Use of Magnetic Resonance Imaging in the Evaluation ofAcute Cholecystitis in Emergency Setting.

Background Acute cholecystitis is one of the commonest surgical disease. The rapid diagnosis at its early stage is one of the crucial factor in patient care and management. Objective To evaluate the role of magnetic resonance imaging (MRI) and magnetic resonance cholangiopancreatography (MRCP) in the diagnosis or exclusion of acute cholecystitis, coexisting choledocholithiasis, and acute pancreatitis in emergency setting. Method This study was conducted in the department of radiodiagnosis B and C teaching hospital, Birtamod, Nepal from July 2016 to November 2019. Patients, clinically diagnosed as acute cholecystitis or biliary condition with positive Murphy's sign with or without jaundice and deranged Liver Function Test, raised Leucocyte counts were evaluated by Magnetic Resonance imaging. The sensitivity, specificity, Positive Productive Value (PPV), Negative Productive Value (NPV) were calculated for the diagnosis of acute cholecystitis. Data was entered and analysed by using SPSS version 20. Result There were 40 patients included in our study. Among them 27 (67.5%) were females and 13 (32.5%) male. The age of the patients ranged from 16 years to 79 years, mean age 49.4 years. Majority of the patients were in the age group of 40-60 years (57.5%). The overall sensitivity, specificity, Positive Productive Value and Negative Productive Value of Magnetic Resonance imaging diagnosis of acute cholecystitis were 100%, 66.6%, 94.4% and 100% respectively. Acute cholecystitis associated with gall stone disease were common and found in 72.5% cases, with sensitivity 96.5%, specificity 27.7%, Positive Productive Value 77.7% and Negative Productive Value 75.0%. Conclusion Magnetic resonance imaging (MRI)/Magnetic resonance cholangiopancreatography (MRCP) is an excellent tool for the evaluation of biliary pathology and can be used for the preoperative evaluation of acute cholecystitis at the emergency setting.

Prevalence of Hepatitis B and C among HIV Infected Patients in Nepal over 1990-2020.

Background Hepatitis B and C (HBV and HCV) are viral infections caused by corresponding viruses. Here in this study we planned to conduct this meta-analysis to pool data on the prevalence and risk factors of HBV and/or HCV among HIV patients in Nepal. Method We used MOOSE guideline for the systemic review of available literature. We searched online databases using appropriate keywords. We used CMA-3 for data synthesis. Odds ratio, and proportion were used to estimate the outcome with a 95% confidence interval where appropriate. We assessed the heterogeneity using the I-squared (I2 ) test. Result We included nine studies for our synthesis. Pooling of data showed HBV in 4.6% (CI: 3.7-5.6), HCV in 19.7% (CI: 10.8-33.0), both HBV and HCV in 1.3% (CI: 0.5-3.7) in HIV affected individuals. Among HBV co-infected HIV positive patients, 59.5% (CI: 25.5-86.3) were male; 76.1% (CI: 30.1-96.0) were married and 43.6% (CI: 3.8-93.8) had a history of intravenous drug use (IVDU). Among HCV co-infected HIV positive individuals 88.3% (CI: 73.6-95.4) were male; 63.6% (CI: 55.4-71.1) were married; 91.5% (CI: 68.6-98.1) were literate; 59.2% (CI: 49.9-67.9) were on ART; and 92.2% (95%CI: 84.9-96.1) had a history of IVDU. Conclusion The pooled prevalence of co-infection with HBV, HCV, and combined HBV and HCV were 4.6%, 19.7% and 1.3% respectively among HIV positive patients. Thus, it is necessary to appropriately screen for HBV and HCV in individuals diagnosed with HIV and high-risk populations. IVDU remains the most common risk factor found in co-infected individuals.

Peptidergic and nitrergic inhibitory neurotransmissions in the hamster jejunum: regulation of vasoactive intestinal peptide release by nitric oxide.

Regulation of vasoactive intestinal peptide (VIP) release by nitric oxide (NO) was investigated in the hamster jejunum. Electrical field stimulation and applied NO (3-100 microM) evoked biphasic hyperpolarizations consisting of an initial transient hyperpolarizing component followed by a second more slowly developing component (late component). The NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (200 microM) abolished the biphasic inhibitory junction potential evoked by electrical field stimulation. The NO scavenger oxyhemoglobin (50 microM) and the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ; 10 microM) abolished both components of the inhibitory junction potentials and the NO-induced hyperpolarizations. VIP(6-28) (1 microM), which abolished VIP (3 microM)-induced hyperpolarizations, also inhibited the late components of the inhibitory junction potentials and the NO-induced hyperpolarizations. ODQ inhibited VIP release and cAMP production by electrical field stimulation and NO application. N(6)-2,0-Dibutyryladenosine 3',5'-cyclic monophosphate (0.1-3 mM) caused a membrane hyperpolarization. These results suggest that NO may stimulate VIP release from enteric nerves in the hamster jejunum. In addition, we propose that NO and NO-stimulated VIP contribute to the early and late components of the inhibitory junction potentials, respectively, in the circular smooth muscle cells of the hamster jejunum.

Cyclic GMP-associated apamin-sensitive nitrergic slow inhibitory junction potential in the hamster ileum.

1. The mediators of non-adrenergic, non-cholinergic (NANC) inhibitory junction potentials (i.j.ps) in the circular smooth muscle cells of the hamster ileum were studied. 2. Electrical field stimulation (EFS; 0.5 ms duration, 15 V) of the intramural nerves with a train of five pulses at 20 Hz evoked a rapidly developing hyperpolarization (fast i.j.p.) followed by a sustained hyperpolarization (slow i.j.p.). 3. NG-nitro-L-arginine methyl ester (L-NAME; 50 - 200 microM) and NG-nitro-L-arginine (L-NNA; 50 - 200 microM), NO synthase inhibitors, inhibited or abolished the EFS-induced fast and slow NANC i.j.ps. The effects of these NO synthase inhibitors were reversed by L-arginine (5 mM) but not by D-arginine (5 mM). 4. Exogenously applied nitric oxide (NO; 1 - 100 microM) induced concentration-dependent hyperpolarizations. 5. Oxyhaemoglobin (5 - 50 microM), NO scavenger, inhibited only the slow i.j.p., and the NO-induced hyperpolarization. 6. 1H-[1,2,4]oxadiazolo[4, 3-a]quinoxaline-1-one (ODQ; 10 microM) and cystamine (10 mM), guanylate cyclase inhibitors, inhibited only the slow i.j.p. Zaprinast (100 microM), a phosphodiesterase type V inhibitor, enhanced the amplitude and duration of the slow i.j.p. 7. Apamin (100 nM), a small conductance Ca2+-activated K+ channel blocker, inhibited only the slow i.j.p., and NO-induced hyperpolarization. A high concentration of 8-bromoguanosine 3':5'-cyclic monophosphate (8-bromo-cGMP; 1 mM)-induced membrane hyperpolarization which was blocked by apamin. 8. These results suggest that NO, or a related compound, may be the inhibitory transmitter underlying the apamin-sensitive NANC slow i.j.p. and cyclic GMP mediates the slow i. j.p. in the hamster ileum. It is also likely that NO, without involvement of guanylate cyclase is associated with the fast i.j.p.

Bradykinin causes endothelium-independent hyperpolarisation and neuromodulation by prostanoid synthesis in hamster mesenteric artery.

The mechanism of bradykinin-induced hyperpolarisation and purinergic neuromodulation was examined in the hamster superior mesenteric artery using intracellular microelectrode techniques. Bradykinin induced a concentration-dependent hyperpolarisation both in endothelium-intact and -denuded preparations. Indomethacin blocked this hyperpolarisation. Prostacyclin and iloprost also hyperpolarised the membrane of mesenteric artery, while prostaglandin E(2) did not evoke any membrane hyperpolarisation. The bradykinin-, prostacyclin- and iloprost-induced hyperpolarisation were inhibited by glibenclamide. Bradykinin also inhibited the amplitude of the purinergic excitatory junction potentials (e.j.p.s), both in endothelium-intact and -denuded preparations. Indomethacin blocked this inhibitory effect. Prostaglandin E(2) inhibited the e.j. p. in a concentration-dependent manner. Focally applied ATP-induced depolarisation was not modified by bradykinin or prostaglandin E(2.) These findings suggest that bradykinin via prostanoids production pre-synaptically, inhibit the amplitude of purinergic e.j.p., resulting inhibitory purinergic neuromodulation. In addition, bradykinin-released prostanoids elicits membrane hyperpolarisation of smooth muscle cells through opening of K(ATP) channels.

Prevalence of Conventional Risk Factors in ST Segment Elevation Myocardial Infarction Patients in Shahid Gangalal National Heart Centre, Nepal.

INTRODUCTION: Smoking, diabetes mellitus, hypertension, and dyslipidemia are labelled as conventional risk factors for coronary artery disease. Prevalence of these risk factors varies across populations. This study aimed to assess the prevalence of these conventional risk factors in patients, who were discharged from our hospital, with the diagnosis of ST elevation myocardial infarction. METHODS: Medical records of 495 ST elevation myocardial infarction patients discharged from our centre in between January 2012 to December 2012 were retrospectively reviewed to evaluate the prevalence of conventional risk factors. RESULTS: Clear dominance (75%) of male patients was seen. Inferior wall myocardial infarction (29.9%) was the most common diagnosis followed by anterior wall myocardial infarction (25.1%). Hypertension (65%), smoking (57.8%) and dyslipidemia (45.5%) were the most common risk factors. Diabetes (31.1%) was the least common. Prevalence of hypertension, dyslipidemia was similar among male and female. Smoking was statistically common in male (76.8%vs 49.5%),though diabetes was common in female (36.5%vs.29.3%) not statistically significant. CONCLUSIONS: Conventional risk factors are common among ST elevation myocardial infarction patients. Early detection and treatment of these risk factors play a vital role for the prevention of coronary artery disease. Much more focus should be stressed on preventive programs throughout the country.

ATP released from perivascular nerves hyperpolarizes smooth muscle cells by releasing an endothelium-derived factor in hamster mesenteric arteries.

1. The interaction between perivascular nerves and endothelium was investigated by measuring the changes in smooth muscle membrane potentials using intracellular microelectrode techniques in hamster mesenteric thin (100-150 microm) and thick (300-350 microm) arteries. 2. In both arteries, nerve stimulation evoked excitatory junction potentials (EJPs) which were strongly inhibited by pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) (0.5-5 microM). This result indicated that the EJPs were induced by the activation of P2X receptors. 3. Transient hyperpolarizations were evoked by trains of pulses at 20 Hz in PPADS (5 microM)-pre-treated thin arteries, but not in the thick arteries. ATP (100 microM) applied to adventitial surfaces mimicked the hyperpolarizations. Both the ATP- and nerve stimulation-induced hyperpolarizations were blocked by cibacron blue F3GA (2-100 microM) and were also abolished after endothelium removal, indicating that the neurally released ATP evoked transient hyperpolarization through the activation of P2Y receptors located on the endothelium. 4. In endothelium-intact preparations, intimal application of uridine 5'-triphosphate (UTP 100 microM), a P2Y2-like receptor agonist, but not 2-methylthio ATP (7 microM), hyperpolarized the smooth muscle. The UTP-induced hyperpolarization was significantly inhibited by cibacron blue F3GA and was abolished after endothelium removal. 5. These results suggest that ATP released from the perivascular nerves may reach the endothelium and activate P2Y2-like receptors to induce the release of an endothelium-derived hyperpolarizing factor in thin arteries.

Enhancement of ATP release in hindlimb sympathetic perivascular nerve of the golden hamster during hibernation.

The present study investigated the effects of hibernation and hibernating body temperature (10 degrees C) on the relative changes that may occur in adrenergic and purinergic perivascular neurotransmission of the golden hamster. The hindlimb resistance vessels and the tibial artery of age-matched controls, cold exposed controls and hibernated hamsters were examined by pharmacological and electrophysiological techniques. At 34 degrees C, electrical field stimulation (EFS; supramaximal voltage, 0.5 ms; for 10 s) in all three groups evoked only twitch responses at 1-5 Hz, which were inhibited by piridoxal phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS), a 2PX receptor antagonist. At 10-50 Hz the twitch responses were followed by sustained contractile responses, which were inhibited by prazosin, an alpha1-adrenoceptor antagonist. These responses were markedly enhanced at higher frequencies in hibernated tissues. At 10 degrees C, EFS evoked only the PPADS-sensitive transient responses in all the three groups, and this was markedly enhanced in hibernated tissues. At 34 degrees C, a single stimulus evoked a PPADS-sensitive excitatory junction potential (EJP) in all three groups but a train of pulses (e.g. approximately 0.5) evoked EJPs and prazosin-sensitive sustained depolarizations. These responses were markedly enhanced in hibernated cells. At 10 degrees C, either a single stimulus or a train of stimuli evoked only transient PPADS-sensitive EJPs, which were markedly enhanced in hibernated cells. The contractile responses and electrical membrane responses to exogenous ATP (1-1000 microM) and noradrenaline (0.1-100 microM) were unchanged in the three groups at 34 and at 10 degrees C. These results suggest that during hibernation enhancement of ATP release from the sympathetic perivascular nerves may occur, leading to an efficient means for maintenance of vascular tone and peripheral resistance.