Observations on some environmental factors connected with fertility in heat stressed cows

A field study was performed using 15 Kibutz dairy herds, in which 4195 cows situated in northern Israel were milked to determine the influence of climatological factors and nutritional regimes on the conception rate during the summer period (July-September). The Overall Conception Rate (OCR) during summer was 28.2% (17.3-41.9%) compared to 40% in the spring (May-June). The conception rate from first inseminations (CRl) was 31.3% during summer and 45.3% during spring. The OCR of the nullipara heifers in the same herds was 59.2% in summer and 60.4% in spring. The OCR in summer was negatively correlated with the minimum temperature (r=-0.53), the relative humidity at 0800 hrs. (r=-0.47), and the relative humidity at 1400 hrs (r=-0.49), whereas the CRl during summer was negatively correlated only with the minimum temperature (r=-0.51). In 12 (13) feeding groups of cows examined in 6 herds, no correlation was found between rectal temperatures and the actual milk productions of the cows. In 14 (15) herds, the milk production in summer was lower than in spring; the decrease varied from 0.9%-18.2% (average 7.8%). A highly significant negative correlation was found between the OCR and the various parameters of protein intake: grams of crude protein/cow/day, grams of crude protein/kg FCM/day, and percentage of protein from total dry matter. Particularly high correlations were found between the OCR and the average amounts of protein/kg FCM/day in milk of all cows (r=-0.84).     

Clinical trial of chromium and yeast supplements on carbohydrate and lipid metabolism in diabetic men

Chromium (Cr) deficiency in experimental animals and in humans sustained by prolonged total parenteral nutrition has been shown to cause diabetes mellitus. Prior trials in humans indicated that Cr supplements, in either inorganic or organic form, may improve carbohydrate utilization. We report here a clinical double-blind, random cross-over trial of inorganic chromium trichloride, a brewer’s yeast that contained Cr as glucose-tolerance-factor (GTF), a brewer’s yeast extract without GTF, and a placebo. Forty-three outpatient diabetic men received three of these supplements for 4 months each. Subgroups included 21 ketosis-prone, 7 ketosis-resistant non-obese, and 15 ketosis-resistant obese men. Cr levels were followed pre- and post-treatment in hair, red blood cells, plasma, and urine. Response of carbohydrate metabolism to treatment was assessed in terms of change in insulin requirements, fasting plasma glucose, plasma cholesterol, and triglycerides, as well as the change in plasma glucose, glucagon, and insulin or C-peptide levels in response to a standard meal. In some men, these parameters were also measured after iv tolbutamide. Both the inorganic and organic oral Cr supplements increased measurable body pools of Cr in hair and red blood cells by about 25%. However, fasting plasma glucose and lipids and the glucose response to either the standard meal or to tolbutamide were not significantly altered by any of the treatments.     

Modulation of locomotor activity by substance P in rats

The effects of intraperitoneally or intracerebrally (DA A-10 area) administered substance P (SP) on locomotor activity of rats were studied in an exact 12-h light/12-h dark cycle changing from dark to light at 6 a.m. SP was administered either at 11 a.m. (light phase, minimal locomotor activity) or at 7 p.m. (dark phase, maximal locomotor activity). The effects of 12.5 micrograms/kg SP intracerebral and 125 micrograms/kg SP intraperitoneal were very similar. In the light phase SP produces excitation but inhibition of locomotion in darkness. Hence, the effect of SP depends on the internal mechanisms controlling motor activity and tends to level off the spontaneous circadian oscillation. We found a long lasting SP effect during both the light and dark period. The present experiments led us to the conclusion that SP has a levelling effect on locomotor activity. Probably this effect might be explained as SP's action on the dopaminergic pathway or dopamine metabolism, because the dopamine content in neurons also has a circadian rhythm.     

Evidence for dysfunction in the regulation of cytosolic Ca2+ in excitation-contraction uncoupled dysgenic muscle

In noncontracting, dysgenic murine muscle, excitation is uncoupled from contraction. To test whether the gene lesion is expressed as a defect in the regulation of the intracellular free Ca2+ levels, cultured normal and dysgenic muscle at various stages of development (proliferative myoblasts, early, late, and mature myotubes) were exposed to increasing increments (0.5-mM steps) of extracellular Ca2+ in ionophore A23187-Ca2+-EGTA-buffered media. Normal and dysgenic muscle at all stages (except myoblast) displayed contractures at approximately 500 microM free Ca2+ and higher. Experiments using finer increments of Ca2+ and different ionophore concentrations indicated an external Ca2+ threshold for contracture at 265 microM Ca2+ for early and late myotubes and 47-78 microM for mature normal and dysgenic myotubes. Low extracellular concentrations of calcium (14 microM and 0.76 nM) caused elongation of both normal and dysgenic myotubes. Mature cells were depolarized by exposure to increasing extracellular K+ and monitored by intracellular recording; normal and dysgenic myotubes showed similar reductions in membrane potentials. Depolarization to -35 mV elicited contractures in normal myotubes, but even depolarization to -9 mV in dysgenic cells elicited no response. Thus steady-state depolarization of dysgenic muscle does not cause contractures, which can, however, be elicited by increasing the intracellular free Ca2+. These results offer new evidence for a possible defect in the regulation of Ca2+ levels in dysgenic muscle.     

Degradation of transplanted mitochondrial proteins by hepatocyte monolayers.

Reductively [3H]methylated rat mitochondria and mitochondrial-outer-membrane vesicles and mitochondrial-outer-membrane vesicles where monoamine oxidase is irreversibly labelled by [3H]pargyline have been transplanted into hepatocytes by poly(ethylene glycol)-mediated organelle or organelle-vesicle cell fusion. During subsequent culture of hepatocyte monolayers for 4-5 days, under conditions which mimic endogenous catabolic rates in vivo the transplanted organelle proteins retain their degradation characteristics observed in vivo (e.g. mitochondria: average t 1/2 72.5 h; monoamine oxidase: t1/2 55 h). In all cases protein degradation with first-order kinetics is only observed after an initial lag period (i.e. 24-30 h after fusion). Transplantation of fluorescein-conjugated organelles showed that the fluorescent material is rapidly internalized (average t1/2 1-6 h) and uniformly distributed in the cytoplasm. During a subsequent 18-24 h period (which corresponds to the lag period for intracellular destruction of transplanted mitochondrial material) the transplanted material is translocated to assume a perinuclear distribution. The destruction of transplanted mitochondrial proteins is compared with endogenous mitoribosomally synthesized proteins (average t1/2 52.5 h). Percoll fractionation of cell homogenates containing transplanted mitochondrial outer membranes where the enzyme monoamine oxidase is irreversibly labelled with [3H]pargyline shows a distribution of enzyme similar to lysosomal acid phosphatase. After transplantation of reductively methylated 3H-labelled mitochondrial-outer-membrane vesicles the cells were treated with leupeptin to alter lysosomal density. This treatment leads to the predominant association of acid phosphatase with dense structures, whereas the 3H-labelled transplanted material predominantly does not change density. Therefore transplanted mitochondrial-outer-membrane proteins are found in intracellular vesicular structures from which the proteins are donated for destruction, at least in part, by a lysosomal mechanism.     

Studies on dissimilatory sulfate-reducing bacteria that decompose fatty acids

Gliding motility, ultrastructure and nutrition of two newly isolated filamentous sulfate-reducing bacteria, strains 5ac10 and 4be13, were investigated. The filaments were always attached to surfaces. Growth was supported by addition of insoluble aluminium phosphate or agar as substrata for gliding movement. Electron microscopy of ultrathin sections revealed cell walls characteristic of Gramnegative bacteria; the undulated structure of the outer membrane may pertain to the translocation mechanism. Intracytoplasmic membranes were present. Acetate, higher fatty acids, succinate or fumarate served as electron donors and carbon sources. Strain 5ac10 grew also with lactate, but not with benzoate that was used only by strain 4be13. Strain 5ac10 was able to grow slowly on H₂ plus CO₂ or formate in the presence of sulfate without additional organic carbon source. The capacity of complete oxidation was shown by stoichiometric measurements with acetate plus sulfate. Both strains contained b- and c-type cytochromes. Desulfoviridin was detected only in strain 5ac10. The two filamentous gliding sulfate reducers are described as new species of a new genus, Desulfonema limicola and Desulfonema magnum.     

Stomatal movement in Zea mays: Shuttle of potassium and chloride between guard cells and subsidiary cells

Summary When stomates of Zea mays open K and Cl migrate from the subsidiary cells into the guard cells; when the stomates close both elements return to the subsidiary cells. Subsidiary cells function as reservoirs for K and Cl. Import of K and Cl into the guard cells and loss of both elements from the guard cells become observable 1 or 2 min after light is turned on or off, both when histochemical methods and the electron-probe microanalyzer are used for detection. Each stomatal complex of maize contains on the average 10±3×10^-13 gram equivalents (eq) of K and 4±1×10^-13 eq of Cl. Guard cells accumulate K in the light and CO₂-free air at an average rate of 10×10^-15 eq K per minute, and Cl at approximately half that rate.     

Genetic control of murine hemagglutinin formation to H-2.5

When B10.D2 (H-2^d) mice are immunized with lymphoid cells from C57B1/10 (H-2 ^d ) and their antisera tested against B10.A (H-2 ^a ) target cells, only antibodies to H-2.5 are measured. The same is true for immunization of DBA/2 (H-2 ^d ) mice when their antisera are absorbed with B10.D2 cells prior to testing. Irrespective of the dose of immunogen administered, the primary hemagglutinin response of B10.D2 mice is significantly lower than that of DBA/2 mice and (B10.D2 × DBA/2)F₁ hybrids, but the secondary responses are similar. The low responsiveness of B10.D2 mice appears to be determined by a single dominant gene with incomplete penetrance; the gene is not linked to eitherH- 2, Hc, or the immunoglobulin allotype loci. In addition, the H-2.5 hemagglutinin response is susceptible to nongenetic influences. When antisera from B10.D2, devoid of H-2.5 hemagglutinins, were assayed in a complement-mediated cytotoxic test, they contained almost as much anti-H-2.5 activity as did the antisera from DBA/2 mice or (B10.D2 × DBA/2)F₁ hybrids. The possibility is discussed that the locus responsible for the deficient primary hemagglutinin response of B 10.D2 may not be determinant-specific but may affect hemagglutinin responses in general.