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Biomedical subjects

R Bhattacharya

Publications and source records attributed to R Bhattacharya.

At least 19 recordsLinked to original sources
PubMed2006

The knee skyline radiograph: its usefulness in the diagnosis of patello-femoral osteoarthritis.

The aim of this study was to determine the usefulness of the skyline radiograph in the diagnosis of patellofemoral osteoarthritis. Additionally, we wanted to assess the usefulness of patello-femoral crepitus as a clinical sign of this condition. Seventy-seven patients scheduled to undergo knee surgery had standard antero-posterior, lateral and skyline X-rays of their affected knee. The presence of clinical patello-femoral crepitus was also documented preoperatively. At the operation, their patellofemoral joints were graded into two groups according to the presence or absence of osteoarthritis. The lateral and skyline view X-rays as well as patello-femoral crepitus were compared individually against the operative findings. The skyline view had a sensitivity of 79% and a specificity of 80%. The lateral view had a sensitivity of 82% and specificity of 65%. Patello-femoral crepitus as a sign had a sensitivity of 89% and a specificity of 82%. There was no statistically significant difference between the two radiological views in terms of sensitivity and specificity in the diagnosis of patellofemoral osteoarthritis. Hence, we cannot recommend the skyline view as a routine radiological investigation in all cases of suspected patellofemoral osteoarthritis.

Humans↗
PubMed2006

Role of computerised tomography in management of intra-articular fractures of the os calcis.

This study aimed to look at the role played by the CT scan in decision making in the management of intra-articular fractures of the calcaneum. Twenty-four patients with intra-articular fractures of the calcaneum were included. Their initial radiographs and CT films were blinded and assessed by three independent observers. Based on this they were selected for operative or non-operative management. The actual management was also recorded. The data were then subjected to statistical analysis to look at the association between the decision from radiograph, that from the CT scan and the actual management undertaken. Non-parametric tests for related samples were performed to look at the association between the actual management and the decisions made by assessing the radiographs and the CT scans. For all three observers, there was no significant difference between the actual management and decisions made by assessing the plain radiographs or the CT scan. There was also no significant difference between the radiograph-based and the CT-based decisions. However, the Cochran Q test showed that there was significant variation among the three observers for the CT-based assessment. Our results, show that the CT scan should only be done when a definite decision is made to operate on a patient, based on plain radiographs. Calcaneal fractures which are selected for non-operative management, based on X rays, should not have a CT scan as a routine as it provides no valuable additional information affecting the management decision.

Calcaneus↗
PubMed2006

Effect of alpha-ketoglutarate on cyanide-induced biochemical alterations in rat brain and liver.

OBJECTIVE: To investigate the biochemical changes in rat brain and liver following acute exposure to a lethal dose of cyanide, and its response to treatment of alpha-ketoglutarate (alpha-KG) in the absence or presence of sodium thiosulfate (STS). METHODS: Female rats were administered 2.0 LD50 potassium cyanide (KCN; oral) in the absence or presence of pre-treatment (-10 min), simultaneous treatment (0 min) or post-treatment (+2-3 min) of alpha-KG (2.0 g/kg, oral) and/or STS (1.0 g/kg, intraperitoneal, -15 min, 0 min or + 2-3 min). At the time of onset of signs and symptoms of KCN toxicity (2-4 min) and at the time of death (5-15 min), various parameters particularly akin to oxidative stress viz. cytochrome oxidase (CYTOX), superoxide dismutase (SOD), glutathione peroxidase (GPx), reduced glutathione (GSH) and oxidized glutathione (GSSG) in brain, and CYTOX, sorbitol dehydrogenase (SDH), alkaline phosphatase (ALP), GSH and GSSG in liver homogenate were measured. RESULTS: At both time intervals brain CYTOX, SOD, GPx, and GSH significantly reduced (percent inhibition compared to control) to 24%, 56%, 77%, and 65%, and 44%, 46%, 78%, and 57%, respectively. At the corresponding time points liver CYTOX and GSH reduced to 74% and 63%, and 44% and 68%, respectively. The levels of GSSG in the brain and liver, and hepatic ALP and SDH were unchanged. Pre-treatment and simultaneous treatment of a-KG alone or with STS conferred significant protection on above variables. Post-treatment was effective in restoring the changes in liver but failed to normalize the changes in the brain. CONCLUSIONS: Oral treatment with alpha-KG alone or in combination with STS has protective effects on cyanide-induced biochemical alterations in rat brain and liver.

Animals↗
PubMed2005

Effect of sub-acute oral cyanide administration in rats: protective efficacy of alpha-ketoglutarate and sodium thiosulfate.

Chronic toxicity of cyanide in humans and animals has been previously described. Alpha-ketoglutarate (alpha-KG) and sodium thiosulfate (STS) are known to confer remarkable protection against acute cyanide poisoning in rodents. Their efficacy against sub-acute or chronic cyanide exposure is not known. The objective of the present study was to assess the sub-acute toxicity of potassium cyanide (KCN) in female rats following oral administration of 7.0 mg/kg (0.5 LD50) for 14 d. The effect of alpha-KG (oral; 1.0 g/kg) and/or STS (intraperitoneal, 1.0 g/kg) on cyanide toxicity was also evaluated. Various hematological and biochemical indices were determined after 7 d of treatment and additional parameters like organ-body weight index (OBI) and histology of brain, heart, lung, liver, kidney and spleen were performed after 14 and 21 d (recovery group) of cyanide exposure. Sub-acute exposure of KCN did not produce any significant change in body weight of the animals, OBI, hematology and the levels of blood urea, creatinine, aspartate aminotransferase, triiodothyronine (T3) and tetraiodothyronine (T4). The levels of temporal glutathione disulfide (GSSG) and hepatic malondialdehyde (MDA), reduced glutathione (GSH) and GSSG were unaffected. However, in KCN treated animals elevated levels of blood glucose and reduced levels of alanine aminotransferase were observed. Activities of cytochrome c oxidase in the brain and rhodanese in the liver were diminished. Reduced levels of GSH and enhanced levels of MDA in brain were observed. Increased levels of blood thiocyanate were observed in all the treatments of KCN. Additionally, KCN also produced various histological changes in the brain, heart, liver and kidney. Although, treatment of alpha-KG and STS alone significantly blunted the toxicity of KCN, concomitant use of both interventions afforded to maximum protection. This study indicates a promising role of alpha-KG and STS for the treatment of prolonged cyanide exposures.

Administration, Oral↗
PubMed2005

Mechanism of ricin-induced apoptosis in human cervical cancer cells.

The mechanism of ricin-induced apoptosis in human cervical cancer cell line HeLa was studied. The present study demonstrated that ricin induces apoptosis of human cervical cancer cells (HeLa) in a time dependent manner with an IC(50) for cell viability of 1 microg/ml. Ricin treatment resulted in a time dependent increase in LDH leakage, DNA fragmentation, percent apoptotic cells, generation of reactive oxygen species and depletion of intracellular glutathione levels. DNA agarose gel electrophoresis showed typical oligonucleosomal length DNA fragmentation. Additionally, DNA diffusion assay was performed to confirm DNA damage and apoptosis. Ricin activated caspase-3 as evidenced by both proteolytic cleavage of procaspase-3 into 20 and 18 kDa subunits, and increased protease activity. Caspase activity was maximum at 4h and led to the cleavage of 116 kDa poly(ADP-ribose) polymerase (PARP), resulting in the 85 kDa cleavage product. Ricin-induced caspase-3 activation also resulted in cleavage of DNA fragmentation factor-45 (DFF45/ICAD) and DFF40 or caspase-activated DNase in HeLa cells. Activation of caspase-3, cleavage of PARP and DNA fragmentation was blocked by pre-treatment with caspase-3 specific inhibitor Ac-DEVD-CHO (100 microM) and broad-spectrum caspase inhibitor Z-VAD-FMK (40 microM). Ricin-induced DNA fragmentation was inhibited by pre-treatment with PARP inhibitors 3-aminobenzamide (100 microM) and DPQ (10 microM). Our results indicate that ricin-induced cell death was mediated by generation of reactive oxygen species and subsequent activation of caspase-3 cascade followed by down stream events leading to apoptotic mode of cell death.

Apoptosis↗
PubMed2005

Sanders classification of fractures of the os calcis. An analysis of inter- and intra-observer variability.

Our study was undertaken to assess the inter- and intra-observer variability of the classification system of Sanders for calcaneal fractures. Five consultant orthopaedic surgeons with different subspecialty interests classified CT scans of 28 calcaneal fractures using this classification system. After six months, they reclassified the scans. Kappa statistics were used to analyse the two groups. The interobserver variability of the classification system was 0.32 (95% confidence interval (CI) 0.26 to 0.38). The subclasses were then combined and assessment of agreement between the general classes as a whole gave a kappa value of 0.33 (95% CI 0.25 to 0.41). The mean kappa value for intra-observer variability of the classification system was 0.42 (95% CI 0.22 to 0.62). When the subclasses were combined, it was 0.45 (95% CI 0.21 to 0.65). Our results show that, despite its popularity, the classification system of Sanders has only fair agreement among users.

Calcaneus↗
PubMed2004

A randomized controlled trial of knifelight and open carpal tunnel release.

A randomized controlled trial was done to compare the results of carpal tunnel decompression using the standard open approach and the Knifelight technique. Twenty-six patients with bilateral carpal tunnel syndrome requiring operation were selected for the study and the operative technique was randomized for the first hand. Six weeks later, the second hand was operated upon using the alternate technique. There was little difference between the two techniques with regard to time taken to return to work, return of grip strength, symptom relief, complications, incidence of pillar pain and patient preference. However, the incidence of scar tenderness was significantly lower with the Knifelight technique.

Carpal Tunnel Syndrome↗
PubMed2003

Different supramolecular hydrogen bond structures and significant changes in magnetic properties in dinuclear mu 2-1,1-N3 copper(II) complexes with very similar tridentate Schiff base blocking ligands.

Three new basal-apical, mu(2)-1,1-azide bridged complexes, [CuL(1)(N(3))](2) (1), [CuL(2)(N(3))](2) (2) and [CuL(3)(N(3))](2) (3) with very similar tridentate Schiff base blocking ligands [L(1) = N-(3-aminopropyl)salicylaldimine, L(2) = 7-amino-4-methyl-5-azahept-3-en-2-one and L(3) = 8-amino-4-methyl-5-azaoct-3-en-2-one) have been synthesised and their molecular structures determined by X-ray crystallography. In complex 1, there is no inter-dimer H-bonding. However, complexes 2 and 3 form two different supramolecular structures in which the dinuclear entities are linked by strong H-bonds giving one-dimensional systems. Variable-temperature (300-2 K) magnetic susceptibility measurements and magnetization measurements at 2 K reveal that complexes and have antiferromagnetic coupling while has ferromagnetic coupling which is also confirmed by EPR spectra at 4-300 K. Magnetostructural correlations have been made taking into consideration both the azido bridging ligands and the existence of intermolecular hydrogen bonds in complexes 2 and 3.

Journal Article↗
PubMed2002

In vitro and in vivo attenuation of experimental cyanide poisoning by alpha-ketoglutarate.

Treatment of cyanide poisoning generally includes methemoglobin forming agents, like amyl nitrite and/or sodium nitrite (SN), in combination with sodium thiosulphate (STS). However, in many instances of cyanide poisoning, use of nitrites are contraindicated due to their strong vasoactive properties. alpha-Ketoglutarate (alpha-KG) antagonises cyanide by cyanohydrin formation and is considered a promising antidote for cyanide poisoning. In the present study, pre-treatment (30 min) and simultaneous treatment (0 min) of alpha-KG (5 mM) was found to confer significant protection against 5 mM potassium cyanide (KCN) induced cytotoxicity in rat thymocytes as measured by eosin Y exclusion and leakage of intracellular lactate dehydrogenase (LDH), but could not prevent the mitochondrial dysfunction (MTT assay), depletion of cellular GSH (reduced glutathione) and DNA damage. The post-treatment (5 or 30 min) of alpha-KG did not offer any protection on any of the above parameters. Results of in vitro studies were also supported by in vivo data. Pre-treatment of peroral (p.o.) alpha-KG (0.125-2.0 g/kg) exhibited dose and time dependent effects and was found to be effective even when given upto 60 min prior to KCN (p.o.). Addition of STS significantly enhanced the protective efficacy of alpha-KG at all the doses and time intervals. A 10 min pre-treatment of alpha-KG increased the LD(50) of KCN 7.6-fold, which was further increased to 25.6-fold by the addition of both SN and STS. Simultaneous treatment of alpha-KG (2.0 g/kg) increased the LD50 of KCN 5.4-fold which was increased to 18.1-fold by the addition of STS. However, addition of SN did not confer any additional protection. In the presence of SN+STS, a decrease in the dose of alpha-KG exhibited a dose-dependent decrease in protection, but still a >10-fold protection could be observed at 1.0 g/kg dose of alpha-KG. Considering the efficacy and safety of peroral alpha-KG, a promising treatment regimen consisting of alpha-KG+STS or alpha-KG+SN+STS is proposed, depending upon the individual situation.

Animals↗
PubMed2002

Involvement of caspase and reactive oxygen species in cyanobacterial toxin anatoxin-a-induced cytotoxicity and apoptosis in rat thymocytes and Vero cells.

The hepatotoxins and neurotoxins produced by bloom-forming cyanobacteria have been the cause of human and animal health hazards and even death. The most common cyanobacterial neurotoxin is anatoxin-a, and intoxications by these toxins can be fatal through muscular paralysis causing respiratory arrest. We report here anatoxin-a-induced apoptosis in two non-neuronal cells, viz. cultured rat thymocytes and African green monkey kidney cells (Vero). Anatoxin-containing cell-free extracts (ACE) from Anabena flosaquae and purified anatoxin-a were used in the study. The toxin-induced cytotoxicity was characterized by loss of viability, lactate dehydrogenase leakage, loss of mitochondrial function, and DNA fragmentation. The toxin-induced apoptosis was characterized by plasma membrane blebbing, condensed chromatin, nuclear fragmentation and formation of apoptotic bodies. Toxin-treated thymocytes showed typical internucleosomal DNA fragmentation in agarose gel electrophoresis. Ultrastructure studies confirmed the apoptotic morphology in thymocytes. ACE and anatoxin-a showed caspase-3 activation, and pretreatment with the caspase-3-specific tetrapeptide inhibitor, acetyl-Asp-Glu-Val-Asp-aldehyde (Ac-DEVD-CHO) abolished the DNA fragmentation and reduced the incidence of apoptotic cells. The thymocytes also showed dose- and time-dependent toxin-induced generation of reactive oxygen species. The study demonstrates that anatoxin-induced apoptosis is possibly mediated by generation of reactive oxygen species and caspase activation.

Analysis of Variance↗
PubMed2002

Promising role of alpha-ketoglutarate in protecting against the lethal effects of cyanide.

Treatment of cyanide poisoning generally includes amyl nitrite and/or sodium nitrite (SN) in combination with sodium thiosulphate (STS). However, in many instances of cyanide poisoning, use of nitrites is contraindicated due to their strong vasoactive properties. alpha-Ketoglutarate (alpha-KG) antagonizes cyanide poisoning by cyanohydrin formation. Protective efficacy of graded doses of alpha-KG (p.o.) as pretreatment, simultaneous treatment or post-treatment was evaluated against acute potassium cyanide (KCN) poisoning (p.o.) in female rats. Pretreatment with alpha-KG (0.125-2.0 g/kg) exhibited dose- and time-dependent effects and was found to be effective even when given up to 60 min prior to KCN. Addition of STS significantly enhanced the protective efficacy of alpha-KG at all the doses and time intervals. A 10-min pretreatment with alpha-KG increased the LD50 of KCN by 7-fold, which was further increased 28-fold by the addition of both SN and STS. Simultaneous treatment with alpha-KG (2.0 g/kg) increased the LD50 of KCN by 7-fold, which was doubled by the addition of STS. However, addition of SN did not confer any additional protection. Post-treatment with alpha-KG + STS minimized the mortality by 50% but did not significantly extend the survival time in KCN (2 LD50)-administered rats. KCN (0.75 LD50) inhibited rat brain cytochrome oxidase, which was significantly protected by pretreatment or simultaneous treatment with alpha-KG and STS. Considering the efficacy and safety of peroral alpha-KG, a promising treatment regimen consisting of alpha-KG + STS or alpha-KG + SN + STS is proposed depending upon the situation.

Animals↗
PubMed2001

Protective effects of amifostine and its analogues on sulfur mustard toxicity in vitro and in vivo.

Sulfur mustard (bis(2-chloroethyl)sulfide, SM) is a highly reactive bifunctional alkylating agent that forms sulfonium ions in the body. SM alkylates DNA, leading to DNA strand breaks and cell death in a variety of cell types and tissues. Although several approaches have been proposed to challenge the toxic action(s) of SM, no satisfactory treatment regimen has evolved. The synthetic aminothiol amifostine, earlier known as WR-2721 (S-2-(3-aminopropylamino)ethyl phosphorothioate), has been extensively used as a chemical radioprotector for the normal tissues in cancer radiotherapy and chemotherapy. SM is known as a radiomimetic agent and this prompted us to evaluate the protective efficacy of amifostine (2.5 mM) and three of its analogues, DRDE-06 (S-2 (3-aminopropylamino) ethyl phenyl sulfide), DRDE-07 (S-2 (2-aminoethylamino) ethyl phenyl sulfide), and DRDE-08 (S-2 (4-aminobutylamino) ethyl phenyl sulfide), against SM toxicity in rat liver slices. Of the four agents tested, a 30-min pretreatment of amifostine and DRDE-07 enhanced the LC50 (a concentration producing 50% leakage of lactate dehydrogenase (LDH) or alanine aminotransferase (ALT)) of SM by 5.9- and 3.3-fold for LDH and 10.2- and 5.5-fold for ALT, respectively. Except DNA fragmentation, both these agents significantly attenuated the loss of intracellular K(+) and mitochondrial integrity (MTT assay), depletion of GSH levels, and histopathology produced by a toxic concentration (80 microM) of SM. However, when amifostine and DRDE-07 were introduced 2 h after SM, no significant protection was observed. SM (77.5 or 155 mg/kg) was also applied dermally on female albino mice and challenged by 0.20 LD50 (po) of amifostine, DRDE-06, DRDE-07, or DRDE-08 at -30 min, 0 min, or +6 h. Protection was observed only when the agents were administered at -30 min or 0 min; posttreatment (+6 h) did not offer any protection. The magnitude of in vivo protection was in the following order: DRDE-07 >or= amifostine > DRDE-08 > DRDE-06. Gas chromatographic analysis showed that there was no direct chemical interaction between SM and the antidotes. The po LD50s of amifostine, DRDE-06, DRDE-07, and DRDE-08 were 1049, 1345, 1248, and 951 mg/kg, respectively. Both in vitro and in vivo data indicate promising roles of amifostine and DRDE-07 as prophylactic agents against SM poisoning.

Amifostine↗
PubMed2001

1 alpha,25-Dihydroxyvitamin D(3) inhibits rat liver ultrastructural changes in diethylnitrosamine-initiated and phenobarbital promoted rat hepatocarcinogenesis.

The active metabolite of vitamin D, 1 alpha,25-dihydroxyvitamin D(3)[1,25(OH)(2)D(3)] has been receiving increasing attention and has come to the forefront of cancer chemoprevention research as being a regulator of cellular growth, differentiation and death. In the present study, attempts have been made to investigate the in vivo chemopreventive effect of 1,25(OH)(2)D(3) in two-stage rat liver carcinogenesis. Hepatocarcinogenesis was initiated with a single intraperitoneal injection of diethylnitrosamine [DEN] (200 mg/kg b. wt.) at week 4. After a brief recovery period of 2 weeks, all the DEN-treated rats were given phenobarbital (0.05%) in the basal diet and continued thereafter till the completion of the experiment. The results of our experiment showed that the rats which received 1,25(OH)(2)D(3) for 14 weeks (0.3 microg/100 microL propylene glycol, per os, twice a week), starting the treatment 4 weeks prior to DEN injection, exhibited maximum protective effect in maintaining the normal cellular architecture of the hepatocytes than the group of rats which received this micronutrient for only 9 weeks. Moreover, continuous supplementation of 1,25(OH)(2)D(3) maintains the concentration of hepatic microsomal cytochrome P-450 like that of normal vehicle control. Thus, long-term supplementation of 1,25(OH)(2)D(3) significantly (P < 0.001) inhibits hepatic cytosolic lipid peroxidation, thereby protecting the cell membranes from free-radical mediated damage. These results suggest that 1,25(OH)(2)D(3) is useful in the inhibition of rat liver carcinogenesis.

Animals↗
PubMed2001

Pharmacological interventions of cyanide-induced cytotoxicity and DNA damage in isolated rat thymocytes and their protective efficacy in vivo.

Cyanide inhibits the mitochondrial respiratory chain enzyme cytochrome oxidase causing histotoxic hypoxia. It is primarily considered as a neurotoxin but its other toxic manifestations are also well documented. Cyanide-induced apoptosis in neuronal cells has also been demonstrated recently. At the same time we also reported that potassium cyanide (KCN) produces extensive cytotoxicity and DNA fragmentation in rat thymocytes. The DNA damage was sensitive to elevated levels of extracellular Ca2+ and was attenuated by Zn2+ (modulator of Ca2+ dependent endonuclease), N-acetylcysteine (free radical scavenger) and diltiazem (Ca2+ channel blocker). In a continuation of this work, in the present study we have shown that the cytotoxicity and DNA fragmentation induced by 5 mM KCN was preceded by loss of mitochondrial integrity (MTT assay and rhodamine-123 staining) and nuclear viability (propidium iodide uptake) which were mediated by generation of reactive oxygen species (DCHF-DA staining). The DNA damage was also accompanied by nuclear fragmentation (Hoechst 33342 staining), a phenomenon that characterises the 'apoptotic' type of cell death. The in vitro toxic insult of KCN was challenged by pre-treatment (0.5 h), simultaneous treatment or post-treatment (0.5-3 h) of various pharmacological agents viz., Trolox (antioxidant), EGTA (Ca2+ modulator) and aurintricarboxylic acid (ATA; Ca2+/Mg2+ dependent endonuclease inhibitor). In addition, Quercetin (antioxidant) was tested as simultaneous treatment alone and was found to be ineffective. On the basis of various biochemical indices and DNA fragmentation (quantitative and qualitative), simultaneous treatment of Trolox was found to be the most effective in attenuating cyanide toxicity in vitro. This protection can be attributed to interventions in oxidative stress-mediated cell injury which is an early event preceding DNA damage. Both EGTA and ATA could not prevent this damage. Trolox also increased the LD(50) of KCN in mice 2.5-fold as compared to 1.8- and 1.6-fold for EGTA and ATA, respectively.

Animals↗
PubMed2001

Extraction of motion strength and motor activity signals from video recordings of neonatal seizures.

This paper presents two methods developed to extract quantitative information from video recordings of neonatal seizures in the form of temporal motion strength and motor activity signals. Motion strength signals are extracted by measuring the area of the body parts that move during the seizure and the relative speed of motion using a combination of spatiotemporal subband decomposition of video, nonlinear filtering, and segmentation. Motor activity signals are extracted by tracking selected anatomical sites during the seizure using a modified version of a feature-tracking procedure developed for video, known as the Kanade-Lucas-Tomasi (KLT) algorithm. The experiments indicate that the temporal signals produced by the proposed methods provide the basis for differentiating myoclonic from focal clonic seizures and distinguishing these types of neonatal seizures from normal infant behaviors.

Algorithms↗