Pain Medicine Education in Emergency Medicine Residency Programs.

Background Pain is a common complaint in the emergency department (ED), yet there is a lack of robust pain curricula in emergency medicine (EM) residency programs. In this study, we investigated pain education in EM residencies and various factors related to educational development. Methodology This was a prospective study collecting online survey results sent to Program Directors, Associate Program Directors, and Assistant Program Directors of EM residencies in the United States. Descriptive analyses with nonparametric tests were performed to investigate relationships between these factors, including educational hours, level of educational collaboration with pain medicine specialists, and multimodal therapy utilization. Results The overall individual response rate was 39.8% (252 out of 634 potential respondents), representing 164 out of 220 identified EM residencies with 110 (50%) Program Directors responding. Traditional classroom lectures were the most common modality for the delivery of pain medicine content. EM textbooks were the most common resource utilized for curriculum development. An average of 5.7 hours per year was devoted to pain education. Up to 46.8% of respondents reported poor or absent educational collaboration with pain medicine specialists. Greater collaboration levels were associated with greater hours devoted to pain education (p = 0.01), perceived resident interest in acute and chronic pain management education (p < 0.001), and resident utilization of regional anesthesia (p = <0.01). Faculty and resident interest in acute and chronic pain management education were similar to each other and high on the Likert scale, with higher scores correlating to greater hours devoted to pain education (p = 0.02 and 0.01, respectively). Faculty expertise in pain medicine was rated the most important factor in improving pain education in their programs. Conclusions Pain education is a necessity for residents to adequately treat pain in the ED, but remains challenging and undervalued. Faculty expertise was identified as a factor limiting pain education among EM residents. Collaboration with pain medicine specialists and recruitment of EM faculty with expertise in pain medicine are ways to improve pain education of EM residents.

Ear fullness characteristics and prognosis in patients with all-frequency sudden sensorineural hearing loss.

OBJECTIVE: This study investigated the characteristics and prognosis of the feeling of ear fullness in patients with unilateral all-frequency sudden sensorineural hearing loss. METHODS: Our study included 56 patients with a diagnosis of unilateral all-frequency sudden sensorineural hearing loss accompanied by a feeling of ear fullness and 48 patients without a feeling of ear fullness. The condition of these patients was prospectively observed. RESULTS: Positive correlations were observed between grading of feeling of ear fullness and hearing loss in patients with a feeling of ear fullness (r = 0.599, p < 0.001). No significant differences were observed in the total effective rate of hearing recovery between patients with and without a feeling of ear fullness after one month of treatment (Z = -0.641, p = 0.521). Eighty-six per cent of patients (48 out of 56) showed complete recovery from the feeling of ear fullness. There was no correlation between feeling of ear fullness recovery and hearing recovery (r = 0.040, p = 0.769). CONCLUSION: The prognosis of feeling of ear fullness is good. There was no correlation between feeling of ear fullness recovery and hearing recovery for all-frequency sudden sensorineural hearing loss patients.

[Characteristics and prognosis of ear fullness feeling in patients with all-frequency sudden deafness].

Objective: The characteristics and prognosis of ear fullness feeling in patients with all-frequency sudden deafness were explored. Method: 104 patients (104 ears) with unilateral all-frequency sudden deafness were collected in study from June 2015 to March 2019, including 50 males and 54 females, the mean age ranged from 23-65 years, and the disease duration ranged from 1-9 days. Of those, 56 patients accompanied with the feeling of ear fullness (FEF) were enrolled into'the ear fullness group', and 48 patients without FEF were included in'the without ear fullness group'. Patients' treatment strategy followed the Chinese Medical Association Guidelines for the diagnosis and treatment of sudden deafness (2015). Moreover, VAS scale scores and subjective grading of FEF were acquired in patients with FEF. We analyzed the clinical characteristics and prognosis of FEF with SPSS 23.0 software. Results: There were no differences between the two groups in terms of age, gender, duration of disease, the side of deaf ear, degree of hearing loss, and auditory brainstem evoked potential results (age,t=1.566; gender,χ(2)=0.001; duration, t=0.057; side,χ(2)=0.033; degree of hearing loss Z=-0.180; ABR,χ(2)=0.001;all P>0.05) . There was a positive correlation between the subjective grading of FEF and the degree of hearing loss in patients with FEF (r=0.599, P<0.001) . The total rate of hearing improvement following one month of treatments in patients with FEF vs with no FEF was 35/56(62.5%) vs 28/48(58.3%) (Z=-0.641, P=0.521). After one month of treatment, the total effective rate of FEF was 94.6%(53/56), and the improvement of FEF had nothing to improvement of hearing (r=0.040, P=0.769) . Conclusions: The degree of hearing loss is positively correlated with the degree of FEF in patients with all-frequency sudden deafness. Hearing recovery is not related to FEF. The recovery effect of FEF is good, and has no correlation with hearing recovery.

Involvement of Streptococcus mutans regulator RR11 in oxidative stress response during biofilm growth and in the development of genetic competence.

AIMS: To identify the genes regulated by RR11, the regulator of the Streptococcus mutans HK/RR11 two-component system. METHODS AND RESULTS: The S. mutans RR11-encoding gene was inactivated, and the effects of gene disruption on the cell's ability to form biofilms under stresses and acquire extracellular DNA were tested. Biofilm was reduced in cells lacking RR11 following exposure to oxidative stress. RR11-defective cells showed approx. 20-fold reduction in transformation efficiency. Microarray used to decipher the RR11-regulated genes in biofilm showed that approx. 5% of the UA159 genome underwent a significant change in expression. RR11 was found to regulate 174 genes, including genes involved in competence, stress-response and cell division. CONCLUSIONS: Target genes controlled by RR11during biofilm growth have been identified by a comparison of transcriptional profiles between an RR11 defective mutant and the parental strain. The results demonstrated that RR11 is involved in the control of diverse cellular processes, including the formation of biofilm under oxidative stress and development of genetic competence. SIGNIFICANCE AND IMPACT OF THE STUDY: The regulator of HK/RR11 system controls a large regulon and is an important regulator involved in stress response during S. mutans biofilm growth enabling the survival and persistence of its progeny in the microbial community.

[The anticonvulsive effect of 4,4-bis(hydroxymethyl)-2-phenyl-2-oxazoline]. / Efecto anticonvulsionante de la 2-fenil-4,4-bis (hidroximetil)-2-oxazolina.

INTRODUCTION: Certain compounds belonging to the family of the 2-aryl oxazolines have been reported to act on the central nervous system with a number of different effects and applications, which make them useful as depressants, anaesthetics, anticonvulsants, and so on. AIMS: Our aim was to study the possible effect of 4,4-bis(hydroxymethyl)-2-phenyl-2-oxazoline (OX), obtained by chemical synthesis using microwaves, in two experimental models of epilepsy. MATERIALS AND METHODS: Two models were used: one involving (repeated stimulation) electroconvulsive shock in mice and the other consisted in inducing audiogenic seizures in Mongolian gerbils. Recordings were performed of the potentials in the dentate gyrus (DG) generated in response to electrical stimulation of the entorhinal cortex in anaesthetised gerbils, using the stereotactic technique. RESULTS: A 150 mg/kg dose of OX lowered the number of electrical pulses required to induce the tonic seizures triggered by the electroshock, as well as their duration. This same dose blocked the seizures induced by audiogenic stimuli in the gerbils and significantly reduced their severity (degrees of seizures) and occurrence. OX diminished, in a dose-dependent manner, the amplitude of the excitatory post-synaptic potential and that of the population spike, triggered by stimulating the entorhinal cortex in the DG. CONCLUSIONS: OX acts as an antiepileptic agent and its mechanism of action could be related to the inhibiting effect it exerts on the entorhinal cortex-DG synapses in the hippocampus.

Efecto anticonvulsionante de la 2-fenil-4, 4-bis (hidroximetil)-2-oxazolina / The anticonvulsive efecto of 4, 4-Bis (Hydroxymethyl)-2-phenyl-2oxazoline

Introduction. Certain compounds belonging to the family of the 2-aryl oxazolines have been reported to act on the central nervous system with a number of different effects and applications, which make them useful as depressants, anaesthetics, anticonvulsants, and so on. Aims. Our aim was to study the possible effect of 4,4-bis(hydroxymethyl)-2-phenyl-2-oxazoline (OX), obtained by chemical synthesis using microwaves, in two experimental models of epilepsy. Materials and methods. Two models were used: one involving (repeated stimulation) electroconvulsive shock in mice and the other consisted in inducing audiogenic seizures in Mongolian gerbils. Recordings were performed of the potentials in the dentate gyrus (DG) generated in response to electrical stimulation of the entorhinal cortex in anaesthetised gerbils, using the stereotactic technique. Results. A 150 mg/kg dose of OX lowered the number of electrical pulses required to induce the tonic seizures triggered by the electroshock, as well as their duration. This same dose blocked the seizures induced by audiogenic stimuli in the gerbils and significantly reduced their severity (degrees of seizures) and occurrence. OX diminished, in a dose-dependent manner, the amplitude of the excitatory post-synaptic potential and that of the population spike, triggered by stimulating the entorhinal cortex in the DG. Conclusions. OX acts as an antiepileptic agent and its mechanism of action could be related to the inhibiting effect it exerts on the entorhinal cortex-DG synapses in the hippocampus (AU)

Introducción. Algunos compuestos de la familia de las 2- aril-oxazolinas se han descrito como sustancias activas sobre el sistema nervioso central, con efectos y aplicaciones diversas, como depresores, anestésicos, anticonvulsionantes, etc. Objetivo. Estudiar el posible efecto de la 2-fenil-4,4-bis (hidroximetil)-2-oxazolina (OX) obtenida por síntesis química bajo microondas en dos modelos de epilepsia experimental. Materiales y métodos. Se emplearon el modelo de choque electroconvulsivo –por estimulación repetitiva– en ratones y el de crisis audiogénica en el gerbo mongol. Se incluyó el registro de los potenciales del giro dentado (GD) en respuesta a la estimulación eléctrica de la corteza entorrinal en el gerbo anestesiado mediante la técnica estereotáctica. Resultados. La dosis de 150 mg/kg de OX redujo el número de pulsos eléctricos necesarios para inducir la crisis tónica producida por el choque eléctrico, así como su duración. Esta misma dosis bloqueó las crisis inducidas por el estímulo audiogénico en el gerbo y disminuyó significativamente su gravedad (grados de crisis) y aparición. La OX redujo, en forma dependiente de la dosis, la amplitud del potencial postsináptico excitatorio y de la espiga de población, provocada por la estimulación de la corteza entorrinal en el GD. Conclusiones. La OX posee un efecto antiepiléptico cuyo mecanismo podría estar relacionado con su acción inhibitoria sobre la sinapsis corteza entorrinal-GD en el hipocampo (AU)

Efecto anticonvulsionante de la 2-fenil-4, 4-bis (hidroximetil)-2 oxazolina / s. t

Certain compounds belonging to the family of the 2-aryl oxazolines have been reported to act on the central nervous system with a number of different effects and applications, which make them useful as depressants, anaesthetics, anticonvulsants, and so on. AIMS. Our aim was to study the possible effect of 4,4-bis(hydroxymethyl)-2-phenyl-2-oxazoline (OX), obtained by chemical synthesis using microwaves, in two experimental models of epilepsy...(AU)

Efecto anticonvulsionante de la 2-fenil-4, 4-bis (hidroximetil)-2-oxazolina / The anticonvulsive effect of 4, 4-bis(hydroxymethyl)-2-phenyl-2-oxazoline

Introducción. Algunos compuestos de la familia de las 2- aril-oxazolinas se han descrito como sustancias activas sobre el sistema nervioso central, con efectos y aplicaciones diversas, comodepresores, anestésicos, anticonvulsionantes, etc. Objetivo. Estudiar el posible efecto de la 2-fenil-4,4-bis (hidroximetil)-2-oxazolina (OX)obtenida por síntesis química bajo microondas en dos modelos deepilepsia experimental. Materiales y métodos. Se emplearon el modelode choque electroconvulsivo –por estimulación repetitivaen ratones y el de crisis audiogénica en el gerbo mongol. Se incluyó el registro de los potenciales del giro dentado (GD) en respuesta a la estimulación eléctrica de la corteza entorrinal en el gerbo anestesiado mediante la técnica estereotáctica. Resultados. La dosis de 150 mg/kg de OX redujo el número de pulsos eléctricos necesarios parainducir la crisis tónica producida por el choque eléctrico, así comosu duración. Esta misma dosis bloqueó las crisis inducidas por el estímulo audiogénico en el gerbo y disminuyó significativamente su gravedad (grados de crisis) y aparición. La OX redujo, en forma dependiente de la dosis, la amplitud del potencial postsináptico excitatorio y de la espiga de población, provocada por la estimulación dela corteza entorrinal en el GD. Conclusiones. La OX posee un efectoantiepiléptico cuyo mecanismo podría estar relacionado con su acción inhibitoria sobre la sinapsis corteza entorrinal-GD en el hipocampo(AU)

Introduction. Certain compounds belonging to the family of the 2-aryl oxazolines have been reported to act on the central nervous system with a number of different effects and applications, which make them useful as depressants, anaesthetics, anticonvulsants, and so on. Aims. Our aim was to study the possible effect of 4,4-bis(hydroxymethyl)-2-phenyl-2-oxazoline (OX), obtained by chemical synthesis using microwaves, in two experimental models of epilepsy. Materials and methods. Two models were used: one involving (repeated stimulation) electroconvulsive shock in mice and the other consistedin inducing audiogenic seizures in Mongolian gerbils. Recordings were performed of the potentials in the dentate gyrus (DG) generated in response to electrical stimulation of the entorhinal cortex in anaesthetised gerbils, using the stereotactictechnique. Results. A 150 mg/kg dose of OX lowered the number of electrical pulses required to induce the tonic seizures triggered by the electroshock, as well as their duration. This same dose blocked the seizures induced by audiogenic stimuli in the gerbils and significantly reduced their severity (degrees of seizures) and occurrence. OX diminished, in a dose-dependentmanner, the amplitude of the excitatory post-synaptic potential and that of the population spike, triggered by stimulating the entorhinal cortex in the DG. Conclusions. OX acts as an antiepileptic agent and its mechanism of action could be related to the inhibiting effect it exerts on the entorhinal cortex-DG synapses in the hippocampus(AU)

T cell regulation of p62(dok) (Dok1) association with Crk-L.

In addition to engagement of the T cell receptor-CD3 complex, T lymphocytes can be activated by a variety of cell surface molecules including the approximately 50-kDa surface receptor CD2. While the majority of biochemical signaling elements are triggered by either CD2 or TcR-CD3 receptors, a small number of proteins are engaged by only one receptor. Recently, p62(dok) (Dok1), a member of the Dok family of adapter molecules, has been reported to be activated by CD2 and not by CD3 engagement. Here we have examined the role of p62(dok) in CD2-dependent signaling in Jurkat T cells. As previously reported, we find that ligation of the CD2 molecule by mitogenic pairs of anti-CD2 mAbs led to phosphorylation of p62(dok). While CD2-induced p62(dok) tyrosine phosphorylation was independent of both the p36/38 membrane adapter protein linker of activated T cells (LAT) and the ZAP70/Syk family of kinases, it was dependent upon the Src family of kinases including Lck and Fyn. We find further that CD2 engagement induced the association of tyrosine-phosphorylated p62(dok) to Crk-L. The CD2-dependent association of p62(dok) to Crk-L was independent of expression of the ZAP70/Syk family of kinases. Of note, while T cell receptor-CD3 engagement did not induce either p62(dok) phosphorylation or Crk-L association in Jurkat T cells, it did inhibit CD2-dependent p62(dok)-Crk-L complexes; this TcR-CD3-mediated regulation was dependent upon ZAP70 kinase activity. Our data suggest that phosphorylation of p62(dok) and its interaction with other signaling proteins may depend upon integrated signals emanating from the CD2 receptor, utilizing a ZAP70/LAT-independent pathway, and the TcR-CD3 receptor, which is ZAP70/Syk-dependent.

Inhibition of acute-, latent-, and chronic-phase human immunodeficiency virus type 1 (HIV-1) replication by a bistriazoloacridone analog that selectively inhibits HIV-1 transcription.

Nanomolar concentrations of temacrazine (1,4-bis[3-(6-oxo-6H-v-triazolo[4,5,1-de]acridin-5-yl)amino-propyl ]piperazine) were discovered to inhibit acute human immunodeficiency virus type 1 (HIV-1) infections and suppress the production of virus from chronically and latently infected cells containing integrated proviral DNA. This bistriazoloacridone derivative exerted its mechanism of antiviral action through selective inhibition of HIV-1 transcription during the postintegrative phase of virus replication. Mechanistic studies revealed that temacrazine blocked HIV-1 RNA formation without interference with the transcription of cellular genes or with events associated with the HIV-1 Tat and Rev regulatory proteins. Although temacrazine inhibited the in vitro 3' processing and strand transfer activities of HIV-1 integrase, with a 50% inhibitory concentration of approximately 50 nM, no evidence of an inhibitory effect on the intracellular integration of proviral DNA into the cellular genome during the early phase of infection could be detected. Furthermore, temacrazine did not interfere with virus attachment or fusion to host cells or the enzymatic activities of HIV-1 reverse transcriptase or protease, and the compound was not directly virucidal. Demonstration of in vivo anti-HIV-1 activity by temacrazine identifies bistriazoloacridones as a new class of pharmaceuticals that selectively blocks HIV-1 transcription.

Inhibition of multiple phases of human immunodeficiency virus type 1 replication by a dithiane compound that attacks the conserved zinc fingers of retroviral nucleocapsid proteins.

The human immunodeficiency virus type 1 (HIV-1) nucleocapsid p7 protein contains two retrovirus-type zinc finger domains that are required for multiple phases of viral replication. Chelating residues (three Cys residues and one His residue) of the domains are absolutely conserved among all strains of HIV-1 and other retroviruses, and mutations in these residues in noninfectious virions. These properties establish the zinc finger domains as logical targets for antiviral chemotherapy. Selected dithiobis benzamide (R-SS-R) compounds were previously found to inhibit HIV-1 replication by mediating an electrophilic attack on the zinc fingers. Unfortunately, reaction of these disulfide-based benzamides with reducing agents yields two monomeric structures (two R-SH structures) that can dissociated and no longer react with the zinc fingers, suggesting that in vivo reduction would inactivate the compounds. Through an extensive drug discovery program of the National Cancer Institute, a nondissociable tethered dithiane compound (1,2-dithiane-4,5-diol, 1,1-dioxide, cis; NSC 624151) has been identified. This compound specifically attacks the retroviral zinc fingers, but not other antiviral targets. The lead compound demonstrated broad antiretroviral activity, ranging from field isolates and drug-resistant strains of HIV-1 to HIV-2 and simian immunodeficiency virus. The compound directly inactivated HIV-1 virions and blocked production of infectious virus from cells harboring integrated proviral DNA. NSC 624151 provides a scaffold from which medicinal chemists can develop novel compounds for the therapeutic treatment of HIV infection.

Human immunodeficiency virus type-1 (HIV-1) replication is unaffected by human secretory leukocyte protease inhibitor.

Human secretory leukocyte protease inhibitor (SLPI), a serine protease inhibitor found concentrated in secretory fluids, has been postulated to participate in the body's natural defense against infection by the human immunodeficiency virus type-1 (HIV-1) by affecting trypsin-like enzymes on the surface of target cells. SLPI was evaluated for potential antiviral activity against laboratory, clinical and monocytotropic strains of HIV-1 in human T-cell lines, peripheral blood lymphocytes and monocyte/macrophage cultures. SLPI was tested in a single cycle of infection assay and under conditions in which SLPI was preincubated both with target cells and with virus and then maintained during the virus-to-cell adsorption phase and throughout the entire culture period. However, SLPI did not exert anti-HIV activity under any experimental conditions, and mechanistic studies showed SLPI to have no inhibitory activity on HIV-1 binding, reverse transcriptase or protease. Thus, SLPI exhibited no suggestive anti-HIV-1 activity.

Inhibitors of HIV nucleocapsid protein zinc fingers as candidates for the treatment of AIDS.

Strategies for the treatment of human immunodeficiency virus-type 1 (HIV-1) infection must contend with the obstacle of drug resistance. HIV-1 nucleocapsid protein zinc fingers are prime antiviral targets because they are mutationally intolerant and are required both for acute infection and virion assembly. Nontoxic disulfide-substituted benzamides were identified that attack the zinc fingers, inactivate cell-free virions, inhibit acute and chronic infections, and exhibit broad antiretroviral activity. The compounds were highly synergistic with other antiviral agents, and resistant mutants have not been detected. Zinc finger-reactive compounds may offer an anti-HIV strategy that restricts drug-resistance development.

The site of antiviral action of 3-nitrosobenzamide on the infectivity process of human immunodeficiency virus in human lymphocytes.

The C-nitroso compound 3-nitrosobenzamide, which has been shown to remove zinc from the retroviral-type zinc finger of p7NC nucleocapsid proteins, inhibits acute infection of human immunodeficiency virus type 1 in cultured human lymphocytes. The attachment of the virus to lymphocytes and the activities of critical viral enzymes, such as reverse transcriptase, protease, and integrase, are not affected by 3-nitrosobenzamide. However, the process of reverse transcription to form proviral DNA is effectively abolished by the drug, identifying the mode of action of 3-nitrosobenzamide as interrupting the role of p7NC in accurate proviral DNA synthesis during the infectious phase of the virus life cycle.

Inhibition of proteolytic processing of the polyproteins of cowpea mosaic virus by hemin.

Cleavages of the polyproteins synthesized from cowpea mosaic virus (CPMV) B RNA and M RNA in rabbit reticulocyte lysates are inhibited by hemin. Cleavage of the CPMV B RNA-encoded 200K polyprotein and of the M RNA-encoded 60K intermediary precursor protein were most sensitive to hemin inhibition, while cleavages of other precursor proteins were less sensitive. A significant observation was that at a hemin concentration of 25 microM, but not at higher concentrations, the 60K protein was cleaved to yield the two viral capsid proteins. This cleavage reaction has not been observed in vitro previously.

Inhibition of bacterially expressed HIV protease activity determined by an in vitro cleavage assay with MuLV Pr65gag.

HIV protease is a virally coded enzyme that cleaves gag as well as gag-pol precursor polyproteins into functional products needed for virus assembly. A pUC plasmid containing an HIV insert starting at the 5' end of the pol gene and ending just inside the intergrase coding sequence was expressed in E. coli. It provided an 11 kD gene product (protease) that specifically cleaved the Gazdar MuLV Pr65gag precursor into Pr40gag (p30 + p10) and Pr27gag (p15 + p12) intermediates, as well as lower molecular weight gag-encoded products. These were detected by immunoblotting with either MuLV anti-p30 or p12 sera. Using cleavage of MuLV Pr65gag as an assay system, pepstatin A, fusidic acid, and cerulenin were observed to inhibit HIV protease cleavage by greater than 50% at concentrations of 0.1, 0.2-0.5, and 0.5 mM, respectively.

Inhibition of cleavage of a plant viral polyprotein by an inhibitor activity present in wheat germ and cowpea embryos.

In rabbit reticulocyte lysate, the bottom component RNA of cowpea mosaic virus directs the synthesis of a 200,000-molecular-weight precursor protein (200K protein) that is cleaved during synthesis by a reticulocyte enzyme to form a 32K protein and a 170K protein. Cleavage of the 200K protein was found to be effectively inhibited by inhibitor activity in wheat germ and cowpea embryo extracts. The inhibitor was nondialyzable, precipitatable by ammonium sulfate, and partially stable at high temperatures. The activity appeared to be specific in that it caused no inhibition of the secondary cleavage reactions (cleavage of the 170K protein) at concentrations that were sufficient to cause complete inhibition of the primary cleavage reaction (cleavage of the 200K protein).

Callosal projections in the visual cortex and the vertical meridian of the visual field in the albino rat.

Studies using electrophysiological and HRP-labeling techniques showed that the lateral border of physiologically determined primary visual cortex coincides with the cytoarchiectonically defined area 17/18a border. The dense callosal projections are distributed in a zone, about 1.5 mm wide, along this border, which lies in the callosal zone, about 1/4-1/3 of the zone width from its lateral limit. There are two representations of the vertical meridian of the visual field, one in the proper of area 17, about 1/3 of the zone width from its medial limit, the other in area 18a, at about the lateral zone limit.

Binocular responses in the superior colliculus of the albino rat.

The retinotopic map for the contralateral eye is similar to that found in the pigmented rats and in other rodents. Cells which had ipsilateral responses were recorded in a fairly large area in the rostral portion of the tectum. Their receptive fields lay from about 40 degrees in the contralateral hemifield to about 40 degrees in the ipsilateral hemifield. The ipsilateral response of a binocular cell is similar in almost every respect to its counterpart in the opposite eye except being very weak and that the receptive field is usually smaller. Most binocular cells are distributed in the Stratum griseum superficiale (SGS) and the Stratum opticum (SO). Less binocular cells recorded in the Stratum griseum intermediale (SGI) have more scattered distribution both in the size and in the position of the receptive field.

Study on the genome of cauliflower mosaic virus (Xinjiang isolate). Restriction mapping of virion and cloned viral DNA.

The genomic DNA of CaMV (Xinjiang isolate) was mapped on the virion DNA with a number of restriction endonucleases by double digestions and partial digestions of one-end 32P-labelled fragments. It contained the unique sites of BglI, SalI and XhoI. BamHI and HhaI each cut it at two sites, EcoRI at five sites (three of which were located), HpaII at seven sites, BglII at eight sites, and HaeIII at ten sites. The sites of all the enzymes used above, as well as HindIII which cut at ten sites were also mapped on the cloned CaMV DNA. Virion DNA and cloned viral DNA gave the same results in the number and location of cleavage sites of the restriction enzymes tested on both DNAs. Like most of the other isolates, CaMV-Xinjiang isolate has three single-stranded discontinuities. From the digestion patterns of SalI, XhoI, EcoRI and HhaI, it is concluded that the restriction map of CaMV-XJ genome is closely related to that of BKMV isolate from East Germany.