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The amounts of kinin-releasing enzymes in the venoms of Crotalus atrox, Crotalus adamanteus, Crotalus scutulatus scutulatus and Agkistrodon piscivorus piscivorus were measured by determining the amounts of kinin released from a sheep kininogen substrate by means of a specific radioimmunoassay. Four monospecific and two commercial polyspecific antivenom IgG samples were tested for their ability to reduce the kinin-releasing activities of the four crotalid venoms measured in vitro. All of the antivenom IgG samples were able to neutralize venom kininogenase activity to varying extents. On of the commercial polyspecific antivenoms was of equal or higher potency than the corresponding monospecific antivenoms for three of the venoms tested, indicating a high degree of cross-neutralization. F(ab')2 and especially Fab fragments of that polyspecific antivenom IgG were also effective in reducing the kinin-releasing activities of the four crotalid venoms.

Picroliv (active principle from Picrorrhiza kurroa), its major components picroside I, catalpol, kutkoside I, kutkoside, andrographolide (active constituent of Andrographis paniculata), silymarin and Phyllanthus niruri extract were tested for the presence of anti hepatitis B virus surface antigen (anti HBs) like activity. HBsAg positive serum samples obtained from hepatitis B virus (HBV) associated acute and chronic liver diseases and healthy HBsAg carriers were used to evaluate the anti-HBs like activity of compounds/extract. The latter were mixed with serum samples and incubated at 37 degrees C overnight followed by HBsAg screening in the Elisa system. A promising anti-HBsAg like activity was noted in picroliv (and its major components) catalpol, P. niruri which differed from the classical viral neutralization. Picroliv also inhibited purified HBV antigens (HBsAg and HBsAg) prepared from healthy HBsAg carriers. The in vitro testing system appears to be a suitable model to identify an agent active against HBV, prior to undertaking detailed studies.

A technique for reducing congenital gigantism of the toes which has been used successfully in four patients is described.

A case of abdominal pain caused by irritation of a segment of jejunum and another due to irritation of the ureter are reported. In both cases the cause of the irritation was established to be osteophytic growth from the 4th lumbar vertebra. After its excision the symptoms disappeared in both cases. To the best of our knowledge, osteophytes have not been reported before to be the cause of intestinal and ureteric pain, and its is therefore urged that in cases of intractable pain these must be considered as a possible cause.

The delayed-type hypersensitivity (DTH) to Japanese encephalitis virus (JEV) and the suppressor cells controlling it and the antibody-forming cells in inbred Swiss mice have been studied. JEV induces DTH, with a peak response at day 7 following infection which persists at low levels at least up to 119 days. Suppressor activity appeared on day 18. It was transferable by immune spleen cells. Treatment of spleen cells with anti-Thy-1.2 antisera and complement abrogated the suppressor activity. The homogenate of the spleen was equally effective in mediating suppression of DTH and the humoral response as measured by direct antibody plaque-forming cell (IgM-PFC) assay. The suppressor activity was antigen-specific both on DTH and T helper for antibody response as the immune responses against SRBC or Coxsackie B4 virus were not suppressed. The suppressor cells were sensitive to cyclophosphamide treatment when the drug was given 48 hr before their appearance. It is, therefore, concluded that in JEV infection of mice, antigen-specific suppressor T cells are generated, both for DTH and IgM antibody, which are cyclophosphamide-sensitive and mediate suppression through soluble product(s).

An 11-year-old girl with complex seizures was started on valproic acid (VPA) in addition to clonazepam and ethosuximide. Shortly thereafter, she developed marked hyperammonemia that was worsened by a protein load. The hyperammonemia improved somewhat when protein was not given, and it resolved on discontinuation of the valproic acid. No associated changes in serum transaminases or bilirubin were observed. Isolated hyperammonemia may occur soon after VPA ingestion and appears to be a relatively infrequent, reversible side effect. The mechanism of hyperammonemia probably differs from other manifestations of hepatotoxicity, such as elevated transaminases or frank hepatic failure.

Adoptive transfer of spleen cells obtained from mice primed with Japanese encephalitis virus (JEV) suppressed IgM antibody plaque forming cells (PFC) against JEV in the spleen. Similar suppression of PFC was also shown in vitro by adding primed spleen cells to JEV-stimulated spleen cell cultures. The suppressor activity appeared sharply in the third week after priming and persisted up to 6 weeks. By using various cell separation procedures it was found that the suppressor activity resided in the T cell enriched fraction and not in B cells or macrophages. Sensitivity of the cells to treatment with anti-Thy 1.2 antiserum and complement confirmed that suppressor cells were T lymphocytes. It was noted that the suppression was effective against dengue virus antigen also. Our findings thus show generation of suppressor T lymphocytes in JEV-infected mice.

Following intraperitoneal inoculation, Japanese encephalitis virus replicated in peritoneal macrophages, appeared on day 3 in the splenic macrophages of the perifollicular region and later in cells of the periarteriolar lymphoid sheath (PALS) as shown by indirect immunofluorescence. Productive JEV infection was observed both in macrophages and T-cells. Morphological study of spleen during JEV infection revealed proliferative changes, with increased number of macrophages from day 3 p.i. in the perifollicular region followed by accumulation of polymorphonuclear leucocytes which reached a maximum on day 9 p.i. The T dependent areas were considerably enlarged by day 9 and gradually reduced in size by week 3. At later periods germinal centres appeared in the T independent area and were prominent by day 15. The cells containing virus antigen disappeared with the appearance of germinal centres, thus indicating the role of the latter also in virus clearance.

Persistent and latent Japanese encephalitis virus (JEV) infection was studied in pregnant and non-pregnant mice. Following intraperitoneal inoculation into pregnant mice JEV persisted for 16 weeks in contrast to 4 weeks in non-pregnant mice. This was followed by a higher frequency of latent infection in pregnant mice. The virus could be reactivated during pregnancy or by cyclophosphamide treatment, the latter being more effective.

Since Japanese encephalitis virus (JEV) induces the generation of suppressor T cells in mouse spleen which, through the production of a soluble suppressor factor (SF), suppress IgM plaque-forming cells (IgM-PFC) the present study was undertaken to further characterize these suppressor cells and the SF. The suppressor cells were Ly1-2+ and sensitive to hydrocortisone and a high dose of irradiation. SF was trypsin-sensitive, thermolabile and non-dialysable, and passed through a 450-nm filter. This SF was shown to be a low molecular weight substance, with an approximate MW of 18,000 daltons.

Japanese encephalitis virus (JEV) infection induces suppressor T-cells (Ts1) which suppress both the humoral (Ts-PFC) and cell mediated (Ts-DTH) immune response by producing soluble suppressor factors. This study shows that in the JEV model, both TS-PFC and Ts-DTH mediate suppression by recruiting a second subpopulation of suppressor T-cells, the Ts2-PFC and Ts2-DTH. The signal between Ts1 and Ts2 is transmitted by macrophages (M phi). The suppressor factors are adsorbed by peritoneal or splenic M phi. Both heat-killed and live M phi are capable of adsorbing suppressor factors but only live M phi are capable of presenting the signal to T-cells. Thus these are at least two generations of suppressor T-cells in the JEV-specific suppressor pathway and the presence of M phi is obligatory for transmission of the signal.

Intraperitoneal inoculation with Japanese encephalitis virus (JEV) induces the generation of T suppressor cells for delayed type hypersensitivity (Ts-DTH) in Swiss albino mice. The Ts-DTH are hydrocortisone resistant, partially sensitive to X-irradiation and the membrane phenotype of Ts cells is Ly I+. Ts-DTH suppression is mediated through the production of soluble suppressor factor (SF-DTH). SF-DTH is non-dialysable but passes through 450 nm filter and does not sediment after centrifugation at 100,000 g for 2 h; chromatography on Sephadex G-100 indicates an approximate molecular weight of 12,000.

Anterior temporal (AT) and sphenoidal (SP) electrodes as well as standard 10-20 electrodes were used to evaluate patients with recent onset complex partial seizures. A total of 58 epileptiform foci were found in 80 patients. AT electrodes significantly improved detection of foci in comparison with 10-20 electrodes. SP electrodes resulted in a small, non-significant increase in detection in comparison to AT electrodes. AT electrodes may be substituted for basal electrodes for the purpose of diagnosis in the majority of patients with recent onset complex partial seizures.

Latent Japanese encephalitis virus (JEV) infection was shown in inapparently congenitally infected Swiss albino mice after their mothers had been given JEV intraperitoneally during pregnancy. Only one of 37 (2.7%) of the baby mice showed persistence of infectious virus at 5 weeks of age. Reactivation of JEV in Swiss albino mice was demonstrated by stimulation with allogeneic spleen cells from Parks strain mice at 21 weeks of age; reactivation was demonstrated in 41% of the inapparently infected mice. The spleen cells of congenitally infected mice had depressed [3H]thymidine uptake following stimulation with concanavalin A, and depressed ability to induce a graft-versus-host response.

The generation of secondary suppressor T (Ts) cells has been studied during latent Japanese encephalitis virus (JEV) infection of mice. The mice infected with JEV 27 weeks earlier, on challenge with the homologous virus, showed accelerated generation of secondary Ts cells; these appeared on Day 6, with peak activity on Day 8, and lasted for 27 days. The secondary Ts cells were Thy1.2+, Ly1-2+, antigen-specific, and acted in a dose-dependent manner. The secondary Ts cells could also be generated by reactivation of the JEV in latently infected mice. The findings thus show the presence of memory suppressor T cells in mice latently infected with JEV that can be stimulated to produce secondary Ts cells by exogenous or endogenous virus challenge. This phenomenon could help to persistence of the virus.