Conventional B-2 cell-derived plasma cells are surface Ig negative, CD19low/negative and express high levels of the plasma cell marker Acalabrutinib nmr CD138 and slightly higher level of CD43 than B-1 cells (Fig. 5 and 40). BM B-1 cells, >80% of which spontaneously secrete IgM in vitro (Fig. 4C), are surface IgM+IgDlow/negative, and express relatively high levels of CD19 but are CD138− (Figs. 2, 3, 5). Our data are consistent with earlier reports on the phenotype of IgM-secreting B cells 25, 33 and through the use of the allotype chimeras we now identify these BM cells

unequivocally as B-1 cells (Figs. 3 and 4). In addition, as we show here (Figs. 1 and 4), these cells produce antibodies that recognize influenza virus, a specificity we have previously linked to B-1 cell-derived antibodies 5, 26, 27. Staining with antibodies recognizing a B-1a cell-specific Ig-idiotype (T-15) binding to phosphorylcholine, as well as staining with phosphatidylcholine-containing liposomes identified small numbers of BM B-1 cells (data not shown), further confirming their similarity to known B-1 cells with regard to specificity. Notably, these RXDX-106 cells are distinct from the IgMloIgDhi

sinusoidal BM B cells, which were described recently as rapid IgM secreters following challenge with blood-borne T-independent antigens 42. FACS-sorting experiments did Epothilone B (EPO906, Patupilone) not reveal significant spontaneous IgM secretion among IgMloIgDhi B cells in our

non-challenged mice (Fig. 2). In contrast to BM and spleen, PerC B-1 cells from BALB/c mice or from allotype chimeras were not significant sources of spontaneous IgM secretion (Figs. 1 and 4). Thus, our data are consistent with several in vivo studies that indicated the inability of PerC B-1 cells to produce natural IgM 33, 36, 37. It is remarkable, however, that PerC B-1 cells secrete or shed small amounts of IgM, resulting in large numbers of pinhead-size ELISPOTs (Fig. 1), also noted by others 31, 32, without significant amounts of secreted product amassing in the culture supernatants (Figs. 1 and 3). Such “leakiness” of B cells was not noted for cells harvested from any other tissue, for example the PLNs (Fig. 1). This might explain the apparent discrepancies in the literature regarding IgM secretion by PerC B-1 cells 31–37. Counting of these very small dots by PerC B-1 cells, might lead to an over-estimation of the ability of these cells to secrete significant amounts of natural IgM.

All animal experiments were approved by the local federal government. Third-stage larvae (L3) of N. brasiliensis were washed extensively in sterile 0·9% saline (37°) and injected subcutaneously (500 organisms) into mice. Mice were given antibiotics

contained in water (2 g/l neomycin sulphate, 100 mg/l polymyxin B sulphate, Sigma-Aldrich, St Louis, MO) for Apoptosis inhibitor the first 5 days after infection. Worm expulsion was determined by counting adult worms in the small intestine on day 9 after infection. Eggs in faecal pellets were counted using McMaster counting chambers. Single-cell suspensions were generated from lymph nodes, spleen or PBS-perfused lung samples that had been cut into small pieces and mechanically dispersed using a 70-μm nylon strainer (BD Falcon, Bedford, MA). Samples were washed once in FACS buffer (PBS / 2% fetal bovine serum /1 mg/ml sodium azide), incubated with anti-CD16/CD32 blocking monoclonal antibody (mAb; 2.4G2) for 5 min at room temperature, and stained click here with diluted

mAb mixtures. The following mAbs were used: phycoerythrin (PE)-Cy5.5-labelled anti-CD4 (clone RM4-5), biotinylated anti-CD11a (M17/4), PE-labelled anti-CD25 (PC61.5), allophycocyanin (APC)-labelled anti-CD29 (eBioHMb1-1), PE-labelled anti-CD44 (IM7), PE- or APC-labelled anti-DO11.10 TCR (KJ1-26), APC-labelled anti-Vα2 (B20.1) and PE-labelled anti-TCR-Vα8.3 (B21.14) were all purchased from eBioscience (San Diego, CA). Biotinylated

anti-CD62 ligand (CD62L; MEL-14) and PE-labelled anti-CD69 were purchased from Invitrogen-Caltag (Carlsbad, CA). Biotinylated anti-TCR-Vα3.2 (RR3-16), anti-TCR-Vα11.1/11.2 (RR8-1), anti-TCR-Vβ3 (KJ25), anti-TCR-Vβ4 (KT4), anti-TCR-Vβ5.1/5.2 (MR9-4), anti-TCR-Vβ6 (RR4-7), anti-TCR-Vβ8.1/8.2 (MR5-2), anti-TCR-Vβ14 (14-2), the FITC-labelled mouse Vβ TCR screening panel and PE-labelled anti-Siglec-F (E50-2440) were purchased from BD Biosciences (San Jose, CA). Biotinylated anti-IgE (23G3) was purchased from Southern Biotechnology Associates (Birmingham, AL). An APC-labelled streptavidin (Southern Biotechnology Associates) was used to visualize biotinylated mAbs. Samples were acquired on a FACSCalibur or FACS Canto II instrument (BD Immunocytometry Systems, San Jose, CA) and analysed using FlowJo software (Tree Star, Ashland, OR). T cells from mediastinal lymph nodes of Sucrase N. brasiliensis-infected mice were stimulated with 1 μg/ml ionomycin and 40 ng/ml PMA and subjected to an IL-4 cytokine secretion assay detection kit according to the manufacturer’s instructions (Miltenyi Biotec, Bergisch Gladbach, Germany). In brief, cytokine released from the cell is captured on the cell surface and can be detected directly with a PE-labelled mAb. Serum IgE levels were analysed using a purified anti-mouse IgE mAb (R35-72) for coating and a biotinylated rat anti-mouse IgE mAb (R35-118) for detection. Both mAbs were purchased from BD Biosciences.

tuberculosis27–30. This analysis showed that while many genes for apoptosis-promoting proteins are upregulated in the cells of TB patients, so are some negative regulators, such as FLIPS and FLIPL (Fig. 5). It is possible that these negative regulators are able to reduce the degree of apoptosis induced – or push cell death towards necrosis instead, to the possible benefit of the pathogen 56–58. More striking, however, is the data on PBMC separated on the basis of CD14, which indicate that surface expression of the receptor responsible for initiating the extrinsic pathway of apoptosis is Smoothened Agonist not equal in the different cell types. Figure 1 shows

that monocytic cells from TB patients – and only from TB patients – express a lower ratio of mRNA TNF-α receptors compared with the T-cell-containing fraction – and the increased shedding of TNF-α receptors into the plasma of TB patients (Fig. 2) may attenuate the effect of TNF-α even further 31. Similarly, the increase

in the pro-apoptotic molecule Caspase 8 seen in blood from TB patients (Fig. 4A) is not seen in monocytes (Fig. 4B) where if anything, expression is decreased compared with controls. If we compare the ratio of the markers analyzed in CD14+ and CD14− subsets (Table 1), it can be very clearly seen that the balance of expression of genes for the TNF-α receptors and Caspase 8 is strongly altered in TB patients, reflecting a significant shift away from expression in the monocyte-containing subset. We can therefore hypothesize that in active TB the increased apoptosis this website we see in PBMC falls disproportionately on the non-monocytic cells – including the T-cell compartment. This hypothesis is compatible with the in vitro data already published showing inhibition of apoptosis in infected macrophages by virulent M. tuberculosis (but not avirulent mycobacteria) check details 27, 28, 55, 59–63. It is also consistent with multiple reports suggesting that upregulation of Fas/FasL in vivo is specifically associated with T-cell death in TB 38, 64–67. A bias in cell death towards activated T cells in

TB patients might explain the anergy seen in advanced TB patients, which appears to be TNF-α related 68, 69. Finally, if TNF-α-driven apoptosis of T cells plays a role in M. tuberculosis pathogenesis, it would also provide an interesting explanation for why blocking TNF-α with Etanercept (soluble TNF receptor) in TB patients undergoing treatment, led to an increase in CD4T cell numbers 70. We have tested some aspects of this hypothesis by infecting human THP-1 cells with virulent M. tuberculosis or avirulent M. tuberculosis and BCG in vitro and measuring expression of the same genes as we have tested here. These experiments have confirmed both the overall anti-apoptotic effect of virulent M. tuberculosis infection of monocytes, at the same time as it drives activation of many of the genes we see upregulated in patients – including the TNF-α/TNFR axis (Abebe et al., submitted).

There is evidence that ACEi are efficacious at reducing BP and subsequent CVD and all-cause mortality in patients with mild, moderate and severe renal impairment. There is currently little evidence about the comparative effectiveness of other agents in preventing cardiovascular mortality and morbidity in this patient population. Post-hoc analyses of ACEi trials have shown that the treatment effects of ACEi on cardiovascular outcomes are consistent in patients with and without CKD.

ACEi appear therefore a reasonable first choice for prevention of CVD in this population. The evidence about the cardiovascular protective effects of ARB in CKD patients is scarce. However, they have been shown to confer renal protection in patients with diabetic nephropathy

and are therefore a sensible alternative if ACEi are not tolerated in this population. Head to head studies JAK/stat pathway have reported similar cardiovascular outcomes with different classes of agents in people with CKD, although the power to detect meaningful Inhibitor Library purchase differences is limited. ACEi, ARB, CCB and diuretics are therefore all reasonable choices for people with CKD. Renin angiotensin system blockade with ACEi or ARB is likely to have renal benefits in people with proteinuria and should therefore be preferred in this population (see separate guideline). There is little evidence about the efficacy in preventing CVD of different combinations of BP-lowering drugs in people with CKD. If BP targets are not met, the choice of a second agent should be based on individual patient factors, tolerability, and side-effects. a. We recommend that an ACEi or angiotensin receptor antagonist be prescribed for patients with CKD (or kidney transplant) and heart failure (1B). d. We suggest that patients receiving dialysis who have heart failure should be prescribed an ACEi or angiotensin receptor antagonist Alanine-glyoxylate transaminase (2D). For patients with CKD (or kidney transplant) symptomatic on the recommended agents, the following therapies could be considered as a third

agent (ungraded): Aldosterone antagonists have mortality benefit in people without CKD, but this may be attenuated in CKD and offset by greater toxicity Angiotensin receptor antagonist added to the ACEi reduces hospitalization but not mortality in people without CKD, but there are no data in CKD and potential increased toxicity Polyunsaturated fatty acid (PUFA), vasodilators and digoxin have all been studied in heart failure patients, but there is insufficient data to recommend for or against their use in heart failure patients with CKD receiving ACEi and beta-blocker therapy Diuretic therapy should be prescribed as required to control volume state with careful monitoring of kidney function and electrolytes (ungraded).

For cancer patients, the attraction of using a physical strategy such as electroporation, rather than viral vectors, is to avoid immunological blockade due to pre-existing or developing immunity against the viral components 44, 45. Electroporation is being tested in clinical Decitabine trials with clear evidence for amplification of immunity, including in patients with PCa 46. Our focus is on peptide-specific DNA vaccines, and for PSMA these are superior to full-length sequence, possibly due to the fact that PSMA is a large molecule and may

be expressed poorly, or responses may have targeted as-yet unidentified peptides. In this study, we have used the native membrane-spanning sequence, a prerequisite for including PSMA27, and this could also affect antigen processing. We did not explore the therapeutic induction of anti-PSMA immunoglobulin

by the full-length vaccines due to the problem of rapid internalization reported by others 15. Candidate target peptides have been reported in PSMA but the important question of whether they are naturally presented by PSMA-expressing AZD6244 manufacturer tumor cells has been difficult to answer. This is due mainly to the reliance for assays on T cells expanded from the blood of patients or normal subjects, a technically demanding and uncertain strategy. Limitations of this technique have been illustrated by the controversy over whether or not a peptide from PSA (PSA154–163) is processed and presented from the endogenous molecule 47. Testing in HLA-A*0201 transgenic mice is a useful alternative since it both provides a clear index of immunogenicity and generates CD8+ T cells to test against target tumor

cells, either mouse or human 27. Transduction of target cells with the chimeric HLA-A*0201 transgene (HHD) allows the detection of T cells of a range of avidities which can then reveal if the candidate peptides are presented by the selected tumor cells. This has been the basis of our selection of peptides for testing of our DNA fusion vaccines, now in clinical trial for patients with chronic myeloid leukemia using two separate WT1 STK38 peptides 27. For PCa, this approach reveals that PSMA27 and PSMA663 peptides are presented and validates their use in clinical trials. On the contrary, PSMA711 is less well presented and this might account for the relatively weak performance in affecting outcome in clinical trials 18. In our view, this preclinical information is necessary and sufficient to move our DNA vaccines into clinical trials. We have tested PSMA27 in a phase I/II clinical trial of our DNA fusion vaccine (p.DOM-PSMA27) in patients with PCa. Thirty patients were vaccinated with or without electroporation. Antibody responses against the DOM protein were detected in 21 out of 30 patients, with electroporation clearly enhancing levels induced 46. Peptide-specific CD8+ T-cell responses were induced in 17 out of 30 patients (57%) with a lower but still likely benefit of electroporation 34.

All three patients who received these surgical interventions reached full recovery from fungal

pleural infections (two due to Aspergillus spp.). In summary, drainage with chest tubes and in some cases surgical (thoracoscopic) debridement is indicated in Aspergillus pleural empyema, which occurs mostly after pneumonectomies.[86-91] Aspergillus arthritis is a rare clinical disease most frequently present in immunocompromised patients. Knee and shoulder are the joints most frequently affected; however, the wrist and sacroiliac joint have also been reported. The infection of Idasanutlin research buy joints by Aspergillus spp. is caused mostly by haematogenous spread in disseminated IA; however, cases have been reported after medical injections into the joint.[57] Contamination and infection during surgery have also been reported in patients without underlying immunosuppression or other predisposing risk factors. Diagnostic imaging, such as magnetic resonance imaging which can show bone marrow oedema, should be performed early. Positron emission tomography-computed tomography may show uptake of 18-Fluoro-deoxiglucose (standard uptake value 9.0 against

the contralateral side 1.5) in the suspected joint, confirming the presence of articular and extra-articular inflammation. Clinical presentation consists of pain, swelling and instability in the affected joint. Drainage check details should be performed to gain synovial fluid for diagnostic methods. While debridement Branched chain aminotransferase and drainage are indicated in Aspergillus arthritis, joint replacement can only be recommended in selected cases.[92-94, 94-100] Steinfeld et al. [99] reported of two cases of Aspergillus arthritis of the knee that were managed by surgical intervention after the poor response to antifungal therapy alone. Arthroscopic debridement with a motorised shaver was performed and both patients showed good response. In immunocompetent patients with Aspergillus arthritis, antifungal therapy without surgical intervention has been reported to result in full recovery.[96]

In Aspergillus prosthetic joint infection change of prosthesis may help to save the extremity.[100, 101] Aspergillus skin and soft-tissue infections primarily occur in immunocompromised patients. However, primary cutaneous aspergillosis has recently also been reported on a tattoo in an immunocompetent patient who underwent home tattooing.[102] In immunocompromised patients, IA can manifest in skin and soft tissue, either as primary cutaneous Aspergillus infection or as secondary cutaneous manifestations of an underlying disseminated Aspergillus infection. Primary cutaneous aspergillosis mostly arises around intravenous line site, burns, bruises or surgical wounds, which represent potential ports of entry in patients with neutropenia.

Preserved capillary density of dorsal finger skin in treated hypertensive patients with or without type 2 diabetes. Microcirculation 19: 554–562, 2012. Objectives:  Capillary rarefaction is a hallmark of untreated hypertension. Recent data indicate that rarefaction may be reversed by antihypertensive treatment in nondiabetic hypertensive patients. Despite the frequent association of diabetes with

hypertension, nothing is known on the capillary density of treated diabetic patients with hypertension. Methods:  We enrolled 21 normotensive healthy, 25 hypertensive only, and 21 diabetic (type 2) hypertensive subjects. Selleckchem Afatinib All hypertensive patients were treated with a blocker of the renin-angiotensin system, and a majority had a home blood pressure ≤135/85 mmHg. Capillary density was assessed with

videomicroscopy on dorsal finger skin and with laser Doppler imaging on forearm skin (maximal vasodilation elicited by local heating). Results:  There was no difference between www.selleckchem.com/products/dinaciclib-sch727965.html any of the study groups in either dorsal finger skin capillary density (controls 101 ± 11 capillaries/mm2, nondiabetic hypertensive 99 ± 16, diabetic hypertensive 96 ± 18, p > 0.5) or maximal blood flow in forearm skin (controls 666 ± 114 perfusion units, nondiabetic hypertensive 612 ± 126, diabetic hypertensive 620 ± 103, p > 0.5). Conclusions:  Irrespective of the presence or not of type 2 diabetes, capillary density is normal in hypertensive patients with reasonable control of blood pressure achieved with a blocker of the renin-angiotensin system. “
“Please cite this paper as: Henricson,

Tesselaar, Baiat, Nilsson and Sjöberg (2011). Local Heating as a Predilatation Method for Measurement of Vasoconstrictor Responses with Racecadotril Laser-Doppler Flowmetry. Microcirculation 18(3), 214–220. Studying microvascular responses to iontophoresis of vasoconstricting drugs contributes to a better understanding of the regulatory mechanisms of cutaneous vessels, but measuring these responses with laser-Doppler flowmetry at basal blood flow conditions is technically challenging. This study aimed to investigate whether the measurement of cutaneous vasoconstrictor responses to noradrenaline (NA) and phenylephrine (PE), delivered by iontophoresis, is facilitated by predilatation of the microvascular bed using local heating. We used different drug delivery rates (100 s × 0.12 mA, 200 s × 0.06 mA, 300 s × 0.04 mA) to investigate whether predilatation affects the local drug dynamics by an increased removal of drugs from the skin. In a predilatated vascular bed, iontophoresis of NA and PE resulted in a significant decrease in perfusion from the thermal plateau (p < 0.001). The decrease was 25–33%, depending on drug delivery rate. In unheated skin, a significant vasoconstriction was observed (p < 0.001), with 17% and 14% decrease from baseline for NA and PE, respectively.

[12]. It is therefore unlikely that the constitutive NKG2D ligand expression is caused by a low-grade inflammatory

activity against the commensal bacteria. The NKG2D ligands were detected using recombinant NKG2D and the specific nature of the NKG2D ligands were investigated by RT-PCR which showed that only Rae-1 had a similar expression pattern as the flow I-BET-762 manufacturer cytometry results, whereas H60c merely showed a tendency toward this. Hence, not all NKG2G ligands on IECs seem to be regulated by the gut microbiota. We further found a striking downregulation of IEC NKG2D ligand expression in vancomycin-treated mice, which contradicted the findings in ampicillin-treated and germ-free mice. Vancomycin is a well-known anti-Gram-positive antibiotic but also inhibits many Gram-negative Firmicutes species [36], most likely as a result of an ancient evolutionary co-dependency of certain Gram-positive

and Gram-negative bacteria. However, we previously observed a manyfold increase of A. muciniphila in feces from vancomycin-treated nonobese diabetic mice which constituted almost 90% of the remaining microbiota [35]. This species has been suggested to possess an anti-inflammatory protective effect against inflammatory bowel disease [39], and recent findings in gnotobiotic mice mono-colonized with A. muciniphila suggest a transcriptional host response upon colonization that involves immune tolerance against commensal gut bacteria [40]. see more It is thus tempting to speculate that the dominance of this single species in vancomycin-treated mice is linked to the decreased NKG2D ligand expression on IECs, especially as we found high levels of A. muciniphila in the vancomycin-treated mice which corresponded with low levels of NKG2D ligand expression whereas increased expression of A. muciniphila was not observed

in the ampicillin-treated mice. We also found that dietary XOS propagated A. muciniphila, and in parallel to the data obtain in the vancomycin-treated mice, XOS feeding also caused a marked reduction in the IEC NKG2D ligand expression. The nature and mechanisms behind this interesting correlation, as well as specifying other microbes that may Nitroxoline modulate NKG2D ligands, need further investigation in, for example gnotobiotic mice. The commensal microbiota can affect NKG2D ligand expression by several different mechanisms, which may not necessarily be mutually exclusive. For instance, the commensal bacteria may establish a regulatory milieu in the intestine, with increased expression of immuno-inhibitory cytokines such as TGF-β and IL-10. In this regard, it is notable that both TGF-β and IL-10 have been shown to downregulate NKG2D ligand surface expression [41, 42]. In agreement with this, IL-10 KO mice were shown to have an increase in IEC NKG2D ligand expression.

007) (Fig. 4B). Histological analysis did not reveal any differences

in CNS pathology between knockout and control groups with severe PD98059 mw mononuclear cell infiltrate and axonal demyelination in CNS lesions in both groups (not shown). These studies suggest that Mog expression is regulated by AIRE and this can influence the development of MOG35–55-induced EAE. As a therapeutic strategy that is in line with our previous studies 29, we asked whether AIRE-induced MOG expression in chimeric mice following transplantation of Aire transduced BM would prevent or reduce the development of EAE. Cohorts of lethally irradiated C57BL/6 mice were transplanted with non-manipulated BM cells or BM cells transduced with selleck inhibitor either pAire, pProII or pMog retrovirus. Ten weeks after transplantation, mice were immunised with MOG35–55 peptide and monitored for EAE development. Chimeric mice ectopically expressing AIRE had a significantly delayed initiation and progression of EAE compared to control groups (Aire versus ProII, p=0.009; versus nBMT, p=0.002; versus WT control, p=0.001) (Fig. 4C). There was no difference between the control groups (all p values>0.2) except for the positive control group that ectopically expressed MOG directly and did not develop EAE (Aire versus Mog, p=0.002). The absence of EAE in MOG chimeric mice confirms our published data that mice transplanted with Mog-transduced BM are resistant to EAE induction

29. These observations suggest that ectopic expression of AIRE promotes elevated levels of MOG expression in BM derived cells and

that this can delay the development of EAE following MOG35–55 immunisation. The ability to genetically manipulate the BM compartment and promote ectopic Adenosine triphosphate antigen expression and immune tolerance has been demonstrated in a number of settings 26–28, 40. We have recently shown that transduced BM cells encoding Mog led to ectopic expression of MOG in BM-derived cells and immune tolerance with complete resistance to EAE induction 29. It is well established that the transcription factor AIRE is associated with the expression of a large array of TRA in the thymus 4, 5 and to a lesser extent in the periphery 13. Furthermore, mice and humans lacking AIRE have a greater incidence of autoimmune conditions 4, 17–19. We therefore asked whether the ectopic expression of AIRE could be used to promote the ectopic expression of target autoantigens and whether this could influence the susceptibility to MOG-induced EAE. While AIRE expression in vivo is predominantly restricted to thymic medullary cells, it has also been detected outside the thymus in dendritic cells and peripheral lymphoid organs 13, 16. Following the in vitro transduction of a number of cell lines of thymic, dendritic cell and macrophage origin with an Aire-encoding retrovirus, we observed that indeed the expression of TRA was upregulated in an AIRE-dependent manner.

Presence of alternative splicing or post-translational modifications in proteins (such as glycosylation, phosphorylation, proteolytic processing, lipid modification, etc.) explains these basic numerical differences. Interestingly, fluids such as semen appear, in the context of protein identification and relation to function, really complex, ranging from few relevant proteins in spermatozoa towards hundreds

in SP.15 Moreover, the fact that ejaculation is in many species fractionated adds a new dimension to the action of SP proteins (and their interaction) on sperm function and on female reactivity. This paper attempts to review aspects of the composition of the seminal plasma of mammals, with a particular focus on its proteomics and the CH5424802 order differential functions this fluid would play in relation to sperm function and signalling to the female, with an ultimate focus on its role in modulating fertility. As already mentioned, collection of a naturally fractionated ejaculate (as in humans, pigs or horses) into a single vial represents a non-physiological situation, because such bulk ejaculate where all fluids mix at a single time does

not exist in vivo. During coitus, individuals from these exemplified species deliver spurts of fluid Lenvatinib in a sequential manner and to a specific location in the female. In primates and some artiodactila, sperm deposition is performed tuclazepam deep in the vagina, in front of the cervical opening or in the vaginal fornix while in other species of ungulates, sperm deposition occurs intracervically or even intrauterine.2 The first secretion (pre-ejaculate) presented to the urethra is that of the urethral and/or bulbourethral glands (Littré and Cowper for human, a secretion

containing mainly mucin, sialic acid, galactose and salts in a slightly viscous, clearly aqueous fluid). This is followed by the emission of spermatozoa from the caudae epididymides to the urethra accompanied by secretion from the prostate, followed by ejaculation proper (e.g. expulsion of semen into the female) in a series of spurts. The initial spurts are usually called the sperm-rich fraction of the ejaculate, because most spermatozoa are present there,16 with a blend of the acidic cauda epididymides and ampullar fluids together with the slightly acidic citrate and zinc-rich prostate fluid, which also contains specific peptides and proteins [as acid phosphatase and prostate-specific antigen (PSA) in humans]. In the following spurts, there is a gradual dominance of secretion from the seminal vesicles (rich in fructose, peptides, proteins, prostaglandins (PGs), etc., which is clearly basic in nature)2,17 as well as gradual diminution of sperm numbers.