Occupational malaria and health risk among select occupational health care employee groups in an urban hospital at Tirupati, A.P.

Epidemiological studies on occupational environments are very meagre in the developing countries like India. For this reason an attempt was made in the present investigation to see the occupational risk of malaria among health care workers of Sri Venkateswara Ramnarayan Ruia Government General Hospital (SVRRGGH), Tirupati, Andhra Pradesh. The cohort studies revealed association between exposure to occupational (hospital) environment and malaria among hospital staff. Retrospective cohort studies were made. 1,454 subjects namely hospital staff exposed to occupational environment included civil assistant surgeons and physicians, the students of medicine, the students of nursing, permanent nursing staff and the class IV employees (class IV included janitorial, male nursing orderlies, female nursing orderlies, attenders, laundry workers and the rest). Retrospective epidemiological studies were carried out for four years on the cohorts and the hospital staff. The data showed statistically significant relative risk and attributable risk for malaria. Physicians and civil assistant surgeons showed no incidence of malaria. The relative risk for malaria in the class IV employees was 1.27, 0, 5.8 and 2.9 for the years 1995-98. The students of nursing showed 4.2, 2.42, 3.3 and 0 relative risk for malaria, whereas the students of medicine showed 2, 2, 2 and 1.6 for the years 1995 to 1998. The attributable risk was ranged from 21.76-82.70, 58.75-76.17, 50-80 for the class IV employees, the students of nursing and the students of medicine retrospectively. These results provide an evidence for an association between occupational environment and malaria for the hospital staff and is more prevalent among certain groups of the hospital staff.

Mechanisms of fatigue in normal intercostal muscle and muscle from patients with myasthenia gravis.

Fatigue mechanisms in normal intercostal muscle and muscle from patients with myasthenia gravis (MG) were evaluated by monitoring the compound muscle action potential (CMAP) and tetanic tension responses to repetitive nerve or muscle stimulation in vitro. When fatigue was induced by nerve stimulation at 30 Hz for 0.5 s every 2.5 s, about half of the original tension decreased after 30 min in normal muscle and 5 min in MG muscle. Analysis of the changes in area of CMAPs and tension indicated that impairment of neuromuscular transmission, muscle membrane excitation, and excitation-contraction (E-C) coupling and contractility accounted for 40%, 29%, and 31% of fatigue in normal muscle, and 83%, 0%, and 17% of fatigue in MG muscle. When fatigue was induced by muscle stimulation at 30 Hz, tension declined by a quarter after 30 min in normal muscle, but by a half after 17 min in MG muscle. Impairment of muscle membrane excitation and E-C coupling and contractility accounted for 58% and 42% of fatigue in normal muscle, and 22% and 78% of fatigue in MG muscle. Thus, fatigue of normal muscle is caused by impairment of at least four processes, and enhanced fatigue of MG muscle is caused by greater impairment of neuromuscular transmission, E-C coupling, and contractility.

Peripheral mechanisms of fatigue in muscles of normal and dystrophic mice.

We evaluated the contribution of different processes to fatigue of normal and dystrophic mouse muscles using an in vitro electromyography chamber. Fatigue was induced by repetitive nerve stimulation at 30 Hz for 0.5 s, every 2.5 s until tension decreased by about 50%. We monitored the compound nerve action potential (AP), compound muscle AP, and isometric tension responses to nerve stimulation, and compound muscle AP and tension responses to direct muscle stimulation. In normal mice, about 50% reduction in nerve-evoked tension occurred by 2.4 min in extensor digitorum longus (EDL), 4.8 min in diaphragm, and 9 min in soleus. Analysis of the responses revealed that the fatigue was caused by failure of more than one process in all muscles, and failure of nerve conduction did not contribute to fatigue in any muscle. Failure of neuromuscular transmission, muscle membrane excitation, and excitation-contraction (E-C) coupling and contractility accounted for 55, 45, and 0%, respectively, of the fatigue in EDL, for 21, 74, and 5% of the fatigue in diaphragm, and for 2, 54, and 44% of the fatigue in soleus. In dystrophic mice, while about 50% reduction in nerve-evoked tension occurred by 8.1 min in EDL and 5.6 min in diaphragm, only 29% reduction in tension occurred by 80 min in soleus. Failure of neuromuscular transmission, muscle membrane excitation, E-C coupling and contractility accounted for 22, 63 and 15% of the fatigue in EDL, for 21, 79, and 0% of the fatigue in diaphragm, and for 15, 59, and 26% of the fatigue in soleus. The proportion of slow-twitch oxidative fibers was more than normal in dystrophic EDL, but the same as normal in dystrophic diaphragm and soleus. The slower onset of fatigue was attributable to lesser failure of neuromuscular transmission in dystrophic EDL, and to lesser failure of E-C coupling and contractility in dystrophic soleus.

Responses of intercostal muscle biopsies from normal subjects and patients with myasthenia gravis.

In order to evaluate the mechanisms of weakness in muscles of patients with myasthenia gravis (MG), intercostal muscle biopsies were obtained from 9 normal subjects and 6 MG patients, and the compound muscle action potential (AP) and tension responses to nerve and muscle stimulation, and contracture responses on exposure to caffeine, were monitored in vitro. In normal muscle, on stimulation of the nerve or muscle at 30 to 100 Hz, the AP responses showed decrement in amplitude, one-third of which was attributable to failure of neuromuscular transmission and two-thirds to failure of muscle membrane excitation. On stimulation at 1 to 5 Hz, the AP responses showed very little decrement, while the contractile responses showed significant fade in tension, due to failure of E-C coupling or contractility. In muscle from patients with generalized MG, stimulation of the nerve at all frequencies (1 to 100 Hz) caused much greater decrement in APs and fade in tension responses than in normal muscle, due mainly to failure of neuromuscular transmission. However, at 100 Hz, 40% of the decrement in APs was due to failure of muscle membrane excitation, and at 1 to 5 Hz, 40% of the fade in tension was due to failure of E-C coupling or contractility, as in normal muscle. On direct stimulation the contraction and half-relaxation times were slower and the tetanic tension was smaller than in normal muscle, especially in the MG patient with thymoma. Caffeine-induced contractures were smaller in MG muscle than in normal muscle. These results indicate that while the weakness of MG muscle is due mainly to failure of neuromuscular transmission, it is also partly due to reduced E-C coupling or contractility.

Effect of Cleistanthus collinus leaf extract on neuromuscular function of the isolated mouse phrenic nerve-diaphragm.

Cleistanthus collinus is a toxic plant whose leaves have been used for homicidal or suicidal purposes. Since the toxic effects include muscle cramps and weakness, the effect of the leaf extract on the electrical and mechanical responses to nerve and muscle stimulation was studied in the isolated phrenic nerve-diaphragm preparation of the mouse. Following a 1 hr exposure to 0.015% leaf extract, the response of the compound nerve action potential to supramaximal nerve stimulation was reduced by 38%. The compound muscle action potential was reduced by 97%, and isometric tension by 99%. In response to direct muscle stimulation the compound muscle action potential and isometric tension were reduced by 38%. There was only an 11% reduction in resting membrane potential, but a 51% reduction in the amplitude of miniature endplate potentials. Endplate potentials could be evoked by nerve stimulation without prior treatment of the muscle with curare or a high concentration of magnesium. These studies indicate that the leaf extract markedly inhibits muscle contraction by reducing excitability of the nerve and muscle membranes, and by blocking neuromuscular transmission, without affecting excitation-contraction coupling or contractility of the muscle fibers.

Colorimetric determination of dimethoate or omethoate.

A simple, sensitive and rapid colorimetric method is described for determining dimethoate [O,O-dimethyl-S-(N-methylcarbanoylmethyl)phosphorodithioate] and omethoate by an enzymatic method using pig liver acetone powder as enzyme source and p-nitrobenzenediazonium fluoroborate as the chromogenic reagent. This colorimetric method is more sensitive than non-enzymatic methods. Inhibition can be detected at ng levels and amounts ranging from 50 to 1000 ng of omethoate and from 1 to 10 mug of dimethoate can be estimated.

Histamine and selected antihistamine regulation of glutamate dehydrogenase and acetylcholinesterase in sheep and medulla oblongata.

The effects of histamine acid phosphate and selected antihistamines, both separately and together are studied on the enzyme-substrate relationships of glutamate dehdrogenase and acetylcholinesterase of sheep liver and brain homogenates.