Correction to: Development of typological classification and its relationship to microdifferentiation in ethnic India

Prostate cancer (PCa) represents the most frequently diagnosed cancer in men. Cisplatin, also known as cis-diamminedichloroplatinum (DDP), is a standard chemotherapeutic agent used to treat PCa, and DDP resistance remains one important obstacle inDDP-based chemotherapy. In our research, we found miR-425-5p was down-regulated in PCa and even lower in DDP-resistantPCa determined by quantitative polymerase chain reaction; in contrast, GSK3b mRNA expression was upregulated in PCa andeven higher in DDP-resistant PCa. Moreover, there was a modest but significant inverse correlation between the expression ofGSK3b mRNA and miR-425-5p. Functional experiments showed that miR-425-5p mimic inhibited DDP resistance as evidencedby a promoted apoptosis rate (flow cytometry) and suppressed cell viability (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide assay) and expressions of MDR1 and MRP1 (western blotting) in DU145/DDP and PC3/DDP cells. Luciferase reporterassay and RNA immunoprecipitation identified GSK3b was a potential target of miR-425-5p. The effect of miR-425-5p mimic onDDP resistance was partially reversed by pcDNA-GSK3b. Mechanically, miR-425-5p mimic reduced expression of b-catenin,cyclin D1 and C-myc, which was further blocked when GSK3b overexpressed. In vivo experiments, recovery of GSK3bprevented xenograft tumor growth and DDP resistance in the presence of miR-425-5p mimic. To sum up, miR-425-5p upregulation might sensitize human PCa to DDP by targeting GSK3b and inactivating the Wnt/b-catenin signaling pathway

Efficacy of magnesium sulphate in aluminium phosphide poisoning--comparison of two different dose schedules.

The results of an open randomised study on the efficacy of magnesium sulphate therapy in aluminium phosphide poisoning are presented. One hundred and fifty five patients divided in three groups and matched for age, sex, dose, duration and severity of poisoning constituted the subject matter. Significant hypomagnesemia was observed in patients who did not receive magnesium sulphate (group 1). Two dose schedules of MgSO4 therapy were tried. The dose schedule No.1 given to patients of group 2 did not raise the magnesium levels significantly as compared to controls (group 4). The difference in the mortality between groups 1 & 2 was also not significant. On the other hand, the dose schedule No.2 given to patients of group 3 raised the magnesium levels significantly and these remained above normal limits throughout the observed period. This dose schedule brought down the mortality significantly than dose schedule No.1 (p < 0.001). It was also found that dose schedule No.2 has been effective in reducing the mortality irrespective of dose of pesticide consumed and its efficacy was due to rapid rise in magnesium levels. It is suggested that hypomagnesemia might be responsible for high mortality of patients of aluminium phosphide poisoning and its correction has beneficial effect on the management and ultimate favourable outcome of the illness.

A clinico-investigative profile in Graves' ophthalmopathy.

A clinico-investigative profile was studied in 30 patients with Graves' Ophthalmopathy (GO) (15 each with early and late). In accordance to the thyroid status 63.3% of patients were hyperthyroid and 36.7% euthyroid. There was slight female preponderence, with ratio being 1.5:1. Exophthalmometric readings were significantly high in GO patients as compared to controls. However, no significant diagnostic role of postural exophthalmometry was seen. Positional tonometery may have respectable place among the tests for early diagnosis of GO; however, it could not differentiate between hyperthyroid and euthyroid cases. Further the role of ultrasonography, if available could not be overemphasized.

Magnesium levels in acute cardiotoxicity due to aluminium phosphide poisoning.

Significant hypomagnesemia and hypomagnocytia were observed in patients of aluminium phosphide (AIP) poisoning having evidence of acute cardiotoxicity while magnesium levels were normal in patients of AIP poisoning without shock or cardiotoxicity as well as in controls. There was a direct relationship between electrocardiographic findings and low magnesium levels. The mortality was also related directly to hypomagnesemia. The dose of pesticide also influenced the mortality adversely. Autopsied heart showed changes of toxic myocarditis on histopathology.

Lung transfer components in hyperthyroidism.

Pulmonary functions were studied in twenty hyperthyroid non smoker patients. Their FVC, PEFR and MVV were significantly lowered while FEV1/FVC% and EFR25-75% were normal. Amongst the diffusion functions, Tlco, Dm and VA were reduced and VC increased, though these changes were not statistically significant. After the achievement of euthyroid state, statistically significant increase was seen in FVC, PEFR, MVV, Tlco120, Dm and VA with significant decrease in Vc from the basal levels. FEV1/FVC% and EFR25-75% were not affected. These observations suggest that the principal abnormalities in pulmonary functions in the hyperthyroid state are increased pulmonary capillary blood volume and respiratory myopathy, which are reversed as euthyroid state is achieved.

Reversion of ventricular and supraventricular tachycardia by magnesium sulphate therapy in aluminium phosphide poisoning. Report of two cases.

Two patients with aluminium phosphide poisoning developed supraventricular tachycardia and ventricular tachycardia (one each). These reverted successfully with magnesium sulphate therapy.

Incidence & outcome of aluminium phosphide poisoning in a hospital study.

A total of 418 patients with aluminium phosphide poisoning admitted during January 1981 to December 1987, were studied and analysed for various clinical parameters. A steady increase in the number of patients was seen during the last 7 yr. Maximum number belonged to the younger generation and nature of poisoning was suicidal in most of these patients. Dose of poison consumed varied, but most patients consumed two tablets (6 g). A wide range of symptoms and signs was seen, the commonest being gastrointestinal manifestations and shock. Cardiac arrhythmias and conduction disturbances were seen in 38.2 per cent patients. The overall mortality was 77.2 per cent. Indices of a bad prognosis included poor response to dopamine infusion and continuous increase in its dosage, chest infections, adult respiratory distress syndrome and disseminated intravascular coagulation. The complications noticed were pericarditis, congestive cardiac failure, acute gastrointestinal haemorrhage and acute respiratory arrest. Histopathology of various organs showed changes suggestive of cellular hypoxia but the mechanism of ECG changes and of the complications could not be elucidated.

Electrocardiographic abnormalities in aluminium phosphide poisoning with special reference to its incidence, pathogenesis, mortality and histopathology.

Ninety-five patients out of total 190 cases of aluminium phosphide (ALP) poisoning, who exhibited ECG changes were studied for incidence, type and pattern of ECG abnormalities, their effect on mortality and their relationship with histopathology of heart. Its incidence in the present study was 50%. The arrhythmias, conduction disturbances and ischaemic pattern occurred more or less in equal frequency. Certain ECG abnormalities which had not been reported previously ie, early repolarisation syndrome, varied sino-atrial blocks, bradycardia-tachycardia syndrome and electrical alternans were observed in this study. The clinical profile of these cases was similar irrespective of whether patients had ECG abnormalities or not. Shock was the cardinal feature. There was no effect of ECG abnormalities on mortality. The mortality which was otherwise high, depended upon severity of poisoning, dose of poison consumed, duration of shock, failure of response of shock to resuscitative measures and severe hypomagnesaemia. The pathogenesis of ECG abnormalities is still obscure. Hypomagnesaemia was observed in all the 18 cases studied, irrespective of ECG abnormalities. However, these were common when hypomagnesaemia was severe. Hypoxaemia and shock were not the contributory factors for these abnormalities. Autopsy revealed stereotyped histopathological changes of toxic myocarditis independent of ECG findings.

Jaccoud's arthritis.

A 16 year old girl with multivalvular heart disease and recurrent episodes of polyarthritis with correctable deformities of hands and feet fitting into that of Jaccoud's arthritis is reported. The condition is rare and often difficult to differentiate from rheumatoid arthritis.

Aluminium phosphide poisoning. Two cases with rare presentation.

We report two cases of aluminium phosphide poisoning who presented with rare manifestations, one with bleeding diathesis, hepatitis and acute tubular necrosis and the other with acute respiratory failure.

Plasma renin activity in shock due to aluminium phosphide poisoning.

Plasma renin activity (PRA) was estimated in 30 patients with aluminium phosphide (AIP) poisoning (study group) admitted in shock. Ten patients in shock other than due to AIP poisoning (Group II A) and 20 normal healthy subjects (Group II B) served as controls. The PRA was significantly higher in the study group and group II A as compared to normal healthy subjects (p less than 0.001). Significantly higher PRA was found in the study group as compared to Group II A (p less than 0.001). The initial higher PRA continued to rise further in the study group but it started decreasing in Group II A as the duration of shock advanced. Continuation of shock in AIP poisoning was probably due to slow release of toxic PH3 gas, which was detected by positive silver nitrate paper test. The rise in PRA was directly proportional to the dose of pesticide consumed. There was direct relationship of mortality with increased PRA. Angiotensin converting enzyme inhibitors may have a role in combating shock in AIp poisoning.

Significance of heart rate response in shock due to aluminium phosphide poisoning.

Mixed heart rate response has been observed in shock due to aluminium phosphide poisoning. Bradycardia observed in 9 of 30 cases studied indicated transient vagotonia and it reversed with atropine. Both tachycardiac bradycardiac responses were associated with significant increase in the mortality.

Adrenocortical involvement in aluminium phosphide poisoning.

The effect of aluminium phosphide (AlP) which is a systemic poison on the adrenal cortex was studied in 30 patients of AlP poisoning. A significant rise in the plasma cortisol level (greater than 1048 nmol/l) was observed in the twenty patients. Mortality was 50 per cent. Autopsy study could be undertaken only in 10 patients. Histopathology showed mild to moderate changes. In the rest (10 patients), the adrenal cortex was critically involved and the cortisol level failed to rise beyond normal levels (less than 690 nmol/l). The histopathology revealed severe changes (complete lipid depletion, haemorrhage, necrosis etc.) and all these patients died. In the critically ill patients, the cortisol levels remained low because of severe adreno-cortical involvement. The changes in the adrenal cortex could be due to shock or to cellular toxic effect of phosphine. The histopathological changes in various viscera showed congestion, edema and cellular infiltration. In the heart, there were patchy areas of necrosis, while the liver showed fatty changes and the lungs showed, in addition areas of gray/red hepatization. There was no adrenal apoplexy or extensive haemorrhage that could explain shock in these patients. Cardiogenic shock could not be confirmed due to lack of facilities for haemodynamic monitoring, but there was histopathological evidence in support of cardiovascular shock.

Adult respiratory distress syndrome following aluminium phosphide ingestion. Report of 4 cases.

Four cases of adult respiratory distress syndrome (ARDS) following aluminium phosphide ingestion (ALP) are being reported. The dose of the intoxicant varied from 2 tablets (6.0 gm) to 3 tablets (9.0 gm). All patients had shock at admission and developed ARDS within 6 hours. The exhalation of Phosphine, (PH3) detected by positive silver nitrate paper test, was the possible noxious triggering factor in our cases. The cases are being reported because of their rare occurrence.

Insulin response and glucose tolerance in survivors of myocardial infarction.

Insulin response and glucose tolerance was studied in 25 adult patients who had survived acute myocardial infarction 2-24 months prior to study. The results were compared with 15 age and sex matched healthy controls. Mean fasting glucose and serum insulin levels were normal in both groups. These values were significantly higher in patient group during glucose tolerance test (GTT) done after 75 g of glucose load. Eight patients (32%) had abnormal glucose tolerance and hyperinsulinaemia. Another 6 patients had hyperinsulinaemia (total 14 patients--56%). This is thought to be due to co-existent potential diabetes in these patients. The frequency of abnormal GTT or hyperinsulinaemia was not related to serum cholesterol levels but showed a positive correlation with serum triglyceride levels.

Spot diagnosis of aluminium phosphide ingestion: an application of a simple test.

Silver nitrate impregnated paper test was performed with the gastric fluid and in breath in 50 patients of aluminium phosphide poisoning. The test was 100% positive with gastric fluid but was positive in 50% patients in breath. The test is simple, reliable and sensitive method to detect phosphine (PH3) for bed side diagnosis of aluminium phosphide (AIP) ingestion.