Profitability of scheduled commercial banks in Inida - a case analysis

The banking system, which constitutes the core of the financial sector, plays a crucial role in transmitting monetary policy impulses to the entire economic system. Its efficiency and development, therefore, are vitalfor enhancing the growth and improving the chancesfor price stability'. In view of the importance of improving the profitability performance of the banking sector in recent years, a census study has been adopted by covering all Indian scheduled commercial banks in India which have been divided into three groups, namely, SB I group. Nationalised Banks group and Private Banks group with two sessions viz., Period 1 and Period II by dividing the 10 years study period into firstfive years and last five years. Hie scope of the study is wider in nature. Vie study identified certain factors, which are prominent to hike the profitability of the banks. The step-wise multiple regression has been adopted by the researcher. An analysis ofthe SBIgroup reveals that in both the period ofstudy, the variable provisions and contingencies to total expenses showed a prominent place.. The nationalized banks group showed a position of provisions and contingencies to total expenses in the first halfof the study period and Capital A dequacy Ratio during the second halfof the study period. In relation to the Private Banks group, it has changed from Other interest expenses ratio to Capital Adequacy ratio. The study makes emphasis with regard to initiating monitoring and controlling mechanism on certain important ratios which are inevitable one to enhance the profitability of scheduled commercial banks

A Dangerous Twist of the 'T' Wave: A Case of Wellens' Syndrome

Wellens’ syndrome is a condition in which electrocardiographic (ECG) changes indicate critical proximal left anterior descending artery narrowing occurring during the chest pain-free period. Due to the severity of the obstruction, if such cases are managed by early invasive revascularisation therapy, a major threat in the form of a massive myocardial infarction or sudden death may be averted. We present the case of a patient with previous chest pain, whose ECG showing subtle ischemic changes was initially overlooked. A repeat ECG taken during the painless period showed a biphasic T wave, suggestive of Wellen’s’ syndrome. This was confirmed by an immediate coronary angiogram

A case of hoarseness of voice following COVID-19 infection

Mucormycosis is a fatal angio-invasive fungal infection associated with a high mortality. Apart from the traditional risk factors, COVID-19 infection and steroid therapy for the same have been recently identified to predispose to this life-threatening infection. Usual presentations of mucormycosis include rhino-orbito-cerebral, pulmonary, gastrointestinal, renal and cutaneous involvement. We report an unusual case of mediastinal involvement by mucormycosis in a patient recovering from moderate COVID-19 pneumonia. Early diagnosis, prompt initiation of antifungal therapy accompanied by timely surgical debridement were pivotal in averting morbidity and mortality in this patient

Methylation mediated silencing of TMS1/ASC gene in prostate cancer

BACKGROUND: Transcriptional silencing associated with aberrant promoter methylation has been established as an alternate pathway for the development of cancer by inactivating tumor suppressor genes. TMS1 (Target of Methylation induced Silencing), also known as ASC (Apoptosis Speck like protein containing a CARD) is a tumor suppressor gene which encodes for a CARD (caspase recruitment domain) containing regulatory protein and has been shown to promote apoptosis directly and by activation of downstream caspases. This study describes the methylation induced silencing of TMS1/ASC gene in prostate cancer cell lines. We also examined the prevalence of TMS1/ASC gene methylation in prostate cancer tissue samples in an effort to correlate race and clinico-pathological features with TMS1/ASC gene methylation. RESULTS: Loss of TMS1/ASC gene expression associated with complete methylation of the promoter region was observed in LNCaP cells. Gene expression was restored by a demethylating agent, 5-aza-2'deoxycytidine, but not by a histone deacetylase inhibitor, Trichostatin A. Chromatin Immunoprecipitation (ChIP) assay showed enrichment of MBD3 (methyl binding domain protein 3) to a higher degree than commonly associated MBDs and MeCP2. We evaluated the methylation pattern in 66 prostate cancer and 34 benign prostatic hyperplasia tissue samples. TMS1/ASC gene methylation was more prevalent in prostate cancer cases than controls in White patients (OR 7.6, p 0.002) while no difference between the cases and controls was seen in Black patients (OR 1.1, p 0.91). CONCLUSION: Our study demonstrates that methylation-mediated silencing of TMS1/ASC is a frequent event in prostate cancer, thus identifying a new potential diagnostic and prognostic marker for the treatment of the disease. Racial differences in TMS1/ASC methylation patterns implicate the probable role of molecular markers in determining in susceptibility to prostate cancer in different ethnic groups

Acute fatty liver of pregnancy: an update on mechanisms

Acute fatty liver of pregnancy (AFLP), characterized by hepatic microvesicular steatosis, is a sudden catastrophic illness occurring almost exclusively in the third trimester of pregnancy. Defective fatty acid oxidation in the fetus has been shown to be associated with this disease. Since the placenta has the same genetic makeup as the fetus and as AFLP patients generally recover following delivery, we hypothesized that the placenta might be involved in pathogenesis of this disease. In an animal model of hepatic microvesicular steatosis (using sodium valproate), we found that microvesicular steatosis results in mitochondrial structural alterations and oxidative stress in subcellular organelles of the liver. In placentas from patients with AFLP, we observed placental mitochondrial dysfunction and oxidative stress in subcellular organelles. In addition, defective placental fatty acid oxidation results in accumulation of toxic mediators such as arachidonic acid. Escape of these mediators into the maternal circulation might affect the maternal liver resulting in microvesicular steatosis

N-Butyl­pyridine-4-thio­carboxamide

In the title mol­ecule, C10H14N2S, the n-butyl chain assumes a trans zigzag conformation. The dihedral angle between the pyridine ring and the thio­amide plane is 23.38 (8)°. The mol­ecules in the crystal structure are linked by an inter­molecular N—H⋯N hydrogen bond

Single-agent arsenic trioxide in the treatment of newly diagnosed acute promyelocytic leukemia: durable remissions with minimal toxicity

Arsenic trioxide, as a single agent, has proven efficacy in inducing molecular remission in patients with acute promyelocytic leukemia (APL). There is limited long-term outcome data with single-agent As2O3 in the management of newly diagnosed cases of APL. Between January 1998 to December 2004, 72 newly diagnosed cases of APL were treated with a regimen of single-agent As2O3 at our center. Complete hematologic remission was achieved in 86.1%. At a median follow-up of 25 months (range: 8-92 months), the 3-year Kaplan-Meier estimate of EFS, DFS, and OS was 74.87% ± 5.6%, 87.21% ± 4.93%, and 86.11% ± 4.08%, respectively. Patients presenting with a white blood cell (WBC) count lower than 5 × 109/L and a platelet count higher than 20 × 109/L at diagnosis (n = 22 [30.6%]) have an excellent prognosis with this regimen (EFS, OS, and DFS of 100%). The toxicity profile, in the majority, was mild and reversible. After remission induction, this regimen was administered on an outpatient basis. Single-agent As2O3, as used in this series, in the management of newly diagnosed cases of APL, is associated with responses comparable with conventional chemotherapy regimens. Additionally, this regimen has minimal toxicity and can be administered on an outpatient basis after remission induction

3-Amino­phenyl naphthalene-1-sulfonate

In the title compound, C16H13NO3S, the plane of the naphthalene ring system forms a dihedral angle of 64.66 (10)° with the benzene ring. The mol­ecular structure is stabilized by weak intra­molecular C—H⋯O inter­actions and the crystal packing is stabilized by weak inter­molecular N—H⋯O and C—H⋯O inter­actions and by π–π stacking inter­actions of the inversion-related naphthalene units [centroid–centroid distance of 3.7373 (14) Å]

JunB Mediates Basal- and TGFβ1-Induced Smooth Muscle Cell Contractility

Smooth muscle contraction is a dynamic process driven by acto-myosin interactions that are controlled by multiple regulatory proteins. Our studies have shown that members of the AP-1 transcription factor family control discrete behaviors of smooth muscle cells (SMC) such as growth, migration and fibrosis. However, the role of AP-1 in regulation of smooth muscle contractility is incompletely understood. In this study we show that the AP-1 family member JunB regulates contractility in visceral SMC by altering actin polymerization and myosin light chain phosphorylation. JunB levels are robustly upregulated downstream of transforming growth factor beta-1 (TGFβ1), a known inducer of SMC contractility. RNAi-mediated silencing of JunB in primary human bladder SMC (pBSMC) inhibited cell contractility under both basal and TGFβ1-stimulated conditions, as determined using gel contraction and traction force microscopy assays. JunB knockdown did not alter expression of the contractile proteins α-SMA, calponin or SM22α. However, JunB silencing decreased levels of Rho kinase (ROCK) and myosin light chain (MLC20). Moreover, JunB silencing attenuated phosphorylation of the MLC20 regulatory phosphatase subunit MYPT1 and the actin severing protein cofilin. Consistent with these changes, cells in which JunB was knocked down showed a reduction in the F:G actin ratio in response to TGFβ1. Together these findings demonstrate a novel function for JunB in regulating visceral smooth muscle cell contractility through effects on both myosin and the actin cytoskeleton

N-(5-Bromo-2-chloro­benz­yl)-N-cyclo­propyl­naphthalene-2-sulfonamide

In the title compound, C20H17BrClNO2S, the dihedral angle between the benzene ring and the naphthalene plane is 8.95 (8)°. The crystal packing is stabilized by weak inter­molecular C—H⋯O, C—H⋯Cl and π–π [centroid–centroid distance = 3.8782 (16) Å] inter­actions