A REVIEW ON HYPO HIDROTIC EFFECT OF SIDDHA FORMULATION - KUNGUMAPOO MATHIRAI

Hyperhidrosis is a condition present with excess sweating of palms on the hands, soles of the feet, forehead and axillae. This is socially embarrassing. There are few herbs to treat hyperhidrosis in Siddha system of medicine. The drug Kungumapoo Mathirai is being used in Siddha system of medicine for many years to treat hyperhidrosis. The ingredients used in the preparation of Kungumapoo Mathirai are Crocus sativus, Zingiberofficinale, Piper nigrum, Piper cubeba, Costus speciosus, Carum capticum, Piper longum, Syzygium aromaticu, Elettaria cardomom, Korosanai (Oxbile), Vengaram (Sodium biborate), Lingam (Red sulphide of mercury), Sambrani poo (Dry powder of Styrax benzoin). This article reviews the hypo hydration effect of the drug Kungumapoo Mathirai and its ingredients. This review will help to get much information on hypohydrosis effect of the chemical constituents of the drug. The antioxidant properties of the ingredients which is acting as hypo hydrating agent and their mechanism in controlling the nervous excitement by reducing the action potential in detail. The use of herbal drugs is becoming more popular due to the adverse effects of synthetic Anticholenergics and Antispasmodic drugs which are used to treat hyperhidrosis worldwide. Excellence of Siddha, formulated each and every medicines on the basis of Thiridhosa theory and five elemental theory, which are the basic principles of Siddha medicine. The basic theory of Siddha formulation Kungumapoo Mathirai is also explained here

Emmanuel Farber: In Memoriam (1918–2014)

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Immuno-affinity Purification of Insect Cell Expressed Rabies Virus Glycoprotein using a Conformational Specific Monoclonal Antibody

.Rabies is a disease of nervous system and causes progressive encephalitis with fatal outcome. The conformation-dependent epitopes on the glycoprotein (G) of rabies virus (RV) is responsible for the induction of virus neutralizing antibodies which is ultimately required to get complete protection from viral challenge. Therefore, a suitable chromatography technique is necessary to purify the tag free recombinant rabies virus glycoprotein (rRVG) without altering its immunogenic epitopes. The present study was undertaken to purify the rRVG using a conformational specific anti-rabies virus glycoprotein (RVG) mAb, M5B4, which binds to the natively folded G. The mAb had shown a significant kinetic interaction with RVG. The mAb immobilized onto the NHS-activated Sepharose 4 fast flow™ was used for the purification of rRVG by immuno-affinity chromatography (IAC). The bound rRVG was eluted in IAC using 0.1M glycine with pH 2.5 and the identity of the purified protein was confirmed by MALDI-TOF. The IAC purified rRVG induced neutralizing antibody response and 83% of the immunized mice were protected against intra-cerebral rabies virus challenge. The results indicate that the mAb based IAC method can be an effective purification technique for tag free rRVG with significant level of purity, without compromising the protein’s immunogenic potential

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial

Background: Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events. Methods: The REstart or STop Antithrombotics Randomised Trial (RESTART) was a prospective, randomised, open-label, blinded endpoint, parallel-group trial at 122 hospitals in the UK. We recruited adults (≥18 years) who were taking antithrombotic (antiplatelet or anticoagulant) therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage, discontinued antithrombotic therapy, and survived for 24 h. Computerised randomisation incorporating minimisation allocated participants (1:1) to start or avoid antiplatelet therapy. We followed participants for the primary outcome (recurrent symptomatic intracerebral haemorrhage) for up to 5 years. We analysed data from all randomised participants using Cox proportional hazards regression, adjusted for minimisation covariates. This trial is registered with ISRCTN (number ISRCTN71907627). Findings: Between May 22, 2013, and May 31, 2018, 537 participants were recruited a median of 76 days (IQR 29–146) after intracerebral haemorrhage onset: 268 were assigned to start and 269 (one withdrew) to avoid antiplatelet therapy. Participants were followed for a median of 2·0 years (IQR [1·0– 3·0]; completeness 99·3%). 12 (4%) of 268 participants allocated to antiplatelet therapy had recurrence of intracerebral haemorrhage compared with 23 (9%) of 268 participants allocated to avoid antiplatelet therapy (adjusted hazard ratio 0·51 [95% CI 0·25–1·03]; p=0·060). 18 (7%) participants allocated to antiplatelet therapy experienced major haemorrhagic events compared with 25 (9%) participants allocated to avoid antiplatelet therapy (0·71 [0·39–1·30]; p=0·27), and 39 [15%] participants allocated to antiplatelet therapy had major occlusive vascular events compared with 38 [14%] allocated to avoid antiplatelet therapy (1·02 [0·65–1·60]; p=0·92). Interpretation: These results exclude all but a very modest increase in the risk of recurrent intracerebral haemorrhage with antiplatelet therapy for patients on antithrombotic therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage. The risk of recurrent intracerebral haemorrhage is probably too small to exceed the established benefits of antiplatelet therapy for secondary prevention

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial

Background: Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events. Methods: The REstart or STop Antithrombotics Randomised Trial (RESTART) was a prospective, randomised, open-label, blinded endpoint, parallel-group trial at 122 hospitals in the UK. We recruited adults (≥18 years) who were taking antithrombotic (antiplatelet or anticoagulant) therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage, discontinued antithrombotic therapy, and survived for 24 h. Computerised randomisation incorporating minimisation allocated participants (1:1) to start or avoid antiplatelet therapy. We followed participants for the primary outcome (recurrent symptomatic intracerebral haemorrhage) for up to 5 years. We analysed data from all randomised participants using Cox proportional hazards regression, adjusted for minimisation covariates. This trial is registered with ISRCTN (number ISRCTN71907627). Findings: Between May 22, 2013, and May 31, 2018, 537 participants were recruited a median of 76 days (IQR 29–146) after intracerebral haemorrhage onset: 268 were assigned to start and 269 (one withdrew) to avoid antiplatelet therapy. Participants were followed for a median of 2·0 years (IQR [1·0– 3·0]; completeness 99·3%). 12 (4%) of 268 participants allocated to antiplatelet therapy had recurrence of intracerebral haemorrhage compared with 23 (9%) of 268 participants allocated to avoid antiplatelet therapy (adjusted hazard ratio 0·51 [95% CI 0·25–1·03]; p=0·060). 18 (7%) participants allocated to antiplatelet therapy experienced major haemorrhagic events compared with 25 (9%) participants allocated to avoid antiplatelet therapy (0·71 [0·39–1·30]; p=0·27), and 39 [15%] participants allocated to antiplatelet therapy had major occlusive vascular events compared with 38 [14%] allocated to avoid antiplatelet therapy (1·02 [0·65–1·60]; p=0·92). Interpretation: These results exclude all but a very modest increase in the risk of recurrent intracerebral haemorrhage with antiplatelet therapy for patients on antithrombotic therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage. The risk of recurrent intracerebral haemorrhage is probably too small to exceed the established benefits of antiplatelet therapy for secondary prevention

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial

BACKGROUND: Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events. METHODS: The REstart or STop Antithrombotics Randomised Trial (RESTART) was a prospective, randomised, open-label, blinded endpoint, parallel-group trial at 122 hospitals in the UK. We recruited adults (≥18 years) who were taking antithrombotic (antiplatelet or anticoagulant) therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage, discontinued antithrombotic therapy, and survived for 24 h. Computerised randomisation incorporating minimisation allocated participants (1:1) to start or avoid antiplatelet therapy. We followed participants for the primary outcome (recurrent symptomatic intracerebral haemorrhage) for up to 5 years. We analysed data from all randomised participants using Cox proportional hazards regression, adjusted for minimisation covariates. This trial is registered with ISRCTN (number ISRCTN71907627). FINDINGS: Between May 22, 2013, and May 31, 2018, 537 participants were recruited a median of 76 days (IQR 29-146) after intracerebral haemorrhage onset: 268 were assigned to start and 269 (one withdrew) to avoid antiplatelet therapy. Participants were followed for a median of 2·0 years (IQR [1·0- 3·0]; completeness 99·3%). 12 (4%) of 268 participants allocated to antiplatelet therapy had recurrence of intracerebral haemorrhage compared with 23 (9%) of 268 participants allocated to avoid antiplatelet therapy (adjusted hazard ratio 0·51 [95% CI 0·25-1·03]; p=0·060). 18 (7%) participants allocated to antiplatelet therapy experienced major haemorrhagic events compared with 25 (9%) participants allocated to avoid antiplatelet therapy (0·71 [0·39-1·30]; p=0·27), and 39 [15%] participants allocated to antiplatelet therapy had major occlusive vascular events compared with 38 [14%] allocated to avoid antiplatelet therapy (1·02 [0·65-1·60]; p=0·92). INTERPRETATION: These results exclude all but a very modest increase in the risk of recurrent intracerebral haemorrhage with antiplatelet therapy for patients on antithrombotic therapy for the prevention of occlusive vascular disease when they developed intracerebral haemorrhage. The risk of recurrent intracerebral haemorrhage is probably too small to exceed the established benefits of antiplatelet therapy for secondary prevention. FUNDING: British Heart Foundation

ANTI-QUORUM SENSING POTENTIAL OF LIMONIA ACIDISSIMA (L.) AGAINST VIBRIO HARVEYI KUMB-VA4

 Objective: This study aims to investigate the quorum-sensing inhibition (QSI) potential of Limonia acidissima L. against the biofilm forming Vibrio harveyi isolated from freshwater fish.Methods: The present study evaluated the anti-QS activity of the L. acidissima methanol and ethyl acetate (LA-M and LA-EA) fruit extracts using Chromobacterium violaceum ATCC 12472 (wild) and C. violaceum CV026 (mutant) as biomonitor strains and biofilm formation using the crystal violet assay. Vibrio sp. were isolated from freshwater-cultured fishes and screened for biofilm formation property. Strong biofilm forming isolate were subjected to molecular characterization. Limonia fruit pulp was subjected to methanol and ethyl acetate extraction using cold percolation method and yield was calculated. In parallel to determining the QSI properties of the extract, minimum inhibitory concentration (MIC), biofilm inhibition concentration (BIC), antibiofilm properties, and metabolic activity of LA-M and LA-EA against the biofilm forming V. harveyi KUMB-VA4 was determined.Results: The results of the present study demonstrated that the overall yield of methanol and ethyl acetate extract was 12.84% and 9.3% (w/w), respectively. Strong biofilm forming Vibrio isolate KUMB-VA4 was obtained from infected freshwater fishes and was subjected to molecular characterization. MIC of LA-M was 1510 μg/ml and LA-EA was observed to be 3000 μg/ml against the test pathogen, respectively. Biofilm inhibition assay revealed a BIC of LA-M at 250 μg/ml and LA-EA at 500 μg/ml. Both the plant extracts significantly reduced the biofilm formation of V. harveyi KUMB-VA4 and the metabolic activity in a dose-dependent manner. Light microscopy and scanning electron microscopy revealed that LA-M and LA-EA significantly altered 68.6% and 54.5% of the biofilm architecture at BIC. The QSI assay revealed that LA-M effectively reduced the violacein production of the biomonitor strains at sub-BIC (100–500 μg/ml) to 80% than LA-EA (43%) in a strong dose-dependent fashion.Conclusions: The present study revealed the QSI property of Limonia acidissima against the biofilm forming V. harveyi isolated from infected fish

1′-Benzylspiro[chromene-2,4′-piperidine]-4-carbonitrile

In the title compound, C21H20N2O, the piperidine ring adopts a chair conformation while the pyran ring adopts a screw-boat conformation. The piperidine ring forms dihedral angles of 65.75 (3) and 67.79 (5)° with the chroman and methyl-substituted benzene rings, respectively. The crystal structure features weak C—H...π and π–π [centroid–centroid distance = 3.8098 (8) Å] interactions