Denial may be adaptive during hospitalization for acute coronary disease. We studied the impact of denial in 48 patients referred to a tertiary care center for treatment of unstable angina. Using the Hackett-Cassem Denial Scale, we divided the group into 25 high deniers and 23 low deniers. The two groups were comparable in baseline demographic and social data, coronary risk factors, cardiac history, medical treatment, vital signs, and cardiac catheterization results (number of diseased vessels and ejection fraction). Compared to low deniers, high deniers had half as many episodes of angina during hospitalization (1.3 vs. 2.5; p less than 0.03, t = 2.2, df = 46) and were more likely to reach medical stabilization, i.e., pain free for 36 hr (92% vs. 65%, p less than 0.03, Fisher exact probability test). Intravenous nitroglycerin drips were also required less often in high deniers (32% vs. 78%, p = 0.002, Fisher exact). Two myocardial infarctions and one death occurred, all in low deniers. We conclude that denial independently predicts better medical outcome during acute hospitalization for unstable angina.

ECIRS is a novel and excellent approach for the treatment of simultaneous renal and ureteral calculi with stone clearance and morbidity profile comparable to traditional prone PCNL. We believe that the advantage provided by this approach to the surgeon, patient, and anesthetist may lead to widespread adaptability of this technique in the management of complex urolithiasis.

Objective To study the role of miRNA-181a and augmenter of liver regeneration in TGF-β-induced fibrosis in hepatic stellate cells. Methods LX2 cells were treated with 20 ng/ml TGF-β for 24 h. miRNA-181a, ALR plasmid and empty vectors were transfected using siPORT NeoFx reagent. Cells were harvested after 48 h or 72 h of transfection for protein or RNA analysis. Western blotting was performed for ALR, TGF-β receptor II (TGFβ-RII), collagen 1A1 (COLL1A1), alpha-smooth muscle cell actin (α-SMA), rac1, E-cadherin and β-actin. Quantitative RT-PCR was performed for ALR, GAPDH, miRNA-181a or 5S rRNA. Results TGF-β induced the expression of miRNA-181a, which in turn down-regulated ALR thereby induced the fibrosis markers, such as COLL1A1, α-SMA and rac1 in hepatic stellate cells. Over-expression of miRNA-181a down-regulated expression of ALR and up-regulated expression of fibrosis markers. On the other hand, ALR over-expression resulted in a decrease in miRNA-181a expression and fibrosis markers. Over-expression of ALR also inhibited the expression of TGFβ-RII and increased expression E-cadherin. Conclusion TGF-β induced miRNA-181a, which in turn induced fibrosis, at least in part, by inhibiting ALR. ALR inhibited TGF-β action by decreasing the expression of TGFβ-RII, thereby inhibiting miRNA-181a expression and fibrosis markers. ALR could serve as a potential molecule to inhibit liver fibrosis.

Bellini duct carcinoma of kidney derives from collecting duct and is associated with an aggressive course and extremely poor prognosis. Here, we report an interesting case of Collecting Duct Carcinoma (CDC) with Inferior Vena Cava (IVC) thrombus and large retroperitoneal lymph nodes and diffuse desmoplastic reaction. The patient underwent left open radical nephrectomy with IVC thrombectomy and regional lymphadenectomy. Based on morphological and immunohistochemical analysis, diagnosis of collecting duct (Bellini duct) carcinoma was made. Presently, patient is on adjuvant chemotherapy with gemcitabine and cisplatin and under follow-up.

Post-infective pseudoaneurysm of the left ventricle in children is very rare, with only five cases reported in English medical literature so far. Patients usually have a short history of infection by Staphylococcus aureus. Timely surgical intervention has generally a good outcome. We present a case of post-infectious pseudoaneurysm in a 2-year-old girl with a review of literature.

Butyrate, a histone deacetylase inhibitor, has several therapeutic applications, including cancer. However, the effect of butyrate in HBV replication is not known so far. It was hypothesized that butyrate might inhibit HBV replication and host cell proliferation via SIRT-1. It was found that the increased expression of SIRT-1 in Hep G2.2.15 cells (HBV expressing cells) than Hep G2 cells. Next the expression of SIRT-1 and Acetylated p53 (Ac-p53) were measured in the liver biopsy samples of chronic hepatitis B (CHB) patients with high viral load and compared to CHB patients with low viral load and found that there was a high SIRT-1 expression and a low Ac-p53 levels in CHB patients with high viral load compared to CHB patients with low viral load. Incubation of butyrate inhibited SIRT-1 expression and cell proliferation. Inhibition of SIRT-1 by butyrate or SIRT-1 siRNA increased the levels of Ac-p53. The elevated Ac-p53 decreased p-akt, cyclin D1, and thereby inhibited cell proliferation. Incubation of butyrate with Hep G2.2.15 cells also inhibited HBx protein expression, HBV-DNA and hepatitis B surface antigen (HBsAg). Taken together, the data showed that butyrate inhibited HBV replication and cell proliferation by inhibiting SIRT-1 expression in hepatoma cells. K E Y W O R D S anti-viral, butyrate, HBV, p53, replication, SIRT-1 1 | INTRODUCTION Hepatitis B Virus (HBV) is a small double stranded-DNA virus, and its infection is a major health problem worldwide. 1 HBV infection is responsible for chronic liver inflammation (hepatitis), which further progresses to liver cirrhosis and liver failure or hepatocellular carcinoma (HCC). 2 The control of HBV replication is one of the most significant approaches to reduce the chronic HBV infection-linked pathogenicity. To date, there is no treatment available which can completely eradicate HBV infection in the patients. Few chemotherapeutic drugs such as, adefovir, entecavir, lamivudine, and telbivudine target the HBV-DNA polymerase and can reduce the viral replication. 3,4 However, long-term use of these drugs might lead to the increase the viral drug-resistance. 4Recently, use of interferon-alpha (IFN-α) along with the analogues of nucleotide/nucleoside significantly minimized the HBV infection and replication in the HBV infected patients. 5,6 Nevertheless, long-term use of IFN-α and nucleotide/nucleoside therapy tends to develop the drug resistance and causes some side effects in the patients. 7,8 Therefore, there is a need for a potential therapy or the targeted drugs for the anti-HBV therapeutics.SIRT-1 or Sirtuin-1 is a class III histone deacetylase (HDAC), which can deactivate histones or many non-histone proteins including p53, NF-κB, AP-1, and PGC-1α. SIRT-1 modulates several cellular processes such as apoptosis, cell cycle regulation, aging, and gene silencing. 9-11 SIRT-1 is also known to induce HBV replication. 12 SIRT-1 inducer resveratrol had been shown to influence the HBV

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Introduction: A medical record is a systematic documentation of a patient’s medical history and care for legal and future use. A poor quality medical record can negatively affect patient care and safety. The study aims to assess the adequacy of medical records in Bir Hospital, a central hospital.Methods:A cross-sectional study was conducted by analyzing consecutive discharge summaries of patients admitted during a 6 month period in a single unit of a tertiary care center. The discharge summary format of the hospital was taken as the standard and evaluation for adequacy of data entered was assessed. Descriptive statistics were used to analyze various statistical discrepancies. Results: Patient’s condition at discharge was missing in 86 (66.15%). Patient’s address was missing in 21 (16.1%) cases. Almost all the discharge sheets lacked mailing address. Total 96 (73.8%) had use of abbreviations diagnosis. Age and sex were missing in 1 (0.76%). Doctor’s signature was illegible in 103 (79.3%) and missing in 2 (1.5%) summaries. Doctor’s name and their level/position were missing in 118 (90.76%) and 125 (96.1%) respectively. Total 126 patients (96.9%) were not given any instructions on discharge.Conclusions: The discharge summaries analyzed were seen to be inadequate especially in documenting course during the hospital stay, condition at discharge, appropriate instructions and the treating physician’s details. These can probably be addressed by introducing electronic medical records if feasible. Otherwise, the discharge summary should be standardized and doctors should be trained to write legible, complete discharge summaries.Key Words: discharge, hospital, records, summaries