate analysis, BE was associated with increasing age (P = 0.02), white race (P = 0.03), and negative H. pylori status (P = 0.04). Overall, BE was not associated with heartburn, although heartburn was more common in persons with LSBE or circumferential short segments. CONCLUSIONS: LSBE is very uncommon in patients who have no history of heartburn. SSBE is relatively common in persons age > or =40 years with no prior endoscopy, irrespective of heartburn history.     

Interaction of sensory responses with spontaneous depolarization in layer 2/3 barrel cortex

The rodent primary somatosensory cortex is spontaneously active in the form of locally synchronous membrane depolarizations (UP states) separated by quiescent hyperpolarized periods (DOWN states) both under anesthesia and during quiet wakefulness. In vivo whole-cell recordings and tetrode unit recordings were combined with voltage-sensitive dye imaging to analyze the relationship of the activity of individual pyramidal neurons in layer 2/3 to the ensemble spatiotemporal dynamics of the spontaneous depolarizations. These were either brief and localized to an area of a barrel column or occurred as propagating waves dependent on local glutamatergic synaptic transmission in layer 2/3. Spontaneous activity inhibited the sensory responses evoked by whisker deflection, accounting almost entirely for the large trial-to-trial variability of sensory-evoked postsynaptic potentials and action potentials. Subthreshold sensory synaptic responses evoked while a cortical area was spontaneously depolarized were smaller, briefer and spatially more confined. Surprisingly, whisker deflections evoked fewer action potentials during the spontaneous depolarizations despite neurons being closer to threshold. The ongoing spontaneous activity thus regulates the amplitude and the time-dependent spread of the sensory response in layer 2/3 barrel cortex.     

Toll-like Receptor 1 743 A>G, 1805 T>G & Toll-like Receptor 6 745 C>T gene polymorphism and tuberculosis: A case control study of north Indian population from Agra (India)

Infection with Mycobacteriumtuberculosis possibly depends on host genetic factors and is thought to be the major cause of differential susceptibility to the disease. In the present study, 205 pulmonary tuberculosis cases and 127 healthy controls were studied for the association of Toll-like Receptor (TLR) variants (TLR1 variants 743A>G and 1805T>G, and TLR6 variant 745 C>T) in north Indian population. The frequency of heterozygous genotypes (AG) in TB cases (0.47) and HCs (0.61), differed significantly (p value = 0.02). The association of AG genotypes in HCs was adjusted for gender as gender was observed to be a confounder and M−H OR was found to be 0.62 (p = 0.044). On categorizing the cases basing on AFB smear positivity, the heterozygous genotypes (AG) was found to be associated with low bacillary load (scanty and 1+) (P = 0.002). No association was observed for either TLR1 1805 T>G or TLR6 745 C>T polymorphism. Level of serum IL6 was found to be significantly higher among healthy controls with TLR1 GG genotype compared to healthy controls with AA (p = 0.035) and AG (p = 0.005) genotypes. Thus, it may be suggested that the heterozygous condition for TLR1 743 A>G provide resistance from the disease. However, in depth study is required to understand the mechanism for possible protective responses.