Mental health patients in primary health care services in Nepal

Patients attending two primary care settings in Nepal (a village health post and a district hospital outpatient department) were screened for psychiatric morbidity using the Self Reporting Questionnaire. Approximately one-quarter of all patients screened were found to have psychiatric morbidity. Women presenting were found to have higher frequency of "psychiatric caseness" than men. All these psychiatric patients presented with physical complaints, none with psychological, and the most common physical symptoms presented were abdominal pain, headache and cough. Health worker recognition of these cases was 29% in the health post and 0% in the hospital. Conclusions are drawn regarding the need for sufficient and relevant psychiatric teaching in health worker curriculae.     

Tubular Cell and HIV-1 gp120 Interaction Products Promote Migration of Monocytes

Renal interstitial accumulation of monocytes is an important feature of HIV-associated nephropathy. We studied the effects of proximal tubular cell products (TCP) and proximal tubular cell-gp120 interaction products (TC-120IP) on the migration of monocytes across a modified Boyden chamber. TC-120IP promoted (P<0.001) the migration of monocytes when compared with TCP (TCP, 45.0 ± 5.9 vs. TC-120IP, 192.3 ± 39.5 migrated monocytes/field). This effect of TC-120IP on monocyte migration was dose dependent. Anti-MCP-1 (TCP, 24.7 ± 2.6; TC-120IP, 82.3 ± 5.5; TC120-IP + anti-MCP-1 antibody, 46.5 ± 3.5 migrated monocytes/field) as well as anti-TGF- antibodies (TCP, 25.8 ± 3.4; TC120-IP, 80.3 ± 6.9; TC-120IP + anti-TGF- antibody, 43.8 ± 5.6 migrated monocytes/field) partly attenuated TC-120IP-induced migration of monocytes across a filter. Moreover, anti-MCP-1 and anti-TGF antibodies showed an additive inhibitory effect on TC-1201P-induced migration of monocytes across a filter. These results suggest that TC-120IP-induced migration of monocytes may be mediated through the generation of MCP-1 and TGF- by tubular cells. The present study provides the basis for a hypothesis that HIV-1 gp120 protein may be contributing to the infiltration of monocytes in the renal interstitium of patients with HIV-associated nephropathy.     

Morphine Stimulates Mesangial Cell TNF-α and Nitrite Production

Background: Intravenous opiate abusers are susceptible to develop heroin and HIV-associated nephropathies; however, the role of opiates in the development of these kidney lesions is not clear. Patients with opiate addiction are prone to recurrent infections. Methods: The effect of morphine was studied on the generation of TNF- with or without LPS (lipopolysaccharide) by cultured mouse mesangial cells. In addition, the effect of morphine was evaluated on mesangial cell nitrite production. To evaluate the role of opiate receptors, we studied the effect of naloxone and naltrexone on mesangial cell TNF- and nitrite production. To determine the role of TNF- on mesangial cell nitrite production, we examined the effect of anti-TNF- antibody on morphine-induced nitrite production. Assay of TNF- and nitrite production was carried by ELISA and Griess method respectively. Results: Morphine alone did not enhance the generation of TNF- by mesangial cells, however, an enhanced (P < 0.001) TNF- production was observed when mesangial cells were first treated with morphine for 18 h and then activated further with LPS. Maximum release of TNF- was seen at a concentration of 10^–12 M of morphine. Opiate receptor antagonists (naloxone and naltrexone) inhibited the effect of morphine. Morphine also amplified (P < 0.0002) the effect of LPS on mesangial cell nitrite production. Anti-TNF- antibody attenuated morphine induced nitrite generation. Conclusion: We conclude that morphine stimulates the generation of TNF- by LPS-activated mesangial cells. This effect of morphine seems to be opiate receptor mediated and has a downstream effect in the form of mesangial cell nitrite generation. The present in vitro study provides the basis for a hypothesis that morphine may be playing a role in the development of heroin and HIV-associated nephropathies.     

Morphine stimulates superoxide formation by glomerular mesangial cells

Focal glomerulosclerosis is the predominant glomerular lesion in heroin addicts. We studied whether morphine, a metabolite of heroin, could directly affect the formation of superoxide by glomerular mesangial cells. Mesangial cells preincubated with morphine (10^–8 M) showed a higher (P<0.001) production of superoxide when compared to control cells (control) 401±21 vs. morphine 610±41 nM/mg protein/h). This effect of morphine on mesangial cells was dose dependent. Naloxone, an opiate antagonist, attenuated morphine-induced formation of Superoxide by mesangial cells [control, 317±4; morphine (10^–8 M), 573±9; and naloxone (10^–8 M) + morphine (10^–8 M), 333±6 nM/mg protein/h]. We conclude that morphine enhances formation of superoxide by mesangial cells and this effect of morphine seems to be mediated through opiate receptors. Since superoxide has been demonstrated to cause mesangiolysis, we propose that morphine may be playing a role in the induction of mesangial injury in patients with opiate abuse.This work was supported by National Institute of Health Grant R01-DA-06753.     

Morphine modulates cathepsin B and L activity in isolated glomeruli and mesangial cells

Altered matrix degradation may be playing a role in the development of initial mesangial expansion and subsequent glomerulosclerosis in persons with heroin abuse. We studied whether morphine, a metabolite of heroin, had any effect on lysosomal content of cathepsin B and L in mesangial cells. Morphine (10^–6 M) increased (P<0.01) mesangial cathepsin B and L activity (control, 22.1+2.2 vs. morphine, 31.4+1.4 mol NMec/g protein,N=5). Morphine (10^–6 M) also increased (P<0.01) glomerular cathepsin B and L activity (control, 0.1+0.01 vs. morphine, 2.2±0.2 pmol NMec/g protein,N=3). This effect of morphine occurred in a dose-dependent manner. These results suggest that morphine enhances cathepsin B and L activity in mesangial cells and isolated glomeruli. This effect of morphine may enhance capacity of mesangial cells to degrade increased amount of mesangial macromolecules.     

Three-Dimensional Echocardiographic Reconstruction of the Left Ventricle by a Transesophageal Tomographic Technique: In Vitro and In Vivo Validation of its Volume Measurement

Accurate determination of left ventricular (LV) volume has important therapeutic and prognostic implications in patients with cardiac disease. Volume estimations by two-dimensional techniques are not very accurate due to geometric assumptions. OBJECTIVES: To validate LV volume determinations by a new transesophageal three-dimensional echocardiographic technique. We performed three-dimensional reconstruction of the LV using an echo-computed tomographic (CT) technique based on serial pullback parallel slice imaging technique in both in vitro and in vivo settings. Fourteen latex balloons with various sizes (30-235 mL) and shapes (conical, pear shaped, round, elliptical, and aneurysms in various locations) filled with known volumes of water were imaged in a water bath. From the static three-dimensional image, the LV long axis was defined and the LV was sectioned perpendicular to this axis into 2-mm slices. The volume of each slice was calculated with the observer blinded to the actual volume as the product of the slice thickness and the manually traced perimeter of the slice and the LV volume as the sum of the volumes of the slices (Simpson's method). The calculated LV volume closely correlated with the actual volume (r = 0.99, P < 0.0001, calculated volume = 1.06x - 11.3, Deltavolume = -5.7 +/- 10.0 cc). Using the same system, transesophageal echocardiographic (TEE) images of the LV were obtained in 15 patients gated to respiration and ECG. Satisfactory dynamic three-dimensional reconstruction of the LV was possible in ten patients. The three-dimensional LV volumes (systolic and diastolic) using Simpson's method correlated well with those obtained from biplane or multiplane TEE images using the area length method (r = 0.89, p < 0.0001, y = 12.7 + 0.84x, Deltavolume = 1.3 +/- 18.1 cc). The LV major-axis diameters by the two methods showed very close correlations as well (r = 0.86, P < 0.0001, y = 19 + 0.74x, Deltadiameter = 1.0 +/- 7.2 mm). We conclude that three-dimensional LV volume calculation by the echo-CT technique is intrinsically sound, is independent of LV geometry, and with some limitations, is applicable in vivo. (ECHOCARDIOGRAPHY, Volume 13, November 1996)     

Two year audit of perinatal mortality at Kathmandu Medical College Teaching Hospital.

Introduction: Perinatal mortality rate is a sensitive indicator of quality of care provided to women in pregnancy, at and after child birth and to the newborns in the first week of life. Regular perinatal audit would help in identifying all the factors that play a role in causing perinatal deaths and thus help in appropriate interventions to reduce avoidable perinatal deaths. Aims and objectives: This study was carried out to determine perinatal mortality rate (PMR) and the factors responsible for perinatal deaths at KMCTH in the two year period from November 2003 to October 2005 (Kartik 2060 B.S. to Ashoj 2062). Methodology: This is a prospective study of all the still births and early neonatal deaths in KMCTH during the two year period from November 2003 to October 2005. Details of each perinatal death were filled in the standard perinatal death audit forms of the Department of Pediatrics, KMCTH. Perinatal deaths were analyzed according to maternal characteristics like maternal age, parity, type of delivery and fetal characteristics like sex, birth weight and gestational age and classify neonatal deaths according to Wigglesworth's classification and comparison made with earlier similar study. Results: Out of the 1517 total births in the two year period, 22 were still births (SB) and 10 were early neonatal deaths (ENND). Out of the 22 SB, two were of < 1 kg in weight and out of 10 ENND, one was of <1 kg. Thus, perinatal mortality rate during the study period was 19.1 and extended perinatal mortality rate was 21.1 per 1000 births. The important causes of perinatal deaths were extreme prematurity, birth asphyxia, congenital anomalies and associated maternal factors like antepartum hemorrhage and most babies were of very low birth weight. According to Wigglesworth's classification, 43.8% of perinatal deaths were in Group I, 12.5% in Group II, 28.1% in Group III, 12.5% in Group IV and 12.5% in Group V. Discussion: The perinatal death audit done in KMCTH for 1 year period from September 2002 to August 2003 showed perinatal mortality rate of 30.7 and extended perinatal mortality rate of 47.9 per 1000 births. There has been a significant reduction in the perinatal mortality rate in the last 2 years at KMCTH. Main reasons for improvement in perinatal mortality rate were improvement in care of both the mothers and the newborns and the number of births have also increased significantly in the last 2 years without appropriate increase in perinatal deaths. Conclusion: Good and regular antenatal care, good care at the time of birth including appropriate and timely intervention and proper care of the sick neonates are important in reducing perinatal deaths. Prevention of preterm births, better care and monitoring during the intranatal period and intensive care of low birth weight babies would help in further reducing perinatal deaths. Key words: Perinatal mortality rate (PMR), still births, early neonatal death (ENND), Total perinatal death (PND).