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Biomedical subjects

A Bhalla

Publications and source records attributed to A Bhalla.

At least 37 records · Page 2Linked to original sources
PubMed2001

Seasonal variations in incidence of severe and complicated malaria in central India.

The geographical position and climate of India is favorable for the transmission of malarial infection. The maximum prevalence of malaria in most parts of India is from July to November months. Rainfall provides mosquitoes, a breeding ground giving rise to epidemics. We studied the seasonal variation in cases of severe and complicated malaria presenting at MGIMS, Sevagram, Wardha (Vidarbha region in Maharashtra) over a period of three years. The findings of peak of malaria observed during September-November during three years period points to the fact that the increase in vector breeding after rainy season is responsible for the upsurge in the malarial cases during these months. This also indicates that this area (Vidarbha) has an unstable transmission of malaria.

Humans↗
PubMed2001

Video game epilepsy.

Reflex epilepsy is the commonest form of epilepsy in which seizures are provoked by specific external stimulus. Photosensitive reflex epilepsy is provoked by environmental flicker stimuli. Video game epilepsy is considered to be its variant or a pattern sensitive epilepsy. The mean age of onset is around puberty and boys suffer more commonly as they are more inclined to play video games. Television set or computer screen is the commonest precipitants. The treatment remains the removal of the offending stimulus along with drug therapy. Long term prognosis in these patients is better as photosensitivity gradually declines with increasing age. We present two such case of epilepsy induced by video game.

Adolescent↗
PubMed2001

Circadian pattern of cardiovascular and cerebrovascular diseases in geriatric population.

OBJECTIVES: Over last 13 years various studies have been done to evaluate the circadian pattern in cardiovascular and cerebrovascular diseases in adults and the existence of such variation in Indian population also has been demonstrated. The data on this variation in geriatric patients does not exist. METHODS: We undertook this prospective observational study at Government Medical College and Hospital, Chandigarh to evaluate the circadian variation in disorders like acute myocardial infarction (AMI), unstable angina (USA), non Q wave MI (non QMI), cerebrovascular accidents (strokes, both ischemic and hemorrhagic) and transient ischemic attacks (TIA). OBSERVATIONS: We studied 158 patients (56.98% males and 43.02% females), mean age was 69 +/- 4 years. 34.17% each had AMI and CVA, 22.78% and USA and 7.59% had NON Q MI, only two patients in our study group had TIAs. We divided 24 hours into four equal quarters each for analysis. RESULTS: We observed that maximum episodes were seen during the period between 6 am till 12 noon 58/158 (36.71%) and a second peak was seen during 6 pm and 12 midnight when 40/158 events were recorded (25.31%). The least number of episodes were seen during the period between 12 midnight till 6 am 22/158 (13.92%). Similar peaking of events was noted for acute myocardial infarction but only one peak was seen for unstable angina. For cerebrovascular accidents two similar peaks were noted between 6 am till 12 noon and 12 noon till 6 pm. CONCLUSIONS: Our study population (geriatric patients) shows the presence of a definitive circadian variation with two comparable peaks. One during the morning hours (6 am-12 noon) and another peak between 6 pm and 12 midnight in patients having acute coronary diseases. In cerebrovascular accidents patients too, similar peaks were noted between 6 am till 12 noon and 12 noon till 6 pm.

Age Distribution↗
PubMed2000

Influence of raised plasma osmolality on clinical outcome after acute stroke.

BACKGROUND AND PURPOSE: Abnormal physiological parameters after acute stroke may induce early neurological deterioration. Studies of the effect of dehydration on stroke outcome are limited. We examined the association of raised plasma osmolality on stroke outcome at 3 months and the change of plasma osmolality with hydration during the first week after stroke. METHODS: Acute stroke patients had their plasma osmolality measured at admission and at days 1, 3, and 7. Maximum plasma osmolality and the area under curve (AUC) were also calculated during the first week. Patients were stratified according to how they were hydrated: orally, intravenously, or both. Outcome included survival at 3 months after stroke. Logistic regression was performed to examine the association between raised plasma osmolality (>296 mOsm/kg) and survival, adjusting for stroke severity. Linear regression was performed to examine the pattern of plasma osmolality across hydration groups. RESULTS: One hundred sixty-seven patients were included. Mean admission (300 mOsm/kg, SD 11.4), maximum (308.1 mOsm/kg, SD 17.1), and AUC (298.3 mOsm/kg, SD 11.7) plasma osmolality were significantly higher in those who died compared with survivors (293.1 mOsm/kg [SD 8.2], 297.7 mOsm/kg [SD 8. 7], and 291.7 mOsm/kg [SD 8.1], respectively; P:<0.0001). Admission plasma osmolality >296 mOsm/kg was significantly associated with mortality (OR 2.4, 95% CI 1.0 to 5.9). In patients hydrated intravenously, there was no significant fall in plasma osmolality compared with patients hydrated orally (P:=0.68). CONCLUSIONS: Raised plasma osmolality on admission is associated with stroke mortality, after correcting for case mix. Correction of dehydration after stroke requires a more systematic approach. Trials are required to determine whether correcting dehydration after stroke improves outcome.

Acute Disease↗
PubMed2000

The three subfamilies of leucine-rich repeat-containing G protein-coupled receptors (LGR): identification of LGR6 and LGR7 and the signaling mechanism for LGR7.

Glycoprotein hormone receptors, including LH receptor, FSH receptor, and TSH receptor, belong to the large G protein-coupled receptor (GPCR) superfamily but are unique in having a large ectodomain important for ligand binding. In addition to two recently isolated mammalian LGRs (leucine-rich repeat-containing, G protein-coupled receptors), LGR4 and LGR5, we further identified two new paralogs, LGR6 and LGR7, for glycoprotein hormone receptors. Phylogenetic analysis showed that there are three LGR subgroups: the known glycoprotein hormone receptors; LGR4 to 6; and a third subgroup represented by LGR7. LGR6 has a subgroup-specific hinge region after leucine-rich repeats whereas LGR7, like snail LGR, contains a low density lipoprotein (LDL) receptor cysteine-rich motif at the N terminus. Similar to LGR4 and LGR5, LGR6 and LGR7 mRNAs are expressed in multiple tissues. Although the putative ligands for LGR6 and LGR7 are unknown, studies on single amino acid mutants of LGR7, with a design based on known LH and TSH receptor gain-of-function mutations, indicated that the action of LGR7 is likely mediated by the protein kinase A but not the phospholipase C pathway. Thus, mutagenesis of conserved residues to allow constitutive receptor activation is a novel approach for the characterization of signaling pathways of selective orphan GPCRs. The present study also defines the existence of three subclasses of leucine-rich repeat-containing, G protein-coupled receptors in the human genome and allows future studies on the physiological importance of this expanding subgroup of GPCR.

Amino Acid Sequence↗
PubMed1999

Therapeutic advances in acute ischaemic stroke.

No drug has yet been shown to be unequivocally effective for acute stroke. Over the past decade, however, there has been an explosion in stroke research resulting in the development of novel therapeutic approaches. Therapies to improve arterial recanalisation and agents used to protect the brain from neurotoxic cellular damage are currently being evaluated. Tight control of physiological parameters may also limit neuronal damage. It is likely that within the next few years effective therapy will become available that will need a major change in the way that services are provided for stroke patients in the acute phase of their illness.

Brain Ischemia↗
PubMed1998

T-cell receptor-gamma rearrangement and c-myb methylation in MNNG-exposed Bloom syndrome B-lymphoblastoid cells.

The MNNG-exposed Bloom syndrome (BS) B-lymphoblastoid cell population (BS-MNNG), when analyzed for aberrant genetic variations, showed an illegitimate rearrangement at the TCR-gamma gene and hypermethylation at the c-myb protooncogene. The TCR-gamma rearrangement involved a Vgamma9 segment corresponding to a 4 kb band detected with a Jgamma-specific probe in HindIII-digested DNA samples from BS-MNNG cells only. These variations were not shown by unexposed BS cells or both MNNG-exposed and unexposed normal (GA3) B-lymphoblastoid cells.

B-Lymphocytes↗
PubMed1998

MNNG-transformed Bloom syndrome B-lymphoblastoids for the detection of Hodgkin's lymphoma-associated antigen in 2D Westerns.

Twenty-four hour MNNG-exposed Bloom syndrome (BS) B-lymphoblastoid cells with the potential to form single cell colonies in soft agar and nude mouse tumour (2/6 (33%) showed a simultaneous increase in the Ras-expressing cells (using monoclonal antibody to p21 transforming protein) from 20% (at 24 h) to 85% (on day 30). In contrast, there was an absence of Ras-positive cells in MNNG-exposed fresh lymphocytes (PBMCs) from a healthy subject and a presence of only 11-18% of Ras-positive cells in normal (GA3) and unexposed BS B-lymphoblastoid cells. The Western blot analysis using sera samples from Hodgkin's lymphoma patients showed the presence of proteins of 102 and 68 kDa which in 2D Westerns were observed to be unique to BS-MNNG cells with approximate pIs of 5.3 and 5.7, respectively. It is proposed that BS-MNNG cells provide an interesting in vitro human cell model to generate unique cancer-associated antigen(s) in addition to using this system to understand the primary events associated with neoplastic transformation.

Antigens, Neoplasm↗
PubMed1997

Morbidity and mortality in compensated cirrhosis type C: a retrospective follow-up study of 384 patients.

BACKGROUND & AIMS: Few data are available concerning the long-term prognosis of chronic liver disease associated with hepatitis C virus infection. This study examined the morbidity and survival of patients with compensated cirrhosis type C. METHODS: A cohort of 384 European cirrhotic patients was enrolled at seven tertiary referral hospitals and followed up for a mean period of 5 years. Inclusion criteria were biopsy-proven cirrhosis, abnormal serum aminotransferase levels, absence of complications of cirrhosis, and exclusion of hepatitis A and B viruses and of metabolic, toxic, or autoimmune liver diseases. RESULTS: Antibodies against hepatitis C virus were positive in 98% of 361 patients tested. The 5-year risk of hepatocellular carcinoma was 7% and that of decompensation was 18%. Death occurred in 51 patients (13%), with 70% dying of liver disease. Survival probability was 91% and 79% at 5 and 10 years, respectively. Two hundred five patients (53%) were treated with interferon alfa. After adjustment for clinical and serological differences at baseline between patients treated or not treated with interferon, the 5-year estimated survival probability was 96% and 95% for treated and untreated patients, respectively. CONCLUSIONS: In this cohort of patients, life expectancy is relatively long, in agreement with the morbidity data showing a slowly progressive disease.

Carcinoma, Hepatocellular↗